https://www.wikidoc.org/api.php?action=feedcontributions&user=Caroline+Collis&feedformat=atomwikidoc - User contributions [en]2024-03-28T19:14:02ZUser contributionsMediaWiki 1.40.0https://www.wikidoc.org/index.php?title=Hypertension_in_adolescents&diff=1707119Hypertension in adolescents2021-07-16T14:59:46Z<p>Caroline Collis: </p>
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<div>__NOTOC__<br />
{{SI}}<br />
<br />
{{CMG}}; {{AE}} {{DS}}, {{Jose}}<br />
<br />
{{SK}} <br />
==Overview==<br />
[[Hypertension]] is one of the major risk factor for [[cardiovascular]] diseases. It is often associated with adverse [[cardiac]] and [[vascular]] outcomes. Hypertension in the [[pediatric]] age group often leads to the development of [[cardiovascular]] compromises for the patient, such as [[atherosclerotic]] plaques development, and [[renal]] function loss in the adulthood. To make matters worse, pediatric hypertension is greatly underdiagnosed due to the difficulty in measuring children's [[blood pressure]], and the need to refer to detailed tables of normative values. Thus, cautious monitoring, early diagnosis, and treatment of [[hypertension]] in children is critical to prevent disease progression.<br />
<br />
==Classification==<br />
[[Pediatric]] [[hypertension]] may be classified according to the AAP [[(American Academic of Pediatrics)]]:<ref name="pmid31263043">{{cite journal| author=Weaver DJ| title=Pediatric Hypertension: Review of Updated Guidelines. | journal=Pediatr Rev | year= 2019 | volume= 40 | issue= 7 | pages= 354-358 | pmid=31263043 | doi=10.1542/pir.2018-0014 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31263043 }} </ref><br />
{| class="wikitable"<br />
!<br />
!Age<13 years<br />
!Age>=13 years<br />
|-<br />
|<br />
[[Normal]] [[Blood]] [[pressure]]<br />
|<br />
<90th [[percentile]]<br />
|<br />
<180/<90 mmhg<br />
|-<br />
|<br />
Elevated or High Normal Blood Pressure<br />
|<br />
90th to <95th [[percentile]]<br />
|<br />
120-129/<80 mmHg<br />
|-<br />
|<br />
Stage 1 [[Hypertension]]<br />
|<br />
>95th [[percentile]] to <95th [[percentile]] +12 mmHg<br />
|<br />
130-139/80-89 mmHg<br />
|-<br />
|<br />
Stage 2 [[Hypertension]]<br />
|<br />
>95th [[percentile]] + 12 mmHg<br />
|<br />
>140/90 mmHg<br />
|}<br />
<br />
==Pathophysiology==<br />
*The pathophysiology of [[hypertension]] can be either [[primary]], which is multifactorial, or secondary, in which [[hypertension]] develops as a consequence of other diseases.<br />
*Essential hypertension can be triggered by multiple factors such as: [[obesity]], [[insulin resistance]], activation of [[sympathetic nervous system]], changes in [[sodium]] homeostasis, [[renin-angiotensin-aldosterone system]] changes, disorders in the [[vascular smooth muscle]] structure or function, elevated [[uric acid]] levels, [[fetal programming]] and [[genetic]] factors.<ref name="pmid22941155">{{cite journal| author=Raj M, Krishnakumar R| title=Hypertension in children and adolescents: epidemiology and pathogenesis. | journal=Indian J Pediatr | year= 2013 | volume= 80 Suppl 1 | issue= | pages= S71-6 | pmid=22941155 | doi=10.1007/s12098-012-0851-4 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22941155 }} </ref><br />
<br />
==Causes==<br />
Based on [[etiology]], hypertension in children can be classified into 2 groups:<ref>Khoury, M. and Urbina, E. M. (2021) ‘Hypertension in adolescents: diagnosis, treatment, and implications’, The Lancet Child & Adolescent Health, 5(5), pp. 357–366. doi: 10.1016/S2352-4642(20)30344-8</ref><br />
*1. Primary hypertension - No specific cause known<br />
*2. Secondary hypertension - Common causes include:<ref>Friedman K, Wallis T, Maloney KW, et al. An unusual cause of pediatric hypertension. J Pediatr 2007; 151:206.</ref><br />
<br />
*[[Renal]] diseases<br />
*[[Renal artery stenosis]]<br />
*[[Obstructive sleep apnea]]<ref>Marcus CL, Greene MG, Carroll JL. Blood pressure in children with obstructive sleep apnea. Am J Respir Crit Care Med 1998; 157:1098</ref><br />
*Related to [[drugs]] - [[glucocorticoids]], [[CNS]] [[stimulant]]s<br />
*[[Congenital adrenal hyperplasia]]<br />
*[[Pheochromocytoma]]<br />
*[[Hyperthyroidism]]<br />
*[[Coarctation]] of the [[aorta]]<br />
<br />
=== Common causes of pediatric hypertension by pediatric age group ===<br />
These conditions are displayed in order of prevalence<ref name="pmid11223345">{{cite journal| author=Flynn JT| title=Evaluation and management of hypertension in childhood. | journal=Prog Pediatr Cardiol | year= 2001 | volume= 12 | issue= 2 | pages= 177-188 | pmid=11223345 | doi=10.1016/s1058-9813(00)00071-0 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11223345 }} </ref><ref name="pmid10218072">{{cite journal| author=Bartosh SM, Aronson AJ| title=Childhood hypertension. An update on etiology, diagnosis, and treatment. | journal=Pediatr Clin North Am | year= 1999 | volume= 46 | issue= 2 | pages= 235-52 | pmid=10218072 | doi=10.1016/s0031-3955(05)70115-2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10218072 }} </ref><ref name="pmid15844381">{{cite journal| author=Flynn JT| title=Hypertension in adolescents. | journal=Adolesc Med Clin | year= 2005 | volume= 16 | issue= 1 | pages= 11-29 | pmid=15844381 | doi=10.1016/j.admecli.2004.10.002 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15844381 }} </ref><br />
<br />
'''One to six years:'''<br />
* [[Renal parenchymal disease]]; [[renal vascular disease]]; endocrine causes; [[coarctation of the aorta]]; [[essential hypertension]]<br />
'''Six to twelve years:'''<br />
* [[Renal parenchymal disease]]; [[essential hypertension]]; [[renal vascular disease]]; endocrine causes; [[coarctation of the aorta]]; [[iatrogenic]] illness<br />
'''Twelve to eighteen years'''<br />
* [[Essential hypertension]]; [[iatrogenic]] illness; [[renal parenchymal disease]]; [[renal vascular disease]]; endocrine causes; [[coarctation of the aorta]]<br />
<br />
==Differentiating Hypertension in Adolescents From Other Diseases==<br />
<br />
Hypertension in [[adolescent]]s may be a symptom of other underlying and undiagnosed conditions. Thus, these patients require a detailed medical assessment. Secondary causes were discussed above and include: [[renal]] diseases, [[drugs]], [[adrenal]] diseases and [[hyperthyroidism]].<br />
<br />
==Epidemiology and Demographics==<br />
*According to the [[WHO]], an estimated 1.13 billion people worldwide have [[hypertension]]. <br />
*[[Hypertension]] commonly affects individuals older than 65 years of age, especially living in low or middle-income countries.<br />
*In a study from the University of Texas' McGovern Medical School, the [[prevalence]] of pediatric elevated [[hypertension]] from 10 to 17 years of age was 16.3%, stage 1 [[hypertension]] was 10.6% and stage 2 [[hypertension]] 2.4%.<ref name="pmid30571555">{{cite journal| author=Bell CS, Samuel JP, Samuels JA| title=Prevalence of Hypertension in Children. | journal=Hypertension | year= 2019 | volume= 73 | issue= 1 | pages= 148-152 | pmid=30571555 | doi=10.1161/HYPERTENSIONAHA.118.11673 | pmc=6291260 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30571555 }} </ref><br />
*Higher prevalence was noted in patients who were classified as [[obese]] or [[overweight]].<ref name="pmid30571555">{{cite journal| author=Bell CS, Samuel JP, Samuels JA| title=Prevalence of Hypertension in Children. | journal=Hypertension | year= 2019 | volume= 73 | issue= 1 | pages= 148-152 | pmid=30571555 | doi=10.1161/HYPERTENSIONAHA.118.11673 | pmc=6291260 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30571555 }} </ref><br />
* [[Prevalence]] of childhood hypertension has increased from 1994 to 2018.<ref name="pmid31589252">{{cite journal| author=Song P, Zhang Y, Yu J, Zha M, Zhu Y, Rahimi K | display-authors=etal| title=Global Prevalence of Hypertension in Children: A Systematic Review and Meta-analysis. | journal=JAMA Pediatr | year= 2019 | volume= 173 | issue= 12 | pages= 1154-1163 | pmid=31589252 | doi=10.1001/jamapediatrics.2019.3310 | pmc=6784751 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31589252 }} </ref><br />
*A [[systematic review]] estimated that in 2015, the [[prevalence]] of childhood hypertension was 4.32% among children aged 6 years. Patients aged 19 years had a [[prevalence]] of 3.28%. The peak of [[prevalence]] in [[hypertension]] occurred at age 14 years.<ref name="pmid31589252">{{cite journal| author=Song P, Zhang Y, Yu J, Zha M, Zhu Y, Rahimi K | display-authors=etal| title=Global Prevalence of Hypertension in Children: A Systematic Review and Meta-analysis. | journal=JAMA Pediatr | year= 2019 | volume= 173 | issue= 12 | pages= 1154-1163 | pmid=31589252 | doi=10.1001/jamapediatrics.2019.3310 | pmc=6784751 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31589252 }} </ref><br />
<br />
==Risk Factors==<br />
*The most common risk factor in the development of hypertension in adolescents is [[obesity]]. <br />
*Non-modifiable risk factors include [[obstructive sleep apnea]], [[diabetes]], [[low birth weight]], [[gender]], [[race]], [[genetic inheritance]], [[socioeconomic status]], [[premature birth]], use of [[umbilical artery catheter]]s and [[family history]] of [[cardiovascular disease]].<ref name="pmid27335997">{{cite journal| author=Ewald DR, Haldeman PhD LA| title=Risk Factors in Adolescent Hypertension. | journal=Glob Pediatr Health | year= 2016 | volume= 3 | issue= | pages= 2333794X15625159 | pmid=27335997 | doi=10.1177/2333794X15625159 | pmc=4784559 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27335997 }} </ref><br />
*Modifiable risk factors include: [[decongestants]], use of [[nose]] or [[eye]] drops, [[oral contraceptives]], [[antidepressants]], [[bronchodilators]], [[salt]] intake, [[dietary habits]], [[excess adiposity]], [[physical level activity]], [[secondhand smoke]], [[poor sleep quality]], [[short sleep duration]].<ref name="pmid27335997">{{cite journal| author=Ewald DR, Haldeman PhD LA| title=Risk Factors in Adolescent Hypertension. | journal=Glob Pediatr Health | year= 2016 | volume= 3 | issue= | pages= 2333794X15625159 | pmid=27335997 | doi=10.1177/2333794X15625159 | pmc=4784559 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27335997 }} </ref><br />
<br />
==Screening==<br />
<br />
*According to the U.S. Preventive Services Task Force (USPSTF), [[screening]] for [[hypertension]] in asymptomatic children and adolescents is not recommended.<ref name="pmid30277729">{{cite journal| author=Riley M, Hernandez AK, Kuznia AL| title=High Blood Pressure in Children and Adolescents. | journal=Am Fam Physician | year= 2018 | volume= 98 | issue= 8 | pages= 486-494 | pmid=30277729 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30277729 }} </ref><br />
*According to the 2017 American Academy of Pediatrics guidelines, [[screening]] for [[hypertension]] in asymptomatic children and adolescents is recommended annually beginning at three years of age.<ref name="pmid30277729">{{cite journal| author=Riley M, Hernandez AK, Kuznia AL| title=High Blood Pressure in Children and Adolescents. | journal=Am Fam Physician | year= 2018 | volume= 98 | issue= 8 | pages= 486-494 | pmid=30277729 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30277729 }} </ref><br />
*According to the 2016 European Society of Hypertension guidelines, [[screening]] for [[hypertension]] in asymptomatic children and adolescents is recommended every two years beginning at three years of age.<ref name="pmid30277729">{{cite journal| author=Riley M, Hernandez AK, Kuznia AL| title=High Blood Pressure in Children and Adolescents. | journal=Am Fam Physician | year= 2018 | volume= 98 | issue= 8 | pages= 486-494 | pmid=30277729 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30277729 }} </ref><br />
<br />
==Natural History, Complications, and Prognosis==<br />
*If left untreated, children with hypertension may progress to develop [[atherosclerotic heart disease]] in adulthood. They have also increased risk of cardiovascular disease and [[mortality]] as well as [[left ventricular hypertrophy]].<br />
*Renal complications such as [[chronic kidney disease]] may develop.<br />
*Ophthalmologic compromise is also a possible with [[hypertensive retinopathy]] being a potential complication.<br />
*Children and adolescents with severe hypertension are at risk of developing hypertensive encephalopathy, seizures, cerebrovascular accidents, and congestive heart failure.<ref name="pmid16719248">{{cite journal| author=Luma GB, Spiotta RT| title=Hypertension in children and adolescents. | journal=Am Fam Physician | year= 2006 | volume= 73 | issue= 9 | pages= 1558-68 | pmid=16719248 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16719248 }} </ref><br />
<br />
==Diagnosis==<br />
===Diagnostic Study of Choice===<br />
<br />
*The diagnostic study of choice for diagnosing hypertension in adolescents is the attainment of accurate blood pressure measurement in children and adolescents. <br />
*It can be challenging due to the variance of the measurements with different cuff sizes, anxiety, patient positioning, caffeine intake, and activity levels.<br />
*To choose an adequate cuff size, one must pick an inflatable bladder that is at least 40% of the arm circumference and a bladder length that is 80% to 100% of the arm circumference.<ref name="pmid30277729">{{cite journal| author=Riley M, Hernandez AK, Kuznia AL| title=High Blood Pressure in Children and Adolescents. | journal=Am Fam Physician | year= 2018 | volume= 98 | issue= 8 | pages= 486-494 | pmid=30277729 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30277729 }} </ref><br />
<br />
===History and Symptoms===<br />
*The majority of children with hypertension are asymptomatic.<br />
*Common symptoms of [[hypertensive emergencies]] include [[headache]], [[altered sensorium]], [[seizures]], [[vomiting]], focal [[neurologic]] complaints and [[visual]] disturbances.<ref>Flynn JT, Kaelber DC, Baker-Smith CM, et al. Clinical Practice Guideline for Screening and Management of High Blood Pressure in Children and Adolescents. Pediatrics 2017; 140.</ref><br />
<br />
===Physical Examination===<br />
<br />
*Common [[physical examination]] findings of hypertension include [[retinal]] [[vascular]] changes on [[fundoscopy]], [[cardiac heave]], and laterally displaced point of maximal impulse ([[PMI]]) due to [[left ventricular hypertrophy]] (LVH). <ref>Flynn JT, Kaelber DC, Baker-Smith CM, et al. Clinical Practice Guideline for Screening and Management of High Blood Pressure in Children and Adolescents. Pediatrics 2017; 140.</ref><br />
<br />
===Laboratory Findings===<br />
<br />
*There are no [[diagnostic]] laboratory findings associated with hypertension. <br />
*To evaluate for end-organ damage, hypertension causes or hypertension-associated conditions that may increase the cardiovascular risk the following exams may be useful:<br />
**[[Lipid profile]]<br />
**[[Complete blood count]]<br />
**[[Fasting glucose]] or [[A1C level]]<br />
**[[ALT]] and [[AST]]<br />
**[[Drug screening]]<br />
**Measurement of serum [[blood urea nitrogen]] (BUN)<br />
**[[Plasma]] [[renin]]<br />
**[[Aldosterone]] activity<br />
**[[Creatinine]]<br />
**[[Electrolytes]]<br />
**[[Urinalysis]]<br />
<br />
===Electrocardiogram===<br />
*An ECG is not helpful in the diagnosis of [[hypertension]]. <br />
*Findings on an ECG suggestive of hypertension include [[left ventricular hypertrophy]], [[ST depression]] and [[T wave inversion]].<br />
<br />
===X-ray===<br />
*A chest [[X-ray]] is not helpful in the [[diagnosis]] of hypertension. <br />
*There are findings on an x-ray suggestive of hypertension-associated complications, which include increased [[cardiothoracic ratio]], secondary to [[left ventricular hypertrophy]].<br />
<br />
===Echocardiography or Ultrasound===<br />
<br />
*There are no [[echocardiography]]/[[ultrasound]] findings diagnostic of hypertension. <br />
*However, an echocardiography/ultrasound may be helpful in the diagnosis of [[complications]] of hypertension, which include [[left ventricular hypertrophy]] and [[renovascular disease]].<ref>Chhadia S, Cohn RA, Vural G, Donaldson JS. Renal Doppler evaluation in the child with hypertension: a reasonable screening discriminator? Pediatr Radiol 2013; 43:1549..</ref><br />
<br />
===CT scan===<br />
*There are no CT scan findings diagnostic of hypertension.<br />
*It can diagnose some causes of hypertension such as [[coarctation of aorta]] or adrenal disease.<br />
<br />
===MRI===<br />
*There are no MRI scan findings diagnostic of hypertension.<br />
*It can diagnose some causes of hypertension such as [[coarctation of aorta]] or adrenal disease.<br />
<br />
===Other Imaging Findings===<br />
*There are no other imaging findings associated with hypertension.<br />
<br />
===Other Diagnostic Studies===<br />
*There are no other diagnostic studies associated with hypertension.<br />
<br />
==Treatment==<br />
The AAP guideline recommends keeping systolic and diastolic pressure under 90th percentile or <130/80 mmHg in patients aged 13 or older to prevent any cardiovascular events. <br />
<br />
===Medical Therapy===<br />
<br />
====Lifestyle modifications====<br />
*All children and adolescents with [[hypertension]] should change their lifestyle for the better.<ref name="pmid30277729">{{cite journal| author=Riley M, Hernandez AK, Kuznia AL| title=High Blood Pressure in Children and Adolescents. | journal=Am Fam Physician | year= 2018 | volume= 98 | issue= 8 | pages= 486-494 | pmid=30277729 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30277729 }} </ref><br />
*Such changes include: weight reduction if [[obese]] or [[overweight]], regular physical activity, healthy diet ([[DASH diet]]), avoidance of substance use, stress reduction, family-based interventions (involving the whole family on such lifestyle changes can dramatically increase therapeutic adherence).<ref name="pmid30277729">{{cite journal| author=Riley M, Hernandez AK, Kuznia AL| title=High Blood Pressure in Children and Adolescents. | journal=Am Fam Physician | year= 2018 | volume= 98 | issue= 8 | pages= 486-494 | pmid=30277729 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30277729 }} </ref><br />
<br />
====Pharmacological treatment====<br />
*The mainstay of [[treatment]] for [[hypertension]] in adolescents is [[pharmacotherapy]]. Pharmacological therapy is reserved for those patient who have symptomatic or persistent [[hypertension]] despite [[lifestyle modification]], stage 2 [[hypertension]] without modifiable factors, or [[hypertension]] secondary to [[chronic kidney disease]] or [[diabetes]].<ref name="pmid30277729">{{cite journal| author=Riley M, Hernandez AK, Kuznia AL| title=High Blood Pressure in Children and Adolescents. | journal=Am Fam Physician | year= 2018 | volume= 98 | issue= 8 | pages= 486-494 | pmid=30277729 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30277729 }} </ref><br />
*First line medication generally include [[angiotensin converting enzyme inhibitors]] ([[ACEIs]]), [[angiotensinogen receptor blockers]] ([[ARBs]]), long acting [[calcium channel blocker]]s (CCBs) and [[thiazide]] [[diuretics]].<ref>Lurbe E, Agabiti-Rosei E, Cruickshank JK, et al. 2016 European Society of Hypertension guidelines for the management of high blood pressure in children and adolescents. J Hypertens 2016; 34: 1887–920.</ref><br />
*[[Beta-blockers]] are not considered first line agents.<ref name="pmid30277729">{{cite journal| author=Riley M, Hernandez AK, Kuznia AL| title=High Blood Pressure in Children and Adolescents. | journal=Am Fam Physician | year= 2018 | volume= 98 | issue= 8 | pages= 486-494 | pmid=30277729 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30277729 }} </ref><br />
*Black patients may benefit from medications other than [[angiotensin converting enzyme inhibitors]].<ref name="pmid30277729">{{cite journal| author=Riley M, Hernandez AK, Kuznia AL| title=High Blood Pressure in Children and Adolescents. | journal=Am Fam Physician | year= 2018 | volume= 98 | issue= 8 | pages= 486-494 | pmid=30277729 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30277729 }} </ref><br />
*[[Calcium channel blockers]] and [[hydrochlorothiazide]] are appropriate choices for female adolescents at risk for pregnancy.<ref name="pmid30277729">{{cite journal| author=Riley M, Hernandez AK, Kuznia AL| title=High Blood Pressure in Children and Adolescents. | journal=Am Fam Physician | year= 2018 | volume= 98 | issue= 8 | pages= 486-494 | pmid=30277729 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30277729 }} </ref><br />
*Start at the lowest dose and titrate every 2-4 weeks until blood pressure goal is reached.<ref name="pmid30277729">{{cite journal| author=Riley M, Hernandez AK, Kuznia AL| title=High Blood Pressure in Children and Adolescents. | journal=Am Fam Physician | year= 2018 | volume= 98 | issue= 8 | pages= 486-494 | pmid=30277729 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30277729 }} </ref><br />
<br />
==Surgery==<br />
[[Surgery]] is not the first-line [[treatment]] option for children with hypertension. [[Surgery]] is usually reserved for children with select [[adrenal]] disease or [[coarctation of aorta]].<br />
<br />
==Primary prevention==<br />
Effective measures for the [[primary prevention]] of primary hypertension in children include [[low sodium]] intake, adhering to the [[DASH diet]], maintaining appropriate [[body weight]], and regular physical activities.<br />
<br />
==Secondary prevention==<br />
There are no established measures for the [[secondary prevention]] of hypertension in children.<br />
<br />
==References==<br />
{{reflist|2}}<br />
<br />
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[[Category: Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Hepatitis_C_overview&diff=1703740Hepatitis C overview2021-06-11T13:07:38Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{#widget:SchemaSnippet}}<br />
{{Hepatitis C}}<br />
{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[User:YazanDaaboul|Yazan Daaboul]], [[User:Sergekorjian|Serge Korjian]]<br />
<br />
==Overview==<br />
[[Hepatitis C virus]] (HCV) is a single-stranded [[RNA virus]] that causes [[liver damage]]. Initially discovered in 1989, HCV was found to be a [[bloodborne infection]] that develops into a [[chronic]] state in most cases. Although the exact [[pathogenesis]] and life cycle of HCV are not well understood, it has been demonstrated that impaired [[innate immunity|innate]] and [[adaptive immunity]] to acute HCV may contribute to the development of chronic [[infection]]. While the [[transfusion]] of blood and [[blood]] products along with injectable therapy were considered the most common [[risk factors]] for HCV in the past, the use of [[intravenous drug use (recreational)|illegal intravenous drugs]] is currently the most important [[risk factor]]. In the absence of treatment, chronic HCV leads to [[liver cirrhosis]] several years after the initial [[infection]], a course complicated by decompensated [[liver failure]] or [[hepatocellular carcinoma]]. Other extra-hepatic manifestations are also common. Specific patient populations should be screened for HCV first using HCV [[serological testing]] or, rarely, directly by measuring [[HCV RNA]] in patients who have had previous HCV exposure, treatment-induced clearance, or [[immunosuppression]]. The [[diagnosis]] is made when tests for [[anti-HCV]] and [[HCV RNA]] both return positive results. Measures to slow the progression of [[liver disease]], such as [[vaccines]] against other diseases and increased awareness of the risks associated with the use of [[alcohol]] or drugs that injure the [[liver]] should be taken following [[diagnosis]]. Classically, [[interferon]] (IFN) therapy was used to treat HCV, followed by the use of [[ribavirin]]. More recently, [[protease inhibitors]] emerged as effective drugs of choice for HCV [[infection]].<br />
<br />
==Historical Perspective==<br />
The discovery of the hepatitis C virus was made based on early findings of [[patients]] with [[signs]] and [[symptoms]] of [[viral hepatitis]] lacking positive serologies for hepatitis A or B. These [[patients]] were originally described in 1974-5 as having "non-A, non-B viral hepatitis" (NANBH). It was not until 1989 that [[hepatitis C virus]] (HCV) was truly discovered when Qui-Lim Choo and colleagues successfully isolated the first [[cDNA]] clone 5-1-1 derived from the NANBH [[genome]]. The first [[interferon-alpha]] (INF-a) to treat HCV was developed in 1986 and approved in 1991. Approximately 10-15 years later, global efforts to reduce the burden of HCV were launched; worldwide campaigns were led by the [[World Health Organization]] ([[WHO]]) and [[Centers for Disease Control and Prevention]] ([[CDC]]).<br />
<br />
==Pathophysiology==<br />
In cases of isolated acute HCV infection, the host [[immune system]] stimulates the [[secretion]] of [[interferon-alpha]] and the activation of [[natural killer cells]], which is followed by the activation of the [[adaptive immune system]]. [[Chronic HCV]] is characterized by the impairment of these mechanisms. Eventually, chronic HCV infection leads to local [[inflammation]] and [[fibrogenesis]], which causes [[hepatic]] injury and [[cirrhosis]]. [[Hepatocellular carcinoma]], a known [[complication]] of chronic HCV infection, arises in cases of [[cirrhosis]]; the role of oncogenic proteins of HCV in the [[pathogenesis]] of [[hepatocellular carcinoma]] has yet to be elucidated.<br />
<br />
==Causes==<br />
The hepatitis C virus (HCV) is the causative agent of hepatitis C. It is a member of the genus ''[[Hepacivirus]]'' that belongs to the ''[[Flaviviridae]]'' family. It is an enveloped, single-stranded [[RNA virus]]. The RNA [[genome]] acts as a template for [[viral replication]] and eventually, [[protein biosynthesis]]. Humans are considered the only natural hosts for HCV. The [[virus]] is primarily transmitted by exposure to contaminated [[blood]].<br />
<br />
==Classification==<br />
HCV can be classified based on the isolated [[genotype]] and subtype. Six major genotypes have been identified. Several new genotypes and subtypes were recently discovered.<br />
<br />
==Epidemiology and Demographics==<br />
[[Hepatitis C]] is a major health problem that affects approximately 2 to 4 million people in the United States, 5 to 10 million people in Europe, and 12 million people in India. Approximately 150,000 new cases occur annually in the United States and in Western Europe, although [[incidence]] rates are difficult to estimate with accuracy given the [[asymptomatic]] nature of early stages of the disease. While the [[prevalence]] of the disease appears to be declining, hepatitis C is still highly prevalent in specific areas of the world. Egypt is the country with the highest prevalence of [[HCV]], HCV-associated [[cirrhosis]], and [[hepatocellular carcinoma]], and the [[prevalence]] tends to increase with age, suggesting ongoing new cases of HCV. Approximately one-fourth of all cases of [[cirrhosis]] and [[hepatocellular carcinoma]] are attributed to HCV worldwide. Hepatitis C affects males and females equally.<br />
<br />
==Risk Factors==<br />
[[Risk factors]] for hepatitis C include [[intravenous drug use]] (most important), multiple [[blood]] [[transfusions]] prior to 1992, [[injection (medicine)|therapeutic injections]] for [[hemophilia]] prior to 1987, and work in the healthcare field (given that exposure to contaminated [[blood]] products is the most important mode of transmission).<br />
<br />
Other, less common [[risk factors]] include occupational exposure to blood, such as contaminated needle sticks, [[Hemodialysis]], solid organ [[transplantation]] from infected donors, birth to infected mother (in cases of detectable maternal [[HCV PCR]] at [[delivery]]), sexual intercourse with an infected partner, sexual intercourse with multiple partners, [[HIV]] infection, and [[tattoo]]s or [[piercing]]s with infected needle sticks.<br />
==Screening==<br />
People living in regions highly prevalent with HCV and who have engaged in high-risk behaviors should be screened. Screening by [[serological testing]], confirmed by [[Nucleic acid amplification technique|nucleic acid amplification]] ([[Nucleic acid amplification technique|NAT]]) for [[HCV|HCV RNA]], is required. Additionally, screening for other [[Bloodborne infection|bloodborne infections]], such as [[HBV]] and [[HIV]], is required once a diagnosis is made. The ideal frequency of testing in these patients is unclear and should be personalized according to the frequency of a patient's exposure to risk.<br />
<br />
==Differentiating Hepatitis C from other Diseases==<br />
Hepatitis C must be differentiated from other diseases that cause [[hepatic]] injury and abnormal [[liver function tests]] such as other viral hepatitides ([[Hepatitis A]], [[Hepatitic B]], and Hepatitis E), and non-viral etiologies (e.g., [[alcoholic liver disease]], non-alcoholic [[steatohepatitis]], drug-induced liver injury, [[autoimmune hepatitis]], and [[hepatocellular carcinoma]]).<br />
<br />
==Natural History and Prognosis==<br />
The majority of individuals infected with [[HCV]] will become chronic carriers. The most common [[complications]] of HCV are [[hepatic]], including [[liver cirrhosis]] years after the onset of [[infection]] and the consequent development of [[hepatocellular carcinoma]]. Other classical extrahepatic manifestations, such as [[cryoglobulinemia]], [[lichen planus]], [[membranoproliferative glomerulonephritis]], and [[porphyria cutanea tarda]] are also complications of chronic HCV [[infection]]. Treatment is necessary for [[patients]] with chronic stable HCV [[infection]]; otherwise, prognosis is poor and progression of the disease may be fatal.<br />
<br />
==Treatment==<br />
The treatment of hepatitis C has changed dramatically over the past decade. Whereas relatively new [[protease inhibitor]]s [[telaprevir]] and [[boceprevir]] were added to the regular regimen of [[IFN]] and [[ribavirin]] in 2011 to treat [[patients]] with genotype 1 HCV, newer oral agents [[sofosbuvir]] and [[simeprevir]] have demonstrated greater efficacy in viral clearance along with a better safety profile. New guidelines from the AASLD and the IDSA have endorsed the use of these oral agents (particularly [[sofosbuvir]]) as first-line agents in the treatment of chronic HCV in both relapsers and treatment-naive patients.<br />
<br />
[[Category:Gastroenterology]]<br />
[[Category:FinalQCRequired]]<br />
[[Category:Emergency mdicine]]<br />
[[Category:Disease]]<br />
[[Category:Up-To-Date]]<br />
[[Category:Infectious disease]]<br />
[[Category:Hepatology]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_surgery&diff=1703613Pulmonary hypertension surgery2021-06-09T17:37:37Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}, Richard Channick, M.D.; '''Assistant Editor(s)-in-Chief:''' [[User:Ralph Matar|Ralph Matar]]; [[User:Lisa Prior|Lisa Prior]]; [[Ann Slater|Ann Slater, R.N.]]; {{Rim}}; {{Jose}}<br />
<br />
==Overview==<br />
Patients with severe [[pulmonary hypertension classification#WHO Functional Classification|WHO functional class II or III]] pulmonary hypertension (PH) refractory to medical therapy are candidates for surgical intervention, such as [[atrial septostomy]] or [[lung transplantation]]. [[Pulmonary thromboendarterectomy]] (PTE) is a surgical procedure that is used for chronic [[thromboembolic]] pulmonary hypertension.<br />
<br />
==Surgery==<br />
Surgical intervention such as [[atrial septostomy]] or [[lung transplantation]] should be considered among patients with pulmonary arterial hypertension (PAH) who fail to improve on optimal therapy or when medical therapy is unavailable.<ref name="pmid19713419">{{cite journal| author=Galiè N, Hoeper MM, Humbert M, Torbicki A, Vachiery JL, Barbera JA et al.| title=Guidelines for the diagnosis and treatment of pulmonary hypertension: the Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS), endorsed by the International Society of Heart and Lung Transplantation (ISHLT). | journal=Eur Heart J | year= 2009 | volume= 30 | issue= 20 | pages= 2493-537 | pmid=19713419 | doi=10.1093/eurheartj/ehp297 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19713419 }} </ref><br />
<br />
Failure of clinical improvement among PAH patients with [[pulmonary hypertension classification#WHO Functional Classification|WHO functional class II or III]] is defined as either:<ref name="pmid19713419">{{cite journal| author=Galiè N, Hoeper MM, Humbert M, Torbicki A, Vachiery JL, Barbera JA et al.| title=Guidelines for the diagnosis and treatment of pulmonary hypertension: the Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS), endorsed by the International Society of Heart and Lung Transplantation (ISHLT). | journal=Eur Heart J | year= 2009 | volume= 30 | issue= 20 | pages= 2493-537 | pmid=19713419 | doi=10.1093/eurheartj/ehp297 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19713419 }} </ref><br />
* A stable and unsatisfactory clinical status, or<br />
* An unstable and deteriorating status<br />
<br />
Failure of clinical improvement among PAH patients with [[pulmonary hypertension classification#WHO Functional Classification|WHO functional class IV]] is defined as either:<ref name="pmid19713419">{{cite journal| author=Galiè N, Hoeper MM, Humbert M, Torbicki A, Vachiery JL, Barbera JA et al.| title=Guidelines for the diagnosis and treatment of pulmonary hypertension: the Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS), endorsed by the International Society of Heart and Lung Transplantation (ISHLT). | journal=Eur Heart J | year= 2009 | volume= 30 | issue= 20 | pages= 2493-537 | pmid=19713419 | doi=10.1093/eurheartj/ehp297 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19713419 }} </ref><br />
* Absence of quick improvement to a WHO functional class III or less, or<br />
* A stable and unsatisfactory clinical status<br />
<br />
===Atrial Septostomy===<br />
* [[Atrial septostomy]] is a surgical procedure that creates a shunt between the right and left [[atria]]. <br />
* It relieves pressure on the right side of the heart, but at the cost of lower oxygen levels in blood ([[hypoxia]]). It is best performed in experienced centers.<br />
* Graded balloon dilatation of [[atrial septostomy]] is the recommended type of [[atrial septostomy]].<ref name="pmid9708453">{{cite journal| author=Sandoval J, Gaspar J, Pulido T, Bautista E, Martínez-Guerra ML, Zeballos M et al.| title=Graded balloon dilation atrial septostomy in severe primary pulmonary hypertension. A therapeutic alternative for patients nonresponsive to vasodilator treatment. | journal=J Am Coll Cardiol | year= 1998 | volume= 32 | issue= 2 | pages= 297-304 | pmid=9708453 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9708453 }} </ref> <br />
* [[Atrial septostomy]] might be considered among PH patients with [[pulmonary hypertension classification#WHO Functional Classification|WHO functional class IV]] and [[right heart failure]] refractory to therapy.<ref name="pmid17426198">{{cite journal| author=Kurzyna M, Dabrowski M, Bielecki D, Fijalkowska A, Pruszczyk P, Opolski G et al.| title=Atrial septostomy in treatment of end-stage right heart failure in patients with pulmonary hypertension. | journal=Chest | year= 2007 | volume= 131 | issue= 4 | pages= 977-83 | pmid=17426198 | doi=10.1378/chest.06-1227 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17426198 }} </ref> <br />
* [[Atrial septostomy]] should also be considered among PH patients who have [[Eisenmenger's syndrome]], idiopathic PAH, and those awaiting [[lung transplantation]].<ref name="pmid19713419">{{cite journal| author=Galiè N, Hoeper MM, Humbert M, Torbicki A, Vachiery JL, Barbera JA et al.| title=Guidelines for the diagnosis and treatment of pulmonary hypertension: the Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS), endorsed by the International Society of Heart and Lung Transplantation (ISHLT). | journal=Eur Heart J | year= 2009 | volume= 30 | issue= 20 | pages= 2493-537 | pmid=19713419 | doi=10.1093/eurheartj/ehp297 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19713419 }} </ref><br />
<br />
===Lung Transplantation===<br />
* [[Lung transplantation]] is considered in the treatment of patients with idiopathic PH, PH associated with [[congenital heart disease]], or [[pulmonary veno-occlusive disease]] (PVOD) who fail to improve on optimal medical therapy. <br />
* Combined [[Lung transplantation|lung]] and [[heart transplantation]] might be considered in selected patients.<ref name="pmid19713419">{{cite journal| author=Galiè N, Hoeper MM, Humbert M, Torbicki A, Vachiery JL, Barbera JA et al.| title=Guidelines for the diagnosis and treatment of pulmonary hypertension: the Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS), endorsed by the International Society of Heart and Lung Transplantation (ISHLT). | journal=Eur Heart J | year= 2009 | volume= 30 | issue= 20 | pages= 2493-537 | pmid=19713419 | doi=10.1093/eurheartj/ehp297 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19713419 }} </ref><br />
* According to the Registry of the International Society for Heart and Lung Transplantation, the survival rates following [[lung transplantation]] are 61%, 49%, and 25 % at 3, 5, and 10 years respectively.<ref name="pmid16890108">{{cite journal| author=Trulock EP, Edwards LB, Taylor DO, Boucek MM, Keck BM, Hertz MI et al.| title=Registry of the International Society for Heart and Lung Transplantation: twenty-third official adult lung and heart-lung transplantation report--2006. | journal=J Heart Lung Transplant | year= 2006 | volume= 25 | issue= 8 | pages= 880-92 | pmid=16890108 | doi=10.1016/j.healun.2006.06.001 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16890108 }} </ref><br />
*If patients present with rapidly progressing disease, [[pulmonary transplantation]] should be considered earlier.<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
===Pulmonary Thromboendarterectomy===<br />
* [[Pulmonary thromboendarterectomy]] (PTE) is a surgical procedure that is used for the treatment of chronic [[thromboembolic]] pulmonary hypertension. <br />
* It is the surgical removal of an organized [[thrombus]] along with the lining of the [[pulmonary artery]]. <br />
* [[PTE]] is a large and very difficult procedure that is currently performed in a few select centers. Case series show remarkable success in most patients.<br />
* Treatment for [[hypoxic]] and miscellaneous varieties of PH have not been established. However, studies of several agents are currently enrolling patients. Many physicians will treat these diseases with the same medications as for PAH, until better options become available.<br />
<br />
==References==<br />
{{reflist|2}}<br />
{{WH}}<br />
{{WS}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_secondary_prevention&diff=1703612Pulmonary hypertension secondary prevention2021-06-09T17:35:40Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}<br />
<br />
==Overview==<br />
The recommended measures for secondary prevention are avoiding pregnancy, rigorous follow up in case of pregnancy, avoiding unnecessary surgeries, multidisciplinary care in case of necessary surgery, avoiding high altitude, supplemental oxygen to ensure a target oxygen saturation of 91% in case of exposure to high altitude, and up-to-date immunizations against [[influenza]] and [[pneumococcal pneumonia]].<br />
<br />
==Secondary prevention==<br />
Shown below are recommended measures for patients with PAH:<ref name="pmid24937180">{{cite journal| author=Taichman DB, Ornelas J, Chung L, Klinger J, Lewis S, Mandel J et al.| title=Pharmacological Therapy for Pulmonary Arterial Hypertension in Adults: CHEST Guideline. | journal=Chest | year= 2014 | volume= | issue= | pages= | pmid=24937180 | doi=10.1378/chest.14-0793 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24937180 }} </ref><br />
* Avoid pregnancy <br />
* Rigorous follow up in case of pregnancy<br />
* Avoid unnecessary surgeries<br />
* Multidisciplinary care in case of necessary surgery<br />
* Avoid high altitude<br />
* Supplemental oxygen in order to ensure a target oxygen saturation of 91% in case of exposure to high altitude<br />
* Up-to-date immunizations against [[influenza]] and [[pneumococcal pneumonia]]<br />
<br />
==References==<br />
{{Reflist|2}}<br />
{{WH}}<br />
{{WS}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_screening&diff=1703611Pulmonary hypertension screening2021-06-09T17:34:41Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}} '''Assistant Editor(s)-in-Chief:''' {{Jose}}; [[User:Ralph Matar|Ralph Matar]]<br />
==Overview==<br />
<br />
Patients with a known [[BMPR2]] [[mutation]], [[scleroderma]], and [[portal hypertension]] undergoing evaluation for [[liver transplantation]] should receive periodic screening for pulmonary hypertension (PH) through [[echocardiography]]. <br />
<br />
==Screening==<br />
* Studies have not shown an impact on outcomes with [[pulmonary hypertension]] [[screening]];<br />
* Despite that, there is an expert consensus that some groups of patients must be screened for [[pulmonary hypertension]] such as:<br />
**Patients with [[scleroderma]] spectrum disorders (especially the ones with corrected [[DLCO]] less than 80%);<br />
**Patients with mutations for a heritable form of [[PAH]];<br />
**Patients with portal hypertension being considered for organ transplantation;<br />
* These patients must be screened annually with [[echocardiography]].<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
===Summary===<br />
Shown below is a table summarizing the recommended screening in several medical conditions associated with elevated risk for PH.<ref>ACCF/AHA 2009 Expert Consensus Document on Pulmonary Hypertension</ref><ref>ACCF/AHA 2009 Expert Consensus Document on Pulmonary Hypertension</ref><br />
<br />
{| style="cellpadding=0; cellspacing= 0; width: 600px;"<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF; width: 40%" align="center" |'''Condition''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF; width: 60%" align="center" |'''Recommended screening'''<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #DCDCDC" align="left" |''' Known [[BMPR2]] [[mutation]]''' || style="font-size: 100; padding: 0 5px; background: #F5F5F5" align="left" |[[Echocardiogram]] (yearly)<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #DCDCDC" align="left" |'''BMPR2 [[mutation]] in a first degree relative''' || style="font-size: 100; padding: 0 5px; background: #F5F5F5" align="left" |[[Genetic counseling]] <br> [[BMPR2]] genotyping<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #DCDCDC" align="left" |'''Family history for PAH in 2 or more relatives'''|| style="font-size: 100; padding: 0 5px; background: #F5F5F5" align="left" | [[Genetic counseling]] <br> [[BMPR2]] genotyping<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #DCDCDC" align="left" |'''[[Systemic sclerosis]]'''|| style="font-size: 100; padding: 0 5px; background: #F5F5F5" align="left" |[[Echocardiogram]] (yearly)<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #DCDCDC" align="left" |'''[[Portal hypertension]]''' || style="font-size: 100; padding: 0 5px; background: #F5F5F5" align="left" |[[Echocardiogram]] if orthotopic liver transplantation is in consideration<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #DCDCDC" align="left" |'''[[Sickle cell disease]]''' || style="font-size: 100; padding: 0 5px; background: #F5F5F5" align="left" |[[Echocardiogram]] (yearly)<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #DCDCDC" align="left" |'''Previous use of [[fenfluramine]]''' || style="font-size: 100; padding: 0 5px; background: #F5F5F5" align="left" |[[Echocardiogram]] in case of symptoms<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #DCDCDC" align="left" |'''[[Congenital heart disease]]''' || style="font-size: 100; padding: 0 5px; background: #F5F5F5" align="left" |[[Echocardiogram]] at the time of diagnosis<br />
|}<br />
<br />
===Echocardiography findings===<br />
[[Echocardiography]] findings that are suggestive of PH include:<ref>ACCF/AHA 2009 Expert Consensus Document on Pulmonary Hypertension</ref><br />
# Enlargement of the size of [[right atrium]] and [[right ventricle]]<br />
# Decrease in the function of the [[right ventricle]]<br />
# Displacement of the [[interventricular septum]]<br />
# [[Tricuspid regurgitation]]<br />
# Presence of [[pericardial effusion]]<br />
<br />
==References==<br />
{{Reflist|2}}<br />
{{WikiDoc Help Menu}}<br />
{{WikiDoc Sources}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_risk_factors&diff=1703610Pulmonary hypertension risk factors2021-06-09T17:20:06Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}; '''Assistant Editor(s)-in-Chief:''' [[User:Ralph Matar|Ralph Matar]]; {{Rim}}<br />
<br />
==Overview==<br />
Pulmonary hypertension (PH) is a multifactorial disease involving genetic and environmental risk factors. Risk factors for pulmonary arterial hypertension include [[BMPR2]] [[mutation]], [[connective tissue disease]], [[HIV infection]], [[portal hypertension]], [[fenfluramine]] use, and [[congenital heart disease]] with a [[shunt]]. [[Left heart]] and [[lung]] diseases are risk factors for PH. Patients with a [[hypercoagulable state]] (such as the presence of [[lupus anticoagulant]], deficiency of [[protein C]], [[protein S]], or [[antithrombin III]], [[inflammation#Chronic inflammation|chronic inflammatory disorders]], [[myeloproliferative syndrome]]s, and [[splenectomy]]) are at an increased risk for chronic [[thromboembolic]] pulmonary hypertension.<br />
<br />
==Risk Factors==<br />
Risk factors of pulmonary hypertension are divided as follows:<ref name="McLaughlin-2009">{{Cite journal | last1 = McLaughlin | first1 = VV. | last2 = Archer | first2 = SL. | last3 = Badesch | first3 = DB. | last4 = Barst | first4 = RJ. | last5 = Farber | first5 = HW. | last6 = Lindner | first6 = JR. | last7 = Mathier | first7 = MA. | last8 = McGoon | first8 = MD. | last9 = Park | first9 = MH. | title = ACCF/AHA 2009 expert consensus document on pulmonary hypertension: a report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents and the American Heart Association: developed in collaboration with the American College of Chest Physicians, American Thoracic Society, Inc., and the Pulmonary Hypertension Association. | journal = Circulation | volume = 119 | issue = 16 | pages = 2250-94 | month = Apr | year = 2009 | doi = 10.1161/CIRCULATIONAHA.109.192230 | PMID = 19332472 }}</ref><br />
<br />
===Pulmonary Arterial Hypertension===<br />
* [[BMPR2]] gene mutation<br />
* [[ALK1]] gene mutation<br />
* [[Connective tissue disease]]<br />
* [[HIV]] infection<br />
* [[Portal hypertension]]<br />
* [[Congenital heart disease]]<br />
* [[Schistosomiasis]]<br />
* Chronic [[hemolytic anemia]]<br />
* [[Drug]]s and [[toxin]]s<br />
<br />
Shown below is a table summarizing the list of drugs associated with PAH:<br />
<br />
{| style="cellpadding=0; cellspacing= 0; width: 600px;"<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF; width: 25%" align="center" |Definite risk || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF; width: 25%" align="center" |Possible risk || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF; width: 25%" align="center" |Likely risk || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF; width: 25%" align="center" |Unlikely risk<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #F5F5F5" align="left" |<br />
* [[Aminorex]] <br />
* [[Fenfluramine]] <br />
* [[Dexfenfluramine]] <br />
* Toxic rapeseed oil <br />
* [[Benfluorex]]<br />
| style="font-size: 100; padding: 0 5px; background: #F5F5F5" align="left" |<br />
* [[Cocaine]] <br />
* [[Phenylpropanolamine]]<br />
* [[St John's wort]] <br />
* [[Chemotherapy]] <br />
* [[Selective serotonin reuptake inhibitor]]s <br />
* [[Pergolide]]<br />
| style="font-size: 100; padding: 0 5px; background: #F5F5F5" align="left" |<br />
* [[Amphetamine]] <br />
* [[L-tryptophan]] <br />
* [[Methamphetamine]]<br />
| style="font-size: 100; padding: 0 5px; background: #F5F5F5" align="left" |<br />
* [[Oral contraceptive]]<br />
* [[Estrogen|Estrogen therapy]]<br />
* [[Smoking]]<br />
|}<br />
<br />
===Pulmonary hypertension due to Left Heart Disease===<br />
* [[Systolic dysfunction]]<br />
* [[Diastolic dysfunction]]<br />
* Left [[valvular disease]]<br />
<br />
===Pulmonary Hypertension due to Lung Diseases and/or Hypoxia===<br />
* Alveolar [[hypoventilation]] disorders<br />
* Chronic exposure to high altitude<br />
* [[Chronic obstructive pulmonary disease]]<br />
* Developmental abnormalities<br />
* [[Interstitial lung disease]]<br />
* Pulmonary diseases with mixed restrictive and obstructive pattern<br />
* Sleep related breathing problems<br />
<br />
===Chronic Thromboembolic Pulmonary Hypertension===<br />
* [[Pulmonary embolism]]<br />
* [[Hypercoagulability]] ([[lupus anticoagulant]], deficiency of [[protein C]], [[protein S]], or [[antithrombin III]], [[inflammation|chronic inflammatory disorder]]s, [[myeloproliferative syndrome]]s, and [[splenectomy]])<br />
<br />
===PH with Unclear and/or Multifactorial Mechanisms===<br />
* [[Myeloproliferative disease]]<br />
* [[Splenectomy]]<br />
* [[Sarcoidosis]]<br />
* [[Histiocytosis]]<br />
* [[Lymphangioleiomyomatosis]]<br />
* [[Neurofibromatosis]]<br />
* [[Vasculitis]]<br />
* [[Glycogen storage disease]]<br />
* [[Gaucher disease]]<br />
* [[Thyroid]] disorder<br />
* Obstruction by [[tumor]]<br />
* Fibrosing [[mediastinitis]]<br />
* [[Chronic renal failure]] on [[dialysis]]<br />
<br />
==References==<br />
{{Reflist|2}}<br />
{{WikiDoc Help Menu}}<br />
{{WikiDoc Sources}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_primary_prevention&diff=1703609Pulmonary hypertension primary prevention2021-06-09T17:11:35Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}<br />
<br />
==Overview==<br />
Genetic and environmental factors are involved in pulmonary hypertension (PH); therefore, not all cases of PH are preventable. PH that is secondary to other diseases such as [[left heart failure]], chronic [[lung]] disease, chronic [[liver]] disease, and [[collagen vascular disease]]s among others can be prevented by the early and optimal treatment of these medical conditions. Patients who are at an elevated risk for developing pulmonary arterial hypertension (PAH) must be monitored for the occurrence of symptoms of PAH. Patients at risk for PAH include subjects with [[systemic sclerosis]] or with genetic predisposition.<br />
<br />
==Primary Prevention==<br />
*The primary prevention of the pulmonary hypertension is as follows:<ref name="pmid24937180">{{cite journal| author=Taichman DB, Ornelas J, Chung L, Klinger J, Lewis S, Mandel J et al.| title=Pharmacological Therapy for Pulmonary Arterial Hypertension in Adults: CHEST Guideline. | journal=Chest | year= 2014 | volume= | issue= | pages= | pmid=24937180 | doi=10.1378/chest.14-0793 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24937180 }} </ref><br />
**[[Genetic]] and [[Environmental factor|environmental factors]] are involved in pulmonary hypertension (PH); therefore, not all cases of PH are preventable. <br />
**PH that is secondary to other diseases such as [[left heart failure]], chronic [[lung]] disease, chronic [[liver]] disease, and [[collagen vascular disease]]s among others can be prevented by the early and optimal treatment of these medical conditions. <br />
**Patients who are at an elevated risk for developing pulmonary arterial hypertension (PAH) must be monitored for the occurrence of symptoms of PAH. Patients at risk for PAH include subjects with [[systemic sclerosis]] or with a genetic predisposition.<br />
<br />
==References==<br />
{{Reflist|2}}<br />
{{WH}}<br />
{{WS}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_physical_examination&diff=1703608Pulmonary hypertension physical examination2021-06-09T17:10:38Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
'''Editor(s)-in-Chief:''' [[User:C Michael Gibson |C. Michael Gibson, M.S., M.D.]] [mailto:charlesmichaelgibson@gmail.com] ; '''Assistant Editor(s)-in-Chief:''' [[User:Lisa Prior|Lisa Prior]]; [[User:Ralph Matar|Ralph Matar]] <br />
<br />
==Overview==<br />
Pulmonary hypertension (PH) can present with myriad physical findings that may be associated with PH or the underlying cause. Findings associated with pulmonary hypertension are usually connected to right heart failure or right heart overload, while other findings may be associated with underlying cause, such as thoracic deformities which may arise in the setting of [[COPD]], or [[sclerodactyly]] that may be seen in patients with [[scleroderma]]. Some may develop on a spectrum corresponding to the severity of the disease. <br />
<br />
==Physical Examination==<br />
<br />
*There are [[physical examination]] findings associated with [[pulmonary hypertension]], and other findings associated with the causes for development of [[pulmonary hypertension]].<br />
*Common physical examination findings of [[pulmonary hypertension]] include signs of right heart failure such as [[elevated jugular venous pressure]], [[right ventricular paraesternal heave or subxiphoid thrust]], [[loud P2]], [[right-sided S3 or S4]], [[holosystolic tricuspid regurgitant murmur]] (that becomes louder after inspiration due to increased venous return), [[peripheral edema]], [[hepatomegaly]], [[ascites]] and [[pulsatile liver]].<br />
*Common physical examination findings associated with causes for development of [[pulmonary hypertension]] and more specific [[pulmonary hypertension]] findings are detailed below:<br />
<br />
===General Appearance=== <br />
<br />
The appearance of the patient may give clues as to the etiology of the condition. For example in [[Chronic obstructive pulmonary disease|COPD]], one of the most common causes of pulmonary hypertension, the patient may appear short of breath with pursed lips breathing and use of accessory muscles. Later on as the disease gets more severe, the patient may appear [[cyanosis|cyanotic]] with extremities cold to the touch.<ref name="isbn0-7295-3905-9">{{cite book |author=Simon O'Connor MBBS FRACP DDU; Nicholas P. Hirsch MBBS FRCA FRCP |title=Clinical Examination: A Systematic Guide to Physical Diagnosis |publisher=Churchill Livingstone |location=Edinburgh |year=2009 |pages= |isbn=0-7295-3905-9 |oclc= |doi= |accessdate=}}</ref><br />
<br />
===Pulse=== <br />
<br />
The [[Pulse|pulse]] may be diminished. This usually occurs in more severe cases.<ref name="isbn0-7295-3905-9">{{cite book |author=Simon O'Connor MBBS FRACP DDU; Nicholas P. Hirsch MBBS FRCA FRCP |title=Clinical Examination: A Systematic Guide to Physical Diagnosis |publisher=Churchill Livingstone |location=Edinburgh |year=2009 |pages= |isbn=0-7295-3905-9 |oclc= |doi= |accessdate=}}</ref><br />
<br />
===Skin===<br />
* [[Telangiectasia]]: suggestive of [[scleroderma]]<br />
* Digital ulceration: suggestive of [[scleroderma]]<br />
* [[Sclerodactyly]]: suggestive of [[scleroderma]]<br />
* [[Spider nevi]]: suggestive of liver disease<br />
* [[Palmar erythema]]: suggestive of liver disease<br />
* [[Clubbing]]: may be indicative of [[congenital heart disease]] or [[pulmonary veno-occlusive disease]]<ref name="pmid19713419">{{cite journal| author=Galiè N, Hoeper MM, Humbert M, Torbicki A, Vachiery JL, Barbera JA et al.| title=Guidelines for the diagnosis and treatment of pulmonary hypertension: the Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS), endorsed by the International Society of Heart and Lung Transplantation (ISHLT). | journal=Eur Heart J | year= 2009 | volume= 30 | issue= 20 | pages= 2493-537 | pmid=19713419 | doi=10.1093/eurheartj/ehp297 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19713419 }} </ref><br />
<br />
===Jugular Venous Pressure - JVP=== <br />
<br />
Assessment of the [[Jugular venous pressure|JVP]] in pulmonary hypertension involves assessing the 'a' wave (coincides with atrial contraction), the 'v' wave (coincides with atrial filling) and the height of the JVP column above the sternal angle. Physical findings may include:<br />
<br />
* Prominent 'a' wave: due to forced atrial contraction <br />
* Prominent 'v' wave: later if [[Tricuspid regurgitation|tricuspid regurgitation]] develops with [[right ventricular failure]]<br />
* Elevated [[JVP]]: can be present if [[right ventricular failure]] develops<br />
* Postive [[Kussmaul's sign]]: [[JVP]] elevation during inspiration (the opposite of what normally happens) because of [[right ventricular failure]]<ref name="isbn0-7295-3905-9">{{cite book |author=Simon O'Connor MBBS FRACP DDU; Nicholas P. Hirsch MBBS FRCA FRCP |title=Clinical Examination: A Systematic Guide to Physical Diagnosis |publisher=Churchill Livingstone |location=Edinburgh |year=2009 |pages= |isbn=0-7295-3905-9 |oclc= |doi= |accessdate=}}</ref><br />
* Positive [[Hepatojugular reflux|abdominojugular reflux]]: [[JVP]] rises and remains elevated during a period of over 10 seconds whilst abdominal pressure is applied. This may be present if [[right ventricular failure]] develops.<ref name="isbn0-7295-3905-9">{{cite book |author=Simon O'Connor MBBS FRACP DDU; Nicholas P. Hirsch MBBS FRCA FRCP |title=Clinical Examination: A Systematic Guide to Physical Diagnosis |publisher=Churchill Livingstone |location=Edinburgh |year=2009 |pages= |isbn=0-7295-3905-9 |oclc= |doi= |accessdate=}}</ref><br />
<br />
===Lungs===<br />
* [[Lung]] exam is generally normal.<br />
* [[Crackles]] upon inspirations are indicative of [[interstitial lung disease]].<br />
<br />
===Cardiovascular===<br />
<br />
A complete [[precordium|precordial]] assessment of pulmonary hypertension involves [[Palpation of the precordium|palpating the precordium]] for [[Heave|heaves]] and thrills and auscultating to assess first and second heart sounds, splitting of the second heart sound and determining if there are any added [[Heart sounds|heart sounds]] or murmurs. Physical findings may include the following:<br />
<br />
====Palpation====<br />
<br />
* Left parasternal heave: due to hyperdynamic [[right ventricle]]<br />
* Palpable P2: correlates with severe disease <ref name="isbn0-7295-3905-9">{{cite book |author=Simon O'Connor MBBS FRACP DDU; Nicholas P. Hirsch MBBS FRCA FRCP |title=Clinical Examination: A Systematic Guide to Physical Diagnosis |publisher=Churchill Livingstone |location=Edinburgh |year=2009 |pages= |isbn=0-7295-3905-9 |oclc= |doi= |accessdate=}}</ref><br />
<br />
====Auscultation====<br />
<br />
=====First and second heart sound (S1,S2)=====<br />
<br />
* Loud P2 component of S2: this is due to the forceful closure of the valve because of increased pulmonary pressure. It can be heard mostly in the pulmonary area (upper right sternal border). If it is evident at the cardiac apex, this indicates more severe disease. It is best appreciated on inspiration.<ref name="isbn0-7817-7012-2">{{cite book |author=Thompson, Paul Richard; Topol, Eric J.; Califf, Robert M.; Prystowsky, Eric N.; Thomas, James Alan |title=Textbook of cardiovascular medicine |publisher=Lippincott Williams & Wilkins |location=Hagerstwon, MD |year=2007 |pages= |isbn=0-7817-7012-2 |oclc= |doi= |accessdate=}}</ref><br />
<br />
=====Splitting of S2=====<br />
<br />
* Narrowed splitting of S2: in chronic pulmonary hypertension, pulmonary artery compliance decreases leading to earlier pulmonary valve closure and narrowed splitting.<ref name="isbn0-07-055417-X">{{cite book |author=Alexander, R. McNeill; Hurst, J. Willis; Schlant, Robert C. |title=The Heart, arteries and veins |publisher=McGraw-Hill, Health Professions Division |location=New York |year=1994 |pages= |isbn=0-07-055417-X |oclc= |doi= |accessdate=}}</ref><br />
* Widened splitting of S2: widened splitting may occur later if right ventricular failure or bundle branch block develops.<ref name="isbn0-7817-7012-2">{{cite book |author=Thompson, Paul Richard; Topol, Eric J.; Califf, Robert M.; Prystowsky, Eric N.; Thomas, James Alan |title=Textbook of cardiovascular medicine |publisher=Lippincott Williams & Wilkins |location=Hagerstwon, MD |year=2007 |pages= |isbn=0-7817-7012-2 |oclc= |doi= |accessdate=}}</ref><br />
<br />
=====Extra Heart Sounds===== <br />
* S4: due to right ventricular hypertrophy and therefore reduced compliance secondary to pulmonary hypertension. It is increased with inspiration.<br />
* S3: if right ventricular failure develops. Increased with inspiration.<ref name="isbn0-7295-3905-9">{{cite book |author=Simon O'Connor MBBS FRACP DDU; Nicholas P. Hirsch MBBS FRCA FRCP |title=Clinical Examination: A Systematic Guide to Physical Diagnosis |publisher=Churchill Livingstone |location=Edinburgh |year=2009 |pages= |isbn=0-7295-3905-9 |oclc= |doi= |accessdate=}}</ref><br />
<br />
=====Additional Sounds===== <br />
* Systolic pulmonary ejection click: increased with inspiration<br />
<br />
=====Murmurs===== <br />
* Ejection midsystolic murmur: increased with [[inspiration]]<br />
* Diastolic murmur (Graham-Steele murmur): indicates [[pulmonary regurgitation]]<br />
* Pansystolic murmur: indicates [[tricuspid regurgitation]] and developing [[right ventricular failure]]<ref name="isbn0-7020-2993-9">{{cite book |author=Clark, Michael; Kumar, Parveen J. |title=Kumar and Clark's clinical medicine |publisher=Elsevier Saunders |location=St. Louis, Mo |year=2009 |pages= |isbn=0-7020-2993-9 |oclc= |doi= |accessdate=}}</ref><br />
<br />
===Abdomen=== <br />
<br />
Findings in the abdomen include:<br />
<br />
* [[Ascites]]: indicates right ventricular failure<br />
* Painful [[hepatomegaly]]: indicates right ventricular failure<br />
* Pulsatile liver: due to tricuspid regurgitation <ref name="isbn0-7295-3905-9">{{cite book |author=Simon O'Connor MBBS FRACP DDU; Nicholas P. Hirsch MBBS FRCA FRCP |title=Clinical Examination: A Systematic Guide to Physical Diagnosis |publisher=Churchill Livingstone |location=Edinburgh |year=2009 |pages= |isbn=0-7295-3905-9 |oclc= |doi= |accessdate=}}</ref><br />
<br />
===Extremities=== <br />
<br />
* [[Edema]]: indicates [[right ventricular failure]]<ref name="isbn0-7295-3905-9">{{cite book |author=Simon O'Connor MBBS FRACP DDU; Nicholas P. Hirsch MBBS FRCA FRCP |title=Clinical Examination: A Systematic Guide to Physical Diagnosis |publisher=Churchill Livingstone |location=Edinburgh |year=2009 |pages= |isbn=0-7295-3905-9 |oclc= |doi= |accessdate=}}</ref><br />
* [[Cool extremities]]: indicates severe disease<br />
<br />
==References==<br />
{{Reflist|2}}<br />
{{WikiDoc Help Menu}}<br />
{{WikiDoc Sources}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_pathophysiology&diff=1703607Pulmonary hypertension pathophysiology2021-06-09T16:56:05Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}; '''Assistant Editor(s)-in-Chief:''' [[User:Ralph Matar|Ralph Matar]]; [[User:Rim Halaby|Rim Halaby]] {{Jose}}<br />
==Overview==<br />
Pulmonary hypertension (PH) is a pathological condition of the pulmonary vasculature present in several disease states that presents with elevated mean pulmonary artery pressure (PAP) as measured by [[right heart catheterization]] at rest. The factors that are in involved in the pathophysiology of the increase in the mean pulmonary arterial pressure are: increase in pulmonary [[vascular resistance]], increase in the right-side cardiac output and increase in the [[mean pulmonary venous pressure]]. Pulmonary arterial hypertension is characterized by [[endothelial]] dysfunction resulting from an imbalance between [[apoptosis]] and proliferation of pulmonary artery smooth muscle cells favoring the proliferation. The other types of [[pulmonary hypertension]] are caused by hemodynamic changes that result in increased [[pulmonary blood pressure]] or architectural changes to the lung or its [[vasculature]] that result in the same outcome.<br />
<br />
==Pathophysiology==<br />
The pathophysiology of pulmonary hypertension<ref name="pmid15059929">{{cite journal |vauthors=Marcos E, Fadel E, Sanchez O, Humbert M, Dartevelle P, Simonneau G, Hamon M, Adnot S, Eddahibi S |title=Serotonin-induced smooth muscle hyperplasia in various forms of human pulmonary hypertension |journal=Circ. Res. |volume=94 |issue=9 |pages=1263–70 |date=May 2004 |pmid=15059929 |doi=10.1161/01.RES.0000126847.27660.69 |url=}}</ref><ref name="pmid10024307">{{cite journal |vauthors=Eddahibi S, Fabre V, Boni C, Martres MP, Raffestin B, Hamon M, Adnot S |title=Induction of serotonin transporter by hypoxia in pulmonary vascular smooth muscle cells. Relationship with the mitogenic action of serotonin |journal=Circ. Res. |volume=84 |issue=3 |pages=329–36 |date=February 1999 |pmid=10024307 |doi= |url=}}</ref><ref name="pmid26479975">{{cite journal |vauthors=Huber LC, Bye H, Brock M |title=The pathogenesis of pulmonary hypertension--an update |journal=Swiss Med Wkly |volume=145 |issue= |pages=w14202 |date=2015 |pmid=26479975 |doi=10.4414/smw.2015.14202 |url=}}</ref><ref name="pmid23457160">{{cite journal |vauthors=Peacock A |title=Pulmonary hypertension |journal=Eur Respir Rev |volume=22 |issue=127 |pages=20–5 |date=March 2013 |pmid=23457160 |doi=10.1183/09059180.00006912 |url=}}</ref><ref name="pmid24267295">{{cite journal |vauthors=Tuder RM, Stacher E, Robinson J, Kumar R, Graham BB |title=Pathology of pulmonary hypertension |journal=Clin. Chest Med. |volume=34 |issue=4 |pages=639–50 |date=December 2013 |pmid=24267295 |doi=10.1016/j.ccm.2013.08.009 |url=}}</ref><ref name="pmid24951761">{{cite journal |vauthors=Michelakis ED |title=Pulmonary arterial hypertension: yesterday, today, tomorrow |journal=Circ. Res. |volume=115 |issue=1 |pages=109–14 |date=June 2014 |pmid=24951761 |doi=10.1161/CIRCRESAHA.115.301132 |url=}}</ref><ref name="pmid21110189">{{cite journal |vauthors=Douwes JM, Berger RM |title=The maze of vasodilator response criteria |journal=Pediatr Cardiol |volume=32 |issue=2 |pages=245–6 |date=February 2011 |pmid=21110189 |doi=10.1007/s00246-010-9849-8 |url=}}</ref><ref name="pmid25593290">{{cite journal |vauthors=Ranchoux B, Antigny F, Rucker-Martin C, Hautefort A, Péchoux C, Bogaard HJ, Dorfmüller P, Remy S, Lecerf F, Planté S, Chat S, Fadel E, Houssaini A, Anegon I, Adnot S, Simonneau G, Humbert M, Cohen-Kaminsky S, Perros F |title=Endothelial-to-mesenchymal transition in pulmonary hypertension |journal=Circulation |volume=131 |issue=11 |pages=1006–18 |date=March 2015 |pmid=25593290 |doi=10.1161/CIRCULATIONAHA.114.008750 |url=}}</ref><ref name="pmid27045138">{{cite journal |vauthors=Hopper RK, Moonen JR, Diebold I, Cao A, Rhodes CJ, Tojais NF, Hennigs JK, Gu M, Wang L, Rabinovitch M |title=In Pulmonary Arterial Hypertension, Reduced BMPR2 Promotes Endothelial-to-Mesenchymal Transition via HMGA1 and Its Target Slug |journal=Circulation |volume=133 |issue=18 |pages=1783–94 |date=May 2016 |pmid=27045138 |pmc=4856565 |doi=10.1161/CIRCULATIONAHA.115.020617 |url=}}</ref><ref name="pmid11401896">{{cite journal |vauthors=Jobe AH, Bancalari E |title=Bronchopulmonary dysplasia |journal=Am. J. Respir. Crit. Care Med. |volume=163 |issue=7 |pages=1723–9 |date=June 2001 |pmid=11401896 |doi=10.1164/ajrccm.163.7.2011060 |url=}}</ref><br />
<br />
PH is defined as an elevated mean pulmonary artery pressure (PAP) ≥ 25 mmHg as measured by right heart catheterization at rest. The elevation in PAP results from an elevation in the pulmonary vascular resistance caused by a multifactorial pathogenesis involving genetic and environmental factors.<br />
<br />
Pulmonary hypertension has several pathophysiologic mechanisms depending on the underlying etiology. Nevertheless, the following sequence of events is almost always present:<br />
<br />
*Vasoconstriction (ocurring early in the disease); <br />
*Thrombosis (during the evolution of the disease); <br />
*Remodeling (then takes place and becomes the most important factor).<ref name="pmid26479975">{{cite journal| author=Huber LC, Bye H, Brock M, Swiss Society of Pulmonary Hypertension| title=The pathogenesis of pulmonary hypertension--an update. | journal=Swiss Med Wkly | year= 2015 | volume= 145 | issue= | pages= w14202 | pmid=26479975 | doi=10.4414/smw.2015.14202 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26479975 }} </ref><br />
**An initiating factor leads to increased resistance in the pulmonary vasculature causing narrowing of the [[vessels]] and impaired [[blood flow]].<br />
**As a consequence, the right [[ventricle]] adapts by increasing right ventricular [[systolic]] pressures to preserve the [[cardiac output]] from the right heart. <br />
**Over time, increasing right ventricular [[systolic]] pressures will subsequently result in chronic changes in the [[pulmonary circulation]] and the affected blood vessels progressively become [[Fibrosis|stiffer and thicker]], further increasing the blood pressure within the lungs and impairing blood flow. <br />
**In addition, the increased workload of the heart causes thickening and enlargement of the [[right ventricle]], making the heart less able to pump blood through the lungs, causing right [[heart failure]]. Factors that might affect the ability of the right ventricle to adapt to an increased pulmonary vascular resistance are:<br />
*** Age of the patient at onset<br />
*** Rapidity of onset of pulmonary hypertension<br />
*** Coexisting [[hypoxemia]]<br />
<br />
==Pulmonary Arterial Hypertension==<br />
===Molecular and Cellular Changes===<br />
* Pulmonary arterial hypertension is characterized by [[endothelial]] dysfunction resulting from an imbalance between [[apoptosis]] and proliferation of pulmonary artery smooth muscle cells favoring the proliferation. <br />
* There is also thickened and disordered [[adventitia]] due to excessive amounts of adventitial [[metalloproteinase]]s. <br />
* Several pathways are implicated in development of vascular remodeling, which is the hallmark of pathologic changes in pulmonary hypertension:<br />
1. '''''Vasoconstriction-mediated remodeling'''''<br />
* Imbalance of vasoactive signals is suggested in the pathogenesis of remodeling. <br />
* Reduced levels of vasodilatory mediators, in particular [[PGI2|prostaglandin I<sub>2</sub>]], [[nitric oxide]], and [[cGMP|cyclic guanine monophosphate]], and elevated levels of vasocontricting molecules such as [[endothelin 1]], [[thromboxane]], and [[5-hydroxytryptamine]] contribute to alterations in the vascular tone.<br />
* Down regulation of the [[voltage-gated potassium channel]]s has also been linked with altered pulmonary vascular tone, dysregulation of cellular homeostasis, and induction of proliferative sequelae in vascular [[smooth muscle cell]]s.<br />
* Patients with [[PAH]] seem to have higher concentrations of serum [[endothelin-1]] (a potent vasoconstrictor) than controls.<ref name="pmid26479975">{{cite journal| author=Huber LC, Bye H, Brock M, Swiss Society of Pulmonary Hypertension| title=The pathogenesis of pulmonary hypertension--an update. | journal=Swiss Med Wkly | year= 2015 | volume= 145 | issue= | pages= w14202 | pmid=26479975 | doi=10.4414/smw.2015.14202 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26479975 }} </ref><br />
* May occur in response to [[hypoxia]];<br />
* May be related to [[calcium channel]] dysfunction - in fact, there are mutations in the [[ion channels]] (KCNK3) which predispose to [[hereditary PAH]];<br />
* May be reversible - patients treated early in the disease with [[calcium channel blockers]] seem to have a much better prognosis.<ref name="pmid26479975">{{cite journal| author=Huber LC, Bye H, Brock M, Swiss Society of Pulmonary Hypertension| title=The pathogenesis of pulmonary hypertension--an update. | journal=Swiss Med Wkly | year= 2015 | volume= 145 | issue= | pages= w14202 | pmid=26479975 | doi=10.4414/smw.2015.14202 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26479975 }} </ref><br />
2. '''''Thrombosis-mediated remodeling'''''<br />
* Many [[coagulopathies]] were described in patients with [[PAH]], such as increased [[von Willebrand factor]] activity, [[protein C]] and [[protein S deficiency]].<ref name="pmid8797416">{{cite journal| author=Welsh CH, Hassell KL, Badesch DB, Kressin DC, Marlar RA| title=Coagulation and fibrinolytic profiles in patients with severe pulmonary hypertension. | journal=Chest | year= 1996 | volume= 110 | issue= 3 | pages= 710-7 | pmid=8797416 | doi=10.1378/chest.110.3.710 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8797416 }} </ref><ref name="pmid9877507">{{cite journal| author=Hoeper MM, Sosada M, Fabel H| title=Plasma coagulation profiles in patients with severe primary pulmonary hypertension. | journal=Eur Respir J | year= 1998 | volume= 12 | issue= 6 | pages= 1446-9 | pmid=9877507 | doi=10.1183/09031936.98.12061446 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9877507 }} </ref><br />
* [[Thrombin]] plays a key role in mediating vascular remodeling by activating [[platelet]], upregulating [[angiogenesis]]-related genes (including [[tissue factor|tissue factor [TF]]], [[basic fibroblast growth factor|basic fibroblast growth factor [bFGF]]], and [[matrix metalloproteinase]]-2), and transactivating [[vascular endothelial growth factor|vascular endothelial growth factor (VEGF)]] by inducing the production of [[reactive oxygen species|reactive oxygen species (ROS)]] and the expression of the [[Hypoxia inducible factors|hypoxia inducible factor-1 alpha]].<br />
* Upregulation of TF in the vasculature leads to initiation of coagulation cascade and migration and proliferation of [[smooth muscle cell]]s upon vascular injury. <br />
* In addition, [[platelet activation]] by [[thrombin]] results in the release of granules containing substances that promote [[mitogenesis]] and [[vasoconstriction]] including [[VEGF]], [[bFGF]], [[platelet-derived growth factor]], and [[serotonin]], which also contribute to increased endothelial cell migration and proliferation.<br />
3. '''''Proliferation-mediated remodeling'''''<br />
* The pathogenic pathway of lung vasculature remodeling in PH is not fully understood;<br />
* It is regulated by a variety of growth factors, cytokines, mytogens, ion channels, neurotransmitters viruses, transcription factors and receptors, the most studied being the [[bone morphogenetic protein receptor type II]] (BMPR2).<br />
* BMPR2 loss-of-function mutations were found in 70% of patients with hereditary PAH and in 20% of patients with idiopathic PAH;<ref name="pmid25612240">{{cite journal| author=Momose Y, Aimi Y, Hirayama T, Kataoka M, Ono M, Yoshino H | display-authors=etal| title=De novo mutations in the BMPR2 gene in patients with heritable pulmonary arterial hypertension. | journal=Ann Hum Genet | year= 2015 | volume= 79 | issue= 2 | pages= 85-91 | pmid=25612240 | doi=10.1111/ahg.12096 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25612240 }} </ref><ref name="pmid16429403">{{cite journal| author=Aldred MA, Vijayakrishnan J, James V, Soubrier F, Gomez-Sanchez MA, Martensson G | display-authors=etal| title=BMPR2 gene rearrangements account for a significant proportion of mutations in familial and idiopathic pulmonary arterial hypertension. | journal=Hum Mutat | year= 2006 | volume= 27 | issue= 2 | pages= 212-3 | pmid=16429403 | doi=10.1002/humu.9398 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16429403 }} </ref><br />
* Anecdotal reports have stated that [[imatinib]] has been able to cause significant improvement of PAH patients;<ref name="pmid16192491">{{cite journal| author=Ghofrani HA, Seeger W, Grimminger F| title=Imatinib for the treatment of pulmonary arterial hypertension. | journal=N Engl J Med | year= 2005 | volume= 353 | issue= 13 | pages= 1412-3 | pmid=16192491 | doi=10.1056/NEJMc051946 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16192491 }} </ref><br />
* [[Serotonin]] exerts both vasoconstrictive and mitogenic effects on [[smooth muscle cell]]s (SMC). <br />
* Serotonin m bind to 5-hydroxytryptamine 1A and 2B receptors or may enter SMC via [[SERT|serotonin transporter]] which induces generation of [[reactive oxygen species|ROS]], [[rho kinase]], and [[MAPK|mitogen-activated protein kinases]]. <br />
* This in turn leads to the expression of [[growth factor]]s and proliferation. [[Bone morphogenetic protein|Bone morphogenetic protein (BMP)]] is also involved in the SMC proliferation. <br />
* Upon binding of BMP to its heterodimerized receptors, a group of cytoplasmic proteins known as receptor-mediated [[Smad]]s are phosphorylated and translocated to the nucleus where they upregulate genes related to anti-proliferation. <br />
* Serotonin is shown to antagonize the BMP/Smad pathway thus facilitating the proliferation of [[smooth muscle cell]]s.<br />
4. '''''Inflammation-mediated remodeling'''''<br />
* Influx of inflammatory effector cells is stimulated by the release of chemokines such as [[CCL5]] and [[CX3CL1]]. <br />
* On the other hand, [[endothelial cell]] and [[smooth muscle cell]] dysfunction contributes to the release of vasomotor and [[growth factor]]s, activation of [[transcription factor]]s, influx of [[calcium]], and dysfunction of [[mitochondria]]. <br />
* The net effect is a shift of balance in favor of proliferation and suppressed [[apoptosis]], leading to remodeling of the pulmonary vasculature.<br />
Shown below is an image depicting remodeling in pulmonary arterial hypertension.<br />
<br />
[[File:Pathophysiology of pulmonary hypertension.png|661x661px]]<br />
<br />
===Genetic Mutations===<br />
====TGF-β Receptor Pathway====<br />
* The bone morphogenetic protein receptor II (BMPR2) gene encodes a [[serine]]/[[threonine]] [[kinase]] that functions as a receptor for bone morphogenetic proteins which forms a heterodimer cytoplasmic complex of two type II and two type I receptors. The downstream signaling involves activation of SMAD transcription factor which mediates anti-proliferation in smooth muscle cells.<br />
<br />
* Activin-like kinase 1 gene mutations are detected in patients with [[hereditary hemorrhagic telangiectasia]] and pulmonary arterial hypertension. Mutation would cause growth-promoting alterations.<br />
<br />
====Serotoninergic Pathway====<br />
* 5- Hydroxytryptamine (serotonin) transporter mutations have also been associated with the proliferation of [[smooth muscle cell]]s of pulmonary arteries.<ref name="pmid11602621">{{cite journal| author=Eddahibi S, Humbert M, Fadel E, Raffestin B, Darmon M, Capron F et al.| title=Serotonin transporter overexpression is responsible for pulmonary artery smooth muscle hyperplasia in primary pulmonary hypertension. | journal=J Clin Invest | year= 2001 | volume= 108 | issue= 8 | pages= 1141-50 | pmid=11602621 | doi=10.1172/JCI12805 | pmc=PMC209526 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11602621 }} </ref><br />
<br />
==Genetics==<br />
'''Familial PAH''' often results from a [[mutation]] in the bone morphogenic protein receptor-2 (BMPR2) and is inherited as an [[autosomal dominant]] disease with incomplete [[penetrance]] and anticipation.<ref name="Rich-1987">{{Cite journal | last1 = Rich | first1 = S. | last2 = Dantzker | first2 = DR. | last3 = Ayres | first3 = SM. | last4 = Bergofsky | first4 = EH. | last5 = Brundage | first5 = BH. | last6 = Detre | first6 = KM. | last7 = Fishman | first7 = AP. | last8 = Goldring | first8 = RM. | last9 = Groves | first9 = BM. | title = Primary pulmonary hypertension. A national prospective study. | journal = Ann Intern Med | volume = 107 | issue = 2 | pages = 216-23 | month = Aug | year = 1987 | doi = | PMID = 3605900 }}</ref><br />
==Associated conditions==<br />
*PAH is also associated with:<ref>ACCF/AHA 2009 Expert Consensus Document on Pulmonary Hypertension</ref><br />
#[[Congenital heart disease]] (30% of untreated cases)<br />
#[[Connective tissue diseases]] (12% of patients with [[scleroderma]] and up to 21% of patients with [[rheumatoid arthritis]])<br />
#[[HIV]] (0.5%)<br />
#[[Portal hypertension]] (2-6%)<br />
#[[Sickle cell disease]] (20 to 40%)<br />
#[[Systemic lupus erythematosus]] (4 to 14%)<br />
#[[Hemoglobinopathies]]<br />
#[[Myeloproliferative disorders]]<br />
#Drugs and toxins<br />
==Histopathology==<br />
PH is a pathological condition present in different disease states that share similar clinical manifestation and some common histopathological features. Shown below is a table that summarizes the classification of PH based on histopathology findings.<ref name="pmid15194175">{{cite journal| author=Pietra GG, Capron F, Stewart S, Leone O, Humbert M, Robbins IM et al.| title=Pathologic assessment of vasculopathies in pulmonary hypertension. | journal=J Am Coll Cardiol | year= 2004 | volume= 43 | issue= 12 Suppl S | pages= 25S-32S | pmid=15194175 | doi=10.1016/j.jacc.2004.02.033 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15194175 }} </ref><br />
{| style="cellpadding=0; cellspacing= 0; width: 600px;"<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''Class''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''Histopathological findings'''<ref name="pmid15194175">{{cite journal| author=Pietra GG, Capron F, Stewart S, Leone O, Humbert M, Robbins IM et al.| title=Pathologic assessment of vasculopathies in pulmonary hypertension. | journal=J Am Coll Cardiol | year= 2004 | volume= 43 | issue= 12 Suppl S | pages= 25S-32S | pmid=15194175 | doi=10.1016/j.jacc.2004.02.033 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15194175 }} </ref><br />
! style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |Images<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |'''Pulmonary arteriopathy''' || style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |'''''Constrictive lesions in pulmonary arteries''''' <br><br />
* Medial hypertrophy <br />
* Intimal thickening <br />
* Adventitial thickening <br><br />
'''''Complex lesions in pulmonary arteries''''' <br><br />
* Plexiform lesions <br />
* Dilatation lesions <br />
* [[Arteritis]] <br><br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |[[File:Pulmonary hypertension arteriopathy intimal and medial thickening.jpg|thumb]][[File:Pulmonary hypertension arteriopathy adventitial thickening.jpg|thumb]][[File:Pulmonary hypertension arteriopathy intimal and adventitial thickening.jpg|thumb]]<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |'''Pulmonary arteriopathy with venous-venular changes''' || style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" | ''Changes similar to pulmonary arteriopathy'' <br> PLUS<br> ''Changes in venules and veins''<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |[[File:Pulmonary hypertension arteriopathy medial muscle layer thickening.jpg|thumb]][[File:Pulmonary hypertension Plexiform lesion 2.jpg|thumb]]<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width:50%" align="left" |'''Pulmonary occlusive venopathy''' <br> (with or without arteriopathy) || style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |'''''Changes in venules and veins''''' <br><br />
* Diffuse fibrotic occlusion<br />
* Intimal thickening <br />
* Medial thickening <br />
* Adventitial thickening <br><br />
'''''Changes in the capillaries''''' <br />
* Dilatation <br />
* Congestion <br><br />
'''''Changes in the interstitium''''' <br />
* [[Edema]] <br />
* [[Fibrosis]] <br />
* [[Hemosiderosis]]<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |'''Pulmonary microvasculopathy''' <br> (with or without arteriopathy and/on venopathy)|| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |'''''Changes in the capillaries''''' <br />
* Localized capillary proliferation <br><br />
'''''Changes in the interstitium''''' <br />
* [[Edema]] <br />
* [[Fibrosis]] <br />
* [[Hemosiderosis]]<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |[[File:Pulmonary hypertension Pulmonary capillary hemangiomatosis.jpg|thumb]][[File:Pulmonary hypertension pulmonary capillary hemangiomatosis.jpg|thumb]]<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |'''Unclassified''' || style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" | ''Non specific changes''<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |<br />
|}<br />
<br />
==Gallery==<br />
'''The images below are courtesy of Dr. Yale Rosen (''Source:Wikimedia Commons'').'''<br />
<br />
<gallery><br />
Image:Pulmonary hypertension arteriopathy intimal and medial thickening.jpg|Marked intimal and medial thickening<br />
<br />
Image:Pulmonary hypertension arteriopathy medial muscle layer thickening.jpg|Medial muscle layer thickening involving multiple pulmonary arteries.<br />
<br />
Image:Pulmonary hypertension associated with vasculitis fibrinoid necrosis.jpg|This arteriole exhibits fibrinoid necrosis.<br />
<br />
Image:Pulmonary hypertension arteriopathy medial thickening.jpg|Pronounced thickening of the medial muscle layer.<br />
<br />
Image:Pulmonary hypertension arteriopathy intimal and medial thickening.jpg|Marked intimal and medial thickening.<br />
<br />
Image:Pulmonary hypertension arteriopathy intimal thickening.jpg|This artery exhibits marked intimal thickening The red-staining cells in the intima are probably myofibroblasts. Masson trichrome stain.<br />
<br />
Image:Pulmonary hypertension arteriopathy adventitial thickening.jpg|Marked adventitial thickening. Masson trichrome stain.<br />
<br />
Image:Pulmonary hypertension arteriopathy intimal and adventitial thickening.jpg|This artery exhibits marked intimal thickening as well as adventitial thickening. The red-staining cells in the intima are probably myofibroblasts. Masson trichrome stain.<br />
<br />
Image:Pulmonary hypertension arteriopathy adventitial thickening and hemangiomatosis.jpg|Pulmonary hypertension associated with pulmonary hemangiomatosis. A muscular pulmonary artery surrounded by angiomatous vessels exhibits marked intimal and adventitial thickening.<br />
<br />
Image:Pulmonary hypertension arteriopathy intimal and medial thickening 2.jpg|There is thickening of the medial muscle layer as well as mild intimal thickening.<br />
<br />
Image:Pulmonary hypertension pulmonary capillary hemangiomatosis.jpg|Alveolar capillary proliferation as well as the proliferation of larger blood vessels, probably venules.<br />
<br />
Image:Pulmonary hypertension associated vasculitis fibrinoid necrosis 2.jpg|This artery exhibits vasculitis characterized by focal necrosis of the wall accompanied by inflammation.<br />
<br />
Image:Pulmonary hypertension Plexiform and dilatation lesions.jpg|A large dilatation lesion is present on the right side of this image adjacent to an angiomatoid lesion.<br />
<br />
Image:Pulmonary hypertension Plexiform and dilatation lesions 2.jpg|Two angiomatoid lesions are present. A large dilatation lesion is a present adjacent to the angiomatoid lesion that is located just above center.<br />
<br />
Image:Pulmonary hypertension Plexiform lesion.jpg|There is angiomatoid (plexiform) lesion.<br />
<br />
Image:Pulmonary hypertension Plexiform lesion 2.jpg|The appearance suggests multiple lesions but a single lesion cannot be excluded. Note the destruction of the arterial wall at the site of the angiomatoid lesion. Destructive arterial changes are frequently associated with angiomatoid lesions. There is an elastic stain.<br />
<br />
Image:Pulmonary hypertension Plexiform lesion 3 and associated inflammation.jpg|This angiomatoid lesion is accompanied by inflammation which is frequently associated with these lesions.<br />
<br />
Image:Pulmonary hypertension Pulmonary capillary hemangiomatosis.jpg|There is a proliferation of alveolar wall capillaries which are markedly dilated.<br />
<br />
Image:Pulmonary hypertension Plexiform and dilatation lesions 4.jpg|A dilatation lesion is seen in the left lower quadrant adjacent to the angiomatoid lesion. There is an elastic stain.<br />
<br />
Image:Pulmonary hypertension Plexiform and dilatation lesions 5.jpg|This angiomatoid lesion contains multiple thrombi within the vascular spaces. A large dilatation lesion is a present adjacent to the bottom of the angiomatoid lesion.<br />
<br />
Image:Pulmonary hypertension Plexiform and dilatation lesions 6.jpg|A dilatation lesion is present adjacent to the right side of the angiomatoid lesion.<br />
<br />
Image:Pulmonary hypertension Plexiform and dilatation lesions 7.jpg|There is a disappearance of the arterial wall at the site of the angiomatoid lesions. Arterial wall destruction is a frequent finding in association with angiomatoid lesions. A dilatation lesion encircles the angiomatoid lesion<br />
<br />
</gallery><br />
<br />
==References==<br />
{{reflist|2}}<br />
<br />
{{WH}}<br />
{{WS}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_overview&diff=1703603Pulmonary hypertension overview2021-06-09T15:58:30Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}, Richard Channick, M.D.; '''Assistant Editor(s)-in-Chief:''' [[User:Lisa Prior|Lisa Prior]], [[Ann Slater|Ann Slater, R.N.]]; {{Jose}}<br />
<br />
==Overview==<br />
'''Pulmonary hypertension''' (PH) is a condition of elevated blood pressure (>25 mmHg at rest) within the [[pulmonary artery]] of the [[lungs]], leading to myriad symptoms including [[dypsnea|shortness of breath]], [[dizziness]], [[syncope]], [[chest pain]], [[tachycardia]] and leg swelling. PH has several differing etiologies and is a progressive and fatal disease if left untreated. PH is classified by the World Health Organization (WHO) into 5 different groups, which will be discussed later on this page. Treatment is generally targeted toward the underlying etiology of disease. “Pulmonary arterial hypertension” (PAH) refers to group 1 [[PH]] in the updated WHO classification and “pulmonary hypertension” (PH) refers to any of group 2 PH through group 5 PH. PH is also used when referring to all five groups collectively.<br />
<br />
==Historical Perspective==<br />
[[Pulmonary hypertension]] was first described by [[Ernst von Romberg]], a German physician, in 1891.<br />
<br />
==Classification==<br />
[[Pulmonary hypertension]] may be classified according to the mechanism leading to its development into 5 groups: [[pulmonary arterial hypertension]], [[pulmonary hypertension due to left heart disease]], [[pulmonary hypertension due to chronic lung diseases and/or hypoxia]], and [[pulmonary hypertension due to embolic disease]] and [[miscellaneous]] causes.<br />
<br />
==Pathophysiology==<br />
Pulmonary hypertension (PH) is a pathological condition of the pulmonary vasculature present in several disease states that presents with elevated [[mean pulmonary artery pressure]] (PAP) as measured by [[right heart catheterization]] at rest. The factors that are involved in the pathophysiology of the increase in the mean pulmonary arterial pressure are: increase in pulmonary [[vascular resistance]], increase in the right-side cardiac output, and increase in the [[mean pulmonary venous pressure]]. [[Pulmonary arterial hypertension]] is characterized by [[endothelial]] dysfunction resulting from an imbalance between [[apoptosis]] and proliferation of pulmonary artery [[smooth muscle cells]] favoring the [[proliferation]]. The other types of [[pulmonary hypertension]] are caused by hemodynamic changes that result in increased [[pulmonary blood pressure]] or architectural changes to the lung or its [[vasculature]] that result in the same outcome.<br />
<br />
==Causes==<br />
<br />
The World Health Organization (WHO) has classified PH based on etiology into five distinct groups: Group 1 (pulmonary arterial hypertension - which may be related to heritable [[PAH]] due to genetic defects, connective tissue diseases such as [[rheumatoid arthritis]], [[systemic lupus erythematosus]], [[Raynaud Disease]], and mixed connective tissue disease, [[HIV]], drugs and toxins, and parasitic infections such as [[schistosomiasis]]), Group 2 (PH due to left heart failure), Group 3 (PH due to [[chronic lung disease]] and/or [[hypoxemia]]), Group 4 (PH due to [[chronic thromboembolic disease]]), and Group 5 (PH due to multifactorial mechanisms such as [[chronic hemolytic anemia]], [[sarcoidosis]], [[chronic kidney disease]], and [[myeloproliferative disorders]]).<br />
<br />
==Differentiating Pulmonary hypertension from Other Diseases==<br />
One of the most common initial presentations of patients with [[pulmonary hypertension]] is [[dyspnea]]; therefore, the differential diagnosis is very broad. As the disease progresses with time, more symptoms related to [[right ventricular hypertrophy]] and [[Right ventricular failure|failure]] occur; which further narrows down the differential diagnosis.<br />
<br />
==Epidemiology and Demographics==<br />
[[Pulmonary arterial hypertension]] has been considered as a disease of young women. The [[mean]] age of patients in the U.S. registry was 36 years old and the overall female-to-male [[ratio]] was 1.7:1. The [[prevalence]] of pulmonary hypertension is approximately 1.5-5 per 100,000 individuals.<br />
<br />
==Risk Factors==<br />
Pulmonary hypertension (PH) is a multifactorial disease involving genetic and environmental risk factors. Risk factors for pulmonary arterial hypertension include [[BMPR2]] [[mutation]], [[connective tissue disease]], [[HIV infection]], [[portal hypertension]], [[fenfluramine]] use, and [[congenital heart disease]] with [[shunt]]. [[Left heart]] and [[lung]] diseases are risk factors for PH. Patients with a [[hypercoagulable state]] (such as the presence of [[lupus anticoagulant]], deficiency of [[protein C]], [[protein S]], or [[antithrombin III]], [[Inflammation#Chronic inflammation|chronic inflammatory disorders]], [[Myeloproliferative syndrome|myeloproliferative syndromes]], and [[splenectomy]]) are at an increased risk for chronic [[thromboembolic]] pulmonary hypertension.<br />
<br />
==Screening==<br />
Patients with a known [[BMPR2]] [[mutation]], [[scleroderma]], and [[portal hypertension]] undergoing evaluation for [[liver transplantation]] should receive periodic screening for pulmonary hypertension (PH) through a thorough assessment of the presence of symptoms, physical examination, a [[chest X ray]], [[electrocardiography]], and an [[echocardiogram]]. Additional investigation with [[right heart catheterization]] should be performed if screening is suggestive of the presence of PH.<br />
<br />
==Natural History, Complications and Prognosis==<br />
The most common initial symptoms of [[pulmonary hypertension]] are [[dyspnea]], [[fatigue]], and [[syncope]]. There was an estimated median survival of 2.8 years for symptomatic patients who do not receive any treatment, with the most common cause of death as [[cor pulmonale]], but survival rates have been increasing as new forms of treatment become available. Despite such advances, [[prognosis]] is still poor.<br />
<br />
==Diagnosis==<br />
===Diagnostic Study of Choice===<br />
[[Pulmonary hypertension]] is defined by a mean pulmonary arterial pressure higher than 25mmHg. It can be assessed by [[echocardiography]], the diagnostic study of choice due to its low risk and useful information that it can provide, and [[right heart cardiac catheterization]] to confirm the diagnosis.<br />
<br />
===History and Symptoms===<br />
The hallmark of [[pulmonary hypertension]] is [[progressive dyspnea]]. The most common symptoms of [[pulmonary hypertension]] include [[dyspnea]], [[fatigue]], [[chest pain]] and [[syncope]] or [[presyncope]]. [[Ortner syndrome]] may also be seen (characterized by [[hoarseness]] due to compression of the left laryngeal nerve caused by enlargement of the pulmonary artery).<br />
<br />
===Physical Examination===<br />
Pulmonary hypertension (PH) can present with myriad physical findings that may be associated with PH or the underlying cause. Findings associated with pulmonary hypertension are usually associated with right heart failure or right heart overload, while other findings may be associated with underlying cause, such as thoracic deformities which may arise in the setting of [[COPD]], or [[sclerodactyly]] that may be seen in patients with [[scleroderma]]. Some may develop on a spectrum corresponding to the severity of the disease.<br />
<br />
===Laboratory Findings===<br />
There are no specific diagnostic lab findings associated with [[pulmonary hypertension]]. Despite that, several laboratory tests are required in the evaluation of a patient for pulmonary hypertension to assess its severity or possible associated causes. [[Biochemistry]], [[hematology]] and [[thyroid function tests]] are required in all patients with pulmonary hypertension. They are important for the diagnosis of [[chronic hemolytic anemia]], [[myeloproliferative disorder]]s, thyroid disorders and [[chronic renal failure]] on [[dialysis]].<br />
<br />
===ECG===<br />
Elevated pulmonary pressures in pulmonary hypertension (PH) can lead to [[right ventricular hypertrophy]] ([[RVH]]) and [[right atrial enlargement]] which can sometimes be observed on an [[electrocardiogram]] (ECG). The ECG findings of PH include [[right axis deviation]], [[right ventricular]] strain pattern, and [[P pulmonale]]. The ECG findings of PH are neither specific nor sensitive and their absence does not rule out the presence of PH.<br />
<br />
===Chest X Ray===<br />
A [[chest X-ray]] is abnormal in the majority of patients with pulmonary hypertension (PH); however, there is no correlation between the severity of PH and the findings on a chest X-ray. Findings of PH on a [[chest X-ray]] include [[pulmonary artery]] dilatation and right-sided enlargement of the heart. A [[chest X-ray]] allows the exclusion of left heart disease and lung disease that can lead to group 2 and group 3 PH, respectively.<br />
<br />
===CT===<br />
A [[lung]] CT scan is helpful in the differential diagnosis of [[pulmonary hypertension]]. Different types of CT imaging have been used to rule out certain etiologies of [[pulmonary hypertension]] and to evaluate the anatomy of the [[pulmonary vasculature]].<br />
<br />
===MRI===<br />
Thoracic MRI is helpful in the differential diagnosis of [[pulmonary hypertension]] as well as in the evaluation of the right ventricle function. It provides important prognostic indicators when assessing the right ventricle in patients with pulmonary hypertension. Findings that predict poor prognosis are: [[stroke volume]] ≤25ml/m^2, right ventricular [[end-diastolic volume]] ≥84ml/m^2 and left ventricular [[end-diastolic volume]] ≤40ml/m^2.<br />
<br />
===Echocardiography or Ultrasound===<br />
[[Echocardiography]] may demonstrate right ventricular or atrial enlargement with a thickened [[interventricular septum]] in patients with pulmonary hypertension, decreased right ventricular function, or hypertrophy. [[Pulmonary artery systolic pressure]] can also be estimated using echocardiography. Right ventricular afterload may be suggested by a leftward [[septal]] displacement during systole. [[Pericardial effusion]]s and diminished [[left ventricular]] cavity typically portend a dismal prognosis.<br />
<br />
===Other diagnostic studies===<br />
Pulmonary hypertension diagnosis is made using [[right heart cardiac catheterization]]. It is mandatory for diagnosing [[pulmonary arterial hypertension]]. It confirms the diagnosis and evaluates for some causes such as valvular heart diseases. Other studies may also be performed. These studies include [[pulmonary function tests]], overnight oximetry, and ventilation-perfusion studies (which is crucial to rule out [[chronic pulmonary thromboembolism]]).<br />
<br />
==Treatment==<br />
<br />
===Medical Therapy===<br />
The choice of treatment for pulmonary hypertension (PH) requires the assessment of the clinical severity of the disease and the identification of any underlying cause. Patients who have PH secondary to a medical condition such as [[left heart failure]], [[lung]] diseases, or [[Thromboembolism|thromboembolic disease]] (PH group 2, 3, and 4 respectively) should receive treatment for the underlying cause. Patients who have pulmonary arterial hypertension (PAH) must undergo vasoreactivity testing in order to assist in the selection of the optimal therapy which include [[Calcium channel blocker|calcium channel blockers]], [[endothelin receptor antagonist]], [[Phosphodiesterase inhibitor|phosphodiesterase inhibitors]], or [[Prostanoid|prostanoids]].<br />
<br />
===Surgery===<br />
Patients with severe [[Pulmonary hypertension classification#WHO Functional Classification|WHO functional class II or III]] pulmonary hypertension (PH) refractory to medical therapy are candidates for surgical intervention, such as [[atrial septostomy]] or [[lung transplantation]]. [[Pulmonary thromboendarterectomy]] (PTE) is a surgical procedure that is used for chronic [[thromboembolic]] pulmonary hypertension.<br />
<br />
===Primary Prevention===<br />
Genetic and environmental factors are involved in pulmonary hypertension (PH); therefore, not all cases of PH are preventable. PH that is secondary to other diseases such as [[left heart failure]], chronic [[lung]] disease, chronic [[liver]] disease, and [[Collagen vascular disease|collagen vascular diseases]] among others can be prevented by the early and optimal treatment of these medical conditions. Patients who are at elevated risk for developing pulmonary arterial hypertension (PAH) must be monitored for the occurrence of symptoms of PAH. Patients at risk for PAH include subjects with [[systemic sclerosis]] or with genetic predisposition.<br />
<br />
===Secondary Prevention===<br />
The recommended measures for the secondary prevention are avoiding pregnancy, rigorous follow up in case of pregnancy, avoid unnecessary surgeries, multidisciplinary care in case of necessary surgery, avoid high altitude, supplemental oxygen in order to ensure a target oxygen saturation of 91% in case of exposure to high altitude, and up-to-date immunizations against [[influenza]] and [[pneumococcal pneumonia]].<br />
<br />
==References==<br />
{{Reflist|2}}<br />
<br />
{{WH}}<br />
{{WS}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_other_diagnostic_studies&diff=1703602Pulmonary hypertension other diagnostic studies2021-06-09T15:51:00Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}; '''Assistant Editor(s)-in-Chief:''' [[User:Ralph Matar|Ralph Matar]]; [[User:Rim Halaby|Rim Halaby]]<br />
<br />
==Overview==<br />
Pulmonary hypertension diagnosis is made using [[right heart cardiac catheterization]]. It is mandatory for diagnosing [[pulmonary arterial hypertension]]. It confirms the diagnosis and evaluates for some causes such as valvular heart diseases. Other studies may also be performed. These studies include [[pulmonary function tests]], overnight oximetry, and ventilation-perfusion studies (which is crucial to rule out [[chronic pulmonary thromboembolism]]).<br />
<br />
==Key Findings in Right Heart Catheterization in Pulmonary Hypertension ==<br />
*Right heart catheterization allows the determination of:<ref name="pmid26621978">{{cite journal |vauthors=Rosenkranz S, Preston IR |title=Right heart catheterisation: best practice and pitfalls in pulmonary hypertension |journal=Eur Respir Rev |volume=24 |issue=138 |pages=642–52 |date=December 2015 |pmid=26621978 |doi=10.1183/16000617.0062-2015 |url=}}</ref><ref name="pmid25163757">{{cite journal |vauthors=Guo X, Liu M, Ma Z, Wang S, Yang Y, Zhai Z, Wang C, Zhai R |title=Flow characteristics of the proximal pulmonary arteries and vena cava in patients with chronic thromboembolic pulmonary hypertension: correlation between 3.0 T phase-contrast MRI and right heart catheterization |journal=Diagn Interv Radiol |volume=20 |issue=5 |pages=414–20 |date=2014 |pmid=25163757 |pmc=4463330 |doi=10.5152/dir.2014.13501 |url=}}</ref><ref name="pmid25146706">{{cite journal |vauthors=Greiner S, Jud A, Aurich M, Hess A, Hilbel T, Hardt S, Katus HA, Mereles D |title=Reliability of noninvasive assessment of systolic pulmonary artery pressure by Doppler echocardiography compared to right heart catheterization: analysis in a large patient population |journal=J Am Heart Assoc |volume=3 |issue=4 |pages= |date=August 2014 |pmid=25146706 |pmc=4310406 |doi=10.1161/JAHA.114.001103 |url=}}</ref><ref name="pmid23890907">{{cite journal |vauthors=D'Alto M, Romeo E, Argiento P, D'Andrea A, Vanderpool R, Correra A, Bossone E, Sarubbi B, Calabrò R, Russo MG, Naeije R |title=Accuracy and precision of echocardiography versus right heart catheterization for the assessment of pulmonary hypertension |journal=Int. J. Cardiol. |volume=168 |issue=4 |pages=4058–62 |date=October 2013 |pmid=23890907 |doi=10.1016/j.ijcard.2013.07.005 |url=}}</ref><ref name="pmid17174196">{{cite journal |vauthors=Hoeper MM, Lee SH, Voswinckel R, Palazzini M, Jais X, Marinelli A, Barst RJ, Ghofrani HA, Jing ZC, Opitz C, Seyfarth HJ, Halank M, McLaughlin V, Oudiz RJ, Ewert R, Wilkens H, Kluge S, Bremer HC, Baroke E, Rubin LJ |title=Complications of right heart catheterization procedures in patients with pulmonary hypertension in experienced centers |journal=J. Am. Coll. Cardiol. |volume=48 |issue=12 |pages=2546–52 |date=December 2006 |pmid=17174196 |doi=10.1016/j.jacc.2006.07.061 |url=}}</ref><ref name="pmid23260714">{{cite journal |vauthors=Taylor B, Rumbak M, Taylor SP, Solomon D |title=Early versus delayed right heart catheterization in evaluation of pulmonary arterial hypertension |journal=J. Heart Lung Transplant. |volume=32 |issue=1 |pages=137–8 |date=January 2013 |pmid=23260714 |doi=10.1016/j.healun.2012.10.004 |url=}}</ref> <br />
**Presence or absence of pulmonary hypertension, the underlying etiology, and the prognosis.<br />
**Prognostic markers such as right atrial pressure, [[cardiac output]], and [[mean pulmonary artery pressure]]. <br />
**Pulmonary venous pressures by measuring [[pulmonary capillary wedge pressure]] ([[PCWP]]). <br />
*[[Fick’s method]] is reliable in patients with PAH for the measurement of cardiac output:<br />
**Cardiac Output = oxygen consumption/arteriovenous oxygen difference x 100<br />
*Since end-expiratory intrathoracic pressure most closely correlates with atmospheric pressure, it is important that all right ventricular, pulmonary artery, pulmonary wedge, and left ventricular pressures be measured at end-expiration.<br />
<br />
*The causes of pulmonary hypertension can be classified into three categories which are each characterized by different ranges of values recorded by [[right heart catheterization]].<br />
** '''Pre-capillary pulmonary Hypertension''' (involving the [[pulmonary artery]] and arterioles)<br />
***PAH<br />
***[[Congenital heart diseases]] with [[Eisenmenger syndrome]]<br />
***[[Thromboembolism]]<br />
**'''Capillary pulmonary hypertension'''<br />
***Parenchymal lung diseases<br />
**'''Post capillary pulmonary hypertension (passive congestion that leads to elevated capillary wedge pressure)'''<br />
***[[Left heart failure]]<br />
***[[Mitral valve disease|Mitral valve diseases]]<br />
***[[Pulmonary veno-occlusive disease|Pulmonary veno-occlusive diseases]]<br />
<br />
* Accordingly, the expected results by [[right heart catheterization]] are:<br />
**'''Precapillary pulmonary hypertension'''<br />
***Mean pulmonary artery pressure > 25 mm Hg. In primary pulmonary hypertension the [[pulmonary artery]] [[diastolic pressure]] is much higher than the [[pulmonary capillary wedge pressure]]. <br />
***Capillary wedge pressure < 15 mm Hg (knowing that the normal [[PCWP]] or [[left ventricular end diastolic pressure]] (LVEDP) is less than 8 mmHg)<br />
***Cardiac output: normal<br />
**'''Postcapillary pulmonary hypertension'''<br />
***Mean Pulmonary artery pressure > 25 mm Hg<br />
***Capillary wedge pressure > 15 mm Hg. If the pulmonary hypertension is due to [[Left heart failure|left-sided heart failure]], and the pulmonary artery diastolic pressure in the pulmonary capillary wedge pressure will be both similarly elevated. <br />
***Cardiac output: normal or low<br />
<br><br />
[[Image:Elevated_PCWP.png|548x548px]]<br />
[[Image:Elevated_pulmonary_artery_pressure.png|540x540px]]<br />
<br />
==Other Diagnostic Studies==<br />
*The other diagnostic studies are as follows:<ref name="pmid12574693">{{cite journal| author=Presberg KW, Dincer HE| title=Pathophysiology of pulmonary hypertension due to lung disease. | journal=Curr Opin Pulm Med | year= 2003 | volume= 9 | issue= 2 | pages= 131-8 | pmid=12574693 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12574693 }} </ref><ref name="pmid17218563">{{cite journal| author=Minai OA, Pandya CM, Golish JA, Avecillas JF, McCarthy K, Marlow S et al.| title=Predictors of nocturnal oxygen desaturation in pulmonary arterial hypertension. | journal=Chest | year= 2007 | volume= 131 | issue= 1 | pages= 109-17 | pmid=17218563 | doi=10.1378/chest.06-1378 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17218563 }} </ref><br />
**'''[[Pulmonary function tests]]'''<br />
***The aim of [[pulmonary function tests]] is to detect any obstructive or restrictive patten of an underlying lung disease that might be causing the pulmonary hypertension. <br />
**'''Overnight oximetry'''<br />
***Overnights oximetry might be used in some patients with pulmonary hypertension in order to assess the necessity of [[oxygen therapy]] during sleep time. <br />
**'''Ventilation-perfusion studies'''<br />
***Ventilation-perfusion studies are done to rule out any [[thromboembolic]] diseases in the lungs.<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
==References==<br />
{{Reflist|2}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_natural_history&diff=1703601Pulmonary hypertension natural history2021-06-09T15:49:15Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}; '''Assistant Editor(s)-in-Chief: '''[[User:Ralph Matar|Ralph Matar]]; {{Jose}}<br />
<br />
==Overview==<br />
<br />
[[Pulmonary hypertension]] most common initial symptoms are [[dyspnea]], [[fatigue]], and [[syncope]]. There was an estimated median survival of 2.8 years for symptomatic patients who do not receive any treatment, with the most common cause of death as [[cor pulmonale]], but survival rates have been increasing as new forms of treatment become available. Despite such advances, [[prognosis]] is still poor.<br />
<br />
==Natural History==<br />
<br />
*The National Institutes of Health (NIH) Registry estimated a median survival of 2.8 years for symptomatic patients with idiopathic pulmonary hypertension who do not receive any treatment, with the cause of death usually being right ventricular failure ([[cor pulmonale]]).<ref name="pmid3605900">{{cite journal| author=Rich S, Dantzker DR, Ayres SM, Bergofsky EH, Brundage BH, Detre KM et al.| title=Primary pulmonary hypertension. A national prospective study. | journal=Ann Intern Med | year= 1987 | volume= 107 | issue= 2 | pages= 216-23 | pmid=3605900 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3605900 }} </ref> <br />
*The 1, 3,and 5-year survival rates for untreated patients with idiopathic pulmonary hypertension were 68%, 48%, and 34%, respectively.<ref name="pmid3605900">{{cite journal| author=Rich S, Dantzker DR, Ayres SM, Bergofsky EH, Brundage BH, Detre KM et al.| title=Primary pulmonary hypertension. A national prospective study. | journal=Ann Intern Med | year= 1987 | volume= 107 | issue= 2 | pages= 216-23 | pmid=3605900 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3605900 }} </ref><br />
<br />
*The median survival duration was even lower for patients with pulmonary hypertension that was associated with other diseases like [[portal hypertension]], and [[scleroderma]] (2-year survival of 40% if untreated).<br />
<br />
*A recent outcome study of those patients who had started treatment with [[bosentan]] demonstrated that 86% patients were alive at 3 years. <br />
<br />
*With multiple agents now available, combination therapy is increasingly used. Impact of these agents on survival is not known, since many of them have been developed only recently. It would not be unreasonable to expect median survival to extend past 10 years in the near future.<br />
<br />
==Complications==<br />
Complications that can develop as a result of [[pulmonary hypertension]] are:<ref name="pmid15249497" /><br />
* [[Right-sided heart failure]] ([[cor pulmonale]])<br />
* Blood clots<br />
* [[Arrhythmia]]<br />
* [[Hemoptysis]]<br />
<br />
==Prognosis==<br />
The prognosis of [[pulmonary hypertension]] is poor, but good with treatment. Without treatment, [[pulmonary hypertension]] will result in [[cor pulmonale]]. [[Pulmonary hypertension]] is associated with a 7 year mortality of 49%.<br />
<br />
*The long-term [[prognosis]] has been known to be poor, however outcomes have changed dramatically over the last two decades. This may be attributed to the use of newer [[drug therapy]], better overall care, and earlier diagnosis (lead time bias).<br />
<br />
*[[Elevated pulmonary arterial pressure]] on heart catheterization is a predictor of [[mortality]], especially if it is happening not only in the setting of [[myocarditis]] or [[decreased right ventricular ejection fraction]], but also [[COPD]]. Treatment of [[pulmonary hypertension]] in these morbidities does not affect outcomes.<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
*Survival rate at 5 years is 57%.<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
*Persistently elevated [[BNP]] or [[NT-proBNP]] levels, [[PAH]] associated with [[connective tissue disease]] or [[portal hypertension]] indicate poorer prognosis.<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
*Some people with this condition may have [[heart failure]] that could lead to death. Assessment of prognosis in patients with pulmonary arterial hypertension (PAH) is important since it influences both medical therapy and referral for [[transplantation]].<br />
<br />
*Mortality rate is 5.2-5.4 per 100,000 and is more common in African-Americans and women.<br />
<br />
*The most common cause of hospitalization is [[heart failure]].<br />
<br />
*The most common cause of death is [[right ventricular failure]] and not chronic lower [[respiratory disease]] as was once thought.<br />
<br />
*Surprisingly, patients with [[Eisenmenger syndrome]] have a more favorable hemodynamic profile and prognosis than adults with idiopathic or primary pulmonary hypertension.<ref>Hopkins WE,Ochoa LL, Richardson GW, Trulock EP(1996) Comparison of the hemodynamics and survival or patients with severe pulmonary hypertension or Eisenmenger Syndrome.</ref><br />
<br />
===Indicators of Poor Prognosis===<br />
Indicators of poor prognosis include:<br />
* Poor functional class<ref name="pmid15249497">{{cite journal| author=McLaughlin VV, Presberg KW, Doyle RL, Abman SH, McCrory DC, Fortin T et al.| title=Prognosis of pulmonary arterial hypertension: ACCP evidence-based clinical practice guidelines. | journal=Chest | year= 2004 | volume= 126 | issue= 1 Suppl | pages= 78S-92S | pmid=15249497 | doi=10.1378/chest.126.1_suppl.78S | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15249497 }} </ref><br />
* Poor exercise tolerance as assessed by the 6-minute-walk distance (6MWD)<ref name="pmid8532025">{{cite journal| author=Barst RJ, Rubin LJ, Long WA, McGoon MD, Rich S, Badesch DB et al.| title=A comparison of continuous intravenous epoprostenol (prostacyclin) with conventional therapy for primary pulmonary hypertension. | journal=N Engl J Med | year= 1996 | volume= 334 | issue= 5 | pages= 296-301 | pmid=8532025 | doi=10.1056/NEJM199602013340504 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8532025 }} </ref><br />
* Elevated [[brain natriuretic peptide]] ([[BNP]])<ref name="pmid20585012">{{cite journal| author=Benza RL, Miller DP, Gomberg-Maitland M, Frantz RP, Foreman AJ, Coffey CS et al.| title=Predicting survival in pulmonary arterial hypertension: insights from the Registry to Evaluate Early and Long-Term Pulmonary Arterial Hypertension Disease Management (REVEAL). | journal=Circulation | year= 2010 | volume= 122 | issue= 2 | pages= 164-72 | pmid=20585012 | doi=10.1161/CIRCULATIONAHA.109.898122 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20585012 }} </ref> or [[NT-proBNP]] levels.<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
* [[Pericardial effusion]]<ref name="pmid20585012">{{cite journal| author=Benza RL, Miller DP, Gomberg-Maitland M, Frantz RP, Foreman AJ, Coffey CS et al.| title=Predicting survival in pulmonary arterial hypertension: insights from the Registry to Evaluate Early and Long-Term Pulmonary Arterial Hypertension Disease Management (REVEAL). | journal=Circulation | year= 2010 | volume= 122 | issue= 2 | pages= 164-72 | pmid=20585012 | doi=10.1161/CIRCULATIONAHA.109.898122 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20585012 }} </ref><br />
* Persistently elevated right atrial size and pressure<ref name="pmid1863023">{{cite journal| author=D'Alonzo GE, Barst RJ, Ayres SM, Bergofsky EH, Brundage BH, Detre KM et al.| title=Survival in patients with primary pulmonary hypertension. Results from a national prospective registry. | journal=Ann Intern Med | year= 1991 | volume= 115 | issue= 5 | pages= 343-9 | pmid=1863023 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1863023 }} </ref><br />
* Significant right ventricular dysfunction or failure<ref name="pmid20585012">{{cite journal| author=Benza RL, Miller DP, Gomberg-Maitland M, Frantz RP, Foreman AJ, Coffey CS et al.| title=Predicting survival in pulmonary arterial hypertension: insights from the Registry to Evaluate Early and Long-Term Pulmonary Arterial Hypertension Disease Management (REVEAL). | journal=Circulation | year= 2010 | volume= 122 | issue= 2 | pages= 164-72 | pmid=20585012 | doi=10.1161/CIRCULATIONAHA.109.898122 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20585012 }} </ref><br />
* Low [[cardiac index]]<ref name="pmid1863023">{{cite journal| author=D'Alonzo GE, Barst RJ, Ayres SM, Bergofsky EH, Brundage BH, Detre KM et al.| title=Survival in patients with primary pulmonary hypertension. Results from a national prospective registry. | journal=Ann Intern Med | year= 1991 | volume= 115 | issue= 5 | pages= 343-9 | pmid=1863023 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1863023 }} </ref><br />
* Underlying connective tissue disease<ref name="pmid20585012">{{cite journal| author=Benza RL, Miller DP, Gomberg-Maitland M, Frantz RP, Foreman AJ, Coffey CS et al.| title=Predicting survival in pulmonary arterial hypertension: insights from the Registry to Evaluate Early and Long-Term Pulmonary Arterial Hypertension Disease Management (REVEAL). | journal=Circulation | year= 2010 | volume= 122 | issue= 2 | pages= 164-72 | pmid=20585012 | doi=10.1161/CIRCULATIONAHA.109.898122 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20585012 }} </ref><br />
* Decreased predicted carbon monoxide diffusing capacity<ref name="pmid20585012">{{cite journal| author=Benza RL, Miller DP, Gomberg-Maitland M, Frantz RP, Foreman AJ, Coffey CS et al.| title=Predicting survival in pulmonary arterial hypertension: insights from the Registry to Evaluate Early and Long-Term Pulmonary Arterial Hypertension Disease Management (REVEAL). | journal=Circulation | year= 2010 | volume= 122 | issue= 2 | pages= 164-72 | pmid=20585012 | doi=10.1161/CIRCULATIONAHA.109.898122 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20585012 }} </ref><br />
*[[PAH]] associated with [[connective tissue disease]] or [[portal hypertension]].<br />
<br />
==References==<br />
{{Reflist|2}}<br />
{{WikiDoc Help Menu}}<br />
{{WikiDoc Sources}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_MRI&diff=1703600Pulmonary hypertension MRI2021-06-09T15:45:36Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}, '''Assistant Editor(s)-in-Chief:''' [[User:Ralph Matar|Ralph Matar]]; {{Jose}}<br />
==Overview==<br />
Thoracic MRI is helpful in the differential diagnosis of [[pulmonary hypertension]] as well as in the evaluation of the right ventricle function. It provides important prognostic indicators when assessing the right ventricle in patients with pulmonary hypertension. Findings that predict poor prognosis are: [[stroke volume]] ≤25ml/m^2, right ventricular [[end-diastolic volume]] ≥84ml/m^2 and left ventricvular [[end-diastolic volume]] ≤40ml/m^2.<br />
<br />
==Key MRI Findings in [[Pulmonary Hypertension]]==<br />
A MRI is useful for:<ref name="pmid24344668">{{cite journal |vauthors=Alassas K, Mergo P, Ibrahim el-S, Burger C, Safford R, Parikh P, Shapiro B |title=Cardiac MRI as a diagnostic tool in pulmonary hypertension |journal=Future Cardiol |volume=10 |issue=1 |pages=117–30 |date=January 2014 |pmid=24344668 |doi=10.2217/fca.13.97 |url=}}</ref><ref name="pmid25145313">{{cite journal |vauthors=Lungu A, Wild JM, Capener D, Kiely DG, Swift AJ, Hose DR |title=MRI model-based non-invasive differential diagnosis in pulmonary hypertension |journal=J Biomech |volume=47 |issue=12 |pages=2941–7 |date=September 2014 |pmid=25145313 |doi=10.1016/j.jbiomech.2014.07.024 |url=}}</ref><ref name="pmid25161042">{{cite journal |vauthors=Ohira H, Beanlands RS, Davies RA, Mielniczuk L |title=The role of nuclear imaging in pulmonary hypertension |journal=J Nucl Cardiol |volume=22 |issue=1 |pages=141–57 |date=February 2015 |pmid=25161042 |doi=10.1007/s12350-014-9960-y |url=}}</ref><ref name="pmid23863980">{{cite journal |vauthors=Kreitner KF, Wirth GM, Krummenauer F, Weber S, Pitton MB, Schneider J, Mayer E, Dueber C |title=Noninvasive assessment of pulmonary hemodynamics in patients with chronic thromboembolic pulmonary hypertension by high temporal resolution phase-contrast MRI: correlation with simultaneous invasive pressure recordings |journal=Circ Cardiovasc Imaging |volume=6 |issue=5 |pages=722–9 |date=September 2013 |pmid=23863980 |doi=10.1161/CIRCIMAGING.112.000276 |url=}}</ref><ref name="pmid24756429">{{cite journal |vauthors=Wirth G, Brüggemann K, Bostel T, Mayer E, Düber C, Kreitner KF |title=Chronic thromboembolic pulmonary hypertension (CTEPH) - potential role of multidetector-row CT (MD-CT) and MR imaging in the diagnosis and differential diagnosis of the disease |journal=Rofo |volume=186 |issue=8 |pages=751–61 |date=August 2014 |pmid=24756429 |doi=10.1055/s-0034-1366425 |url=}}</ref><br />
*Accurate evaluation of the size, morphology and function of the [[right ventricle]].<br />
**A MRI has similar abilities to those of an [[echocardiography]] in the diagnosis and treatment of patients with pulmonary hypertension. <br />
<br />
*Detection of shunts contributing to pulmonary hypertension.<br />
<br />
*Detection of acute and chronic pulmonary [[thromboembolic]] disease.<br />
<br />
*Differentiation between the pulmonary [[vasculature]] and [[mediastinal]] [[adenopathy]] when used for contrast enhancement.<br />
<br />
*Follow-up for right heart [[hemodynamics]]. <br />
**Poor right ventricular function is indicated by the following according to the ACCF/AHA 2009 expert consensus document on pulmonary hypertension:<br />
*** [[Stroke volume]] ≤25ml/m^2.<br />
***Right ventricular [[end-diastolic volume]] ≥84ml/m^2( Most appropriate marker of right ventricular failure in the follow-up.)<br />
***Left ventricular [[end-diastolic volume]] ≤40ml/m^2<br />
<br />
*Pulmonary artery stiffness measured by relative cross sectional area change ≤16% also has implications on mortality rate.<br />
<br />
===MRI Limitations include===<br />
*Inability to perform breath hold<br />
<br />
*[[Claustrophobia]]<br />
<br />
*Incompatible hardware such as neurostimulators, [[cochlear implant]]s, aneurysm clips, cardiac pacemakers and [[defibrillator]]s<br />
<br />
*Limited availability and cost<br />
<br />
*Difficulty in assessing PA pressures<br />
<br />
==References==<br />
{{Reflist|2}}<br />
{{WikiDoc Help Menu}}<br />
{{WikiDoc Sources}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]<br />
[[Category:Radiology]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_medical_therapy&diff=1703598Pulmonary hypertension medical therapy2021-06-09T15:07:49Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}; '''Assistant Editor(s)-in-Chief:''' [[User:Ralph Matar|Ralph Matar]], [[User:Rim Halaby|Rim Halaby]]; {{Jose}}<br />
<br />
==Overview==<br />
The choice of treatment for pulmonary hypertension (PH) requires the assessment of the clinical severity of the [[disease]] and the identification of any underlying [[Causes|cause]]s. [[Patients]] who have PH secondary to a medical condition such as [[left heart failure]], [[lung]] diseases, or [[thromboembolism|thromboembolic disease]] (PH group 2, 3, and 4 respectively) should receive treatment for the underlying cause. [[Patients]] who have pulmonary arterial hypertension (PAH) must undergo vasoreactivity testing in order to assist in the selection of the optimal therapy which includes [[calcium channel blocker]]s, [[endothelin receptor antagonist]], [[phosphodiesterase inhibitor]]s, or [[prostanoid]]s.<br />
<br />
==Medical Therapy==<br />
<br />
*If [[pulmonary hypertension]] is secondary to another disease, treatment is largely focused on treating the underlying disease.<br />
*[[Oxygen]] is indicated for all [[causes]] of PH to maintain an oxygen saturation above 90% at exertion, rest or while sleeping. It is not effective in advanced [[Eisenmenger syndrome]].<br />
*[[Diuretics]] should be considered if there is important [[right heart dysfunction]].<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
===Treatment of PH due to Left Heart Disease===<br />
<br />
*Treatment must focus on [[left heart dysfunction]];<br />
*[[Prostacyclin analogues]], [[phosphodiesterase type 5 (PDE5) inhibitors]], [[endothelin-receptor antagonists]], and [[soluble guanylate cyclase]] (SGC) stimulators.<br />
*PH due to [[mitral valve dysfunction]] usually returns to normal after correction of the [[mitral valve disease]]<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref>.<br />
<br />
===Treatment of PH due to Lung Disease===<br />
<br />
*Only [[oxygen]] is proven to be effective;<br />
*Avoid periods of [[hypoxia]] and treat underlying disease;<br />
*There is no benefit in the use of [[pulmonary]] [[vasodilators]] in such cases.<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
===Treatment of PH due to Chronic Thromboembolic Disease===<br />
<br />
*Pulmonary [[thromboendarterectomy]] (PTE) may be curative;<br />
*[[Balloon pulmonary angioplasty]] may be recommended if [[patients]] are not candidates for (PTE) or if residual hypertension is still significant;<br />
*[[Riociguat]] may be effective for refractory cases or cases unsuitable for surgical treatment.<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
===Treatment Algorithm for PAH===<br />
<br />
*A [[right heart catheterization]] is essential to confirm the diagnosis of PH and should always be performed prior to the initiation of therapy.<br />
*If [[left heart failure]] is excluded as a cause of PH, then [[vasodilator]] testing must be performed to assist in the selection of the optimal therapy.<br />
*In the vasoreactivity test, a short acting [[vasodilator]] ([[prostanoid]]s, inhaled [[NO]], [[adenosine]]) is administered and the change in pulmonary arterial pressure (PAP) is assessed.<br />
*A fall in the mean PAP by more than 10 and less than 40 mmHg is considered a positive result. [[Patients]] who have a positive vasodilator response are started on oral [[calcium channel blocker]]s.<br />
*[[Calcium channel blocker]]s should not be administered to [[patients]] who are non-reactive to the vasoreactivity test. '''''[[Calcium channel blocker]] should not be used in patients with Eisenmenger syndrome.'''''<br />
*[[Patients]] who do not have a positive vasodilator response require other specific medical therapy as described below.<ref name="pmid19749199">{{cite journal| author=Task Force for Diagnosis and Treatment of Pulmonary Hypertension of European Society of Cardiology (ESC). European Respiratory Society (ERS). International Society of Heart and Lung Transplantation (ISHLT). Galiè N, Hoeper MM, Humbert M et al.| title=Guidelines for the diagnosis and treatment of pulmonary hypertension. | journal=Eur Respir J | year= 2009 | volume= 34 | issue= 6 | pages= 1219-63 | pmid=19749199 | doi=10.1183/09031936.00139009 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19749199 }} </ref><br />
<br />
Shown below is an algorithm depicting the optimal therapy for a patient with PAH.<ref name="pmid19749199">{{cite journal| author=Task Force for Diagnosis and Treatment of Pulmonary Hypertension of European Society of Cardiology (ESC). European Respiratory Society (ERS). International Society of Heart and Lung Transplantation (ISHLT). Galiè N, Hoeper MM, Humbert M et al.| title=Guidelines for the diagnosis and treatment of pulmonary hypertension. | journal=Eur Respir J | year= 2009 | volume= 34 | issue= 6 | pages= 1219-63 | pmid=19749199 | doi=10.1183/09031936.00139009 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19749199 }} </ref> <br />
<br />
{{Family tree/start}}<br />
{{Familytree | | | | | | | A01 | | | | | | | | A01= '''Supportive treatment:'''<br><div style="width:12em; text-align:left">[[Diuretics]] <br>+/-<br> [[Oxygen therapy]] <br>+/-<br>[[Oral anticoagulation therapy]] <br> +/-<br>[[Digoxin]] </div>}}<br />
{{Familytree | | | | | | | |!| | | | | | | | | }}<br />
{{Familytree | | | | | | | B01 | | | | | | | | B01= <div style="width:12em; text-align:left">'''What is the result of the acute vasoreactivity test?''' </div>}}<br />
{{Familytree | | | |,|-|-|-|^|-|-|-|.| | | | | }}<br />
{{Familytree | | | C01 | | | | | | C02 | | | | C01= Vasoreactive| C02= Non vasoreactive}}<br />
{{Familytree | | | |!| | | | | | | |!| | | | | }}<br />
{{Familytree | | | D01 | | |F|~|~| D02 | | | | D01= <div style="width:12em; text-align:left">What is the WHO functional class (FC)?</div>| D02= <div style="width:12em; text-align:left">What is the WHO functional class (FC)? </div>}}<br />
{{Familytree | | | |!| | | |:| |,|-|^|-|-|-|-|-|.| }}<br />
{{Familytree | | | E01 | | |:| E02 | | E03 | | E04 | E01= WHO FC I, II, or III| E02= WHO FC II| E03= WHO FC III| E04= WHO FC IV}}<br />
{{Familytree | | | |!| | | |:| |!| | | |!| | | |!| }}<br />
{{Familytree | | | F01 | | |:| F02 | | F03 | | F04 | F01= <div style="width:12em; text-align:left">Administer: <br> ❑ [[Calcium channel blocker]]</div>| F02= <div style="width:12em; text-align:left">Administer: <br> ❑ Endothelin receptor antagonist, or <br> ❑ Phosphodiesterase 5 inhibitor <br> ❑ Soluble guanylate cyclase stimulator </div>| F03= <div style="width:12em; text-align:left">Administer: <br> ❑ Endothelin receptor antagonist, or <br> ❑ Phosphodiesterase 5 inhibitor, or <br> ❑ Soluble guanylate cyclase stimulator, or <br> ❑ Prostanoids </div>| F04= Administer: <br> ❑ [[Prostanoid]]s}}<br />
{{Familytree | | | |!| | | |:| |`|-|-|-|+|-|-|-|'| }}<br />
{{Familytree | | | G01 | | |:| | | | | G02 | | | | | G01= <div style="width:12em; text-align:left">Is there a sustained response? </div>| G02= <div style="width:12em; text-align:left">Is there a sustained response? </div>}}<br />
{{Familytree | |,|-|^|-|.| |:| | | | | |!| | | | | }}<br />
{{Familytree | H01 | | H02 |J| | | | | H03 | | | | H01= Yes| H02= No| H03= <div style="width:12em; text-align:left">If no, administer combination therapy </div>}}<br />
{{Familytree | |!| | | | | | | | | | | |!| | | | | }}<br />
{{Familytree | I01 | | | | | | | | | | I02 | | | | I01= <div style="width:12em; text-align:left">Continue with [[calcium channel blockers]]s </div>|I02= <div style="width:12em; text-align:left">Is there a sustained response? </div>}}<br />
{{Familytree | | | | | | | | | | | | | |!| | | | | }}<br />
{{Familytree | | | | | | | | | | | | | J01 | | | | J01= <div style="width:12em; text-align:left">If no, lung transplantation </div>}}<br />
{{Familytree/end}}<br />
<br />
==Supportive Therapy==<br />
The supportive therapy for [[patients]] with pulmonary hypertension includes:<br />
<br />
*[[Diuretics]]: for [[right ventricular]] failure and [[fluid retention]].<br />
*[[Oxygen therapy]]: continuous [[oxygen therapy]] is needed for patients with oxygen saturation less than 90%.<br />
*[[Oral anticoagulation therapy]]: to decrease the risk of [[venous thromboembolism]] in [[patients]] with idiopathic PAH, heritable PAH, anorexigenic related PH, and possibly in associated PAH.<br />
*[[Digoxin]]: to improve cardiac muscle contractility in case of [[right heart failure]] and low [[cardiac output]] as well as to slow the ventricular rate in case of atrial [[tachycardia]].<br />
<br />
==Specific Drug Therapies in Treatment-Naïve PAH Patients==<br />
===WHO Functional Class I===<br />
[[Patients]] with WHO functional class I PAH or those at elevated risk of developing PAH, as in the case of [[systemic sclerosis]], should be monitored for the occurrence of PAH-related symptoms.<br />
<br />
===WHO Functional Class II===<br />
<br />
*Symptomatic patients with positive acute vasoreactivity testing should be administered a trial of [[calcium channel blocker]]s ([[amlodipine]], [[nifedipine]], or [[diltiazem]]) when no contraindications are present and in the absence of [[right heart failure]].<ref name="pmid24937180">{{cite journal| author=Taichman DB, Ornelas J, Chung L, Klinger J, Lewis S, Mandel J et al.| title=Pharmacological Therapy for Pulmonary Arterial Hypertension in Adults: CHEST Guideline. | journal=Chest | year= 2014 | volume= | issue= | pages= | pmid=24937180 | doi=10.1378/chest.14-0793 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24937180 }} </ref><br />
<br />
*[[Patients]] among whom [[calcium channel blocker]] trial failed to improve the clinical status or those who are not candidates for [[calcium channel blocker]]s should receive monotherapy with one of the following:<ref name="pmid24937180">{{cite journal| author=Taichman DB, Ornelas J, Chung L, Klinger J, Lewis S, Mandel J et al.| title=Pharmacological Therapy for Pulmon<br />
ary Arterial Hypertension in Adults: CHEST Guideline. | journal=Chest | year= 2014 | volume= | issue= | pages= | pmid=24937180 | doi=10.1378/chest.14-0793 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24937180 }} </ref><br />
**[[Endothelin receptor antagonist]] ([[bosentan]], [[ambrisentan]], [[macitentan]])<br />
**[[Phosphodiesterase-5 inhibitor|Phosphodiesterase 5 inhibitors]] ([[sildenafil]] and [[tadalafil]])<br />
**Soluble guanylate cyclase stimulator ([[riociguat]])<br />
<br />
*[[Prostanoid|Prostanoids]] are not indicated for the treatment of patients with WHO functional class II PAH.<ref name="pmid24937180">{{cite journal| author=Taichman DB, Ornelas J, Chung L, Klinger J, Lewis S, Mandel J et al.| title=Pharmacological Therapy for Pulmonary Arterial Hypertension in Adults: CHEST Guideline. | journal=Chest | year= 2014 | volume= | issue= | pages= | pmid=24937180 | doi=10.1378/chest.14-0793 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24937180 }} </ref><br />
<br />
===WHO Functional Class III===<br />
<br />
*Symptomatic [[patients]] with positive acute vasoreactivity testing should be administered a trial of [[calcium channel blocker]]s ([[amlodipine]], [[nifedipine]], or [[diltiazem]]) when no contraindications are present and in the absence of [[right heart failure]].<ref name="pmid24937180">{{cite journal| author=Taichman DB, Ornelas J, Chung L, Klinger J, Lewis S, Mandel J et al.| title=Pharmacological Therapy for Pulmonary Arterial Hypertension in Adults: CHEST Guideline. | journal=Chest | year= 2014 | volume= | issue= | pages= | pmid=24937180 | doi=10.1378/chest.14-0793 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24937180 }} </ref><br />
<br />
*[[Patients]] among whom [[calcium channel blocker]] trial failed to improve the clinical status or those who are not candidates for [[calcium channel blocker]]s should receive monotherapy with one of the following:<ref name="pmid24937180">{{cite journal| author=Taichman DB, Ornelas J, Chung L, Klinger J, Lewis S, Mandel J et al.| title=Pharmacological Therapy for Pulmonary Arterial Hypertension in Adults: CHEST Guideline. | journal=Chest | year= 2014 | volume= | issue= | pages= | pmid=24937180 | doi=10.1378/chest.14-0793 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24937180 }} </ref><br />
**[[Endothelin receptor antagonist]] ([[bosentan]], [[ambrisentan]], [[macitentan]])<br />
**[[Phosphodiesterase-5 inhibitor|Phosphodiesterase 5 inhibitors]] ([[sildenafil]] and [[tadalafil]])<br />
**Soluble guanylate cyclase stimulator ([[riociguat]])<br />
<br />
*[[Patients]] with WHO class III PAH whose disease is rapidly progressing and associated with poor [[prognostic]] markers, should be administered parenteral [[prostanoid]] as initial therapy instead of oral therapy.<ref name="pmid24937180">{{cite journal| author=Taichman DB, Ornelas J, Chung L, Klinger J, Lewis S, Mandel J et al.| title=Pharmacological Therapy for Pulmonary Arterial Hypertension in Adults: CHEST Guideline. | journal=Chest | year= 2014 | volume= | issue= | pages= | pmid=24937180 | doi=10.1378/chest.14-0793 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24937180 }} </ref><br />
**IV [[epoprostenol]]<br />
**IV [[treprostinil]]<br />
**Continuous SC [[treprostinil]]<br />
<br />
*[[Patients]] with WHO class III PAH whose symptoms are not improved on the initial therapy with either [[endothelin receptor antagonist]] or [[Phosphodiesterase-5 inhibitor|phosphodiesterase 5 inhibitors]] should receive any of the following as an add-on to their initial therapy:<ref name="pmid24937180">{{cite journal| author=Taichman DB, Ornelas J, Chung L, Klinger J, Lewis S, Mandel J et al.| title=Pharmacological Therapy for Pulmonary Arterial Hypertension in Adults: CHEST Guideline. | journal=Chest | year= 2014 | volume= | issue= | pages= | pmid=24937180 | doi=10.1378/chest.14-0793 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24937180 }} </ref><br />
**Inhaled [[treprostinil]] (3 inhalations (18 μg) every 6 hours, can titrate up to 9 inhalations (54 μg) every 6 hours)<br />
**Inhaled [[Iloprost]]<br />
<br />
*[[Patients]] with WHO class III PAH and rapid progression of the disease despite initial therapy with one or more oral medication should be administered parenteral or inhaled [[prostanoid]]s.<ref name="pmid24937180">{{cite journal| author=Taichman DB, Ornelas J, Chung L, Klinger J, Lewis S, Mandel J et al.| title=Pharmacological Therapy for Pulmonary Arterial Hypertension in Adults: CHEST Guideline. | journal=Chest | year= 2014 | volume= | issue= | pages= | pmid=24937180 | doi=10.1378/chest.14-0793 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24937180 }} </ref><br />
<br />
===WHO Functional Class IV===<br />
<br />
*The initial treatment for patients with WHO class IV PAH is a monotherapy with a parenteral [[prostanoid]]:<ref name="pmid24937180">{{cite journal| author=Taichman DB, Ornelas J, Chung L, Klinger J, Lewis S, Mandel J et al.| title=Pharmacological Therapy for Pulmonary Arterial Hypertension in Adults: CHEST Guideline. | journal=Chest | year= 2014 | volume= | issue= | pages= | pmid=24937180 | doi=10.1378/chest.14-0793 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24937180 }} </ref><br />
**Continuous IV [[epoprostenol]]<br />
**Continuous IV [[treprostinil]]<br />
**Continuous SC [[treprostinil]]<br />
<br />
*If the [[patient]] refuses or is unable to receive parenteral therapy, the alternative treatment is a combination of inhaled [[prostanoid]] ([[iloprost]] or [[treprostinil]]) and [[endothelin receptor antagonist]] ([[bosentan]]).<ref name="pmid24937180">{{cite journal| author=Taichman DB, Ornelas J, Chung L, Klinger J, Lewis S, Mandel J et al.| title=Pharmacological Therapy for Pulmonary Arterial Hypertension in Adults: CHEST Guideline. | journal=Chest | year= 2014 | volume= | issue= | pages= | pmid=24937180 | doi=10.1378/chest.14-0793 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24937180 }} </ref><br />
<br />
==Combination Therapies in Patients on Established PAH Treatment==<br />
[[Patients]] with WHO functional class III or IV whose clinical status is unacceptable despite monotherapy should receive an add-on to their treatment:<ref name="pmid24937180">{{cite journal| author=Taichman DB, Ornelas J, Chung L, Klinger J, Lewis S, Mandel J et al.| title=Pharmacological Therapy for Pulmonary Arterial Hypertension in Adults: CHEST Guideline. | journal=Chest | year= 2014 | volume= | issue= | pages= | pmid=24937180 | doi=10.1378/chest.14-0793 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24937180 }} </ref><br />
<br />
*If already on [[endothelin receptor antagonist]], add:<br />
**Inhaled [[iloprost]], or<br />
**Inhaled [[treprostinil]]<br />
**Soluble guanylate cyclase stimulator [[riociguat]] (if already on either [[bosentan]] or [[ambrisentan]])<br />
<br />
*If already on [[Phosphodiesterase-5 inhibitor|phosphodiesterase 5 inhibitor]], add:<br />
**Inhaled [[iloprost]], or<br />
**Inhaled [[treprostinil]], or<br />
**[[Macitentan]]<br />
<br />
*If already on inhaled [[prostanoid]], add:<br />
**[[Macitentan]], or<br />
**Soluble guanylate cyclase stimulator ( [[riociguat]])<br />
<br />
*If already on IV [[epoprostenol]]:<br />
**Up titrate IV [[epoprostenol]], or<br />
**Add [[sildenafil]]<br />
**Do not initiate [[bosentan]] simultaneously<br />
<br />
Patients with WHO functional class III or IV whose clinical status is unacceptable despite dual therapy with two classes of PAH specific medications should receive a third class added on to their treatment.<ref name="pmid24937180">{{cite journal| author=Taichman DB, Ornelas J, Chung L, Klinger J, Lewis S, Mandel J et al.| title=Pharmacological Therapy for Pulmonary Arterial Hypertension in Adults: CHEST Guideline. | journal=Chest | year= 2014 | volume= | issue= | pages= | pmid=24937180 | doi=10.1378/chest.14-0793 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24937180 }} </ref><br />
<br />
==List of All Specific Drug Therapies==<br />
Shown below is a table summarizing the class of recommendation and level of evidence for the different specific drug therapies by the WHO functional class of PAH according to the 2009 Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS), endorsed by the International Society of Heart and Lung Transplantation (ISHLT).<ref name="pmid19713419">{{cite journal| author=Galiè N, Hoeper MM, Humbert M, Torbicki A, Vachiery JL, Barbera JA et al.| title=Guidelines for the diagnosis and treatment of pulmonary hypertension: the Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS), endorsed by the International Society of Heart and Lung Transplantation (ISHLT). | journal=Eur Heart J | year= 2009 | volume= 30 | issue= 20 | pages= 2493-537 | pmid=19713419 | doi=10.1093/eurheartj/ehp297 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19713419 }} </ref><br />
<br />
{| style="cellpadding=0; cellspacing= 0; width: 600px;"<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align="center" |'''Medication'''<br />
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align="center" |'''WHO-FC II'''<br />
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align="center" |'''WHO-FC III'''<br />
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align="center" |'''WHO-FC IV'''<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |'''Calcium channel blockers'''<br />
| style="font-size: 100%; background: #F5F5F5" align="left" |I-C<br />
| style="font-size: 100%; background: #F5F5F5" align="left" |I-C<br />
| style="font-size: 100%; background: #F5F5F5" align="left" | --<br />
|-<br />
| colspan="4" style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |'''Endothelin receptor antagonsit'''<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |Ambrisentan<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |I-A<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |I-A<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |IIa-C<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |Bosentan<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |I-A<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |I-A<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |IIa-C<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |Sitaxentan<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |IIa-C<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |I-A<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |IIa-C<br />
|-<br />
| colspan="4" style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |'''Phosphodiesterase 5 inhibitor'''<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |Sildenafil<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |I-A<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |I-A<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |IIa-C<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |Tadalafil<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |I-B<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |I-B<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |IIa-C<br />
|-<br />
| colspan="4" style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |'''Prostanoids'''<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |Beraprost<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" | --<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |IIb-B<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" | --<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |Epoprostenol (IV)<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" | --<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |I-A<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |I-A<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |Iloprost (inhaled)<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" | --<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |I-A<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |IIa-C<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |Iloprost (IV)<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" | --<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |IIa-C<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |IIa-C<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |Treprostinil (subcutaneous)<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" | --<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |I-B<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |IIa-C<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |Treprostinil (IV)<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" | --<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |IIa-C<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |IIa-C<br />
|-<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |Treprostinil (Inhaled)<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" | --<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |I-B<br />
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |IIa-C<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |'''Initial drugs combination therapy'''<br />
| style="font-size: 100%; background: #F5F5F5" align="left" | --<br />
| style="font-size: 100%; background: #F5F5F5" align="left" | --<br />
| style="font-size: 100%; background: #F5F5F5" align="left" |IIa-C<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |'''Sequential drugs combination therapy'''<br />
| style="font-size: 100%; background: #F5F5F5" align="left" |IIa-C<br />
| style="font-size: 100%; background: #F5F5F5" align="left" |IIa-B<br />
| style="font-size: 100%; background: #F5F5F5" align="left" |IIa-B<br />
|}<br />
<br />
===Endothelin Receptor Antagonist===<br />
There has been a clear role for endothelin system in the pathogenesis of PAH. Endothelin-1 exerts vasoconstrictor and mitogenic effects by binding to two different receptor isoforms: ET-A and ET-B. It is blocked by these antagonists at the vascular smooth muscle.<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
FDA approved endothelin receptor antagonists are [[bosentan]], [[ambrisentan]], and [[macitentan]]<br />
<br />
*[[Bosentan]]: 62.5 mg PO bid for 4 weeks, then 125mg PO bid if there is no change in liver function tests;<br />
**Antagonizes both ET-A and ET-B receptors and was shown to improve haemodynamics, exercise capacity, functional class and delay progression of disease. It is started at 62.5 mg BID and up-titrated to 125 mg BID after 4 weeks.<br />
*[[Macitentan]]: 10mg PO qd; <br />
**Antagonizes both ET-A and ET-B receptors.<br />
*[[Ambrisentan]]: 5–10 mg PO qd;<br />
**Selective ET-A receptor antagonist. Proven to be efficacious on improving symptoms, exercise capacity, hemodynamics, and time to clinical worsening.<br />
*[[Sitaxentan]]: 100mg PO qd;<br />
**Selectively orally active ET-A receptor antagonist was also shown to improve exercise capacity and hemodynamics.<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
[[Side effects]]: <br />
<br />
*[[Hepatotoxicity]], [[headache]], [[edema]], [[anemia]].<br />
*Do not use in pregnancy.<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
===Phosphodiesterase Type-5 Inhibitors===<br />
Inhibiting cGMP-degrading enzymes leads to increased levels of cGMP and subsequently improved vasodilation. All phosphodiesterase inhibitors originally approved for the treatment of erectile dysfunction cause significant pulmonary vasodilation:<br />
<br />
*[[Sildenafil]]:: 20 mg PO tid;<br />
**Daily Maximum effect is observed after 60min from administration of the drug. It's orally active, potent and a selective type-5 phosphodiesterase inhibitor. Favorable effects on symptoms, hemodynamics and exercise capacity were shown in several studies.<br />
*[[Tadalafil]]: 40 mg PO qd;<br />
**Maximum effects observed after 75-90min. Single daily dose is available. Studies showed favorable results on symptoms, hemodynamics, exercise capacity, and times to clinical worsening when the largest dose was used.<br />
<br />
[[Side effects]]: <br />
<br />
*Headache, dyspepsia, flushing, epistaxis, hypotension.<br />
*Do not use them with [[nitrates]].<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
===Prostanoids===<br />
[[Prostacyclin]]s are potent vasodilators and potent inhibitors of [[platelet]] aggregation in vascular beds. Patients with PAH have been shown to have low levels [[prostacyclin]] levels, so stable analogues of [[prostacyclin]] have been made for that purpose. These drugs increase intracellular production of [[cAMP]].<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
FDA approved prostanoids are [[epoprostenol]], [[iloprost]], and [[treprostinil]].<br />
<br />
*[[Epoprostenol]]: (start at 2ng/kg/min and titrate according patient symptoms and exercise capacity)<br />
*[[Iloprost]]: 2.5-5mcg inhaled 6-9 times daily<br />
*[[Treprostinil]]: different delivery methods are currently available.<br />
*[[Selexipag]]: 200mcg PO bid up to maximum dose of 1600mcg bid or patients' tolerance.<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
Side effects:<br />
<br />
*[[Headache]], [[masticatory jaw pain]], [[hypotension]], [[flushing]], [[nausea]], [[diarrhea]], [[rash]].<br />
*[[Cough]] may occur if inhaled;<br />
*Risk of [[cellulitis]].<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
===Soluble Guanylate Cyclase Stimulator===<br />
<br />
*[[Riociguat]]: initiate 0.5-1mg PO tid, increase by 0.5mg every 2 weeks until 2.5mg tid is reached or up to the level where patient's tolerance allows.<br />
<br />
Side effects:<br />
<br />
*Hypotension, dyspepsia;<br />
*Do not use in pregnancy.<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
===Calcium Channel Blockers===<br />
[[Calcium channel blockers]] use must be limited to a few selected patients. These medications are effective for patients who present at the time of heart catheterization with a positive vasoreactivity response. Less than 10% of patients have any improvement and this response is a strong predictor of better prognosis.<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref> Their mode of action is characterized by a decrease in [[smooth muscle]] hypertrophy, hyperplasia and vasoconstriction. [[CCB]] should be started at a low dose and then progressively increase it:<ref name="pmid19749199">{{cite journal| author=Task Force for Diagnosis and Treatment of Pulmonary Hypertension of European Society of Cardiology (ESC). European Respiratory Society (ERS). International Society of Heart and Lung Transplantation (ISHLT). Galiè N, Hoeper MM, Humbert M et al.| title=Guidelines for the diagnosis and treatment of pulmonary hypertension. | journal=Eur Respir J | year= 2009 | volume= 34 | issue= 6 | pages= 1219-63 | pmid=19749199 | doi=10.1183/09031936.00139009 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19749199 }} </ref><br />
<br />
*[[Nifedipine]]: Starting dose 30 mg bid; target dose: 120-240 mg/day<br />
*[[Diltiazem]]: Starting dose 60 mg tid; target dose: 240-720 mg/day<br />
*[[Amlodipine]]: Starting dose 2.5 mg qd; target dose: 20 mg/day<br />
<br />
[[Nifedipine]] and [[amlodipine]] are preferred in cases of relative [[bradycardia]], whereas [[diltiazem]] is preferred in cases of relative [[tachycardia]].<br />
<br />
Patients who are started on CCB should receive a follow up within the next 3 to 4 months to assess for CCB efficacy and tolerability.<ref name="pmid19749199">{{cite journal| author=Task Force for Diagnosis and Treatment of Pulmonary Hypertension of European Society of Cardiology (ESC). European Respiratory Society (ERS). International Society of Heart and Lung Transplantation (ISHLT). Galiè N, Hoeper MM, Humbert M et al.| title=Guidelines for the diagnosis and treatment of pulmonary hypertension. | journal=Eur Respir J | year= 2009 | volume= 34 | issue= 6 | pages= 1219-63 | pmid=19749199 | doi=10.1183/09031936.00139009 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19749199 }} </ref><br />
<br />
==Treatment Consideration in Other Types of PH==<br />
<br />
*There is no clear recommendations regarding the medical therapy in pulmonary veno-occlusive disease and pulmonary capillary haemangiomatosis. Caution should be taken with the administration of [[vasodilators]], particularly [[prostanoid]]s, due to the increased risk of pulmonary edema.<ref name="pmid9603154">{{cite journal| author=Humbert M, Maître S, Capron F, Rain B, Musset D, Simonneau G| title=Pulmonary edema complicating continuous intravenous prostacyclin in pulmonary capillary hemangiomatosis. | journal=Am J Respir Crit Care Med | year= 1998 | volume= 157 | issue= 5 Pt 1 | pages= 1681-5 | pmid=9603154 | doi=10.1164/ajrccm.157.5.9708065 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9603154 }} </ref><ref name="pmid19118230">{{cite journal| author=Montani D, Price LC, Dorfmuller P, Achouh L, Jaïs X, Yaïci A et al.| title=Pulmonary veno-occlusive disease. | journal=Eur Respir J | year= 2009 | volume= 33 | issue= 1 | pages= 189-200 | pmid=19118230 | doi=10.1183/09031936.00090608 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19118230 }} </ref><br />
<br />
*Patients with PH secondary to [[left heart failure]] should receive an optimal therapy for their heart failure problem. The medications for PH are not contraindicated among these patients.<br />
<br />
*Long term [[oxygen therapy]] is the treatment of choice among patients with PH secondary to lung diseases. These patients should not be administered [[vasodilators]] because they cause inhibit [[hypoxic]] [[vasoconstriction]] in the pulmonary circulation.<br />
<br />
*Patients with chronic [[thromboembolic]] pulmonary hypertension require a life long administration of [[anticoagulation therapy]].<br />
<br />
==General Measures==<br />
====Exercise====<br />
<br />
*Rehabilitation of sedentary individuals is crucial. [[Patients]] must be encouraged to maintain physical activity despite [[PAH]] symptoms. Mild [[dyspnea]] is acceptable, but [[chest pain]], near [[syncope]], severe [[breathlessness]] should be avoided.<br />
*[[Isometric exercises]] should be discouraged.<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
====Pregnancy====<br />
<br />
*[[Patients]] with PAH should avoid [[pregnancy]]. [[Patients]] on PAH specific should receive dual [[contraceptive]]. [[Oral contraceptive|Estrogen-containing contraceptives]] should be avoided because they increase the risk of [[venous thromboembolism]].<br />
*If [[pregnancy]] occurs, a multidisciplinary team should take care of the [[patients]]. [[Bosentan]], [[ambrisentan]], [[macitentan]], and [[riociguat]] are contraindicated in [[pregnancy]].<br />
<br />
====Altitude and Air Travel====<br />
<br />
*[[Patients]] with PAH should avoid high altitude. In case of exposure to high altitude or travel, patients should receive supplemental [[oxygen therapy]] (oxygen saturation >92%)<br />
<br />
====Vaccination====<br />
[[Patients]] with PAH should have an up-to-date [[vaccination]] against [[influenza]] and [[pneumococcus]].<br />
<br />
====General anesthesia====<br />
<br />
*[[Epidural]] rather than [[General anaesthesia|general anesthesia]] should be administered for surgical procedures given the potential for [[Hypotension (patient information)|hypotension]].<br />
<br />
====Oxygen====<br />
<br />
*In-flight [[oxygen]] should be considered for those patients who have an oxygen saturation <12%.<br />
<br />
====Anticoagulation====<br />
<br />
*[[Anticoagulation]] should be considered in [[patients]] with pulmonary hypertension in the absence of [[Hemoptysis (patient information)|hemoptysis]].<br />
<br />
====Phlebotomy====<br />
<br />
*[[Phlebotomy]] should be used if the [[hemoglobin]] is greater than 20 and/or the [[hematocrit]] is greater than 65% or if [[symptoms]] of hyper viscosity develop.<br />
<br />
===Contraindicated medications===<br />
{{MedCondContrAbs<br />
<br />
|MedCond =Pulmonary hypertension|Esmolol}}<br />
<br />
==ESC/ERS (2009) Recommendations for the Treatment of Pulmonary Hypertension (DO NOT EDIT) <ref name="pmid22015568">{{cite journal| author=Nakanishi N, European Society of Cardiology. European Respiratory Society| title=2009 ESC/ERS pulmonary hypertension guidelines and connective tissue disease. | journal=Allergol Int | year= 2011 | volume= 60 | issue= 4 | pages= 419-24 | pmid=22015568 | doi=10.2332/allergolint.11-RAI-0362 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22015568 }} </ref>==<br />
<br />
===General Measures (DO NOT EDIT) <ref name="pmid22015568">{{cite journal| author=Nakanishi N, European Society of Cardiology. European Respiratory Society| title=2009 ESC/ERS pulmonary hypertension guidelines and connective tissue disease. | journal=Allergol Int | year= 2011 | volume= 60 | issue= 4 | pages= 419-24 | pmid=22015568 | doi=10.2332/allergolint.11-RAI-0362 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22015568 }} </ref>===<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LightGreen" |[[European society of cardiology#Classes of Recommendations|Class I]]<br />
|-<br />
| bgcolor="LightGreen" |<nowiki>"</nowiki>'''1.''' It is recommended to avoid pregnancy in patients with PAH. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LightGreen" |<nowiki>"</nowiki>'''2.''' Immunization of PAH patients against [[influenza]] and pneumococcal infections is recommended. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LightCoral" |[[European society of cardiology#Classes of Recommendations|Class III]]<br />
|-<br />
| bgcolor="LightCoral" |<nowiki>"</nowiki>'''1.''' Excessive physical activity that leads to distressing symptoms is not recommended in patients with PAH. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LemonChiffon" |[[European society of cardiology#Classes of Recommendations|Class IIa]]<br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''1.''' Physically deconditioned PAH patients should be considered for supervised exercise rehabilitation. ''([[European society of cardiology#Level of Evidence|Level of Evidence: B]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''2.''' Psychosocial support should be considered in patients with PAH. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''3.''' In-flight oxygen administration should be considered for patients in WHO-FC III and IV and those with arterial oxygen pressure consistently less than 60mmHg [[CAD|coronary disease]]. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''4.''' [[Epidural anesthesia]] instead of [[general anesthesia]] should be utilized if possible for elective surgery. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
===Supportive Therapy (DO NOT EDIT) <ref name="pmid22015568">{{cite journal| author=Nakanishi N, European Society of Cardiology. European Respiratory Society| title=2009 ESC/ERS pulmonary hypertension guidelines and connective tissue disease. | journal=Allergol Int | year= 2011 | volume= 60 | issue= 4 | pages= 419-24 | pmid=22015568 | doi=10.2332/allergolint.11-RAI-0362 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22015568 }} </ref>===<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LightGreen" |[[European society of cardiology#Classes of Recommendations|Class I]]<br />
|-<br />
| bgcolor="LightGreen" |<nowiki>"</nowiki>'''1.''' Diuretic treatment is indicated in PAH patients with signs of [[RV failure]] and fluid retention. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LightGreen" |<nowiki>"</nowiki>'''2.''' Continuous long-term [[oxygen therapy]] is indicated in [[PAH]] patients when arterial oxygen pressure is consistently less than 60mmHg. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LemonChiffon" |[[European society of cardiology#Classes of Recommendations|Class IIa]]<br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''1.''' Oral [[anticoagulant]] treatment should be considered in patients with IPAH, heritable PAH, and PAH due to use of anorexigens. ''([[European society of cardiology#Level of Evidence|Level of Evidence: B]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LemonChiffon" |[[European society of cardiology#Classes of Recommendations|Class IIb]]<br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''1.''' Oral [[anticoagulant]] treatment should be considered in patients with APAH. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''2.''' [[Digoxin]] may be considered in patients with PAH who develop [[atrial tachyarrhythmias]] to slow ventricular rate. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
===PAH Associated with Congenital Cardiac Shunts (DO NOT EDIT) <ref name="pmid22015568">{{cite journal| author=Nakanishi N, European Society of Cardiology. European Respiratory Society| title=2009 ESC/ERS pulmonary hypertension guidelines and connective tissue disease. | journal=Allergol Int | year= 2011 | volume= 60 | issue= 4 | pages= 419-24 | pmid=22015568 | doi=10.2332/allergolint.11-RAI-0362 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22015568 }} </ref>===<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LightGreen" |[[European society of cardiology#Classes of Recommendations|Class I]]<br />
|-<br />
| bgcolor="LightGreen" |<nowiki>"</nowiki>'''1.''' Bosentan (Endothelin receptor antagonist) is indicated in WHO-FC III patients with [[Eisenmenger syndrome]]. ''([[European society of cardiology#Level of Evidence|Level of Evidence: B]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LightCoral" |[[European society of cardiology#Classes of Recommendations|Class III]]<br />
|-<br />
| bgcolor="LightCoral" |<nowiki>"</nowiki>'''1.''' The use of CCB is not recommended in patients with [[Eisenmenger's syndrome]]. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LemonChiffon" |[[European society of cardiology#Classes of Recommendations|Class IIa]]<br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''1.''' Other endothelin receptor antagonist, [[phosphodiesterase inhibitors]], and [[prostanoid]]s should be considered in patients with [[Eisenmenger's syndrome]]. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''2.''' In the absence of significant [[hemoptysis|haemoptysis]], oral coagulant treatment should be considered in patients with PA thrombosis or signs of [[heart failure]]. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''3.''' The use of supplemental [[oxygen therapy]] should be considered in cases in which it produces a consistent increase in arterial oxygen saturation and reduces symptoms. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''4.''' If symptoms of [[hyperviscosity]] are present, [[phlebotomy]] with isovolumic replacement should be considered usually when the [[hematocrit|haematocrit]] is > 65%. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LemonChiffon" |[[European society of cardiology#Classes of Recommendations|Class IIb]]<br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''1.''' Combination therapy may be considered in patients with [[Eisenmenger's syndrome]]. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
===PAH Associated with Connective Tissue Diseases (CTD) (DO NOT EDIT) <ref name="pmid22015568">{{cite journal| author=Nakanishi N, European Society of Cardiology. European Respiratory Society| title=2009 ESC/ERS pulmonary hypertension guidelines and connective tissue disease. | journal=Allergol Int | year= 2011 | volume= 60 | issue= 4 | pages= 419-24 | pmid=22015568 | doi=10.2332/allergolint.11-RAI-0362 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22015568 }} </ref>===<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LightGreen" |[[European society of cardiology#Classes of Recommendations|Class I]]<br />
|-<br />
| bgcolor="LightGreen" |<nowiki>"</nowiki>'''1.''' In patients with PAH associated with CTD the same treatment algorithm as in patients with IPAH is recommended. ''([[European society of cardiology#Level of Evidence|Level of Evidence: A]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LightGreen" |<nowiki>"</nowiki>'''2.''' Echocardiographic screening for the detection of PH is recommended in symptomatic patients with [[scleroderma]] spectrum of diseases. ''([[European society of cardiology#Level of Evidence|Level of Evidence: B]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LightGreen" |<nowiki>"</nowiki>'''3.''' Echocardiographic screening for the detection of PH is recommended in symptomatic patients with all other CTDs. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LightGreen" |<nowiki>"</nowiki>'''4.''' [[Right heart catheterization]] is indicated in all cases of suspected PAH associated with CTDs, in particular if specific drug therapy is considered. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LemonChiffon" |[[European society of cardiology#Classes of Recommendations|Class IIa]]<br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''1.''' Oral anticoagulation should be considered on an individual basis. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LemonChiffon" |[[European society of cardiology#Classes of Recommendations|Class IIb]]<br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''1.''' Echocardiographic screening for the detection of PH is recommended in symptomatic patients with scleroderma spectrum of diseases. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
===PAH Associated with Portal Hypertension (DO NOT EDIT) <ref name="pmid22015568">{{cite journal| author=Nakanishi N, European Society of Cardiology. European Respiratory Society| title=2009 ESC/ERS pulmonary hypertension guidelines and connective tissue disease. | journal=Allergol Int | year= 2011 | volume= 60 | issue= 4 | pages= 419-24 | pmid=22015568 | doi=10.2332/allergolint.11-RAI-0362 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22015568 }} </ref>===<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LightGreen" |[[European society of cardiology#Classes of Recommendations|Class I]]<br />
|-<br />
| bgcolor="LightGreen" |<nowiki>"</nowiki>'''1.''' Echocardiographic screening for the detection of PH is recommended in symptomatic patients with [[liver diseases]] and/or in candidates for [[liver transplantation]]. ''([[European society of cardiology#Level of Evidence|Level of Evidence: B]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LightCoral" |[[European society of cardiology#Classes of Recommendations|Class III]]<br />
|-<br />
| bgcolor="LightCoral" |<nowiki>"</nowiki>'''1.''' Anticoagulation is not recommended in patients with increased risk of [[bleeding]]. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LightCoral" |<nowiki>"</nowiki>'''2.''' Significant PAH is a contraindication to [[liver transplantation]] if mean PAP is .35 mmHg and/or [[pulmonary vascular resistance]] is > 250 dynes.s.cm^-5 ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LemonChiffon" |[[European society of cardiology#Classes of Recommendations|Class IIa]]<br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''1.''' In patients with pulmonary arterial hypertension associated with [[portal hypertension]] the same treatment algorithm as in patients with idiopathic pulmonary hypertension should be considered, taking into consideration co-morbidities. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
===PAH Associated with Human Immunodeficiency Virus Infection (DO NOT EDIT) <ref name="pmid22015568">{{cite journal| author=Nakanishi N, European Society of Cardiology. European Respiratory Society| title=2009 ESC/ERS pulmonary hypertension guidelines and connective tissue disease. | journal=Allergol Int | year= 2011 | volume= 60 | issue= 4 | pages= 419-24 | pmid=22015568 | doi=10.2332/allergolint.11-RAI-0362 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22015568 }} </ref>===<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LightGreen" |[[European society of cardiology#Classes of Recommendations|Class I]]<br />
|-<br />
| bgcolor="LightGreen" |<nowiki>"</nowiki>'''1.''' [[Echocardiography]] is indicated in patients with unexplained [[dyspnea]] to detect HIV-related cardiovascular complications. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LightCoral" |[[European society of cardiology#Classes of Recommendations|Class III]]<br />
|-<br />
| bgcolor="LightCoral" |<nowiki>"</nowiki>'''1.''' [[Anticoagulation]] is not recommended in patients with increased risk of bleeding. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LemonChiffon" |[[European society of cardiology#Classes of Recommendations|Class IIa]]<br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''1.''' In patients with pulmonary arterial hypertension associated with [[HIV|HIV-infection]] the same treatment algorithm as in patients with idiopathic pulmonary hypertension should be considered, taking into consideration co-morbidities and drug-drug interactions. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
===PAH Associated with Pulmonary Veno-Occlusive Disease(PVOD) (DO NOT EDIT) <ref name="pmid22015568">{{cite journal| author=Nakanishi N, European Society of Cardiology. European Respiratory Society| title=2009 ESC/ERS pulmonary hypertension guidelines and connective tissue disease. | journal=Allergol Int | year= 2011 | volume= 60 | issue= 4 | pages= 419-24 | pmid=22015568 | doi=10.2332/allergolint.11-RAI-0362 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22015568 }} </ref>===<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LightGreen" |[[European society of cardiology#Classes of Recommendations|Class I]]<br />
|-<br />
| bgcolor="LightGreen" |<nowiki>"</nowiki>'''1.''' Referral of patients with [[Pulmonary vein stenosis|PVOD]] to a transplant center for evaluation is indicated as soon as the diagnosis is established. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LemonChiffon" |[[European society of cardiology#Classes of Recommendations|Class IIa]]<br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''1.''' Patients with [[Pulmonary vein stenosis|PVOD]] should be managed only in centers with extensive experience in pulmonary arterial hypertension due to the risk of lung edema after the initiation of PAH-specific drug therapy. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
===PH Associated with Left Heart Disease (DO NOT EDIT) <ref name="pmid22015568">{{cite journal| author=Nakanishi N, European Society of Cardiology. European Respiratory Society| title=2009 ESC/ERS pulmonary hypertension guidelines and connective tissue disease. | journal=Allergol Int | year= 2011 | volume= 60 | issue= 4 | pages= 419-24 | pmid=22015568 | doi=10.2332/allergolint.11-RAI-0362 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22015568 }} </ref>===<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LightGreen" |[[European society of cardiology#Classes of Recommendations|Class I]]<br />
|-<br />
| bgcolor="LightGreen" |<nowiki>"</nowiki>'''1.''' The optimal treatment of the underlying left heart disease is recommended in patients with pulmonary hypertension due to left heart disease. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LightCoral" |[[European society of cardiology#Classes of Recommendations|Class III]]<br />
|-<br />
| bgcolor="LightCoral" |<nowiki>"</nowiki>'''1.''' The use of PAH specific drug therapy is not recommended in patients with pulmonary hypertension due to left [[heart disease]]. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LemonChiffon" |[[European society of cardiology#Classes of Recommendations|Class IIa]]<br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''1.''' Patient with "out of proportion" pulmonary hypertension due to left heart disease should be enrolled in randomized controlled trials targeting pulmonary hypertension specific drugs. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LemonChiffon" |[[European society of cardiology#Classes of Recommendations|Class IIb]]<br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''1.''' Increased left-sided filling pressures may be estimated by [[Doppler echocardiography]]. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''2.''' Invasive measurements of [[pulmonary wedge pressure]] of left ventricular end-diastolic pressure may be required to confirm the diagnosis of pulmonary hypertension due to left heart disease. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''3.''' [[Right heart catheterization]] may be considered in patients with echocardiographic signs suggesting severe pulmonary hypertension in patients with left heart disease. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
===PH Associated with Lung Disease (DO NOT EDIT) <ref name="pmid22015568">{{cite journal| author=Nakanishi N, European Society of Cardiology. European Respiratory Society| title=2009 ESC/ERS pulmonary hypertension guidelines and connective tissue disease. | journal=Allergol Int | year= 2011 | volume= 60 | issue= 4 | pages= 419-24 | pmid=22015568 | doi=10.2332/allergolint.11-RAI-0362 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22015568 }} </ref>===<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LightGreen" |[[European society of cardiology#Classes of Recommendations|Class I]]<br />
|-<br />
| bgcolor="LightGreen" |<nowiki>"</nowiki>'''1.''' Echocardiography is recommended as a screening tool for the assessment of PH due to lung diseases. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LightGreen" |<nowiki>"</nowiki>'''2.''' [[Right heart catheterization]] is recommended for a definite diagnosis of pulmonary hypertension due to [[lung diseases]]. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LightGreen" |<nowiki>"</nowiki>'''3.''' The optimal treatment of the underlying lung disease including long-term [[oxygen therapy]] in patients with chronic [[hypoxemia]] is recommended in patients with pulmonary hypertension due to [[lung diseases]]. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LightCoral" |[[European society of cardiology#Classes of Recommendations|Class III]]<br />
|-<br />
| bgcolor="LightCoral" |<nowiki>"</nowiki>'''1.''' The use of PAH specific drug therapy is not recommended in patients with pulmonary hypertension due to [[lung disease]]s. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LemonChiffon" |[[European society of cardiology#Classes of Recommendations|Class IIa]]<br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''1.''' Patients with "out of proportion" pulmonary hypertension due to lung diseases should be enrolled in randomized controlled trials targeting PAH-specific drugs. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
===PH Associated with Chronic Thromboembolic Pulmonary Hypertension(CTEPH) (DO NOT EDIT) <ref name="pmid22015568">{{cite journal| author=Nakanishi N, European Society of Cardiology. European Respiratory Society| title=2009 ESC/ERS pulmonary hypertension guidelines and connective tissue disease. | journal=Allergol Int | year= 2011 | volume= 60 | issue= 4 | pages= 419-24 | pmid=22015568 | doi=10.2332/allergolint.11-RAI-0362 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22015568 }} </ref>===<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LightGreen" |[[European society of cardiology#Classes of Recommendations|Class I]]<br />
|-<br />
| bgcolor="LightGreen" |<nowiki>"</nowiki>'''1.''' The diagnosis of CTEPH is based on the presence of pre-capillary pulmonary hypertension(mean PAH>25mmHg,PWP<15mmHg,Pulmonary vascular resistance>2 Wood units) in patients with multiple chronic/organized occlusive thrombi/emboli in the elastic pulmonary arteries (main, lobar, segmental, subsegmental). ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LightGreen" |<nowiki>"</nowiki>'''2.''' In patients with CTEPH, lifelong anticoagulation is indicated. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LightGreen" |<nowiki>"</nowiki>'''3.''' Surgical pulmonary endarterectomy is the recommended treatment for patients with CTEPH. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LemonChiffon" |[[European society of cardiology#Classes of Recommendations|Class IIa]]<br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''1.''' Once perfusion scanning and/or [[CT angiography]] show signs compatible with CTEPH, the patient should be referred to a center with expertise in surgical pulmonary endarterectomy. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''2.''' The selection of patients for surgery should be based on the extent and location of the organized thrombi, on the degree of pulmonary hypertension, and on the presence of co-morbidities. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LemonChiffon" |[[European society of cardiology#Classes of Recommendations|Class IIb]]<br />
|-<br />
| bgcolor="LemonChiffon" |<nowiki>"</nowiki>'''1.''' PAH-specific drug therapy may be indicated in selected CTEPH patients such as patients not candidates for surgery or patients with residual pulmonary hypertension after pulmonary endarterectomy. ''([[European society of cardiology#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
===PAH Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death (DO NOT EDIT) <ref name="pmid16935995">{{cite journal| author=Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M et al.| title=ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. | journal=Circulation | year= 2006 | volume= 114 | issue= 10 | pages= e385-484 | pmid=16935995 | doi=10.1161/CIRCULATIONAHA.106.178233 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16935995}}</ref>===<br />
<br />
{| class="wikitable"<br />
|-<br />
| colspan="1" style="text-align:center; background:LightCoral" |[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class III]] (Harm)<br />
|-<br />
| bgcolor="LightCoral" |<nowiki>"</nowiki>'''1.''' Prophylactic antiarrhythmic therapy generally is not indicated for primary prevention of SCD in patients with pulmonary arterial hypertension or other pulmonary conditions. ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: C]])'' <nowiki>"</nowiki><br />
|}<br />
<br />
==References==<br />
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[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_laboratory_tests&diff=1703587Pulmonary hypertension laboratory tests2021-06-09T14:19:29Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}; '''Assistant Editor(s)-in-Chief:''' [[User:Ralph Matar|Ralph Matar]]; {{Jose}}<br />
<br />
==Overview==<br />
There are no specific [[diagnostic]] [[Laboratory|lab]] findings associated with [[pulmonary hypertension]]. Despite that, several [[laboratory]] tests are required in the evaluation of a [[patient]] for pulmonary hypertension to assess its severity or possible associated causes. [[Biochemistry]], [[hematology]] and [[thyroid function tests]] are required in all [[patients]] with pulmonary hypertension. They are important for the [[diagnosis]] of [[chronic hemolytic anemia]], [[myeloproliferative disorder]]s, [[thyroid disorders]] and [[chronic renal failure]] on [[dialysis]].<br />
<br />
==Laboratory Findings==<br />
<br />
*[[Biochemistry]], [[hematology]] and [[thyroid function tests]] are required in all [[patients]] with pulmonary hypertension. They are important for the [[diagnosis]] of [[chronic hemolytic anemia]], [[myeloproliferative disorder]]s, [[thyroid disorders]], and [[chronic renal failure]] on [[dialysis]].<br />
*[[Serologic]] testing to detect [[connective tissue diseases]] ([[systemic sclerosis]]), [[HIV]], and [[hepatitis]].<br />
**[[Systemic sclerosis]] is an important [[disease]] to exclude in pulmonary hypertension because this systemic disease is a [[risk factor]] for the development of pulmonary arterial hypertension. Anti-Scl-70, [[Anti-centromere antibodies|anti-centromere]], and U3-RNP markers are typically positive.<br />
*[[Liver function tests]] should be done to exclude [[portal hypertension]].<br />
<br />
===Other Biomarkers===<br />
<br />
===Brain natriuretic peptide (BNP) and N-terminal fragment of BNP (NT-proBNP)===<br />
<br />
*[[Brain natriuretic peptide]] (BNP) is elevated in pulmonary hypertension of various classes:<br />
**1.1. Idiopathic PAH (IPAH)<br />
**1.4.1 PAH associated with [[connective tissue disease]]<br />
**1.4.4 [[Congenital heart diseases]] (with systemic-to-pulmonary shunts)<br />
**3.1 Pulmonary hypertension due to [[chronic obstructive pulmonary disease]]<br />
**3.2 Pulmonary hypertension due to [[interstitial lung disease]]<br />
**4. Chronic thromboembolic pulmonary hypertension (CTEPH)<br />
**5.3 Pulmonary hypertension with metabolic disorders such as [[Gaucher disease]]<br />
<br />
*BNP levels correlate with hemodynamic parameters, exercise capacity, and [[New York heart association functional classification|NYHA functional class]] and bear [[prognostic]] significance in IPAH, in pulmonary hypertension due to lung diseases, and in chronic [[thromboembolic]] pulmonary hypertension.<ref name="Nagaya-2000">{{Cite journal | last1 = Nagaya | first1 = N. | last2 = Nishikimi | first2 = T. | last3 = Uematsu | first3 = M. | last4 = Satoh | first4 = T. | last5 = Kyotani | first5 = S. | last6 = Sakamaki | first6 = F. | last7 = Kakishita | first7 = M. | last8 = Fukushima | first8 = K. | last9 = Okano | first9 = Y. | title = Plasma brain natriuretic peptide as a prognostic indicator in patients with primary pulmonary hypertension. | journal = Circulation | volume = 102 | issue = 8 | pages = 865-70 | month = Aug | year = 2000 | doi = | PMID = 10952954 }}</ref><ref name="Kucher-2003">{{Cite journal | last1 = Kucher | first1 = N. | last2 = Printzen | first2 = G. | last3 = Goldhaber | first3 = SZ. | title = Prognostic role of brain natriuretic peptide in acute pulmonary embolism. | journal = Circulation | volume = 107 | issue = 20 | pages = 2545-7 | month = May | year = 2003 | doi = 10.1161/01.CIR.0000074039.45523.BE | PMID = 12742987 }}</ref><ref name="ten Wolde-2003">{{Cite journal | last1 = ten Wolde | first1 = M. | last2 = Tulevski | first2 = II. | last3 = Mulder | first3 = JW. | last4 = Söhne | first4 = M. | last5 = Boomsma | first5 = F. | last6 = Mulder | first6 = BJ. | last7 = Büller | first7 = HR. | title = Brain natriuretic peptide as a predictor of adverse outcome in patients with pulmonary embolism. | journal = Circulation | volume = 107 | issue = 16 | pages = 2082-4 | month = Apr | year = 2003 | doi = 10.1161/01.CIR.0000070020.79932.DB | PMID = 12707233 }}</ref><ref name="Leuchte-2006">{{Cite journal | last1 = Leuchte | first1 = HH. | last2 = Baumgartner | first2 = RA. | last3 = Nounou | first3 = ME. | last4 = Vogeser | first4 = M. | last5 = Neurohr | first5 = C. | last6 = Trautnitz | first6 = M. | last7 = Behr | first7 = J. | title = Brain natriuretic peptide is a prognostic parameter in chronic lung disease. | journal = Am J Respir Crit Care Med | volume = 173 | issue = 7 | pages = 744-50 | month = Apr | year = 2006 | doi = 10.1164/rccm.200510-1545OC | PMID = 16415273 }}</ref><br />
*N-terminal fragment of BNP (NT-proBNP) has been studied as an alternative [[biomarker]] to BNP in various classes of pulmonary hypertension.<br />
*Higher NT-proBNP and peak oxygen uptake were shown to be independent predictors of mortality and a supramedian NT-proBNP level indicated a significantly lower survival.<ref name="Andreassen-2006">{{Cite journal | last1 = Andreassen | first1 = AK. | last2 = Wergeland | first2 = R. | last3 = Simonsen | first3 = S. | last4 = Geiran | first4 = O. | last5 = Guevara | first5 = C. | last6 = Ueland | first6 = T. | title = N-terminal pro-B-type natriuretic peptide as an indicator of disease severity in a heterogeneous group of patients with chronic precapillary pulmonary hypertension. | journal = Am J Cardiol | volume = 98 | issue = 4 | pages = 525-9 | month = Aug | year = 2006 | doi = 10.1016/j.amjcard.2006.02.061 | PMID = 16893710 }}</ref><ref name="Fijalkowska-2006">{{Cite journal | last1 = Fijalkowska | first1 = A. | last2 = Kurzyna | first2 = M. | last3 = Torbicki | first3 = A. | last4 = Szewczyk | first4 = G. | last5 = Florczyk | first5 = M. | last6 = Pruszczyk | first6 = P. | last7 = Szturmowicz | first7 = M. | title = Serum N-terminal brain natriuretic peptide as a prognostic parameter in patients with pulmonary hypertension. | journal = Chest | volume = 129 | issue = 5 | pages = 1313-21 | month = May | year = 2006 | doi = 10.1378/chest.129.5.1313 | PMID = 16685024 }}</ref><br />
<br />
===Cyclic guanosine monophosphate (cGMP)===<br />
<br />
*[[Cyclic guanosine monophosphate]] ([[cGMP]]) is produced by the activation of guanylate cyclase and can be viewed as an indirect marker of [[nitric oxide]] production.<br />
*Plasma [[cGMP]] levels are higher in [[patients]] with pulmonary hypertension and decrease after inhalation of [[iloprost]].<ref name="Wiedemann-2001">{{Cite journal | last1 = Wiedemann | first1 = R. | last2 = Ghofrani | first2 = HA. | last3 = Weissmann | first3 = N. | last4 = Schermuly | first4 = R. | last5 = Quanz | first5 = K. | last6 = Grimminger | first6 = F. | last7 = Seeger | first7 = W. | last8 = Olschewski | first8 = H. | title = Atrial natriuretic peptide in severe primary and nonprimary pulmonary hypertension: response to iloprost inhalation. | journal = J Am Coll Cardiol | volume = 38 | issue = 4 | pages = 1130-6 | month = Oct | year = 2001 | doi = | PMID = 11583893 }}</ref><br />
*A significant correlation between baseline plasma [[cGMP]] and severity of pulmonary arterial hypertension has also been reported.<br />
*[[Nitric oxide]] inhalation provoked a prompt increase in [[cGMP]] production, however, the magnitude of [[cGMP]] release is not linked with a decrease in pulmonary [[vascular resistance]].<ref name="Ghofrani-2002">{{Cite journal | last1 = Ghofrani | first1 = HA. | last2 = Wiedemann | first2 = R. | last3 = Rose | first3 = F. | last4 = Weissmann | first4 = N. | last5 = Schermuly | first5 = RT. | last6 = Quanz | first6 = K. | last7 = Grimminger | first7 = F. | last8 = Seeger | first8 = W. | last9 = Olschewski | first9 = H. | title = Lung cGMP release subsequent to NO inhalation in pulmonary hypertension: responders versus nonresponders. | journal = Eur Respir J | volume = 19 | issue = 4 | pages = 664-71 | month = Apr | year = 2002 | doi = | PMID = 11998996 }}</ref><br />
<br />
===D-dimer===<br />
<br />
*[[D-dimer]] is a degradation product of cross-linked fibrin and may represent microvascular [[thrombosis]] which is implicated in the pathogenesis of pulmonary hypertension.<br />
*[[D-dimer]] has been shown to be increased and correlates with disease severity as measured by [[NYHA classification|NYHA class]], resting [[oxygen saturation]], and mean pulmonary artery pressure.<br />
*There was also an inverse correlation between [[d-dimer]] levels and one-year survival in [[patients]] with primary pulmonary hypertension.<ref name="Shitrit-2002">{{Cite journal | last1 = Shitrit | first1 = D. | last2 = Bendayan | first2 = D. | last3 = Rudensky | first3 = B. | last4 = Izbicki | first4 = G. | last5 = Huerta | first5 = M. | last6 = Fink | first6 = G. | last7 = Kramer | first7 = MR. | title = Elevation of ELISA d-dimer levels in patients with primary pulmonary hypertension. | journal = Respiration | volume = 69 | issue = 4 | pages = 327-9 | month = | year = 2002 | doi = 63270 | PMID = 12169745 }}</ref><ref name="Shitrit-2002-02">{{Cite journal | last1 = Shitrit | first1 = D. | last2 = Bendayan | first2 = D. | last3 = Bar-Gil-Shitrit | first3 = A. | last4 = Huerta | first4 = M. | last5 = Rudensky | first5 = B. | last6 = Fink | first6 = G. | last7 = Kramer | first7 = MR. | title = Significance of a plasma D-dimer test in patients with primary pulmonary hypertension. | journal = Chest | volume = 122 | issue = 5 | pages = 1674-8 | month = Nov | year = 2002 | doi = | PMID = 12426270 }}</ref><br />
<br />
==References==<br />
{{Reflist|2}}<br />
<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_history_and_symptoms&diff=1703586Pulmonary hypertension history and symptoms2021-06-09T14:17:12Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}; '''Assistant Editor(s)-in-Chief:''' [[User:Lisa Prior|Lisa Prior]]; {{Jose}}<br />
<br />
==Overview==<br />
The hallmark of [[pulmonary hypertension]] is [[progressive dyspnea]]. The most common symptoms of [[pulmonary hypertension]] include [[dyspnea]], [[fatigue]], [[chest pain]] and [[syncope]] or [[presyncope]]. [[Ortner syndrome]] may also be seen (characterized by [[hoarseness]] due to compression of the left laryngeal nerve caused by enlargement of the pulmonary artery).<br />
<br />
==History==<br />
The history should be focused on the areas including:<ref name="pmid12716138">{{cite journal |author=Budev MM, Arroliga AC, Jennings CA |title=Diagnosis and evaluation of pulmonary hypertension |journal=Cleve Clin J Med |volume=70 Suppl 1 |issue= |pages=S9–17 |year=2003 |month=April |pmid=12716138 |doi= |url=}}</ref><br />
* The average time from the onset of the initial symptoms of PH to the diagnosis is approximately 2 years.<ref name="pmid3605900">{{cite journal |author=Rich S, Dantzker DR, Ayres SM, ''et al.'' |title=Primary pulmonary hypertension. A national prospective study |journal=Ann. Intern. Med. |volume=107 |issue=2 |pages=216–23 |year=1987 |month=August |pmid=3605900 |doi= |url=}}</ref> This can be attributed primarily due to the non-specificity of symptoms and the considerable overlap with symptoms of other pulmonary and cardiovascular diseases. Therefore, a detailed clinical history must be obtained. <br />
* Pulmonary arterial hypertension (PAH) does not typically present with [[orthopnea]] or [[paroxysmal nocturnal dyspnea]], while pulmonary venous hypertension typically does.<br />
* Also, a history of exposure to [[cocaine]], [[methamphetamine]], [[alcohol]] leading to [[cirrhosis]], and smoking leading to [[emphysema]] are considered significant.<br />
<br />
* Many conditions are associated with PH and symptoms suggestive of [[Liver|hepatic disease]], [[Congenital heart disease|congenital heart disease]], [[Thyroid disease|thyroid diseases]], and diseases that cause [[Hypoxia|hypoxia]] must be considered in the clinical history. <br />
* If the patient complains of [[Snoring|snoring]] and [[Somnolence|daytime sleepiness]], then [[Sleep apnea|obstructive sleep apnea]] (OSA) under [[Pulmonary hypertension|group 3 hypoxic PH]] may be a likely culprit.<br />
* A cluster of associated symptoms such as skin changes, [[Raynaud's phenomenon]] and [[Arthralgia|joint pain]] may point towards a [[Connective tissue disease|connective tissue disorder]] under [[Pulmonary hypertension|group 1 PAH]] as the underlying cause. <br />
* A history of [[deep vein thrombosis]] or [[pulmonary embolism]] may lead one to consider [[Pulmonary hypertension|group 4 chronic thromboembolic PH]].<ref name="isbn0-07-121971-4">{{cite book |author=Carolyn H. Welsh; Michael E. Hanley |title=Current diagnosis & treatment in pulmonary medicine |publisher=Lange Medical Books / McGraw-Hill |location=New York |year=2003 |pages= |isbn=0-07-121971-4 |oclc= |doi= |accessdate=}}</ref> <br />
*It is important to gather a comprehensive medication history including use of over-the-counter medications and herbal supplements as well as illicit drug use as many substances are associated with [[Pulmonary hypertension|group 1 PAH]]. <br />
* It is also wise to discern if the patient is high risk for [[Human Immunodeficiency Virus|HIV]] exposure as it has been shown that PH disease course is accelerated in HIV-affected patients.<br />
* Finally, a family history should be examined to see if there is a hereditary component at play.<br />
<br />
==Symptoms==<br />
Symptoms of pulmonary hypertension include:<ref name="pmid12716138" /><br />
*Progressive [dyspnea]] (~85%)<br />
*[[Fatigue]] (~26%)<br />
*[[Chest pain]] (~22%)<br />
*[[Lower extremity edema]] (~20%)<br />
**As systemic venous hypertension develops secondary to a failing right ventricle, [[Edema|leg swelling]] may be a feature of the condition in addition to upper right abdominal discomfort (from hepatic congestion) and abdominal swelling ([[Ascites|ascites]]).<ref name="isbn0-07-121971-4">{{cite book |author=Carolyn H. Welsh; Michael E. Hanley |title=Current diagnosis & treatment in pulmonary medicine |publisher=Lange Medical Books / McGraw-Hill |location=New York |year=2003 |pages= |isbn=0-07-121971-4 |oclc= |doi= |accessdate=}}</ref><br />
*[[Syncope]] or [[presyncope]](~17%)<br />
*[[Raynaud's phenomenon]] (~10%)<br />
**Anginal [[Chest pain|chest pain]] is thought to be due to increased myocardial oxygen demand in a strained right heart that is either hypertrophied or dilated. <br />
**However, there have also been reports of angina due to decreased [[Myocardium|myocardial]] oxygen supply from compression of the left main [[Coronary circulation|coronary artery]] by a dilated pulmonary artery.<ref name="pmid10190427">{{cite journal |author=Kawut SM, Silvestry FE, Ferrari VA, ''et al.'' |title=Extrinsic compression of the left main coronary artery by the pulmonary artery in patients with long-standing pulmonary hypertension |journal=Am. J. Cardiol. |volume=83 |issue=6 |pages=984–6, A10 |year=1999 |month=March |pmid=10190427 |doi= |url=}}</ref> <br />
*[[Syncope|Near Syncope]] (~5%)<br />
**[[Syncope]] can occur through either reduced [[Cardiac output|cardiac output]], [[Cardiac arrhythmia|arrhythmias]] or ventricular [[Ischemia|ischemia]] and indicates pulmonary hypertension is severe. <br />
*[[Palpitation|Palpitations]] (~5%)<br />
*[[Cough]] (rare)<br />
*[[Hemoptysis]] (rare)<br />
*[[Hoarseness]] (rare)<ref name="pmid3605900">{{cite journal |author=Rich S, Dantzker DR, Ayres SM, ''et al.'' |title=Primary pulmonary hypertension. A national prospective study |journal=Ann. Intern. Med. |volume=107 |issue=2 |pages=216–23 |year=1987 |month=August |pmid=3605900 |doi= |url=}}</ref><br />
**Hoarseness ([[Ortner's syndrome]]) is thought to be due to compression of the left [[Recurrent laryngeal nerve|recurrent laryngeal nerve]] between a dilated pulmonary artery and the [[Aorta|aorta]].<ref name="pmid12716138">{{cite journal |author=Budev MM, Arroliga AC, Jennings CA |title=Diagnosis and evaluation of pulmonary hypertension |journal=Cleve Clin J Med |volume=70 Suppl 1 |issue= |pages=S9–17 |year=2003 |month=April |pmid=12716138 |doi= |url=}}</ref><br />
<br />
==WHO Functional Classification==<br />
Clinically, a patient may be categorized based on the severity of symptoms into a particular class using the WHO modified functional classification system for [[Pulmonary hypertension|pulmonary hypertension]] (modified from [[Congestive heart failure classification|NYHA functional classification system]] for heart failure). The baseline WHO functional classification is used for the assessment of the severity of PH in order to tailor the choice of therapy. Shown below is a table summarizing the different functional classes.<ref>Rich S, Rubin LJ, Abenhail L, et al. Executive summary from the World Symposium on Primary Pulmonary Hypertension 1998, Evian, France, September 6-10, 1998. Geneva: The World Health Organization.</ref><br />
<br />
{| style="cellpadding=0; cellspacing= 0; width: 600px;"<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''Class''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''Description'''<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 30%" align="left" | '''I''' || style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |<br />
* No limitation of usual physical activity<br />
* No increased [[dyspnea]], [[fatigue]], [[chest pain]], or presyncope upon ordinary physical activity<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 30%" align="left" |'''II''' || style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |<br />
* Mild limitation of physical activity<br />
* No discomfort at rest <br />
* Increased [[dyspnea]], [[fatigue]], [[chest pain]], or presyncope upon normal physical activity<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 30%" align="left" |'''III''' || style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |<br />
* Marked limitation of physical activity<br />
* No discomfort at rest<br />
* Increased [[dyspnea]], [[fatigue]], [[chest pain]], or presyncope upon less than ordinary activity<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 30%" align="left" |'''IV''' || style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |<br />
* Inability to perform any physical activity at rest with/without signs of right ventricular failure<br />
* Dyspnea and/or fatigue may be present at rest<br />
* Increased [[dyspnea]], [[fatigue]], [[chest pain]], or presyncope by almost any physical activity<br />
|}<br />
<br />
==References==<br />
{{Reflist|2}}<br />
{{WikiDoc Help Menu}}<br />
{{WikiDoc Sources}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_historical_perspective&diff=1703584Pulmonary hypertension historical perspective2021-06-09T14:01:34Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}: {{AE}} {{Jose}}<br />
==Overview==<br />
[[Pulmonary hypertension]] was first described by [[Ernst von Romberg]], a German physician, in 1891.<br />
==Historical Perspective==<br />
*[[Pulmonary hypertension]] was first described by [[Ernst von Romberg]], a German physician, in 1891.<br />
* In 1929, Werner Forssman demonstrated that it was possible to perform [[Right heart catheterization|right-sided catheterization]] in humans by performing [[catheterization]] on himself.<br />
* In 1951, Dresdale coined the term primary pulmonary hypertension after describing series of cases of this new pathology. He also investigated the effects of [[tolzoline]] in a woman with [[pulmonary arterial hypertension]] causing a sudden reduction in pulmonary vascular resistance.<br />
*In the late 1960s, there was an epidemic of [[pulmonary arterial hypertension]] induced by aminorex, which sparked interest in the disease.<br />
*[[Pulmonary hypertension]] was first classified into primary and secondary in 1973 during the World Health Organization (WHO) meeting on PH in Geneva, Switzerland.<br />
*[[Bosentan]] was approved to treat [[pulmonary hypertension]] in 2001, and [[sildenafil]] was approved in 2005.<ref name="pmid19561874">{{cite journal| author=Barst RJ| title=Pulmonary hypertension: past, present and future. | journal=Ann Thorac Med | year= 2008 | volume= 3 | issue= 1 | pages= 1-4 | pmid=19561874 | doi=10.4103/1817-1737.37832 | pmc=2700428 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19561874 }} </ref><br />
<br />
==References==<br />
{{reflist|2}}<br />
<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_epidemiology_and_demographics&diff=1703583Pulmonary hypertension epidemiology and demographics2021-06-09T13:59:04Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}; {{AE}} [[User:Ralph Matar|Ralph Matar]]; {{Jose}}<br />
<br />
== Overview ==<br />
<br />
Pulmonary arterial hypertension has been considered as a disease of young women. The mean age of patients in the U.S. registry was 36 years and the overall female-to-male ratio was 1.7:1.<br />
<br />
==Epidemiology and Demographics==<br />
<br />
===Incidence===<br />
* While previously considered a rare disease, the most recent evidence from a French registry suggests that the [[incidence]] of new cases of pulmonary arterial hypertension is 0.20-0.30 cases per 100,000 individuals.<ref name="Rich-1987">{{Cite journal | last1 = Rich | first1 = S. | last2 = Dantzker | first2 = DR. | last3 = Ayres | first3 = SM. | last4 = Bergofsky | first4 = EH. | last5 = Brundage | first5 = BH. | last6 = Detre | first6 = KM. | last7 = Fishman | first7 = AP. | last8 = Goldring | first8 = RM. | last9 = Groves | first9 = BM. | title = Primary pulmonary hypertension. A national prospective study. | journal = Ann Intern Med | volume = 107 | issue = 2 | pages = 216-23 | month = Aug | year = 1987 | doi = | PMID = 3605900 }}</ref><br />
<br />
===Prevalence===<br />
* The [[prevalence]] of pulmonary hypertension is approximately 1.5-5 per 100,000 individuals.<ref name="pmid33710842">{{cite journal| author=Levine DJ| title=Pulmonary arterial hypertension: updates in epidemiology and evaluation of patients. | journal=Am J Manag Care | year= 2021 | volume= 27 | issue= 3 Suppl | pages= S35-S41 | pmid=33710842 | doi=10.37765/ajmc.2021.88609 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33710842 }} </ref><br />
<br />
===Age===<br />
* Pulmonary hypertension usually develops between the ages of 20 and 60, but it can occur at any age. The mean age of patients in the U.S. registry was approximately 36 years old.<ref name="Rich-1987">{{Cite journal | last1 = Rich | first1 = S. | last2 = Dantzker | first2 = DR. | last3 = Ayres | first3 = SM. | last4 = Bergofsky | first4 = EH. | last5 = Brundage | first5 = BH. | last6 = Detre | first6 = KM. | last7 = Fishman | first7 = AP. | last8 = Goldring | first8 = RM. | last9 = Groves | first9 = BM. | title = Primary pulmonary hypertension. A national prospective study. | journal = Ann Intern Med | volume = 107 | issue = 2 | pages = 216-23 | month = Aug | year = 1987 | doi = | PMID = 3605900 }}</ref><br />
<br />
===Gender===<br />
* The female-to-male ratio for PH is approximately 1.7:1.<ref name="Rich-1987">{{Cite journal | last1 = Rich | first1 = S. | last2 = Dantzker | first2 = DR. | last3 = Ayres | first3 = SM. | last4 = Bergofsky | first4 = EH. | last5 = Brundage | first5 = BH. | last6 = Detre | first6 = KM. | last7 = Fishman | first7 = AP. | last8 = Goldring | first8 = RM. | last9 = Groves | first9 = BM. | title = Primary pulmonary hypertension. A national prospective study. | journal = Ann Intern Med | volume = 107 | issue = 2 | pages = 216-23 | month = Aug | year = 1987 | doi = | PMID = 3605900 }}</ref><br />
* Idiopathic pulmonary hypertension (IPAH), which is more prevalent in women (3x more common), was considered the most common type of pulmonary arterial hypertension in a French registry. Usually it affects women between 30-60 years old.<ref name="pmid33710842">{{cite journal| author=Levine DJ| title=Pulmonary arterial hypertension: updates in epidemiology and evaluation of patients. | journal=Am J Manag Care | year= 2021 | volume= 27 | issue= 3 Suppl | pages= S35-S41 | pmid=33710842 | doi=10.37765/ajmc.2021.88609 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33710842 }} </ref><br />
*Males often face a worse prognosis.<ref name="pmid33710842">{{cite journal| author=Levine DJ| title=Pulmonary arterial hypertension: updates in epidemiology and evaluation of patients. | journal=Am J Manag Care | year= 2021 | volume= 27 | issue= 3 Suppl | pages= S35-S41 | pmid=33710842 | doi=10.37765/ajmc.2021.88609 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33710842 }} </ref><br />
<br />
==References==<br />
<br />
{{Reflist|2}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_electrocardiogram&diff=1703582Pulmonary hypertension electrocardiogram2021-06-09T13:57:35Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
'''Editor(s)-in-Chief:''' [[User:C Michael Gibson |C. Michael Gibson, M.S., M.D.]] [mailto:charlesmichaelgibson@gmail.com]; '''Assistant Editor(s)-in-Chief:''' [[User:Lisa Prior|Lisa Prior]]<br />
<br />
==Overview==<br />
Elevated pulmonary pressures in pulmonary hypertension (PH) can lead to [[right ventricular hypertrophy]] ([[RVH]]) and [[right atrial enlargement]] which can sometimes be observed on an [[electrocardiogram]] (ECG). The ECG findings of PH include [[right axis deviation]], [[right ventricular]] strain pattern, and [[P pulmonale]]. The ECG findings of PH are neither specific nor sensitive and their absence does not rule out the presence of PH.<br />
<br />
==Electrocardiogram==<br />
===ECG Findings Suggestive of RVH in Pulmonary Hypertension===<br />
<br />
*[[Right axis deviation]]<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
*[[Right atrial enlargement]]<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
*[[Right ventricular hypertrophy]]<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
*R/S ratio > 1 in V1<br />
*R wave > 7mm in V1<br />
*rSR' complex in V1 with R' > 10mm <br />
*qR complex in V1<br />
*Right ventricular strain pattern: [[ST segment]] and [[T wave]] inversion in V1-V3 and occasionally in inferior leads (II, III, AVF)<br />
*[[Right bundle branch block]]: [[QRS]] duration > 0.12 seconds, rSR' in leads V1 & V2, wide slurred [[S wave]]s in lateral leads (V5, V6, I)<ref name="isbn0-7637-6405-1">{{cite book |author=O'Keefe, James |title=The Complete Guide to ECGS |publisher=Jones & Bartlett Pub |location= |year=2008 |pages= |isbn=0-7637-6405-1 |oclc= |doi= |accessdate=}}</ref><br />
<br />
===ECG Findings Suggestive of Right Atrial Enlargement===<br />
<br />
*[[P pulmonale]]: P wave amplitude >2.5mm in inferior leads (II, III, AVF) or >1.5mm in V1/V2<br />
*[[P wave]] axis shifted rightward >70°<ref name="isbn0-7637-6405-1">{{cite book |author=O'Keefe, James |title=The Complete Guide to ECGS |publisher=Jones & Bartlett Pub |location= |year=2008 |pages= |isbn=0-7637-6405-1 |oclc= |doi= |accessdate=}}</ref><br />
<br />
===Use of the Electrocardiogram as a Prognostic Tool===<br />
<br />
A number of studies have indicated that a qR pattern in V1 and a tall [[P wave]] in lead I points to a worse outcome in patients with PH.<ref name="pmid11834666">{{cite journal |author=Bossone E, Paciocco G, Iarussi D, ''et al.'' |title=The prognostic role of the ECG in primary pulmonary hypertension |journal=Chest |volume=121 |issue=2 |pages=513–8 |year=2002 |month=February |pmid=11834666 |doi= |url=}}</ref> However up to 13% of patients with significant pulmonary hypertension were shown to have normal ECG findings indicating lack of sensitivity and casting doubt on its use as a prognostic indicator.<ref name="pmid12171826">{{cite journal |author=Ahearn GS, Tapson VF, Rebeiz A, Greenfield JC |title=Electrocardiography to define clinical status in primary pulmonary hypertension and pulmonary arterial hypertension secondary to collagen vascular disease |journal=Chest |volume=122 |issue=2 |pages=524–7 |year=2002 |month=August |pmid=12171826 |doi= |url=}}</ref><br />
<br />
===EKG Examples===<br />
Shown below is an example of right ventricular hypertrophy and right atrial enlargement in a patient with chronic PH. Note [[P pulmonale]] that is a [[P wave]] amplitude >2.5mm in inferior leads (II, III, AVF) and the [[T wave inversion]] in leads II, III, aVF, V2, V3, V4, V5.<br />
<br />
[[Image:Pulhtn1.jpg|center|500px]]<br />
<br />
==References==<br />
{{Reflist|2}}<br />
{{WH}}<br />
{{WS}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_echocardiography_or_ultrasound&diff=1703581Pulmonary hypertension echocardiography or ultrasound2021-06-09T13:55:10Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}, Richard Channick, M.D.; '''Assistant Editor(s)-in-Chief:''' [[User:Ralph Matar|Ralph Matar]]; {{Jose}}<br />
<br />
==Overview==<br />
[[Echocardiography]] may demonstrate right ventricular or atrial enlargement with a thickened [[interventricular septum]] in patients with pulmonary hypertension, decreased right ventricular function, or hypertrophy. [[Pulmonary artery systolic pressure]] can also be estimated using echocardiography. Right ventricular afterload may be suggested by a leftward [[septal]] displacement during systole. [[Pericardial effusion]]s and diminished [[left ventricular]] cavity typically portend a dismal prognosis.<br />
<br />
==Echocardiography==<br />
Once pulmonary hypertension is suspected in a patient, a [[TTE|transthoracic echocardiogram]] should be done to assess right heart functions including: <br />
*Pulmonary arterial pressure<br />
*[[Tricuspid regurgitation]]<br />
*Increased velocity of [[pulmonary valve regurgitation]] and short acceleration time of [[right ventricle]] ejection into the [[pulmonary artery]]<br />
*Enlarged right heart chambers<br />
*Abnormal shape and function (displacement) of [[interventricular septum]]<br />
*Right ventricular wall hypertrophy<br />
*Dilated main [[pulmonary artery]]<br />
*[[Pericardial effusion]]<br />
*Doppler echocardiographic index (Tei index or myocardial performance index) which is the sum of both isovolumetric contraction and relaxation intervals, divided by the ejection time<br />
<br />
'''Echocardiographic assessment'''<br />
*The most important initial parameter for evaluation using echocardiography is the pulmonary artery systolic pressure (PASP), which can be estimated using echocardiography. <br />
*Its evaluation is limited when an accurate tricuspid regurgitation envelope can't be measured. <br />
*Signs of right ventricular or atrial enlargement, decreased right ventricular function or hypertrophy are more important than PASP because they indicate a more severe disease with cardiac compromise. <br />
*Leftward deviation of the interventricular septum, the "D sign" is correlated with poorer prognosis.<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
Shown below is a table summarizing the criteria to estimate the likelihood of the presence of PH based on echocardiography findings.<ref name="pmid19713419">{{cite journal| author=Galiè N, Hoeper MM, Humbert M, Torbicki A, Vachiery JL, Barbera JA et al.| title=Guidelines for the diagnosis and treatment of pulmonary hypertension: the Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS), endorsed by the International Society of Heart and Lung Transplantation (ISHLT). | journal=Eur Heart J | year= 2009 | volume= 30 | issue= 20 | pages= 2493-537 | pmid=19713419 | doi=10.1093/eurheartj/ehp297 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19713419 }} </ref><br />
<br />
{| style="cellpadding=0; cellspacing= 0; width: 600px;"<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''Likelihood of the Presence of PH''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''Criteria''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''Class, Level of Evidence'''<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 20%" align="left" | '''Unlikely''' || style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 50%" align="left" |Tricuspid regurgitation velocity ≤2.8 m/s <br> ''AND'' <BR> Pulmonary artery systolic pressure ≤36 mmHg <br> ''AND'' <BR> Absence of other echocardiography findings suggestive of PH || style="padding: 0 5px; font-size: 100%; background: #F5F5F5" align="left" | [[EHS ESC guidelines classification scheme|Class I, Level of Evidence B]]<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 20%" align="left" |'''Possible''' || style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 50%" align="left" |Tricuspid regurgitation velocity ≤2.8 m/s <br> ''AND'' <BR> Pulmonary artery systolic pressure 37-50 mmHg <br> ''AND'' <BR> Presence of other echocardiography findings suggestive of PH || style="padding: 0 5px; font-size: 100%; background: #F5F5F5" align="left" | [[EHS ESC guidelines classification scheme|Class IIa, Level of evidence C]]<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 20%" align="left" |'''Possible''' || style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 50%" align="left" |Tricuspid regurgitation velocity 2.9-3,4 m/s <br> ''AND'' <BR> Pulmonary artery systolic pressure ≤36 mmHg <br> ''AND'' <BR> Presence or absence of other echocardiography findings suggestive of PH || style="padding: 0 5px; font-size: 100%; background: #F5F5F5" align="left" |[[EHS ESC guidelines classification scheme|Class IIa, Level of Evidence C]]<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 20%" align="left" |'''Likely''' || style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 50%" align="left" |Tricuspid regurgitation velocity >3.4 m/s <br> ''AND'' <BR> Pulmonary artery systolic pressure >50 mmHg <br> ''AND'' <BR> Presence or absence of other echocardiography findings suggestive of PH|| style="padding: 0 5px; font-size: 100%; background: #F5F5F5" align="left" |[[EHS ESC guidelines classification scheme|Class I, Level of evidence B]]<br />
|-<br />
|}<br />
<br />
Echocardiography plays a pivotal role in the diagnosis of PH due to [[left heart failure]]. [[Echocardiographic]] findings characteristic of [[left ventricular]] [[diastolic dysfunction]] are:<ref name="pmid19555862">{{cite journal| author=Hoeper MM, Barberà JA, Channick RN, Hassoun PM, Lang IM, Manes A et al.| title=Diagnosis, assessment, and treatment of non-pulmonary arterial hypertension pulmonary hypertension. | journal=J Am Coll Cardiol | year= 2009 | volume= 54 | issue= 1 Suppl | pages= S85-96 | pmid=19555862 | doi=10.1016/j.jacc.2009.04.008 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19555862 }} </ref><br />
* [[Left atrial]] enlargement<br />
* Concentric remodeling of the [[left ventricle]]<br />
* [[Left ventricular hypertrophy]]<br />
* Findings suggestive of increased [[left ventricular]] filling pressure<br />
<br />
===Video showing Top 10 echocardiographic findings in moderate to severe pulmonary hypertension=== <br />
Disclaimer: Adapted from Billy Cathey RDCS:Pulmonary hypertension 2D findings:<br />
{{#ev:youtube|3yOdNyTH07g}}<br />
'''Abbreviations''':<br />
*RVE: Right ventricular enlargement<br />
*RVH: Right ventricular hypertrophy<br />
*RAE: Right atrial enlargement<br />
*TR: [[Tricuspid regurgitation]]<br />
*PFO: Patent [[foramen ovale]]<br />
*RVSP: Right ventricular systolic pressure<br />
*SPAP: Systolic [[pulmonary artery]] pressure<br />
*RVOT: Right ventricular outflow tract<br />
*IVC: [[Inferior vena cava]]<br />
<br />
==References==<br />
{{Reflist|2}}<br />
{{WikiDoc Help Menu}}<br />
{{WikiDoc Sources}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]<br />
[[Category:Radiology]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_differential_diagnosis&diff=1703580Pulmonary hypertension differential diagnosis2021-06-09T13:52:40Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
[[Image:Home_logo1.png|right|250px|link=https://www.wikidoc.org/index.php/Pulmonary_hypertension]]<br />
{{CMG}}; '''Assistant Editor(s)-in-Chief:''' [[User:Ralph Matar|Ralph Matar]], [[User:Rim Halaby|Rim Halaby]]<br />
<br />
==Overview==<br />
One of the most common initial presentations of patients with pulmonary hypertension is [[dyspnea]]; therefore, the differential diagnosis is very broad. As the disease progresses with time, more symptoms related to [[right ventricular hypertrophy]] and [[Right ventricular failure|failure]] occur; which further narrows down the differential diagnosis.<br />
<br />
==Differential Diagnosis==<br />
<br />
* [[Left heart failure|Left-sided heart failure]]<br />
* [[Coronary heart disease|Coronary artery disease]] <br />
* [[Portal hypertension]]<br />
<br />
==Differentiating Pulmonary Arterial Hypertension from Other Diseases==<br />
<br />
Major entities in the differential diagnosis of pulmonary arterial hypertension are:<ref name="pmid19051731">{{cite journal| author=Doi S| title=[Differential diagnosis of pulmonary hypertension]. | journal=Nihon Rinsho | year= 2008 | volume= 66 | issue= 11 | pages= 2127-32 | pmid=19051731 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19051731 }} </ref><br />
<br />
* [[thromboembolism|Chronic pulmonary thromboembolism]]<br />
* [[Mitral stenosis]]<br />
* Left atrial tumors<br />
* Pulmonary [[veno-occlusive disease]]<br />
<br />
==Differentiating Shortness of Breath or Dyspnea from other Diseases==<br />
* The underlying causes of dyspnea are classified as [[acute]] causes and [[chronic]] causes based on the disease course. Different causes of dyspnea include [[pulmonary]] ([[Upper airway|upper]] and [[Lower respiratory|lower airway]]), [[cardiovascular]], [[central nervous system]], [[toxic]] and [[metabolic]], and [[systemic]] diseases.<br />
'''Diseases that cause shortness of breath have to be differentiated upon the following table'''<ref name="pmid28098068">{{cite journal| author=Berliner D, Schneider N, Welte T, Bauersachs J| title=The Differential Diagnosis of Dyspnea. | journal=Dtsch Arztebl Int | year= 2016 | volume= 113 | issue= 49 | pages= 834-845 | pmid=28098068 | doi=10.3238/arztebl.2016.0834 | pmc=5247680 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28098068 }} </ref><br />
<br />
'''''To review the differential diagnosis of dyspnea and fever, [[Dyspnea and Fever|click here]]'''.''<br />
<br />
'''''To review the differential diagnosis of dyspnea and chest pain, [[Dyspnea and Chest pain|click here]]'''.''<br />
<br />
'''''To review the differential diagnosis of dyspnea and cough, [[Dyspnea and Cough|click here]]'''.''<br />
<br />
'''''To review the differential diagnosis of dyspnea and jugular vein distention, [[Dyspnea and Jugular vein distention|click here]]'''.''<br />
<br />
'''''To review the differential diagnosis of dyspnea and cyanosis or clubbing, [[Dyspnea and Cyanosis or Clubbing|click here]]'''.''<br />
<br />
'''''To review the differential diagnosis of dyspnea and loss of consciousness or agitation, [[Dyspnea and Loss of consciousness or Agitation|click here]]'''.''<br />
<br />
'''''To review the differential diagnosis of dyspnea with normal auscultation, [[Dyspnea with Normal auscultation|click here]]'''.'' <br />
<br />
'''''To review the differential diagnosis of dyspnea with stridor, [[Dyspnea with Stridor|click here]]'''.''<br />
<br />
'''''To review the differential diagnosis of dyspnea with wheezing, [[Dyspnea with Wheezing|click here]]'''.''<br />
<br />
'''''To review the differential diagnosis of dyspnea with crackle, [[Dyspnea with Crackle|click here]]'''.''<br />
<br />
'''''To review the differential diagnosis of dyspnea with rhonchi, [[Dyspnea with Rhonchi|click here]]'''.''<br />
<br />
'''''To review the differential diagnosis of dyspnea, fever,''''' '''''and cough, [[Dyspnea, Fever, and Cough|click here]]'''.''<br />
<br />
'''''To review the differential diagnosis of dyspnea, fever,''''' '''''and chest pain, [[Dyspnea, Fever, and Chest pain|click here]]'''.''<br />
<br />
'''''To review the differential diagnosis of dyspnea, cough, and cyanosis or clubbing [[Dyspnea, Cough, and Cyanosis or Clubbing|click here]]'''.''<br />
<br />
'''''To review the differential diagnosis of dyspnea, fever,''''' '''''chest pain,''''' '''''cough,''''' '''''and cyanosis or clubbing''''' '''''[[Dyspnea, Fever, Chest pain, Cough, and Cyanosis or Clubbing|click here]]'''.''<br />
<br />
<small>'''''Abbreviations:''''' '''ABG ('''[[arterial blood gas]]'''); ACE ('''[[Angiotensin-converting enzyme|angiotensin converting enzyme]]'''); BMI ('''[[body mass index]]'''); CBC ('''[[Complete blood counts|complete blood count]]'''); CSF ('''[[cerebrospinal fluid]]'''); CXR ('''[[chest X-ray]]'''); DOE ('''dyspnea on [[exercise]]'''); ECG ('''[[electrocardiogram]]'''); FEF ('''[[Spirometry|forced expiratory flow rate]]'''); FEV1 ('''[[forced expiratory volume]]'''); FVC ('''[[forced vital capacity]]'''); JVD ('''[[jugular vein distention]]''');''' '''MCV ('''[[mean corpuscular volume]]'''); Plt ('''[[platelet]]'''); RV ('''[[residual volume]]'''); SIADH ('''[[syndrome of inappropriate antidiuretic hormone]]'''); TSH ('''[[thyroid stimulating hormone]]'''); Vt ('''[[tidal volume]]''');''' '''WBC ('''[[White blood cells|white blood cell]]''');'''</small> <br />
<small><small><br />
<br />
{| <br />
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"<br />
! colspan="3" rowspan="3" |Organ system<br />
! rowspan="3" |Diseases<br />
! colspan="13" |Clinical manifestations<br />
! colspan="5" rowspan="2" |Diagnosis<br />
! rowspan="3" |Other features<br />
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"<br />
! colspan="8" |Symptoms<br />
! colspan="5" |Physical exam<br />
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"<br />
!Loss of consciousness<br />
!Agitation<br />
!Weight loss<br />
!Fever<br />
!Chest pain<br />
!Cough<br />
!Orthopnea<br />
!DOE<br />
!Cyanosis<br />
!Clubbing<br />
!JVD<br />
!Peripheral edema<br />
!Auscultation<br />
!CBC<br />
!ABG<br />
!Imaging<br />
!Spirometry<br />
!Gold standard<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
! rowspan="33" |Acute Dyspnea<br />
! rowspan="18" |[[Respiratory system]]<br />
! rowspan="7" |[[Head]] and [[Neck]],<br />
Upper [[airway]]<br />
![[Angioedema]]<ref name="pmid28405953">{{cite journal| author=Bernstein JA, Cremonesi P, Hoffmann TK, Hollingsworth J| title=Angioedema in the emergency department: a practical guide to differential diagnosis and management. | journal=Int J Emerg Med | year= 2017 | volume= 10 | issue= 1 | pages= 15 | pmid=28405953 | doi=10.1186/s12245-017-0141-z | pmc=5389952 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28405953 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]], ↑[[CO2]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |N/A<br />
! style="background: #F5F5F5; padding: 5px;" |[[Physical examination|Physical exam]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Generalized edema]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Anaphylaxis]]<ref name="pmid21293765">{{cite journal| author=Bjornsson HM, Graffeo CS| title=Improving diagnostic accuracy of anaphylaxis in the acute care setting. | journal=West J Emerg Med | year= 2010 | volume= 11 | issue= 5 | pages= 456-61 | pmid=21293765 | doi= | pmc=3027438 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21293765 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Scattered [[wheezing]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |N/A<br />
! style="background: #F5F5F5; padding: 5px;" |[[Vital sign]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Type 1 hypersensitivity]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Aspiration]]<ref name="pmid25581840">{{cite journal| author=O'Horo JC, Rogus-Pulia N, Garcia-Arguello L, Robbins J, Safdar N| title=Bedside diagnosis of dysphagia: a systematic review. | journal=J Hosp Med | year= 2015 | volume= 10 | issue= 4 | pages= 256-65 | pmid=25581840 | doi=10.1002/jhm.2313 | pmc=4607509 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25581840 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Diminished [[breath sounds]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Atelectasis]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]], ↑[[Residual volume|RV]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Bronchoscopy]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Choking]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Croup]]<ref name="pmid23939212">{{cite journal| author=Bjornson CL, Johnson DW| title=Croup in children. | journal=CMAJ | year= 2013 | volume= 185 | issue= 15 | pages= 1317-23 | pmid=23939212 | doi=10.1503/cmaj.121645 | pmc=3796596 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23939212 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Stridor]]<br />
! style="background: #F5F5F5; padding: 5px;" |↑[[WBC]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Steeple sign]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Physical examination|Physical exam]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Barking cough]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Epiglottitis]]<ref name="pmid17104162">{{cite journal| author=Negus VE| title=The Function of the Epiglottis. | journal=J Anat | year= 1927 | volume= 62 | issue= Pt 1 | pages= 1-8 | pmid=17104162 | doi= | pmc=1250045 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17104162 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Stridor]]<br />
! style="background: #F5F5F5; padding: 5px;" |↑[[WBC]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Thumbprint sign|Thumb sign]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Laryngoscopy]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Drooling]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Rhinosinusitis]]<ref name="pmid214901812">{{cite journal| author=Meltzer EO, Hamilos DL| title=Rhinosinusitis diagnosis and management for the clinician: a synopsis of recent consensus guidelines. | journal=Mayo Clin Proc | year= 2011 | volume= 86 | issue= 5 | pages= 427-43 | pmid=21490181 | doi=10.4065/mcp.2010.0392 | pmc=3084646 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21490181 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↑[[WBC]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Air fluid level<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Physical examination|Physical exam]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Headache]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Vocal cord paralysis|Vocal cord dysfunction]]<ref name="pmid8828523">{{cite journal |vauthors=Wood RP, Milgrom H |title=Vocal cord dysfunction |journal=J. Allergy Clin. Immunol. |volume=98 |issue=3 |pages=481–5 |date=September 1996 |pmid=8828523 |doi= |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Stridor]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓ [[FVC]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Laryngoscopy]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Choking]] sensation<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
! rowspan="11" |[[Chest]] and [[Pleurae|Pleura]],<br />
Lower [[airway]]<br />
![[Asthma attack]]<ref name="pmid19858243">{{cite journal| author=Hodder R, Lougheed MD, Rowe BH, FitzGerald JM, Kaplan AG, McIvor RA| title=Management of acute asthma in adults in the emergency department: nonventilatory management. | journal=CMAJ | year= 2010 | volume= 182 | issue= 2 | pages= E55-67 | pmid=19858243 | doi=10.1503/cmaj.080072 | pmc=2817338 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19858243 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Wheeze]]<br />
! style="background: #F5F5F5; padding: 5px;" |↑ [[Eosinophil]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Respiratory alkalosis]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓ [[FEV1]], [[Peak expiratory flow|PEF]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Physical examination|Physical exam]] and<br />
[[Spirometry]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Chest pain]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
!'''[[Atelectasis]]'''<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Diminished [[breath sounds]], [[Wheeze]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]], Normal/↓[[CO2]]<br />
! style="background: #F5F5F5; padding: 5px;" |Collapsed lung lobe, [[Fissure|fissures]]<nowiki/>displacement <br />
! style="background: #F5F5F5; padding: 5px;" |↓ [[FVC]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[CT scan|Chest CT scan]] <br />
! style="background: #F5F5F5; padding: 5px;" |[[Surgical procedure]], [[Aspiration]], <br />
[[Mechanical ventilation]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Bronchitis]]<ref name="CantinBankier2009">{{cite journal|last1=Cantin|first1=Luce|last2=Bankier|first2=Alexander A.|last3=Eisenberg|first3=Ronald L.|title=Bronchiectasis|journal=American Journal of Roentgenology|volume=193|issue=3|year=2009|pages=W158–W171|issn=0361-803X|doi=10.2214/AJR.09.3053}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Rhonchi]] <br />
! style="background: #F5F5F5; padding: 5px;" |↑[[WBC]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Physical examination|Physical exam]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Rhonchi]] relieved by [[Dextromethorphan|cough]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Bronchospasm]]<ref name="pmid23015953">{{cite journal| author=Molis MA, Molis WE| title=Exercise-induced bronchospasm. | journal=Sports Health | year= 2010 | volume= 2 | issue= 4 | pages= 311-7 | pmid=23015953 | doi=10.1177/1941738110373735 | pmc=3445098 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23015953 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Wheeze]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]], ↑[[CO2]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]], ↑[[Residual volume|RV]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Physical examination|Physical exam]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Allergic reaction]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Bronchiolitis]]<ref name="pmid23562737">{{cite journal |vauthors=Holbro A, Lehmann T, Girsberger S, Stern M, Gambazzi F, Lardinois D, Heim D, Passweg JR, Tichelli A, Bubendorf L, Savic S, Hostettler K, Grendelmeier P, Halter JP, Tamm M |title=Lung histology predicts outcome of bronchiolitis obliterans syndrome after hematopoietic stem cell transplantation |journal=Biol. Blood Marrow Transplant. |volume=19 |issue=6 |pages=973–80 |year=2013 |pmid=23562737 |doi=10.1016/j.bbmt.2013.03.017 |url=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Wheeze]] and [[Crackles]]<br />
! style="background: #F5F5F5; padding: 5px;" |↑[[WBC]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Bronchovascular markings<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Clinical]] assessment<br />
! style="background: #F5F5F5; padding: 5px;" |[[Respiratory syncytial virus|Respiratory syncytial virus (RSV)]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[COPD exacerbation resident survival guide|COPD exacerbation]]<ref name="pmid25177479">{{cite journal| author=Qureshi H, Sharafkhaneh A, Hanania NA| title=Chronic obstructive pulmonary disease exacerbations: latest evidence and clinical implications. | journal=Ther Adv Chronic Dis | year= 2014 | volume= 5 | issue= 5 | pages= 212-27 | pmid=25177479 | doi=10.1177/2040622314532862 | pmc=4131503 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25177479 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Wheeze]], [[Rhonchi]], and [[Crackles]]<br />
! style="background: #F5F5F5; padding: 5px;" |↑[[WBC]], ↑[[RBC]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Respiratory alkalosis]]<br />
! style="background: #F5F5F5; padding: 5px;" |Hyperexpansion<br />
! style="background: #F5F5F5; padding: 5px;" |↓ [[FEV1]]/[[FVC]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Clinical]] assessment<br />
! style="background: #F5F5F5; padding: 5px;" |[[Chronic bronchitis|Acute '''exacerbations''' of chronic bronchitis (AECB)]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Lung carcinoma]]<ref name="pmid22054876">{{cite journal| author=Dela Cruz CS, Tanoue LT, Matthay RA| title=Lung cancer: epidemiology, etiology, and prevention. | journal=Clin Chest Med | year= 2011 | volume= 32 | issue= 4 | pages= 605-44 | pmid=22054876 | doi=10.1016/j.ccm.2011.09.001 | pmc=3864624 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22054876 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Wheeze]] and [[Crackles]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Mass lesion, [[hilar lymphadenopathy]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]], ↑[[Residual volume|RV]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Bronchoscopy]] <br />
! style="background: #F5F5F5; padding: 5px;" |Paraneoplastic syndromes, such as [[Syndrome of inappropriate antidiuretic hormone|SIADH]] and [[Lambert-Eaton myasthenic syndrome|Lambert-Eaton]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Pneumonia]]<ref name="pmid25165554">{{cite journal| author=Simonetti AF, Viasus D, Garcia-Vidal C, Carratalà J| title=Management of community-acquired pneumonia in older adults. | journal=Ther Adv Infect Dis | year= 2014 | volume= 2 | issue= 1 | pages= 3-16 | pmid=25165554 | doi=10.1177/2049936113518041 | pmc=4072047 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25165554 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Wheeze]], [[Rhonchi]], and [[Crackles]]<br />
! style="background: #F5F5F5; padding: 5px;" |↑[[WBC]], [[neutrophilia]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Consolidation (medicine)|Lobar consolidation]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Chest X-ray]] and CT Scan<br />
! style="background: #F5F5F5; padding: 5px;" |[[productive cough]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Pneumothorax]]<ref name="pmid17621614">{{cite journal| author=Currie GP, Alluri R, Christie GL, Legge JS| title=Pneumothorax: an update. | journal=Postgrad Med J | year= 2007 | volume= 83 | issue= 981 | pages= 461-5 | pmid=17621614 | doi=10.1136/pgmj.2007.056978 | pmc=2600088 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17621614 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Diminished [[breath sounds]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]], ↑[[CO2]]<br />
! style="background: #F5F5F5; padding: 5px;" |Radiolucency without [[lung]] marking<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]]<br />
! style="background: #F5F5F5; padding: 5px;" |CXR and [[Computed tomography|Chest CT scan]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Tracheal deviation]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Pulmonary embolism]]<ref name="pmid23940438">{{cite journal| author=Bĕlohlávek J, Dytrych V, Linhart A| title=Pulmonary embolism, part I: Epidemiology, risk factors and risk stratification, pathophysiology, clinical presentation, diagnosis and nonthrombotic pulmonary embolism. | journal=Exp Clin Cardiol | year= 2013 | volume= 18 | issue= 2 | pages= 129-38 | pmid=23940438 | doi= | pmc=3718593 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23940438 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Respiratory alkalosis]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Lung|Pulmonary]] [[CT angiography]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Pleuritic chest pain]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Rib fractures]] ([[flail chest]])<ref name="pmid27984449">{{cite journal |vauthors=Swart E, Laratta J, Slobogean G, Mehta S |title=Operative Treatment of Rib Fractures in Flail Chest Injuries: A Meta-analysis and Cost-Effectiveness Analysis |journal=J Orthop Trauma |volume=31 |issue=2 |pages=64–70 |date=February 2017 |pmid=27984449 |doi=10.1097/BOT.0000000000000750 |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Respiratory acidosis]]<br />
! style="background: #F5F5F5; padding: 5px;" |Fracture marks<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Chest X-ray]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Pneumothorax]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
! colspan="2" rowspan="5" |[[Cardiovascular system]]<br />
![[Acute myocardial ischemia]]<ref name="pmid18307844">{{cite journal| author=Bruyninckx R, Aertgeerts B, Bruyninckx P, Buntinx F| title=Signs and symptoms in diagnosing acute myocardial infarction and acute coronary syndrome: a diagnostic meta-analysis. | journal=Br J Gen Pract | year= 2008 | volume= 58 | issue= 547 | pages= 105-11 | pmid=18307844 | doi=10.3399/bjgp08X277014 | pmc=2233977 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18307844 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Cardiac troponin I (cTnI) and T (cTnT)|Cardiac troponin I]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Nausea and vomiting]], Positive pertinent risk factors, such as [[hypertension]], [[diabetes]], and [[smoking]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Acute heart failure]]<ref name="GagginJanuzzi20132">{{cite journal|last1=Gaggin|first1=Hanna K.|last2=Januzzi|first2=James L.|title=Biomarkers and diagnostics in heart failure|journal=Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease|volume=1832|issue=12|year=2013|pages=2442–2450|issn=09254439|doi=10.1016/j.bbadis.2012.12.014}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |[[S4|S]]3<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Respiratory alkalosis]]<br />
! style="background: #F5F5F5; padding: 5px;" |↑ [[Cardiothoracic ratio]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[B-type natriuretic peptide|B-type natriuretic peptide (BNP)]] and [[N-terminal pro b-type natriuretic peptide|N-terminal proBNP (NT-proBNP)]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Excessive sweating]], [[high blood pressure]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Pericardial tamponade]]<ref name="pmid12481882">{{cite journal |vauthors=van Steijn JH, Sleijfer DT, van der Graaf WT, van der Sluis A, Nieboer P |title=How to diagnose cardiac tamponade |journal=Neth J Med |volume=60 |issue=8 |pages=334–8 |year=2002 |pmid=12481882 |doi= |url=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Muffled heart sounds]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Water bottle appearance [[Cardiomegaly|enlarged heart]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Echocardiography]]<br />
! style="background: #F5F5F5; padding: 5px;" |Fluid accumulation in [[pericardium]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Tachyarrhythmia]]<ref name="pmid18307844" /><br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |High [[pulse rate]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[ECG]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Palpitation]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Pulmonary edema]]<ref name="MartindaleNoble2013">{{cite journal|last1=Martindale|first1=Jennifer L.|last2=Noble|first2=Vicki E.|last3=Liteplo|first3=Andrew|title=Diagnosing pulmonary edema|journal=European Journal of Emergency Medicine|volume=20|issue=5|year=2013|pages=356–360|issn=0969-9546|doi=10.1097/MEJ.0b013e32835c2b88}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |Basal [[Crackles|crackle]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Respiratory alkalosis]]<br />
! style="background: #F5F5F5; padding: 5px;" |Bat wing pattern, air bronchograms<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]], ↑[[Residual volume|RV]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Coronary catheterization|Cardiac Catheterization]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Tachypnea]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
! colspan="2" rowspan="3" |[[Central nervous system]]<br />
![[Stroke]]<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Intracranial hemorrhage|Intracranial infarct or hemorrhage]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Brain]] [[MRI]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Paralysis]] or [[Paresthesias|paresthesia]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Encephalitis]]<ref name="pmid15489354">{{cite journal| author=Debiasi RL, Tyler KL| title=Molecular methods for diagnosis of viral encephalitis. | journal=Clin Microbiol Rev | year= 2004 | volume= 17 | issue= 4 | pages= 903-25, table of contents | pmid=15489354 | doi=10.1128/CMR.17.4.903-925.2004 | pmc=523566 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15489354 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↑[[WBC]], [[neutrophilia]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[CSF]] [[PCR]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Confusion]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Traumatic brain injury]]<ref name="pmid22033563">{{cite journal| author=McAllister TW| title=Neurobiological consequences of traumatic brain injury. | journal=Dialogues Clin Neurosci | year= 2011 | volume= 13 | issue= 3 | pages= 287-300 | pmid=22033563 | doi= | pmc=3182015 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22033563 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Respiratory acidosis]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Intracerebral hemorrhage]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Ct scan|Brain CT scan]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Lucid interval]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
! colspan="2" rowspan="4" |[[Toxic]]/[[Metabolic]]<br />
![[Organophosphate poisoning]]<ref name="pmid25425841">{{cite journal| author=Peter JV, Sudarsan TI, Moran JL| title=Clinical features of organophosphate poisoning: A review of different classification systems and approaches. | journal=Indian J Crit Care Med | year= 2014 | volume= 18 | issue= 11 | pages= 735-45 | pmid=25425841 | doi=10.4103/0972-5229.144017 | pmc=4238091 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25425841 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Wheeze]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]], ↑[[CO2]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Blood test]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Salivation]], [[Lacrimation]], [[Emesis]], [[Miosis]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Salicylate poisoning]]<ref name="pmid20440389">{{cite journal| author=Chin RL, Olson KR, Dempsey D| title=Salicylate toxicity from ingestion and continued dermal absorption. | journal=Cal J Emerg Med | year= 2007 | volume= 8 | issue= 1 | pages= 23-5 | pmid=20440389 | doi= | pmc=2859737 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20440389 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Metabolic acidosis]], [[Respiratory alkalosis]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Blood test]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Vomiting]], [[Tinnitus]], [[Confusion]], [[Hyperthermia]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Carbon monoxide poisoning]]<ref name="pmid18710551">{{cite journal| author=Lane TR, Williamson WJ, Brostoff JM| title=Carbon monoxide poisoning in a patient with carbon dioxide retention: a therapeutic challenge. | journal=Cases J | year= 2008 | volume= 1 | issue= 1 | pages= 102 | pmid=18710551 | doi=10.1186/1757-1626-1-102 | pmc=2533003 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18710551 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Wheeze]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Carboxyhemoglobin]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]], ↑[[CO2]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |N/A<br />
! style="background: #F5F5F5; padding: 5px;" |[[Carboxyhemoglobin|Carboxyhemoglobin (HbCO)]] level<br />
! style="background: #F5F5F5; padding: 5px;" |[[Headache]], [[Dizziness]], [[Weakness]], [[Vomiting]], [[Confusion]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Diabetic ketoacidosis]]<ref name="pmid23547550">{{cite journal |vauthors=Westerberg DP |title=Diabetic ketoacidosis: evaluation and treatment |journal=Am Fam Physician |volume=87 |issue=5 |pages=337–46 |date=March 2013 |pmid=23547550 |doi= |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Scattered [[wheeze]], [[Kussmaul breathing|Kussmaul's respiration]]<br />
! style="background: #F5F5F5; padding: 5px;" |↑[[WBC]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Metabolic acidosis]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Blood test]] ([[acidosis]], [[hyperglycemia]], [[ketonemia]])<br />
! style="background: #F5F5F5; padding: 5px;" |[[Vomiting]], [[Abdominal pain]], [[Weakness]], [[Confusion]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
! colspan="2" rowspan="3" |[[Systemic]]<br />
![[Panic attack]]<ref name="pmid16627512">{{cite journal| author=Taylor CB| title=Panic disorder. | journal=BMJ | year= 2006 | volume= 332 | issue= 7547 | pages= 951-5 | pmid=16627512 | doi=10.1136/bmj.332.7547.951 | pmc=1444835 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16627512 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Clinical]] assessment<br />
! style="background: #F5F5F5; padding: 5px;" |[[Anxiety|Severe anxiety]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Pregnancy]]<ref name="pmid28805596">{{cite journal |vauthors=Lee SY, Chien DK, Huang CH, Shih SC, Lee WC, Chang WH |title=Dyspnea in pregnancy |journal=Taiwan J Obstet Gynecol |volume=56 |issue=4 |pages=432–436 |date=August 2017 |pmid=28805596 |doi=10.1016/j.tjog.2017.04.035 |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↑[[WBC]], [[RBC]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]], ↑[[CO2]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]], ↑[[Residual volume|RV]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Human chorionic gonadotropin|βhCG]]<br />
! style="background: #F5F5F5; padding: 5px;" |Missed period, Hyperemesis<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Sepsis]]<ref name="pmid27216810">{{cite journal| author=Askim Å, Mehl A, Paulsen J, DeWan AT, Vestrheim DF, Åsvold BO et al.| title=Epidemiology and outcome of sepsis in adult patients with Streptococcus pneumoniae infection in a Norwegian county 1993-2011: an observational study. | journal=BMC Infect Dis | year= 2016 | volume= 16 | issue= | pages= 223 | pmid=27216810 | doi=10.1186/s12879-016-1553-8 | pmc=4877975 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27216810 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↑[[WBC]], [[neutrophilia]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]], ↑[[CO2]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[SIRS|SIRS criteria]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Chills]], [[Confusion]]<br />
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"<br />
! colspan="3" rowspan="3" |Organ system<br />
! rowspan="3" |Diseases<br />
! colspan="13" |Clinical manifestations<br />
! colspan="5" rowspan="2" |Diagnosis<br />
! rowspan="3" |Other features<br />
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"<br />
! colspan="8" |Symptoms<br />
! colspan="5" |Physical exam<br />
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"<br />
!Loss of consciousness<br />
!Agitation<br />
!Weight loss<br />
!Fever<br />
!Chest pain<br />
!Cough<br />
!Orthopnea<br />
!DOE<br />
!Cyanosis<br />
!Clubbing<br />
!JVD<br />
!Peripheral edema<br />
!Auscultation<br />
!CBC<br />
!ABG<br />
!Imaging<br />
!Spirometry<br />
!Gold standard<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
! rowspan="41" |Chronic Dyspnea<br />
! rowspan="18" |[[Respiratory system]]<br />
! rowspan="4" |[[Head]] and [[Neck]],<br />
<br />
Upper [[airway]]<br />
![[Goiter]]<ref name="pmid22430090">{{cite journal |vauthors=Stang MT, Armstrong MJ, Ogilvie JB, Yip L, McCoy KL, Faber CN, Carty SE |title=Positional dyspnea and tracheal compression as indications for goiter resection |journal=Arch Surg |volume=147 |issue=7 |pages=621–6 |date=July 2012 |pmid=22430090 |doi=10.1001/archsurg.2012.96 |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Blood test]] ([[TSH]], [[T4]])<br />
! style="background: #F5F5F5; padding: 5px;" |[[Weight gain]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Laryngeal cancer|Laryngeal adenocarcinoma]]<ref name="pmid7956433">{{cite journal |vauthors=Schwenk NR, Schapira RM, Byrd JC |title=Laryngeal carcinoma presenting as platypnea |journal=Chest |volume=106 |issue=5 |pages=1609–11 |date=November 1994 |pmid=7956433 |doi= |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Stridor]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]], ↑[[CO2]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Retropharyngeal space|Retropharyngeal tissue]] thickness<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Laryngoscopy]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Choking]] sensation<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Vocal cord paralysis]]<ref name="pmid8828523" /><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Stridor]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Pharyngeal constrictor|Pharyngeal constrictor muscles]] thinning, [[uvular]] deviation<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Laryngoscopy]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Choking]] sensation<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Tracheal stenosis]]<ref name="pmid23748638">{{cite journal |vauthors=Conti V, Calia N, Pasquini C, Zardi S, Finetti C, Stomeo F, Ravenna F |title=[Chronic cough and worsening dyspnea: a case of idiopathic tracheal stenosis] |language=Italian |journal=Recenti Prog Med |volume=104 |issue=4 |pages=156–8 |date=April 2013 |pmid=23748638 |doi=10.1701/1271.14026 |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Stridor]], [[Stertorous]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]], ↑[[CO2]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Soft tissue]] thickening internal to normal-appearing [[Trachea|tracheal cartilage]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Bronchoscopy]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Respiratory distress]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
! rowspan="14" |[[Chest]] and [[Pleura]],<br />
Lower [[airway]]<br />
![[Bronchial asthma]]<ref name="pmid19858243" /><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Wheeze]]<br />
! style="background: #F5F5F5; padding: 5px;" |↑ [[Eosinophil]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Respiratory alkalosis]], [[Metabolic acidosis]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Pulmonary]] hyperinflation,<br />
<br />
[[Bronchial]] wall thickening<br />
! style="background: #F5F5F5; padding: 5px;" |↓ [[FEV1]]/[[FVC]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Spirometry]] before and after [[bronchodilator]]<br />
! style="background: #F5F5F5; padding: 5px;" |Paroxysmal [[respiratory distress]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Bronchiectasis]]<ref name="CantinBankier2009" /><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Rhonchi]], [[Wheezing]], [[Crackles]]<br />
! style="background: #F5F5F5; padding: 5px;" |↑[[WBC]], [[neutrophilia]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]], ↑[[CO2]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Bronchiectasis chest x ray|Tram-track opacities]]<br />
! style="background: #F5F5F5; padding: 5px;" |↑ [[FEV1]]/[[FVC]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Computed tomography|High resolution computed tomography (HRCT)]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Productive cough|Chronic productive cough]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[COPD]]<ref name="pmid25177479" /><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Wheeze|Expiratory wheeze]]<br />
! style="background: #F5F5F5; padding: 5px;" |↑ [[RBC]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Respiratory alkalosis]], [[Metabolic acidosis]]<br />
! style="background: #F5F5F5; padding: 5px;" |↑ Bronchovascular markings, [[Cardiomegaly]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓ [[FEV1]]/[[FVC]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Physical examination|Physical exam]] and<br />
[[Spirometry]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Heavy smoking]] history<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Emphysema]]<ref name="pmid18453358">{{cite journal| author=Sharafkhaneh A, Hanania NA, Kim V| title=Pathogenesis of emphysema: from the bench to the bedside. | journal=Proc Am Thorac Soc | year= 2008 | volume= 5 | issue= 4 | pages= 475-7 | pmid=18453358 | doi=10.1513/pats.200708-126ET | pmc=2645322 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18453358 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Wheeze|Expiratory wheeze]], Hyperinflation<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Respiratory alkalosis]], [[Metabolic acidosis]]<br />
! style="background: #F5F5F5; padding: 5px;" |Flattening of [[diaphragm]], vertical [[heart]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓ [[FEV1]]/[[FVC]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Physical examination|Physical exam]] and<br />
[[Spirometry]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Barrel chest]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Pulmonary hypertension]]<ref name="pmid20407377">{{cite journal |vauthors=Sajkov D, Petrovsky N, Palange P |title=Management of dyspnea in advanced pulmonary arterial hypertension |journal=Curr Opin Support Palliat Care |volume=4 |issue=2 |pages=76–84 |date=June 2010 |pmid=20407377 |doi=10.1097/SPC.0b013e328338c1e0 |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |Accentuated [[S2]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Hypoxia]] and [[acidosis]]<br />
! style="background: #F5F5F5; padding: 5px;" |Enlarged [[Pulmonary arteries|'''pulmonary''' arteries]]<br />
! style="background: #F5F5F5; padding: 5px;" |↑[[Physiologic]] [[Residual volume|RV]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Cardiac catheterization]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Syncope]],<br />
<br />
[[Ascites]], [[Pleural effusion]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Interstitial lung disease]]<ref name="pmid2060395">{{cite journal |vauthors=Baughman RP, Shipley RT, Loudon RG, Lower EE |title=Crackles in interstitial lung disease. Comparison of sarcoidosis and fibrosing alveolitis |journal=Chest |volume=100 |issue=1 |pages=96–101 |year=1991 |pmid=2060395 |doi= |url=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Rhonchi]], [[Wheezing]], [[Crackles]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]], ↑[[CO2]]<br />
! style="background: #F5F5F5; padding: 5px;" |Peripheral [[pulmonary]] infiltrative opacification <br />
! style="background: #F5F5F5; padding: 5px;" |↑ [[FEV1]]/[[FVC]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Computed tomography|High resolution computed tomography (HRCT)]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Pneumoconiosis]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Sarcoidosis]]<ref name="pmid14518232">{{cite journal |vauthors=Moher D, Cole CW, Hill GB |title=Epidemiology of abdominal aortic aneurysm: the effect of differing definitions |journal=Eur J Vasc Surg |volume=6 |issue=6 |pages=647–50 |date=November 1992 |pmid=1451823 |doi= |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Crackles]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]], ↑[[CO2]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Hilar lymphadenopathy|Hilar adenopathy]]<br />
! style="background: #F5F5F5; padding: 5px;" |↑ [[FEV1]]/[[FVC]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Computed tomography|High resolution computed tomography (HRCT)]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Hypercalcemia]], high [[Angiotensin-converting enzyme|ACE]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Alveolitis]]<ref name="pmid15692967">{{cite journal |vauthors=Khanna D, Clements PJ, Furst DE, Chon Y, Elashoff R, Roth MD, Sterz MG, Chung J, FitzGerald JD, Seibold JR, Varga J, Theodore A, Wigley FM, Silver RM, Steen VD, Mayes MD, Connolly MK, Fessler BJ, Rothfield NF, Mubarak K, Molitor J, Tashkin DP |title=Correlation of the degree of dyspnea with health-related quality of life, functional abilities, and diffusing capacity for carbon monoxide in patients with systemic sclerosis and active alveolitis: results from the Scleroderma Lung Study |journal=Arthritis Rheum. |volume=52 |issue=2 |pages=592–600 |date=February 2005 |pmid=15692967 |doi=10.1002/art.20787 |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Basal [[Crackles|crackle]]<br />
! style="background: #F5F5F5; padding: 5px;" |↑[[WBC]], [[neutrophilia]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" | Basal reticulonodular opacification <br />
! style="background: #F5F5F5; padding: 5px;" |↑ [[FEV1]]/[[FVC]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Computed tomography|High resolution computed tomography (HRCT)]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Dry cough]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Bronchiolitis obliterans]]<ref name="pmid23562737" /><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Wheeze|Expiratory wheeze]]<br />
! style="background: #F5F5F5; padding: 5px;" |↑[[WBC]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]], ↑[[CO2]]<br />
! style="background: #F5F5F5; padding: 5px;" |Hyperinflation, Reticulonodular opacities<br />
! style="background: #F5F5F5; padding: 5px;" |↓ [[FEV1]]/[[FVC]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Biopsy|Lung biopsy]]<br />
! style="background: #F5F5F5; padding: 5px;" |Complication of [[Hematopoietic stem cell transplantation|allogeneic hematopoietic stem cell transplantation]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Cystic fibrosis]]<ref name="ZieglerRovedder2009">{{cite journal|last1=Ziegler|first1=Bruna|last2=Rovedder|first2=Paula Maria Eidt|last3=Dalcin|first3=Paulo de Tarso Roth|last4=Menna-Barreto|first4=Sérgio Saldanha|title=Padrões ventilatórios na espirometria em pacientes adolescentes e adultos com fibrose cística|journal=Jornal Brasileiro de Pneumologia|volume=35|issue=9|year=2009|pages=854–859|issn=1806-3713|doi=10.1590/S1806-37132009000900006}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Rhonchi]], [[Wheezing]], [[Crackles]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Metabolic alkalosis]]<br />
! style="background: #F5F5F5; padding: 5px;" |Thick-walled [[bronchiectasis]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓ [[Forced expiratory volume|FEF<sub>75%</sub>]]/[[FVC]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Sweat test]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Congenital absence of the vas deferens|Absent vas deferens]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Pleural effusion]]<ref name="pmid25978627">{{cite journal |vauthors=Thomas R, Jenkins S, Eastwood PR, Lee YC, Singh B |title=Physiology of breathlessness associated with pleural effusions |journal=Curr Opin Pulm Med |volume=21 |issue=4 |pages=338–45 |date=July 2015 |pmid=25978627 |pmc=5633324 |doi=10.1097/MCP.0000000000000174 |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Egophony|Egophony ("E-to-A" change)]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Blunting of the [[Costophrenic angle|costophrenic]] and cardiophrenic angle<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]], ↑[[Residual volume|RV]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Pleural effusion causes|Light's criteria]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tactile fremitus]], Asymmetrical [[chest expansion]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Pulmonary shunt|Pulmonary right-to-left shunt]]<ref name="pmid19335916">{{cite journal| author=Vodoz JF, Cottin V, Glérant JC, Derumeaux G, Khouatra C, Blanchet AS et al.| title=Right-to-left shunt with hypoxemia in pulmonary hypertension. | journal=BMC Cardiovasc Disord | year= 2009 | volume= 9 | issue= | pages= 15 | pmid=19335916 | doi=10.1186/1471-2261-9-15 | pmc=2671488 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19335916 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Diminished [[breath sounds]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]], ↑[[CO2]], [[Respiratory acidosis]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]], ↑[[Residual volume|RV]] <br />
([[physiological]])<br />
! style="background: #F5F5F5; padding: 5px;" |[[CT angiography|Pulmonary CT angiography]]<br />
! style="background: #F5F5F5; padding: 5px;" |Chronic [[hypoxemia]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Diaphragmatic paralysis]]<ref name="pmid27929389">{{cite journal| author=Dubé BP, Dres M| title=Diaphragm Dysfunction: Diagnostic Approaches and Management Strategies. | journal=J Clin Med | year= 2016 | volume= 5 | issue= 12 | pages= | pmid=27929389 | doi=10.3390/jcm5120113 | pmc=5184786 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27929389 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Unilateral or bilateral [[Diaphragmatic dysfunction|diaphragmatic flattening]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]], ↑[[Residual volume|RV]]<br />
([[anatomical]])<br />
! style="background: #F5F5F5; padding: 5px;" |[[CXR]] confirmed by [[fluoroscopic]] sniff test<br />
! style="background: #F5F5F5; padding: 5px;" |[[Respiratory insufficiency]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Tuberculosis]]<ref name="pmid16709993">{{cite journal| author=Campbell IA, Bah-Sow O| title=Pulmonary tuberculosis: diagnosis and treatment. | journal=BMJ | year= 2006 | volume= 332 | issue= 7551 | pages= 1194-7 | pmid=16709993 | doi=10.1136/bmj.332.7551.1194 | pmc=1463969 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16709993 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Rhonchi]], [[Wheezing]], [[Crackles]]<br />
! style="background: #F5F5F5; padding: 5px;" |↑[[WBC]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]], ↑[[CO2]]<br />
! style="background: #F5F5F5; padding: 5px;" |Patchy [[Consolidation (medicine)|consolidation]] or poorly defined linear and nodular [[Opacity|opacities]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Restrictive Lung Disease|Restrictive]], [[Obstructive lung disease|obstructive]], or mixed<br />
! style="background: #F5F5F5; padding: 5px;" |[[Interferon-γ release assays|IFN-γ release assay (IGRA)]]<br />
<br />
[[Acid fast|Acid-fast staining]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Night sweat]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
! colspan="2" rowspan="7" |[[Cardiovascular system]]<br />
![[Constrictive pericarditis]]<ref name="pmid12481882" /><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Muffled heart sounds]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Calcification|Calcifications]] <br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Computed tomography|Chest CT scan]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Syncope]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Restrictive cardiomyopathy]]<ref name="pmid118386552">{{cite journal |vauthors=Nakamura M, Satoh M, Kowada S, Satoh H, Tashiro A, Sato F, Masuda T, Hiramori K |title=Reversible restrictive cardiomyopathy due to light-chain deposition disease |journal=Mayo Clin. Proc. |volume=77 |issue=2 |pages=193–6 |date=February 2002 |pmid=11838655 |doi=10.4065/77.2.193 |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Dilatation of the [[inferior vena cava]] and [[right atrium]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Right ventricular]] [[biopsy]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Weight gain]],<br />
<br />
[[Nausea]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Valvular heart disease]]<ref name="pmid18307844" /><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Cardiac murmur]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Dilatation of [[Heart chamber|heart chambers]] <br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Echocardiography]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Syncope]], [[Palpitation]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Bradyarrhythmia]]<ref name="pmid28266824">{{cite journal |vauthors=Barstow C, McDivitt JD |title=Cardiovascular Disease Update: Bradyarrhythmias |journal=FP Essent |volume=454 |issue= |pages=18–23 |date=March 2017 |pmid=28266824 |doi= |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[ECG]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Syncope]], [[Palpitation]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Pericardial effusion]]<ref name="pmid23236323">{{cite journal| author=Jung HO| title=Pericardial effusion and pericardiocentesis: role of echocardiography. | journal=Korean Circ J | year= 2012 | volume= 42 | issue= 11 | pages= 725-34 | pmid=23236323 | doi=10.4070/kcj.2012.42.11.725 | pmc=3518705 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23236323 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Muffled heart sounds]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Fluid density around the [[heart]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[M-mode echo: principles and classic findings|M-mode]] and [[Doppler echocardiography|2-dimensional Doppler echocardiography]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Hoarseness]], [[Palpitation]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Coronary heart disease]]<ref name="pmid18307844" /><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Cardiac troponin I (cTnI) and T (cTnT)|Cardiac troponin I]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Nausea]], [[Lightheadedness]], [[Sweating]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Ventricular septal defect|Intracardiac shunt]]<ref name="pmid193359162">{{cite journal| author=Vodoz JF, Cottin V, Glérant JC, Derumeaux G, Khouatra C, Blanchet AS et al.| title=Right-to-left shunt with hypoxemia in pulmonary hypertension. | journal=BMC Cardiovasc Disord | year= 2009 | volume= 9 | issue= | pages= 15 | pmid=19335916 | doi=10.1186/1471-2261-9-15 | pmc=2671488 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19335916 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Cardiac murmur|Cardiac continuous murmur]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]]<br />
! style="background: #F5F5F5; padding: 5px;" |Dilatation of [[Heart chamber|heart chambers]] <br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Echocardiography]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Syncope]], [[Palpitation]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
! colspan="2" rowspan="4" |[[Neuromuscular disease]]<br />
![[Amyotrophic lateral sclerosis]]<ref name="pmid17029274">{{cite journal |vauthors=Lechtzin N, Lange DJ, Davey C, Becker B, Mitsumoto H |title=Measures of dyspnea in patients with amyotrophic lateral sclerosis |journal=Muscle Nerve |volume=35 |issue=1 |pages=98–102 |date=January 2007 |pmid=17029274 |doi=10.1002/mus.20669 |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↑[[WBC]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]], ↑[[Residual volume|RV]]<br />
! style="background: #F5F5F5; padding: 5px;" |Revised El Escorial criteria (clinical)<br />
! style="background: #F5F5F5; padding: 5px;" |[[Muscle weakness]], [[Dysphagia]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Polymyositis]]/[[dermatomyositis]]<ref name="pmid1246203">{{cite journal |vauthors=Schwarz MI, Matthay RA, Sahn SA, Stanford RE, Marmorstein BL, Scheinhorn DJ |title=Interstitial lung disease in polymyositis and dermatomyositis: analysis of six cases and review of the literature |journal=Medicine (Baltimore) |volume=55 |issue=1 |pages=89–104 |date=January 1976 |pmid=1246203 |doi= |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↑[[WBC]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]], ↑[[Residual volume|RV]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Muscle biopsy]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Muscle weakness]], [[Dermatomyositis physical examination|Heliotrope]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Mitochondrial disease|Mitochondrial diseases]]<ref name="pmid21813873">{{cite journal| author=Heinicke K, Taivassalo T, Wyrick P, Wood H, Babb TG, Haller RG| title=Exertional dyspnea in mitochondrial myopathy: clinical features and physiological mechanisms. | journal=Am J Physiol Regul Integr Comp Physiol | year= 2011 | volume= 301 | issue= 4 | pages= R873-84 | pmid=21813873 | doi=10.1152/ajpregu.00001.2011 | pmc=3197343 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21813873 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Wheeze]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[WBC]], [[Platelet|Plt]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]], ↑[[Residual volume|RV]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Muscle biopsy]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Myalgia|Muscle pain]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[McArdle disease|Glycolytic enzyme defects (e.g., McArdle)]]<ref name="pmid7603522">{{cite journal |vauthors=Tarui S |title=Glycolytic defects in muscle: aspects of collaboration between basic science and clinical medicine |journal=Muscle Nerve Suppl |volume=3 |issue= |pages=S2–9 |date= 1995 |pmid=7603522 |doi= |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]], ↑[[Residual volume|RV]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Muscle biopsy]] (ragged red fibers)<br />
! style="background: #F5F5F5; padding: 5px;" |[[Myoglobinuria]],<br />
<br />
[[Muscle weakness]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
! colspan="2" rowspan="2" |[[Toxic]]/[[Metabolic]]<br />
![[Metabolic acidosis]]<ref name="pmid8350272">{{cite journal| author=Lane R, Adams L| title=Metabolic acidosis and breathlessness during exercise and hypercapnia in man. | journal=J Physiol | year= 1993 | volume= 461 | issue= | pages= 47-61 | pmid=8350272 | doi= | pmc=1175244 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8350272 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Metabolic acidosis]], [[Respiratory alkalosis]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Arterial blood gas|ABG]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Confusion]], [[Vomiting]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Renal failure]]<ref name="pmid12035070">{{cite journal |vauthors=DePalo LR |title=Fatal dyspnea in a patient with renal failure |journal=Mt. Sinai J. Med. |volume=69 |issue=3 |pages=113–20 |date=May 2002 |pmid=12035070 |doi= |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓ [[RBC]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Metabolic acidosis]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Creatinine|Cr]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Nausea]], [[Vomiting]], [[Oliguria]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
! colspan="2" rowspan="6" |[[Systemic]]<br />
![[Anemia]]<ref name="pmid23559772">{{cite journal| author=Sengupta A, Saha K, Jash D, Banerjee SN| title=Dyspnea with anemia turned out to be a case of hereditary hemorrhagic telangiectasia. | journal=Asian J Transfus Sci | year= 2013 | volume= 7 | issue= 1 | pages= 75-8 | pmid=23559772 | doi=10.4103/0973-6247.106745 | pmc=3613670 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23559772 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓ [[RBC]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Hemoglobin|HGB]], [[MCV]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Weakness]], [[Fatigue]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Anxiety]]<ref name="pmid15200799">{{cite journal |vauthors=Bailey PH |title=The dyspnea-anxiety-dyspnea cycle--COPD patients' stories of breathlessness: "It's scary /when you can't breathe" |journal=Qual Health Res |volume=14 |issue=6 |pages=760–78 |date=July 2004 |pmid=15200799 |doi=10.1177/1049732304265973 |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Psychological|Psychological interview]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Sweating]], [[Palpitation]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Ascites]]<ref name="pmid24336542">{{cite journal| author=Perri GA| title=Ascites in patients with cirrhosis. | journal=Can Fam Physician | year= 2013 | volume= 59 | issue= 12 | pages= 1297-9; e538-40 | pmid=24336542 | doi= | pmc=3860926 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24336542 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Peritoneal fluid accumulation<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]], ↑[[Residual volume|RV]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Medical ultrasonography|Abdominal ultrasound]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Abdominal distention]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Depression]]<ref name="pmid16516455">{{cite journal |vauthors=Neuman A, Gunnbjörnsdottir M, Tunsäter A, Nyström L, Franklin KA, Norrman E, Janson C |title=Dyspnea in relation to symptoms of anxiety and depression: A prospective population study |journal=Respir Med |volume=100 |issue=10 |pages=1843–9 |date=October 2006 |pmid=16516455 |doi=10.1016/j.rmed.2006.01.016 |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Psychological|Psychological interview]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Depressed mood]], [[fatigue]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Kyphoscoliosis]]<ref name="pmid26083538">{{cite journal| author=Qiabi M, Chagnon K, Beaupré A, Hercun J, Rakovich G| title=Scoliosis and bronchial obstruction. | journal=Can Respir J | year= 2015 | volume= 22 | issue= 4 | pages= 206-8 | pmid=26083538 | doi= | pmc=4530852 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26083538 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Wheeze]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Deviated [[vertebral column]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]], ↑[[Residual volume|RV]]<br />
([[anatomical]])<br />
! style="background: #F5F5F5; padding: 5px;" |[[X ray|Standing lateral spine radiograph]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Low back pain]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Obesity]]<ref name="pmid12090884">{{cite journal |vauthors=Sin DD, Jones RL, Man SF |title=Obesity is a risk factor for dyspnea but not for airflow obstruction |journal=Arch. Intern. Med. |volume=162 |issue=13 |pages=1477–81 |date=July 2002 |pmid=12090884 |doi= |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]], ↑[[Residual volume|RV]]<br />
([[anatomical]])<br />
! style="background: #F5F5F5; padding: 5px;" |[[Body mass index|BMI]]<br />
! style="background: #F5F5F5; padding: 5px;" |Low [[stamina]],<br />
[[Sweating]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
! colspan="2" rowspan="4" |[[Autoimmune]]<br />
![[Churg-Strauss syndrome]]<ref name="pmid22554368">{{cite journal |vauthors=Uyar M, Elbek O, Bakır K, Kibar Y, Bayram N, Dikensoy Ö |title=Churg-Strauss syndrome related to montelukast |journal=Tuberk Toraks |volume=60 |issue=1 |pages=56–8 |date= 2012 |pmid=22554368 |doi= |url= |author=}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |Scattered [[wheezing]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |Areas of [[parenchymal]] opacification<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]], ↑[[Residual volume|RV]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Biopsy]] <br />
! style="background: #F5F5F5; padding: 5px;" |[[Fatigue]],[[Numbness]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Microscopic polyangiitis]]<ref name="pmid26266064">{{cite journal| author=Tilanus A, Van der Niepen P, Geers C, Wissing KM| title=Pulmonary Limited MPO-ANCA Microscopic Polyangiitis and Idiopathic Lung Fibrosis in a Patient with a Diagnosis of IgA Nephropathy. | journal=Case Rep Nephrol | year= 2015 | volume= 2015 | issue= | pages= 378170 | pmid=26266064 | doi=10.1155/2015/378170 | pmc=4525752 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26266064 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |Scattered [[wheezing]]<br />
! style="background: #F5F5F5; padding: 5px;" |↑[[WBC]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]], ↑[[CO2]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Tidal volume|Vt]], ↑[[Residual volume|RV]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Histological]] confirmation<br />
! style="background: #F5F5F5; padding: 5px;" |[[Skin lesions]], [[Nerve damage]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Wegener's granulomatosis]]<ref name="pmid23034218">{{cite journal| author=Cardenas-Garcia J, Farmakiotis D, Baldovino BP, Kim P| title=Wegener's granulomatosis in a middle-aged woman presenting with dyspnea, rash, hemoptysis and recurrent eye complaints: a case report. | journal=J Med Case Rep | year= 2012 | volume= 6 | issue= | pages= 335 | pmid=23034218 | doi=10.1186/1752-1947-6-335 | pmc=3492078 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23034218 }}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+/-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |[[Wheezing]], [[Crackles]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓ [[RBC]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓[[Oxygen|O2]], ↑[[CO2]]<br />
! style="background: #F5F5F5; padding: 5px;" |Cavitate [[nodules]], ground-glass opacity<br />
! style="background: #F5F5F5; padding: 5px;" |↓ [[FEV1]]/[[FVC]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Biopsy]] demonstrating a [[granulomatous]] [[vasculitis]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Rhinosinusitis|Chronic rhinosinusitis]] <br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
![[Goodpasture disease|Goodpasture's disease]]<ref name="BalDas2014">{{cite journal|last1=Bal|first1=Amanjit|last2=Das|first2=Ashim|last3=Gupta|first3=Dheeraj|last4=Garg|first4=Mandeep|title=Goodpasture’s Syndrome and p-ANCA Associated Vasculitis in a Patient of Silicosiderosis: An Unusual Association|journal=Case Reports in Pulmonology|volume=2014|year=2014|pages=1–7|issn=2090-6846|doi=10.1155/2014/398238}}</ref><br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |+<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" |-<br />
! style="background: #F5F5F5; padding: 5px;" | Bilateral coarse [[crepitations]]<br />
! style="background: #F5F5F5; padding: 5px;" |↓ [[RBC]], [[Hemoglobin|HGB]], [[Hematocrit|HCT]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" | Like [[Pulmonary edema chest x ray|pulmonary edema]]<br />
! style="background: #F5F5F5; padding: 5px;" |Normal<br />
! style="background: #F5F5F5; padding: 5px;" |[[Kidney]] [[biopsy]]<br />
! style="background: #F5F5F5; padding: 5px;" |[[Hematuria]],<br />
[[Hemoptysis]]<br />
|- style="background: #DCDCDC; padding: 5px; text-align: center;" |<br />
|}<br />
</small></small><br />
<br />
==References==<br />
{{Reflist|2}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_diagnostic_study_of_choice&diff=1703579Pulmonary hypertension diagnostic study of choice2021-06-09T13:43:57Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}, Richard Channick, M.D.; '''Assistant Editor(s)-in-Chief:''' [[User:Ralph Matar|Ralph Matar]], [[User:Lisa Prior|Lisa Prior]], [[Ann Slater|Ann Slater, R.N.]]; {{Jose}}<br />
<br />
==Overview==<br />
[[Pulmonary hypertension]] is defined by a mean pulmonary arterial pressure higher than 25mmHg. It can be assessed by [[echocardiography]], the diagnostic study of choice due to its low risk and useful information that it can provide, and [[right heart cardiac catheterization]] to confirm the diagnosis. <br />
<br />
==Diagnosis==<br />
* The diagnostic approach to PH aims to:<ref name="Shitrit-2002">{{Cite journal | last1 = Shitrit | first1 = D. | last2 = Bendayan | first2 = D. | last3 = Rudensky | first3 = B. | last4 = Izbicki | first4 = G. | last5 = Huerta | first5 = M. | last6 = Fink | first6 = G. | last7 = Kramer | first7 = MR. | title = Elevation of ELISA d-dimer levels in patients with primary pulmonary hypertension. | journal = Respiration | volume = 69 | issue = 4 | pages = 327-9 | month = | year = 2002 | doi = 63270 | PMID = 12169745 }}</ref><ref name="Shitrit-2002-02">{{Cite journal | last1 = Shitrit | first1 = D. | last2 = Bendayan | first2 = D. | last3 = Bar-Gil-Shitrit | first3 = A. | last4 = Huerta | first4 = M. | last5 = Rudensky | first5 = B. | last6 = Fink | first6 = G. | last7 = Kramer | first7 = MR. | title = Significance of a plasma D-dimer test in patients with primary pulmonary hypertension. | journal = Chest | volume = 122 | issue = 5 | pages = 1674-8 | month = Nov | year = 2002 | doi = | PMID = 12426270 }}</ref><ref name="pmid3605900">{{cite journal| author=Rich S, Dantzker DR, Ayres SM, Bergofsky EH, Brundage BH, Detre KM et al.| title=Primary pulmonary hypertension. A national prospective study. | journal=Ann Intern Med | year= 1987 | volume= 107 | issue= 2 | pages= 216-23 | pmid=3605900 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3605900 }} </ref><ref name="pmid12716138">{{cite journal |author=Budev MM, Arroliga AC, Jennings CA |title=Diagnosis and evaluation of pulmonary hypertension |journal=Cleve Clin J Med |volume=70 Suppl 1 |issue= |pages=S9–17 |year=2003 |month=April |pmid=12716138 |doi= |url=}}</ref><ref name="isbn0-07-121971-4">{{cite book |author=Carolyn H. Welsh; Michael E. Hanley |title=Current diagnosis & treatment in pulmonary medicine |publisher=Lange Medical Books / McGraw-Hill |location=New York |year=2003 |pages= |isbn=0-07-121971-4 |oclc= |doi= |accessdate=}}</ref><ref name="Wiedemann-2001">{{Cite journal | last1 = Wiedemann | first1 = R. | last2 = Ghofrani | first2 = HA. | last3 = Weissmann | first3 = N. | last4 = Schermuly | first4 = R. | last5 = Quanz | first5 = K. | last6 = Grimminger | first6 = F. | last7 = Seeger | first7 = W. | last8 = Olschewski | first8 = H. | title = Atrial natriuretic peptide in severe primary and nonprimary pulmonary hypertension: response to iloprost inhalation. | journal = J Am Coll Cardiol | volume = 38 | issue = 4 | pages = 1130-6 | month = Oct | year = 2001 | doi = | PMID = 11583893 }}</ref><ref name="pmid11834666">{{cite journal |author=Bossone E, Paciocco G, Iarussi D, ''et al.'' |title=The prognostic role of the ECG in primary pulmonary hypertension |journal=Chest |volume=121 |issue=2 |pages=513–8 |year=2002 |month=February |pmid=11834666 |doi= |url=}}</ref><ref name="pmid10190427">{{cite journal |author=Kawut SM, Silvestry FE, Ferrari VA, ''et al.'' |title=Extrinsic compression of the left main coronary artery by the pulmonary artery in patients with long-standing pulmonary hypertension |journal=Am. J. Cardiol. |volume=83 |issue=6 |pages=984–6, A10 |year=1999 |month=March |pmid=10190427 |doi= |url=}}</ref><ref name="isbn0-7295-3905-9">{{cite book |author=Simon O'Connor MBBS FRACP DDU; Nicholas P. Hirsch MBBS FRCA FRCP |title=Clinical Examination: A Systematic Guide to Physical Diagnosis |publisher=Churchill Livingstone |location=Edinburgh |year=2009 |pages= |isbn=0-7295-3905-9 |oclc= |doi= |accessdate=}}</ref><ref name="pmid19713419">{{cite journal| author=Galiè N, Hoeper MM, Humbert M, Torbicki A, Vachiery JL, Barbera JA et al.| title=Guidelines for the diagnosis and treatment of pulmonary hypertension: the Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS), endorsed by the International Society of Heart and Lung Transplantation (ISHLT). | journal=Eur Heart J | year= 2009 | volume= 30 | issue= 20 | pages= 2493-537 | pmid=19713419 | doi=10.1093/eurheartj/ehp297 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19713419 }} </ref><ref name="isbn0-7817-7012-2">{{cite book |author=Thompson, Paul Richard; Topol, Eric J.; Califf, Robert M.; Prystowsky, Eric N.; Thomas, James Alan |title=Textbook of cardiovascular medicine |publisher=Lippincott Williams & Wilkins |location=Hagerstwon, MD |year=2007 |pages= |isbn=0-7817-7012-2 |oclc= |doi= |accessdate=}}</ref><ref name="Nagaya-2000">{{Cite journal | last1 = Nagaya | first1 = N. | last2 = Nishikimi | first2 = T. | last3 = Uematsu | first3 = M. | last4 = Satoh | first4 = T. | last5 = Kyotani | first5 = S. | last6 = Sakamaki | first6 = F. | last7 = Kakishita | first7 = M. | last8 = Fukushima | first8 = K. | last9 = Okano | first9 = Y. | title = Plasma brain natriuretic peptide as a prognostic indicator in patients with primary pulmonary hypertension. | journal = Circulation | volume = 102 | issue = 8 | pages = 865-70 | month = Aug | year = 2000 | doi = | PMID = 10952954 }}</ref><ref name="Kucher-2003">{{Cite journal | last1 = Kucher | first1 = N. | last2 = Printzen | first2 = G. | last3 = Goldhaber | first3 = SZ. | title = Prognostic role of brain natriuretic peptide in acute pulmonary embolism. | journal = Circulation | volume = 107 | issue = 20 | pages = 2545-7 | month = May | year = 2003 | doi = 10.1161/01.CIR.0000074039.45523.BE | PMID = 12742987 }}</ref><ref name="ten Wolde-2003">{{Cite journal | last1 = ten Wolde | first1 = M. | last2 = Tulevski | first2 = II. | last3 = Mulder | first3 = JW. | last4 = Söhne | first4 = M. | last5 = Boomsma | first5 = F. | last6 = Mulder | first6 = BJ. | last7 = Büller | first7 = HR. | title = Brain natriuretic peptide as a predictor of adverse outcome in patients with pulmonary embolism. | journal = Circulation | volume = 107 | issue = 16 | pages = 2082-4 | month = Apr | year = 2003 | doi = 10.1161/01.CIR.0000070020.79932.DB | PMID = 12707233 }}</ref><ref name="Leuchte-2006">{{Cite journal | last1 = Leuchte | first1 = HH. | last2 = Baumgartner | first2 = RA. | last3 = Nounou | first3 = ME. | last4 = Vogeser | first4 = M. | last5 = Neurohr | first5 = C. | last6 = Trautnitz | first6 = M. | last7 = Behr | first7 = J. | title = Brain natriuretic peptide is a prognostic parameter in chronic lung disease. | journal = Am J Respir Crit Care Med | volume = 173 | issue = 7 | pages = 744-50 | month = Apr | year = 2006 | doi = 10.1164/rccm.200510-1545OC | PMID = 16415273 }}</ref><br />
** Confirm the diagnosis of PH<br />
** Determine the classification group of PH<br />
** Specify the possible etiology for PH, if present<br />
** Evaluate the hemodynamic status of the patient<br />
<br />
===Diagnostic Study of Choice===<br />
* Echocardiography is the diagnostic study of choice, as it can:<br />
**Estimate the pulmonary artery systolic pressure (PSAP);<br />
**Evaluate for possible causes of [[pulmonary hypertension]];<br />
**Assess the presence of right atrial or ventricular enlargement, hypertrophy, or decreased right ventricular function;<br />
**May also evaluate left heart chambers, especially if they are causing [[pulmonary hypertension]];<br />
<br />
*Although pulmonary arterial pressure can be estimated on the basis of [[echocardiography]], pressure sampling with a [[Swan-Ganz catheter]] provides the most definite measurement. PAOP and PVR cannot be measured directly with [[echocardiography]]. <br />
* '''Therefore the diagnosis of PAH requires a [[cardiac catheterization]]'''. A [[Swan-Ganz catheter]] can also measure the [[cardiac output]], which is far more important in measuring disease severity than the pulmonary arterial pressure.<br />
* Normal pulmonary arterial pressure in a person living at sea level has a mean value between 12 and 16 mm Hg. Definite pulmonary hypertension is present when mean pressures at rest exceed 25 mm Hg. If mean pulmonary artery pressure rises above 30 mm Hg (4000 Pa) with exercise, that is also considered pulmonary hypertension.<br />
<br />
=== Diagnostic criteria ===<br />
A diagnosis of PAH requires the presence of pulmonary hypertension with two other conditions.<br />
* Pulmonary artery occlusion pressure (PAOP or PCWP) must be less than 15 mm Hg (2000 Pa)<br />
* Pulmonary vascular resistance (PVR) must be greater than 3 Wood units (240 dyn•s•cm<sup>-5</sup> or 2.4 mN•s•cm<sup>-5</sup>).<br />
<br />
== References ==<br />
{{Reflist|2}}<br />
{{WikiDoc Help Menu}}<br />
{{WikiDoc Sources}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_CT&diff=1703578Pulmonary hypertension CT2021-06-09T13:42:04Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}, Richard Channick, M.D.; '''Assistant Editor(s)-in-Chief:''' [[User:Ralph Matar|Ralph Matar]], [[User:Lisa Prior|Lisa Prior]], [[Ann Slater|Ann Slater, R.N.]]; {{Jose}}<br />
==Overview==<br />
A [[lung]] CT scan is helpful in the differential diagnosis of [[pulmonary hypertension]]. Different types of CT imaging have been used to rule out certain etiologies of pulmonary hypertension and to evaluate the anatomy of the pulmonary vasculature.<br />
<br />
==CT==<br />
*Contrast-enhanced images may show intraluminal abnormalities in the arteries and veins, which are useful for confirming etiologies such as [[thromboembolism|thromboembolic]] disease.<br />
*[[High-resolution CT]] (HRCT) scanning of the chest has a role in the evaluation of pulmonary hypertension in patients with suspected diffuse lung disease, like in patients with [[scleroderma]], [[interstitial lung disease]], and [[histiocytosis X]].<br />
*A [[spiral CT scan]] in a patient with pulmonary hypertension can also reveal enlarged pulmonary arteries and an absence of [[thrombosis]]. <br />
**The normal upper limit for the diameter of the pulmonary artery is 28.6 mm. A value greater than 28.6 mm suggests increased pressure in the pulmonary system.<ref>Pulmonary Hypertension Imaging,Author: Davinder Jassal, MD, FACC, FRCPC; Chief Editor: Eugene C Lin, MD</ref><br />
* A CT scan is 100% specific for the diagnosis of pulmonary veno-occlusive disease (PVOD).<ref name="pmid15208112">{{cite journal| author=Resten A, Maitre S, Humbert M, Rabiller A, Sitbon O, Capron F et al.| title=Pulmonary hypertension: CT of the chest in pulmonary venoocclusive disease. | journal=AJR Am J Roentgenol | year= 2004 | volume= 183 | issue= 1 | pages= 65-70 | pmid=15208112 | doi=10.2214/ajr.183.1.1830065 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15208112 }} </ref> The characteristics findings of PVOD on CT scan are:<ref name="pmid15208112">{{cite journal| author=Resten A, Maitre S, Humbert M, Rabiller A, Sitbon O, Capron F et al.| title=Pulmonary hypertension: CT of the chest in pulmonary venoocclusive disease. | journal=AJR Am J Roentgenol | year= 2004 | volume= 183 | issue= 1 | pages= 65-70 | pmid=15208112 | doi=10.2214/ajr.183.1.1830065 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15208112 }} </ref><br />
** Subpleural thickened septal lines<br />
** Centrilobular ground-glass opacities (vs panlobular opacities in idiopathic pulmonary arterial hypertension)<br />
** [[Adenopathy]]<br />
<br />
===Multi Sliced CT===<br />
<br />
Images shown below are courtesy of RadsWiki and copylefted.<br />
<br />
<div align="left"><br />
<gallery heights="175" widths="175"><br />
Image:Pulmonary-artery-hypertension-101.jpg|Pulmonary hypertension. Note increase in diameter of pulmonary artery.<br />
Image:Pulmonary-artery-hypertension-102.jpg|Pulmonary hypertension. Note increase in diameter of pulmonary artery.<br />
</gallery><br />
</div><br />
<br />
===CT-Scan of a Patient with Advanced Histiocytosis X Associated With Severe Pulmonary Hypertension<ref>Severe Pulmonary Hypertension in Histiocytosis X,Am. J. Respir. Crit. Care Med., Volume 161, Number 1, January 2000, 216-223</ref>===<br />
<gallery><br />
Image:Ct-scan for a patient with advanced Histiocytosis X associated with severe pulmonary hypertension.jpeg|CT-scan for a patient with advanced histiocytosis X associated with severe pulmonary hypertension.<br />
</gallery><br />
<br />
==References==<br />
{{Reflist|2}}<br />
{{WH}}<br />
{{WS}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]<br />
[[Category:Radiology]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_classification&diff=1703577Pulmonary hypertension classification2021-06-09T13:34:52Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}, Richard Channick, M.D.; '''Assistant Editor(s)-in-Chief:''' [[User:Ralph Matar|Ralph Matar]]; Lisa Prior, [[Ann Slater|Ann Slater, R.N.]]; {{Rim}}; {{Jose}}<br />
<br />
==Overview==<br />
[[Pulmonary hypertension]] may be classified according to the mechanism leading to its development into 5 groups: [[pulmonary arterial hypertension]], [[pulmonary hypertension due to left heart disease]], [[pulmonary hypertension due to chronic lung diseases and/or hypoxia]], and [[pulmonary hypertension due to embolic disease]], and [[miscellaneous]] causes.<br />
<br />
==Classification==<br />
*[[Pulmonary hypertension]] was first classified into [[primary]] and [[secondary]] in 1973 during the [[World Health Organization]] (WHO) meeting on PH in Geneva, Switzerland.<ref name="WHO1973">Hatano S, Strasser T. Primary Pulmonary Hypertension. Report on a WHO Meeting. October 15–17, 1973, Geneva: World Health Organization, 1975.</ref><br />
*Pulmonary hypertension can be classified following different methods such as using the [[WHO]] clinical criteria, the hemodynamic findings, and the histopathological findings. The most common method of classification is using the disease mechanism, established by the World Health Organization, which is discussed below in detail.<br />
<br />
==WHO - Clinical Classification==<br />
* [[Pulmonary hypertension]] was first classified into [[primary]] and [[secondary]] in 1973 during the [[World Health Organization]] (WHO) meeting on PH in Geneva, Switzerland.<ref name="WHO1973">Hatano S, Strasser T. Primary Pulmonary Hypertension. Report on a WHO Meeting. October 15–17, 1973, Geneva: World Health Organization, 1975.</ref><br />
* The classification of the disease has been progressively updated since then and the latest version was defined in 2018, during the 6th World Symposium on Pulmonary Hypertension.<br />
* It is currently used by the U.S. Food and Drug Administration (FDA) and the European Medicines Agency (EMA) for the labeling of new drugs approved for the treatment of [[pulmonary hypertension]].<br />
<br />
*The latest classification method categorizes [[pulmonary hypertension]] into 5 groups:<br />
** Group I - Pulmonary arterial hypertension<br />
** Group II - Pulmonary hypertension due to left heart disease <br />
** Group III - Pulmonary hypertension due to chronic lung diseases and/or hypoxia <br />
** Group IV - Pulmonary hypertension due to embolic disease<br />
** Group V - Miscellaneous causes (e.g., sarcoidosis, lymphatic obstruction)<br />
<br />
===WHO Classification===<br />
Shown below is a table with the detailed classification of [[pulmonary hypertension]].<ref name="pmid24355639">{{cite journal| author=Simonneau G, Gatzoulis MA, Adatia I, Celermajer D, Denton C, Ghofrani A et al.| title=Updated clinical classification of pulmonary hypertension. | journal=J Am Coll Cardiol | year= 2013 | volume= 62 | issue= 25 Suppl | pages= D34-41 | pmid=24355639 | doi=10.1016/j.jacc.2013.10.029 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24355639 }} </ref><br />
<br />
<span style="font-size: 80%;">''Abbreviations:'' BMPR, bone morphogenic protein receptor type II; CAV1, caveolin-1; ENG, endoglin; HIV, human immunodeficiency virus.</span><br />
<br />
{| style="cellpadding=0; cellspacing= 0; width: 600px;"<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''Group 1. Pulmonary arterial hypertension (PAH)'''<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |'''1.1. Idiopathic PAH''' <br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |'''1.2. Heritable PAH''' <br><br />
1.2.1 [[BMPR2]] <br><br />
1.2.2 [[ALK-1]], [[Endoglin|ENG]], [[SMAD9]], [[CAV1]], [[KCNK3]] <br><br />
1.2.3 Unknown<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |'''1.3 Drug and toxin-induced''' <br><br />
''Definite'' (an epidemic or large multicenter epidemiological studies demonstrating an association between a drug and PAH) <br><br />
*[[Aminorex]] <br />
*[[Fenfluramine]] <br />
*[[Dexfenfluramine]] <br />
*Toxic [[rapeseed oil]] <br />
*[[Benfluorex]] <br />
*[[SSRI]]s <br><br />
''Likely'' (a single case-control study demonstrating an association or a multiple-case series) <br><br />
*[[Amphetamine]]s <br />
*L-[[Tryptophan]] <br />
*[[Methamphetamine]]s <br />
*[[Dasatinib]] <br><br />
''Possible'' (drugs with similar mechanisms of action as those in the definite or likely category but which have not yet been studied) <br><br />
*[[Cocaine]] <br />
*[[Phenylpropanolamine]] <br />
*[[St. John's wort|St. John's Wort]] <br />
*[[Chemotherapeutic agent]]s <br />
*[[Interferon]] α and β <br />
*[[Amphetamine]]-like drugs <br><br />
''Unlikely'' (one in which a drug has been studied in epidemiological studies and an association with PAH has not been demonstrated) <br><br />
*[[Oral contraceptive]]s <br />
*[[Estrogen]] <br />
*[[Cigarette smoking]]<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |'''1.4 Associated with:''' <br><br />
1.4.1 [[Connective tissue disease]] <br><br />
1.4.2 [[HIV infection]] <br><br />
1.4.3 [[Portal hypertension]] <br><br />
1.4.4 [[Congenital heart disease]]s <br><br />
1.4.5 [[Schistosomiasis]] <br><br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''1’ Pulmonary veno-occlusive disease (PVOD) and/or pulmonary capillary hemangiomatosis (PCH)'''<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''1’’ Persistent pulmonary hypertension of the newborn (PPHN)'''<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''Group 2. Pulmonary hypertension due to left heart disease'''<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |2.1 [[Left ventricular systolic dysfunction]]<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |2.2 [[diastolic dysfunction|Left ventricular diastolic dysfunction]]<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |2.3 [[Valvular disease]]<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |2.4 [[Congenital heart disease|Congenital]]/acquired left heart inflow/outflow tract obstruction and congenital [[cardiomyopathies]]<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''Group 3. Pulmonary hypertension due to lung diseases and/or hypoxia'''<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |3.1 [[Chronic obstructive pulmonary disease]]<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |3.2 [[Interstitial lung disease]]<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |3.3 Other pulmonary diseases with mixed restrictive and obstructive pattern<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |3.4 Sleep-disordered breathing<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |3.5 Alveolar [[hypoventilation]] disorders<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |3.6 Chronic exposure to high altitude<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |3.7 Developmental lung diseases<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''Group 4. Chronic thromboembolic pulmonary hypertension (CTEPH)'''<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''Group 5. Pulmonary hypertension with unclear multifactorial mechanisms'''<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |5.1 Hematologic disorders: chronic [[hemolytic anemia]], [[myeloproliferative disorder]]s, [[splenectomy]]<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |5.2 Systemic disorders: [[sarcoidosis]], [[Langerhans cell histiocytosis|pulmonary histiocytosis]], [[lymphangioleiomyomatosis]]<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |5.3 Metabolic disorders: [[glycogen storage disease]], [[Gaucher disease]], [[thyroid]] disorders<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align="left" |5.4 Others: [[tumor]] obstruction, fibrosing [[mediastinitis]], [[chronic renal failure]], segmental PH<br />
|}<br />
<br />
==Classification Based on Hemodynamical Findings==<br />
<br />
<span style="font-size: 80%;">'''Abbreviations:''' '''PAP:''' Pulmonary artery pressure; '''PWP:''' pulmonary wedge pressure </span><br />
<br />
{| style="cellpadding=0; cellspacing= 0; width: 600px;"<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''Type of pulmonary hypertension''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''Possible clinical class''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''Mean PAP''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''PWP'''<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |'''Pre-capillary''' || style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |Class I <br>Class III <br>Class IV <br>Class V || style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |≥ 25 mmHg || style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |≤ 15 mmHg<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |'''Post-capillary''' || style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |Class II || style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |≥ 25 mmHg || style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |> 15 mmHg<br />
|}<br />
<br />
<br />
==Classification Based on Histopathological Findings==<br />
PH is a pathological condition present in different disease states that share similar clinical manifestations and some common histopathological features. Shown below is a table that summarizes the classification of PH based on histopathology findings.<ref name="pmid15194175">{{cite journal| author=Pietra GG, Capron F, Stewart S, Leone O, Humbert M, Robbins IM et al.| title=Pathologic assessment of vasculopathies in pulmonary hypertension. | journal=J Am Coll Cardiol | year= 2004 | volume= 43 | issue= 12 Suppl S | pages= 25S-32S | pmid=15194175 | doi=10.1016/j.jacc.2004.02.033 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15194175 }} </ref><br />
{| style="cellpadding=0; cellspacing= 0; width: 600px;"<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''Class''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF" align="left" |'''Histopathological findings'''<ref name="pmid15194175">{{cite journal| author=Pietra GG, Capron F, Stewart S, Leone O, Humbert M, Robbins IM et al.| title=Pathologic assessment of vasculopathies in pulmonary hypertension. | journal=J Am Coll Cardiol | year= 2004 | volume= 43 | issue= 12 Suppl S | pages= 25S-32S | pmid=15194175 | doi=10.1016/j.jacc.2004.02.033 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15194175 }} </ref><br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |'''Pulmonary arteriopathy''' || style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |Constrictive lesions in pulmonary arteries:<br />
* Medial hypertrophy <br />
* Intimal thickening <br />
* Adventitial thickening <br />
Complex lesions in pulmonary arteries:<br />
* Plexiform lesions <br />
* Dilatation lesions <br />
* [[Arteritis]] <br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |'''Pulmonary arteriopathy with venous-venular changes''' || style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" | Changes similar to pulmonary arteriopathy <br> PLUS<br> Changes in venules and veins<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width:50%" align="left" |'''Pulmonary occlusive venopathy''' <br> (with or without arteriopathy) || style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |Changes in venules and veins:<br />
* Diffuse fibrotic occlusion<br />
* Intimal thickening <br />
* Medial thickening <br />
* Adventitial thickening <br />
Changes in the capillaries:<br />
* Dilatation <br />
* Congestion <br />
Changes in the interstitium <br />
* [[Edema]] <br />
* [[Fibrosis]] <br />
* [[Hemosiderosis]]<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |'''Pulmonary microvasculopathy''' <br> (with or without arteriopathy and/on venopathy)|| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |Changes in the capillaries: <br />
* Localized capillary proliferation <br />
Changes in the interstitium <br />
* [[Edema]] <br />
* [[Fibrosis]] <br />
* [[Hemosiderosis]]<br />
|-<br />
| style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" |'''Unclassified''' || style="padding: 0 5px; font-size: 100%; background: #F5F5F5;" align="left" | Non specific changes<br />
|}<br />
<br />
==References==<br />
{{Reflist|2}}<br />
{{WikiDoc Help Menu}}<br />
{{WikiDoc Sources}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_chest_x_ray&diff=1703576Pulmonary hypertension chest x ray2021-06-09T13:31:14Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}, Richard Channick, M.D.; '''Assistant Editor(s)-in-Chief:''' [[User:Ralph Matar|Ralph Matar]]; {{Jose}}<br />
==Overview==<br />
<br />
A [[chest X-ray]] is abnormal in the majority of patients with pulmonary hypertension (PH); however, there is no correlation between the severity of PH and the findings on a chest X-ray. Findings of PH on a [[chest X-ray]] include [[pulmonary artery]] dilatation and right-sided enlargement of the heart. A [[chest X-ray]] may suggest that there is no compromise of the left heart if normal and allows for initial assessment of lung disease that can lead to group 2 and group 3 PH, respectively.<br />
<br />
==Chest X Ray==<br />
Findings of PH on a chest X-ray include:<ref name="pmid26552229">{{cite journal |vauthors=Korobkova IZ, Lazutkina VK, Nizovtsova LA, Riden TV |title=[Radiographic assessment of pulmonary hypertension: Methodical aspects] |language=Russian |journal=Vestn Rentgenol Radiol |volume= |issue=4 |pages=45–53 |date=2015 |pmid=26552229 |doi= |url=}}</ref><ref name="pmid24311231">{{cite journal |vauthors=Pienn M, Kovacs G, Tscherner M, Avian A, Johnson TR, Kullnig P, Stollberger R, Olschewski A, Olschewski H, Bálint Z |title=Non-invasive determination of pulmonary hypertension with dynamic contrast-enhanced computed tomography: a pilot study |journal=Eur Radiol |volume=24 |issue=3 |pages=668–76 |date=March 2014 |pmid=24311231 |doi=10.1007/s00330-013-3067-8 |url=}}</ref><ref name="pmid23912192">{{cite journal |vauthors=Cordova FC, D'Alonzo G |title=Sarcoidosis-associated pulmonary hypertension |journal=Curr Opin Pulm Med |volume=19 |issue=5 |pages=531–7 |date=September 2013 |pmid=23912192 |doi=10.1097/MCP.0b013e328363f4a3 |url=}}</ref><br />
* [[Hilar]] pulmonary arterial dilation<br />
* Loss of peripheral blood vessel markings<br />
* Enlarged right atrium, right ventricle and [[pulmonary arteries]] in advanced diseases.<ref name="pmid33844574">{{cite journal| author=Poch D, Mandel J| title=Pulmonary Hypertension. | journal=Ann Intern Med | year= 2021 | volume= 174 | issue= 4 | pages= ITC49-ITC64 | pmid=33844574 | doi=10.7326/AITC202104200 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33844574 }} </ref><br />
<br />
Shown below are chest X-ray images of patients with PH.<br />
<gallery><br />
Image:336139-361242-1175.jpg|This is a posteroanterior radiograph revealing enlarged pulmonary arteries in a patient with [[atrial septal defect]].<br />
Image:Pulmon4.gif<br />
Image:CXR for a patient with advanced [[Histiocytosis X]] associated with severe pulmonary hypertension.jpeg|Chest x-ray for a patient with advanced Histiocytosis X associated with severe pulmonary hypertension<br />
</gallery><br />
<br />
==References==<br />
{{Reflist|2}}<br />
{{WikiDoc Help Menu}}<br />
{{WikiDoc Sources}}<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]<br />
[[Category:Radiology]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Pulmonary_hypertension_causes&diff=1703575Pulmonary hypertension causes2021-06-09T13:29:49Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Pulmonary hypertension}}<br />
{{CMG}}; {{AE}} [[User:Ralph Matar|Ralph Matar]]; {{MM}}; {{Jose}}<br />
<br />
==Overview==<br />
[[Pulmonary hypertension]] may be caused by either [[left heart failure]] (the most common cause) or other somewhat common causes such as [[HIV]], [[systemic sclerosis]], [[portal hypertension]], [[congenital heart disease]], and [[sickle cell disease]].<br />
The World Health Organization (WHO) has classified PH based on etiology into five distinct groups: Group 1 (pulmonary arterial hypertension), Group 2 ([[PH]] due to [[left heart failure]]), Group 3 ([[PH]] due to [[chronic lung disease]] and/or [[hypoxemia]]), Group 4 ([[PH]] due to [[chronic thromboembolic disease]]), and Group 5 ([[PH]] due to multifactorial mechanisms).<br />
<br />
==Causes==<br />
<br />
===Life Threatening Causes===<br />
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. <br />
*Pulmonary hypertension itself is not a life-threatening condition, but it is progressively fatal if left untreated. [[Pulmonary embolism|Pulmonary embolism]] and [[left heart failure|acute left heart failure]] are two causes of pulmonary hypertension that can be quickly fatal.<br />
<br />
===Common Causes===<br />
The most common cause of pulmonary hypertension is [[left heart failure]] leading to pulmonary venous hypertension. Other common causes of pulmonary arterial hypertension (PAH) include:<ref name="pmid14985486">{{cite journal| author=Gladwin MT, Sachdev V, Jison ML, Shizukuda Y, Plehn JF, Minter K et al.| title=Pulmonary hypertension as a risk factor for death in patients with sickle cell disease. | journal=N Engl J Med | year= 2004 | volume= 350 | issue= 9 | pages= 886-95 | pmid=14985486 | doi=10.1056/NEJMoa035477 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14985486 }} </ref><ref name="pmid23852284">{{cite journal| author=Nayak NC, Chitale AR| title=Indian childhood cirrhosis (ICC) & ICC-like diseases: the changing scenario of facts versus notions. | journal=Indian J Med Res | year= 2013 | volume= 137 | issue= 6 | pages= 1029-42 | pmid=23852284 | doi= | pmc=PMC3734708 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23852284 }} </ref><ref name="pmid9776954">{{cite journal| author=Schultze AE, Roth RA| title=Chronic pulmonary hypertension--the monocrotaline model and involvement of the hemostatic system. | journal=J Toxicol Environ Health B Crit Rev | year= 1998 | volume= 1 | issue= 4 | pages= 271-346 | pmid=9776954 | doi=10.1080/10937409809524557 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9776954 }} </ref><ref name="pmid23741096">{{cite journal| author=Kashyap S, Mohapatra PR| title=Pulmonary alveolar microlithiasis. | journal=Lung India | year= 2013 | volume= 30 | issue= 2 | pages= 143-7 | pmid=23741096 | doi=10.4103/0970-2113.110424 | pmc=PMC3669555 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23741096 }} </ref><br />
*[[Cor pulmonale]] ([[right heart failure]] due to [[pulmonary disease]])<br />
*[[Congestive heart failure]]<br />
*[[Congenital heart disease]]<br />
*[[Chronic pulmonary thromboembolism]]<br />
*[[COPD]]<br />
*[[Pulmonary Hypertension|Familial Pulmonary Hypertension]]<br />
*[[HIV]]<br />
*[[Interstitial lung disease]]<br />
*[[Mitral stenosis]]<br />
*[[Obstructive sleep apnea]]<br />
*[[Portal hypertension]]<br />
*[[Pickwickian syndrome]]<br />
*[[Diseases of the valvular structures|Right-sided valvular disease]]<br />
*[[Systemic sclerosis]]<br />
*[[Systemic lupus erythematosus]]<br />
*[[Sickle cell disease]]<br />
*[[Stimulant drugs]] such as amphetamines<br />
<br />
====Idiopathic Pulmonary Arterial Hypertension====<br />
When none of the causes on this page can be found, the disease is termed idiopathic pulmonary arterial hypertension ([[IPAH]]).<br />
<br />
=== Causes by Organ System ===<br />
<br />
{| style="width:70%; height:100px" border="1"<br />
| style="width:25%" bgcolor="LightSteelBlue" ; border="1" | '''Cardiovascular'''<br />
| style="width:75%" bgcolor="Beige" ; border="1" | [[ASD|Atrial septal defect]], [[cor triatriatum]], [[left heart failure]], [[Fallot tetralogy]], [[persistent fetal circulation]], [[mitral valve stenosis]], [[mitral valve insufficiency]], [[ventricular septal defect]] <br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Chemical / poisoning'''<br />
| bgcolor="Beige" | [[Coal workers' pneumoconiosis]]<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Dermatologic'''<br />
| bgcolor="Beige" | [[Neurofibromatosis]], [[systemic lupus erythematosus]]<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Drug and Toxin Side Effect'''<br />
| bgcolor="Beige" | Definite: [[Aminorex]], [[Carfilzomib]], [[benfluorex]], [[dexfenfluramine]], [[Diethylpropion]], [[fenfluramine]], toxic [[rapeseed]] oil, [[benfluorex]], <br> Likely: [[Amphetamines]], L-[[tryptophan]], [[methamphetamine]] <br> Possible: [[Cocaine]], [[Lorcaserin]], [[Pegylated interferon alfa-2b]], [[phentermine]], [[phenylpropanolamine]], [[pergolide]],[[Protamine sulfate]],[[St John's wort]], [[chemotherapeutic agents]], [[SSRI]], [[Aprotinin]]<br />
<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Ear Nose Throat'''<br />
| bgcolor="Beige" | [[Pickwickian syndrome]]<br />
|- <br />
|- bgcolor="LightSteelBlue"<br />
| '''Endocrine'''<br />
| bgcolor="Beige" | [[Thyroid diseases]]<br />
|- <br />
|- bgcolor="LightSteelBlue"<br />
| '''Environmental'''<br />
| bgcolor="Beige" | [[High altitude sickness|High Altitude (chronically)]]<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Gastroenterologic'''<br />
| bgcolor="Beige" | [[Portal hypertension]]<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Genetic'''<br />
| bgcolor="Beige" | [[Alveolar capillary dysplasia|Alveolar capillary dysplasia with misalignment of pulmonary veins]], [[cholesterol ester storage disease]], [[cystic fibrosis]], [[Gaucher disease]], Indian familial childhood cirrhosis<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Hematologic'''<br />
| bgcolor="Beige" | [[Myeloproliferative disorders]], [[paroxysmal nocturnal haemoglobinuria]], [[polycythemia vera]], [[splenectomy]], [[sickle cell disease]]<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Iatrogenic'''<br />
| bgcolor="Beige" | No underlying cause<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Infectious Disease'''<br />
| bgcolor="Beige" | [[ Kaposi's sarcoma-associated herpesvirus|HHV-8]], [[schistosoma japonicum]] and [[schistosoma mansoni]]<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Musculoskeletal / Ortho'''<br />
| bgcolor="Beige" | [[Scoliosis|Idiopathic spinal scoliosis]]<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Neurologic'''<br />
| bgcolor="Beige" | No underlying cause<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Nutritional / Metabolic'''<br />
| bgcolor="Beige" | No underlying cause<br />
<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Obstetric/Gynecologic'''<br />
| bgcolor="Beige" | No underlying cause<br />
<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Oncologic'''<br />
| bgcolor="Beige" | No underlying causes<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Opthalmologic'''<br />
| bgcolor="Beige" | No underlying causes<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Overdose / Toxicity'''<br />
| bgcolor="Beige" | [[Diethylpropion]], monocrotaline, [[phentermine]], [[radiation exposure]] (fibrosing [[mediastinitis]] and [[pulmonary fibrosis]]).<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Psychiatric'''<br />
| bgcolor="Beige" | No underlying causes<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Pulmonary'''<br />
| bgcolor="Beige" | [[Idiopathic pulmonary hemosiderosis]], [[sarcoidosis]], [[primary pulmonary hypertension]], [[pulmonary fibrosis]], [[alveolar capillary dysplasia|alveolar capillary dysplasia with misalignment of pulmonary veins]], [[cystic fibrosis]], [[pulmonary embolism]], [[tropical pulmonary eosinophilia]], [[pulmonary capillary hemangiomatosis]], [[bronchiectasis]],[[bronchopulmonary dysplasia]], [[chronic obstructive pulmonary disease]], pulmonary alveolar microlithiasis, [[pulmonary fibrosis]], [[Langerhans cell histiocytosis]],[[interstitial lung disease]].<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Renal / Electrolyte'''<br />
| bgcolor="Beige" | [[renal failure|Chronic renal failure]] on [[dialysis]]<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Rheum / Immune / Allergy'''<br />
| bgcolor="Beige" | [[Vasculitis]], [[Churg-Strauss syndrome]], [[sarcoidosis]], [[systemic sclerosis]], [[systemic lupus erythematosus]].<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Sexual'''<br />
| bgcolor="Beige" | No underlying causes<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Trauma'''<br />
| bgcolor="Beige" | No underlying causes<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Urologic'''<br />
| bgcolor="Beige" | No underlying causes<br />
|-<br />
|- bgcolor="LightSteelBlue"<br />
| '''Miscellaneous'''<br />
| bgcolor="Beige" | [[Gaucher disease]], [[glycogen storage diseases]], [[scoliosis|idiopathic spinal scoliosis]], <br />
|-<br />
|}<br />
<br />
=== Causes in Alphabetical Order ===<br />
{{columns-list|<br />
* [[Alveolar capillary dysplasia|Alveolar capillary dysplasia with misalignment of pulmonary veins]]<br />
* [[Atrial Septal Defects]]<br />
* [[Bronchiectasis]]<br />
* [[Bronchopulmonary dysplasia]]<br />
* [[Cholesterol ester storage disease]]<br />
* [[hemolytic anemia|Chronic hemolytic anemia]]<br />
* [[Chronic obstructive pulmonary disease]]<br />
* [[renal failure|Chronic renal failure]] on [[dialysis]]<br />
* [[Churg-Strauss syndrome]]<br />
* [[Coal workers' pneumoconiosis]]<br />
* [[Cor triatriatum]]<br />
* [[Cystic fibrosis]]<br />
* [[Diastolic heart failure|Diastolic dysfunction]]<br />
* [[Diethylpropion]]<br />
* [[Fallot tetralogy]]<br />
* [[Fetal circulation, persistent]]<br />
* [[Fibrosing Mediastinitis|Fibrosing mediastinitis]]<br />
* [[Gaucher disease]]<br />
* [[Glycogen storage diseases]]<br />
* [[High altitude sickness|High Altitude(chronically)]]<br />
* [[Idiopathic pulmonary haemosiderosis]]<br />
* Indian familial childhood cirrhosis<br />
* [[Interstitial Lung Disease]]<br />
* [[Scoliosis|Idiopathic spinal scoliosis]]<br />
* [[Langerhans cell histiocytosis]]<br />
* [[Mitral valve insufficiency]]<br />
* [[Mitral valve stenosis]]<br />
* Monocrotaline poisoning<br />
* [[Myeloproliferative disorders]]<br />
* [[Neurofibromatosis]]<br />
* [[Obstructive sleep apnea]]<br />
* [[Paroxysmal nocturnal haemoglobinuria]]<br />
*[[Pergolide]]<br />
* [[Phentermine|Phentermine poisoning]]<br />
* [[Pickwickian syndrome]]<br />
* [[Portal hypertension]]<br />
* [[Polycythemia vera]]<br />
* Pulmonary alveolar microlithiasis<br />
* [[Pulmonary capillary hemangiomatosis]]<br />
* [[Pulmonary embolism]]<br />
* [[Pulmonary fibrosis]]<br />
* [[Pulmonary veno-occlusive disease]]<br />
* [[Sarcoidosis]]<br />
* [[Schistosoma japonicum]]<br />
* [[Schistosoma mansoni]]<br />
* [[Sickle cell disease]]<br />
* [[Splenectomy]]<br />
* [[Systemic lupus erythematosus]]<br />
* [[Systolic dysfunction]]<br />
* [[Tropical pulmonary eosinophilia]]<br />
* [[Vasculitis]]<br />
* [[Ventricular septal defect]]<br />
}}<br />
<br />
=== Causes by Clinical Classification ===<br />
<br />
<u>'''Class 1:'''</u> Pulmonary arterial hypertension<br />
# [[Pulmonary hypertension|Idiopathic pulmonary arterial hypertension]]<br />
# Heritable ([[BMPR2]], [[ALK-1]], [[ENG]], [[SMAD9]], [[CAV1]], [[KCNK3]])<br />
# Drug and toxin induced<br />
:* [[Aminorex]]<br />
:* [[Fenfluramine]]<br />
:* [[Dexfenfluramine]]<br />
:* Toxic [[rapeseed oil]]<br />
:* [[Benfluorex]]<br />
:* [[SSRI]]s<br />
<br />
<u>'''Class 2:'''</u> Pulmonary hypertension due to left heart disease<br />
# [[Left ventricular systolic dysfunction]]<br />
# [[diastolic dysfunction|Left ventricular diastolic dysfunction]]<br />
# [[Valvular disease]]<br />
# Congenital/acquired left heart inflow/outflow tract obstruction and congenital cardiomyopathies<br />
<br />
<u>'''Class 3:'''</u> Pulmonary hypertension due to lung diseases and/or hypoxia<br />
# [[Chronic obstructive pulmonary disease]]<br />
# [[Interstitial lung disease]]<br />
# Other pulmonary diseases with mixed [[Restrictive lung disease|restrictive]] and [[Obstructive Lung Disease|obstructive]] pattern<br />
# Sleep-disordered breathing<br />
# Alveolar hypoventilation disorders<br />
# Chronic exposure to high altitude<br />
# Developmental lung diseases<br />
<br />
<u>'''Class 4:'''</u> Chronic thromboembolic pulmonary hypertension<br />
<br />
<u>'''Class 5:'''</u> Pulmonary hypertension with unclear multifactorial mechanisms<br />
#'''Hematologic disorders''': Chronic [[hemolytic anemia]], [[Myeloproliferative disorders]], [[splenectomy]],<br />
#'''Systemic disorders''': [[Sarcoidosis]], [[Langerhans cell histiocytosis|pulmonary histiocytosis]], [[lymphangioleiomyomatosis]]<br />
#'''Metabolic disorders''': [[Glycogen storage disease]], [[Gaucher disease]], [[thyroid disorders]]<br />
#'''Miscellaneous''': Tumoral obstruction, fibrosing [[mediastinitis]], [[chronic renal failure]], segmental PH<br />
<br />
==References==<br />
{{Reflist|2}}<br />
<br />
[[Category:Medicine]]<br />
[[Category:Cardiology]]<br />
[[Category:Pulmonology]]<br />
[[Category:Emergency medicine]]<br />
[[Category:Up-To-Date]]<br />
<br />
<br />
{{WikiDoc Help Menu}}<br />
{{WikiDoc Sources}}</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Atopic_dermatitis_risk_factors&diff=1703508Atopic dermatitis risk factors2021-06-08T20:16:01Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Atopic dermatitis}}<br />
{{CMG}}; {{AE}} {{S.S}}<br />
<br />
==Overview==<br />
Atopic dermatitis is a multifactorial, [[chronic]] inflammatory skin disease as a result of interactions between various [[Genetics|genetic]], [[immune]], and environmental factors. The most important [[risk factor]] for the development of atopic dermatitis is a [[family history]] or personal history of [[atopy]] including [[asthma]], [[allergic rhinitis]], [[food allergy]].<br />
<br />
==Risk Factors==<br />
The most potent [[risk factor]] in the development of atopic dermatitis is a [[family history]] or personal history of [[atopy]].<br />
===Common Risk Factors===<br />
<br />
*Common [[Risk factor|risk factors]] in the development of atopic dermatitis include:<br />
**Family history of atopic dermatitis or other [[atopy]]<ref name="pmid19785611">{{cite journal |vauthors=Wen HJ, Chen PC, Chiang TL, Lin SJ, Chuang YL, Guo YL |title=Predicting risk for early infantile atopic dermatitis by hereditary and environmental factors |journal=Br. J. Dermatol. |volume=161 |issue=5 |pages=1166–72 |date=November 2009 |pmid=19785611 |doi=10.1111/j.1365-2133.2009.09412.x |url=}}</ref><br />
***70% of atopic dermatitis [[patients]] have a positive family history of atopic diseases<br />
***Risk of developing atopic dermatitis is 2- to 3-fold higher in children with 1 atopic parent <ref name="pmid2353830">{{cite journal |vauthors=Küster W, Petersen M, Christophers E, Goos M, Sterry W |title=A family study of atopic dermatitis. Clinical and genetic characteristics of 188 patients and 2,151 family members |journal=Arch. Dermatol. Res. |volume=282 |issue=2 |pages=98–102 |date=1990 |pmid=2353830 |doi= |url=}}</ref><br />
***Risk of developing atopic dermatitis is 3- to 5-fold higher in children with both atopic parents <ref name="pmid23538302">{{cite journal |vauthors=Küster W, Petersen M, Christophers E, Goos M, Sterry W |title=A family study of atopic dermatitis. Clinical and genetic characteristics of 188 patients and 2,151 family members |journal=Arch. Dermatol. Res. |volume=282 |issue=2 |pages=98–102 |date=1990 |pmid=2353830 |doi= |url=}}</ref><br />
**Loss of function [[mutations]] in the ''[[filaggrin]]'' ([[Filaggrin|''FLG'') gene]]<ref name="pmid16550169">{{cite journal |vauthors=Palmer CN, Irvine AD, Terron-Kwiatkowski A, Zhao Y, Liao H, Lee SP, Goudie DR, Sandilands A, Campbell LE, Smith FJ, O'Regan GM, Watson RM, Cecil JE, Bale SJ, Compton JG, DiGiovanna JJ, Fleckman P, Lewis-Jones S, Arseculeratne G, Sergeant A, Munro CS, El Houate B, McElreavey K, Halkjaer LB, Bisgaard H, Mukhopadhyay S, McLean WH |title=Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis |journal=Nat. Genet. |volume=38 |issue=4 |pages=441–6 |date=April 2006 |pmid=16550169 |doi=10.1038/ng1767 |url=}}</ref><br />
***Risk for earlier-onset atopic dermatitis<br />
***Risk for severe and persistent atopic dermatitis<br />
**Personal history of [[atopy]] ([[asthma]], [[allergic rhinitis]], [[food allergy]]) <ref name="pmid20579595">{{cite journal |vauthors=Suh KY |title=Food allergy and atopic dermatitis: separating fact from fiction |journal=Semin Cutan Med Surg |volume=29 |issue=2 |pages=72–8 |date=June 2010 |pmid=20579595 |doi=10.1016/j.sder.2010.03.007 |url=}}</ref><br />
** Environmental factors predisposing individuals to the development of atopic dermatitis include:<ref name="pmid23452057">{{cite journal |vauthors=Garmhausen D, Hagemann T, Bieber T, Dimitriou I, Fimmers R, Diepgen T, Novak N |title=Characterization of different courses of atopic dermatitis in adolescent and adult patients |journal=Allergy |volume=68 |issue=4 |pages=498–506 |date=April 2013 |pmid=23452057 |doi=10.1111/all.12112 |url=}}</ref><br />
***Temperature (colder climates with low [[humidity]])<br />
***Ultraviolet radiation<br />
***Air pollution<br />
***Water hardness<br />
***Household hygiene<br />
===Less Common Risk Factors===<br />
<br />
*Less common [[Risk factor|risk factors]] in the development of atopic dermatitis include:<br />
**[[Infections]]<br />
***Children who are frequently exposed to [[infections]], carry an increased probability of developing atopic dermatitis and other [[Allergic disorders|allergic diseases]].<ref name="pmid117993642">{{cite journal |vauthors=McKeever TM, Lewis SA, Smith C, Collins J, Heatlie H, Frischer M, Hubbard R |title=Early exposure to infections and antibiotics and the incidence of allergic disease: a birth cohort study with the West Midlands General Practice Research Database |journal=J. Allergy Clin. Immunol. |volume=109 |issue=1 |pages=43–50 |date=January 2002 |pmid=11799364 |doi= |url=}}</ref><br />
***During [[pregnancy]], exposure to [[antibiotics]] and [[infections]] is a crucial risk factor for the development of [[Atopy|atopic march]] diseases.<ref name="pmid122314922">{{cite journal |vauthors=McKeever TM, Lewis SA, Smith C, Hubbard R |title=The importance of prenatal exposures on the development of allergic disease: a birth cohort study using the West Midlands General Practice Database |journal=Am. J. Respir. Crit. Care Med. |volume=166 |issue=6 |pages=827–32 |date=September 2002 |pmid=12231492 |doi=10.1164/rccm.200202-158OC |url=}}</ref><br />
**House renovation<br />
***Mothers who have been living in a renovated areas during [[pregnancy]] has increased risk of developing [[atopic diseases]] in the children.<ref name="pmid197856112">{{cite journal |vauthors=Wen HJ, Chen PC, Chiang TL, Lin SJ, Chuang YL, Guo YL |title=Predicting risk for early infantile atopic dermatitis by hereditary and environmental factors |journal=Br. J. Dermatol. |volume=161 |issue=5 |pages=1166–72 |date=November 2009 |pmid=19785611 |doi=10.1111/j.1365-2133.2009.09412.x |url=}}</ref><br />
**[[Vaccination]]<br />
***Recent published studies has observed a significantly higher risk of [[asthma]] and [[atopic diseases]] in non-vaccinated children vs vaccinated children.<ref name="pmid15853947">{{cite journal |vauthors=Martignon G, Oryszczyn MP, Annesi-Maesano I |title=Does childhood immunization against infectious diseases protect from the development of atopic disease? |journal=Pediatr Allergy Immunol |volume=16 |issue=3 |pages=193–200 |date=May 2005 |pmid=15853947 |doi=10.1111/j.1399-3038.2005.00254.x |url=}}</ref><br />
**High domestic water [[calcium carbonate]] levels in infancy<ref name="pmid27241890">{{cite journal |vauthors=Perkin MR, Craven J, Logan K, Strachan D, Marrs T, Radulovic S, Campbell LE, MacCallum SF, McLean WH, Lack G, Flohr C |title=Association between domestic water hardness, chlorine, and atopic dermatitis risk in early life: A population-based cross-sectional study |journal=J. Allergy Clin. Immunol. |volume=138 |issue=2 |pages=509–16 |date=August 2016 |pmid=27241890 |doi=10.1016/j.jaci.2016.03.031 |url=}}</ref><br />
**Higher level of parental education<ref name="pmid20444159">{{cite journal |vauthors=Weber AS, Haidinger G |title=The prevalence of atopic dermatitis in children is influenced by their parents' education: results of two cross-sectional studies conducted in Upper Austria |journal=Pediatr Allergy Immunol |volume=21 |issue=7 |pages=1028–35 |date=November 2010 |pmid=20444159 |doi=10.1111/j.1399-3038.2010.01030.x |url=}}</ref><br />
**Living in urban areas<ref name="pmid20331459">{{cite journal |vauthors=Schram ME, Tedja AM, Spijker R, Bos JD, Williams HC, Spuls PI |title=Is there a rural/urban gradient in the prevalence of eczema? A systematic review |journal=Br. J. Dermatol. |volume=162 |issue=5 |pages=964–73 |date=May 2010 |pmid=20331459 |doi=10.1111/j.1365-2133.2010.09689.x |url=}}</ref><br />
**Exposure to [[antibiotics]] in [[infancy]]<ref name="pmid23782060">{{cite journal |vauthors=Tsakok T, McKeever TM, Yeo L, Flohr C |title=Does early life exposure to antibiotics increase the risk of eczema? A systematic review |journal=Br. J. Dermatol. |volume=169 |issue=5 |pages=983–91 |date=November 2013 |pmid=23782060 |doi=10.1111/bjd.12476 |url=}}</ref><br />
**Active and passive exposure to tobacco<ref name="pmid27542586">{{cite journal |vauthors=Kantor R, Kim A, Thyssen JP, Silverberg JI |title=Association of atopic dermatitis with smoking: A systematic review and meta-analysis |journal=J. Am. Acad. Dermatol. |volume=75 |issue=6 |pages=1119–1125.e1 |date=December 2016 |pmid=27542586 |pmc=5216172 |doi=10.1016/j.jaad.2016.07.017 |url=}}</ref><br />
**Itching causes scratching which leads to dysfunction of the epidermal skin barrier.<br />
***[[Risk factors]] which aggravate itching include [[sweating]], [[dry skin]], [[emotional stress]], hot water, and certain foods.<br />
**[[Stress]] can result into increased levels of [[Cortisol|glucocorticosteroids]] in blood, which further leads to dysfunction of skin barrier by affecting the integrity and adhesion of the [[stratum corneum]].<ref name="pmid18606083">{{cite journal |vauthors=Arndt J, Smith N, Tausk F |title=Stress and atopic dermatitis |journal=Curr Allergy Asthma Rep |volume=8 |issue=4 |pages=312–7 |date=July 2008 |pmid=18606083 |doi= |url=}}</ref><br />
<br />
==References==<br />
<br />
{{Reflist|2}}<br />
<br />
[[Category:Autoimmune diseases]]<br />
[[Category:Dermatology]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Atopic_dermatitis_physical_examination&diff=1703505Atopic dermatitis physical examination2021-06-08T20:12:32Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Atopic dermatitis}}<br />
<br />
{{CMG}};{{AE}}{{S.S}}<br />
<br />
==Overview==<br />
Atopic dermatitis is a chronic or relapsing [[hypersensitive]] manifestation of the [[skin]]. Common physical examination findings of atopic dermatitis include [[pruritus]], [[Eczema|eczematous]] lesions, [[xerosis]] and [[lichenification]]. The lesions are usually age-specific and can be at various stages of development. The lesions can involve any area of the body in severe cases, but usually, it is uncommon to find lesions in the [[axillary]], [[gluteal]], or [[groin]] area.<br />
<br />
==Physical Examination==<br />
The clinical presentation of atopic dermatitis is highly variable, depending upon the patient's age and disease activity.<ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
<br />
===Appearance of the Patient===<br />
*Patients with atopic dermatitis usually appear normal. <br />
<br />
===Vital Signs===<br />
<br />
*Vitals signs in atopic dermatitis patients are usually within normal limits.<br />
<br />
===Skin===<br />
'''Primary findings''':<br />
* Primary findings are present in all cases of atopic dermaitis.<ref name="Thestrup-Pedersen2000">{{cite journal|last1=Thestrup-Pedersen|first1=K.|title=Clinical aspects of atopic dermatitis|journal=Clinical and Experimental Dermatology|volume=25|issue=7|year=2000|pages=535–543|issn=0307-6938|doi=10.1046/j.1365-2230.2000.00696.x}}</ref><br />
** Atopic [[Itch]]: Severe pruritus- cardinal feature of atopic dermatitis (must be present)<br />
** Atopic [[xerosis]]: Dry skin, especially during winters <br />
** Atopic [[eczema]]: Location of lesions has age-specific patterns <br />
** Stigmata of AD <br />
'''Other findings''':<br />
* Symmetrical [[lesions]]<br />
* Constant scratching may lead to [[lichenification]]<br />
<br />
* An acute eczematoid eruption (with erythematous [[papules]]) appears after patients scratch their skin.<br />
* Most severe form of atopic dermatitis can include [[erythroderma]]<br />
'''Typical morphology and distribution''':<br />
* [[Eczema|Eczematous]] dermatitis:<ref>{{cite journal|title=Japanese Dermatological Association Criteria for the diagnosis of atopic dermatitis|journal=The Journal of Dermatology|volume=29|issue=6|year=2002|pages=398–398|issn=03852407|doi=10.1111/j.1346-8138.2002.tb00292.x}}</ref>erythema is more frequently violaceous or even invisible in Black patients. The<br />
lesions are characterized by papules, papulovesicles, edema, crusting, and scaling <br />
{| class="wikitable"<br />
|+<br />
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Acute atopic dermatitis'''<br />
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Subacute or chronic atopic dermatitis'''<br />
|-<br />
|<br />
* [[Erythema]], [[Exudate|exudates]], [[papules]], [[vesicles]], scales and crusts<br />
* Can usually get infected with ''[[Staphylococcus aureus]]''<br />
* Lesions are intensely pruritic <br />
|<br />
* Infiltrated [[erythema]], [[prurigo]], scales and crusts<br />
* Lesions are dry or excoriated [[erythematous]] [[papules]]<br />
* [[Lichenification]] and fissuring may develop over time<br />
|}<br />
'''Age-specific patterns''':<br />
{| class="wikitable"<br />
|+<br />
! colspan="3" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Infants and young children(zero to two years)'''<br />
|-<br />
|<br />
* Earliest lesions:<ref name="pmid97349034">{{cite journal |vauthors=Rudikoff D, Lebwohl M |title=Atopic dermatitis |journal=Lancet |volume=351 |issue=9117 |pages=1715–21 |date=June 1998 |pmid=9734903 |doi=10.1016/S0140-6736(97)12082-7 |url=}}</ref><ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
** Presents with [[erythema]] and exudation of the creases([[Antecubital fossa|antecubital]] and [[Popliteal fossa|popliteal fossae]])<br />
<br />
* Over the following few weeks:<br />
** Highly pruritic, red, scaly and crusted lesions, usually localized to the cheeks, the forehead and scalp, and the [[extensors]] of the lower legs<br />
* Lesions are ill-defined, [[erythematous]], scaly, and crusted (eczematous) patches and [[plaques]].<br />
* Most commonly involved areas:<br />
** Scalp, cheeks and [[extensor]] side of the extremities.<br />
** Flexural areas, especially the neck fold<br />
* Midline of the face and the tip of the nose is spared (Yamamoto’s sign)<br />
* Diaper area is generally spared<br />
* [[Lichenification]] is uncommon in infancy<br />
|-<br />
! colspan="3" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Older children and adolescents (2 to 16 years)'''<br />
|-<br />
|<br />
* [[Lichenification]] is characteristic of childhood atopic dermatitis<br />
<br />
* Areas involved: <br />
** Flexural areas, particularly the [[Antecubital fossa|antecubital]] and [[Popliteal fossa|popliteal fossae]], and buttock-thigh creases<br />
** [[Volar|Volar aspect]] of the wrists and ankles<br />
** "Atopic dirty neck" - neck and sides of the neck may show a reticulate pigmentation<br />
* Thickened plaques show [[lichenification]] and [[excoriation]]<br />
* [[Xerosis]] is generalized<br />
* Dennie-Morgan folds (i.e. increased folds below the eye) along with [[erythema]] and scaling around the eyes<br />
* Centrofacial pallor<br />
* Dry skin and fissuring behind the ears or on the earlobe (infra-auricular and retro-auricular fissuring)<br />
* In African-American patients, papulonodular lesions are prominent with post-inflammatory [[hyperpigmentation]]<br />
|-<br />
! colspan="3" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Adults (from puberty onward)'''<br />
|-<br />
|<br />
* Lesions are more localized and lichenified<ref name="pmid18402293">{{cite journal |vauthors=Kulthanan K, Samutrapong P, Jiamton S, Tuchinda P |title=Adult-onset atopic dermatitis: a cross-sectional study of natural history and clinical manifestation |journal=Asian Pac. J. Allergy Immunol. |volume=25 |issue=4 |pages=207–14 |date=December 2007 |pmid=18402293 |doi= |url=}}</ref><ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
* Areas involved:<br />
** Facial involvement is common, especially in the forehead and periorbital regions.<br />
** [[Lichenification]] occurs in skin flexures such as wrists, hands, ankles, feet, fingers, and toes<br />
<br />
* Atopic dirty neck: A brown macular ring around the neck may be present (localized deposition of [[amyloid]])<br />
* [[Xerosis]] is prominent<br />
|}<br />
'''Associated symptoms with atopic dermatitis''':<ref name="RotheGrant-Kels19963">{{cite journal|last1=Rothe|first1=Marti Jill|last2=Grant-Kels|first2=Jane M|title=Diagnostic criteria for atopic dermatitis|journal=The Lancet|volume=348|issue=9030|year=1996|pages=769–770|issn=01406736|doi=10.1016/S0140-6736(05)65206-3}}</ref><ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
{| class="wikitable"<br />
|+<br />
! colspan="3" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Atopic stigmata'''<br />
(associated cutaneous findings seen in atopic dermatitis patients)<br />
|-<br />
|<br />
* Atypical vascular responses<br />
** Centrofacial pallor<br />
** Delayed blanch response<br />
* Skin<br />
** [[Keratosis pilaris]]<br />
** Palmar hyperlinearity<br />
** [[Pityriasis alba]]<br />
** [[Ichthyosis]]<br />
* [[Ocular]]/periorbital<br />
** Periorbital darkening and Dennie-Morgan infraorbital folds<br />
** Hertoghe's sign- thinning or absence of the lateral portion of the eyebrows<br />
* Other <br />
** Infra-auricular and retro-auricular fissuring<br />
** Nipple [[eczema]]<br />
** White dermographism<br />
** Perifollicular accentuation<br />
|}<br />
'''Clinical phenotypes of atopic dermatitis:'''<br />
* Localized and morphological variants of atopic dermatitis are present in both children and adults.<br />
* These variants can present as only clinical features of atopic dermatitis or can present in association with age-related manifestations.<br />
{| class="wikitable"<br />
|+<br />
! colspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Different phenotypes of atopic dermatitis<ref name="pmid21054785">{{cite journal |vauthors=Pugliarello S, Cozzi A, Gisondi P, Girolomoni G |title=Phenotypes of atopic dermatitis |journal=J Dtsch Dermatol Ges |volume=9 |issue=1 |pages=12–20 |date=January 2011 |pmid=21054785 |doi=10.1111/j.1610-0387.2010.07508.x |url=}}</ref> <br />
|-<br />
| colspan="2" |<br />
* Acute vs chronic eczema<br />
* Intrinsic vs extrinsic atopic eczema <br />
* Early onset vs late-onset<br />
* Mild vs severe eczema<br />
* Increased [[IgE]] vs non-atopic<br />
* [[Staphylococcus aureus|''Staphylococcus aureus'']] infection/colonization, disseminated viral or fungal infections e.g. [[Molluscum contagiosum|''Molluscum contagiosum'']], [[Malassezia furfur|''Malassezia'']]<br />
* Associated with [[ichthyosis]], [[keratosis pilaris]], palmar hyperlinearity, early-onset, severe and persistent eczema (FLG null genotype)<br />
|-<br />
! style="background: #7d7d7d; color: #FFFFFF; text-align: center;" |Localized variants<br />
! style="background: #7d7d7d; color: #FFFFFF; text-align: center;" |Morphological variants<br />
|-<br />
|<br />
* Hand eczema<br />
* Juvenile [[palmar]] and [[plantar]] dermatitis<br />
* Eyelid dermatitis<br />
* Atopic [[cheilitis]] <br />
* Periorificial dermatitis<br />
* Nipple dermatitis<br />
|<br />
* Nummular eczema<br />
<br />
* [[Prurigo|Atopic prurigo]]<br />
<br />
* [[Lichen planus]]-like <br />
<br />
* [[Pityriasis alba|Pit]]<span class="_ _1 current-selection"></span>[[Pityriasis alba|yriasis alba]]<span class="_ _1 current-selection"></span><br />
|}<br />
* '''Localized variants''':<ref name="pmid21054785" /><br />
** Atopic hand eczema:<ref name="pmid16956463">{{cite journal |vauthors=Simpson EL, Thompson MM, Hanifin JM |title=Prevalence and morphology of hand eczema in patients with atopic dermatitis |journal=Dermatitis |volume=17 |issue=3 |pages=123–7 |date=September 2006 |pmid=16956463 |doi= |url=}}</ref><ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
*** Atopic hand eczema typically affects [[volar]] wrists and [[dorsum]] of the hands<ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
*** One-third of patients with atopic hand eczema, also reports foot eczema<ref name="pmid25716740">{{cite journal |vauthors=Brans R, Hübner A, Gediga G, John SM |title=Prevalence of foot eczema and associated occupational and non-occupational factors in patients with hand eczema |journal=Contact Derm. |volume=73 |issue=2 |pages=100–7 |date=August 2015 |pmid=25716740 |doi=10.1111/cod.12370 |url=}}</ref><br />
*** Common in adults with past medical history of history of atopic dermatitis, and currently do not have dermatitis in typical areas (i.e. flexural)<br />
*** Most common in adults exposed to wet environments <br />
** Eyelid eczema:<ref name="pmid24314387">{{cite journal |vauthors=Wolf R, Orion E, Tüzün Y |title=Periorbital (eyelid) dermatides |journal=Clin. Dermatol. |volume=32 |issue=1 |pages=131–40 |date=2014 |pmid=24314387 |doi=10.1016/j.clindermatol.2013.05.035 |url=}}</ref><br />
*** Some patients of atopic dermatitis, may present with eyelid eczema alone<br />
*** Associated with [[lichenification]] and presence of Dennie-Morgan lines<br />
** Atopic cheilitis:<br />
*** Also known as lip eczema or cheilitis sicca<br />
*** Presents as dryness, peeling, and fissuring of the lips <br />
** Juvenile papular dermatitis:<ref name="pmid83084">{{cite journal |vauthors=Rasmussen JE |title=Sutton's summer prurigo of the elbows |journal=Acta Derm. Venereol. |volume=58 |issue=6 |pages=547–9 |date=1978 |pmid=83084 |doi= |url=}}</ref><br />
*** Primarily occurs in the spring and summer - associated with [[pollinosis]] <br />
*** Localized mainly to the elbows and knees <br />
** Juvenile [[palmar]] and [[plantar]] dermatitis<br />
*** Painful variant of atopic dermatitis <br />
*** Localized on the anterior part of the sole <br />
* '''Morphological variants''':<ref name="pmid21054785" /><br />
** [[Nummular dermatitis|Nummular]] (discoid eczema):<br />
*** Sharply demarcated patches and plaques with inflammation of skin <br />
*** Secondarily infection with [[Staphylococcus aureus|''Staphylococcus aureus'']] common <br />
*** Commonly affected areas- extremities and buttocks<br />
*** Very difficult to treat<br />
<br />
=== HEENT ===<br />
* In patients with atopic dermatitis, eczematous lesions can be present on the face, depending on the age of the patients.<br />
<gallery><br />
Image:Atopic Dermatitis01.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis05.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis06.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis11.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis12.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis13.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis16.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis17.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis18.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis19.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis32.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis20.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis21.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis22.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis23.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis24.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis27.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis28.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis29.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis31.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis01.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis05.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis06.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis11.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis12.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis13.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis16.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis17.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis18.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis19.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis20.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis01.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis05.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis06.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis11.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis12.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis13.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis16.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis17.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis18.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis19.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Skin atopic dermatitis2.jpg|Atopic dermatitis<br />
</gallery><br />
<br />
===Neck===<br />
* Neck examination of patients with atopic dermatitis is usually normal.<br />
* Eczematous lesions can be present depending on the age of the patients.<br />
<br />
===Lungs===<br />
* Pulmonary examination of patients with atopic dermatitis is usually normal.<br />
<br />
===Heart===<br />
* Cardiovascular examination of patients with atopic dermatitis is usually normal.<br />
<br />
===Abdomen===<br />
* Abdominal examination of patients with atopic dermatitis is usually normal.<br />
<br />
===Back===<br />
* In patients with atopic dermatitis, eczematous lesions can be present on the trunk, depending on the age of the patients.<br />
<gallery><br />
Image:Atopic Dermatitis07.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis08.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis09.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis10.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis14.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
</gallery><br />
<br />
===Genitourinary===<br />
* Genitourinary examination of patients with atopic dermatitis is usually normal.<br />
<br />
===Neuromuscular===<br />
* Neuromuscular examination of patients with atopic dermatitis is usually normal.<br />
<br />
===Extremities===<br />
* In patients with atopic dermatitis, eczematous lesions can be present on extremities, depending on the age of the patients.<br />
<gallery><br />
Image:Atopic Dermatitis02.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis03.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis04.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis15.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis25.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis26.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis33.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis34.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Atopic Dermatitis36.jpg|Atopic Dermatitis. ''[http://www.atlasdermatologico.com.br/ Adapted from Dermatology Atlas.]''<br />
Image:Skin atopic dermatitis.jpg|Atopic dermatitis<br />
</gallery><br />
<br />
(Images courtesy of Charlie Goldberg, M.D.)<br />
<br />
<div align="left"><br />
<gallery heights="175" widths="175"><br />
<br />
</gallery><br />
</div><br />
<br />
==References==<br />
{{Reflist|2}}<br />
<br />
[[Category:Autoimmune diseases]]<br />
[[Category:Dermatology]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Atopic_dermatitis_pathophysiology&diff=1703504Atopic dermatitis pathophysiology2021-06-08T20:08:09Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Atopic dermatitis}}<br />
<br />
{{CMG}}; {{AE}} {{S.S}}<br />
<br />
==Overview==<br />
<br />
[[Atopic dermatitis]] is a [[chronic]] [[inflammatory]] [[skin disorder]] with an [[Immunology|immunologic]] background and occurs in patients with a personal or [[family history]] of [[atopy]] (i.e. [[asthma]] or [[allergic rhinitis]]). It is caused by either a skin barrier dysfunction or [[immune]] dysregulation of the [[Adaptive immunity|adaptive]] and [[innate immune response]] leading to an enhanced [[IgE]]-mediated, systemic [[Th2 response]]. The skin barrier is invaded by [[exogenous]] substances, including [[allergens]], [[irritants]] and [[microbes]]; and the tightly packed structure of the [[stratum corneum]] is further compromised. Systemically, a dysfunctional [[Innate immune system|innate]] and [[adaptive immune response]] causes further damage to the [[epidermis]]. <br />
<br />
==Pathophysiology==<br />
===Physiology===<br />
The normal physiology of [[atopic dermatitis]] can be understood as follows:<br />
<br />
'''Epidermal barrier function:'''<br />
<br />
*'''Epidermis''': It directly interfaces with the [[Environment (biophysical)|environment]] and acts as the 1st line of defense. It is primarily dependent on the structure and composition of the most outermost layer of the skin, i.e. [[stratum corneum]]. It protects the body from [[irritants]], [[allergens]], [[microbes]], and [[pathogens]] from invading the skin as well as preventing the excess water loss. The epidermis consists of:<ref name="pmid25131691">{{cite journal |vauthors=Elias PM, Wakefield JS |title=Mechanisms of abnormal lamellar body secretion and the dysfunctional skin barrier in patients with atopic dermatitis |journal=J. Allergy Clin. Immunol. |volume=134 |issue=4 |pages=781–791.e1 |date=October 2014 |pmid=25131691 |pmc=4186911 |doi=10.1016/j.jaci.2014.05.048 |url=}}</ref><br />
**Tightly packed corneocytes layers in the [[stratum corneum]]<br />
**Intercellular lipid bilayers<br />
**Corneocytes layers embedded in the [[extracellular matrix]] derived from [[lipid]] [[Lamellae (zoology)|lamellae]]<br />
**Natural moisturizing factors (NMF), maintaining the water retention in the [[stratum corneum]]<br />
**[[Antimicrobial peptides]]<br />
*'''Filaggrin proteins:''' It is encoded by [[Filaggrin|filaggrin gene ''FLG'']] on [[chromosome]] 1q21 (contains the genes of the [[epidermal differentiation complex]] (EDC)) and is the main component required to form corneocytes in the [[stratum corneum]].<ref name="pmid19386895">{{cite journal |vauthors=Sandilands A, Sutherland C, Irvine AD, McLean WH |title=Filaggrin in the frontline: role in skin barrier function and disease |journal=J. Cell. Sci. |volume=122 |issue=Pt 9 |pages=1285–94 |date=May 2009 |pmid=19386895 |pmc=2721001 |doi=10.1242/jcs.033969 |url=}}</ref><ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
**Pro-[[filaggrin]] is required for the formation of [[dense]] [[cytoplasmic]] [[granules]], which along with other [[Protein|proteins]], forms the corneocytes that acts as a primary unit for the barrier function of the [[skin]].<br />
**Pro-[[filaggrin]] undergoes extensive [[phosphorylation]] and [[dephosphorylation]], to produce [[filaggrin]] [[Monomer|monomers]] to interact and aggregate with the [[keratin]] filaments and permits extensive crosslinking, to form a highly insoluble [[keratin]] matrix.<ref name="pmid193868952">{{cite journal |vauthors=Sandilands A, Sutherland C, Irvine AD, McLean WH |title=Filaggrin in the frontline: role in skin barrier function and disease |journal=J. Cell. Sci. |volume=122 |issue=Pt 9 |pages=1285–94 |date=May 2009 |pmid=19386895 |pmc=2721001 |doi=10.1242/jcs.033969 |url=}}</ref><br />
**The degraded products of [[filaggrin]] protein are one of the major components of natural moisturizing factors (NMF), which prevents excess water loss from the [[stratum corneum]].<br />
**The degraded products of [[filaggrin]] protein also maintain the [[Acid|acidic]] [[pH]] of the [[stratum corneum]], required to regulate the activity of [[enzymes]].<br />
*'''Proteins related to tight junctions''': These [[transmembrane proteins]] are present in the [[stratum granulosum]] of the [[epidermis]] and come together to form [[tight junctions]] which includes the [[Claudins|claudin-1]], [[occludin]], junctional [[adhesion]] molecule.<ref name="pmid211635152">{{cite journal |vauthors=De Benedetto A, Rafaels NM, McGirt LY, Ivanov AI, Georas SN, Cheadle C, Berger AE, Zhang K, Vidyasagar S, Yoshida T, Boguniewicz M, Hata T, Schneider LC, Hanifin JM, Gallo RL, Novak N, Weidinger S, Beaty TH, Leung DY, Barnes KC, Beck LA |title=Tight junction defects in patients with atopic dermatitis |journal=J. Allergy Clin. Immunol. |volume=127 |issue=3 |pages=773–86.e1–7 |date=March 2011 |pmid=21163515 |pmc=3049863 |doi=10.1016/j.jaci.2010.10.018 |url=}}</ref><br />
*'''Other proteins''': [[Filaggrin]]-2, [[corneodesmosin]], [[desmoglein-1]], desmocollin-1, [[Transglutaminase|transglutaminase-3]] are also part of skin barrier related proteins.<ref name="pmid21211653">{{cite journal |vauthors=Broccardo CJ, Mahaffey S, Schwarz J, Wruck L, David G, Schlievert PM, Reisdorph NA, Leung DY |title=Comparative proteomic profiling of patients with atopic dermatitis based on history of eczema herpeticum infection and Staphylococcus aureus colonization |journal=J. Allergy Clin. Immunol. |volume=127 |issue=1 |pages=186–93, 193.e1–11 |date=January 2011 |pmid=21211653 |pmc=3059191 |doi=10.1016/j.jaci.2010.10.033 |url=}}</ref><br />
<br />
'''Immune response:'''<br />
<br />
*'''Cutaneous immune response''': Acts as the first-line barrier and constitutes the rapid response mechanism to the invading [[Allergens|allergen]] or [[pathogen]].<ref name="pmid20109730">{{cite journal |vauthors=Barnes KC |title=An update on the genetics of atopic dermatitis: scratching the surface in 2009 |journal=J. Allergy Clin. Immunol. |volume=125 |issue=1 |pages=16–29.e1–11; quiz 30–1 |date=January 2010 |pmid=20109730 |pmc=2874322 |doi=10.1016/j.jaci.2009.11.008 |url=}}</ref> It recognizes the [[microbes]] through receptors known as [[pattern recognition receptors]] (PRRs). The cutaneous immune response includes the following 4 elements:<ref name="pmid233742592">{{cite journal |vauthors=Kuo IH, Yoshida T, De Benedetto A, Beck LA |title=The cutaneous innate immune response in patients with atopic dermatitis |journal=J. Allergy Clin. Immunol. |volume=131 |issue=2 |pages=266–78 |date=February 2013 |pmid=23374259 |doi=10.1016/j.jaci.2012.12.1563 |url=}}</ref><br />
**''Physical:'' [[Stratum corneum]] and the [[tight junctions]] in [[stratum granulosum]] forms the physical barrier. The maintenance and repair of [[epithelial]] barriers are mediated th<nowiki/>rough the activation of [[Pattern recognition receptors|PRR]]<nowiki/>s by the [[innate immune system]].<ref name="pmid15236188">{{cite journal |vauthors=Cario E, Gerken G, Podolsky DK |title=Toll-like receptor 2 enhances ZO-1-associated intestinal epithelial barrier integrity via protein kinase C |journal=Gastroenterology |volume=127 |issue=1 |pages=224–38 |date=July 2004 |pmid=15236188 |doi= |url=}}</ref><br />
**''Chemical:'' Chemical constitutes antimicrobial proteins including [[antimicrobial peptides]] (AMPs), S100 proteins, [[cytokines]] as well as [[chemokines]], innate lymphoid cells group 2 (ILC-2), [[toll-like receptors]] (TLRs), [[keratinocytes]], filaggrin degraded products, and [[neutrophils]].<ref name="pmid23374259">{{cite journal |vauthors=Kuo IH, Yoshida T, De Benedetto A, Beck LA |title=The cutaneous innate immune response in patients with atopic dermatitis |journal=J. Allergy Clin. Immunol. |volume=131 |issue=2 |pages=266–78 |date=February 2013 |pmid=23374259 |doi=10.1016/j.jaci.2012.12.1563 |url=}}</ref><ref name="pmid232231422">{{cite journal |vauthors=Kuo IH, Carpenter-Mendini A, Yoshida T, McGirt LY, Ivanov AI, Barnes KC, Gallo RL, Borkowski AW, Yamasaki K, Leung DY, Georas SN, De Benedetto A, Beck LA |title=Activation of epidermal toll-like receptor 2 enhances tight junction function: implications for atopic dermatitis and skin barrier repair |journal=J. Invest. Dermatol. |volume=133 |issue=4 |pages=988–98 |date=April 2013 |pmid=23223142 |pmc=3600383 |doi=10.1038/jid.2012.437 |url=}}</ref><br />
**''[[Microbiome|Microbiome]]'': The microbiome consists of skin-resident normal microbial flora including [[bacteria]], [[fungi]], and [[viruses]]. It provides protection against invading [[microbes]] and [[pathogens]], and modulates the balance between [[inflammation]] and [[immune responses]].<ref name="pmid279740402">{{cite journal |vauthors=Lynch SV, Pedersen O |title=The Human Intestinal Microbiome in Health and Disease |journal=N. Engl. J. Med. |volume=375 |issue=24 |pages=2369–2379 |date=December 2016 |pmid=27974040 |doi=10.1056/NEJMra1600266 |url=}}</ref><br />
**''Immunological'': Immune response includes both [[Innate immune response|non-specific]] and immediate response ([[innate immunity]]) and highly specific and late response ([[adaptive immunity]]).<br />
*'''Adaptive Immune response''':<ref name="pmid20109730" /><br />
**The character and magnitude of the [[Adaptive immune response|adaptive immune]] system is determined by the innate immune response by interactions with the epidermal elements and activation of TLRs.<ref name="pmid19078985">{{cite journal |vauthors=De Benedetto A, Agnihothri R, McGirt LY, Bankova LG, Beck LA |title=Atopic dermatitis: a disease caused by innate immune defects? |journal=J. Invest. Dermatol. |volume=129 |issue=1 |pages=14–30 |date=January 2009 |pmid=19078985 |doi=10.1038/jid.2008.259 |url=}}</ref><br />
*'''Thymic stromal lymphopoietin:'''<br />
**<nowiki/> [[Thymic stromal lymphopoietin]] ([[TSLP]]) is considered as a master switch for [[allergic inflammation]], and is highly expressed by [[epithelial cells]] and epidermal [[keratinocytes]].<ref name="pmid16432252">{{cite journal |vauthors=Liu YJ |title=Thymic stromal lymphopoietin: master switch for allergic inflammation |journal=J. Exp. Med. |volume=203 |issue=2 |pages=269–73 |date=February 2006 |pmid=16432252 |pmc=2118215 |doi=10.1084/jem.20051745 |url=}}</ref><ref name="pmid22270071">{{cite journal |vauthors=Takai T |title=TSLP expression: cellular sources, triggers, and regulatory mechanisms |journal=Allergol Int |volume=61 |issue=1 |pages=3–17 |date=March 2012 |pmid=22270071 |doi=10.2332/allergolint.11-RAI-0395 |url=}}</ref><br />
**<nowiki/>It is an [[Interleukin 7|IL-7]]-like [[cytokine]], which stimulates the differentiation of naïve [[T helper cells]] into [[Th2 response|inflammatory Th2 cells]].<ref name="pmid164322522">{{cite journal |vauthors=Liu YJ |title=Thymic stromal lymphopoietin: master switch for allergic inflammation |journal=J. Exp. Med. |volume=203 |issue=2 |pages=269–73 |date=February 2006 |pmid=16432252 |pmc=2118215 |doi=10.1084/jem.20051745 |url=}}</ref><br />
<br />
===Pathogenesis===<br />
<br />
It is understood that atopic dermatitis is the result of either skin barrier dysfunction or immune dysregulation.<ref name="pmid21682749">{{cite journal |vauthors=Boguniewicz M, Leung DY |title=Atopic dermatitis: a disease of altered skin barrier and immune dysregulation |journal=Immunol. Rev. |volume=242 |issue=1 |pages=233–46 |date=July 2011 |pmid=21682749 |pmc=3122139 |doi=10.1111/j.1600-065X.2011.01027.x |url=}}</ref><br />
<br />
'''Epidermal barrier dysfunction (outside-in hypothesis):'''<ref name="pmid183290874">{{cite journal |vauthors=Elias PM, Hatano Y, Williams ML |title=Basis for the barrier abnormality in atopic dermatitis: outside-inside-outside pathogenic mechanisms |journal=J. Allergy Clin. Immunol. |volume=121 |issue=6 |pages=1337–43 |date=June 2008 |pmid=18329087 |pmc=2706021 |doi=10.1016/j.jaci.2008.01.022 |url=}}</ref><br />
<br />
*The major factors causing abnormal skin barrier include loss-of-function mutations in the [[filaggrin]] gene (FLG) resulting in:<ref name="pmid22521249">{{cite journal |vauthors=Morizane S, Yamasaki K, Kajita A, Ikeda K, Zhan M, Aoyama Y, Gallo RL, Iwatsuki K |title=TH2 cytokines increase kallikrein 7 expression and function in patients with atopic dermatitis |journal=J. Allergy Clin. Immunol. |volume=130 |issue=1 |pages=259–61.e1 |date=July 2012 |pmid=22521249 |pmc=3387356 |doi=10.1016/j.jaci.2012.03.006 |url=}}</ref><ref name="pmid22951058">{{cite journal |vauthors=Margolis DJ, Apter AJ, Gupta J, Hoffstad O, Papadopoulos M, Campbell LE, Sandilands A, McLean WH, Rebbeck TR, Mitra N |title=The persistence of atopic dermatitis and filaggrin (FLG) mutations in a US longitudinal cohort |journal=J. Allergy Clin. Immunol. |volume=130 |issue=4 |pages=912–7 |date=October 2012 |pmid=22951058 |pmc=3462287 |doi=10.1016/j.jaci.2012.07.008 |url=}}</ref><ref name="pmid23374260">{{cite journal |vauthors=McAleer MA, Irvine AD |title=The multifunctional role of filaggrin in allergic skin disease |journal=J. Allergy Clin. Immunol. |volume=131 |issue=2 |pages=280–91 |date=February 2013 |pmid=23374260 |doi=10.1016/j.jaci.2012.12.668 |url=}}</ref><br />
**Filaggrin protein deficiency<ref name="pmid19720210">{{cite journal |vauthors=Howell MD, Kim BE, Gao P, Grant AV, Boguniewicz M, DeBenedetto A, Schneider L, Beck LA, Barnes KC, Leung DY |title=Cytokine modulation of atopic dermatitis filaggrin skin expression |journal=J. Allergy Clin. Immunol. |volume=124 |issue=3 Suppl 2 |pages=R7–R12 |date=September 2009 |pmid=19720210 |doi=10.1016/j.jaci.2009.07.012 |url=}}</ref><br />
**[[Tight junction]] abnormalities<ref name="pmid21163515">{{cite journal |vauthors=De Benedetto A, Rafaels NM, McGirt LY, Ivanov AI, Georas SN, Cheadle C, Berger AE, Zhang K, Vidyasagar S, Yoshida T, Boguniewicz M, Hata T, Schneider LC, Hanifin JM, Gallo RL, Novak N, Weidinger S, Beaty TH, Leung DY, Barnes KC, Beck LA |title=Tight junction defects in patients with atopic dermatitis |journal=J. Allergy Clin. Immunol. |volume=127 |issue=3 |pages=773–86.e1–7 |date=March 2011 |pmid=21163515 |pmc=3049863 |doi=10.1016/j.jaci.2010.10.018 |url=}}</ref><br />
**More [[alkaline]] surface pH<ref name="pmid18329087">{{cite journal |vauthors=Elias PM, Hatano Y, Williams ML |title=Basis for the barrier abnormality in atopic dermatitis: outside-inside-outside pathogenic mechanisms |journal=J. Allergy Clin. Immunol. |volume=121 |issue=6 |pages=1337–43 |date=June 2008 |pmid=18329087 |pmc=2706021 |doi=10.1016/j.jaci.2008.01.022 |url=}}</ref><br />
**[[Microbial]] colonization<br />
**Altered [[Proteases|protease]] activity in the [[stratum corneum]]<ref name="pmid16815133">{{cite journal |vauthors=Cork MJ, Robinson DA, Vasilopoulos Y, Ferguson A, Moustafa M, MacGowan A, Duff GW, Ward SJ, Tazi-Ahnini R |title=New perspectives on epidermal barrier dysfunction in atopic dermatitis: gene-environment interactions |journal=J. Allergy Clin. Immunol. |volume=118 |issue=1 |pages=3–21; quiz 22–3 |date=July 2006 |pmid=16815133 |doi=10.1016/j.jaci.2006.04.042 |url=}}</ref><br />
<br />
*Skin barrier abnormalities lead to the increased permeability of the [[epidermis]].<br />
**This leads to entry of [[antigens]] or [[pathogens]] resulting in [[microbial]] colonization, most notably by ''[[staphylococcus aureus]]'' and [[herpes simplex virus (HSV)]].<br />
**This sequence of events results in the production of inflammatory [[cytokines]] and impaired production of [[antimicrobial peptides]].<ref name="pmid23712284">{{cite journal |vauthors=Leung DY |title=New insights into atopic dermatitis: role of skin barrier and immune dysregulation |journal=Allergol Int |volume=62 |issue=2 |pages=151–61 |date=June 2013 |pmid=23712284 |doi=10.2332/allergolint.13-RAI-0564 |url=}}</ref><br />
<br />
*Skin barrier abnormalities also lead to increased [[Transepidermal water loss|trans-epidermal water loss]], and decreased levels of [[Ceramide|ceramides]] and water binding.<ref name="pmid19494826">{{cite journal| author=Cork MJ, Danby SG, Vasilopoulos Y, Hadgraft J, Lane ME, Moustafa M et al.| title=Epidermal barrier dysfunction in atopic dermatitis. | journal=J Invest Dermatol | year= 2009 | volume= 129 | issue= 8 | pages= 1892-908 | pmid=19494826 | doi=10.1038/jid.2009.133 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19494826 }} </ref><ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
<br />
*Severe atopic dermatitis has been associated with higher levels of [[Transepidermal water loss|trans-epidermal water loss]].<ref name="pmid21137118">{{cite journal |vauthors=Flohr C, England K, Radulovic S, McLean WH, Campbel LE, Barker J, Perkin M, Lack G |title=Filaggrin loss-of-function mutations are associated with early-onset eczema, eczema severity and transepidermal water loss at 3 months of age |journal=Br. J. Dermatol. |volume=163 |issue=6 |pages=1333–6 |date=December 2010 |pmid=21137118 |doi= |url=}}</ref><br />
<br />
'''Immune dysregulation (inside-out’ hypothesis):'''<ref name="pmid183290872">{{cite journal |vauthors=Elias PM, Hatano Y, Williams ML |title=Basis for the barrier abnormality in atopic dermatitis: outside-inside-outside pathogenic mechanisms |journal=J. Allergy Clin. Immunol. |volume=121 |issue=6 |pages=1337–43 |date=June 2008 |pmid=18329087 |pmc=2706021 |doi=10.1016/j.jaci.2008.01.022 |url=}}</ref><br />
<br />
*'''Innate immune response:'''<br />
**Pathogens or tissue damage activate pattern recognition receptors including [[toll-like receptors]] (TLRs), which further induces a release of inflammatory mediators<nowiki/>, including [[Antimicrobial peptides|AMP]]<nowiki/>s, [[cytokines]], and [[chemokines]].<ref name="pmid23223142">{{cite journal |vauthors=Kuo IH, Carpenter-Mendini A, Yoshida T, McGirt LY, Ivanov AI, Barnes KC, Gallo RL, Borkowski AW, Yamasaki K, Leung DY, Georas SN, De Benedetto A, Beck LA |title=Activation of epidermal toll-like receptor 2 enhances tight junction function: implications for atopic dermatitis and skin barrier repair |journal=J. Invest. Dermatol. |volume=133 |issue=4 |pages=988–98 |date=April 2013 |pmid=23223142 |pmc=3600383 |doi=10.1038/jid.2012.437 |url=}}</ref><br />
**Defective cutaneous [[Innate immune system|innate immune]]-mediated epidermal barrier repair and maintenance may alter skin-resident normal microbial flora and lead to severe [[inflammation]] as demonstrated with atopic dermatitis patients colonized with [[Staphylococcus aureus|s''taphylococcus aureus'']]''.''<ref name="pmid22310478">{{cite journal |vauthors=Kong HH, Oh J, Deming C, Conlan S, Grice EA, Beatson MA, Nomicos E, Polley EC, Komarow HD, Murray PR, Turner ML, Segre JA |title=Temporal shifts in the skin microbiome associated with disease flares and treatment in children with atopic dermatitis |journal=Genome Res. |volume=22 |issue=5 |pages=850–9 |date=May 2012 |pmid=22310478 |pmc=3337431 |doi=10.1101/gr.131029.111 |url=}}</ref><br />
**In intact skin barrier, [[Antimicrobial peptides|antimicrobial peptides (AMPs)]] are regulated by [[cytokines]], [[Interleukin 17|IL-17]], and [[Interleukin 22|IL- 22]], which are secreted by [[T helper 17 cell|Th17]] and [[T helper cell|Th22]] cells. This effect is suppressed in patients with atopic dermatitis.<ref name="pmid21315950">{{cite journal |vauthors=Macias ES, Pereira FA, Rietkerk W, Safai B |title=Superantigens in dermatology |journal=J. Am. Acad. Dermatol. |volume=64 |issue=3 |pages=455–72; quiz 473–4 |date=March 2011 |pmid=21315950 |doi=10.1016/j.jaad.2010.03.044 |url=}}</ref><br />
*'''Adaptive immune response:'''<br />
**Increased [[allergen]] penetration through the damaged [[epidermis]] leading to a [[Th2 response|Th2]]-type milieu is thought to explain the critical link between the barrier defect of atopic dermatitis patients with FLG mutations and Th2 polarization.<ref name="pmid216827492">{{cite journal |vauthors=Boguniewicz M, Leung DY |title=Atopic dermatitis: a disease of altered skin barrier and immune dysregulation |journal=Immunol. Rev. |volume=242 |issue=1 |pages=233–46 |date=July 2011 |pmid=21682749 |pmc=3122139 |doi=10.1111/j.1600-065X.2011.01027.x |url=}}</ref><br />
**Enhanced expression of [[Th2 response|Th2]], [[Th17]], and Th22 cytokines, characterize the [[acute]] initiation of atopic dermatitis lesions.<ref name="pmid25282559">{{cite journal |vauthors=Leung DY, Guttman-Yassky E |title=Deciphering the complexities of atopic dermatitis: shifting paradigms in treatment approaches |journal=J. Allergy Clin. Immunol. |volume=134 |issue=4 |pages=769–79 |date=October 2014 |pmid=25282559 |pmc=4186710 |doi=10.1016/j.jaci.2014.08.008 |url=}}</ref><ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
**Epidermal barrier function is regulated through [[Th2]] and Th22 cytokines ([[Interleukin 4|IL-4]], [[Interleukin 13|IL-13,]] [[Interleukin 31|IL-31]], and [[Interleukin 22|IL-22]]) by:<ref name="pmid252825593">{{cite journal |vauthors=Leung DY, Guttman-Yassky E |title=Deciphering the complexities of atopic dermatitis: shifting paradigms in treatment approaches |journal=J. Allergy Clin. Immunol. |volume=134 |issue=4 |pages=769–79 |date=October 2014 |pmid=25282559 |pmc=4186710 |doi=10.1016/j.jaci.2014.08.008 |url=}}</ref><ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
***Stimulating epidermal [[hyperplasia]]<br />
***Inhibiting the expression of terminal keratinocyte differentiation genes (eg, ''FLG'', [[loricrin]], [[involucrin]])<br />
***Suppressing the production of [[Antimicrobial peptides|AMPs]]<br />
*'''Thymic stromal lymphopoietin:'''<br />
**Defective skin barrier and enhanced [[epidermal]] [[protease]] activity, which is reported in atopic dermatitis, promote [[TSLP]] production and [[Th2 response]], leading to atopic dermatitis-like [[inflammation]].<ref name="pmid222700712">{{cite journal |vauthors=Takai T |title=TSLP expression: cellular sources, triggers, and regulatory mechanisms |journal=Allergol Int |volume=61 |issue=1 |pages=3–17 |date=March 2012 |pmid=22270071 |doi=10.2332/allergolint.11-RAI-0395 |url=}}</ref><br />
**''[[TSLP]]'' polymorphisms have been linked to the severity of atopic dermatitis.<br />
**[[TSLP]] genetic variants are associated with atopic dermatitis and [[eczema herpeticum]].<ref name="pmid20466416">{{cite journal |vauthors=Gao PS, Rafaels NM, Mu D, Hand T, Murray T, Boguniewicz M, Hata T, Schneider L, Hanifin JM, Gallo RL, Gao L, Beaty TH, Beck LA, Leung DY, Barnes KC |title=Genetic variants in thymic stromal lymphopoietin are associated with atopic dermatitis and eczema herpeticum |journal=J. Allergy Clin. Immunol. |volume=125 |issue=6 |pages=1403–1407.e4 |date=June 2010 |pmid=20466416 |pmc=2925504 |doi=10.1016/j.jaci.2010.03.016 |url=}}</ref><br />
**In patients with defective skin barrier due to [[Filaggrin|FLG]] mutations, [[TSLP]] genetic variants are associated with reduced [[probability]] of having persistent atopic dermatitis.<ref name="pmid24401911">{{cite journal |vauthors=Margolis DJ, Kim B, Apter AJ, Gupta J, Hoffstad O, Papadopoulos M, Mitra N |title=Thymic stromal lymphopoietin variation, filaggrin loss of function, and the persistence of atopic dermatitis |journal=JAMA Dermatol |volume=150 |issue=3 |pages=254–9 |date=March 2014 |pmid=24401911 |pmc=4414492 |doi=10.1001/jamadermatol.2013.7954 |url=}}</ref><br />
<br />
==Genetics==<br />
Recent studies have established a strong genetic association of atopic dermatitis. Twin studies have indicated high [[heritability]] of atopic dermatitis with a [[Concordance (genetics)|concordance]] rate of 72–86 % for [[monozygotic twins]] compared with 21–23 % for [[dizygotic twins]].<ref name="pmid27004062">{{cite journal |vauthors=Al-Shobaili HA, Ahmed AA, Alnomair N, Alobead ZA, Rasheed Z |title=Molecular Genetic of Atopic dermatitis: An Update |journal=Int J Health Sci (Qassim) |volume=10 |issue=1 |pages=96–120 |date=January 2016 |pmid=27004062 |pmc=4791162 |doi= |url=}}</ref><br />
<br />
Genes involved in the pathogenesis of atopic dermatitis include:<ref name="pmid270040623">{{cite journal |vauthors=Al-Shobaili HA, Ahmed AA, Alnomair N, Alobead ZA, Rasheed Z |title=Molecular Genetic of Atopic dermatitis: An Update |journal=Int J Health Sci (Qassim) |volume=10 |issue=1 |pages=96–120 |date=January 2016 |pmid=27004062 |pmc=4791162 |doi= |url=}}</ref><br />
{| class="wikitable"<br />
|+<br />
! colspan="3" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Genes involved in the pathogenesis of atopic dermatitis<br />
|-<br />
| colspan="2" style="background: #7d7d7d; color: #FFFFFF; text-align: center;" |'''Filaggrin Gene mutation'''<br />
|<br />
*Located on [[chromosome]] 1q21 [[Epidermal differentiation complex|(epidermal differentiation complex]]) loss-of-function mutations in the filaggrin gene FLG, is strongly associated with a broad range of skin and [[allergic]] diseases including atopic dermatitis.<ref name="pmid21991953">{{cite journal |vauthors=Irvine AD, McLean WH, Leung DY |title=Filaggrin mutations associated with skin and allergic diseases |journal=N. Engl. J. Med. |volume=365 |issue=14 |pages=1315–27 |date=October 2011 |pmid=21991953 |doi=10.1056/NEJMra1011040 |url=}}</ref><br />
*Mutation in this gene is also responsible for [[ichthyosis vulgaris]] and [[pachyonychia congenita]].<ref name="pmid17657246">{{cite journal |vauthors=Liao H, Waters AJ, Goudie DR, Aitken DA, Graham G, Smith FJ, Lewis-Jones S, McLean WH |title=Filaggrin mutations are genetic modifying factors exacerbating X-linked ichthyosis |journal=J. Invest. Dermatol. |volume=127 |issue=12 |pages=2795–8 |date=December 2007 |pmid=17657246 |doi=10.1038/sj.jid.5700971 |url=}}</ref><br />
*The common genetic variant R510X and 2282del4 are very strongly associated with atopic dermatitis.<ref name="pmid16550169">{{cite journal |vauthors=Palmer CN, Irvine AD, Terron-Kwiatkowski A, Zhao Y, Liao H, Lee SP, Goudie DR, Sandilands A, Campbell LE, Smith FJ, O'Regan GM, Watson RM, Cecil JE, Bale SJ, Compton JG, DiGiovanna JJ, Fleckman P, Lewis-Jones S, Arseculeratne G, Sergeant A, Munro CS, El Houate B, McElreavey K, Halkjaer LB, Bisgaard H, Mukhopadhyay S, McLean WH |title=Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis |journal=Nat. Genet. |volume=38 |issue=4 |pages=441–6 |date=April 2006 |pmid=16550169 |doi=10.1038/ng1767 |url=}}</ref><br />
*FLG [[gene mutation]] is associated with developing [[atopic dermatitis]] at an early age(≤8 years) but is not associated with late childhood or adulthood atopic dermatitis.<ref name="pmid25314673">{{cite journal |vauthors=Rupnik H, Rijavec M, Korošec P |title=Filaggrin loss-of-function mutations are not associated with atopic dermatitis that develops in late childhood or adulthood |journal=Br. J. Dermatol. |volume=172 |issue=2 |pages=455–61 |date=February 2015 |pmid=25314673 |doi=10.1111/bjd.13477 |url=}}</ref><br />
|-<br />
| colspan="2" style="background: #7d7d7d; color: #FFFFFF; text-align: center;" |'''SPINK5 and LEKTI gene'''<br />
|<br />
*Located on [[chromosome]] 5q32, [[SPINK5|Serine Protease Inhibitor Kazal-Type 5 (SPINK5]]) gene encodes a [[protease inhibitor]] lymphoepithelial Kazal-type-Related Inhibitor ([[LEKTI]]), which is involved in converting profilaggrin into [[filaggrin]] and is responsible for marinating the permeability of the normal skin.<ref name="pmid270040622">{{cite journal |vauthors=Al-Shobaili HA, Ahmed AA, Alnomair N, Alobead ZA, Rasheed Z |title=Molecular Genetic of Atopic dermatitis: An Update |journal=Int J Health Sci (Qassim) |volume=10 |issue=1 |pages=96–120 |date=January 2016 |pmid=27004062 |pmc=4791162 |doi= |url=}}</ref><br />
*[[LEKTI]] deficiency leads to enhanced cleavage of intercellular attachments, decreased corneocyte [[cohesion]] and impaired skin barrier function.<ref name="pmid168151332">{{cite journal |vauthors=Cork MJ, Robinson DA, Vasilopoulos Y, Ferguson A, Moustafa M, MacGowan A, Duff GW, Ward SJ, Tazi-Ahnini R |title=New perspectives on epidermal barrier dysfunction in atopic dermatitis: gene-environment interactions |journal=J. Allergy Clin. Immunol. |volume=118 |issue=1 |pages=3–21; quiz 22–3 |date=July 2006 |pmid=16815133 |doi=10.1016/j.jaci.2006.04.042 |url=}}</ref><br />
|-<br />
| colspan="2" style="background: #7d7d7d; color: #FFFFFF; text-align: center;" |'''MHC (or HLA) genes'''<br />
|<br />
*Major [[histocompatibility]] complex or [[human leukocyte antigen]]<br />
|-<br />
| colspan="2" style="background: #7d7d7d; color: #FFFFFF; text-align: center;" |'''Innate Immune system genes''':<br />
|<br />
*CARD4 (or [[NOD1]]) gene: [[Caspase]] recruitment domain–containing protein (CARD) 4<br />
*[[CARD15]] (or [[NOD2]]) gene<br />
*[[Monocyte]] differentiation antigen (or [[CD14|CD14)]] gene<br />
*MBL2 gene: [[Mannose-binding lectin pathway|mannose-binding lectin]] '''('''MBL2) gene<br />
*[[Toll-like receptors|Toll-like receptor]]( [[TLR2]], [[TLR4]], [[TLR6]] and [[TLR 9]]) genes<br />
*DEFB1 gene: human β-defensin 1<br />
|-<br />
| rowspan="2" style="background: #7d7d7d; color: #FFFFFF; text-align: center;" |'''Adaptive immune system genes'''<br />
| style="background: #DCDCDC; text-align: center;" |'''Cytokines and related genes''':<br />
|<br />
*[[Interleukin 4|IL-4]] gene<br />
*IL-4Rα gene<br />
*[[STAT6]] gene (Signal transducer and activator of transcription )<br />
*[[Interleukin 10|IL-10]] gene<br />
*[[Interleukin 6|IL-6]] gene<br />
*[[Tumor necrosis factor-alpha|TNF-α]] gene<br />
*[[TNF]]-β gene<br />
*[[IL-1]]α gene<br />
*[[IL-β]] gene<br />
*[[IFNγ]] gene<br />
*IL-1RL1<br />
*[[Interleukin 5|IL-5]] gene<br />
*[[Interleukin 12|IL-12]] β gene<br />
*IL-12R β<br />
*[[Interleukin 13|IL-13]] gene<br />
*IL-18 gene<br />
*TGF-β1 gene<br />
*[[GM-CSF]] gene<br />
*[[IL-9]] gene<br />
*[[IL-9R]] gene<br />
|-<br />
| style="background: #DCDCDC; text-align: center;" |'''Chemokines and related genes''':<br />
|<br />
*[[CCL5]] gene: [[Chemokine]] (C-Cmotif) ligand 5<br />
*[[CCL11]] gene<br />
*[[CCL17]] gene<br />
*[[CCR3 (gene)|CCR3]] gene<br />
*[[CCR4]] gene<br />
*[[CMA1]] gene: [[Mast cell]] [[chymase]] 1<br />
|-<br />
| colspan="2" style="background: #7d7d7d; color: #FFFFFF; text-align: center;" |'''Drug-metabolizing genes'''<br />
|<br />
*[[GST]] genes: [[glutathione]] S-transferase<br />
*[[NAT-2]] gene: N-acetyl transferase<br />
|-<br />
| colspan="2" style="background: #7d7d7d; color: #FFFFFF; text-align: center;" |'''Other genes'''<br />
|<br />
*[[CTLA-4]]<br />
*KLK<br />
*[[RUNX1]] gene<br />
*[[IRF2]] gene<br />
*[[FCER1B]] gene<br />
*[[PHF11]] gene<br />
|-<br />
| colspan="3" |Adapted from ''Molecular Genetic of Atopic dermatitis: An Update''<ref name="pmid270040624">{{cite journal |vauthors=Al-Shobaili HA, Ahmed AA, Alnomair N, Alobead ZA, Rasheed Z |title=Molecular Genetic of Atopic dermatitis: An Update |journal=Int J Health Sci (Qassim) |volume=10 |issue=1 |pages=96–120 |date=January 2016 |pmid=27004062 |pmc=4791162 |doi= |url=}}</ref><br />
|}<br />
<br />
==Associated Conditions==<br />
<br />
'''Conditions associated with atopic dermatitis:'''<br />
<br />
*[[Atopic]] triad <ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
**[[Atopic dermatitis]]<br />
**[[Allergic rhinitis]]<br />
**[[Asthma]]<br />
*Food-induced [[urticaria]]/[[anaphylaxis]]<br />
*[[Ichthyosis vulgaris]]<br />
*[[Ocular]] comorbidities<br />
**[[Atopic keratoconjunctivitis]]<br />
**[[Vernal keratoconjunctivitis]]<br />
*[[Wiskott-Aldrich syndrome]]<br />
**[[Thrombocytopenia]]<br />
**[[Eczema]] (atopic dermatitis)<br />
**Recurrent [[Infection|infections]]<br />
*[[Hyper-IgE syndrome]]:<br />
**[[Eczema]] (atopic dermatitis)<br />
**High serum [[IgE]]<br />
**Recurrent cold abscesses<br />
*[[Anemia]]<br />
*[[Psychiatric]] [[disorders]]<br />
**[[Depression]]<br />
**[[Anxiety]]<br />
**[[Suicidal|Suicid]]<nowiki/>[[Suicidal|al]] ideations<br />
**[[Attention deficit hyperactivity disorder]]<br />
*[[Angina pectoris]]<br />
<br />
==Gross Pathology==<br />
On [[gross pathology]], characteristic findings of atopic dermatitis include:<ref name="MihmSoter19762">{{cite journal|last1=Mihm|first1=Martin C|last2=Soter|first2=Nicholas A|last3=Dvorak|first3=Harold F|last4=Austen|first4=K Frank|title=The Structure Of Normal Skin And The Morphology Of Atopic Eczema|journal=Journal of Investigative Dermatology|volume=67|issue=3|year=1976|pages=305–312|issn=0022202X|doi=10.1111/1523-1747.ep12514346}}</ref><br />
<br />
*'''Acute atopic dermatitis''':<br />
**[[Erythema]]<br />
**[[Edema]]<br />
**Vesiculation with oozing<br />
*'''Chronic atopic dermatitis:'''<br />
**Lichenified plaques<br />
**Prominent skin markings<br />
<br />
==Microscopic Pathology==<br />
On microscopic [[histopathological]] analysis, characteristic findings of [[atopic dermatitis]] include:<ref name="MihmSoter19763">{{cite journal|last1=Mihm|first1=Martin C|last2=Soter|first2=Nicholas A|last3=Dvorak|first3=Harold F|last4=Austen|first4=K Frank|title=The Structure Of Normal Skin And The Morphology Of Atopic Eczema|journal=Journal of Investigative Dermatology|volume=67|issue=3|year=1976|pages=305–312|issn=0022202X|doi=10.1111/1523-1747.ep12514346}}</ref><br />
<br />
*'''Acute vesicular lesions''': <br />
**[[Epidermal]] psoriasiform [[hyperplasia]]<br />
**Marked intercellular [[edema]] with spongiotic vesiculation<br />
**Marked perivenular infiltrate<br />
**Epidermal infiltrate, consisting predominately of a lymphohistiocytic infiltrate in the dermis<br />
*'''Chronic lichenified plaque''':<br />
**[[Hyperkeratosis]]<br />
**Psoriasiform hyperplasia<br />
**Dyskeratosis<br />
**Marked thickening of the [[papillary]] dermis<br />
**Minimal intercellular [[edema]]<br />
<br />
==References==<br />
{{Reflist|2}}<br />
[[Category:Dermatology]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Atopic_dermatitis_overview&diff=1703491Atopic dermatitis overview2021-06-08T19:32:34Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Atopic dermatitis}}<br />
{{CMG}} {{AE}} {{S.S}} [[Ogechukwu Hannah Nnabude, MD]]<br />
<br />
==Overview==<br />
Atopic dermatitis is a [[chronic]] [[inflammatory]] skin disorder that occurs primarily in children, but also affects adults, usually with a personal or [[family history]] of [[atopy]] including [[asthma]], and [[allergic rhinitis]]. Atopic dermatitis presents usually with intense [[pruritus]] and is often associated with elevated levels of [[Immunoglobulin E|immunoglobulin E (IgE)]].<br />
<br />
==Historical Perspective==<br />
The term atopic dermatitis was first coined by Fred Wise and Marion Sulzberger, American [[Dermatologist|dermatologists]], in 1933, and the first widely used [[diagnostic criteria]] for atopic dermatitis was published by Jon Hanifin and Georg Rajka, in 1980.<br />
==Pathophysiology==<br />
Atopic dermatitis is a [[chronic]] [[inflammatory]] [[skin disorder]] with an [[Immunology|immunologic]] background and occurs in patients with a personal or [[family history]] of [[atopy]] (i.e. [[asthma]] or [[allergic rhinitis]]). It is caused by either skin barrier dysfunction or immune dysregulation of the [[Adaptive immunity|adaptive]] and [[innate immune response]] leading to an enhanced [[IgE]]-mediated, systemic [[Th2 response]]. The skin barrier is invaded by [[exogenous]] substances, including [[allergens]], [[irritants]] and [[microbes]]; and the tightly packed structure of the [[stratum corneum]] is further compromised. Systemically, a dysfunctional [[Innate immune system|innate]] and [[adaptive immune response]] causes further damage to the [[epidermis]].<br />
==Causes==<br />
Atopic dermatitis is the result of either skin barrier dysfunction or immune dysregulation due to [[Genetics|genetic]] defects. The most important genetic defect includes [[Mutation|mutations]] in the [[filaggrin]] gene (FLG). <br />
==Differentiating Atopic Dermatitis from other Diseases==<br />
Atopic dermatitis is a chronic [[inflammatory]] skin disorder, which is indistinguishable from other causes of dermatitis. Atopic dermatitis is usually associated with a personal or [[family history]] of [[atopic diseases]] including [[asthma]], allergic rhinitis and [[food allergy]]. The most common clinically similar dermatitis in infancy is [[seborrheic dermatitis]] which includes [[hyperkeratosis]] of the [[Scalp rash|scalp]], also found in atopic dermatitis.<br />
<br />
==Epidemiology and Demographics==<br />
It now affects 10-20% of children and 1-3% of adults in industrialized countries, and its [[prevalence]] there has more than doubled in the past thirty years. Atopic dermatitis [[incidence]] is highest during [[infancy]] and early childhood. The majority of atopic dermatitis patients have onset of symptoms <5 years of age. The [[prevalence]] of atopic dermatitis is approximately 5,000-20,000 cases per 100,000 children worldwide. In 2003, the prevalence of atopic dermatitis was estimated to be 10,700 cases per 100,000 children in the [[United States]].<br />
==Risk Factors==<br />
Atopic dermatitis is a multifactorial, [[chronic]] [[inflammatory]] skin disease as a result of interactions between various [[Genetics|genetic]], [[immune]] and environmental factors. The most important [[risk factor]] for the development of atopic dermatitis is a [[family history]] or personal history of [[atopy]] including [[asthma]], [[allergic rhinitis]], [[food allergy]].<br />
<br />
==Screening==<br />
There is insufficient evidence to recommend routine screening for atopic dermatitis.<br />
==Natural History, Complications and Prognosis==<br />
The symptoms of atopic dermatitis usually start during the first few years of life, and present with [[symptoms]] such as intense [[pruritus]] and chronic and relapsing age dependent [[Eczema|eczematous]] lesions. Common [[complications]] of atopic dermatitis include super-infection with [[Staphylococcus aureus|staphylococcus ''aureus'']]'','' [[herpes simplex virus]], and [[molluscum contagiosum]]; [[Sleep disturbances|sleep problems]] due to intense [[pruritus]], [[ocular]] [[comorbidities]], and topical [[corticosteroids]] leading to [[striae]] formation.<br />
<br />
==Diagnosis==<br />
===Diagnostic Studies===<br />
Due to the variable [[morphology]], distribution of skin lesions, and intermittent clinical features, it is very challenging to define the diagnosis of atopic dermatitis. Atopic dermatitis is primarily diagnosed based on the [[clinical]] presentation. Currently, the most commonly used [[criteria]] worldwide is published by the United Kingdom Working Group and is based upon history, [[morphology]] and distribution of [[Eczema|eczematous]] lesions, and clinical features of atopic dermatitis. In [[patients]] with atopic dermatitis, to rule out other skin [[conditions]], a [[histologic]] examination of a [[skin biopsy]] and other [[laboratory]] tests (eg, [[Immunoglobulin E|serum immunoglobulin E]], [[KOH test|potassium hydroxide preparation]], patch testing, [[genetic testing]]) can be considered. <br />
===History and Symptoms===<br />
The most common [[symptoms]] of atopic dermatitis include [[pruritus]], distribution of [[rash]] in age- specific patters and [[dry skin]]. Patients often have a personal or [[family history]] of [[asthma]] or [[allergic rhinitis]]. [[Patients]] with atopic dermatitis may report a positive history of [[cutaneous]] hyper-reactivity to diverse environmental stimuli and [[Atopy|atopic disorders]].<br />
<br />
===Physical Examination===<br />
Atopic dermatitis is a chronic or relapsing [[hypersensitive]] manifestation of the [[skin]]. Common [[physical examination]] findings of atopic dermatitis include [[pruritus]], [[Eczema|eczematous]] lesions, [[xerosis]] and [[lichenification]]. The lesions are usually age-specific and can be at various stages of development. The lesions can involve any area of the body in severe cases, but usually, it is uncommon to find lesions in the [[axillary]], [[gluteal]], or [[groin]] area.<br />
<br />
===Laboratory Findings===<br />
The diagnosis of atopic dermatitis remains clinical as there is no reliable [[Biomarker|bio-marker]] that can differentiate atopic dermatitis from other skin diseases.<br />
===Other diagnostic studies===<br />
There are no routinely diagnostic studies for atopic dermatitis, but in selected patients to rule out other skin conditions, a [[histologic]] examination of a [[skin biopsy]] and other laboratory tests (eg, [[IgE|serum immunoglobulin E]], [[KOH test|potassium hydroxide preparation]], patch testing, [[genetic testing]]) can be considered.<br />
<br />
==Treatment==<br />
===Medical Therapy===<br />
The mainstay of treatment for atopic dermatitis depends upon the severity of the disease and is treated with a combination of conservative and medical therapy. The goals of treatment include the elimination of aggravating factors, skin barrier function repair, maintaining skin hydration, and pharmacologic treatment of skin [[inflammation]]. [[Pharmacological|Pharmacologic]] medical therapies for atopic dermatitis can be classified according to several severity scales( (i.e [[SCORAD]] index, the Eczema Area, and Severity Index (EASI), and the Patient-Oriented Eczema Measure POEM).<br />
<br />
===Primary Prevention===<br />
Primary prevention applies to patients with a history of other [[atopic diseases]] and have not been diagnosed with atopic dermatitis yet. Its primary goal is to reduce the risk of developing atopic dermatitis in the future. Approaches to reduce the development of atopic dermatitis in children usually include the minimization of [[antibiotics]] administration in infants and infections in [[infants]].<br />
<br />
===Secondary prevention===<br />
Secondary prevention involves protecting and restoring the epidermal skin barrier function including abstaining from using soap, cosmetics, dyes, fragrances, and detergents, washing new clothes before wearing them, avoiding frequent and sudden climate changes, using air humidifiers in winters, avoiding excessive exposure to UV radiation and using SPF sunscreens, regular application of emollients every 6 hours, and stress-reducing therapy<br />
<br />
===Financial costs===<br />
There has been no discussion on the cost-effectiveness of therapy for [[atopic dermatitis]], however, in a retrospective study, the utilization of health care and treatment costs annually were higher for patients with atopic dermatitis than for controls without atopic dermatitis and was associated with the severity of the disease.<br />
===Future or Investigational Therapies===<br />
A more novel form of treatment involves exposure to broad or narrow-band [[ultraviolet light]]. UV radiation exposure has been found to have a localized [[immunomodulatory]] effect on affected [[tissue]]s, and may be used to decrease the severity and frequency of flares. In particular, Meduri et al. have suggested that the usage of UVA1 is more effective in treating acute flares, whereas narrow-band UVB is more effective in long-term management scenarios. However, UV radiation has also been implicated in various types of skin cancer, and thus UV treatment is not without risk.<br />
<br />
[[Category:Autoimmune diseases]]<br />
[[Category:Dermatology]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Atopic_dermatitis_natural_history,_complications_and_prognosis&diff=1703487Atopic dermatitis natural history, complications and prognosis2021-06-08T19:23:21Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Atopic dermatitis}}<br />
<br />
{{CMG}}; {{AE}} {{S.S}}<br />
<br />
==Overview==<br />
The [[symptoms]] of atopic dermatitis usually start during the first few years of life, and present as intense [[pruritus]] and chronic and relapsing age dependent [[Eczema|eczematous]] [[lesions]]. Common [[complications]] of atopic dermatitis include super-infection with [[Staphylococcus aureus|staphylococcus ''aureus'']]'','' [[herpes simplex virus]], and [[molluscum contagiosum]]; [[Sleep disturbances|sleep problems]] due to intense [[pruritus]], [[ocular]] comorbidities, and [[striae]] formation due to long term use of topical [[corticosteroids]].<br />
==Natural History, Complications, and Prognosis==<br />
<br />
===Natural History===<br />
<br />
*The [[symptoms]] of atopic dermatitis usually start during the first few years of life, and present as intense [[pruritus]] and chronic and relapsing age dependent [[Eczema|eczematous]] lesions.<ref name="pmid23452057">{{cite journal |vauthors=Garmhausen D, Hagemann T, Bieber T, Dimitriou I, Fimmers R, Diepgen T, Novak N |title=Characterization of different courses of atopic dermatitis in adolescent and adult patients |journal=Allergy |volume=68 |issue=4 |pages=498–506 |date=April 2013 |pmid=23452057 |doi=10.1111/all.12112 |url=}}</ref><br />
*The majority of infants and children with atopic dermatitis usually grow out of the disease during childhood.<ref name="pmid23301666">{{cite journal |vauthors=Burr ML, Dunstan FD, Hand S, Ingram JR, Jones KP |title=The natural history of eczema from birth to adult life: a cohort study |journal=Br. J. Dermatol. |volume=168 |issue=6 |pages=1339–42 |date=June 2013 |pmid=23301666 |doi=10.1111/bjd.12216 |url=}}</ref><br />
*In severe cases, atopic dermatitis continues or [[relapse]]<nowiki/>s in adulthood.<ref name="pmid234520573">{{cite journal |vauthors=Garmhausen D, Hagemann T, Bieber T, Dimitriou I, Fimmers R, Diepgen T, Novak N |title=Characterization of different courses of atopic dermatitis in adolescent and adult patients |journal=Allergy |volume=68 |issue=4 |pages=498–506 |date=April 2013 |pmid=23452057 |doi=10.1111/all.12112 |url=}}</ref><br />
*The natural history of atopic dermatitis can be categorized into various subtypes according to the clinical features.<br />
**The most common subtype was characterized by the early onset of atopic dermatitis (<2 years) and persistent until adulthood.<ref name="pmid234520574">{{cite journal |vauthors=Garmhausen D, Hagemann T, Bieber T, Dimitriou I, Fimmers R, Diepgen T, Novak N |title=Characterization of different courses of atopic dermatitis in adolescent and adult patients |journal=Allergy |volume=68 |issue=4 |pages=498–506 |date=April 2013 |pmid=23452057 |doi=10.1111/all.12112 |url=}}</ref><br />
*In the sequence of atopy march diseases, atopic dermatitis is the first to commence during infancy, followed by [[allergic rhinitis]], [[food allergy]] and [[asthma]] later in life.<ref name="pmid20674819">{{cite journal |vauthors=Spergel JM |title=From atopic dermatitis to asthma: the atopic march |journal=Ann. Allergy Asthma Immunol. |volume=105 |issue=2 |pages=99–106; quiz 107–9, 117 |date=August 2010 |pmid=20674819 |doi=10.1016/j.anai.2009.10.002 |url=}}</ref><br />
*Atopic dermatitis is a life long [[disease]] with periods of waxing and waning [[Eczema|eczematous]] [[skin lesions]].<ref name="pmid24696036">{{cite journal |vauthors=Margolis JS, Abuabara K, Bilker W, Hoffstad O, Margolis DJ |title=Persistence of mild to moderate atopic dermatitis |journal=JAMA Dermatol |volume=150 |issue=6 |pages=593–600 |date=June 2014 |pmid=24696036 |pmc=4352328 |doi=10.1001/jamadermatol.2013.10271 |url=}}</ref><br />
*<br />
<br />
===Complications===<br />
<br />
*Common complications of atopic dermatitis include:<br />
**Super-infection<br />
***[[Staphylococcus aureus|Staphylococcus ''aureus'']]<ref name="pmid21070347">{{cite journal |vauthors=Matiz C, Tom WL, Eichenfield LF, Pong A, Friedlander SF |title=Children with atopic dermatitis appear less likely to be infected with community acquired methicillin-resistant Staphylococcus aureus: the San Diego experience |journal=Pediatr Dermatol |volume=28 |issue=1 |pages=6–11 |date=2011 |pmid=21070347 |doi=10.1111/j.1525-1470.2010.01293.x |url=}}</ref><ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
***[[Herpes simplex]] virus ( Kaposi varicelliform eruption or [[eczema herpeticum]]) - occurs in <3% of patients<br />
***[[Molluscum contagiosum]]<br />
**[[Sleep disturbances|Sleep problems]] due to intense [[pruritus]]<br />
**[[Ocular]] comorbidities<br />
***[[Atopic keratoconjunctivitis]]<ref name="pmid24342754">{{cite journal |vauthors=Chen JJ, Applebaum DS, Sun GS, Pflugfelder SC |title=Atopic keratoconjunctivitis: A review |journal=J. Am. Acad. Dermatol. |volume=70 |issue=3 |pages=569–75 |date=March 2014 |pmid=24342754 |doi=10.1016/j.jaad.2013.10.036 |url=}}</ref><br />
***[[Vernal keratoconjunctivitis]]<ref name="pmid25744396">{{cite journal |vauthors=Pattnaik L, Acharya L |title=A comprehensive review on vernal keratoconjunctivitis with emphasis on proteomics |journal=Life Sci. |volume=128 |issue= |pages=47–54 |date=May 2015 |pmid=25744396 |doi=10.1016/j.lfs.2015.01.040 |url=}}</ref><br />
***[[Keratoconus]]<br />
***Infectious [[keratitis]]<br />
***[[Blepharitis]]<br />
**Topical [[corticosteroids]] can lead to [[striae]] formation<br />
**[[Atopy]] march: Other atopic disorders such as [[allergic rhinitis]], [[food allergy]] and [[asthma]]<ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
**[[Depression]], [[anxiety]] and [[suicidality]] are among long-term complications of atopic dermatitis.<ref name="pmid23452057">{{cite journal |vauthors=Garmhausen D, Hagemann T, Bieber T, Dimitriou I, Fimmers R, Diepgen T, Novak N |title=Characterization of different courses of atopic dermatitis in adolescent and adult patients |journal=Allergy |volume=68 |issue=4 |pages=498–506 |date=April 2013 |pmid=23452057 |doi=10.1111/all.12112 |url=}}</ref><br />
<br />
===Prognosis===<br />
<br />
*Atopic dermatitis is a [[chronic disease]] with varying subtypes.<ref name="pmid15131576">{{cite journal |vauthors=Illi S, von Mutius E, Lau S, Nickel R, Grüber C, Niggemann B, Wahn U |title=The natural course of atopic dermatitis from birth to age 7 years and the association with asthma |journal=J. Allergy Clin. Immunol. |volume=113 |issue=5 |pages=925–31 |date=May 2004 |pmid=15131576 |doi=10.1016/j.jaci.2004.01.778 |url=}}</ref><br />
*The presence of severe atopic dermatitis and early [[atopic]] sensitization is associated with a particularly poor prognosis.<ref name="pmid151315762">{{cite journal |vauthors=Illi S, von Mutius E, Lau S, Nickel R, Grüber C, Niggemann B, Wahn U |title=The natural course of atopic dermatitis from birth to age 7 years and the association with asthma |journal=J. Allergy Clin. Immunol. |volume=113 |issue=5 |pages=925–31 |date=May 2004 |pmid=15131576 |doi=10.1016/j.jaci.2004.01.778 |url=}}</ref><br />
*[[Mortality]] is unusual in atopic dermatitis.<br />
<br />
==References==<br />
{{Reflist|2}}<br />
[[Category:Autoimmune diseases]]<br />
[[Category:Dermatology]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Atopic_dermatitis_medical_therapy&diff=1703486Atopic dermatitis medical therapy2021-06-08T19:15:20Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Atopic dermatitis}}<br />
<br />
{{CMG}}; {{AE}}{{S.S}}<br />
<br />
==Overview==<br />
The mainstay of treatment for atopic dermatitis depends upon the severity of the [[disease]]. The treatment involves a combination of conservative and medical therapy. The goals of treatment include elimination of aggravating factors, skin barrier function repair, maintaining skin hydration and [[Pharmacological|pharmacologic]] treatment of skin [[inflammation]]. Pharmacologic medical therapies for atopic dermatitis can be classified according to several severity scales including [[SCORAD|SCORAD index]], the eczema area and severity index (EASI), and the patient-oriented eczema measure (POEM).<br />
==Conservative Therapy==<br />
<br />
{| class="wikitable"<br />
|+<br />
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Elimination of exacerbating factors'''<br />
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Maintaining skin hydration'''<br />
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Controlling pruritus'''<br />
|-<br />
|<br />
*Avoid [[trigger]]<nowiki/>s such as low [[humidity]], overheating of skin<ref name="pmid18829806">{{cite journal |vauthors=Krakowski AC, Eichenfield LF, Dohil MA |title=Management of atopic dermatitis in the pediatric population |journal=Pediatrics |volume=122 |issue=4 |pages=812–24 |date=October 2008 |pmid=18829806 |doi=10.1542/peds.2007-2232 |url=}}</ref><br />
*Treat [[stress]] and [[anxiety]]<br />
*Avoid exposure to [[solvents]] and [[detergents]]<br />
*Treat skin [[infections]] such as [[Staphylococcus aureus|S''taphylococcus aureus'']] and [[herpes simplex]].<br />
|<br />
*'''Emollients and moisturizers'''<br />
**Thick creams, [[Ointment|ointments]] (eg, [[petroleum jelly]]) with low/zero water content<ref name="pmid188298062">{{cite journal |vauthors=Krakowski AC, Eichenfield LF, Dohil MA |title=Management of atopic dermatitis in the pediatric population |journal=Pediatrics |volume=122 |issue=4 |pages=812–24 |date=October 2008 |pmid=18829806 |doi=10.1542/peds.2007-2232 |url=}}</ref><br />
**Apply [[emollients]] immediately after lukewarm baths twice daily <ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
*'''Bathing practices'''<br />
**Warm soaking baths or showers using mild or soap-free cleansers<br />
|<br />
*Tepid baths<ref name="pmid188298063">{{cite journal |vauthors=Krakowski AC, Eichenfield LF, Dohil MA |title=Management of atopic dermatitis in the pediatric population |journal=Pediatrics |volume=122 |issue=4 |pages=812–24 |date=October 2008 |pmid=18829806 |doi=10.1542/peds.2007-2232 |url=}}</ref><br />
*Wet dressings (wet wraps)<br />
*Moisturizers containing [[Antipruritic|anti-pruritic]] ingredients such as [[phenol]], [[menthol]], and [[camphor]]<br />
<br />
*<br />
|}<br />
<br />
==Medical Therapy==<br />
<br />
*Pharmacologic medical therapies for atopic dermatitis can be classified according to several severity scales including [[SCORAD|SCORAD index]], the eczema area and severity index (EASI), and the patient-oriented eczema measure (POEM) which includes characteristics of the [[rash]], questions about [[itch]], [[sleep]], impact on daily activities, and persistence of disease.<ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
<br />
===Atopic dermatitis===<br />
<br />
*'''1. Mild atopic dermatitis''':<br />
**'''1.1 [[Topical]] [[corticosteroids]] and [[emollients]] -''' mainstay therapy<br />
***'''1.1.1 Adult'''<br />
****Preferred regimen (1): [[Desonide Topical|Desonide]] 0.05% top. q12h-q24h for 14-28 days<br />
****Preferred regimen (2): [[Hydrocortisone (ointment)|Hydrocortisone]] 2.5% top. q12h-q24h for 14-28 days<ref name="pmid7547394">{{cite journal |vauthors=Aalto-Korte K, Turpeinen M |title=Pharmacokinetics of topical hydrocortisone at plasma level after applications once or twice daily in patients with widespread dermatitis |journal=Br. J. Dermatol. |volume=133 |issue=2 |pages=259–63 |date=August 1995 |pmid=7547394 |doi= |url=}}</ref><br />
****Preferred regimen (3): [[Fluocinolone acetonide]] [[drug name|0.01% top.]] q12h-q24h for 14-28 days<br />
****Alternative regimen (1): [[Tacrolimus]] 0.1% top. q12h ('''0.03% for adults who do not tolerate the higher dose)'''<ref name="pmid9295241">{{cite journal |vauthors=Ruzicka T, Bieber T, Schöpf E, Rubins A, Dobozy A, Bos JD, Jablonska S, Ahmed I, Thestrup-Pedersen K, Daniel F, Finzi A, Reitamo S |title=A short-term trial of tacrolimus ointment for atopic dermatitis. European Tacrolimus Multicenter Atopic Dermatitis Study Group |journal=N. Engl. J. Med. |volume=337 |issue=12 |pages=816–21 |date=September 1997 |pmid=9295241 |doi=10.1056/NEJM199709183371203 |url=}}</ref><br />
****Alternative regimen (2): [[Pimecrolimus]] 1% top. q12h<ref name="pmid92952415">{{cite journal |vauthors=Ruzicka T, Bieber T, Schöpf E, Rubins A, Dobozy A, Bos JD, Jablonska S, Ahmed I, Thestrup-Pedersen K, Daniel F, Finzi A, Reitamo S |title=A short-term trial of tacrolimus ointment for atopic dermatitis. European Tacrolimus Multicenter Atopic Dermatitis Study Group |journal=N. Engl. J. Med. |volume=337 |issue=12 |pages=816–21 |date=September 1997 |pmid=9295241 |doi=10.1056/NEJM199709183371203 |url=}}</ref><br />
****Alternative regimen (3) Crisaborole 2% [[Topical|top.]]<ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
***'''1.1.2 Pediatric'''<br />
****Preferred regimen (1): [[Desonide]] 0.05% top. q12h-q24h for 14-28 days<br />
****Preferred regimen (2): [[Hydrocortisone (ointment)|Hydrocortisone]] 2.5% top. q12h-q24h for 14-28 days<ref name="pmid75473942">{{cite journal |vauthors=Aalto-Korte K, Turpeinen M |title=Pharmacokinetics of topical hydrocortisone at plasma level after applications once or twice daily in patients with widespread dermatitis |journal=Br. J. Dermatol. |volume=133 |issue=2 |pages=259–63 |date=August 1995 |pmid=7547394 |doi= |url=}}</ref><br />
****Preferred regimen (3): [[Fluocinolone acetonide]] [[drug name|0.01% top.]] q12h-q24h for 14-28 days<br />
****Alternative regimen (1): [[Tacrolimus]] 0.03% top. q12h ('''Children (>2years)'''<ref name="pmid92952412">{{cite journal |vauthors=Ruzicka T, Bieber T, Schöpf E, Rubins A, Dobozy A, Bos JD, Jablonska S, Ahmed I, Thestrup-Pedersen K, Daniel F, Finzi A, Reitamo S |title=A short-term trial of tacrolimus ointment for atopic dermatitis. European Tacrolimus Multicenter Atopic Dermatitis Study Group |journal=N. Engl. J. Med. |volume=337 |issue=12 |pages=816–21 |date=September 1997 |pmid=9295241 |doi=10.1056/NEJM199709183371203 |url=}}</ref><br />
****Alternative regimen (2): [[Pimecrolimus]] 1% top. q12h<ref name="pmid92952416">{{cite journal |vauthors=Ruzicka T, Bieber T, Schöpf E, Rubins A, Dobozy A, Bos JD, Jablonska S, Ahmed I, Thestrup-Pedersen K, Daniel F, Finzi A, Reitamo S |title=A short-term trial of tacrolimus ointment for atopic dermatitis. European Tacrolimus Multicenter Atopic Dermatitis Study Group |journal=N. Engl. J. Med. |volume=337 |issue=12 |pages=816–21 |date=September 1997 |pmid=9295241 |doi=10.1056/NEJM199709183371203 |url=}}</ref><br />
****Alternative regimen (3): Crisaborole 2% top.<br />
*'''2 Moderate atopic dermatitis'''<br />
**'''2.1 Topical [[corticosteroids]] and [[emollients]]''' '''-''' mainstay therapy<br />
***'''2.1.1 Adult'''<br />
****Preferred regimen (1): [[Fluocinolone]] 0.025%. q12h-q24h for 14-28 days<br />
****Preferred regimen (2): [[Triamcinolone (topical)|Triamcinolone]] 0.1% top. q12h-q24h for 14-28 days<br />
****Preferred regimen (3): [[Fluocinolone acetonide]] [[drug name|0.025% top.]] q12h-q24h for 14-28 days<br />
****Alternative regimen (1): [[Tacrolimus (topical)|Tacrolimus]] 0.1% top. q12h ('''0.03% for adults who do not tolerate the higher dose)'''<ref name="pmid92952413">{{cite journal |vauthors=Ruzicka T, Bieber T, Schöpf E, Rubins A, Dobozy A, Bos JD, Jablonska S, Ahmed I, Thestrup-Pedersen K, Daniel F, Finzi A, Reitamo S |title=A short-term trial of tacrolimus ointment for atopic dermatitis. European Tacrolimus Multicenter Atopic Dermatitis Study Group |journal=N. Engl. J. Med. |volume=337 |issue=12 |pages=816–21 |date=September 1997 |pmid=9295241 |doi=10.1056/NEJM199709183371203 |url=}}</ref><br />
****Alternative regimen (2): [[Pimecrolimus topical|Pimecrolimus]] 1% top. q12h<ref name="pmid92952417">{{cite journal |vauthors=Ruzicka T, Bieber T, Schöpf E, Rubins A, Dobozy A, Bos JD, Jablonska S, Ahmed I, Thestrup-Pedersen K, Daniel F, Finzi A, Reitamo S |title=A short-term trial of tacrolimus ointment for atopic dermatitis. European Tacrolimus Multicenter Atopic Dermatitis Study Group |journal=N. Engl. J. Med. |volume=337 |issue=12 |pages=816–21 |date=September 1997 |pmid=9295241 |doi=10.1056/NEJM199709183371203 |url=}}</ref><br />
****Alternative regimen (3): [[Crisaborole]] 2% top.<br />
***'''2.1.2 Pediatric'''<br />
****Preferred regimen (1): [[Fluocinolone]] 0.025%. q12h-q24h for 14 days<br />
****Preferred regimen (2): [[Triamcinolone (topical)|Triamcinolone]] 0.1% top. q12h-q24h for 14 days<br />
****Preferred regimen (3): [[Fluocinolone acetonide]] [[drug name|0.025% top.]] q12h-q24h for 14-28 days<br />
****Alternative regimen (1): [[Tacrolimus (topical)|Tacrolimus]] 0.03% top. q12h ('''Children (>2years)'''<ref name="pmid92952414">{{cite journal |vauthors=Ruzicka T, Bieber T, Schöpf E, Rubins A, Dobozy A, Bos JD, Jablonska S, Ahmed I, Thestrup-Pedersen K, Daniel F, Finzi A, Reitamo S |title=A short-term trial of tacrolimus ointment for atopic dermatitis. European Tacrolimus Multicenter Atopic Dermatitis Study Group |journal=N. Engl. J. Med. |volume=337 |issue=12 |pages=816–21 |date=September 1997 |pmid=9295241 |doi=10.1056/NEJM199709183371203 |url=}}</ref><br />
****Alternative regimen (2): [[Pimecrolimus topical|Pimecrolimus]] 1% top. q12h<ref name="pmid92952418">{{cite journal |vauthors=Ruzicka T, Bieber T, Schöpf E, Rubins A, Dobozy A, Bos JD, Jablonska S, Ahmed I, Thestrup-Pedersen K, Daniel F, Finzi A, Reitamo S |title=A short-term trial of tacrolimus ointment for atopic dermatitis. European Tacrolimus Multicenter Atopic Dermatitis Study Group |journal=N. Engl. J. Med. |volume=337 |issue=12 |pages=816–21 |date=September 1997 |pmid=9295241 |doi=10.1056/NEJM199709183371203 |url=}}</ref><br />
****Alternative regimen (3): [[Crisaborole]] 2% top.<br />
*'''3. Severe atopic dermatitis'''<br />
**'''3.1 [[Phototherapy]] or systemic [[immunosuppressant]] treatment''' '''-''' mainstay therapy<br />
***'''3.1.1 Adult'''<br />
****Preferred regimen (1): [[Phototherapy]] [[Ultraviolet light therapy|(Ultraviolet light therapy]]) with [[PUVA therapy|PUVA]] ([[psoralens]] plus ultraviolet A radiation), 3 times a week<br />
****Preferred regimen (2): [[Cyclosporine]] PO 3-5 mg/kg o.d. for 6 weeks ('''monitor BP and serum creatinine q2 weeks for three months, f/u q month)'''<ref name="pmid107273133">{{cite journal |vauthors=Czech W, Bräutigam M, Weidinger G, Schöpf E |title=A body-weight-independent dosing regimen of cyclosporine microemulsion is effective in severe atopic dermatitis and improves the quality of life |journal=J. Am. Acad. Dermatol. |volume=42 |issue=4 |pages=653–9 |date=April 2000 |pmid=10727313 |doi= |url=}}</ref><br />
****Alternative regimen (1): [[Methotrexate]] PO<ref name="pmid195527163">{{cite journal |vauthors=Lyakhovitsky A, Barzilai A, Heyman R, Baum S, Amichai B, Solomon M, Shpiro D, Trau H |title=Low-dose methotrexate treatment for moderate-to-severe atopic dermatitis in adults |journal=J Eur Acad Dermatol Venereol |volume=24 |issue=1 |pages=43–9 |date=January 2010 |pmid=19552716 |doi=10.1111/j.1468-3083.2009.03351.x |url=}}</ref><br />
****Alternative regimen (2): [[Azathioprine]] PO<ref name="pmid121741063">{{cite journal |vauthors=Berth-Jones J, Takwale A, Tan E, Barclay G, Agarwal S, Ahmed I, Hotchkiss K, Graham-Brown RA |title=Azathioprine in severe adult atopic dermatitis: a double-blind, placebo-controlled, crossover trial |journal=Br. J. Dermatol. |volume=147 |issue=2 |pages=324–30 |date=August 2002 |pmid=12174106 |doi= |url=}}</ref><br />
****Alternative regimen (3): Mycophenolate mofetil PO<br />
****Alternative regimen (4): [[Dupilumab]] 600 mg SQ once and then 300 mg SQ every 2 weeks thereafter<ref name="pmid250067193">{{cite journal |vauthors=Beck LA, Thaçi D, Hamilton JD, Graham NM, Bieber T, Rocklin R, Ming JE, Ren H, Kao R, Simpson E, Ardeleanu M, Weinstein SP, Pirozzi G, Guttman-Yassky E, Suárez-Fariñas M, Hager MD, Stahl N, Yancopoulos GD, Radin AR |title=Dupilumab treatment in adults with moderate-to-severe atopic dermatitis |journal=N. Engl. J. Med. |volume=371 |issue=2 |pages=130–9 |date=July 2014 |pmid=25006719 |doi=10.1056/NEJMoa1314768 |url=}}</ref><br />
***'''3.1.2 Pediatric'''<br />
****Preferred regimen (1): [[Phototherapy]] ([[Ultraviolet light]] therapy) with [[PUVA therapy|PUVA]] ( [[psoralens]] plus ultraviolet A radiation), 3 times a week('''older children > 6 years''')<br />
****Alternative regimen (1): [[Cyclosporine (oral)|Cyclosporine]] PO 3 to 5 mg/kg per day o.d. for 6 weeks (monitor '''[[blood pressure]] and [[serum creatinine]]''' every 2 weeks for three months, f/b every month''')'''<ref name="pmid107273134">{{cite journal |vauthors=Czech W, Bräutigam M, Weidinger G, Schöpf E |title=A body-weight-independent dosing regimen of cyclosporine microemulsion is effective in severe atopic dermatitis and improves the quality of life |journal=J. Am. Acad. Dermatol. |volume=42 |issue=4 |pages=653–9 |date=April 2000 |pmid=10727313 |doi= |url=}}</ref><ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
****Alternative regimen (2): [[Azathioprine]] PO<ref name="pmid121741062">{{cite journal |vauthors=Berth-Jones J, Takwale A, Tan E, Barclay G, Agarwal S, Ahmed I, Hotchkiss K, Graham-Brown RA |title=Azathioprine in severe adult atopic dermatitis: a double-blind, placebo-controlled, crossover trial |journal=Br. J. Dermatol. |volume=147 |issue=2 |pages=324–30 |date=August 2002 |pmid=12174106 |doi= |url=}}</ref><br />
****Alternative regimen (3): Mycophenolate mofetil PO<br />
****Alternative regimen (4): [[Dupilumab]] 600 mg SQ once and then 300 mg SQ every 2 weeks thereafter<ref name="pmid250067192">{{cite journal |vauthors=Beck LA, Thaçi D, Hamilton JD, Graham NM, Bieber T, Rocklin R, Ming JE, Ren H, Kao R, Simpson E, Ardeleanu M, Weinstein SP, Pirozzi G, Guttman-Yassky E, Suárez-Fariñas M, Hager MD, Stahl N, Yancopoulos GD, Radin AR |title=Dupilumab treatment in adults with moderate-to-severe atopic dermatitis |journal=N. Engl. J. Med. |volume=371 |issue=2 |pages=130–9 |date=July 2014 |pmid=25006719 |doi=10.1056/NEJMoa1314768 |url=}}</ref><br />
*'''4. Severe refractory atopic dermatitis'''<br />
**'''4.1 Adult'''<br />
***Preferred regimen (1): Intensive [[Topical application|topical]] therapy<br />
****Soak and smear: Soak for 15 minutes in a tub of water. Apply [[Desoximetasone Topical|desoximetasone]] 0.25% top. to the whole body, except the [[groin]], [[axillae]], and [[face]].<br />
****Wet wrap therapy: [[Desoximetasone Topical|Desoximetasone]] 0.25% top. then occluded with wet wraps q12h<br />
***Alternative regimen (1): [[Phototherapy]]: narrowband ultraviolet B or [[Psoralen and ultraviolet A|psoralen plus ultraviolet A]] two to three times per week<br />
***Alternative regimen (2): [[Cyclosporine]] PO 2.5 to 5 mg/kg o.d. ('''C/I -''' '''[[Renal function impairment|abnormal renal function]], uncontrolled [[hypertension]] or [[infection]], and [[malignancy]]''')<ref name="pmid10727313">{{cite journal |vauthors=Czech W, Bräutigam M, Weidinger G, Schöpf E |title=A body-weight-independent dosing regimen of cyclosporine microemulsion is effective in severe atopic dermatitis and improves the quality of life |journal=J. Am. Acad. Dermatol. |volume=42 |issue=4 |pages=653–9 |date=April 2000 |pmid=10727313 |doi= |url=}}</ref><br />
***Alternative regimen (3): [[Prednisone]] 40 to 60 mg o.d. for one week, then taper the dose over the following two to three weeks<br />
***Alternative regimen (4): [[Methotrexate]] 7.5 to 25 mg single weekly dose with folic acid 1 mg o.d.<ref name="pmid195527162">{{cite journal |vauthors=Lyakhovitsky A, Barzilai A, Heyman R, Baum S, Amichai B, Solomon M, Shpiro D, Trau H |title=Low-dose methotrexate treatment for moderate-to-severe atopic dermatitis in adults |journal=J Eur Acad Dermatol Venereol |volume=24 |issue=1 |pages=43–9 |date=January 2010 |pmid=19552716 |doi=10.1111/j.1468-3083.2009.03351.x |url=}}</ref><br />
***Alternative regimen (5): [[Azathioprine]] 2 to 3 mg/kg<ref name="pmid12174106">{{cite journal |vauthors=Berth-Jones J, Takwale A, Tan E, Barclay G, Agarwal S, Ahmed I, Hotchkiss K, Graham-Brown RA |title=Azathioprine in severe adult atopic dermatitis: a double-blind, placebo-controlled, crossover trial |journal=Br. J. Dermatol. |volume=147 |issue=2 |pages=324–30 |date=August 2002 |pmid=12174106 |doi= |url=}}</ref><br />
***Alternative regimen (6): Mycophenolate mofetil 1 to 2 g/day<br />
***Alternative regimen (7): [[Mycophenolic acid]] 720 to 1440 mg/day<br />
***Alternative regimen (8): [[Dupilumab]] 600 mg SQ once and then 300 mg SQ every 2 weeks thereafter<ref name="pmid25006719">{{cite journal |vauthors=Beck LA, Thaçi D, Hamilton JD, Graham NM, Bieber T, Rocklin R, Ming JE, Ren H, Kao R, Simpson E, Ardeleanu M, Weinstein SP, Pirozzi G, Guttman-Yassky E, Suárez-Fariñas M, Hager MD, Stahl N, Yancopoulos GD, Radin AR |title=Dupilumab treatment in adults with moderate-to-severe atopic dermatitis |journal=N. Engl. J. Med. |volume=371 |issue=2 |pages=130–9 |date=July 2014 |pmid=25006719 |doi=10.1056/NEJMoa1314768 |url=}}</ref><br />
**'''4.2 Pediatric'''<br />
***Preferred regimen (1): Intensive topical therapy<br />
****Wet wrap therapy: [[Desoximetasone]] 0.05% top. then occluded with wet wraps q12h-q24h for 2 to 14 days<br />
***Alternative regimen (1) [[Phototherapy]]: narrowband ultraviolet B ([[UVB]]) 3 times per week ('''older children > 6 years''')<ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
***Alternative regimen (2): [[Cyclosporine]] PO 2.5 to 5 mg/kg o.d. for 2-4 months ('''monitor [[Renal function|renal]] and [[Liver function tests|hepatic function]]''')<ref name="pmid107273132">{{cite journal |vauthors=Czech W, Bräutigam M, Weidinger G, Schöpf E |title=A body-weight-independent dosing regimen of cyclosporine microemulsion is effective in severe atopic dermatitis and improves the quality of life |journal=J. Am. Acad. Dermatol. |volume=42 |issue=4 |pages=653–9 |date=April 2000 |pmid=10727313 |doi= |url=}}</ref><br />
***Alternative regimen (3): [[Methotrexate]] 0.5 mg/kg PO single weekly dose with folic acid 1 mg o.d.('''up to a maximum of 25 mg per week''')<ref name="pmid19552716">{{cite journal |vauthors=Lyakhovitsky A, Barzilai A, Heyman R, Baum S, Amichai B, Solomon M, Shpiro D, Trau H |title=Low-dose methotrexate treatment for moderate-to-severe atopic dermatitis in adults |journal=J Eur Acad Dermatol Venereol |volume=24 |issue=1 |pages=43–9 |date=January 2010 |pmid=19552716 |doi=10.1111/j.1468-3083.2009.03351.x |url=}}</ref><br />
***Alternative regimen (4): [[Methylprednisolone]] 0.5 mg/kg o.d. for 1-2 weeks tapered over one month<br />
<br />
'''Other Drugs for atopic dermatitis''':<br />
<br />
*I[[Interferon-γ|nterferon-γ]] sub-q o.d. for 12 weeks<ref name="pmid8432915">{{cite journal |vauthors=Hanifin JM, Schneider LC, Leung DY, Ellis CN, Jaffe HS, Izu AE, Bucalo LR, Hirabayashi SE, Tofte SJ, Cantu-Gonzales G |title=Recombinant interferon gamma therapy for atopic dermatitis |journal=J. Am. Acad. Dermatol. |volume=28 |issue=2 Pt 1 |pages=189–97 |date=February 1993 |pmid=8432915 |doi= |url=}}</ref><br />
*Anti-CD20 therapy<br />
**[[Rituximab]]<ref name="pmid18206507">{{cite journal |vauthors=Simon D, Hösli S, Kostylina G, Yawalkar N, Simon HU |title=Anti-CD20 (rituximab) treatment improves atopic eczema |journal=J. Allergy Clin. Immunol. |volume=121 |issue=1 |pages=122–8 |date=January 2008 |pmid=18206507 |doi=10.1016/j.jaci.2007.11.016 |url=}}</ref><br />
*Anti-IgE<br />
**[[Omalizumab]]<ref name="pmid16384758">{{cite journal |vauthors=Lane JE, Cheyney JM, Lane TN, Kent DE, Cohen DJ |title=Treatment of recalcitrant atopic dermatitis with omalizumab |journal=J. Am. Acad. Dermatol. |volume=54 |issue=1 |pages=68–72 |date=January 2006 |pmid=16384758 |doi=10.1016/j.jaad.2005.09.030 |url=}}</ref><br />
*Anti-TNFα therapy<br />
**[[Infliximab]]<ref name="pmid15761436">{{cite journal |vauthors=Jacobi A, Antoni C, Manger B, Schuler G, Hertl M |title=Infliximab in the treatment of moderate to severe atopic dermatitis |journal=J. Am. Acad. Dermatol. |volume=52 |issue=3 Pt 1 |pages=522–6 |date=March 2005 |pmid=15761436 |doi=10.1016/j.jaad.2004.11.022 |url=}}</ref><br />
*Anti-IL-6 receptor therapy<br />
**[[Tocilizumab]]<ref name="pmid21962991">{{cite journal |vauthors=Navarini AA, French LE, Hofbauer GF |title=Interrupting IL-6-receptor signaling improves atopic dermatitis but associates with bacterial superinfection |journal=J. Allergy Clin. Immunol. |volume=128 |issue=5 |pages=1128–30 |date=November 2011 |pmid=21962991 |doi=10.1016/j.jaci.2011.09.009 |url=}}</ref><br />
<br />
'''Adjuvant treatment:'''<br />
<br />
*[[Primrose Oil|Primrose]] oil<ref name="pmid23633319">{{cite journal |vauthors=Bamford JT, Ray S, Musekiwa A, van Gool C, Humphreys R, Ernst E |title=Oral evening primrose oil and borage oil for eczema |journal=Cochrane Database Syst Rev |volume= |issue=4 |pages=CD004416 |date=April 2013 |pmid=23633319 |doi=10.1002/14651858.CD004416.pub2 |url=}}</ref><br />
*[[Omega-3]]<ref name="pmid18241260">{{cite journal |vauthors=Koch C, Dölle S, Metzger M, Rasche C, Jungclas H, Rühl R, Renz H, Worm M |title=Docosahexaenoic acid (DHA) supplementation in atopic eczema: a randomized, double-blind, controlled trial |journal=Br. J. Dermatol. |volume=158 |issue=4 |pages=786–92 |date=April 2008 |pmid=18241260 |doi=10.1111/j.1365-2133.2007.08430.x |url=}}</ref><br />
*[[Probiotics]]<ref name="pmid22336810">{{cite journal |vauthors=Bath-Hextall FJ, Jenkinson C, Humphreys R, Williams HC |title=Dietary supplements for established atopic eczema |journal=Cochrane Database Syst Rev |volume= |issue=2 |pages=CD005205 |date=February 2012 |pmid=22336810 |doi=10.1002/14651858.CD005205.pub3 |url=}}</ref><br />
*Chinese herbal medicines<br />
*[[Vitamin D|Oral vitamin D]]<ref name="pmid21087229">{{cite journal |vauthors=Peroni DG, Piacentini GL, Cametti E, Chinellato I, Boner AL |title=Correlation between serum 25-hydroxyvitamin D levels and severity of atopic dermatitis in children |journal=Br. J. Dermatol. |volume=164 |issue=5 |pages=1078–82 |date=May 2011 |pmid=21087229 |doi=10.1111/j.1365-2133.2010.10147.x |url=}}</ref><br />
<br />
'''Management of Infections:''' <br />
<br />
*'''Bacterial''' '''infections''': (most common bacteria - [[Staphylococcus aureus|S''taphylococcus aureus'']])<ref name="pmid20670815">{{cite journal |vauthors=Ong PY, Leung DY |title=The infectious aspects of atopic dermatitis |journal=Immunol Allergy Clin North Am |volume=30 |issue=3 |pages=309–21 |date=August 2010 |pmid=20670815 |pmc=2913147 |doi=10.1016/j.iac.2010.05.001 |url=}}</ref><br />
**Clinically infected skin:<br />
***[[Mupirocin]] 2% top. BID for one to two weeks<br />
***More extensive infection: Oral antibiotic therapy with [[cephalosporins]] or penicillinase-resistant penicillins for two weeks.<br />
**Clinically uninfected skin:<br />
***Liquid chlorine bleach- 0.5 cup or 120 ml of 6% bleach in a full bathtub [40 gallons or 150 L] of lukewarm water<ref name="pmid19403473">{{cite journal |vauthors=Huang JT, Abrams M, Tlougan B, Rademaker A, Paller AS |title=Treatment of Staphylococcus aureus colonization in atopic dermatitis decreases disease severity |journal=Pediatrics |volume=123 |issue=5 |pages=e808–14 |date=May 2009 |pmid=19403473 |doi=10.1542/peds.2008-2217 |url=}}</ref><br />
*'''Viral infections:'''<br />
**[[Herpes simplex virus]]:<br />
***[[Acyclovir]] 200 or 400 mg PO five times daily<br />
***[[Famciclovir]] 750 mg BID for one day or 1500 mg as a single dose<br />
**[[Molluscum contagiosum|''Molluscum contagiosum'']] :<br />
***[[Cryotherapy]], curettage, [[cantharidin]], and [[podophyllotoxin]] as first-line therapeutic options.<br />
*'''Fungal infections:'''<br />
**[[Dermatophytes|Dermatophyte]] infections '''-''' [[topical]] or [[oral]] [[antifungals]]<ref name="pmid11421895">{{cite journal |vauthors=Lintu P, Savolainen J, Kortekangas-Savolainen O, Kalimo K |title=Systemic ketoconazole is an effective treatment of atopic dermatitis with IgE-mediated hypersensitivity to yeasts |journal=Allergy |volume=56 |issue=6 |pages=512–7 |date=June 2001 |pmid=11421895 |doi= |url=}}</ref><br />
<br />
'''Controlling pruritus:'''<br />
<br />
*Preferred regimen''':'''<br />
**Sedatives: [[Diphenhydramine]], [[hydroxyzine]], and [[cyproheptadine]]<br />
**Non-sedatives: [[Fexofenadine]], [[cetirizine]] or [[loratadine]]<br />
*Alternative regimen:<br />
**Topical [[doxepin]]<br />
**Topical [[calcineurin]] inhibitors<br />
*** [[Pimecrolimus]] 1% cream or [[tacrolimus]] 0.03% to 0.1%<ref name="pmid92952414" /><ref name="pmid92952418" /><br />
<br />
'''Potential systemic therapies (not yet approved):'''<ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
<br />
* JAK inhibitors:<br />
** Abrocitinib (JAK1)<br />
** Gusacitinib (pan-JAK, SYK)<br />
** Tofacitinib (JAK1 and JAK3)<br />
** Upadacitinib (JAK1)<br />
* Interleukin-13 receptor antibodies <br />
* nterleukin-22 receptor antibody<br />
* Interleukin-31 receptor A antibody <br />
* Interleukin-33 receptor A antibody<br />
* Phosphodiesterase-4 inhibitor <br />
<br />
==References==<br />
<br />
{{Reflist|2}}<br />
<br />
[[Category:Autoimmune diseases]]<br />
[[Category:Dermatology]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Atopic_dermatitis_history_and_symptoms&diff=1703485Atopic dermatitis history and symptoms2021-06-08T19:08:50Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Atopic dermatitis}}<br />
{{CMG}}; {{AE}} {{S.S}}<br />
<br />
==Overview==<br />
The most common [[symptoms]] of atopic dermatitis include [[pruritus]], distribution of [[rash]] in age-specific patterns, and [[dry skin]]. [[Symptoms]] differ depending on age, stage, race/ethnic group, and geographic location. Patients often have a personal or [[family history]] of [[asthma]] or [[allergic rhinitis]]. [[Patients]] with atopic dermatitis may report a positive history of [[cutaneous]] hyper-reactivity to diverse environmental stimuli and [[Atopy|atopic disorders]].<br />
<br />
==History and Symptoms==<br />
===History===<br />
[[Patients]] with atopic dermatitis may have a positive history of:<ref name="pmid23712284">{{cite journal |vauthors=Leung DY |title=New insights into atopic dermatitis: role of skin barrier and immune dysregulation |journal=Allergol Int |volume=62 |issue=2 |pages=151–61 |date=June 2013 |pmid=23712284 |doi=10.2332/allergolint.13-RAI-0564 |url=}}</ref><ref name="pmid97349032">{{cite journal |vauthors=Rudikoff D, Lebwohl M |title=Atopic dermatitis |journal=Lancet |volume=351 |issue=9117 |pages=1715–21 |date=June 1998 |pmid=9734903 |doi=10.1016/S0140-6736(97)12082-7 |url=}}</ref><br />
<br />
*[[Cutaneous]] hyper-reactivity to diverse environmental stimuli including:<br />
**Exposure to food and inhalant [[allergens]]<br />
**Changes in physical environment (including [[humidity]], [[pollution]], etc.)<br />
**[[Irritants]]<br />
**[[Microbial|Microbial infection]]<br />
**[[Stress]]<br />
*[[Atopic]] march: development of clinical [[signs]] during childhood from atopic dermatitis to [[asthma]] to [[allergic rhinitis]].<ref name="pmid20674819">{{cite journal |vauthors=Spergel JM |title=From atopic dermatitis to asthma: the atopic march |journal=Ann. Allergy Asthma Immunol. |volume=105 |issue=2 |pages=99–106; quiz 107–9, 117 |date=August 2010 |pmid=20674819 |doi=10.1016/j.anai.2009.10.002 |url=}}</ref><ref name="pmid206748192">{{cite journal |vauthors=Spergel JM |title=From atopic dermatitis to asthma: the atopic march |journal=Ann. Allergy Asthma Immunol. |volume=105 |issue=2 |pages=99–106; quiz 107–9, 117 |date=August 2010 |pmid=20674819 |doi=10.1016/j.anai.2009.10.002 |url=}}</ref><ref name="pmid16935684">{{cite journal |vauthors=Asher MI, Montefort S, Björkstén B, Lai CK, Strachan DP, Weiland SK, Williams H |title=Worldwide time trends in the prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and eczema in childhood: ISAAC Phases One and Three repeat multicountry cross-sectional surveys |journal=Lancet |volume=368 |issue=9537 |pages=733–43 |date=August 2006 |pmid=16935684 |doi=10.1016/S0140-6736(06)69283-0 |url=}}</ref><br />
**Clinical features of atopic dermatitis usually occur earlier in life.<br />
**[[Asthma]] and [[allergic rhinitis]] usually occur later on in life.<ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
<br />
===Common Symptoms===<br />
Common [[symptoms]] of atopic dermatitis include:<ref name="DeleuranVestergaard2014">{{cite journal|last1=Deleuran|first1=M.|last2=Vestergaard|first2=C.|title=Clinical heterogeneity and differential diagnosis of atopic dermatitis|journal=British Journal of Dermatology|volume=170|year=2014|pages=2–6|issn=00070963|doi=10.1111/bjd.12933}}</ref><ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
<br />
*Severe [[pruritus]]: Can cause [[sleep disturbances]] in children<ref name="pmid7633537">{{cite journal |vauthors=Dahl RE, Bernhisel-Broadbent J, Scanlon-Holdford S, Sampson HA, Lupo M |title=Sleep disturbances in children with atopic dermatitis |journal=Arch Pediatr Adolesc Med |volume=149 |issue=8 |pages=856–60 |date=August 1995 |pmid=7633537 |doi= |url=}}</ref><ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
*Chronic or relapsing skin lesions<br />
*Distribution of rash on:<br />
**Facial and [[extensor]] surfaces in infants and young children<br />
**Flexural [[lichenification]] in older children and adults<br />
<br />
===Less Common Symptoms===<br />
Less common symptoms of atopic dermatitis include:<ref name="pmid9734903">{{cite journal |vauthors=Rudikoff D, Lebwohl M |title=Atopic dermatitis |journal=Lancet |volume=351 |issue=9117 |pages=1715–21 |date=June 1998 |pmid=9734903 |doi=10.1016/S0140-6736(97)12082-7 |url=}}</ref><ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
<br />
*[[Pallor|Facial pallor]]<br />
*[[Dry skin]] especially in winter)<br />
*Nonspecific dermatitis of the hands and feet<br />
*[[Food intolerance]]<br />
*[[Itch]] when sweating<br />
*Difficulty sleeping and diminished productivity has also been reported as atopic dermatitis can cause severe [[pruritus]].<br />
<br />
==References==<br />
{{Reflist|2}}<br />
<br />
[[Category:dermatology]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Atopic_dermatitis_epidemiology_and_demographics&diff=1703484Atopic dermatitis epidemiology and demographics2021-06-08T19:04:24Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Atopic dermatitis}}<br />
<br />
{{CMG}}; {{AE}} <br />
<br />
<br /><br />
<br />
== Overview ==<br />
Atopic dermatitis affects 10-20% of children and 1-3% of adults in industrialized countries. Its [[prevalence]] has doubled in the past thirty years. Atopic dermatitis is significantly associated with African-American individuals and tends to affect metropolitan populations as compared to rural populations.<br />
<br />
==Epidemiology and Demographics==<br />
===Prevalence===<br />
<br />
*The [[prevalence]] of atopic dermatitis is approximately 5,000-20,000 cases per 100,000 children, worldwide.<ref name="pmid9893196">{{cite journal |vauthors=Williams H, Robertson C, Stewart A, Aït-Khaled N, Anabwani G, Anderson R, Asher I, Beasley R, Björkstén B, Burr M, Clayton T, Crane J, Ellwood P, Keil U, Lai C, Mallol J, Martinez F, Mitchell E, Montefort S, Pearce N, Shah J, Sibbald B, Strachan D, von Mutius E, Weiland SK |title=Worldwide variations in the prevalence of symptoms of atopic eczema in the International Study of Asthma and Allergies in Childhood |journal=J. Allergy Clin. Immunol. |volume=103 |issue=1 Pt 1 |pages=125–38 |date=January 1999 |pmid=9893196 |doi= |url=}}</ref><ref name="saito">Saito, Hirohisa. Much Atopy about the Skin: Genome-Wide Molecular Analysis of Atopic Eczema. International Archives of Allergy and Immunology 2005;137:319-325.</ref><br />
*In 2003, the [[prevalence]] of atopic dermatitis was estimated to be 10,700 cases per 100,000 children in the United States.<ref name="pmid20739951">{{cite journal |vauthors=Shaw TE, Currie GP, Koudelka CW, Simpson EL |title=Eczema prevalence in the United States: data from the 2003 National Survey of Children's Health |journal=J. Invest. Dermatol. |volume=131 |issue=1 |pages=67–73 |date=January 2011 |pmid=20739951 |pmc=3130508 |doi=10.1038/jid.2010.251 |url=}}</ref><br />
<br />
===Age===<br />
<br />
*The prevalence of atopic dermatitis is up to 20% in children and up to 3% in adults.<ref name="pmid25925336">{{cite journal |vauthors=Nutten S |title=Atopic dermatitis: global epidemiology and risk factors |journal=Ann. Nutr. Metab. |volume=66 Suppl 1 |issue= |pages=8–16 |date=2015 |pmid=25925336 |doi=10.1159/000370220 |url=}}</ref><ref name="pmid28296746">{{cite journal |vauthors=Wang X, Shi XD, Li LF, Zhou P, Shen YW, Song QK |title=Prevalence and clinical features of adult atopic dermatitis in tertiary hospitals of China |journal=Medicine (Baltimore) |volume=96 |issue=11 |pages=e6317 |date=March 2017 |pmid=28296746 |pmc=5369901 |doi=10.1097/MD.0000000000006317 |url=}}</ref><ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
*The majority of atopic dermatitis patients have onset <5 years of age.<br />
*Atopic dermatitis [[incidence]] is highest during infancy and early childhood.<br />
<br />
===Race===<br />
<br />
*Higher [[prevalence]] of atopic dermatitis was significantly associated with African-American individuals.<ref name="pmid207399512">{{cite journal |vauthors=Shaw TE, Currie GP, Koudelka CW, Simpson EL |title=Eczema prevalence in the United States: data from the 2003 National Survey of Children's Health |journal=J. Invest. Dermatol. |volume=131 |issue=1 |pages=67–73 |date=January 2011 |pmid=20739951 |pmc=3130508 |doi=10.1038/jid.2010.251 |url=}}</ref><ref name="pmid7829705">{{cite journal |vauthors=Williams HC, Pembroke AC, Forsdyke H, Boodoo G, Hay RJ, Burney PG |title=London-born black Caribbean children are at increased risk of atopic dermatitis |journal=J. Am. Acad. Dermatol. |volume=32 |issue=2 Pt 1 |pages=212–7 |date=February 1995 |pmid=7829705 |doi= |url=}}</ref><ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
*Of note, [[patients]] in different racial groups tend to manifest various clinical presentations. For example, trunk lesions of atopic dermatitis may affect all races, but tend to be more clear and have obvious margins in Asians.<br />
<br />
===Gender===<br />
<br />
*Atopic dermatitis affects men and women equally.<br />
<br />
===Region===<br />
<br />
*Atopic dermatitis is a common disease that tends to affect metropolitan populations as compared to rural populations.<ref name="pmid207399512" /><br />
*Higher exposure to air pollution and household hygiene products in metropolitan and developed cities are potential explanations of this observation.<br />
<br />
==References==<br />
<br />
{{Reflist|2}}<br />
<br />
[[Category:Autoimmune diseases]]<br />
[[Category:Dermatology]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Atopic_dermatitis_diagnostic_study_of_choice&diff=1703483Atopic dermatitis diagnostic study of choice2021-06-08T19:01:03Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Atopic dermatitis}}<br />
<br />
{{CMG}}; {{AE}}{{S.S}}, [[Ogechukwu Hannah Nnabude, MD]]<br />
<br />
==Overview==<br />
Due to the variable [[morphology]], distribution of skin [[lesions]], and intermittent clinical features, it is very challenging to define the diagnosis of atopic dermatitis. Atopic dermatitis is primarily diagnosed based on the [[clinical]] presentation. Currently, the most commonly used [[Criterion|criteria]] worldwide is published by the United Kingdom Working Group and is based on history, morphology, and distribution of [[Eczema|eczematous]] [[lesions]], and clinical features of atopic dermatitis. <br />
<br />
==Diagnostic Study of Choice==<br />
<br />
*There is no single diagnostic study of choice for routine diagnosis of atopic dermatitis, but in selected patients, to rule out other skin conditions, histologic examination of a [[skin biopsy]] and other laboratory tests (eg, [[Immunoglobulin E|serum immunoglobulin E]], [[KOH test|potassium hydroxide preparation]], patch testing, [[genetic testing]]) may be considered.<ref name="pmid242904312">{{cite journal |vauthors=Eichenfield LF, Tom WL, Chamlin SL, Feldman SR, Hanifin JM, Simpson EL, Berger TG, Bergman JN, Cohen DE, Cooper KD, Cordoro KM, Davis DM, Krol A, Margolis DJ, Paller AS, Schwarzenberger K, Silverman RA, Williams HC, Elmets CA, Block J, Harrod CG, Smith Begolka W, Sidbury R |title=Guidelines of care for the management of atopic dermatitis: section 1. Diagnosis and assessment of atopic dermatitis |journal=J. Am. Acad. Dermatol. |volume=70 |issue=2 |pages=338–51 |date=February 2014 |pmid=24290431 |pmc=4410183 |doi=10.1016/j.jaad.2013.10.010 |url=}}</ref><br />
<br />
===Diagnostic Criteria:===<br />
<br />
*Atopic dermatitis is primarily diagnosed based on clinical presentation. There are several established criteria for the diagnosis of atopic dermatitis, the earliest and most accepted [[diagnostic criteria]] being the 1980 Hanifin and Rajka criteria that was previously used.<ref name="pmid16086748">{{cite journal |vauthors=Jøhnke H, Vach W, Norberg LA, Bindslev-Jensen C, Høst A, Andersen KE |title=A comparison between criteria for diagnosing atopic eczema in infants |journal=Br. J. Dermatol. |volume=153 |issue=2 |pages=352–8 |date=August 2005 |pmid=16086748 |doi=10.1111/j.1365-2133.2005.06491.x |url=}}</ref><ref>{{cite journal |last1= Hanifin |first1=Jon M. |last2= Rajka |first2=Georg |date= |title=Diagnostic Features of Atopic Dermatitis|url=https://www.medicaljournals.se/acta/content/abstract/10.2340/00015555924447 |journal= Acta Derm Venereol Suppl (Stockh) |volume=60 |issue=92 |pages=44-47 |doi=10.2340/00015555924447 |access-date= }}</ref><br />
*Currently, the most commonly used criteria worldwide is published by United Kingdom Working Group and is based on history, morphology and distribution of eczematous lesions, and clinical features of atopic dermatitis.<ref name="pmid24290431">{{cite journal |vauthors=Eichenfield LF, Tom WL, Chamlin SL, Feldman SR, Hanifin JM, Simpson EL, Berger TG, Bergman JN, Cohen DE, Cooper KD, Cordoro KM, Davis DM, Krol A, Margolis DJ, Paller AS, Schwarzenberger K, Silverman RA, Williams HC, Elmets CA, Block J, Harrod CG, Smith Begolka W, Sidbury R |title=Guidelines of care for the management of atopic dermatitis: section 1. Diagnosis and assessment of atopic dermatitis |journal=J. Am. Acad. Dermatol. |volume=70 |issue=2 |pages=338–51 |date=February 2014 |pmid=24290431 |pmc=4410183 |doi=10.1016/j.jaad.2013.10.010 |url=}}</ref><br />
*The United Kingdom Working Group's criteria includes one mandatory criteria and 3 or more from the 5 major criteria.<ref name="pmid7918017">{{cite journal |vauthors=Williams HC, Burney PG, Pembroke AC, Hay RJ |title=The U.K. Working Party's Diagnostic Criteria for Atopic Dermatitis. III. Independent hospital validation |journal=Br. J. Dermatol. |volume=131 |issue=3 |pages=406–16 |date=September 1994 |pmid=7918017 |doi= |url=}}</ref><br />
<br />
{| class="wikitable"<br />
! colspan="3" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Atopic dermatitis diagnostic criteria<br />
|-<br />
|<br />
*Mandatory criteria:<ref name="pmid7918017" /><br />
**Evidence of [[pruritus]] or report of scratching or rubbing by the parent<br />
*3 or more of the major criteria:<ref name="pmid7918017" /><br />
**History of skin creases involvement including areas around neck and eyes, front of ankles, front of elbows, and back of knees.<br />
**History of [[asthma]] or [[hay fever]] (if children <4 years of age - history of atopic disease in a first-degree relative)<br />
**History of the presence of generally [[dry skin]] in the past year.<br />
**The onset of symptoms in child <2 years of age. This criterion is not recommended if a child <4 years old.<br />
**Visible [[dermatitis]] including flexor surfaces. In children <4 years of age, the criterion can involve dermatitis affecting the cheeks or forehead and outer aspects of the extremities.<br />
|-<br />
|Adapted from ''U.K. Working Party's Diagnostic Criteria''<br />
|}<br />
<br />
*The basis for making decisions about treatment depends on:<ref name="pmid10730763">{{cite journal |vauthors=Emerson RM, Charman CR, Williams HC |title=The Nottingham Eczema Severity Score: preliminary refinement of the Rajka and Langeland grading |journal=Br. J. Dermatol. |volume=142 |issue=2 |pages=288–97 |date=February 2000 |pmid=10730763 |doi= |url=}}</ref><br />
**Presence or absence of [[Sleep disturbances|sleep disturbance]]<br />
**Number and location of involved sites<br />
**Clinical course of the disease<br />
<br />
{| class="wikitable"<br />
! colspan="3" style="background: #4479BA; color: #FFFFFF; text-align: center;" |The American Academy of Dermatology Diagnostic Criteria for Atopic Dermatitis<br />
|-<br />
|<br />
Clinical features and description<ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
<br />
*Essential Features and Description<br />
**Eczema - May be chronic or relapsing with characteristic, age-specific patterns and morphologic features.<br />
***Stages - Acute, subacute, or chronic<br />
***Severity - Mild, moderate, or severe<br />
***Immunoendo cell type - Th2 cells are seen in white and black people, Th2 and Th17 cells are seen in Asians<br />
**[[Pruritus]]<br />
*Important features and description<br />
**Age at onset typically early, between 2 and 6 months of age<br />
**Personal and/or family history of atopy, secondary to IgE reactivity seen in up to 80% of [[patients]].<br />
**[[Xerosis]]<br />
*Associated features and description<br />
**Atypical vascular responses - white dermographism or facial pallor.<br />
**Perifollicular lesions - Keratosis pilaris and perifollicular accentuation.<br />
**[[Ocular]] or periorbital lesions -Hertoghe’s sign<br />
**Regional findings - ichthyosis, Perioral changes, pityriasis alba, periauricular lesions, hyper linear palms.<br />
**Lesions related to chronic scratching - prurigo lesions and lesions Lichenification.<br />
*Associated [[conditions]]<br />
**[[Impetigo]]<br />
**[[Skin abscesses]]<br />
**[[Eczema herpeticum]]<br />
**[[Molluscum contagiosum]] infection<br />
**[[Dermatophytosis]]<br />
**[[Candidiasis]]<br />
**[[Asthma]]<br />
**[[Rhinitis]]<br />
**Rhinoconjunctivitis<br />
**[[Food allergy]]<br />
**[[Inflammatory bowel disease]]<br />
**[[Rheumatoid arthritis]]<br />
**[[Cardiovascular disease]]<br />
**[[Sleep disturbance]]<br />
**[[Anxiety]]<br />
**[[Depression]]<br />
**Suicidality<br />
|}<br />
<br />
==References==<br />
{{Reflist|2}}<br />
[[Category:Dermatology]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Atopic_dermatitis_classification&diff=1703482Atopic dermatitis classification2021-06-08T18:54:31Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Atopic dermatitis}}<br />
{{CMG}}; {{AE}} {{S.S}}<br />
<br />
==Overview==<br />
There is no established system for the classification of [[atopic dermatitis]]. It may be classified into intrinsic [[atopic dermatitis]] and extrinsic [[atopic dermatitis]] according to the means of allergic [[sensitization]]. Intrinsic [[atopic dermatitis]] is associated with normal serum [[IgE]] levels vs elevated total serum [[IgE]] levels.<br />
<br />
==Classification==<br />
<br />
There is no established system for the [[classification]] of [[atopic dermatitis]].<br />
<br />
[[Atopic dermatitis]] may be classified according to the means of allergic [[sensitization]] into:<ref name="pmid12897728">{{cite journal |vauthors=Novak N, Bieber T |title=Allergic and nonallergic forms of atopic diseases |journal=J. Allergy Clin. Immunol. |volume=112 |issue=2 |pages=252–62 |date=August 2003 |pmid=12897728 |doi= |url=}}</ref><ref name="pmid26158358">{{cite journal |vauthors=Karimkhani C, Silverberg JI, Dellavalle RP |title=Defining intrinsic vs. extrinsic atopic dermatitis |journal=Dermatol. Online J. |volume=21 |issue=6 |pages= |date=June 2015 |pmid=26158358 |doi= |url=}}</ref><br />
<br />
*Intrinsic [[atopic dermatitis]]<br />
*Extrinsic [[atopic dermatitis]]<br />
<br />
{| class="wikitable"<br />
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Intrinsic atopic dermatitis<br />
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Extrinsic atopic dermatitis<br />
|-<br />
|<br />
*Normal serum [[IgE]] levels<ref name="pmid16965428">{{cite journal |vauthors=Park JH, Choi YL, Namkung JH, Kim WS, Lee JH, Park HJ, Lee ES, Yang JM |title=Characteristics of extrinsic vs. intrinsic atopic dermatitis in infancy: correlations with laboratory variables |journal=Br. J. Dermatol. |volume=155 |issue=4 |pages=778–83 |date=October 2006 |pmid=16965428 |doi=10.1111/j.1365-2133.2006.07394.x |url=}}</ref><br />
<br />
*No specific [[IgE]] sensitization against<ref name="pmid12861844">{{cite journal |vauthors=Wüthrich B, Schmid-Grendelmeier P |title=The atopic eczema/dermatitis syndrome. Epidemiology, natural course, and immunology of the IgE-associated ("extrinsic") and the nonallergic ("intrinsic") AEDS |journal=J Investig Allergol Clin Immunol |volume=13 |issue=1 |pages=1–5 |date=2003 |pmid=12861844 |doi= |url=}}</ref> <br />
**Environmental [[allergens]]<br />
**[[Food allergens]]<br />
**Skin prick tests<br />
<br />
*No [[filaggrin]] [[mutation]]<br />
*Relative lower levels of [[Interleukin 4|IL-4]] and [[Interleukin 13|IL-13]]<ref name="pmid23777851">{{cite journal |vauthors=Suárez-Fariñas M, Dhingra N, Gittler J, Shemer A, Cardinale I, de Guzman Strong C, Krueger JG, Guttman-Yassky E |title=Intrinsic atopic dermatitis shows similar TH2 and higher TH17 immune activation compared with extrinsic atopic dermatitis |journal=J. Allergy Clin. Immunol. |volume=132 |issue=2 |pages=361–70 |date=August 2013 |pmid=23777851 |pmc=3991240 |doi=10.1016/j.jaci.2013.04.046 |url=}}</ref><br />
*Normal [[eosinophil]] counts and [[eosinophil cationic protein]] levels<ref name="pmid169654283">{{cite journal |vauthors=Park JH, Choi YL, Namkung JH, Kim WS, Lee JH, Park HJ, Lee ES, Yang JM |title=Characteristics of extrinsic vs. intrinsic atopic dermatitis in infancy: correlations with laboratory variables |journal=Br. J. Dermatol. |volume=155 |issue=4 |pages=778–83 |date=October 2006 |pmid=16965428 |doi=10.1111/j.1365-2133.2006.07394.x |url=}}</ref><br />
|<br />
*Elevated total serum [[IgE]] levels<ref name="pmid169654282">{{cite journal |vauthors=Park JH, Choi YL, Namkung JH, Kim WS, Lee JH, Park HJ, Lee ES, Yang JM |title=Characteristics of extrinsic vs. intrinsic atopic dermatitis in infancy: correlations with laboratory variables |journal=Br. J. Dermatol. |volume=155 |issue=4 |pages=778–83 |date=October 2006 |pmid=16965428 |doi=10.1111/j.1365-2133.2006.07394.x |url=}}</ref><br />
<br />
*IgE [[sensitization]] against<ref name="pmid128618442">{{cite journal |vauthors=Wüthrich B, Schmid-Grendelmeier P |title=The atopic eczema/dermatitis syndrome. Epidemiology, natural course, and immunology of the IgE-associated ("extrinsic") and the nonallergic ("intrinsic") AEDS |journal=J Investig Allergol Clin Immunol |volume=13 |issue=1 |pages=1–5 |date=2003 |pmid=12861844 |doi= |url=}}</ref><br />
**Environmental [[allergens]]<br />
**[[Food allergens]]<br />
**Skin prick tests<br />
<br />
*[[Filaggrin]] [[Mutation|mutations]] may be present<ref name="pmid17096018">{{cite journal |vauthors=Weidinger S, Rodríguez E, Stahl C, Wagenpfeil S, Klopp N, Illig T, Novak N |title=Filaggrin mutations strongly predispose to early-onset and extrinsic atopic dermatitis |journal=J. Invest. Dermatol. |volume=127 |issue=3 |pages=724–6 |date=March 2007 |pmid=17096018 |doi=10.1038/sj.jid.5700630 |url=}}</ref><br />
*Increased levels of [[Interleukin 4|IL-4]], [[Interleukin 5|IL-5]] and [[Interleukin 13|IL-13]]<br />
*Increased [[eosinophil]] counts and [[eosinophil cationic protein]] levels<ref name="pmid169654284">{{cite journal |vauthors=Park JH, Choi YL, Namkung JH, Kim WS, Lee JH, Park HJ, Lee ES, Yang JM |title=Characteristics of extrinsic vs. intrinsic atopic dermatitis in infancy: correlations with laboratory variables |journal=Br. J. Dermatol. |volume=155 |issue=4 |pages=778–83 |date=October 2006 |pmid=16965428 |doi=10.1111/j.1365-2133.2006.07394.x |url=}}</ref><br />
|}<br />
<br />
==References==<br />
{{Reflist|2}}<br />
<br />
[[Category:Dermatology]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Atopic_dermatitis_historical_perspective&diff=1700198Atopic dermatitis historical perspective2021-05-07T12:58:05Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Atopic dermatitis}}<br />
<br />
{{CMG}}; {{AE}} {{S.S}}<br />
<br />
==Overview==<br />
In 1933, atopic dermatitis was first coined by two American [[Dermatologist|dermatologists]], Fred Wise and Marion Sulzberger. The first study on the clinical features of [[asthma]] as well as [[allergic rhinitis]] and [[genetics]] was performed by Cooke and Vander in 1916. An association of higher serum [[IgE]] levels was published by Bruno Wüthrich in 1978.<br />
<br />
==Historical Perspective==<br />
<br />
===Discovery===<br />
* One of the very first traces of the relationship between [[allergies]] and genetic factors was described by Hippocrates.<ref name="Mier1975">{{cite journal|last1=Mier|first1=P.D.|title=EARLIEST DESCRIPTION OF THE ATOPIC SYNDROME?|journal=British Journal of Dermatology|volume=92|issue=3|year=1975|pages=359–359|issn=0007-0963|doi=10.1111/j.1365-2133.1975.tb03091.x}}</ref><br />
* In 1816, Willan and Bateman described a disease, “Porrigo larvalis,” which is identified as one of the earliest descriptions of atopic dermatitis.<ref name="pmid16198792">{{cite journal |vauthors=Wallach D, Coste J, Tilles G, Taïeb A |title=The first images of atopic dermatitis: an attempt at retrospective diagnosis in dermatology |journal=J. Am. Acad. Dermatol. |volume=53 |issue=4 |pages=684–9 |date=October 2005 |pmid=16198792 |doi=10.1016/j.jaad.2005.06.045 |url=}}</ref><ref name="WallachTaïeb2014">{{cite journal|last1=Wallach|first1=Daniel|last2=Taïeb|first2=Alain|title=Atopic Dermatitis/Atopic Eczema|volume=100|year=2014|pages=81–96|issn=1660-2242|doi=10.1159/000358606}}</ref><ref name="Levell2000">{{cite journal|last1=Levell|first1=N.J.|title=Thomas Bateman MD FLS 1778-1821|journal=British Journal of Dermatology|volume=143|issue=1|year=2000|pages=9–15|issn=00070963|doi=10.1046/j.1365-2133.2000.03582.x}}</ref><br />
* The first systemic study on the clinical features of [[asthma]] as well as [[allergic rhinitis]] and [[genetics]] was performed by Cooke and Vander in 1916.<ref name="DworetzkyCohen2002">{{cite journal|last1=Dworetzky|first1=Murray|last2=Cohen|first2=Sheldon G.|last3=Blumenthal|first3=Malcolm N.|title=Pioneers and milestones|journal=Journal of Allergy and Clinical Immunology|volume=110|issue=4|year=2002|pages=674–680|issn=00916749|doi=10.1016/S0091-6749(02)70054-7}}</ref><br />
* The association between [[heritable]] [[hypersensitivity]] to [[allergens]] in patients with [[asthma]] and [[hay fever]] and atopic dermatitis was made in 1923 by Arthur Coca and Robert Cooke.<ref name="KramerStrom20172">{{cite journal|last1=Kramer|first1=Owen N.|last2=Strom|first2=Mark A.|last3=Ladizinski|first3=Barry|last4=Lio|first4=Peter A.|title=The history of atopic dermatitis|journal=Clinics in Dermatology|volume=35|issue=4|year=2017|pages=344–348|issn=0738081X|doi=10.1016/j.clindermatol.2017.03.005}}</ref><ref name="pmid12532128">{{cite journal| author=Cohen S, Dworetzky M, Frick OL| title=Coca and Cooke on the classification of hypersensitiveness. | journal=J Allergy Clin Immunol | year= 2003 | volume= 111 | issue= 1 | pages= 205-10 | pmid=12532128 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12532128 }} </ref><br />
* The term atopic dermatitis was first coined from the Greek word, atopos, by Fred Wise and Marion Sulzberger, American [[Dermatologist|dermatologists]], in 1933. Fred Wise and Marion Sulzberger enhanced Arthur Coca and Robert Cooke's concept to include the description of atopic dermatitis.<ref name="WallachTaïeb2014" /><ref name="KramerStrom2017">{{cite journal|last1=Kramer|first1=Owen N.|last2=Strom|first2=Mark A.|last3=Ladizinski|first3=Barry|last4=Lio|first4=Peter A.|title=The history of atopic dermatitis|journal=Clinics in Dermatology|volume=35|issue=4|year=2017|pages=344–348|issn=0738081X|doi=10.1016/j.clindermatol.2017.03.005}}</ref><ref name="Hanifin1982">{{cite journal|last1=Hanifin|first1=Jon M.|title=Atopic dermatitis|journal=Journal of the American Academy of Dermatology|volume=6|issue=1|year=1982|pages=1–13|issn=01909622|doi=10.1016/S0190-9622(82)70001-5}}</ref><ref name="StänderRopper2021">{{cite journal|last1=Ständer|first1=Sonja|last2=Ropper|first2=Allan H.|title=Atopic Dermatitis|journal=New England Journal of Medicine|volume=384|issue=12|year=2021|pages=1136–1143|issn=0028-4793|doi=10.1056/NEJMra2023911}}</ref><br />
*A paper reporting a patient with atopic dermatitis was published by Bruno Wüthrich in 1978, demonstrating on average higher serum [[IgE]] levels compared with controls.<ref name="Thomsen2015">{{cite journal|last1=Thomsen|first1=Simon F.|title=Epidemiology and natural history of atopic diseases|journal=European Clinical Respiratory Journal|volume=2|issue=1|year=2015|pages=24642|issn=2001-8525|doi=10.3402/ecrj.v2.24642}}</ref><br />
* The first widely used diagnostic criteria for atopic dermatitis was published by Jon Hanifin and Georg Rajka, in 1980.<ref>{{cite journal|doi=10.2340/00015555924447}}</ref><br />
* Hanifin and Rajka's criteria was modified by Williams et al. in 1997, to develop the UK Working Party criteria, in which an individual must have itchy skin for 12 months along with other features.<ref name="pmid7918015">{{cite journal |vauthors=Williams HC, Burney PG, Hay RJ, Archer CB, Shipley MJ, Hunter JJ, Bingham EA, Finlay AY, Pembroke AC, Graham-Brown RA |title=The U.K. Working Party's Diagnostic Criteria for Atopic Dermatitis. I. Derivation of a minimum set of discriminators for atopic dermatitis |journal=Br. J. Dermatol. |volume=131 |issue=3 |pages=383–96 |date=September 1994 |pmid=7918015 |doi= |url=}}</ref><br />
*In 2006, [[filaggrin]] gene mutations were first implicated in the [[pathogenesis]] of atopic dermatitis by Palmer et al.<ref name="pmid16550169">{{cite journal |vauthors=Palmer CN, Irvine AD, Terron-Kwiatkowski A, Zhao Y, Liao H, Lee SP, Goudie DR, Sandilands A, Campbell LE, Smith FJ, O'Regan GM, Watson RM, Cecil JE, Bale SJ, Compton JG, DiGiovanna JJ, Fleckman P, Lewis-Jones S, Arseculeratne G, Sergeant A, Munro CS, El Houate B, McElreavey K, Halkjaer LB, Bisgaard H, Mukhopadhyay S, McLean WH |title=Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis |journal=Nat. Genet. |volume=38 |issue=4 |pages=441–6 |date=April 2006 |pmid=16550169 |doi=10.1038/ng1767 |url=}}</ref><br />
<br />
==References==<br />
{{Reflist|2}}<br />
[[Category:Dermatology]]<br />
[[Category:Up-to-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Chest_pain_in_children&diff=1697433Chest pain in children2021-04-16T18:08:53Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
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{| class="infobox" style="float:right;"<br />
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|[[File:Siren.gif|30px|link=Chest pain resident survival guide (pediatrics)]]||<br>||<br><br />
|[[Chest pain resident survival guide (pediatrics)|'''Resident'''<br>'''Survival'''<br>'''Guide''']]<br />
|} <br />
{{SI}} <br />
{{CMG}} {{AE}} {{Mitra}}<br />
<br />
{{SK}} Chest pain in kids, pediatric chest pain<br />
<br />
==Overview==<br />
<br />
Chest pain is a common [[symptom]] in children and adolescents. Despite causing considerable concerns and anxiety in [[patients]] and their families, most cases have [[benign]] and non-[[cardiac]] etiologies. A thorough history and [[physical examination]] can reveal [[diagnoses]] in the majority of [[patients]], necessitating laboratory testing and [[imaging]] studies only in a small subset of [[patients]].<br />
<br />
==Historical Perspective==<br />
There is limited evidence on the historical perspective of chest pain in children. <br />
==Classification==<br />
There is no established system for the classification of chest pain in the pediatric population.<br />
<br />
==Pathophysiology==<br />
*The pathophysiology of chest pain in children depends on the underlying cause.<br />
**For a complete guide on the pathophysiology of [[asthma]], [[Asthma pathophysiology|click here]].<br /><br />
**For a complete guide on the pathophysiology of [[gastroesophageal reflux disease]] ([[GERD]]), [[Gastroesophageal reflux disease pathophysiology|click here]].<br /><br />
**For a complete guide on the pathophysiology of [[pneumothorax]], [[Pneumothorax pathophysiology|click here]].<br /><br />
**For a complete guide on the pathophysiology of [[pulmonary embolism]], [[Pulmonary embolism pathophysiology|click here]].<br /><br />
<br />
==Causes==<br />
The most common causes of [[chest pain]] in children include musculoskeletal, respiratory, psychogenic, and idiopathic.<br />
A comprehensive list of causes of chest pain in children is presented in the table below: <br />
<ref name="pmid23769502">{{cite journal |vauthors=Friedman KG, Alexander ME |title=Chest pain and syncope in children: a practical approach to the diagnosis of cardiac disease |journal=J Pediatr |volume=163 |issue=3 |pages=896–901.e1–3 |date=September 2013 |pmid=23769502 |pmc=3982288 |doi=10.1016/j.jpeds.2013.05.001 |url=}}</ref><ref name="pmid1697801">{{cite journal |vauthors=Aeschlimann A, Kahn MF |title=Tietze's syndrome: a critical review |journal=Clin Exp Rheumatol |volume=8 |issue=4 |pages=407–12 |date=1990 |pmid=1697801 |doi= |url=}}</ref><ref name="Heinz1977">{{cite journal|last1=Heinz|first1=George J.|title=Slipping Rib Syndrome|journal=JAMA|volume=237|issue=8|year=1977|pages=794|issn=0098-7484|doi=10.1001/jama.1977.03270350054023}}</ref><ref name="pmid4000782">{{cite journal |vauthors=Selbst SM |title=Chest pain in children |journal=Pediatrics |volume=75 |issue=6 |pages=1068–70 |date=June 1985 |pmid=4000782 |doi= |url=}}</ref><ref name="Howell1992">{{cite journal|last1=Howell|first1=John M.|title=Xiphodynia: A report of three cases|journal=The Journal of Emergency Medicine|volume=10|issue=4|year=1992|pages=435–438|issn=07364679|doi=10.1016/0736-4679(92)90272-U}}</ref><ref name="Pickering1981">{{cite journal|last1=Pickering|first1=D|title=Precordial catch syndrome.|journal=Archives of Disease in Childhood|volume=56|issue=5|year=1981|pages=401–403|issn=0003-9888|doi=10.1136/adc.56.5.401}}</ref><ref name="pmid1518687">{{cite journal |vauthors=Wiens L, Sabath R, Ewing L, Gowdamarajan R, Portnoy J, Scagliotti D |title=Chest pain in otherwise healthy children and adolescents is frequently caused by exercise-induced asthma |journal=Pediatrics |volume=90 |issue=3 |pages=350–3 |date=September 1992 |pmid=1518687 |doi= |url=}}</ref><ref name="EvangelistaParsons2000">{{cite journal|last1=Evangelista|first1=Juli-anne K.|last2=Parsons|first2=Marytheresa|last3=Renneburg|first3=Anne K.|title=Chest pain in children: diagnosis through history and physical examination|journal=Journal of Pediatric Health Care|volume=14|issue=1|year=2000|pages=3–8|issn=08915245|doi=10.1016/S0891-5245(00)70037-X}}</ref><ref name="BarthRoberts1986">{{cite journal|last1=Barth|first1=Charles W.|last2=Roberts|first2=William C.|title=Left main coronary artery originating from the right sinus of valsalva and coursing between the aorta and pulmonary trunk|journal=Journal of the American College of Cardiology|volume=7|issue=2|year=1986|pages=366–373|issn=07351097|doi=10.1016/S0735-1097(86)80507-1}}</ref><ref name="LipsitzMasia2005">{{cite journal|last1=Lipsitz|first1=Joshua D.|last2=Masia|first2=Carrie|last3=Apfel|first3=Howard|last4=Marans|first4=Zvi|last5=Gur|first5=Merav|last6=Dent|first6=Heather|last7=Fyer|first7=Abby J.|title=Noncardiac chest pain and psychopathology in children and adolescents|journal=Journal of Psychosomatic Research|volume=59|issue=3|year=2005|pages=185–188|issn=00223999|doi=10.1016/j.jpsychores.2005.05.004}}</ref><ref name="LeeGilleland2013">{{cite journal|last1=Lee|first1=Jennifer L.|last2=Gilleland|first2=Jordan|last3=Campbell|first3=Robert M.|last4=Simpson|first4=Patricia|last5=Johnson|first5=Gregory L.|last6=Dooley|first6=Kenneth J.|last7=Blount|first7=Ronald L.|title=Health care utilization and psychosocial factors in pediatric noncardiac chest pain.|journal=Health Psychology|volume=32|issue=3|year=2013|pages=320–327|issn=1930-7810|doi=10.1037/a0027806}}</ref><ref name="pmid2403723">{{cite journal |vauthors=Selbst SM |title=Chest pain in children |journal=Am Fam Physician |volume=41 |issue=1 |pages=179–86 |date=January 1990 |pmid=2403723 |doi= |url=}}</ref><ref>{{cite journal|doi=10.7759/2Fcureus.3690}}</ref><ref>{{cite journal|doi=10.2147/2FOAEM.S29942}}</ref><ref>{{cite journal|doi=10.1007/2Fs00383-011-2874-8}}</ref><ref name="pmid26692880">{{cite journal |vauthors=Chun JH, Kim TH, Han MY, Kim NY, Yoon KL |title=Analysis of clinical characteristics and causes of chest pain in children and adolescents |journal=Korean J Pediatr |volume=58 |issue=11 |pages=440–5 |date=November 2015 |pmid=26692880 |pmc=4675925 |doi=10.3345/kjp.2015.58.11.440 |url=}}</ref><ref>{{cite journal|doi=10.1161/2FCIRCULATIONAHA.113.006702}}</ref><ref name="Swap2005">{{cite journal|last1=Swap|first1=Clifford J.|title=Value and Limitations of Chest Pain History in the Evaluation of Patients With Suspected Acute Coronary Syndromes|journal=JAMA|volume=294|issue=20|year=2005|pages=2623|issn=0098-7484|doi=10.1001/jama.294.20.2623}}</ref><br />
<br />
{| class="wikitable"<br />
|+<br />
|-<br />
| align="center" style="background: #4479BA; color: #FFFFFF " |'''Causes of pediatric [[chest pain]]'''<br />
|-<br />
|'''[[Musculoskeletal]]'''<br />
|-<br />
|<br />
*[[Costochondritis]] <br />
|-<br />
|<br />
*[[Trauma]]<br />
|-<br />
|<br />
*Muscle overuse/strain<br />
|-<br />
|<br />
*[[Tietze's syndrome]]<br />
|-<br />
|<br />
*[[Precordial catch syndrome]]<br />
|-<br />
|'''[[Respiratory]]'''<br />
|-<br />
|<br />
*Severe and/or chronic [[Cough]]<br />
|-<br />
|<br />
*[[Asthma]] (including [[exercise-induced asthma]])/[[bronchospasm]]<br />
|-<br />
|<br />
*Foreign body<br />
|-<br />
|<br />
*[[Pleuritic]]:<br />
**[[Pneumonia]]<br />
**[[Pneumothorax]]<br />
**[[Pulmonary emboli]]<br />
|-<br />
|'''[[Psychogenic]]'''<br />
|-<br />
|<br />
*[[Anxiety]]<br />
|-<br />
|<br />
*[[Hyperventilation]]<br />
|-<br />
|'''[[Gastrointestinal]]'''<br />
|-<br />
|<br />
*[[Gastroesophageal reflux disease]] ([[GERD]])<br />
|-<br />
|<br />
*[[Esophagitis]]<br />
|-<br />
|<br />
*[[Peptic ulcer disease]]<br />
|-<br />
|'''[[Cardiac]]'''<br />
|-<br />
|<br />
*[[Myocarditis]]<br />
|-<br />
|<br />
*[[Pericarditis]]<br />
|-<br />
|<br />
*[[Arrhythmia]]<br />
|-<br />
| <br />
*[[Myocardial ischemia]]:<br />
**Anomalous coronary arteries<br />
**[[Aortic stenosis]]<br />
**[[Hypertrophic obstructive cardiomyopathy]]<br />
**[[Coronary artery disease]]<br />
**[[vasculitis]]:<br />
***[[Kawasaki disease]]<br />
|-<br />
|<br />
*[[Mitral valve prolapse]]<br />
|-<br />
|'''[[Miscellaneous]]'''<br />
|-<br />
|<br />
*[[Herpes Zoster]]<br />
|-<br />
|<br />
*[[Sickle cell vaso-occlusive crisis]] ([[Acute chest syndrome]])<br />
|-<br />
|<br />
*Tumors (chest wall/mediastinal)<br />
|-<br />
|'''[[Idiopathic]]'''<br />
|-<br />
|}<br />
{|<br />
|- <br />
|}<br />
<br />
''For a complete list of causes of [[chest pain in children]] click [[Chest pain resident survival guide (pediatrics)|here]].''<br />
<br />
==Differentiating pediatric chest pain from other Diseases==<br />
*When evaluating pediatric chest pain, serious or life-threatening conditions must be differentiated from benign causes.<br />
*Serious or life-threatening causes of [[chest pain]] in children include: <ref name="pmid20653703">{{cite journal| author=Kane DA, Fulton DR, Saleeb S, Zhou J, Lock JE, Geggel RL| title=Needles in hay: chest pain as the presenting symptom in children with serious underlying cardiac pathology. | journal=Congenit Heart Dis | year= 2010 | volume= 5 | issue= 4 | pages= 366-73 | pmid=20653703 | doi=10.1111/j.1747-0803.2010.00436.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20653703 }} </ref> <ref name="pmid23769502">{{cite journal |vauthors=Friedman KG, Alexander ME |title=Chest pain and syncope in children: a practical approach to the diagnosis of cardiac disease |journal=J Pediatr |volume=163 |issue=3 |pages=896–901.e1–3 |date=September 2013 |pmid=23769502 |pmc=3982288 |doi=10.1016/j.jpeds.2013.05.001 |url=}}</ref><ref name="pmid1697801">{{cite journal |vauthors=Aeschlimann A, Kahn MF |title=Tietze's syndrome: a critical review |journal=Clin Exp Rheumatol |volume=8 |issue=4 |pages=407–12 |date=1990 |pmid=1697801 |doi= |url=}}</ref><ref name="Heinz1977">{{cite journal|last1=Heinz|first1=George J.|title=Slipping Rib Syndrome|journal=JAMA|volume=237|issue=8|year=1977|pages=794|issn=0098-7484|doi=10.1001/jama.1977.03270350054023}}</ref><ref name="pmid4000782">{{cite journal |vauthors=Selbst SM |title=Chest pain in children |journal=Pediatrics |volume=75 |issue=6 |pages=1068–70 |date=June 1985 |pmid=4000782 |doi= |url=}}</ref><ref name="Howell1992">{{cite journal|last1=Howell|first1=John M.|title=Xiphodynia: A report of three cases|journal=The Journal of Emergency Medicine|volume=10|issue=4|year=1992|pages=435–438|issn=07364679|doi=10.1016/0736-4679(92)90272-U}}</ref><ref name="Pickering1981">{{cite journal|last1=Pickering|first1=D|title=Precordial catch syndrome.|journal=Archives of Disease in Childhood|volume=56|issue=5|year=1981|pages=401–403|issn=0003-9888|doi=10.1136/adc.56.5.401}}</ref><ref name="pmid1518687">{{cite journal |vauthors=Wiens L, Sabath R, Ewing L, Gowdamarajan R, Portnoy J, Scagliotti D |title=Chest pain in otherwise healthy children and adolescents is frequently caused by exercise-induced asthma |journal=Pediatrics |volume=90 |issue=3 |pages=350–3 |date=September 1992 |pmid=1518687 |doi= |url=}}</ref><ref name="EvangelistaParsons2000">{{cite journal|last1=Evangelista|first1=Juli-anne K.|last2=Parsons|first2=Marytheresa|last3=Renneburg|first3=Anne K.|title=Chest pain in children: diagnosis through history and physical examination|journal=Journal of Pediatric Health Care|volume=14|issue=1|year=2000|pages=3–8|issn=08915245|doi=10.1016/S0891-5245(00)70037-X}}</ref><ref name="BarthRoberts1986">{{cite journal|last1=Barth|first1=Charles W.|last2=Roberts|first2=William C.|title=Left main coronary artery originating from the right sinus of valsalva and coursing between the aorta and pulmonary trunk|journal=Journal of the American College of Cardiology|volume=7|issue=2|year=1986|pages=366–373|issn=07351097|doi=10.1016/S0735-1097(86)80507-1}}</ref><ref name="LipsitzMasia2005">{{cite journal|last1=Lipsitz|first1=Joshua D.|last2=Masia|first2=Carrie|last3=Apfel|first3=Howard|last4=Marans|first4=Zvi|last5=Gur|first5=Merav|last6=Dent|first6=Heather|last7=Fyer|first7=Abby J.|title=Noncardiac chest pain and psychopathology in children and adolescents|journal=Journal of Psychosomatic Research|volume=59|issue=3|year=2005|pages=185–188|issn=00223999|doi=10.1016/j.jpsychores.2005.05.004}}</ref><ref name="LeeGilleland2013">{{cite journal|last1=Lee|first1=Jennifer L.|last2=Gilleland|first2=Jordan|last3=Campbell|first3=Robert M.|last4=Simpson|first4=Patricia|last5=Johnson|first5=Gregory L.|last6=Dooley|first6=Kenneth J.|last7=Blount|first7=Ronald L.|title=Health care utilization and psychosocial factors in pediatric noncardiac chest pain.|journal=Health Psychology|volume=32|issue=3|year=2013|pages=320–327|issn=1930-7810|doi=10.1037/a0027806}}</ref><ref name="pmid2403723">{{cite journal |vauthors=Selbst SM |title=Chest pain in children |journal=Am Fam Physician |volume=41 |issue=1 |pages=179–86 |date=January 1990 |pmid=2403723 |doi= |url=}}</ref><ref>{{cite journal|doi=10.7759/2Fcureus.3690}}</ref><ref>{{cite journal|doi=10.2147/2FOAEM.S29942}}</ref><ref>{{cite journal|doi=10.1007/2Fs00383-011-2874-8}}</ref><ref name="pmid26692880">{{cite journal |vauthors=Chun JH, Kim TH, Han MY, Kim NY, Yoon KL |title=Analysis of clinical characteristics and causes of chest pain in children and adolescents |journal=Korean J Pediatr |volume=58 |issue=11 |pages=440–5 |date=November 2015 |pmid=26692880 |pmc=4675925 |doi=10.3345/kjp.2015.58.11.440 |url=}}</ref><ref>{{cite journal|doi=10.1161/2FCIRCULATIONAHA.113.006702}}</ref><ref name="Swap2005">{{cite journal|last1=Swap|first1=Clifford J.|title=Value and Limitations of Chest Pain History in the Evaluation of Patients With Suspected Acute Coronary Syndromes|journal=JAMA|volume=294|issue=20|year=2005|pages=2623|issn=0098-7484|doi=10.1001/jama.294.20.2623}}</ref><br />
**[[Aortic dissection]] <br />
**Foreign body aspiration or ingestion <br />
**[[Myocardial ischemia]] <br />
**[[Myocarditis]]<br />
**[[Pericarditis]] <br />
**[[Pericardial effusion]] <br />
**[[Pneumothorax]]/[[tension pneumothorax]]<br />
**[[Pulmonary embolus]] <br />
**[[Status asthmatics]]<br />
<br />
==Epidemiology and Demographics==<br />
*Chest pain accounts for 0.3%-0.6% of emergency department visits, 15% of outpatient visits, and 5.2% of cardiology consultations in the pediatric population. <ref name="pmid26678235">{{cite journal| author=Yeh TK, Yeh J| title=Chest Pain in Pediatrics. | journal=Pediatr Ann | year= 2015 | volume= 44 | issue= 12 | pages= e274-8 | pmid=26678235 | doi=10.3928/00904481-20151110-01 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26678235 }} </ref> <ref name="pmid21111115">{{cite journal| author=Selbst SM| title=Approach to the child with chest pain. | journal=Pediatr Clin North Am | year= 2010 | volume= 57 | issue= 6 | pages= 1221-34 | pmid=21111115 | doi=10.1016/j.pcl.2010.09.003 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21111115 }} </ref><br />
*In children and adolescents aged 10-21 years, chest pain has been reported to cause ≥ 650,000 annual pediatric cardiologist visits. <ref name="pmid26678235">{{cite journal| author=Yeh TK, Yeh J| title=Chest Pain in Pediatrics. | journal=Pediatr Ann | year= 2015 | volume= 44 | issue= 12 | pages= e274-8 | pmid=26678235 | doi=10.3928/00904481-20151110-01 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26678235 }} </ref><br />
<br />
==Risk factors==<br />
Common risk factors in the development of [[chest pain]] in children include: <br />
<ref name="pmid23769502">{{cite journal |vauthors=Friedman KG, Alexander ME |title=Chest pain and syncope in children: a practical approach to the diagnosis of cardiac disease |journal=J Pediatr |volume=163 |issue=3 |pages=896–901.e1–3 |date=September 2013 |pmid=23769502 |pmc=3982288 |doi=10.1016/j.jpeds.2013.05.001 |url=}}</ref><ref name="pmid1697801">{{cite journal |vauthors=Aeschlimann A, Kahn MF |title=Tietze's syndrome: a critical review |journal=Clin Exp Rheumatol |volume=8 |issue=4 |pages=407–12 |date=1990 |pmid=1697801 |doi= |url=}}</ref><ref name="Heinz1977">{{cite journal|last1=Heinz|first1=George J.|title=Slipping Rib Syndrome|journal=JAMA|volume=237|issue=8|year=1977|pages=794|issn=0098-7484|doi=10.1001/jama.1977.03270350054023}}</ref><ref name="pmid4000782">{{cite journal |vauthors=Selbst SM |title=Chest pain in children |journal=Pediatrics |volume=75 |issue=6 |pages=1068–70 |date=June 1985 |pmid=4000782 |doi= |url=}}</ref><ref name="Howell1992">{{cite journal|last1=Howell|first1=John M.|title=Xiphodynia: A report of three cases|journal=The Journal of Emergency Medicine|volume=10|issue=4|year=1992|pages=435–438|issn=07364679|doi=10.1016/0736-4679(92)90272-U}}</ref><ref name="Pickering1981">{{cite journal|last1=Pickering|first1=D|title=Precordial catch syndrome.|journal=Archives of Disease in Childhood|volume=56|issue=5|year=1981|pages=401–403|issn=0003-9888|doi=10.1136/adc.56.5.401}}</ref><ref name="pmid1518687">{{cite journal |vauthors=Wiens L, Sabath R, Ewing L, Gowdamarajan R, Portnoy J, Scagliotti D |title=Chest pain in otherwise healthy children and adolescents is frequently caused by exercise-induced asthma |journal=Pediatrics |volume=90 |issue=3 |pages=350–3 |date=September 1992 |pmid=1518687 |doi= |url=}}</ref><ref name="EvangelistaParsons2000">{{cite journal|last1=Evangelista|first1=Juli-anne K.|last2=Parsons|first2=Marytheresa|last3=Renneburg|first3=Anne K.|title=Chest pain in children: diagnosis through history and physical examination|journal=Journal of Pediatric Health Care|volume=14|issue=1|year=2000|pages=3–8|issn=08915245|doi=10.1016/S0891-5245(00)70037-X}}</ref><ref name="BarthRoberts1986">{{cite journal|last1=Barth|first1=Charles W.|last2=Roberts|first2=William C.|title=Left main coronary artery originating from the right sinus of valsalva and coursing between the aorta and pulmonary trunk|journal=Journal of the American College of Cardiology|volume=7|issue=2|year=1986|pages=366–373|issn=07351097|doi=10.1016/S0735-1097(86)80507-1}}</ref><ref name="LipsitzMasia2005">{{cite journal|last1=Lipsitz|first1=Joshua D.|last2=Masia|first2=Carrie|last3=Apfel|first3=Howard|last4=Marans|first4=Zvi|last5=Gur|first5=Merav|last6=Dent|first6=Heather|last7=Fyer|first7=Abby J.|title=Noncardiac chest pain and psychopathology in children and adolescents|journal=Journal of Psychosomatic Research|volume=59|issue=3|year=2005|pages=185–188|issn=00223999|doi=10.1016/j.jpsychores.2005.05.004}}</ref><ref name="LeeGilleland2013">{{cite journal|last1=Lee|first1=Jennifer L.|last2=Gilleland|first2=Jordan|last3=Campbell|first3=Robert M.|last4=Simpson|first4=Patricia|last5=Johnson|first5=Gregory L.|last6=Dooley|first6=Kenneth J.|last7=Blount|first7=Ronald L.|title=Health care utilization and psychosocial factors in pediatric noncardiac chest pain.|journal=Health Psychology|volume=32|issue=3|year=2013|pages=320–327|issn=1930-7810|doi=10.1037/a0027806}}</ref><ref name="pmid2403723">{{cite journal |vauthors=Selbst SM |title=Chest pain in children |journal=Am Fam Physician |volume=41 |issue=1 |pages=179–86 |date=January 1990 |pmid=2403723 |doi= |url=}}</ref><ref>{{cite journal|doi=10.7759/2Fcureus.3690}}</ref><ref>{{cite journal|doi=10.2147/2FOAEM.S29942}}</ref><ref>{{cite journal|doi=10.1007/2Fs00383-011-2874-8}}</ref><ref name="pmid26692880">{{cite journal |vauthors=Chun JH, Kim TH, Han MY, Kim NY, Yoon KL |title=Analysis of clinical characteristics and causes of chest pain in children and adolescents |journal=Korean J Pediatr |volume=58 |issue=11 |pages=440–5 |date=November 2015 |pmid=26692880 |pmc=4675925 |doi=10.3345/kjp.2015.58.11.440 |url=}}</ref><ref>{{cite journal|doi=10.1161/2FCIRCULATIONAHA.113.006702}}</ref><ref name="Swap2005">{{cite journal|last1=Swap|first1=Clifford J.|title=Value and Limitations of Chest Pain History in the Evaluation of Patients With Suspected Acute Coronary Syndromes|journal=JAMA|volume=294|issue=20|year=2005|pages=2623|issn=0098-7484|doi=10.1001/jama.294.20.2623}}</ref><br />
*Chest trauma<br />
*Muscle overuse/strain<br />
*Prior cardiac disease (including [[congenital heart disease]]) or surgery <br />
*[[Hypercoagulable states]]<br />
*[[Sickle cell disease]]<br />
*Chronic respiratory diseases<br />
*[[Kawasaki disease]]<br />
*[[Familial hyperlipidemia syndromes]]<br />
*[[Substance abuse]] ([[amphetamine]], [[cocaine]], or other stimulants) <br />
*[[Connective tissue diseases]]<br />
<br />
==Screening==<br />
There is insufficient evidence to recommend routine screening for chest pain in children.<br />
<br />
==Natural History, Complications and Prognosis==<br />
*Most cases of chest pain in children are benign, and cardiac causes have been identified in less than 1% of children with chest pain. <ref name="pmid26678235">{{cite journal| author=Yeh TK, Yeh J| title=Chest Pain in Pediatrics. | journal=Pediatr Ann | year= 2015 | volume= 44 | issue= 12 | pages= e274-8 | pmid=26678235 | doi=10.3928/00904481-20151110-01 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26678235 }} </ref> <ref name="pmid24301714">{{cite journal| author=Collins SA, Griksaitis MJ, Legg JP| title=15-minute consultation: a structured approach to the assessment of chest pain in a child. | journal=Arch Dis Child Educ Pract Ed | year= 2014 | volume= 99 | issue= 4 | pages= 122-6 | pmid=24301714 | doi=10.1136/archdischild-2013-303919 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24301714 }} </ref><br />
*Despite having benign etiologies, chest pain in children may contribute to school absences, activity restrictions, and significant anxiety in children and their families. <br />
*The complications of chest pain in children depend on the underlying etiology.<br />
<br />
==Diagnosis==<br />
===Diagnostic Study of Choice===<br />
*A thorough [[history]] and [[physical examination]] will reveal the etiology of [[chest pain]] in the majority of children. <ref name="pmid24301714">{{cite journal| author=Collins SA, Griksaitis MJ, Legg JP| title=15-minute consultation: a structured approach to the assessment of chest pain in a child. | journal=Arch Dis Child Educ Pract Ed | year= 2014 | volume= 99 | issue= 4 | pages= 122-6 | pmid=24301714 | doi=10.1136/archdischild-2013-303919 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24301714 }} </ref><br />
<br />
===History and symptoms===<br />
*A detailed [[history]] is of crucial importance when assessing a child with [[chest pain]] as it can help to make a definitive diagnosis in most pediatric patients with [[chest pain]]. <ref name="pmid23769502">{{cite journal |vauthors=Friedman KG, Alexander ME |title=Chest pain and syncope in children: a practical approach to the diagnosis of cardiac disease |journal=J Pediatr |volume=163 |issue=3 |pages=896–901.e1–3 |date=September 2013 |pmid=23769502 |pmc=3982288 |doi=10.1016/j.jpeds.2013.05.001 |url=}}</ref><ref>{{cite journal|doi=10.3345/2Fkjp.2015.58.11.440}}</ref><ref name="IvesDaubeney2010">{{cite journal|last1=Ives|first1=A.|last2=Daubeney|first2=P. E. F.|last3=Balfour-Lynn|first3=I. M.|title=Recurrent chest pain in the well child|journal=Archives of Disease in Childhood|volume=95|issue=8|year=2010|pages=649–654|issn=0003-9888|doi=10.1136/adc.2008.155309}}</ref><ref name="pmid24301714">{{cite journal| author=Collins SA, Griksaitis MJ, Legg JP| title=15-minute consultation: a structured approach to the assessment of chest pain in a child. | journal=Arch Dis Child Educ Pract Ed | year= 2014 | volume= 99 | issue= 4 | pages= 122-6 | pmid=24301714 | doi=10.1136/archdischild-2013-303919 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24301714 }} </ref><br />
*Particular attention should be paid to the nature of the pain, its characteristics, and associated [[symptom]]s.<br />
*Younger children may interpret a wide range of [[symptom]]s and even unpleasant sensations in their chest wall as [[chest pain]]. A thorough [[history]] may help differentiate true chest pain from these unusual sensations. <br />
*The important characteristics of [[chest pain]] that can help to differentiate the underlying etiology are:<br />
===== [[Musculoskeletal]] =====<br />
*Usually well-localized<br />
*Associated with chest wall [[tenderness]], i.e., reproducible with palpation or gentle pressure<br />
*Worse with movement, [[coughing]], and [[inspiration]]<br />
===== [[Respiratory]] =====<br />
*[[Chest pain]] from [[asthma]] is often interpreted as ‘tightness’. Associated symptoms include [[dyspnea]] ([[shortness of breath]]), [[wheezing]], and dry [[cough]]. In patients with [[exertion-induced asthma]], [[symptom]]s are precipitated with physical activity. <br />
*[[Pleuritic chest pain]] is usually sharp and localized, and positional, i.e., aggravated by [[inspiration]] and [[coughing]]. It may be seen in patients with [[pneumothorax]] and [[pulmonary emboli]]. <br />
===== [[Psychogenic]] =====<br />
*History of [[anxiety disorders]] (e.g. [[panic disorder]]) and/or recent stressful life events.<br />
*[[Hyperventilation]] is a common associated symptom. <br />
===== [[Gastrointestinal]] =====<br />
*[[Retrosternal]] or [[epigastric]] pain<br />
*Typically burning or sharp in nature.<br />
*Eating may exacerbate or improve the pain<br />
*Associates symptoms may include: [[heartburn]], [[dysphagia]], [[nausea]]/[[vomiting]], nocturnal [[cough]]<br />
===== [[Cardiac]] =====<br />
*Usually [[retrosternal]], may radiate to the left arm/jaw region.<br />
*Cardiac [[chest pain]] is typically described as heaviness or crushing pain <br />
*[[Chest pain]] may be precipitated by exertion.<br />
*Associated symptoms include [[presyncope]], [[syncope]], and [[palpitations]].<br />
====== Other important clues in making the diagnosis of [[chest pain]] in children include: ======<br />
*History of underlying medical conditions that may be associated with [[chest pain]] including:<br />
**[[Congenital heart disease]]<br />
**[[Kawasaki disease]]<br />
**[[Sickle cell disease]]<br />
*History of recent [[trauma]], and new or intense physical activity causing muscle overuse/strain<br />
*History or the possibility of recent [[substance abuse]]<br />
*Family history of [[sudden cardiac death]], young-onset [[ischemic heart disease]], and inherited [[arrhythmias]] such as [[long QT syndrome]] or [[Brugada syndrome]]<br />
<br />
===Physical Examination===<br />
*A thorough [[physical examination]] is most often all that is needed to establish a definitive diagnosis in children with [[chest pain]]. <ref name="pmid24301714">{{cite journal| author=Collins SA, Griksaitis MJ, Legg JP| title=15-minute consultation: a structured approach to the assessment of chest pain in a child. | journal=Arch Dis Child Educ Pract Ed | year= 2014 | volume= 99 | issue= 4 | pages= 122-6 | pmid=24301714 | doi=10.1136/archdischild-2013-303919 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24301714 }} </ref> <br />
*Initial assessment should focus on identifying signs of [[cardiorespiratory distress]]. Patients with any of the following findings on [[physical examination]] are more likely to have a serious or life-threatening condition that warrants further diagnostic workup and/or therapeutic intervention:<br />
**[[Dyspnea]], [[tachypnea]], increased work of breathing<br />
**[[Hypoxia]]<br />
**Abnormal [[pulse]] or [[blood pressure]]<br />
**Evidence of [[poor perfusion]]/[[shock]]<br />
**Distended neck veins<br />
**Muffled heart sounds<br />
**Altered mental state<br />
**Therefore, a complete [[physical examination]] should include the following:<br />
**Assessment of [[vital signs]], including [[blood pressure]], [[heart rate]], [[respiratory rate]], and [[oxygen saturations]]<br />
**Assessment of general appearance, including the [[level of consciousness]], color (central or peripheral cyanosis), and evidence of [[anxiety]]/distress, [[dyspnea]], [[tachypnea]], increased work of breathing<br />
**Evaluation of [[peripheral pulses]]<br />
**Inspection of the chest for signs of recent trauma, [[bruising]], deformities or asymmetry, [[intercostal retraction]], and localized swelling (in particular at [[costochondral junctions]])<br />
**Palpation of the chest for chest wall tenderness (in particular at the location of pain), [[crepitus]], [[heaves]], or [[thrills]]<br />
***[[Hooking maneuver]]: hook fingers under lower [[costal margin]] and pull anteriorly- this maneuver will reproduce pain in patients with [[slipping rib syndrome]].<br />
**[[Auscultation]] of lung fields for [[breath sounds]], [[wheeze]], [[crackles]], and [[pleural rub]]. Assessment of [[tactile fremitus]] and transmitted voice sounds ([[egophony]], [[bronchophony]], [[whispered pectoriloquy]]) may be done if there is a clinical suspicion of pulmonary diseases<br />
**[[Auscultation]] of [[precordium]] for [[heart sounds]], [[murmurs]], and [[pericardial rub]]<br />
**Examination of the abdomen for signs of [[tenderness]] (in particular at [[epigastric]] region)<br />
<br />
===Laboratory Findings===<br />
*Laboratory testing is rarely needed in pediatric patients presenting with [[chest pain]]. <ref name="pmid23769502">{{cite journal| author=Friedman KG, Alexander ME| title=Chest pain and syncope in children: a practical approach to the diagnosis of cardiac disease. | journal=J Pediatr | year= 2013 | volume= 163 | issue= 3 | pages= 896-901.e1-3 | pmid=23769502 | doi=10.1016/j.jpeds.2013.05.001 | pmc=3982288 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23769502 }} </ref><br />
*Cardiac [[troponins]] and [[CK-MB]] may be indicated in patients suspected of having cardiac diseases such as [[myocardial infarction]] and [[myocarditis]].<br />
*Additional laboratory tests include [[serum electrolytes]], a [[complete blood count]], [[renal function tests]], and [[liver function tests]].<br />
<br />
===Electrocardiogram===<br />
An [[electrocardiogram]] ([[ECG]]) should be obtained if there is a clinical suspicion of [[cardiac disease]] based upon [[history]] or[[ physical examination]] findings. <ref name="pmid23769502">{{cite journal| author=Friedman KG, Alexander ME| title=Chest pain and syncope in children: a practical approach to the diagnosis of cardiac disease. | journal=J Pediatr | year= 2013 | volume= 163 | issue= 3 | pages= 896-901.e1-3 | pmid=23769502 | doi=10.1016/j.jpeds.2013.05.001 | pmc=3982288 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23769502 }} </ref><br />
<br />
===X-ray===<br />
*A [[chest X-ray]] should be obtained in children in whom a cardiac or pulmonary disorder or foreign body ingestion/or aspiration is suspected based on history and physical examination. <ref name="pmid23769502">{{cite journal| author=Friedman KG, Alexander ME| title=Chest pain and syncope in children: a practical approach to the diagnosis of cardiac disease. | journal=J Pediatr | year= 2013 | volume= 163 | issue= 3 | pages= 896-901.e1-3 | pmid=23769502 | doi=10.1016/j.jpeds.2013.05.001 | pmc=3982288 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23769502 }} </ref><br />
*Useful [[x-ray]] findings and relevant underlying conditions include:<br />
*Signs of [[cardiac enlargement]]: [[heart failure]], [[myocarditis]], [[pericarditis]], or [[pericardial effusion]]<br />
*Enlarged [[aortic root]]: [[aortic dissection]]<br />
*Prominent main [[pulmonary arteries]]: [[pulmonary hypertension]]<br />
*[[Lobar Consolidation]]: pneumonia <br />
*Areas of [[atelectasis]] and [[air trapping]]: [[foreign body aspiration]] <br />
*[[Hyperinflation]]: [[asthma]]<br />
*In addition, [[chest X-ray]] can detect:<br />
**Radio-opaque foreign bodies (eg, button battery, coin, or magnet)<br />
**[[Pneumothorax]]<br />
**[[Pneumomediastinum]]<br />
**[[Pleural effusions]]<br />
<br />
===Echocardiography or Ultrasound===<br />
*In patients with clinical suspicion of cardiac disease, an echocardiographic examination is indicated. [[Echocardiography]] may be helpful in: <ref name="pmid23769502">{{cite journal| author=Friedman KG, Alexander ME| title=Chest pain and syncope in children: a practical approach to the diagnosis of cardiac disease. | journal=J Pediatr | year= 2013 | volume= 163 | issue= 3 | pages= 896-901.e1-3 | pmid=23769502 | doi=10.1016/j.jpeds.2013.05.001 | pmc=3982288 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23769502 }} </ref><br />
**Evaluating cardiac structural abnormalities, and [[ventricular function]] <br />
**Evaluating valvular structure and function<br />
**Measurement of [[pulmonary artery pressure]] and establishing the diagnosis of [[pulmonary hypertension]] <br />
**Assessment of the presence and the size of [[pericardial effusion]] and evaluating the signs of [[tamponade]] (including variation in Doppler peak velocity across the valves during the cardiac cycle, atrial free wall collapse, or paradoxical motion of ventricular septum into the left ventricle during inspiration)<br />
**Diagnosing coronary artery abnormalities, including abnormal origin or course, fistula, aneurysm, and stenosis (caused by [[Kawasaki disease]])<br />
**Diagnosing [[aortic root dissection]]<br />
*In clinically unstable patients, ultrasound may help in the diagnosis of [[pneumothorax]] and [[pericardial effusion]]s and guide interventions (eg, [[chest tube thoracostomy]] or [[pericardiocentesis]]<br />
<br />
===CT scan===<br />
*A CT scan may be helpful in the diagnosis of several [[cardiac diseases]], [[pulmonary diseases]], and foreign body ingestion/aspiration.<br />
<br />
===MRI===<br />
*A MRI may be helpful in the diagnosis of acute [[aortic dissection]].<br />
<br />
===Other Diagnostic Studies===<br />
*A [[24-hour ECG Holter monitoring]] may be used to diagnose [[arrhythmia]]. <ref name="pmid23769502">{{cite journal| author=Friedman KG, Alexander ME| title=Chest pain and syncope in children: a practical approach to the diagnosis of cardiac disease. | journal=J Pediatr | year= 2013 | volume= 163 | issue= 3 | pages= 896-901.e1-3 | pmid=23769502 | doi=10.1016/j.jpeds.2013.05.001 | pmc=3982288 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23769502 }} </ref><br />
*Other imaging studies that may be used in the evaluation of [[chest pain]] include [[V/Q scintigraphy]], [[CT angiography]], and [[upper GI endoscopy]].<br />
<br />
''*For an algorithmic guide on the diagnosis of chest pain in children, [[Chest pain resident survival guide (pediatrics)|click here]].<br />''<br />
<br />
==Treatment==<br />
===Medical Therapy===<br />
''*For a complete guide on the algorithmic approach to the treatment of chest pain in children, [[Chest pain resident survival guide (pediatrics)|click here]].<br /><br />
*The management depends on the clinical status and stability of the patient, patients with severe [[respiratory distress]], hemodynamic instability require rapid care of the (ABC) airway, breathing, and circulation according to the [[Pediatric Advanced Life Support]] ([[PALS]]).<br />
*Medical management of stable patients depends on the underlying etiology of [[chest pain]]: <ref>{{cite journal|doi=10.1136/2Fadc.63.12.1457}}</ref><br />
*[[Costochondritis]] and muscle strain can be treated with [[rest]], [[warm compression]], [[analgesic]], anti-inflammatory agents ([[NSAID]]s)<br />
*[[Pneumonia]] can be treated with [[antibiotics]], [[supplemental oxygen]], and [[mechanical ventilation]] as needed<br />
*[[Gastroesophageal reflux disease]] can be treated with [[H2-blockers]] and [[proton pump inhibitors]] ([[PPIs]]<br />
**For a complete guide on the treatments of [[GERD]], [[Gastroesophageal reflux disease medical therapy|click here]]<br /><br />
*[[Acute chest syndrome]] in patients with [[sickle cell disease]] may be managed with pain control, [[antibiotics]], [[hydration]], [[blood transfusion]], or [[exchange transfusion]]<br />
**For a complete guide on the treatments of [[acute chest syndrome]], [[Acute chest syndrome medical therapy|click here]]<br /><br />
*[[Pulmonary embolism]] requires [[anticoagulant therapy]] or [[thrombolytic]] in hemodynamically unstable children<br />
**For a complete guide on the treatments of [[pulmonary embolism]], [[Pulmonary embolism treatment approach|click here]]<br /><br />
*[[Myocardial ischemia]] and [[myocardial infarction]] should receive anticoagulation, pain management, and catheterization<br />
*[[Heart failure]] should be managed with [[diuretics]], [[ACEIs]], and [[beta-blockers]] if no contraindications<br />
*[[Tachyarrhythmias]] should be managed according to [[Pediatric Advanced Life Support]] ([[PALS]])<br />
*[[Pericarditis]] with [[pericardial effusio]]n requires [[pericardiocentesis]] in patients with [[tamponade]]<br />
**For a complete guide on the treatments of [[pericarditis]], [[Pericarditis treatment|click here]]<br /><br />
<br />
===Surgery===<br />
Surgical intervention may be indicated in patients with: <ref name="pmid29963100">{{cite journal| author=Govindarajan KK| title=Esophageal perforation in children: etiology and management, with special reference to endoscopic esophageal perforation. | journal=Korean J Pediatr | year= 2018 | volume= 61 | issue= 6 | pages= 175-179 | pmid=29963100 | doi=10.3345/kjp.2018.61.6.175 | pmc=6021361 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29963100 }} </ref> <ref name="pmid17007168">{{cite journal| author=Fikar CR| title=Acute aortic dissection in children and adolescents: diagnostic and after-event follow-up obligation to the patient and family. | journal=Clin Cardiol | year= 2006 | volume= 29 | issue= 9 | pages= 383-6 | pmid=17007168 | doi=10.1002/clc.4960290903 | pmc=6654457 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17007168 }} </ref> <ref name="pmid30592692">{{cite journal| author=Williams K, Baumann L, Grabowski J, Lautz TB| title=Current Practice in the Management of Spontaneous Pneumothorax in Children. | journal=J Laparoendosc Adv Surg Tech A | year= 2019 | volume= 29 | issue= 4 | pages= 551-556 | pmid=30592692 | doi=10.1089/lap.2018.0629 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30592692 }} </ref> <ref name="pmid32167851">{{cite journal| author=Pogorelić Z, Gudelj R, Bjelanović D, Jukić M, Elezović Baloević S, Glumac S | display-authors=etal| title=Management of the Pediatric Spontaneous Pneumothorax: The Role of Video-Assisted Thoracoscopic Surgery. | journal=J Laparoendosc Adv Surg Tech A | year= 2020 | volume= 30 | issue= 5 | pages= 569-575 | pmid=32167851 | doi=10.1089/lap.2019.0742 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32167851 }} </ref><br />
*[[Aortic dissection]] <br />
*[[Pneumothorax]] <br />
*[[Pericardial effusion]]<br />
*Esophageal foreign body<br />
* Pulmonary foreign body<br />
<br />
===Primary Prevention===<br />
There are no established measures for the primary prevention of [[chest pain]] in children.<br />
<br />
===Secondary Prevention===<br />
*High-dose [[aspirin]] (80–100 mg/kg/day) and high-dose [[intravenous immunoglobulin]] ([[IVIG]], 2 g/kg) have been suggested to decrease the rate of [[coronary artery aneurysm]]s in children with [[Kawasaki disease]]. <ref name="pmid24730626">{{cite journal| author=Research Committee of the Japanese Society of Pediatric Cardiology. Cardiac Surgery Committee for Development of Guidelines for Medical Treatment of Acute Kawasaki Disease| title=Guidelines for medical treatment of acute Kawasaki disease: report of the Research Committee of the Japanese Society of Pediatric Cardiology and Cardiac Surgery (2012 revised version). | journal=Pediatr Int | year= 2014 | volume= 56 | issue= 2 | pages= 135-58 | pmid=24730626 | doi=10.1111/ped.12317 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24730626 }} </ref><br />
*[[Hydroxyurea]], [[chronic transfusion therapy]], and [[L-glutamine]] may decrease the frequency of acute painful [[vaso-occlusive episodes]], including [[acute chest syndrome]], in patients with [[sickle cell disease]]. <ref name="pmid23861242">{{cite journal| author=Alvarez O, Yovetich NA, Scott JP, Owen W, Miller ST, Schultz W | display-authors=etal| title=Pain and other non-neurological adverse events in children with sickle cell anemia and previous stroke who received hydroxyurea and phlebotomy or chronic transfusions and chelation: results from the SWiTCH clinical trial. | journal=Am J Hematol | year= 2013 | volume= 88 | issue= 11 | pages= 932-8 | pmid=23861242 | doi=10.1002/ajh.23547 | pmc=4631259 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23861242 }} </ref> <ref name="pmid30021096">{{cite journal| author=Niihara Y, Miller ST, Kanter J, Lanzkron S, Smith WR, Hsu LL | display-authors=etal| title=A Phase 3 Trial of l-Glutamine in Sickle Cell Disease. | journal=N Engl J Med | year= 2018 | volume= 379 | issue= 3 | pages= 226-235 | pmid=30021096 | doi=10.1056/NEJMoa1715971 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30021096 }} </ref><br />
<br />
==References==<br />
<br />
[[Category:Pediatrics]]<br />
[[Category:Primary care]]<br />
[[Category:Cardiology]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Spontaneous_coronary_artery_dissection_treatment_approach&diff=1697432Spontaneous coronary artery dissection treatment approach2021-04-16T17:59:51Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Spontaneous coronary artery dissection}}<br />
{{CMG}}; {{AE}} {{Sahar}} {{NRM}}<br><br />
{{SK}} SCAD<br />
==Overview==<br />
Acute management of [[myocardial infarction]] in [[SCAD]] is [[medical therapy]] in approximately 80% of the [[patients]]. [[Myocardial infarction]] in the context of [[SCAD]] is different from the [[myocardial infarction]] in the context of [[atherosclerosis]] and therefore makes it unfavorable for [[revascularization]] approaches. Long-term treatment for [[spontaneous coronary artery dissection]] pursues several main goals including [[antianginal]] therapy, prevention of [[recurrence]], assessment, and management of extra [[coronary]] [[vascular]] abnormalities, and improvement of [[quality of life]]. To improve the quality of life in [[patients]] with [[SCAD]], consider [[cardiac rehabilitation]] referral and manage [[patients]] [[comorbidities]]. <br />
<br />
<br />
==Algorithm for management of acute spontaneous coronary artery dissection: A Scientific Statement From the American Heart Association==<br />
<br />
<div style="font-size: 80%;" align="center"><br />
<br />
<BR><span style="font-size: 1.5em; font-weight: bold;">Algorithm for management of acute spontaneous coronary artery dissection.</span><ref name="HayesKim2018">{{cite journal|last1=Hayes|first1=Sharonne N.|last2=Kim|first2=Esther S.H.|last3=Saw|first3=Jacqueline|last4=Adlam|first4=David|last5=Arslanian-Engoren|first5=Cynthia|last6=Economy|first6=Katherine E.|last7=Ganesh|first7=Santhi K.|last8=Gulati|first8=Rajiv|last9=Lindsay|first9=Mark E.|last10=Mieres|first10=Jennifer H.|last11=Naderi|first11=Sahar|last12=Shah|first12=Svati|last13=Thaler|first13=David E.|last14=Tweet|first14=Marysia S.|last15=Wood|first15=Malissa J.|title=Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement From the American Heart Association|journal=Circulation|year=2018|pages=CIR.0000000000000564|issn=0009-7322|doi=10.1161/CIR.0000000000000564}}</ref><BR><BR><br />
<br />
{{Familytree/start}}<br />
{{Familytree | | | | | | | | | A01 | | | | | | | | |A01=<div style="text-align: left; padding: 5px;">'''Management of [[Acute]] [[Spontaneous Coronary Artery Dissection]]'''</div>}}<br />
{{Familytree | | | |,|-|-|-|-|-|+|-|-|-|-|-|.| | | |}}<br />
{{Familytree | | | B01 | | | | B02 | | | | B03 | | |B01='''Clinically stable <BR>without high-risk [[anatomy]]'''|B02='''Clinically stable with high-risk [[anatomy]]'''<BR>'''(i.e., [[left main]] or [[proximal]] 2-vessel [[dissection]])'''|B03='''Active/[[ongoing ischemia]] <BR>or [[hemodynamic instability]]'''}}<br />
{{Familytree | | | |!| | | | | |!| | | | | |!| | | |}}<br />
{{Familytree | | | C01 | | | | C02 | | | | C03 | | |C01=<div style="text-align: left; padding: 5px;">❑&nbsp;&nbsp;Conservative therapy<BR>❑&nbsp;&nbsp;Monitor as [[inpatient]] 3–5 days</div>|C02=<div style="text-align: left; padding: 5px;">❑&nbsp;&nbsp;Consider [[CABG]]<BR>❑&nbsp;&nbsp;Conservative Rx may be reasonable</div>|C03=<div style="text-align: left; padding: 5px;">❑&nbsp;&nbsp;Consider [[PCI]] if feasible, OR<BR>❑&nbsp;&nbsp;Urgent [[CABG]] (based on technical considerations and local expertise)</div>}}<br />
{{Family tree/end}}<br />
<span style="font-size: 100%;"><br />
'''Abbreviations''':<br />
[[CABG]], [[coronary artery bypass grafting]];<br />
[[PCI]], [[percutaneous coronary intervention]]; <br />
Rx, management.<br />
</span><br />
</div><br />
<br />
==Acute Management==<br />
*Acute management of [[myocardial infarction]] in [[SCAD]] is [[medical therapy]] in approximately 80% of the [[patients]]. [[Myocardial infarction]] in the context of [[SCAD]] is different from the [[myocardial infarction]] in the context of [[atherosclerosis]] and therefore makes it unfavorable for [[revascularization]] approaches.<ref name="KimLongo2020">{{cite journal|last1=Kim|first1=Esther S.H.|last2=Longo|first2=Dan L.|title=Spontaneous Coronary-Artery Dissection|journal=New England Journal of Medicine|volume=383|issue=24|year=2020|pages=2358–2370|issn=0028-4793|doi=10.1056/NEJMra2001524}}</ref><br />
*[[Percutaneous coronary intervention]] ([[PCI]]) can be considered in high risk [[patients]], such as:<br />
**[[Patients]] with following clinical presentations:<br />
***Persistent [[chest pain]] with evidence of worsening [[ischemia]]<br />
***[[Hemodynamic instability]]<br />
***[[Shock]]<br />
***[[Ventricular]] [[arrhythmias]]<br />
**[[Patients]] with following [[vascular]] involvement:<br />
***Multi-vessel proximal dissections <br />
***[[Left main artery]] dissection<br />
***Ostial [[left anterior descending]] [[artery]] [[dissection]]<br />
*Management with [[PCI]] may be associated with several adverse events, including: <br />
** [[Stent]] malposition<br />
** Iatrogenic injury to the [[vessels]]<br />
** [[Hematoma]]<br />
** [[ Coronary]] [[vessel]] occlusion<br />
** [[Coronary]] [[vessel]] anomaly<br />
<br />
==Long-Term Treatment Approach==<br />
* Long-term treatment for spontaneous [[coronary artery]] dissection pursues several main goals:<ref name="KimLongo2020">{{cite journal|last1=Kim|first1=Esther S.H.|last2=Longo|first2=Dan L.|title=Spontaneous Coronary-Artery Dissection|journal=New England Journal of Medicine|volume=383|issue=24|year=2020|pages=2358–2370|issn=0028-4793|doi=10.1056/NEJMra2001524}}</ref><br />
**[[Antianginal]] therapy<br />
**Prevention of recurrence<br />
**Assessment and management of extra [[coronary]] [[vascular]] abnormalities<br />
**Improvement of [[quality of life]]<br />
===Management of [[Chest Pain]]===<br />
* To manage of [[chest pain]] in [[patients]] with [[SCAD]] consider the followings:<ref name="KimLongo2020">{{cite journal|last1=Kim|first1=Esther S.H.|last2=Longo|first2=Dan L.|title=Spontaneous Coronary-Artery Dissection|journal=New England Journal of Medicine|volume=383|issue=24|year=2020|pages=2358–2370|issn=0028-4793|doi=10.1056/NEJMra2001524}}</ref><br />
** [[Antianginal]] [[medications]]<br />
** Consider further testing to rule out underlying [[ischemia]]<br />
** Consider other possible diagnoses<br />
===Prevention=== <br />
* To reduce the risk of [[SCAD]] recurrence, the following should be considered:<ref name="KimLongo2020">{{cite journal|last1=Kim|first1=Esther S.H.|last2=Longo|first2=Dan L.|title=Spontaneous Coronary-Artery Dissection|journal=New England Journal of Medicine|volume=383|issue=24|year=2020|pages=2358–2370|issn=0028-4793|doi=10.1056/NEJMra2001524}}</ref><br />
** [[Beta-blocker]] therapy<br />
** Management of [[hypertension]]<br />
** Maintaining [[physical activity]]<br />
<br />
===Assessment of [[Vascular]] Abnormalities===<br />
* To identify [[patients]] with [[SCAD]]-associated conditions, [[imaging]] with [[CT angiography]] or [[magnetic resonance angiography]] is recommended.<ref name="KimLongo2020">{{cite journal|last1=Kim|first1=Esther S.H.|last2=Longo|first2=Dan L.|title=Spontaneous Coronary-Artery Dissection|journal=New England Journal of Medicine|volume=383|issue=24|year=2020|pages=2358–2370|issn=0028-4793|doi=10.1056/NEJMra2001524}}</ref><br />
<br />
===Improvement in Quality of life===<br />
* To improve the quality of life in [[patients]] with [[SCAD]], consider:<ref name="KimLongo2020">{{cite journal|last1=Kim|first1=Esther S.H.|last2=Longo|first2=Dan L.|title=Spontaneous Coronary-Artery Dissection|journal=New England Journal of Medicine|volume=383|issue=24|year=2020|pages=2358–2370|issn=0028-4793|doi=10.1056/NEJMra2001524}}</ref><br />
**[[Cardiac rehabilitation]] referral <br />
** Manage [[patients]] [[comorbidities]]<br />
<br />
==References==<br />
{{Reflist|2}}<br />
[[Category:Cardiology]]<br />
[[Category:Angiographic Definitions]]<br />
[[Category:Disease]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Spontaneous_coronary_artery_dissection_screening&diff=1697431Spontaneous coronary artery dissection screening2021-04-16T17:57:06Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Spontaneous coronary artery dissection}}<br />
{{CMG}}; {{AE}}{{Sahar}}<br />
<br />
{{SK}} SCAD<br />
<br />
==Overview==<br />
[[SCAD]] usually is the result of an underlying [[vascular]] or [[connective tissue disorders]]. In order to provide the best care to [[patients]] with [[SCAD]], the scientific statement from the American Heart Association (AHA) recommends a detailed review of systems and personal and [[family history]] of [[SCAD]]-associated [[symptoms]] and [[conditions]]. In addition, the AHA statement recommends a complete [[vascular]] exam. Routine [[clinical]] or [[genetic]] [[screening]] of asymptomatic relatives of [[patients]] with [[SCAD]] is not recommended. However, [[genetic]] [[screening]] is recommended in first-degree family members of [[patients]] with [[SCAD]] in whom a monogenic [[vascular]] [[disease]] has been identified.<br />
<br />
==Screening==<br />
[[SCAD]] usually is the result of an underlying [[vascular]] or [[connective tissue disorders]]. In order to provide the best care to [[patients]] with [[SCAD]], the scientific statement from the American Heart Association (AHA) recommends a detailed review of [[systems]] and personal and [[family history]] of [[SCAD]]-associated [[symptoms]] and [[conditions]]. <ref name="HayesKim2018">{{cite journal|last1=Hayes|first1=Sharonne N.|last2=Kim|first2=Esther S.H.|last3=Saw|first3=Jacqueline|last4=Adlam|first4=David|last5=Arslanian-Engoren|first5=Cynthia|last6=Economy|first6=Katherine E.|last7=Ganesh|first7=Santhi K.|last8=Gulati|first8=Rajiv|last9=Lindsay|first9=Mark E.|last10=Mieres|first10=Jennifer H.|last11=Naderi|first11=Sahar|last12=Shah|first12=Svati|last13=Thaler|first13=David E.|last14=Tweet|first14=Marysia S.|last15=Wood|first15=Malissa J.|title=Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement From the American Heart Association|journal=Circulation|volume=137|issue=19|year=2018|issn=0009-7322|doi=10.1161/CIR.0000000000000564}}</ref><br><br />
In addition, the AHA statement recommends a complete [[vascular]] exam with [[palpation]] and [[auscultation]] of the following [[arteries]]:<br />
*[[Abdominal aorta]]<br />
*Cervical [[carotid arteries]]<br />
*Peripheral [[arteries]] of the upper and lower [[extremities]]<br />
===Screening Questions===<br />
The AHA statement recommends a list of questions to rule out [[SCAD]]-associated vasculopathy and [[connective tissue disorders]]: <ref name="HayesKim2018">{{cite journal|last1=Hayes|first1=Sharonne N.|last2=Kim|first2=Esther S.H.|last3=Saw|first3=Jacqueline|last4=Adlam|first4=David|last5=Arslanian-Engoren|first5=Cynthia|last6=Economy|first6=Katherine E.|last7=Ganesh|first7=Santhi K.|last8=Gulati|first8=Rajiv|last9=Lindsay|first9=Mark E.|last10=Mieres|first10=Jennifer H.|last11=Naderi|first11=Sahar|last12=Shah|first12=Svati|last13=Thaler|first13=David E.|last14=Tweet|first14=Marysia S.|last15=Wood|first15=Malissa J.|title=Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement From the American Heart Association|journal=Circulation|volume=137|issue=19|year=2018|issn=0009-7322|doi=10.1161/CIR.0000000000000564}}</ref><br />
{{familytree/start |summary=Sample 10}}{{familytree/start |summary=PE diagnosis Algorithm.}}<br />
{{Family tree/start}}<br />
{{familytree | | | | | B01 | | | | | B01=<div style="float: center; text-align: center; height: 2em; width: 17em; padding:1em;"> '''Screening Questions:'''<br><br />
----<br />
</div>}}<br />
{{familytree | | | | | |!| | | | | |}}<br />
{{familytree | | | | | C01 | | | | | C01=<div style="float: left; text-align: left;"> '''Personal history of the following conditions:'''<br><br />
----<br />
❑ Early-onset [[hypertension]] <br> ❑ [[Stroke]] or [[transient ischemic attack]]<br> ❑ Pulsatile [[tinnitus]]<br> ❑ [[Migraine]] headaches<br> ❑ [[Renal infarction]]<br> ❑ [[Subarachnoid hemorrhage]]<br> ❑ [[Aneurysm]] ([[aortic]], peripheral, [[brain]])<br> ❑ [[Dissection]] ([[aortic]], peripheral)<br> ❑ Rupture of hollow organs ([[intestinal]], [[bladder]], [[uterine]])<br> ❑ [[Pneumothorax]]<br> ❑ Tendon or muscle rupture<br> ❑ [[Joint dislocation]]<br> ❑ Talipes equinovarus ([[clubfoot]])<br> ❑ [[Umbilical hernai|Umbilical]] or [[inguinal hernia]]<br> ❑ [[Scoliosis]] or [[pectus deformity]]<br> ❑ [[Pregnancy]] complications ([[cervical incompetence]], [[hemorrhage]], [[uterine prolapse]], [[hypertension]])<br> ❑ Poor wound healing<br> ❑ [[Ectopia lentis]]<br> ❑ [[Myopia]]<br> ❑ Detached retina, early [[glaucoma]], or early [[cataracts]]<br> ❑ Tall stature<br> ❑ Abnormality of cardiac valve ([[bicuspid aortic valve]], [[mitral valve prolapse]])<br> ❑ [[Systemic inflammatory disease]]<br />
----<br />
<div style="float: left; text-align: left;">'''Family history of the following conditions:'''<br><br />
----<br />
❑ [[Dissection]] ([[coronary]], [[aortic]], peripheral)<br> ❑ Inherited arteriopathy or [[connective tissue disorder]] (eg, vascular [[Ehlers-Danlos syndrome]], [[Marfan syndrome]], Loeys-Dietz syndrome)<br> ❑ [[Fibromuscular dysplasia]]<br> ❑ [[Aneurysm]] ([[aortic]], peripheral, [[brain]])<br> ❑ Early [[stroke]], early [[myocardial infarction]], [[sudden cardiac death]] <br />
----<br />
<div style="float: left; text-align: left;">'''Review of systems (history of any of the following symptoms)'''<br><br />
----<br />
❑ [[Headaches]]<br> ❑ Pulsatile [[tinnitus]]<br> ❑ Postprandial abdominal pain<br> ❑ [[Flank pain]]<br> ❑ [[Claudication]]<br> ❑ [[Easy bruising]]<br> ❑ [[Joint]] hypermobility or laxity</div>}}<br />
{{Family tree/end}}<br />
{|<br />
! colspan="2" style="background:#DCDCDC;" align="center" + |The above table adopted from AHA scientific statement <ref name="HayesKim2018">{{cite journal|last1=Hayes|first1=Sharonne N.|last2=Kim|first2=Esther S.H.|last3=Saw|first3=Jacqueline|last4=Adlam|first4=David|last5=Arslanian-Engoren|first5=Cynthia|last6=Economy|first6=Katherine E.|last7=Ganesh|first7=Santhi K.|last8=Gulati|first8=Rajiv|last9=Lindsay|first9=Mark E.|last10=Mieres|first10=Jennifer H.|last11=Naderi|first11=Sahar|last12=Shah|first12=Svati|last13=Thaler|first13=David E.|last14=Tweet|first14=Marysia S.|last15=Wood|first15=Malissa J.|title=Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement From the American Heart Association|journal=Circulation|volume=137|issue=19|year=2018|issn=0009-7322|doi=10.1161/CIR.0000000000000564}}</ref><br />
|- <br />
|}<br />
===Genetic Screening of Family Members===<br />
* [[Genetic]] [[screening]] is recommended in [[first-degree]] family members of [[patients]] with [[SCAD]] in whom a monogenic [[vascular]] [[disease]] has been identified. <ref name="HayesKim2018">{{cite journal|last1=Hayes|first1=Sharonne N.|last2=Kim|first2=Esther S.H.|last3=Saw|first3=Jacqueline|last4=Adlam|first4=David|last5=Arslanian-Engoren|first5=Cynthia|last6=Economy|first6=Katherine E.|last7=Ganesh|first7=Santhi K.|last8=Gulati|first8=Rajiv|last9=Lindsay|first9=Mark E.|last10=Mieres|first10=Jennifer H.|last11=Naderi|first11=Sahar|last12=Shah|first12=Svati|last13=Thaler|first13=David E.|last14=Tweet|first14=Marysia S.|last15=Wood|first15=Malissa J.|title=Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement From the American Heart Association|journal=Circulation|volume=137|issue=19|year=2018|issn=0009-7322|doi=10.1161/CIR.0000000000000564}}</ref><br />
* Routine [[clinical]] or [[genetic]] [[screening]] of asymptomatic relatives of [[patients]] with [[SCAD]] is not recommended.<br />
<br />
==References==<br />
{{Reflist|2}}<br />
<br />
[[Category:Cardiology]]<br />
[[Category:Angiographic Definitions]]<br />
[[Category:Disease]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Urinary_incontinence_in_children&diff=1696697Urinary incontinence in children2021-04-09T14:24:09Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{| class="infobox bordered" style="width: 15em; text-align: left; font-size: 90%; background:AliceBlue"<br />
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[[Urinary incontinence in children#Overview|Overview]]<br />
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[[Urinary incontinence in children#Historical Perspective|Historical Perspective]]<br />
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[[Urinary incontinence in children#Classification|Classification]]<br />
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[[Urinary incontinence in children#Pathophysiology|Pathophysiology]]<br />
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[[Urinary incontinence in children#Causes|Causes]]<br />
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[[Urinary incontinence in children#Differential Diagnosis|Differential Diagnosis]]<br />
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[[Urinary incontinence in children#Epidemiology and Demographics|Epidemiology and Demographics]]<br />
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[[Urinary incontinence in children#Risk factors|Risk factors]]<br />
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[[Urinary incontinence in children#Natural History, Complications and Prognosis|Natural History, Complications and Prognosis]]<br />
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[[Urinary incontinence in children#Diagnosis|Diagnosis]]<br />
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[[Urinary incontinence in children#Treatment|Treatment]]<br />
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[[Urinary incontinence in children#Prevention|Prevention]]<br />
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<br />
{{CMG}} {{AE}}{{Ifeoma Anaya}}<br />
<br />
{{SK}} [[Urinary incontinence]] in [[Children|kids]]; [[Bedwetting]]; [[Enuresis]]; [[Nocturnal enuresis]]; [[Enuresis]] nocturna; Monosymptomatic [[enuresis]] nocturnal (MEN); Non-monosymtomatic [[enuresis]] nocturnal (non-MEN) <br />
<br />
==Overview==<br />
[[Urinary incontinence]] in [[children]] is a very familiar finding and complaint amongst [[patients]] and their caregivers. The earliest documentation of [[urinary incontinence]] dates back to 1550 BC in the [[Ebers papyrus]]. It is broadly classified into [[physiological]] and [[pathological]] with its various subdivisions, and [[nocturnal enuresis]] can be categorized into primary and [[secondary]]. The [[pathophysiology]] of [[urinary incontinence]] in [[children]], particularly [[enuresis]], can be described as increased [[urine]] production at night, reduced [[Urinary bladder|bladder]] capacity at night, and awakening [[disorder]]. The [[causes]] of [[urinary incontinence]] in [[children]] are identified based on the sub-classification of [[pathological]] [[Urinary incontinence|incontinence]]. Differentials include [[diabetes mellitus]], [[diabetes insipidus]], and [[Urinary tract infections|urinary tract infection]]. [[Children]] achieve the ability to [[control]] their [[Urinary bladder|bladder]] between the ages of 3 and 6 [[Year|years]]. This begins initially during the daytime and nighttime control is achieved much later. [[Nocturnal enuresis]] is seen more frequently in boys. There is no documented [[racial]] predisposition for [[enuresis]]. Some [[risk factors]] include, [[age]] less than 5 [[Year|years]], positive [[family history]], [[family]] size, and [[birth]] order. Certain [[complications]] are poor [[self-esteem]] and inability to socialize with [[Peer support|peers]]. [[Prognosis]] is generally good due to the high chances of spontaneous [[resolution]] at the [[rate]] of 15% per [[year]]. The focus is to eliminate any [[potential]] organic [[Causes|cause]] of [[Urinary incontinence|incontinence]] and to classify and identify the type of functional [[Urinary incontinence|incontinence]] using detailed [[History and Physical examination|history]] and [[Non-invasive (medical)|non-invasive]] [[Procedure|procedures]]. Identify any [[comorbidities]] which are mostly [[psychological]] occurring alongside [[Urinary incontinence|incontinence]]. Fundamental [[diagnosis]] includes taking a detailed [[History and Physical examination|history]] using a standardized [[questionnaire]]. The primary aim of a [[physical examination]] is to look for possible organic [[causes]] of [[Urinary incontinence|incontinence]] and [[comorbidities]]. [[Urinalysis]] is essential to rule out [[urinary tract infections]]. [[Ultrasonography]] is a useful tool when further [[diagnostics]] is required especially in situations of a likely organic [[Causes|cause]] or a [[lack of response]] to [[therapy]]. Uroflowmetry and [[Urodynamics|urodynamic]] studies are additional [[diagnostic]] studies that can be employed. Urotherapy encompasses all non-[[pharmacological]] and non-[[surgical]] [[treatment]] methods employed in the [[treatment]] of [[urinary incontinence]] in [[children]]. [[Desmopressin]] and [[oxybutynin]] are common [[drugs]] used for the [[pharmacological]] management of [[urinary incontinence]] in [[children]]. [[Surgery]] is not routinely employed as a form of [[treatment]] but it might be of importance in correcting some organic [[causes]] of [[urinary incontinence]] in [[children]]. There are no documented primary [[Preventive care|preventive]] measures available for [[urinary incontinence]] in [[children]].<br />
<br />
==Historical Perspective==<br />
<br />
*The earliest documentation of [[urinary incontinence]] dates back to 1550 BC in the [[Ebers papyrus]].<br />
*Pliny the Elder, in 77 AD, wrote about how [[Urinary incontinence|urinary incontinence]] in [[children]] is treated by giving boiled mice in their [[food]].<br />
*Paulus Bagellardus of Padua wrote about the [[distress]] experienced by parents due to [[bedwetting]] when [[infants]] after the age of 3 years 'continue to pass water in the bed' which can sometimes last beyond the period of [[puberty]].<br />
*In 1790, the term '[[enuresis]]' was founded, which means 'to [[urinate]] within' and '[[nocturnal]]' which means 'nighttime occurrence'.<ref name="pmid24578827">{{cite journal| author=Changizi Ashtiyani S, Shamsi M, Cyrus A, Tabatabayei SM| title=Rhazes, a genius physician in the diagnosis and treatment of nocturnal enuresis in medical history. | journal=Iran Red Crescent Med J | year= 2013 | volume= 15 | issue= 8 | pages= 633-8 | pmid=24578827 | doi=10.5812/ircmj.5017 | pmc=3918184 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24578827 }} </ref><br />
*In 1891, Jacobi placed a [[suppository]] into the [[rectum]] several times daily for the [[reinforcement]] of a supposedly weak [[Urinary bladder|bladder]] in order to [[Treatment|treat]] [[enuresis]]. The [[suppository]] was a mixture of old sheep [[fat]] and [[strychnine]].<ref name="Salmon2016">{{cite journal|last1=Salmon|first1=Michael A|title=An Historical Account of Nocturnal Enuresis and its Treatment|journal=Proceedings of the Royal Society of Medicine|volume=68|issue=7|year=2016|pages=443–445|issn=0035-9157|doi=10.1177/003591577506800726}}</ref><br />
*Rhazes, the Persian [[clinician]], identified some [[causes]] of [[enuresis]] in [[children]] such as:<br />
**[[Urinary bladder|Bladder]] [[outlet]] [[muscle]] [[relaxation]]<br />
**Deep [[sleep]]<br />
**Unrestricted [[fluid intake]] prior to [[bedtime]]<ref name="pmid24578827">{{cite journal| author=Changizi Ashtiyani S, Shamsi M, Cyrus A, Tabatabayei SM| title=Rhazes, a genius physician in the diagnosis and treatment of nocturnal enuresis in medical history. | journal=Iran Red Crescent Med J | year= 2013 | volume= 15 | issue= 8 | pages= 633-8 | pmid=24578827 | doi=10.5812/ircmj.5017 | pmc=3918184 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24578827 }} </ref><br />
*Some of his [[treatment]] [[protocols]] included:<br />
**Minimizing [[fluid intake]] before [[bedtime]]<br />
**Intake of [[Substance|substances]] producing [[fluid retention]] and [[body fluid]] losses<br />
**Use of both [[oral]] and [[Injection|injectable]] [[medications]] to the [[bladder]] through the [[urethra]]<ref name="pmid24578827">{{cite journal| author=Changizi Ashtiyani S, Shamsi M, Cyrus A, Tabatabayei SM| title=Rhazes, a genius physician in the diagnosis and treatment of nocturnal enuresis in medical history. | journal=Iran Red Crescent Med J | year= 2013 | volume= 15 | issue= 8 | pages= 633-8 | pmid=24578827 | doi=10.5812/ircmj.5017 | pmc=3918184 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24578827 }} </ref><br />
<br />
==Classification==<br />
<br />
*[[Urinary incontinence]], also known as '[[bedwetting]]' or '[[enuresis]]' can be classified as follows:<br />
<br />
{| class="wikitable"<br />
|+Classification of Urinary Incontinence in Children<br />
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Types of urinary incontinence<br />
! colspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Details<br />
|-<br />
| style="background:#DCDCDC;" + |'''[[Physiological]]<ref name="pmid21977217">{{cite journal| author=Schultz-Lampel D, Steuber C, Hoyer PF, Bachmann CJ, Marschall-Kehrel D, Bachmann H| title=Urinary incontinence in children. | journal=Dtsch Arztebl Int | year= 2011 | volume= 108 | issue= 37 | pages= 613-20 | pmid=21977217 | doi=10.3238/arztebl.2011.0613 | pmc=3187617 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21977217 }} </ref>'''<br />
| colspan="2" |<br />
*It is expected and seen as a norm in the early [[Year|years]].<br />
*Requires a minimum [[age]] of 5 [[Year|years]], at least one [[Event study|event]] in a month, and a minimum [[period]] of 3 months.<br />
*Persisting beyond the [[age]] of 5 years is termed [[pathological]].<br />
*However, there are the 'late developers' who continue to experience [[physiologic]] [[urinary incontinence]] beyond the [[age]] of 5 [[Year|years]].<br />
*[[Clinical]] evaluation of these [[Children|kids]] remains [[normal]].<br />
|-<br />
| rowspan="3" style="background:#DCDCDC;" + |'''[[Pathological]]<ref name="pmid21977217" /><ref name="pmid31844104">{{cite journal| author=Zhu W, Che Y, Wang Y, Jia Z, Wan T, Wen J | display-authors=etal| title=Study on neuropathological mechanisms of primary monosymptomatic nocturnal enuresis in children using cerebral resting-state functional magnetic resonance imaging. | journal=Sci Rep | year= 2019 | volume= 9 | issue= 1 | pages= 19141 | pmid=31844104 | doi=10.1038/s41598-019-55541-9 | pmc=6915704 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31844104 }} </ref><ref name="pmid27703953">{{cite journal| author=Arda E, Cakiroglu B, Thomas DT| title=Primary Nocturnal Enuresis: A Review. | journal=Nephrourol Mon | year= 2016 | volume= 8 | issue= 4 | pages= e35809 | pmid=27703953 | doi=10.5812/numonthly.35809 | pmc=5039962 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27703953 }} </ref>'''<br />
| colspan="2" |'''Organic''': <br />
<br />
*Usually uncommon.<br />
*In-depth investigations needed to be identified more so in cases that have not responded to conventional [[treatment]].<br />
|-<br />
| rowspan="2" |'''Functional or [[psychosomatic]]''': <br />
<br />
*Includes all forms of [[pathological]] [[urinary incontinence]] without [[anatomic]] or [[neurologic]] [[Defect|defects]].<br />
*Manifestations of which have been subdivided into two:<br />
|'''''Monosymtomatic [[enuresis]] (MEN)'':'''<br />
*These children have never had a dry period of >6 months and in the absence of any [[bladder]] [[dysfunction]] or [[symptoms]] suggestive of lower [[urinary tract]] issues.<br />
|-<br />
|'''''Non-monosymptomatic [[enuresis]] Nocturna (Non-MEN)'':'''<br />
*[[Diurnal]] presentation with an [[urge]], frequency, and [[enuresis]].<br />
|}<br />
<br />
*Another form of [[classification]] based on the [[Course (medicine)|course]] of [[nocturnal]] [[enuresis]] is:<br />
**'''Primary [[nocturnal enuresis]]''': 6 consecutive months without ever achieving [[bladder]] control at night. Most common form.<br />
**'''Secondary [[nocturnal enuresis]]''': 6 consecutive months of [[Urinary bladder|bladder]] control attained before a recurrence of [[Urinary incontinence|incontinence]]. Could be related to an organic or [[psychological]] [[Causes|cause]].<ref name="pmid27703953">{{cite journal| author=Arda E, Cakiroglu B, Thomas DT| title=Primary Nocturnal Enuresis: A Review. | journal=Nephrourol Mon | year= 2016 | volume= 8 | issue= 4 | pages= e35809 | pmid=27703953 | doi=10.5812/numonthly.35809 | pmc=5039962 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27703953 }} </ref><br />
<br />
==Pathophysiology==<br />
<br />
*The [[pathophysiology]] of [[urinary incontinence]] in [[children]], particularly [[enuresis]] can be described under three broad [[categories]]:<br />
*'''Increased [[urine]] production at night'''<br />
**The [[Urinary bladder|bladder]] is able to fill up at night as a [[result]] of an [[imbalance]] between the [[urine]] production at night and the [[Urinary bladder|bladder]] capacity. This often leads to frequent awakenings to pass [[urine]] for [[children]] or [[Urinary incontinence|incontinence]] for those with difficulties in waking up.<ref name="pmid11196246">{{cite journal| author=Nevéus T, Läckgren G, Tuvemo T, Hetta J, Hjälmås K, Stenberg A| title=Enuresis--background and treatment. | journal=Scand J Urol Nephrol Suppl | year= 2000 | volume= | issue= 206 | pages= 1-44 | pmid=11196246 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11196246 }} </ref><br />
**[[Nocturnal]] production of the [[antidiuretic hormone]], [[ADH]] is higher when compared to daytime values. Thus, the insufficient production of [[ADH]] in these [[children]] has been identified with a subsequent rise in [[urine]] production, frequency of which is 2 out of 3 children.<ref name="pmid2705537">{{cite journal| author=Rittig S, Knudsen UB, Nørgaard JP, Pedersen EB, Djurhuus JC| title=Abnormal diurnal rhythm of plasma vasopressin and urinary output in patients with enuresis. | journal=Am J Physiol | year= 1989 | volume= 256 | issue= 4 Pt 2 | pages= F664-71 | pmid=2705537 | doi=10.1152/ajprenal.1989.256.4.F664 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2705537 }} </ref><ref name="pmid24955178">{{cite journal| author=Tas T, Cakiroglu B, Hazar AI, Balci MB, Sinanoglu O, Nas Y | display-authors=etal| title=Monosymptomatic nocturnal enuresis caused by seasonal temperature changes. | journal=Int J Clin Exp Med | year= 2014 | volume= 7 | issue= 4 | pages= 1035-9 | pmid=24955178 | doi= | pmc=4057857 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24955178 }} </ref><br />
*'''Reduced [[Urinary bladder|bladder]] capacity at night/Increased [[contractions]] of the [[detrusor muscle]]'''<br />
**Studies have proposed a reduced [[Urinary bladder|bladder]] wall capacity to 70% of the expected values with an increase in the [[Urinary bladder|bladder]] wall thickness on [[ultrasound]] in [[children]] with majorly [[nocturnal enuresis]].<ref name="pmid15118426">{{cite journal| author=Yeung CK, Sreedhar B, Leung VT, Metreweli C| title=Ultrasound bladder measurements in patients with primary nocturnal enuresis: a urodynamic and treatment outcome correlation. | journal=J Urol | year= 2004 | volume= 171 | issue= 6 Pt 2 | pages= 2589-94 | pmid=15118426 | doi=10.1097/01.ju.0000112978.54300.03 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15118426 }} </ref><br />
**In addition to this, there is [[disinhibition]] in [[contractions]] of the [[Urinary bladder|bladder]] wall in about 30% of kids with [[enuresis]].<ref name="pmid8719568">{{cite journal| author=Watanabe H| title=Sleep patterns in children with nocturnal enuresis. | journal=Scand J Urol Nephrol Suppl | year= 1995 | volume= 173 | issue= | pages= 55-6; discussion 56-7 | pmid=8719568 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8719568 }} </ref><br />
*'''Awakening [[Disorder]]'''<br />
**The sudden [[Urinary urgency|urge]] to pass [[urine]] does not occur adequately in [[Children|kids]] that are enuretic.<br />
**[[Chronic]] over-stimulation [[Causality|causing]] a [[down-regulation]] of the voiding center has been surmised by [[Research|researchers]].<ref name="pmid18509134">{{cite journal| author=Yeung CK, Diao M, Sreedhar B| title=Cortical arousal in children with severe enuresis. | journal=N Engl J Med | year= 2008 | volume= 358 | issue= 22 | pages= 2414-5 | pmid=18509134 | doi=10.1056/NEJMc0706528 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18509134 }} </ref><br />
<br />
==Causes==<br />
<br />
*The [[causes]] of [[urinary incontinence]] in [[children]] are identified based on the sub-classification of [[pathological]] [[Urinary incontinence|incontinence]].<br />
*[[Causes]] of MEN are not fully elucidated but are assumed to be as a [[result]] of an interplay between the delayed [[maturation]] of the [[neurological]] [[Urinary bladder|bladder]] and how the [[urine]] production is regulated.<br />
*Non-MEN is subcategorized based on its [[symptoms]] which is predominantly day-time. These [[symptoms]] include:<br />
**[[Overactive bladder]]<br />
**Dis-coordinated [[micturition]]<br />
**Infrequent voiding<br />
*[[Causes]] of organic [[Urinary incontinence|incontinence]] (which is usually [[rare]]) include the following;<br />
**[[Structural biology|Structural]] [[renal]] problems such as:<br />
***[[Ectopic ureter]]<br />
***[[Malformation|Malformed]] [[urethra]]<br />
***Duplex [[kidney]]<br />
**[[Anatomic]] [[neural]] [[disorders]] such as:<br />
***[[Spina bifida]]<br />
***[[Neoplasms]] of the [[nervous system]]<br />
***[[Tethered cord syndrome]]<br />
***[[Sacral agenesis]].<ref name="pmid21977217">{{cite journal| author=Schultz-Lampel D, Steuber C, Hoyer PF, Bachmann CJ, Marschall-Kehrel D, Bachmann H| title=Urinary incontinence in children. | journal=Dtsch Arztebl Int | year= 2011 | volume= 108 | issue= 37 | pages= 613-20 | pmid=21977217 | doi=10.3238/arztebl.2011.0613 | pmc=3187617 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21977217 }} </ref><br />
**[[Obstructive sleep apnea]] ([[Obstructive sleep apnea|OSA]])<br />
**[[Sexual]] [[abuse]]<br />
**[[Pinworm infection|Pinworm infestation]]<br />
<br />
==Differentiating urinary incontinence from other diseases==<br />
<br />
*It must be differentiated from the following:<br />
**[[Diabetes mellitus]]<br />
**[[Diabetes insipidus]]<br />
**[[Urinary tract infections|Urinary tract infection]]<br />
**[[Anxiety disorders|Anxiety disorder]]<br />
**[[Spinal cord]] [[neoplasms]]<br />
**[[Spinal cord]] [[trauma]]<br />
**Small [[Urinary bladder|bladder]]<br />
<br />
==Epidemiology and Demographics==<br />
===Age===<br />
<br />
*[[Children]] usually achieve the ability to [[control]] their [[Urinary bladder|bladder]] function between the [[Age|ages]] of 3 and 6 [[Year|years]].<br />
*This begins initially during the daytime and nighttime control is achieved a lot later.<ref name="pmid21977217">{{cite journal| author=Schultz-Lampel D, Steuber C, Hoyer PF, Bachmann CJ, Marschall-Kehrel D, Bachmann H| title=Urinary incontinence in children. | journal=Dtsch Arztebl Int | year= 2011 | volume= 108 | issue= 37 | pages= 613-20 | pmid=21977217 | doi=10.3238/arztebl.2011.0613 | pmc=3187617 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21977217 }} </ref><br />
*[[Nocturnal enuresis]] is still seen in 15%-20% of five [[Year|year]] old [[Children|kids]] with a spontaneous [[recovery]] [[rate]] of 14% yearly.<ref name="ArdaCakiroglu2016">{{cite journal|last1=Arda|first1=Ersan|last2=Cakiroglu|first2=Basri|last3=Thomas|first3=David T.|title=Primary Nocturnal Enuresis: A Review|journal=Nephro-Urology Monthly|volume=8|issue=4|year=2016|issn=2251-7006|doi=10.5812/numonthly.35809}}</ref><br />
*10% of [[children]] still have [[nocturnal enuresis]] at the [[age]] of 7 [[Year|years]] with daytime [[symptoms]] seen in 2%-9%.<ref name="pmid21977217">{{cite journal| author=Schultz-Lampel D, Steuber C, Hoyer PF, Bachmann CJ, Marschall-Kehrel D, Bachmann H| title=Urinary incontinence in children. | journal=Dtsch Arztebl Int | year= 2011 | volume= 108 | issue= 37 | pages= 613-20 | pmid=21977217 | doi=10.3238/arztebl.2011.0613 | pmc=3187617 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21977217 }} </ref><br />
<br />
===Gender===<br />
<br />
*[[Nocturnal enuresis]] is seen more frequently in boys.<ref name="pmid9202545">{{cite journal| author=Nørgaard JP, Djurhuus JC, Watanabe H, Stenberg A, Lettgen B| title=Experience and current status of research into the pathophysiology of nocturnal enuresis. | journal=Br J Urol | year= 1997 | volume= 79 | issue= 6 | pages= 825-35 | pmid=9202545 | doi=10.1046/j.1464-410x.1997.00207.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9202545 }} </ref><br />
<br />
===Race===<br />
<br />
*There is no documented [[racial]] predisposition for [[enuresis]].<br />
<br />
==Risk Factors==<br />
<br />
*Below is a list of [[risk factors]] associated with [[urinary incontinence]] in [[children]]:<br />
**[[Age]] less than five [[Year|years]]<br />
**Positive [[family history]] (risk is highest when one parent had been a sufferer of [[enuresis]])<br />
**[[Family]] size<br />
**[[Birth]] order<br />
**[[Male]] gender<br />
**Low socioeconomic status<br />
**[[Constipation]]<br />
**History of [[Urinary tract infections|urinary tract infection]]<br />
**History of [[diabetes]]<br />
**[[Psychological]]:<br />
***[[Birth]] of a sibling <ref name="pmid9202545">{{cite journal| author=Nørgaard JP, Djurhuus JC, Watanabe H, Stenberg A, Lettgen B| title=Experience and current status of research into the pathophysiology of nocturnal enuresis. | journal=Br J Urol | year= 1997 | volume= 79 | issue= 6 | pages= 825-35 | pmid=9202545 | doi=10.1046/j.1464-410x.1997.00207.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9202545 }} </ref><br />
***[[ADHD]]<br />
***[[Anxiety]]<br />
***Change of school<br />
***[[New]] home<br />
***[[Divorcee|Divorce]] of [[Parenting|parents]]<br />
<br />
==Natural History, Complications and Prognosis==<br />
<br />
*[[Complications]] include:<br />
**Poor [[self-esteem]]<br />
**Inability to socialize with peers<br />
**[[Mood disorders]]<br />
**[[Stress]]<br />
**General affectation of [[child]] and family's quality of life such as poor academic performance<br />
*[[Prognosis]] is generally good due to the high chances of spontaneous resolution at the [[rate]] of 15% per [[year]].<br />
**As a [[result]] of [[slow]] response to conventional [[treatment]] such as alarm therapy and [[desmopressin]], 20% will remain incontinent by adulthood.<ref name="pmid31424765">{{cite journal| author=| title=StatPearls | journal= | year= 2020 | volume= | issue= | pages= | pmid=31424765 | doi= | pmc= | url= }} </ref><br />
<br />
==Diagnosis==<br />
<br />
*The focus is to eliminate any potential organic [[Causes|cause]] of [[Urinary incontinence|incontinence]] and to classify and identify the type of functional [[Urinary incontinence|incontinence]] using detailed history and [[non-invasive]] [[Procedure|procedures]].<br />
*Identify any [[comorbidities]] which are mostly [[psychological]] occurring alongside [[Urinary incontinence|incontinence]].<ref name="pmid21977217">{{cite journal| author=Schultz-Lampel D, Steuber C, Hoyer PF, Bachmann CJ, Marschall-Kehrel D, Bachmann H| title=Urinary incontinence in children. | journal=Dtsch Arztebl Int | year= 2011 | volume= 108 | issue= 37 | pages= 613-20 | pmid=21977217 | doi=10.3238/arztebl.2011.0613 | pmc=3187617 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21977217 }} </ref><br />
<br />
===Symptoms===<br />
<br />
*Fundamental [[diagnosis]] includes taking a detailed history using a standardized [[questionnaire]]. Some of the important questions to ask include:<br />
**Time of the day [[child]] wets self?<br />
**[[Pattern]] of occurrence (every night or every other night)?<br />
**Place of occurrence (at home)?<br />
**[[Frequency]] of restroom visits during the [[Daytime wetting|day]] and any at night?<br />
**How does the [[child]] pass [[urine]]?<br />
**Any [[Color|colored]] [[Stain|stains]] on pants during the [[Daytime wetting|daytime]]?<br />
**See any holding movements?<br />
**[[Pattern]] of [[Urinary Stream (Decrease)|urine stream]]?<br />
**Any [[Strain|straining]]?<br />
**[[Child|Child's]] [[drinking]] habits especially in the evenings?<br />
**Previous/recurrent [[urinary tract infections]]?<br />
**[[Constipation]]?<br />
**[[Encopresis]]?<br />
**[[Developmental delays]]?<br />
**[[Psychological]] issues?<br />
**Previous [[surgery]]?<br />
**Any [[Stress|stressful]] circumstances recently either at home or school?<br />
**Method of [[treatment]] of [[Urinary incontinence|incontinence]] in the past?<br />
*A [[symptom]] or [[Urinary bladder|bladder]] diary is completed over a [[period]] of 14 days.<br />
<br />
===Physical Examination===<br />
<br />
*Primary aim of a [[physical examination]] is to look for possible organic [[causes]] of [[Urinary incontinence|incontinence]] and [[comorbidities]].<br />
**[[Weight loss]]<br />
**[[Hypertension]] ([[kidney disease]])<br />
**Enlarged [[tonsils]]<br />
**[[Slow]] [[growth]]<br />
**[[Breathing]] through the [[mouth]]<br />
**Spinal [[malformations]] in the [[Lumbosacral trunk|lumbosacral]] [[Region of interest|region]]:<br />
***[[Lipoma]]<br />
***[[Hair]] tufts<br />
***[[Dimple|Dimpled]] [[sacrum]]<br />
***[[Gluteal fold|Gluteal folds]] that [[Appearance|appear]] non-[[Symmetric function|symmetric]]<br />
***[[Hemangiomas]]<br />
**[[Mass]] on [[palpation]] of the [[abdomen]] suggesting [[fecal impaction]]<br />
**[[Genital area|Genital region]]:<br />
***[[Phimosis]]<br />
***[[Urine]] leak<br />
***[[Labial]] synechiae<br />
***[[Vulva|Vulval]] [[inflammation]]<br />
***[[Labial]] [[scars]]<br />
***[[Cremasteric reflex]]<br />
**[[Anal]] [[area]]:<br />
***[[Soiling|Soilage]]<br />
***[[Scratch]] marks/[[Excoriation|excoriations]]<br />
**[[Lower extremities]]:<br />
***Asymmetric [[reflexes]]<br />
***[[Atrophic]] [[muscles]]<br />
***[[Deformities]] on the [[foot]]<br />
**Assess [[developmental milestones]] attained<br />
**Assess [[Child|child's]] [[behavior]] and [[Screening (medicine)|screen]] for any [[behavioral]] [[abnormalities]] using [[Appropriate Use Criteria|appropriate]] [[questionnaires]].<br />
<br />
===Laboratory Findings===<br />
<br />
*[[Urinalysis]]:<br />
**Essential to rule out [[Urinary tract infections|urinary tract infection]]<br />
**Changes in [[urine]] [[specific gravity]] [[Suggestion|suggesting]] [[diabetes insipidus]]<br />
**[[Glucosuria]] for [[diabetes mellitus]]<br />
*[[Lack of response]] to [[therapy]]/[[interventions]] and a [[diagnosis]] of Non-MEN will warrant further work-up<br />
<br />
===Ultrasound===<br />
<br />
*[[Ultrasonography]] is a useful tool when further [[diagnostics]] is required, especially in situations of a likely organic [[Causes|cause]] or a [[lack of response]] to [[therapy]].<br />
*It can [[Anomaly detection|detect anomalies]] in the [[renal system]] such as:<br />
**Increase in thickness of the [[Urinary bladder|bladder]] wall<br />
**Dilated [[ureters]]<br />
**[[Hydronephrosis]]<br />
**[[Ureterocele]]<br />
**Duplex [[kidney]]<br />
**[[Distended abdomen|Distended]] [[rectum]]<ref name="pmid21977217">{{cite journal| author=Schultz-Lampel D, Steuber C, Hoyer PF, Bachmann CJ, Marschall-Kehrel D, Bachmann H| title=Urinary incontinence in children. | journal=Dtsch Arztebl Int | year= 2011 | volume= 108 | issue= 37 | pages= 613-20 | pmid=21977217 | doi=10.3238/arztebl.2011.0613 | pmc=3187617 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21977217 }} </ref><br />
<br />
===CT scan===<br />
<br />
*There are no [[CT scan]] findings [[Association (statistics)|associated]] with [[urinary incontinence]] in [[children]]. However, a [[CT scan]] may be helpful in the [[diagnosis]] of organic [[causes]] whenever a more detailed [[observation]] of [[anatomical]] [[abnormalities]] is required.<br />
<br />
===MRI===<br />
<br />
*There are no [[MRI]] findings [[Association (statistics)|associated]] with [[urinary incontinence]] in [[children]]. However, an [[Magnetic resonance imaging|MRI]] may be helpful in the [[diagnosis]] of organic [[causes]] whenever a more detailed [[observation]] of [[anatomical]] [[abnormalities]] is required.<br />
<br />
===Other Diagnostic Studies===<br />
<br />
*'''Uroflowmetry:''' This shows the [[Urinary bladder|bladder's]] [[pattern]] of voiding. If this [[test]] comes out suspicious, further [[testing]] like the uroflow-[[electromyography]] is required to [[Observation|observe]] [[pelvic floor]] details.<ref name="pmid16753432">{{cite journal| author=Nevéus T, von Gontard A, Hoebeke P, Hjälmås K, Bauer S, Bower W | display-authors=etal| title=The standardization of terminology of lower urinary tract function in children and adolescents: report from the Standardisation Committee of the International Children's Continence Society. | journal=J Urol | year= 2006 | volume= 176 | issue= 1 | pages= 314-24 | pmid=16753432 | doi=10.1016/S0022-5347(06)00305-3 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16753432 }} </ref><br />
*'''[[Urodynamics|Urodynamic studies]]:''' Reveal problems [[Association (statistics)|associated]] with the [[Urinary bladder|bladder]] capacity, and [[compliance]] ([[Detrusor muscle|detrusor muscles]]).<br />
**Valuable for illustrating [[neurogenic]] [[Urinary bladder|bladder]] or issues related to the [[bladder outlet obstruction]].<ref name="pmid15118427">{{cite journal| author=Yeung CK, Sihoe JD, Sit FK, Diao M, Yew SY| title=Urodynamic findings in adults with primary nocturnal enuresis. | journal=J Urol | year= 2004 | volume= 171 | issue= 6 Pt 2 | pages= 2595-8 | pmid=15118427 | doi=10.1097/01.ju.0000112790.72612.0a | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15118427 }} </ref><br />
<br />
==Treatment==<br />
<br />
*[[Treatment]] [[modality]] is based on the following [[Fundamental science|fundamental]] [[Principle (chemistry)|principles]]:<br />
**Encourage both [[patient]] and caregiver to undergo [[therapy]].<br />
**[[Treatment|Treat]] [[Daytime wetting|day-time]] [[symptoms]] prior to night-time in non-MEN.<br />
**[[Fecal]] [[Urinary incontinence|incontinence]] where present should be [[Treatment|treated]] first.<br />
**[[Psychiatric]] [[comorbidities]] should be [[Treatment|treated]] [[Concurrent overlap|concurrently]].<br />
**Higher success [[rates]] documented with combined [[treatment]] [[Modality|modalities]].<br />
**Continuous [[Monitoring competence|monitoring]] of [[treatment]] is highly essential.<ref name="pmid21977217">{{cite journal| author=Schultz-Lampel D, Steuber C, Hoyer PF, Bachmann CJ, Marschall-Kehrel D, Bachmann H| title=Urinary incontinence in children. | journal=Dtsch Arztebl Int | year= 2011 | volume= 108 | issue= 37 | pages= 613-20 | pmid=21977217 | doi=10.3238/arztebl.2011.0613 | pmc=3187617 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21977217 }} </ref><br />
<br />
===Medical Therapy===<br />
<br />
*'''Urotherapy:'''<br />
**This encompasses all the [[treatment]] methods employed in the [[treatment]] of [[urinary incontinence]] in [[children]].<br />
**They are non-[[pharmacological]] and non-[[surgical]] and usually first-line approach.<br />
**It has been proven [[Effective method|effective]] in the management of functional [[urinary incontinence]] and supplementary to [[treatment]] methods of [[Organic Chemistry|organic]] [[urinary incontinence]].<br />
**The components of urotherapy are divided into [[standard]] urotherapy and specific [[interventions]] which may or may not be needed.<br />
**'''[[Standard]] urotherapy''' which is the primary [[treatment]] for the functional type of [[urinary incontinence]] involves the following:<br />
***Extensive [[family]] [[education]] regarding the [[disorder]] and its management.<br />
***[[Suggestions]] on voiding [[behavior]] such as schedules for [[urination]].<br />
***[[Fluid intake]] [[Restriction|restrictions]] and [[nutrition]] in the setting of [[constipation]].<br />
***[[Tracking changes|Tracking]] of the progress of [[treatment]].<br />
**'''Specific [[interventions]]''' that can be occasionally added to [[treatment]] include:<br />
***'''Alarm [[therapy]]:'''<br />
****Most useful for [[disorders]] with awakening.<br />
****It is intended to increase the [[Urinary bladder|bladder]] capacity at night.<br />
****The [[child]] is groomed to awaken prior to [[bedwetting]].<br />
****The [[Ideal solution|ideal]] [[treatment]] for [[children]] < 8 [[Year|years]] with MEN and with good [[support]] from caregivers.<ref name="pmid7962877">{{cite journal| author=Houts AC, Berman JS, Abramson H| title=Effectiveness of psychological and pharmacological treatments for nocturnal enuresis. | journal=J Consult Clin Psychol | year= 1994 | volume= 62 | issue= 4 | pages= 737-45 | pmid=7962877 | doi=10.1037//0022-006x.62.4.737 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7962877 }} </ref><br />
***'''[[Neuromodulation]]:''' [[Transcutaneous electric nerve stimulation|Transcutaneous]] parasacral neurostimulation for [[overactive bladder]] cases.<br />
***'''[[Biofeedback]]:''' Using [[optical]] and [[auditory]] cues to help [[children]] to [[Relaxation|relax]] and empty their [[Urinary bladder|bladder]] in cases of [[micturition]] that are uncoordinated:<ref name="EbilogluErgin2016">{{cite journal|last1=Ebiloglu|first1=Turgay|last2=Ergin|first2=Giray|last3=Irkilata|first3=Hasan Cem|last4=Kibar|first4=Yusuf|title=The biofeedback treatment for non-monosymptomatic enuresis nocturna|journal=Neurourology and Urodynamics|volume=35|issue=1|year=2016|pages=58–61|issn=07332467|doi=10.1002/nau.22678}}</ref><br />
****Anti-[[stress]] program<br />
****[[Pelvic floor]] [[exercise]]<br />
****Self-[[catheterization]]<ref name="pmid21977217">{{cite journal| author=Schultz-Lampel D, Steuber C, Hoyer PF, Bachmann CJ, Marschall-Kehrel D, Bachmann H| title=Urinary incontinence in children. | journal=Dtsch Arztebl Int | year= 2011 | volume= 108 | issue= 37 | pages= 613-20 | pmid=21977217 | doi=10.3238/arztebl.2011.0613 | pmc=3187617 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21977217 }} </ref><br />
**'''[[Pharmacological]] [[treatment]]:'''<br />
***'''[[ADH]] analogs''' such as [[desmopressin|'''desmopressin''']] are helpful in the setting of high [[urine output]] at night. Effective in 70% of cases with complete [[remission]] seen in 25%. [[Relapse]] is however a concern but the [[Coordination|coordinated]] stepwise [[withdrawal]] of [[therapy]] is promising.<br />
***'''[[Anticholinergics]]''' such as '''[[oxybutynin]], and [[propiverine]]''' (preferred due to lower side-effects) are sometimes used in cases of [[overactive bladder]] with [[failure]] to achieve dryness from urotherapy. 65%-87% [[Response rate|response rates]] are [[Reporting results|reported]] with [[Chance|chances]] of [[relapse]] also documented.<br />
***'''[[Botulinum toxin]] A:''' [[Rare|rarely]] indicated.<br />
***'''[[Alpha-blockers]]'''<br />
***'''[[Tricyclic antidepressants]]:''' Have [[lethal]] [[heart]] [[side effects]] and not usually used.<ref name="pmid27703953">{{cite journal| author=Arda E, Cakiroglu B, Thomas DT| title=Primary Nocturnal Enuresis: A Review. | journal=Nephrourol Mon | year= 2016 | volume= 8 | issue= 4 | pages= e35809 | pmid=27703953 | doi=10.5812/numonthly.35809 | pmc=5039962 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27703953 }} </ref><br />
<br />
===Surgery===<br />
<br />
*[[Surgery]] is not routinely employed as a form of [[treatment]]. Might be of importance in [[Corrective|correcting]] some organic [[causes]] of [[urinary incontinence]] in [[children]].<br />
<br />
===Prevention===<br />
<br />
*There are no documented [[Primary prevention|primary preventive]] [[Measure (mathematics)|measures]] available for [[urinary incontinence]] in [[children]].<br />
<br />
==References==<br />
{{Reflist|2}}<br />
<br />
[[Category:Pediatrics]]<br />
[[Category:Primary care]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Urinary_incontinence_resident_survival_guide_(pediatrics)&diff=1696696Urinary incontinence resident survival guide (pediatrics)2021-04-09T12:57:46Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{| class="infobox" style="float:right;"<br />
|-<br />
|[[File:Siren.gif|30px|link=Urinary incontinence resident survival guide (pediatrics)]]||<br>||<br><br />
|[[Urinary incontinence resident survival guide (pediatrics)|'''Resident'''<br>'''Survival'''<br>'''Guide''']]<br />
|}<br />
<br />
{{CMG}} {{AE}} {{Ifeoma Anaya}}<br />
<br />
{{SK}}[[Urinary incontinence]] in kids; [[bedwetting]]; [[enuresis]]; [[nocturnal enuresis]]; [[enuresis]] nocturna; monosymptomatic [[enuresis]] nocturnal (MEN); non-monosymtomatic [[enuresis]] nocturnal (non-MEN) <br />
<br />
{| class="infobox" style="margin: 0 0 0 0; border: 0; float: right; width: 100px; background: #A8A8A8; position: fixed; top: 250px; right: 21px; border-radius: 0 0 10px 10px;" cellpadding="0" cellspacing="0" ;<br />
|-<br />
! style="padding: 0 5px; font-size: 85%; background: #A8A8A8" align="center" |{{fontcolor|#2B3B44|Urinary incontinence resident survival guide (pediatrics) Microchapters}}<br />
|-<br />
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" |[[Urinary incontinence resident survival guide (pediatrics)#Overview|Overview]]<br />
|-<br />
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" |[[Urinary incontinence resident survival guide (pediatrics)#Causes|Causes]]<br />
|-<br />
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" |[[Urinary incontinence resident survival guide (pediatrics)#FIRE: Focused Initial Rapid Evaluation|FIRE]]<br />
|-<br />
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" |[[Urinary incontinence resident survival guide (pediatrics)#Complete Diagnostic Approach|Diagnosis]]<br />
|-<br />
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" |[[Urinary incontinence resident survival guide (pediatrics)#Treatment|Treatment]]<br />
|-<br />
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" |[[Urinary incontinence resident survival guide (pediatrics)#Dos|Dos]]<br />
|-<br />
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" |[[Urinary incontinence resident survival guide (pediatrics)#Don'ts|Don'ts]]<br />
|}<br />
<br />
==Overview==<br />
[[Urinary incontinence]] in [[children]] is a very familiar finding and complaint amongst [[patients]] and their caregivers. It is broadly classified into [[physiological]] and [[pathological]] with its various subdivisions. The [[causes]] of [[urinary incontinence]] in [[children]] are identified based on the sub-classification of [[pathological]] [[Urinary incontinence|incontinence]]. The focus is to eliminate any [[potential]] organic [[Causes|cause]] of [[Urinary incontinence|incontinence]] and to classify and identify the type of functional [[Urinary incontinence|incontinence]] using detailed [[History and Physical examination|history]] and [[Non-invasive (medical)|non-invasive]] [[Procedure|procedures]]. Identify any [[comorbidities]] which are mostly [[psychological]] occurring alongside [[Urinary incontinence|incontinence]]. A fundamental [[diagnosis]] includes taking a detailed [[History and Physical examination|history]] using a standardized [[questionnaire]]. The primary aim of a [[physical examination]] is to look for possible organic [[causes]] of [[Urinary incontinence|incontinence]] and [[comorbidities]]. [[Urinalysis]] is essential to rule out [[urinary tract infections]]. [[Ultrasonography]] is a useful tool when further [[diagnostics]] is required especially in situations of a likely organic [[Causes|cause]] or a lack of response to [[therapy]]. Uroflowmetry and [[Urodynamics|urodynamic]] studies are additional [[diagnostic]] studies that can be employed. Urotherapy encompasses all non-[[pharmacological]] and non-[[surgical]] [[treatment]] methods employed in the [[treatment]] of [[urinary incontinence]] in [[children]]. [[Desmopressin]] and [[oxybutynin]] are common [[drugs]] used for the [[pharmacological]] management of [[urinary incontinence]] in [[children]]. [[Surgery]] is not routinely employed as a form of [[treatment]], it might be of importance in correcting some organic [[causes]] of [[urinary incontinence]] in [[children]].<br />
<br />
==Causes==<br />
===Life Threatening Causes===<br />
<br />
*Life-threatening [[causes]] include [[conditions]] that may [[result]] in death or permanent [[disability]] within 24 hours if left untreated, but are not common. However, there are possible [[causes]] that could result in [[disability]] if left untreated and are considered red flags. These include:<br />
**[[Sexual assault|Sexual abuse]]<br />
**[[Neurological]] [[impairment]] especially of the [[lower extremities]] suggesting possible [[Spinal cord|spinal]] dysraphisms<br />
**[[Diabetes mellitus]]<br />
**[[Diabetes insipidus]]<br />
**[[Urinary tract infections|Urinary tract infection]]<br />
*These are considered to be of particular concern when encountered in practice.<br />
<br />
===Common Causes===<br />
<br />
*These [[causes]] are based on the [[classification]] of [[urinary incontinence]] in [[children]].<br />
<br />
{| class="wikitable"<br />
|+Classification of Urinary Incontinence in Children<br />
! style="background:#4479BA; color: #FFFFFF;" align="center" + |Types of urinary incontinence<br />
! colspan="2" style="background:#4479BA; color: #FFFFFF;" align="center" + |Details<br />
|-<br />
| style="background:#DCDCDC;" + |'''[[Physiological]]<ref name="pmid21977217">{{cite journal| author=Schultz-Lampel D, Steuber C, Hoyer PF, Bachmann CJ, Marschall-Kehrel D, Bachmann H| title=Urinary incontinence in children. | journal=Dtsch Arztebl Int | year= 2011 | volume= 108 | issue= 37 | pages= 613-20 | pmid=21977217 | doi=10.3238/arztebl.2011.0613 | pmc=3187617 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21977217 }} </ref>'''<br />
| colspan="2" |<br />
*It is expected and seen as a norm in the early [[Year|years]].<br />
*Requires a minimum [[age]] of 5 [[Year|years]], at least one [[Event study|event]] in a month, and a minimum [[period]] of 3 months.<br />
*Persisting beyond the [[age]] of 5 [[Year|years]] is termed [[pathological]].<br />
*However, there are the 'late developers' who continue to experience [[physiologic]] [[urinary incontinence]] beyond the [[age]] of 5 [[Year|years]].<br />
*[[Clinical]] evaluation of these [[Children|kids]] remains [[normal]].<br />
|-<br />
| rowspan="3" style="background:#DCDCDC;" + |'''[[Pathological]]<ref name="pmid21977217" /><ref name="pmid31844104">{{cite journal| author=Zhu W, Che Y, Wang Y, Jia Z, Wan T, Wen J | display-authors=etal| title=Study on neuropathological mechanisms of primary monosymptomatic nocturnal enuresis in children using cerebral resting-state functional magnetic resonance imaging. | journal=Sci Rep | year= 2019 | volume= 9 | issue= 1 | pages= 19141 | pmid=31844104 | doi=10.1038/s41598-019-55541-9 | pmc=6915704 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31844104 }} </ref><ref name="pmid27703953">{{cite journal| author=Arda E, Cakiroglu B, Thomas DT| title=Primary Nocturnal Enuresis: A Review. | journal=Nephrourol Mon | year= 2016 | volume= 8 | issue= 4 | pages= e35809 | pmid=27703953 | doi=10.5812/numonthly.35809 | pmc=5039962 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27703953 }} </ref>'''<br />
| colspan="2" |'''Organic''': <br />
<br />
*Usually uncommon.<br />
*In-depth investigations needed to be identified more so in cases that have not responded to [[Conventional medicine|conventional]] [[treatment]].<br />
|-<br />
| rowspan="2" |'''Functional or [[psychosomatic]]''': <br />
<br />
*Includes all forms of [[pathological]] [[urinary incontinence]] without [[anatomic]] or [[neurologic]] [[Defect|defects]].<br />
*Manifestations of which have been subdivided into two:<br />
|'''''Monosymtomatic [[enuresis]] (MEN)'':'''<br />
*These [[Children|kids]] have never had a dry [[period]] of >6 months and in the absence of any [[bladder]] [[dysfunction]] or [[symptoms]] suggestive of lower [[urinary tract]] issues.<br />
|-<br />
|'''''Non-monosymptomatic [[enuresis]] Nocturna (Non-MEN)'':'''<br />
*[[Diurnal]] [[Presenting symptom|presentation]] with an [[urge]], [[frequency]], and [[enuresis]].<br />
|}<br />
<br />
*Another form of [[classification]] based on the [[Course (medicine)|course]] of [[nocturnal]] [[enuresis]] is:<br />
**'''Primary [[nocturnal enuresis]]''': 6 consecutive months without ever achieving [[bladder]] [[control]] at night. Most common form.<br />
**'''Secondary [[nocturnal enuresis]]''': 6 consecutive months of [[Urinary bladder|bladder]] [[control]] attained before a recurrence of [[Urinary incontinence|incontinence]]. Could be related to an organic or [[psychological]] [[Causes|cause]].<ref name="pmid27703953">{{cite journal| author=Arda E, Cakiroglu B, Thomas DT| title=Primary Nocturnal Enuresis: A Review. | journal=Nephrourol Mon | year= 2016 | volume= 8 | issue= 4 | pages= e35809 | pmid=27703953 | doi=10.5812/numonthly.35809 | pmc=5039962 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27703953 }} </ref><br />
<br />
==FIRE: Focused Initial Rapid Evaluation==<br />
<br />
*The [[Focusing|focus]] is to eliminate any [[potential]] organic [[Causes|cause]] of [[Urinary incontinence|incontinence]] and to classify and identify the type of functional [[Urinary incontinence|incontinence]] using detailed [[history]], [[physical examination]] and non-[[invasive]] [[procedures]].<br />
*Identify any [[comorbidities]] which are mostly [[psychological]] occurring alongside [[Urinary incontinence|incontinence]].<ref name="pmid21977217">{{cite journal| author=Schultz-Lampel D, Steuber C, Hoyer PF, Bachmann CJ, Marschall-Kehrel D, Bachmann H| title=Urinary incontinence in children. | journal=Dtsch Arztebl Int | year= 2011 | volume= 108 | issue= 37 | pages= 613-20 | pmid=21977217 | doi=10.3238/arztebl.2011.0613 | pmc=3187617 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21977217 }} </ref><br />
*Features of importance include: <br />
**[[Weight loss]]<br />
**[[Hypertension]] ([[kidney disease]])<br />
**[[Tonsils hypertrophy|Enlarged tonsils]]<br />
**[[Slow]] [[growth]]<br />
**[[Breathing]] through the [[mouth]]<br />
**[[Spinal cord|Spinal]] [[malformations]] in the [[Lumbosacral trunk|lumbosacral region]] such as [[sacral dimple]], [[hair]] tufts<br />
**[[Mass]] on [[palpation]] of the [[abdomen]] suggesting [[fecal impaction]]<br />
**[[Genital area|Genital region]] [[abnormalities]] such as [[labial]] synechiae, [[anal]] [[Soiling|soilage]] and/or [[Excoriation|excoriations]]<br />
**Asymmetric [[reflexes]] of the [[lower extremities]]<br />
**[[Urinalysis]]: Essential to rule out [[Urinary tract infections|urinary tract infection]] and changes in [[urine]] [[specific gravity]] suggesting [[diabetes insipidus]] and [[glucosuria]] for [[diabetes mellitus]]<br />
<br />
==Complete Diagnostic Approach==<br />
*Shown below is an [[algorithm]] [[Summarizing statistical data|summarizing]] the [[diagnosis]] of [[urinary incontinence]] in [[children]] according to the International Children's Continence Society guidelines:<ref name="HjalmasArnold2004">{{cite journal|last1=Hjalmas|first1=K.|last2=Arnold|first2=T.|last3=Bower|first3=W.|last4=Caione|first4=P.|last5=Chiozza|first5=L.M.|last6=von GONTARD|first6=A.|last7=Han|first7=S.W.|last8=Husman|first8=D.A.|last9=Kawauchi|first9=A.|last10=Läckgren|first10=G.|last11=Lottmann|first11=H.|last12=Mark|first12=S.|last13=Rittig|first13=S.|last14=Robson|first14=L.|last15=Walle|first15=J. Vande|last16=Yeung|first16=C.K.|title=NOCTURNAL ENURESIS: AN INTERNATIONAL EVIDENCE BASED MANAGEMENT STRATEGY|journal=Journal of Urology|volume=171|issue=6 Part 2|year=2004|pages=2545–2561|issn=0022-5347|doi=10.1097/01.ju.0000111504.85822.b2}}</ref><br />
<br />
<br />
{{familytree/start}}<br />
{{familytree | | | | | | | | | A01 | | | | | | | | | | | | |A01=•Detailed history:<br>• Questionnaires for [[defecation]] and soiling, voiding, [[wetting]] should be used}}<br />
{{familytree | | | | | | |,|-|-|+|-|-|.| | | | | | | | | | |}}<br />
{{familytree | | | | | | B01 | |!| | B02 | | | | | | | | | | | | |B01=•Establish [[bedwetting]] at night time only|B02=• Preclude day [[symptoms]] ([[urgency]], [[frequency]])<br>• [[Urinary tract infections]]<br>• Other [[disease]] pathologies}}<br />
{{familytree | | | | |,|-|-|-|-|+|-|-|-|-|.| | | | | | | | |}}<br />
{{familytree | | | | C01 | | | C02 | | | C03 | | | | | | | | | | |C01=•Establish nighttime [[urine output]]: first morning void and diapers<br>• [[Fluid intake]]<br>• [[Wetting]] at night|C02=•[[Bladder]] diary:<br>• Keep for at least 3 complete days and nights, [[fluid intake]], [[urine output]] and volumes, [[incontinence]] and [[defecation]] should be documented|C03=•Preclude [[incontinence]] during the day, [[frequency]], [[constipation]]/soiling}}<br />
{{familytree | | | | | | | | | |!| | | | | | | | | | | | | |}}<br />
{{familytree | | | | | | | | | |!| | | | | | | | | | | | | |}}<br />
{{familytree | | | | | | | | | D01 | | | | | | | | | | | | | |D01=•[[Physical examination]]}}<br />
{{familytree | | | | | | |,|-|-|+|-|-|.| | | | | | | | | | |}}<br />
{{familytree | | | | | | E01 | |!| | E02 | | | | | | | | | | | | |E01=•Establish typical [[anatomy]]<br>• [[Normal]] psychomotor [[development]]|E02=•Preclude atypical [[anatomy]](back and [[genital]] regions, [[reflexes]] to rule out [[neurological]] anomalies)}}<br />
{{familytree | | | | | | | | | |!| | | | | | | | | | | | | |}}<br />
{{familytree | | | | | | | | | F01 | | | | | | | | | | | | | |F01=•Additional investigations required with high index of suspicion of other pathologies}}<br />
{{familytree | | | | | | | | | | | | | | | | | | | | | | | |}}<br />
{{familytree/end}}<br />
<br />
==Treatment==<br />
<br />
* Shown below is an [[algorithm]] [[Summarizing statistical data|summarizing]] the [[treatment]] of [[urinary incontinence]] in [[children]] according the International Children's Continence Society guidelines:<ref name="HjalmasArnold2004">{{cite journal|last1=Hjalmas|first1=K.|last2=Arnold|first2=T.|last3=Bower|first3=W.|last4=Caione|first4=P.|last5=Chiozza|first5=L.M.|last6=von GONTARD|first6=A.|last7=Han|first7=S.W.|last8=Husman|first8=D.A.|last9=Kawauchi|first9=A.|last10=Läckgren|first10=G.|last11=Lottmann|first11=H.|last12=Mark|first12=S.|last13=Rittig|first13=S.|last14=Robson|first14=L.|last15=Walle|first15=J. Vande|last16=Yeung|first16=C.K.|title=NOCTURNAL ENURESIS: AN INTERNATIONAL EVIDENCE BASED MANAGEMENT STRATEGY|journal=Journal of Urology|volume=171|issue=6 Part 2|year=2004|pages=2545–2561|issn=0022-5347|doi=10.1097/01.ju.0000111504.85822.b2}}</ref><br />
{{familytree/start}}<br />
{{familytree | | A01 |-|-| A02 |-| A03 | | | | | | |A01=•[[Nocturnal]] wet episodes only from history and [[bladder]] diary?|A02=No|A03=Consider a different [[diagnosis]]}}<br />
{{familytree | | |!| | | | | | | | | | | | | | }}<br />
{{familytree | | G01 | | | | | | | | | | | | | |G01=Yes}}<br />
{{familytree | | |!| | | | | | | | | | | | | | }}<br />
{{familytree | | B01 |-|-| B02 |-| B03 | | | | | |B01=•[[Normal]] [[physical examination]]?|B02=No|B03=Consider a different [[diagnosis]]}}<br />
{{familytree | | |!| | | | | | | | | | | | | | }}<br />
{{familytree | | H01 | | | | | | | | | | | | | |H01=Yes}}<br />
{{familytree | | |!| | | | | | | | | | | | | | }}<br />
{{familytree | | C01 |-|-|-|-|-|-|.| | | | | | |C01=•Difficulty waking up at night?}}<br />
{{familytree | | |!| | | | | | | F01 | | | | |F01=•'''[[Treatment]] options''':<br>• [[Patient]] [[education]], regular [[fluid intake]] and [[urination]], optimistic attitude<br>• Plus [[behavior]] modification like alarm<br>• [[Desmopressin]] alone or with [[alarm]]<br>• Contemplate [[antimuscarinics]] alone or in combination}}<br />
{{familytree | | |)|-|-| D01 |-|'|!| | | | | | |D01=•Increased [[nocturnal]] [[urine output]]}}<br />
{{familytree | | |!| | | | | | | |!| | | | | | }}<br />
{{familytree | | |!| | | | | | | |!| | | | | | }}<br />
{{familytree | | |`|-| E01 |-|-|-|'| | | | | | |E01=•Multiple nightly wet episodes}}<br />
{{familytree | | | | | | | | | | | | | | | | | }}<br />
{{familytree | | | | | | | | | | | | | | | | | }}<br />
{{familytree/end}}<br />
<br />
==Dos==<br />
<br />
*Encourage both [[patient]] and caregiver to undergo [[therapy]] and [[Education|educate]] extensively about the [[causes]] and [[Course (medicine)|course]] of [[illness]] in order to ensure adherence to [[treatment]] [[Modality|modalities]].<br />
*[[Treatment|Treat]] day-time [[symptoms]] prior to night-time in non-MEN.<br />
*[[Fecal]] [[Urinary incontinence|incontinence]] whenever present should be [[Treatment|treated]] first.<br />
*[[Psychiatric]] [[comorbidities]] should be [[Treatment|treated]] [[Concurrent overlap|concurrently]].<br />
*Higher success [[rates]] documented with combined [[treatment]] [[Modality|modalities]].<br />
*Continuous monitoring of [[treatment]] is highly essential.<ref name="pmid21977217">{{cite journal| author=Schultz-Lampel D, Steuber C, Hoyer PF, Bachmann CJ, Marschall-Kehrel D, Bachmann H| title=Urinary incontinence in children. | journal=Dtsch Arztebl Int | year= 2011 | volume= 108 | issue= 37 | pages= 613-20 | pmid=21977217 | doi=10.3238/arztebl.2011.0613 | pmc=3187617 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21977217 }} </ref><br />
<br />
==Don'ts==<br />
<br />
*Never forget to rule out [[Sexual assault|sexual abuse]] as a potential [[cause]] of [[urinary incontinence]] especially in [[secondary]] presentations. Failure to identify this is a catastrophic [[medical]] mistake as it is too important to neglect.<ref>https://www.merckmanuals.com/professional/pediatrics/incontinence-in-children/urinary-incontinence-in-children#v1106778</ref><br />
<br />
==References==<br />
{{Reflist|2}}<br />
<br />
[[Category:Projects]]<br />
[[Category:Resident survival guide]]<br />
[[Category:Pediatrics]]<br />
[[Category:Primary care]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Metabolic_alkalosis_resident_survival_guide&diff=1696016Metabolic alkalosis resident survival guide2021-04-02T15:32:14Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
<br />
<br />
{{WikiDoc CMG}}; {{AE}} {{MMT}}<br />
<br />
{{SK}} Approach to Metabolic alkalosis, Metabolic alkalosis management, Metabolic alkalosis work-up<br />
==Overview==<br />
The normal [[physiological]] pH of [[blood]] is 7.35 to 7.45. An increase above this range is known to be [[Alkalosis]]. [[Metabolic Alkalosis]] is defined as a [[disease]] state where the [[blood pH]] is more than 7.45 due to secondary metabolic processes. The primary [[PH buffer|pH]] buffers in maintaining [[chemical equilibrium]] of physiological [[Blood pH]] are [[alkaline]] [[Bicarbonate|Bicarbonate ions(HCO3]]) and [[acidic]] [[Carbon dioxide|carbon dioxide(CO2)]]. When there is an increased amount of [[Bicarbonate|Bicarbonate(HCO3)]] in the body or a decreased amount of [[carbon dioxide]] or a loss of [[hydrogen ions]], it causes [[alkalosis]]. [[Metabolic alkalosis]] occurs due to the trapping of [[Bicarbonate|Bicarbonate ions]] (HCO3) or loss of [[hydrogen ions]] in the body due to some [[metabolic]] causes for example- [[Gastrointestinal|gastrointestinal loss]] of [[hydrogen ions]], [[Intracellular|intracellular shifting]] of [[hydrogen ions]], [[renal]] [[hydrogen]] loss, increased [[Bicarbonate|bicarbonate ions]] in [[extracellular]] [[Compartments|compartment]], [[Diuretic|diuretic i]]<nowiki/>nduced [[alkalosis]] or [[contraction alkalosis]]. Patient with normal [[renal physiology]] will compensate this increased amount of [[bicarbonate]] through excretion. But impaired [[renal function]] [[secondary]] to [[Chloride|chloride depletion]], [[hypokalemia]], [[hyperaldosteronism]], reduced [[Glomerular filtration rate|glomerular function rate]], reduced [[Effective circulating volume|effective arterial blood volume]] ([[EABV|EABV)]]) in [[heart failure]] or [[cirrhosis]] will lead to [[metabolic alkalosis]]. When the [[physiologic]] [[blood pH]] is above 7.45, it triggers the [[Respiratory centre of the medulla|respiratory center]] to cause [[hypoventilation]], thus decreased [[Carbon dioxide|PCO2]] leading to [[Compensatory responses for acid-base disorders|compensatory]] [[respiratory acidosis]]. The [[PCO2]]elevates from 0.5 to 0.7 mmHg per 1.0 [[mill mole]] elevation in plasma [[bicarbonate]] [[concentration]]. In severe [[Metabolic alkalosis]] PCO2 can reach 60 mmHg. The mortality rate with [[metabolic alkalosis]] is 45% with [[arterial]] [[blood]] pH 7.55 to 80% with [[arterial]] blood pH of 7.65. [[Treatment]] is usually supportive based on cause of the disease.<br />
<br />
==Causes==<br />
===Life Threatening Causes===<br />
Life-threatening causes of severe [[Metabolic alkalosis|metabolic alkalosis (]]<nowiki/>pH 7.55 to 7.65) may result in death (45% to 80%) or permanent disability within 24 hours if left untreated.<ref name="pmid20436691">{{cite journal |vauthors=Tripathy S |title=Extreme metabolic alkalosis in intensive care |journal=Indian J Crit Care Med |volume=13 |issue=4 |pages=217–20 |date=October 2009 |pmid=20436691 |pmc=2856150 |doi=10.4103/0972-5229.60175 |url=}}</ref> <br />
<br />
*[[Gastric acidity reduced|Loss of gastric acid]]<br />
*[[Loop diuretics|Loop]] or [[thiazide diuretics]]<br />
<br />
===Common Causes===<br />
<br />
*'''[[Chloride]] depletion''' o[[Gastrointestinal|r '''Gastrointestinal''']] '''loss of [[hydrogen]]'''<br />
**[[Gastrointestinal tract|GI]] loss: [[Vomiting]] (most commonly seen in [[pyloric stenosis]]), [[Nasogastric tube|NG suction]] , [[Zollinger-Ellison syndrome|Zollinger-ellison]] syndrome, [[Bulimia nervosa|Bulimia]].<ref name="pmid1928424">{{cite journal |vauthors=Galla JH, Gifford JD, Luke RG, Rome L |title=Adaptations to chloride-depletion alkalosis |journal=Am J Physiol |volume=261 |issue=4 Pt 2 |pages=R771–81 |date=October 1991 |pmid=1928424 |doi=10.1152/ajpregu.1991.261.4.R771 |url=}}</ref><br />
**[[Diuretic|Diuretics]]: [[Loop diuretic|Loop]] and [[thiazide diuretics]].<br />
**[[Diarrhea]]: [[Villous adenoma]]<ref name="pmid5927076">{{cite journal |vauthors=Babior BM |title=Villous adenoma of the colon. Study of a patient with severe fluid and electrolyte disturbances |journal=Am J Med |volume=41 |issue=4 |pages=615–21 |date=October 1966 |pmid=5927076 |doi=10.1016/0002-9343(66)90223-3 |url=}}</ref>, [[congenital chloride diarrhea]]<ref name="pmid8896562">{{cite journal |vauthors=Höglund P, Haila S, Socha J, Tomaszewski L, Saarialho-Kere U, Karjalainen-Lindsberg ML, Airola K, Holmberg C, de la Chapelle A, Kere J |title=Mutations of the Down-regulated in adenoma (DRA) gene cause congenital chloride diarrhoea |journal=Nat Genet |volume=14 |issue=3 |pages=316–9 |date=November 1996 |pmid=8896562 |doi=10.1038/ng1196-316 |url=}}</ref><br />
**[[Cystic fibrosis]].<ref name="pmid7618650">{{cite journal |vauthors=Pedroli G, Liechti-Gallati S, Mauri S, Birrer P, Kraemer R, Foletti-Jäggi C, Bianchetti MG |title=Chronic metabolic alkalosis: not uncommon in young children with severe cystic fibrosis |journal=Am J Nephrol |volume=15 |issue=3 |pages=245–50 |date=1995 |pmid=7618650 |doi=10.1159/000168839 |url=}}</ref><br />
**[[Chloride]] deficient [[Infant formula|infant formula.]]<br />
**Gastrocystoplasty <ref name="pmid7609133">{{cite journal |vauthors=Plawker MW, Rabinowitz SS, Etwaru DJ, Glassberg KI |title=Hypergastrinemia, dysuria-hematuria and metabolic alkalosis: complications associated with gastrocystoplasty |journal=J Urol |volume=154 |issue=2 Pt 1 |pages=546–9 |date=August 1995 |pmid=7609133 |doi=10.1097/00005392-199508000-00066 |url=}}</ref><br />
**Post hypercapneic [[metabolic alkalosis]].<br />
*'''[[Potassium]] depletion''' or '''[[Mineralocorticoids]] excess''' or '''[[Renal]] loss of [[hydrogen]]'''<br />
**Dietary [[potassium]] depletion.<ref name="pmid8648937">{{cite journal |vauthors=Sabatini S |title=The cellular basis of metabolic alkalosis |journal=Kidney Int |volume=49 |issue=3 |pages=906–17 |date=March 1996 |pmid=8648937 |doi=10.1038/ki.1996.125 |url=}}</ref><br />
**[[Primary Hyperaldosteronism|Primary hyperaldosteronism]]: [[Conn syndrome]] or [[adenoma]], [[hyperplasia]], [[carcinoma]], [[renin]] or [[glucocorticoid]] responsive.<br />
**[[Secondary hyperaldosteronism]]: [[Renovascular hypertension|Reno vascular hypertension]], [[edema]] ([[cirrhosis]], [[heart failure]], [[Nephrotic syndrome|nephrotic syndrome)]], [[Juxtaglomerular apparatus|juxtaglomerular cell]]([[Renin-secreting tumors|renin producing) tumor]], [[renal cell carcinoma]], [[hemangiopericytoma]], [[nephroblastoma]]<br />
**[[Mineralocorticoid]] excess due to primary decorticosterone excess ([[11β-hydroxylase deficiency|11 beta]], [[17 alpha-hydroxylase deficiency|17 alpha hydroxylase deficienc]]<nowiki/>y), [[licorice]]([[glycyrrhetinic acid]]), [[Liddle's syndrome|liddle syndrome]].<ref name="pmid1731223">{{cite journal |vauthors=Lifton RP, Dluhy RG, Powers M, Rich GM, Cook S, Ulick S, Lalouel JM |title=A chimaeric 11 beta-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension |journal=Nature |volume=355 |issue=6357 |pages=262–5 |date=January 1992 |pmid=1731223 |doi=10.1038/355262a0 |url=}}</ref> <ref name="pmid9452995">{{cite journal |vauthors=Warnock DG |title=Liddle syndrome: an autosomal dominant form of human hypertension |journal=Kidney Int |volume=53 |issue=1 |pages=18–24 |date=January 1998 |pmid=9452995 |doi=10.1046/j.1523-1755.1998.00728.x |url=}}</ref><br />
**[[Bartter syndrome|Bartter]] and [[Gitelman syndrome]]. <ref name="pmid9767561">{{cite journal |vauthors=Kurtz I |title=Molecular pathogenesis of Bartter's and Gitelman's syndromes |journal=Kidney Int |volume=54 |issue=4 |pages=1396–410 |date=October 1998 |pmid=9767561 |doi=10.1046/j.1523-1755.1998.00124.x |url=}}</ref><br />
**[[Laxative]]<br />
*'''Reduced [[Glomerular filtration rate]]'''<br />
**[[Chronic kidney disease]]<br />
*'''[[Extracellular fluid|ECF volume]] depletion/ [[Volume depletion|Volume contraction]]'''<br />
**[[Hypovolemia]] or [[Diuresis|massive diuresis]] with [[loop diuretics]].<br />
*'''Miscellanous'''<br />
**[[Hypercalcemia]] due to [[Milk-alkali syndrome]] or [[bone metastasis]].<br />
**Massive [[blood transfusion]].<br />
**[[Acetate]] containing [[Colloid|colloid sollution]].<br />
**[[Exogenous]] [[alkali]] admintration.<br />
**Combined [[antacid]] and cation exchange resin administration.<br />
**Sodium [[Penicillin|penicillins]].<br />
<br />
==Diagnosis==<br />
Shown below is an [[algorithm]] summarizing the [[diagnosis]] and [[treatment]] of [[Metabolic alkalosis|Metabolic Alkalosis]].<ref name="pmid20436691">{{cite journal |vauthors=Tripathy S |title=Extreme metabolic alkalosis in intensive care |journal=Indian J Crit Care Med |volume=13 |issue=4 |pages=217–20 |date=October 2009 |pmid=20436691 |pmc=2856150 |doi=10.4103/0972-5229.60175 |url=}}</ref> <br />
{{familytree/start |summary=Sample 1}}<br />
{{familytree | | | | | | | | | | | | A01 | | | | | |A01='''History''': • H/O [[Cystic fibrosis]]/[[Congenital adrenal hyperplasia]]/[[CHF]]/[[Uncontrolled HTN]]?<br>• Excess [[antacid]] consumption?<br>• [[Calcium]] over supplementation?<br>• [[Beta lactum antibiotic]] use?<br>• Recent or current [[diuretic]] use?<br>• [[Vomiting]] or [[diarrhea]]?<br>• massive use of [[licorice]]?<br>• H/O recent [[hypercapneic]] [[respiratory failure]]?}}<br />
{{familytree | | | | | | | | | | | | |!| | | | | | | | }}<br />
{{familytree | | | | | | | | | | | | B01 | | | | | |B01='''Physical Examination''': •'''General [[appearance]]''': [[Restlessness]]/ [[Irritable]]/[[lethargic]]?<br>• '''[[Skin]]''': decreased or normal [[turgor]]?<br>• '''[[HEENT]]''': [[Headache]]/[[Dizziness]]?<br>• '''[[CVS]]''': [[Dysrhythmia]]/[[Tachycardia]]?<br>• '''[[Respiratory]]''': [[Hypoxemia]], [[Compensatory]] [[hypoventilation]], [[Pulmonary]] [[microatelactasis]], Increased [[V/Q mismatch]]<br>• '''[[GI]]''': [[Nausea]]/[[vomiting]]/[[diarrhea]]?<br>• '''[[GU]]''': [[Urine output]], [[frequency]]?<br>• '''[[CNS]]''': [[Confusion]], loss of [[consciousness]]/[[Mental obtundation]], [[Neuromuscular excitability]]/[[Muscle cramps]], [[Tremor]], [[tingling]] and [[numbness]] in [[extremities]], [[Weakness]]? }}<br />
{{familytree | | | | | | | | | | | | |!| | | | | | | | }}<br />
{{familytree | | | | | | | | | | | | C01 | | | | | |C01='''[[Laboratory Tests]]''' •[[ABG]](pH >7.45, [[HCO3]] >26 mEq/L, [[PCO2]] compensates for increased [[HCO3]] by decreasing)<br>• [[Basic metabolic panel]]<br>• [[Serum Aldosterone]] And [[renin]]<br>• [[Urine analysis]], [[Urine pH]], [[Urine Chloride]] and [[sodium]]<br>• [[Chest]] [[X-ray]]<br>• [[Abdominal]] [[USG]]/[[CT]] to rule out [[mass]]}}<br />
{{familytree | | | | | |,|-|-|-|-|-|-|+|-|-|-|-|-|-|.| }}<br />
{{familytree | | | | | D01 | | | | | D02 | | | | | D03 |D01='''Expanded [[EABV]](No sign of [[volume depletion]] or [[Saline]] unresponsive)''' •'''[[Treatment]]''': Treat underlying cause.|D02='''Contracted [[EABV]](sign of [[volume depletion]] or [[saline]] responsive)''' •'''[[Treatment]]''': Replace [[volume]] with [[NaCl]] if depleted, correct [[electrolyte imbalance]], reduction of [[gastric secretion]] by [[H2 blocker]] or [[PPI]], discontinue [[diuretics]], [[Acetazolamide]], [[NH4Cl]] and [[HCl]] should be reserved for severe cases. |D03='''Rule out by [[history]]''' •'''[[Treatment]]''': According to cause with discontinuation of offending agents. }}<br />
{{familytree | | | | | |!| | | | | | |!| | |,|-|-|-|^|-|-|-|-|.|}}<br />
{{familytree | | | | | |!| | | | | | |!| | E01 | | | | | | | E02 |E01=[[Transient]]|E02=[[Renal failure]] with ingestion}}<br />
{{familytree | | | | | |!| | | | | | |!| | |!| | | | | | | | |!| | }}<br />
{{familytree | | | | | |!| | | | | | |!| | F01 | | | | | | | F02 |F01=• [[IV]] [[HCO3]]<br>• Acute correction of [[hypercapnea]]|F02=• [[Milk-alkali syndrome]]<br>• [[HCO3]] ingesion }}<br />
{{familytree | | | | | |!| | |,|-|-|-|^|-|-|-|-|.|}}<br />
{{familytree | | | | | |!| | G01 | | | | | | | G02 |G01='''[[GI]] loss(low [[urine Cl]])'''|G02='''[[Renal]] loss(high [[urine Cl]])'''}}<br />
{{familytree | | | | | |!| | |!| | | | | | | | |!| | }}<br />
{{familytree | | | | | |!| | H01 | | | | | | | H02 |H01=• '''[[Gastric]]''': [[Vomiting]], [[NG suction]]<br>• '''[[Lower]] [[bowel]]''': [[Villous adenoma]], [[chloridorrhea]], [[laxative]] abuse|H02=• [[Non-reabsorbed]] ions: [[Penicillin]]<br>• ='''Impaired [[tubular]] [[transport]]''': [[Loop]] and [[thiazide diuretics]], [[Barrter's]] and [[Gitelman's]] disease, [[Hypomagnesaemia]] }}<br />
{{familytree | |,|-|-|-|+|-|-|-|.|}}<br />
{{familytree | E01 | | E02 | | E03 | |E01='''High [[Renin]], High [[aldosterone]]''':• [[Malignant hypertension]]<br>• [[renovascular hypertension]]<br>• [[Renin secretin tumor]]|E02='''Low [[Renin]], High [[aldosterone]]''':• [[Aldosterone secreting tumor]]<br>• [[Adrenal hyperplasia]]<br>• [[Glucocorticoid]] remediable [[aldosteronism]] |E03='''Low [[Renin]], Low [[Aldosterone]]''':• [[Licorice]]<br>• [[Liddle's syndrome]]<br>• [[Enzyme]] deficiency}}<br />
{{familytree/end}}<br />
<br />
==Dos==<br />
*Maintenance of airway, breathing, circulation if there is an unstable patient.<ref name="pmid9767561">{{cite journal |vauthors=Kurtz I |title=Molecular pathogenesis of Bartter's and Gitelman's syndromes |journal=Kidney Int |volume=54 |issue=4 |pages=1396–410 |date=October 1998 |pmid=9767561 |doi=10.1046/j.1523-1755.1998.00124.x |url=}}</ref><br />
*Correction of the underlying cause for [[Bicarbonate|HCO3]] production.<br />
*Removal of inciting factors that reabsorb [[Bicarbonate|HCO3]].<br />
*Patient should be monitored carefully with [[Oxygen saturation|SaO2]], vital signs monitor and [[the electrocardiogram|EKG]].<br />
*Consider [[Respiratory|respiratory suppor]]<nowiki/>t in hypoxemic patient.<br />
<br />
==Don'ts==<br />
<br />
*Avoid [[hyperventilation]] as it will worsen [[Alkalosis|alkalemia]].<ref name="pmid9767561">{{cite journal |vauthors=Kurtz I |title=Molecular pathogenesis of Bartter's and Gitelman's syndromes |journal=Kidney Int |volume=54 |issue=4 |pages=1396–410 |date=October 1998 |pmid=9767561 |doi=10.1046/j.1523-1755.1998.00124.x |url=}}</ref><br />
<br />
==References==<br />
{{Reflist|2}}<br />
<br />
<br />
[[Category:Resident survival guide]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Hepatitis_survival_guide&diff=1696009Hepatitis survival guide2021-04-02T15:20:54Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
<br />
{{WikiDoc CMG}}; {{AE}} {{MSJ}}<br />
{| class="infobox" style="margin: 0 0 0 0; border: 0; float: right; width: 100px; background: #A8A8A8; position: fixed; top: 250px; right: 21px; border-radius: 0 0 10px 10px;" cellpadding="0" cellspacing="0" ;<br />
|-<br />
! style="padding: 0 5px; font-size: 85%; background: #A8A8A8" align="center" |{{fontcolor|#2B3B44|Hepatitis Survival Guide Microchapters}}<br />
|-<br />
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" |[[Hepatitis survival guide#Overview|Overview]]<br />
|-<br />
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" |[[Hepatitis survival guide#Causes|Causes]]<br />
|-<br />
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" |[[Hepatitis survival guide#Diagnosis|Diagnosis]]<br />
|-<br />
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" |[[Hepatitis survival guide#Treatment|Treatment]]<br />
|-<br />
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" |[[Hepatitis survival guide#Dos|Dos]]<br />
|}<br />
<br />
==Overview==<br />
This section provides a short and straight-to-the-point overview of [[acute hepatitis]]. [[Acute hepatitis]] is defined as an acute [[inflammation]] of the [[hepatocytes]] resulting in deranged [[liver function]]s and [[hepatocyte]] injury. It can be due to infective or non-infective causes. The most common infective [[causes]] included [[hepatitis]] [[viruse]]s (including [[Hepatitis A]], B, C, D, and E). The non-infective causes include [[medications]], [[alcohol]], and [[autoimmune hepatitis]]. The treatment is mainly supportive. Regular monitoring should be done to look for adequate resolution of [[infection]], [[signs]] of [[hepatic failure]], [[encephalopathy]], or chronic disease.<br />
<br />
==Causes==<br />
===Life Threatening Causes===<br />
Life-threatening causes include conditions that may result in death or permanent disability within 24 hours if left untreated.<br />
<br />
*[[Acetaminophen]] overdose<br />
*[[Heat stroke]]<br />
*[[Mushroom]] [[poisoning]]<br />
<br />
===Common Causes===<br />
<br />
*[[Hepatitis A]]<ref name="pmid31405537">{{cite journal| author=Kwong S, Meyerson C, Zheng W, Kassardjian A, Stanzione N, Zhang K | display-authors=etal| title=Acute hepatitis and acute liver failure: Pathologic diagnosis and differential diagnosis. | journal=Semin Diagn Pathol | year= 2019 | volume= 36 | issue= 6 | pages= 404-414 | pmid=31405537 | doi=10.1053/j.semdp.2019.07.005 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31405537 }} </ref><br />
*[[Hepatitis B]]<br />
*[[Hepatitis D]]<br />
*[[Hepatitis E]]<br />
*[[Autoimmune hepatitis]]<br />
*[[Epstein Barr virus]]<br />
*[[Cytomegalovirus]]<br />
*[[Herpes simplex]] [[virus]]<br />
*[[Alcohol]]ic [[hepatitis]] <ref name="pmid31219169">{{cite journal| author=Hosseini N, Shor J, Szabo G| title=Alcoholic Hepatitis: A Review. | journal=Alcohol Alcohol | year= 2019 | volume= 54 | issue= 4 | pages= 408-416 | pmid=31219169 | doi=10.1093/alcalc/agz036 | pmc=6671387 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31219169 }} </ref><br />
*[[Antibiotic]]s<ref name="pmid27956449">{{cite journal| author=Katarey D, Verma S| title=Drug-induced liver injury. | journal=Clin Med (Lond) | year= 2016 | volume= 16 | issue= Suppl 6 | pages= s104-s109 | pmid=27956449 | doi=10.7861/clinmedicine.16-6-s104 | pmc=6329561 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27956449 }} </ref><br />
*[[Anticonvulsant]] [[drug]]s<br />
<br />
==Diagnosis==<br />
Shown below is an algorithm summarizing the diagnosis of [[hepatitis]]<ref name="pmid11159575">{{cite journal| author=Ryder SD, Beckingham IJ| title=ABC of diseases of liver, pancreas, and biliary system: Acute hepatitis. | journal=BMJ | year= 2001 | volume= 322 | issue= 7279 | pages= 151-3 | pmid=11159575 | doi=10.1136/bmj.322.7279.151 | pmc=1119417 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11159575 }} </ref><ref name="pmid31855397">{{cite journal| author=| title=StatPearls | journal= | year= 2020 | volume= | issue= | pages= | pmid=31855397 | doi= | pmc= | url= }} </ref>.<br />
{{familytree/start |summary=PE diagnosis Algorithm.}}<br />
{{familytree | | | | A01 | | | A01=<div style="float: left; text-align: left;">[[Patient]]s commonly present with:<br />
* [[Anorexia|Loss of appetite]]<br />
* [[Nausea]]<br />
* [[Vomiting]]<br />
* Right upper quadrant [[abdominal pain]]<br />
* [[Muscle ache]]s<br />
* [[Fatigue]]<br />
* [[Icterus]]<br />
* Dark-colored [[urine]]<br />
* Clay-colored [[stool]] and [[diarrhea]]<br />
* [[Artharalgia]]<br />
* [[Pruritis]]<br />
* [[Urticaria]] <br />
* [[Fever]]}}<br />
{{familytree | | | | |!| | | | }}<br />
{{familytree | | | | B01 | | | B01=<div style="float: left; text-align: left;"> On physical examination there can be:<br />
* [[Jaundice]]<br />
* [[Hepatomegaly]]<br />
* [[Splenomegaly]] }}<br />
{{familytree | | | | |!| | | | }}<br />
{{familytree | | | | C01 | | |C01= Perform [[liver function test]]s and abdominal [[ultrasound]]}}<br />
{{familytree | | | | |!| | | | }}<br />
{{familytree | | | | D01 | | |D01=<div style="float: left; text-align: left;"> The following results are suggestive of acute [[hepatitis]]:<br />
* Elevated serum [[bilirubin]] levels<br />
* Elevated levels of transaminases [[enzyme]]s including [[Alanine aminotransferase]] and [[Aspartate aminotransferase]] greater than five folds the normal reference values.<br />
* Mild elevation or normal value of [[Alkaline phosphatase]] and [[Gamma-glutamyl transpeptidase]]. Marked elevation of these enzymes show peri-ampullary or [[biliary obstruction]]. }}<br />
{{familytree | | | | |!| | | | }}<br />
{{familytree | | | | E01 | | |E01= <div style="float: left; text-align: left;">Perform Viral titers and [[antigen]] detection tests:<br />
* IgM levels for [[HAV]]<br />
* IgM levels for [[HBV]] core [[antigen]]<br />
* Serological assay to detect [[antibody]] levels for [[HCV]]<br />
* IgM levels for [[HDV]] }}<br />
{{familytree/end}}<br />
<br />
==Treatment==<br />
Shown below is an algorithm summarizing the treatment of [[acute hepatitis]]<ref name="pmid11159575">{{cite journal| author=Ryder SD, Beckingham IJ| title=ABC of diseases of liver, pancreas, and biliary system: Acute hepatitis. | journal=BMJ | year= 2001 | volume= 322 | issue= 7279 | pages= 151-3 | pmid=11159575 | doi=10.1136/bmj.322.7279.151 | pmc=1119417 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11159575 }} </ref><ref name="pmid11794193">{{cite journal| author=Jaeckel E, Cornberg M, Wedemeyer H, Santantonio T, Mayer J, Zankel M | display-authors=etal| title=Treatment of acute hepatitis C with interferon alfa-2b. | journal=N Engl J Med | year= 2001 | volume= 345 | issue= 20 | pages= 1452-7 | pmid=11794193 | doi=10.1056/NEJMoa011232 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11794193 }} </ref>.<br />
{{familytree/start |summary=PE diagnosis Algorithm.}}<br />
{{familytree | | | | | | | | A01 |A01=<div style="float: left; text-align: left;">Look for severe clinical [[symptoms]] like [[nausea]], [[vomiting]], [[hepatic encephalopathy]], i.e., changes in [[sleep]] pattern, [[altered mental status]], agitated behavior, and lab finding of [[hepatic failure]], i.e., prolonged [[prothrombin]] time and elevated [[serum]] [[bilirubin]] levels. }} <br />
{{familytree | | | | |,|-|-|-|^|-|-|-|-|.| | | }}<br />
{{familytree | | | B01 | | | | | | | | B02 | | |B01= No |B02= Yes }}<br />
{{familytree |,|-|-|-|+|-|-|-|-|.| | | |!| | |}}<br />
{{familytree |C01| |C02| | |C03| |C04| |C01=<div style="float: left; text-align: left;"> For [[Hepatitis A]]:<br />
* Supportive treatment. Give patients anti-[[emetics]], [[antipyretic]]s, and [[proton pump inhibitors]]. <br />
* Maintain adequate hydration with oral or [[intravenous fluid]]. <br />
* Regular monitoring of [[INR]] and [[LFT]]s to assess [[liver]] function. |C02=<div style="float: left; text-align: left;">For [[Hepatitis B]]:<br />
* Supportive treatment. <br />
* All family members and close contacts should be screened for the [[infection]]. <br />
* [[Hepatitis B]] surface [[antigen]] should be rechecked at regular intervals to assess the chronicity of [[infection]]. |C03=<div style="float: left; text-align: left;">For [[Hepatitis C]]: Early [[Interferon alpha]] therapy should be initiated as it results in undetectable viral levels with sustained anti-viral action. |C04= Requires hospitalization with regular monitoring }}<br />
{{familytree/end}}<br />
<br />
==Dos==<br />
<br />
*The [[ALT]] and [[Aspartate transaminase|AST]] levels on average raise to the thousands in acute hepatitis indicating hepatocellular injury. <br />
*[[Alkaline phosphatase]] can also be raised showing a cholestatic picture. Serum total bilirubin levels are elevated with an increase in conjugated bilirubin levels. <ref name="pmid22947525">{{cite journal| author=Mackinney-Novelo I, Barahona-Garrido J, Castillo-Albarran F, Santiago-Hernández JJ, Méndez-Sánchez N, Uribe M | display-authors=etal| title= Clinical course and management of acute hepatitis A infection in adults. | journal=Ann Hepatol | year= 2012 | volume= 11 | issue= 5 | pages= 652-7 | pmid=22947525 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22947525 }} </ref><br />
*[[AST]] and [[ALT]] levels in [[alcoholic hepatitis]] are usually below 300 iu/L and rarely over 500.<br />
*Drug-induced hepatitis is indistinguishable from viral hepatitis as it also shows [[AST]] and [[ALT]] levels in the thousands.<br />
*[[Abdominal]] [[ultrasound]] is also done in initial management of acute hepatitis [[patients]]. It might show increase in the [[liver]] span, changes in [[echogenicity]], texture, acalculous [[cholecystitis]] and [[splenomegaly]]. <ref name="pmid22947525">{{cite journal| author=Mackinney-Novelo I, Barahona-Garrido J, Castillo-Albarran F, Santiago-Hernández JJ, Méndez-Sánchez N, Uribe M | display-authors=etal| title= Clinical course and management of acute hepatitis A infection in adults. | journal=Ann Hepatol | year= 2012 | volume= 11 | issue= 5 | pages= 652-7 | pmid=22947525 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22947525 }} </ref><br />
<br />
==References==<br />
{{Reflist|2}}<br />
<br />
[[Category:Resident survival guide]]<br />
[[Category:Primary care]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Abortion&diff=1696005Abortion2021-04-02T15:08:58Z<p>Caroline Collis: </p>
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<div>__NOTOC__<br />
{{SI}}<br />
<br />
{{CMG}}; {{AE}} {{nuha}}<br />
<br />
{{SK}}Pregnancy loss, miscarriage, spontaneous abortion <br />
<br />
==Overview==<br />
Abortion is the [[Termination of pregnancy|termination]] of [[pregnancy]] before 20 weeks of [[gestation]], which was first described by an ancient Egyptian medical text as the Ebers Papyrus in 1550 BCE. Abortion is classified as threatened, complete, incomplete, inevitable, septic or missed. [[Chromosome abnormality|Chromosomal abnormalities]] is the most common [[Causes|cause]] of sporadic abortion that occur as early as 4-8 weeks [[gestation]], or it could be due to either [[infectious]], [[Immunological|immunologic]], and environmental factors. [[Fetal]] causes of abortion are [[Genetics|genetic]] or [[chromosomal abnormalities]] while maternal causes include age, [[antiphospholipid syndrome]], severe hypertension, or [[systemic lupus erythematosus]] ([[SLE]]). [[Risk factors]] for abortion include non-modifiable [[Risk factors|risk factor]]<nowiki/>s like advanced age >35 years and previous pregnancy loss. Modifiable [[risk factors]] include [[obesity]], [[infections]], acute and chronic stress, [[medication]] and [[Substance abuse|substance use]], [[cocaine]], [[alcohol]], [[tobacco]] and [[caffeine]]. [[Complications]] of abortion include [[infection]], post abortion traid, [[Uterine|uterine perforation]], [[Septic Shock|septic abortion]], [[Shock|cervical shock]], cervical [[laceration]], and [[Disseminated intravascular coagulation|disseminated intravascular coagulation (DIC)]]. The [[prognosis]] of abortion depends on the [[gestational age]]. The younger the [[gestational age]], the lower the risk of [[complications]].<br />
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==Historical Perspective==<br />
<br />
*Abortion means termination of a [[pregnancy]] and it has been known since ancient times.<br />
*Abortion was first described by an ancient Egyptian medical text as the Ebers Papyrus in 1550 BCE, which suggested that an abortion can be induced with the use of a plant-fiber [[tampon]] coated with honey and crushed dates.<ref name="urlThe Ancient History of Abortion and When it Began">{{cite web |url=https://www.thoughtco.com/when-did-abortion-begin-721090 |title=The Ancient History of Abortion and When it Began |format= |work= |accessdate=}}</ref><br />
*During the ancient Egyptian, Persian, and Roman eras, abortion was practiced although it was never explicitly mentioned in any book of the Judeo-Christian Bible.<ref name="urlThe Ancient History of Abortion and When it Began">{{cite web |url=https://www.thoughtco.com/when-did-abortion-begin-721090 |title=The Ancient History of Abortion and When it Began |format= |work= |accessdate=}}</ref><br />
*In the fourth century BCE, Niddah 23a, a chapter of the Babylonian Talmud, reviews abortion as determining whether a woman is "unclean" and permitting abortion during early pregnancy.<ref name="urlThe Ancient History of Abortion and When it Began">{{cite web |url=https://www.thoughtco.com/when-did-abortion-begin-721090 |title=The Ancient History of Abortion and When it Began |format= |work= |accessdate=}}</ref><br />
<br />
" A woman can only abort something in the shape of a stone, and that can only be described as a lump."<br />
<br />
*In 11th century BCE, the Code of Assura, <nowiki>'' a harsh set of laws restricting women in general''</nowiki> was the earliest legal ban on abortion by forcing the death penalty on married women who obtain abortions without permission of their husbands.<ref name="urlInternet History Sourcebooks">{{cite web |url=https://sourcebooks.fordham.edu/ancient/1075assyriancode.asp |title=Internet History Sourcebooks |format= |work= |accessdate=}}</ref><br />
*In the fifth century BCE, the Hippocratic Oath prohibited physicians from inducing elective abortions.<ref name="urlThe Hippocratic Oath in Roe v. Wade | by Tara Mulder | EIDOLON">{{cite web |url=https://eidolon.pub/the-hippocratic-oath-in-roe-v-wade-ded59eedfd8f |title=The Hippocratic Oath in Roe v. Wade &#124; by Tara Mulder &#124; EIDOLON |format= |work= |accessdate=}}</ref><br />
*In the 19th century, surgical abortions became common and Hegar dilator in 1879 invented dilation-and-curettage (D&C).<ref name="urlThe Ancient History of Abortion and When it Began4">{{cite web |url=https://www.thoughtco.com/when-did-abortion-begin-721090 |title=The Ancient History of Abortion and When it Began |format= |work= |accessdate=}}</ref><br />
*On November 18, 1920, the Commissariats of Health and Justice legalized abortion in Soviet hospitals.<ref name="urldocshare03.docshare.tips">{{cite web |url=http://docshare03.docshare.tips/files/28921/289218791.pdf |title=docshare03.docshare.tips |format= |work= |accessdate=}}</ref><ref name="Endres1971">{{cite journal|last1=Endres|first1=Richard J.|title=Abortion in perspective|journal=American Journal of Obstetrics and Gynecology|volume=111|issue=3|year=1971|pages=436–439|issn=00029378|doi=10.1016/0002-9378(71)90791-5}}</ref><br />
*In 1970, Hawaii, New York, Alaska and Washington declared their abortion laws. Hawaii was the first state to legalize abortions and New York allowed abortions up to the 24th week of pregnancy.<ref name="urldocshare03.docshare.tips2">{{cite web |url=http://docshare03.docshare.tips/files/28921/289218791.pdf |title=docshare03.docshare.tips |format= |work= |accessdate=}}</ref><br />
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==Classification==<br />
<br />
Abortion can be classified into the following:<ref name="pmid564967">{{cite journal| author=Rushton DI| title=Simplified classification of spontaneous abortions. | journal=J Med Genet | year= 1978 | volume= 15 | issue= 1 | pages= 1-9 | pmid=564967 | doi=10.1136/jmg.15.1.1 | pmc=1012814 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=564967 }} </ref> <ref name="pmid28964589">{{cite journal| author=Ganatra B, Gerdts C, Rossier C, Johnson BR, Tunçalp Ö, Assifi A | display-authors=etal| title=Global, regional, and subregional classification of abortions by safety, 2010-14: estimates from a Bayesian hierarchical model. | journal=Lancet | year= 2017 | volume= 390 | issue= 10110 | pages= 2372-2381 | pmid=28964589 | doi=10.1016/S0140-6736(17)31794-4 | pmc=5711001 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28964589 }} </ref><ref name="pmid5914126">{{cite journal| author=Fujikura T, Froehlich LA, Driscoll SG| title=A simplified anatomic classification of abortions. | journal=Am J Obstet Gynecol | year= 1966 | volume= 95 | issue= 7 | pages= 902-5 | pmid=5914126 | doi=10.1016/0002-9378(66)90537-0 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=5914126 }} </ref><br />
{| style="border: 0px; font-size: 90%; margin: 3px;" align="center"<br />
! rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Abortion type}}<br />
! rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Characteristics}}<br />
|-<br />
| rowspan="1;" style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" |Early Threatened<br />
| style="padding: 5px 5px; background: #F5F5F5;" |Abortion before 12 weeks [[gestation]]<br />
[[Symptoms]]: the variable amount of [[bleeding]] <br />
<br />
[[Cervix]]: closed <br />
<br />
[[Ultrasound]]: viable [[pregnancy]]<br />
|-<br />
| rowspan="1;" style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" |Late Inevitable<br />
| style="padding: 5px 5px; background: #F5F5F5;" |Abortion between 12 and 20 weeks [[gestation]]<br />
[[Symptoms]]: [[vaginal bleeding]] and [[abdominal pain]] <br />
<br />
[[Cervix]]:dilated/ open <br />
<br />
[[Ultrasound]]: product of [[conception]] seen at or above the [[cervix]]. <br />
|-<br />
| rowspan="1;" style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" |Spontaneous<br />
| style="padding: 5px 5px; background: #F5F5F5;" |Non-induced abortion<br />
|-<br />
| rowspan="1;" style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" |Missed<br />
| style="padding: 5px 5px; background: #F5F5F5;" |Undetected death of an [[embryo]] or a [[fetus]] that is not expelled and that causes no [[bleeding]] (also called a blighted [[ovum]], [[Anembryonic gestation|anembryonic]] pregnancy, or [[Embryonic|intrauterine embryonic demise]])<br />
[[Symptoms]]: variable, [[asymptomatic]], [[Vaginal bleeding|light vaginal bleeding]]<br />
<br />
[[Cervix]]: closed<br />
<br />
[[Ultrasound]]: Nonviable [[fetus]]<br />
|-<br />
| rowspan="1;" style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" |Inevitable<br />
| style="padding: 5px 5px; background: #F5F5F5;" |[[Vaginal bleeding]] or rupture of the [[membranes]] accompanied by dilation of the [[cervix]]<br />
[[Symptoms]]: [[Vaginal bleeding]], [[Uterine|uterine cramps]], <br />
<br />
[[Cervix]]: Open <br />
<br />
[[Ultrasound]]: Intrauterine fetus with possible heartbeats, ruptured or collapsed [[gestational sac]]<br />
|-<br />
| rowspan="1;" style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" |Incomplete<br />
| style="padding: 5px 5px; background: #F5F5F5;" |Expulsion of some products of [[conception]]<br />
[[Symptoms]]: [[Vaginal bleeding]] with large clots or tissue, [[uterine]] cramps, some products of [[conception]] can be visualized in the [[Cervical os|dilated cervical os]] <br />
<br />
[[Cervix]]: Open <br />
<br />
[[Ultrasound]]: products of [[conception]] in the [[cervix]]<br />
|-<br />
| rowspan="1;" style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" |Threatened<br />
| style="padding: 5px 5px; background: #F5F5F5;" |[[Vaginal bleeding]] occurring before 20 weeks [[gestation]] without cervical dilation and indicating that [[Spontaneous abortions|spontaneous abortion]] may occur<br />
[[Symptom|Symptoms]]: the variable amount of [[bleeding]] <br />
<br />
[[Cervix]]: closed <br />
<br />
[[Ultrasound]]: viable pregnancy <br />
|-<br />
| rowspan="1;" style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" |Septic<br />
| style="padding: 5px 5px; background: #F5F5F5;" |Serious [[infection]] of the [[uterine]] contents during or shortly before or after an abortion. Usually after induced abortion and rarely after [[spontaneous abortion]]<br />
[[Symptoms]]: [[fever]], [[malaise]], signs of [[sepsis]], foul [[vaginal discharge]], [[cervical motion tenderness]], [[uterine]] tenderness, can be life-threatening <br />
<br />
[[Cervix]]: open <br />
<br />
[[Ultrasound]]: retained products of [[conception]]<br />
|-<br />
| rowspan="1;" style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" |Complete<br />
| style="padding: 5px 5px; background: #F5F5F5;" |Expulsion of all products of [[conception]]<br />
[[Symptoms]]: variable, [[asymptomatic]] <br />
<br />
[[Cervix]]: closed, and the [[uterus]] should be contracted. <br />
<br />
[[Ultrasound]]: [[uterus]] is empty <br />
|-<br />
| rowspan="1;" style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" |Recurrent or habitual<br />
| style="padding: 5px 5px; background: #F5F5F5;" |≥ 2 to 3 consecutive spontaneous abortions<br />
|-<br />
| rowspan="1;" style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" |Therapeutic<br />
| style="padding: 5px 5px; background: #F5F5F5;" |Termination of pregnancy because the woman’s life or health is endangered or because the [[fetus]] is dead or has malformations incompatible with life.<br /><br />
|-<br />
| rowspan="1;" style="padding: 5px 5px; background: #DCDCDC; font-weight: bold;" |Induced<br />
| style="padding: 5px 5px; background: #F5F5F5;" |Termination of [[pregnancy]] for medical or elective reasons<br />
|-<br />
<br />
|}<br />
<br />
<br />
==Pathophysiology==<br />
<br />
*[[Chromosome abnormality|Chromosomal abnormalities]] is the most common cause of sporadic abortion that occurs as early as 4-8 weeks [[gestation]], for instance [[aneuploidy]], [[mosaicism]], [[translocation]], [[Inversion (kinesiology)|inversion]], [[Deletion (genetics)|deletion]], or fragile sites.<ref name="pmid11821293">{{cite journal| author=Stephenson MD, Awartani KA, Robinson WP| title=Cytogenetic analysis of miscarriages from couples with recurrent miscarriage: a case-control study. | journal=Hum Reprod | year= 2002 | volume= 17 | issue= 2 | pages= 446-51 | pmid=11821293 | doi=10.1093/humrep/17.2.446 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11821293 }}</ref><br />
*[[First trimester|First-trimester]] [[pregnancy loss]] could be due to either [[infectious]], [[Immunological|immunologic]], and [[Environmental factor|environmental]] factors.<br />
*Immunologic factors is not well defined. Several theories suggest that [[Pregnancy loss|early pregnancy loss]] could be due to: <ref name="pmid12858110">{{cite journal| author=Kallen CB, Arici A| title=Immune testing in fertility practice: truth or deception? | journal=Curr Opin Obstet Gynecol | year= 2003 | volume= 15 | issue= 3 | pages= 225-31 | pmid=12858110 | doi=10.1097/00001703-200306000-00003 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12858110 }}</ref><ref name="pmid10889838">{{cite journal| author=Hill JA, Choi BC| title=Maternal immunological aspects of pregnancy success and failure. | journal=J Reprod Fertil Suppl | year= 2000 | volume= 55 | issue= | pages= 91-7 | pmid=10889838 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10889838 }}</ref><br />
**[[Allogeneic]] factors.<br />
**Lack of the immunological protection of the [[Embryo|embryos]], such as [[complement]] [[Regulatory protein|regulatory proteins]] (eg, [[Mannose-binding lectin pathway|mannose-binding lectin]], and [[HLA-DR]], [[HLA-G]] or [[HLA-E]])<br />
**Increased activity of [[uterine]] [[Natural killer cells|natural killer (uNK) cells]].<br />
**[[Alloimmunization]] to [[blood]] group antigen P.<ref name="pmid17199881">{{cite journal| author=Hanafusa N, Noiri E, Yamashita T, Kondo Y, Suzuki M, Watanabe Y | display-authors=etal| title=Successful treatment by double filtrate plasmapheresis in a pregnant woman with the rare P blood group and a history of multiple early miscarriages. | journal=Ther Apher Dial | year= 2006 | volume= 10 | issue= 6 | pages= 498-503 | pmid=17199881 | doi=10.1111/j.1744-9987.2006.00393.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17199881 }}</ref><br />
*Anatomic distortion of [[uterus]] may be associated with early or second [[trimester]] [[pregnancy loss]], eg: [[fibroids]], [[polyps]], [[adhesions]], or septa depending on the size and position.<br />
*The mechanism of [[pregnancy loss]] due to [[septate uterus]] is not clearly understood, one theory suggests that poor blood supply to the septum leads to poor implantation.<ref name="pmid10632403">{{cite journal| author=Homer HA, Li TC, Cooke ID| title=The septate uterus: a review of management and reproductive outcome. | journal=Fertil Steril | year= 2000 | volume= 73 | issue= 1 | pages= 1-14 | pmid=10632403 | doi=10.1016/s0015-0282(99)00480-x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10632403 }}</ref><br />
*[[Factor XIII|FXIII]] and [[fibrinogen]] play an essential role in [[placental]] [[implantation]] and maintenance of [[pregnancy]], that is why a deficiency of [[Factor XIII|factor XIII (FXIII)]] and [[fibrinogen]] are associated with [[pregnancy loss]].<ref name="pmid12709920">{{cite journal| author=Inbal A, Muszbek L| title=Coagulation factor deficiencies and pregnancy loss. | journal=Semin Thromb Hemost | year= 2003 | volume= 29 | issue= 2 | pages= 171-4 | pmid=12709920 | doi=10.1055/s-2003-38832 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12709920 }}</ref><br />
*It is thought that [[Miscarriage risk factors|miscarriage risk]] is associated with low plasma levels of the [[Kisspeptin|hormone kisspeptin]].<ref name="pmid25127195">{{cite journal| author=Jayasena CN, Abbara A, Izzi-Engbeaya C, Comninos AN, Harvey RA, Gonzalez Maffe J | display-authors=etal| title=Reduced levels of plasma kisspeptin during the antenatal booking visit are associated with increased risk of miscarriage. | journal=J Clin Endocrinol Metab | year= 2014 | volume= 99 | issue= 12 | pages= E2652-60 | pmid=25127195 | doi=10.1210/jc.2014-1953 | pmc=4255122 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25127195 }}</ref><br />
*The mechanism of abortion in cases of [[Polycystic ovary syndrome|PCOS]] is unknown, however it could be related to elevated serum [[Luteinizing hormone|luteinizing hormone (LH)]] levels, high [[testosterone]] and [[androstenedione]] concentrations or [[insulin]] resistance<ref name="pmid12215322">{{cite journal| author=Craig LB, Ke RW, Kutteh WH| title=Increased prevalence of insulin resistance in women with a history of recurrent pregnancy loss. | journal=Fertil Steril | year= 2002 | volume= 78 | issue= 3 | pages= 487-90 | pmid=12215322 | doi=10.1016/s0015-0282(02)03247-8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12215322 }}</ref><br />
<br />
<br /><br />
<br />
==Causes==<br />
'''Early Pregnancy Loss'''<ref name="pmid27842992">{{cite journal| author=Pereza N, Ostojić S, Kapović M, Peterlin B| title=Systematic review and meta-analysis of genetic association studies in idiopathic recurrent spontaneous abortion. | journal=Fertil Steril | year= 2017 | volume= 107 | issue= 1 | pages= 150-159.e2 | pmid=27842992 | doi=10.1016/j.fertnstert.2016.10.007 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27842992 }}</ref><ref name="pmid29932168">{{cite journal| author=Barut MU, Bozkurt M, Kahraman M, Yıldırım E, Imirzalioğlu N, Kubar A | display-authors=etal| title=Thrombophilia and Recurrent Pregnancy Loss: The Enigma Continues. | journal=Med Sci Monit | year= 2018 | volume= 24 | issue= | pages= 4288-4294 | pmid=29932168 | doi=10.12659/MSM.908832 | pmc=6045916 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29932168 }}</ref><br />
<br />
[[Fetal]] [[causes]]:<br />
<br />
*[[Genetics|Genetic]] or [[chromosomal abnormalities]] (45,X [[karyotype]], [[Trisomies]] ([[Trisomy 16]] is the most common), [[aneuploidy]], [[mosaicism]], [[translocation]], [[Inversion (kinesiology)|inversion]], [[Deletion (genetics)|deletion]], fragile sites)<br />
*[[Teratogenic]] and [[mutagenic]] factors.<br />
*<br />
<br />
[[Maternal]] [[causes]]:<br />
<br />
*[[Genetics|Genetic]]: Maternal age is directly related to the [[aneuploidy]] risk,<br />
*Parental [[Chromosome abnormality|chromosomal anomaly]] [[balanced translocation]]<br />
<br />
*[[Corpus luteum|Corpus luteum deficiency]]<br />
*Active infection such as [[rubella virus]], [[cytomegalovirus]]<br />
<br />
*[[Antiphospholipid syndrome]]<br />
*[[Hypertensive crisis|Severe hypertension]]<br />
*[[Systemic lupus erythematosus|Systemic lupus erythematosus (SLE)]]<br />
*[[Renal disease]]<br />
*Poorly controlled [[diabetes mellitus]]<br />
*[[Polycystic ovary syndrome]]<br />
<br />
==Differentiating abortion from other Diseases==<br />
Abortion should be differentiated from other causes of [[bleeding]] with cramping in early [[pregnancy]]:<ref name="urlMiscarriage - StatPearls - NCBI Bookshelf">{{cite web |url=https://www.ncbi.nlm.nih.gov/books/NBK532992/#!po=5.55556 |title=Miscarriage - StatPearls - NCBI Bookshelf |format= |work= |accessdate=}}</ref><br />
<br />
*Related to [[Pregnancy]] <br />
**[[Ectopic pregnancy]]<br />
**[[Hematoma|Subchorionic hematoma]]<br />
**[[Hydatidiform mole|Hydatidiform mole]]<br />
*Unrelated to [[pregnancy]]<br />
**[[Infection]] (cervicitis)<br />
**[[Polyps]]<br />
**[[Fibroids]]<br />
<br />
==Epidemiology and Demographics==<br />
<br />
*The [[incidence]] of abortion worldwide was estimated to be 35 per 1,000 women ages 15 to 44 from 2010 to 2014.<ref name="pmid27179755">{{cite journal| author=Sedgh G, Bearak J, Singh S, Bankole A, Popinchalk A, Ganatra B | display-authors=etal| title=Abortion incidence between 1990 and 2014: global, regional, and subregional levels and trends. | journal=Lancet | year= 2016 | volume= 388 | issue= 10041 | pages= 258-67 | pmid=27179755 | doi=10.1016/S0140-6736(16)30380-4 | pmc=5498988 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27179755 }}</ref><br />
*The rate in resource-rich countries was 27 per 1,000 and in resource-limited countries was 37 per 1,000. The [[incidence]] was highest in the Caribbean (65 per 1,000), and the lowest in North America (17 per 1,000). <ref name="pmid28094905">{{cite journal| author=Jones RK, Jerman J| title=Abortion Incidence and Service Availability In the United States, 2014. | journal=Perspect Sex Reprod Health | year= 2017 | volume= 49 | issue= 1 | pages= 17-27 | pmid=28094905 | doi=10.1363/psrh.12015 | pmc=5487028 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28094905 }}</ref><br />
*In the United States, one in four women will have an abortion during their [[reproductive]] life.<ref name="pmid28094905" /><br />
*The [[incidence]] of abortion is approximately 31%, the true [[incidence]] of abortion is difficult to ascertain, as many losses are not recognized<ref name="pmid30894356">{{cite journal| author=Magnus MC, Wilcox AJ, Morken NH, Weinberg CR, Håberg SE| title=Role of maternal age and pregnancy history in risk of miscarriage: prospective register based study. | journal=BMJ | year= 2019 | volume= 364 | issue= | pages= l869 | pmid=30894356 | doi=10.1136/bmj.l869 | pmc=6425455 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30894356 }}</ref><ref name="pmid33931702">{{cite journal| author=Wilcox AJ, Weinberg CR, O'Connor JF, Baird DD, Schlatterer JP, Canfield RE | display-authors=etal| title=Incidence of early loss of pregnancy. | journal=N Engl J Med | year= 1988 | volume= 319 | issue= 4 | pages= 189-94 | pmid=3393170 | doi=10.1056/NEJM198807283190401 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3393170 }}</ref><br />
*The rate of abortion is influenced by maternal age and history of prior [[pregnancy loss]].<ref name="pmid308943562">{{cite journal| author=Magnus MC, Wilcox AJ, Morken NH, Weinberg CR, Håberg SE| title=Role of maternal age and pregnancy history in risk of miscarriage: prospective register based study. | journal=BMJ | year= 2019 | volume= 364 | issue= | pages= l869 | pmid=30894356 | doi=10.1136/bmj.l869 | pmc=6425455 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30894356 }}</ref> 15% of women experience sporadic abortion, 2% of pregnant women experience two consecutive abortion and only 0.4 to 1% have three consecutive abortion. <ref name="pmid3073445">{{cite journal| author=Salat-Baroux J| title=[Recurrent spontaneous abortions]. | journal=Reprod Nutr Dev | year= 1988 | volume= 28 | issue= 6B | pages= 1555-68 | pmid=3073445 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3073445 }}</ref><br />
*The [[incidence]] of abortions in the United States were highest in women ages 20 to 24 (19.1 per 1,000 women) and 25 to 29 (18.5 per 1,000 women)<ref name="pmid33237897">{{cite journal| author=Kortsmit K, Jatlaoui TC, Mandel MG, Reeves JA, Oduyebo T, Petersen E | display-authors=etal| title=Abortion Surveillance - United States, 2018. | journal=MMWR Surveill Summ | year= 2020 | volume= 69 | issue= 7 | pages= 1-29 | pmid=33237897 | doi=10.15585/mmwr.ss6907a1 | pmc=7713711 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33237897 }}</ref><br />
*Most abortions were done in women who were unmarried (85%) and had one or more children (59%).<ref name="pmid33237897" /><br />
*Abortion rates in individuals of non-Hispanic White were 38.7, 20.0 for Hispanic, and 7.7 for other races per 1,000 women. <ref name="pmid33237897" /><br />
*In the United States in 2018, 78% of abortions occur at 9 weeks or earlier, 92% at 13 weeks or earlier, and 8% at or after 14 weeks.<ref name="pmid332378972">{{cite journal| author=Kortsmit K, Jatlaoui TC, Mandel MG, Reeves JA, Oduyebo T, Petersen E | display-authors=etal| title=Abortion Surveillance - United States, 2018. | journal=MMWR Surveill Summ | year= 2020 | volume= 69 | issue= 7 | pages= 1-29 | pmid=33237897 | doi=10.15585/mmwr.ss6907a1 | pmc=7713711 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33237897 }}</ref><br />
<br />
==Risk Factors==<br />
'''Non-modifiable [[risk factors]] include''': <ref name="pmid30400160">{{cite journal| author=Hu X, Miao M, Bai Y, Cheng N, Ren X| title=Reproductive Factors and Risk of Spontaneous Abortion in the Jinchang Cohort. | journal=Int J Environ Res Public Health | year= 2018 | volume= 15 | issue= 11 | pages= | pmid=30400160 | doi=10.3390/ijerph15112444 | pmc=6266092 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30400160 }}</ref><br />
<br />
*Advanced age >35 years, the most significant risk factor because of the associated fetal [[chromosomal abnormalities]].<br />
*Extremes of age<br />
*Advanced paternal age<br />
*Previous [[pregnancy loss]] increases the risk of later [[pregnancy loss]].<ref name="pmid308943563">{{cite journal| author=Magnus MC, Wilcox AJ, Morken NH, Weinberg CR, Håberg SE| title=Role of maternal age and pregnancy history in risk of miscarriage: prospective register based study. | journal=BMJ | year= 2019 | volume= 364 | issue= | pages= l869 | pmid=30894356 | doi=10.1136/bmj.l869 | pmc=6425455 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30894356 }}</ref><br />
<br />
'''Modifiable [[risk factors]] include:'''<br />
<br />
*[[Obesity]]<ref name="pmid18068166">{{cite journal| author=Metwally M, Ong KJ, Ledger WL, Li TC| title=Does high body mass index increase the risk of miscarriage after spontaneous and assisted conception? A meta-analysis of the evidence. | journal=Fertil Steril | year= 2008 | volume= 90 | issue= 3 | pages= 714-26 | pmid=18068166 | doi=10.1016/j.fertnstert.2007.07.1290 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18068166 }}</ref><br />
*[[Infection]] (eg: [[Parvovirus B19]] infection,[[syphilis]], [[Cytomegalovirus infection|cytomegalovirus (CMV) infection]])<ref name="pmid29628283">{{cite journal| author=Frazier T, Hogue CJR, Bonney EA, Yount KM, Pearce BD| title=Weathering the storm; a review of pre-pregnancy stress and risk of spontaneous abortion. | journal=Psychoneuroendocrinology | year= 2018 | volume= 92 | issue= | pages= 142-154 | pmid=29628283 | doi=10.1016/j.psyneuen.2018.03.001 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29628283 }}</ref><ref name="pmid26499091">{{cite journal| author=Rasti S, Ghasemi FS, Abdoli A, Piroozmand A, Mousavi SG, Fakhrie-Kashan Z| title=ToRCH "co-infections" are associated with increased risk of abortion in pregnant women. | journal=Congenit Anom (Kyoto) | year= 2016 | volume= 56 | issue= 2 | pages= 73-8 | pmid=26499091 | doi=10.1111/cga.12138 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26499091 }}</ref><ref name="pmid23476094">{{cite journal| author=Gomez GB, Kamb ML, Newman LM, Mark J, Broutet N, Hawkes SJ| title=Untreated maternal syphilis and adverse outcomes of pregnancy: a systematic review and meta-analysis. | journal=Bull World Health Organ | year= 2013 | volume= 91 | issue= 3 | pages= 217-26 | pmid=23476094 | doi=10.2471/BLT.12.107623 | pmc=3590617 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23476094 }}</ref><br />
*Pre-gestational [[diabetes]] increases the risk of miscarriage two- to threefold.<ref name="pmid24292565">{{cite journal| author=Tennant PW, Glinianaia SV, Bilous RW, Rankin J, Bell R| title=Pre-existing diabetes, maternal glycated haemoglobin, and the risks of fetal and infant death: a population-based study. | journal=Diabetologia | year= 2014 | volume= 57 | issue= 2 | pages= 285-94 | pmid=24292565 | doi=10.1007/s00125-013-3108-5 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24292565 }}</ref><br />
*Hyper- and [[hypothyroidism]] <ref name="pmid26837268">{{cite journal| author=Maraka S, Ospina NM, O'Keeffe DT, Espinosa De Ycaza AE, Gionfriddo MR, Erwin PJ | display-authors=etal| title=Subclinical Hypothyroidism in Pregnancy: A Systematic Review and Meta-Analysis. | journal=Thyroid | year= 2016 | volume= 26 | issue= 4 | pages= 580-90 | pmid=26837268 | doi=10.1089/thy.2015.0418 | pmc=4827301 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26837268 }}</ref><br />
*Acute and chronic stress<ref name="pmid29530382">{{cite journal| author=Li Y, Margerison-Zilko C, Strutz KL, Holzman C| title=Life Course Adversity and Prior Miscarriage in a Pregnancy Cohort. | journal=Womens Health Issues | year= 2018 | volume= 28 | issue= 3 | pages= 232-238 | pmid=29530382 | doi=10.1016/j.whi.2018.02.001 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29530382 }}</ref><br />
*[[Medication]] and substance use, examples are [[non-steroidal anti-inflammatory drug|NSAIDs]] ([[ibuprofen]] and [[diclofenac]]), [[cocaine]], [[methamphetamines]]<ref name="pmid21896698">{{cite journal| author=Nakhai-Pour HR, Broy P, Sheehy O, Bérard A| title=Use of nonaspirin nonsteroidal anti-inflammatory drugs during pregnancy and the risk of spontaneous abortion. | journal=CMAJ | year= 2011 | volume= 183 | issue= 15 | pages= 1713-20 | pmid=21896698 | doi=10.1503/cmaj.110454 | pmc=3193112 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21896698 }} [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=&cmd=prlinks&id=22411163 Review in: Evid Based Nurs. 2012 Jul;15(3):76-7]</ref><br />
<br />
*[[Alcohol]], [[tobacco]] and [[caffeine]]<ref name="pmid24810392">{{cite journal| author=Avalos LA, Roberts SC, Kaskutas LA, Block G, Li DK| title=Volume and type of alcohol during early pregnancy and the risk of miscarriage. | journal=Subst Use Misuse | year= 2014 | volume= 49 | issue= 11 | pages= 1437-45 | pmid=24810392 | doi=10.3109/10826084.2014.912228 | pmc=4183196 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24810392 }}</ref><ref name="pmid9929522">{{cite journal| author=Ness RB, Grisso JA, Hirschinger N, Markovic N, Shaw LM, Day NL | display-authors=etal| title=Cocaine and tobacco use and the risk of spontaneous abortion. | journal=N Engl J Med | year= 1999 | volume= 340 | issue= 5 | pages= 333-9 | pmid=9929522 | doi=10.1056/NEJM199902043400501 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9929522 }}</ref><ref name="pmid26329421">{{cite journal| author=Chen LW, Wu Y, Neelakantan N, Chong MF, Pan A, van Dam RM| title=Maternal caffeine intake during pregnancy and risk of pregnancy loss: a categorical and dose-response meta-analysis of prospective studies. | journal=Public Health Nutr | year= 2016 | volume= 19 | issue= 7 | pages= 1233-44 | pmid=26329421 | doi=10.1017/S1368980015002463 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26329421 }}</ref><ref name="pmid29739005">{{cite journal| author=Lee SW, Han YJ, Cho DH, Kwak HS, Ko K, Park MH | display-authors=etal| title=Smoking Exposure in Early Pregnancy and Adverse Pregnancy Outcomes: Usefulness of Urinary Tobacco-Specific Nitrosamine Metabolite 4-(Methylnitrosamino)-1-(3-Pyridyl)-1-Butanol Levels. | journal=Gynecol Obstet Invest | year= 2018 | volume= 83 | issue= 4 | pages= 365-374 | pmid=29739005 | doi=10.1159/000485617 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29739005 }}</ref><br />
<br />
==Screening==<br />
There is insufficient evidence to recommend routine screening for abortion.<br />
<br />
==Natural History, Complications, and Prognosis==<br />
<br />
*Complications of spontaneous abortion and therapeutic abortions include the following:<ref name="pmid24962349">{{cite journal| author=Lim LM, Singh K| title=Termination of pregnancy and unsafe abortion. | journal=Best Pract Res Clin Obstet Gynaecol | year= 2014 | volume= 28 | issue= 6 | pages= 859-69 | pmid=24962349 | doi=10.1016/j.bpobgyn.2014.05.005 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24962349 }}</ref><br />
**[[Complications]] of [[anesthesia]]<br />
**Post abortion triad ([[pain]], [[bleeding]], [[low-grade fever]]) caused by retained products of [[conception]].<br />
**Retained products of [[conception]]<br />
**[[Uterine|Uterine perforation]]<ref name="pmid22048784">{{cite journal| author=Koshiba A, Koshiba H, Noguchi T, Iwasaku K, Kitawaki J| title=Uterine perforation with omentum incarceration after dilatation and evacuation/curettage: magnetic resonance imaging findings. | journal=Arch Gynecol Obstet | year= 2012 | volume= 285 | issue= 3 | pages= 887-90 | pmid=22048784 | doi=10.1007/s00404-011-2127-z | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22048784 }}</ref><br />
**[[Septic Shock|Septic abortion]]<ref name="pmid20046250">{{cite journal| author=Saultes TA, Devita D, Heiner JD| title=The back alley revisited: sepsis after attempted self-induced abortion. | journal=West J Emerg Med | year= 2009 | volume= 10 | issue= 4 | pages= 278-80 | pmid=20046250 | doi= | pmc=2791734 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20046250 }}</ref><br />
**[[Shock|Cervical shock]]<br />
**Cervical [[laceration]]<br />
**[[Disseminated intravascular coagulation|Disseminated intravascular coagulation (DIC)]]<br />
*Prognosis of abortion depends on the [[gestational age]]. The younger the [[gestational age]], the lower the risk of [[complications]]. The highest risk of death is from a [[Septic Shock|septic abortion]]; the majority of these cases are a result of illegal abortions in developing countries.<ref name="urlMiscarriage - StatPearls - NCBI Bookshelf2">{{cite web |url=https://www.ncbi.nlm.nih.gov/books/NBK532992/#!po=5.55556 |title=Miscarriage - StatPearls - NCBI Bookshelf |format= |work= |accessdate=}}</ref><br />
<br />
==Diagnosis==<br />
===Diagnostic Study of Choice===<br />
<br />
*[[Ultrasound]] shows no intrauterine [[pregnancy]] or loss of previously seen [[Cardiac|cardiac activity]] is diagnostic if the intrauterine [[pregnancy]] is confirmed by [[ultrasound]] in a previous visit.<ref name="urlUpToDate">{{cite web |url=https://www.uptodate.com/contents/pregnancy-loss-miscarriage-risk-factors-etiology-clinical-manifestations-and-diagnostic-evaluation?search=miscarriage&source=search_result&selectedTitle=2~150&usage_type=default&display_rank=2#H3674675200 |title=UpToDate |format= |work= |accessdate=}}</ref><br />
<br />
*The diagnosis of early pregnancy loss (EPL) occurs if the initial transvaginal ultrasound shows intrauterine pregnancy without [[Fetal circulation|fetal]] [[cardiac]] activity and is based on the criteria made by the Society of Radiologists in Ultrasound Multi-specialty Panel on Early First Trimester [[Diagnosis]] of [[Miscarriage]] and Exclusion of a Viable Intrauterine [[Pregnancy]], which include:<ref name="pmid24106937">{{cite journal| author=Doubilet PM, Benson CB, Bourne T, Blaivas M, Society of Radiologists in Ultrasound Multispecialty Panel on Early First Trimester Diagnosis of Miscarriage and Exclusion of a Viable Intrauterine Pregnancy. Barnhart KT | display-authors=etal| title=Diagnostic criteria for nonviable pregnancy early in the first trimester. | journal=N Engl J Med | year= 2013 | volume= 369 | issue= 15 | pages= 1443-51 | pmid=24106937 | doi=10.1056/NEJMra1302417 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24106937 }}</ref><br />
**A [[gestational sac]] ≥25 mm in mean diameter that does not contain a [[yolk sac]] or [[embryo]]<br />
**An [[embryo]] with a crown-rump length (CRL) ≥7 mm that does not have [[cardiac]] activity<br />
**After a [[Pelvis|pelvic]] [[ultrasound]] shows a gestational sac without a [[yolk sac]], absence of an [[embryo]] with a [[heartbeat]] in ≥2 weeks<br />
**After a [[Pelvis|pelvic]] [[ultrasound]] shows a [[gestational sac]] with a [[yolk sac]], absence of an [[embryo]] with a [[heartbeat]] in ≥11 days<br />
**Findings that are suspicious for, but not [[diagnostic]] of, [[pregnancy loss]] include:<br />
***CRL <7 mm and no [[heartbeat]].<br />
***Mean sac diameter of 16 to 24 mm and no [[embryo]].<br />
***Absence of [[embryo]] with a [[heartbeat]] 7 to 13 days after a [[scan]] that showed a [[gestational sac]] without a [[yolk sac]]<br />
***Absence of [[embryo]] with a heartbeat 7 to 10 days after a scan that showed a [[gestational sac]] with a [[yolk sac]]<br />
***Absence of [[embryo]] ≥6 weeks after [[Menstrual cycle|last menstrual period]]<br />
***[[Amnion|Empty amnion]] (amnion seen adjacent to [[yolk sac]] with no visible [[embryo]])<br />
***Enlarged [[yolk sac]] (>7 mm)<br />
***Small [[gestational sac]] in relation to the size of the [[embryo]] (<5 mm difference between mean sac diameter and CRL)<br />
<br />
===History and Symptoms===<br />
<br />
*Constitutional symptoms including [[fever]] or [[chills]], suggesting septic abortion.<br />
*The history should include when was the date of last menstrual period (LMP), estimated length of [[gestation]], [[bleeding disorders]], previous [[miscarriage]].<br />
<br />
*The symptoms that raise suspicion of abortion are: <br />
**[[Vaginal bleeding]] (the volume of bleeding varies) and [[Abdominal cramping|suprapubic abdominal cramping]] (especially during passage of gestational tissue), passage of clot is an important sign.<br />
**Loss or reduction of [[pregnancy]] symptoms, such as decreased [[Mastalgia|breast tenderness]], [[nausea and vomiting]].<br />
*Asymptomatic discovered incidentally or on routine [[ultrasound]] in early [[pregnancy]].<br />
<br />
===Physical Examination===<br />
<br />
*'''Vital signs'''<br />
<br />
Depends on the amount of [[bleeding]], if severe, the patient will be [[Hemodynamically unstable|hemodynamically unstable.]]<br />
<br />
*'''Pelvic examination''' <br />
**Bimanual examination to determine the status of [[cervix]] and to estimate the [[gestational age]], [[adnexal]] [[tenderness]] or masses or [[cervical motion tenderness]] to exclude [[Ectopic pregnancy|ectopic pregnancy.]]<br />
**[[Speculum|Speculum examination]] to see the source and quantity of [[bleeding]] and whether [[bleeding]] coming from the [[cervix]] and an open [[cervical os]].<br />
**Common [[physical examination]] findings of threatened [[miscarriage]] include vital signs should be within reference ranges, soft and non-tender [[abdomen]], and closed [[Cervical os|internal cervical os]].<br />
**Common [[physical examination]] findings of incomplete [[miscarriage]] include enlarged and soft [[uterus]], dilated and effaced [[cervix]], and products of [[conception]] may be partially present in the [[uterus]], at the [[external os]], or may be present in the [[vagina]].<br />
**Common [[physical examination]] findings of complete miscarriage include a [[Cervix|closed cervix]], and the [[uterus]] should be contracted.<br />
**Common [[physical examination]] findings of missed miscarriage include normal [[vital signs]], the [[uterus]] is small for [[gestational age]], absent fetal [[Heart rate|heart tones]] on [[sonogram]] and [[Cervix|closed cervix]].<br />
<br />
===Laboratory Findings===<br />
<br />
*Laboratory studies may include the following:<ref name="pmid16217116">{{cite journal| author=Murray H, Baakdah H, Bardell T, Tulandi T| title=Diagnosis and treatment of ectopic pregnancy. | journal=CMAJ | year= 2005 | volume= 173 | issue= 8 | pages= 905-12 | pmid=16217116 | doi=10.1503/cmaj.050222 | pmc=1247706 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16217116 }}</ref><br />
**Urine [[Pregnancy test|pregnancy test.]]<br />
**[[Complete blood count]] with differential, [[hemoglobin]] and [[hematocrit]].<br />
**[[Blood type]] and [[Rh factor|Rh factor.]]<br />
*[[Serum]] [[Human chorionic gonadotropin|hCG]] and [[progesterone]] have limited utility in the [[diagnostic]] evaluation of abortion. In general, the [[diagnosis]] of [[pregnancy loss]] is made by an [[Ultrasound (disambiguation)|ultrasound]] (U/S) once the presence of intrauterine [[gestational sac]] is confirmed.<ref name="pmid16217116" /><br />
*An intrauterine [[pregnancy]] may be seen with ([[transvaginal ultrasound]]) (TVUS) at a [[Human chorionic gonadotropin|ß-hCG]] level of 1500-2000 IU/L. However, indeterminate [[pregnancy]] on [[Transvaginal ultrasound|TVUS]] should undergo [[Human chorionic gonadotropin|ß-hCG]] level testing and if [[Human chorionic gonadotropin|ß-hCG]] levels <1500 repeat hCG in 2 days, if [[Human chorionic gonadotropin|ß-hCG]] levels >1500, do [[Transvaginal ultrasound|TVUS]] again.<ref name="pmid16217116" /><br />
*[[Ultrasound (disambiguation)|U/S]] is the most accurate [[diagnostic]] modality in the confirmation of a viable [[pregnancy]] during the [[First trimester|first trimester.]]<br />
*An empty [[uterus]] revealed by U/S in a pregnant woman with positive [[beta-hCG]], suggests a very [[Early pregnancy factor|early pregnancy]] < 3 wk, a completed miscarriage, or an [[ectopic pregnancy]].<ref name="pmid16217116" /><br />
<br />
===Electrocardiogram===<br />
There are no [[ECG]] findings associated with abortion.<br />
<br />
===X-ray===<br />
There are no [[x-ray]] findings associated with abortion.<br />
<br />
===Abdominal/ trans-vaginal Ultrasound <ref name="pmid10696563">{{cite journal| author=Helm TN, Wirth PB, Helm KF| title=Inexpensive digital photography in clinical dermatology and dermatologic surgery. | journal=Cutis | year= 2000 | volume= 65 | issue= 2 | pages= 103-6 | pmid=10696563 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10696563 }}</ref><ref name="pmid1873233X">{{cite journal| author=Schmidt ML, Smith HE, Gamerman S, DiMichele D, Glazer S, Scott JP| title=Prolonged recombinant activated factor VII (rFVIIa) treatment for severe bleeding in a factor-IX-deficient patient with an inhibitor. | journal=Br J Haematol | year= 1991 | volume= 78 | issue= 3 | pages= 460-3 | pmid=1873233X | doi=10.1111/j.1365-2141.1991.tb04468.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1873233 }}</ref>===<br />
<br />
*Findings on an [[ultrasound]] suggestive of nonviable [[pregnancy]] include [[gestational sac]] >25-mm mean sac diameter on [[Sonogram|transabdominal sonogram]]; >16-mm MSD on endovaginal [[sonogram]] without a detectable [[embryo]], [[embryo]] without a [[heartbeat]], hyperechoic material within the uterine cavity.<br />
*An incomplete miscarriage on [[ultrasound]] shows [[gestational sac]] misshaped or collapsed, an irregular complex mass within the [[endometrial]] or cervical canal may be present or echogenic material in the endometrial canal.<br />
*A complete miscarriage may demonstrate an empty [[uterus]] noted on [[transvaginal ultrasound]].<br />
<br />
===CT scan===<br />
There are no [[CT scan]] findings associated with abortion. However, a [[CT scan]] may be helpful in the [[diagnosis]] of [[complications]] like [[uterine rupture]].<ref name="pmid22383917">{{cite journal| author=Themistoklis SN, Chrysovalantis V, Stylianos A, Nikolaos KL, Efthymia A| title=CT Diagnosis of an Abortion-Related Retroperitoneal Space Abscess. | journal=J Clin Med Res | year= 2011 | volume= 3 | issue= 5 | pages= 268-9 | pmid=22383917 | doi=10.4021/jocmr509w | pmc=3279491 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22383917 }}</ref><br />
<br />
===MRI===<br />
The use of a [[MRI]] in maternal emergency obstetric conditions is relatively limited, a [[MRI]] has a role where [[Sonogram|USG]] is indeterminate, particularly in [[ectopic pregnancy]].<ref name="pmid27081223">{{cite journal| author=Gupta R, Bajaj SK, Kumar N, Chandra R, Misra RN, Malik A | display-authors=etal| title=Magnetic resonance imaging - A troubleshooter in obstetric emergencies: A pictorial review. | journal=Indian J Radiol Imaging | year= 2016 | volume= 26 | issue= 1 | pages= 44-51 | pmid=27081223 | doi=10.4103/0971-3026.178292 | pmc=4813073 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27081223 }}</ref> <br />
<br />
===Other Imaging Findings===<br />
There are no other [[imaging]] findings associated with abortion.<br />
<br />
===Other Diagnostic Studies===<br />
There are no other [[diagnostic]] studies associated with abortion.<br />
<br />
==Treatment==<br />
<br />
===Expectant management===<br />
<br />
*Waiting for [[pregnancy]] tissue to pass recommended only in the [[first trimester]], after 13 weeks, [[medication]] management in a health facility or surgical management should be considered.<br />
*[[Pain management]] in the [[first trimester]] is typically [[Non-steroidal anti-inflammatory drug|nonsteroidal anti-inflammatory drugs]] for [[pain]].<br />
*Follow-up to confirm complete passage of gestational tissue by [[ultrasound]].<br />
*Incomplete [[uterine]] emptying still require [[uterine]] aspiration.<br />
*Administer [[Rho(D) Immune Globulin|RhoGAM]] to women with [[Rh incompatibility (patient information)|Rh-negative]] and is experiencing [[vaginal bleeding]]<br />
<br />
===Medical Therapy===<br />
<br />
*'''Up to 13 weeks of gestation''':<ref name="pmid29874535">{{cite journal| author=Schreiber CA, Creinin MD, Atrio J, Sonalkar S, Ratcliffe SJ, Barnhart KT| title=Mifepristone Pretreatment for the Medical Management of Early Pregnancy Loss. | journal=N Engl J Med | year= 2018 | volume= 378 | issue= 23 | pages= 2161-2170 | pmid=29874535 | doi=10.1056/NEJMoa1715726 | pmc=6437668 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29874535 }}</ref><ref name="urlMiscarriage - StatPearls - NCBI Bookshelf4">{{cite web |url=https://www.ncbi.nlm.nih.gov/books/NBK532992/#!po=5.55556 |title=Miscarriage - StatPearls - NCBI Bookshelf |format= |work= |accessdate=}}</ref><br />
**[[mifepristone]] followed by [[misoprostol]] 24 hours later.<br />
**'''Dose:''' [[mifepristone]] 200 mg orally followed in 24 hours by [[misoprostol]] 800 mcg per [[vagina]] (typically given as four 200 mcg tablets).<br />
**[[Antibiotics]] are not recommended for routine medication management of abortion.<ref name="urlapps.who.int">{{cite web |url=https://apps.who.int/iris/bitstream/handle/10665/70914/9789241548434_eng.pdf?sequence=1 |title=apps.who.int |format= |work= |accessdate=}}</ref><br />
**[[Pain]] management with [[Non-steroidal anti-inflammatory drug|nonsteroidal anti-inflammatory drug (NSAID)]] prior to using [[misoprostol]].<ref name="urlapps.who.int" /><br />
**[[Misoprostol]] alone regemin 800 mcg per [[vagina]] (typically four 200 mcg tablets). For patients who do not have complete expulsion after a single dose, a second dose can be given. Between 9 and 12 weeks, the [[World Health Organization|World Health Organization (WHO)]] recommends an initial 800 mcg dose of [[misoprostol]] followed by 400 mcg every three hours until expulsion.<ref name="urlapps.who.int" /><br />
<br />
*'''13 to 20 weeks of gestation'''<br />
**Regardless of the gestational age, medication management of [[pregnancy loss]] includes [[mifepristone]] and [[misoprostol]]. The difference is that the [[misoprostol]] dose is often reduced and repeated, and should be done in a health facility.<br />
<br />
{| class="wikitable"<br />
|+Guideline for safe abortion according to [[WHO]]<ref name="urlapps.who.int" /><br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Recommended methods for medical abortion<br />
|-<br />
|'''The recommended method for medical abortion is [[mifepristone]] followed by [[misoprostol]].'''<br />
|-<br />
|[[Gestational age]] up to 9 weeks the recommended method for medical abortion is [[mifepristone]] followed 1 to 2 days later by [[misoprostol]]<br />
|-<br />
|[[Dosage|Dosages]] and recommendation <br />
<br />
*[[Mifepristone]] should always be administered orally. The recommended dose is 200 mg.<br />
*Administration of [[misoprostol]] is recommended 1 to 2 days (24 to 48 hours) following ingestion of [[mifepristone]].<br />
**For [[vaginal]], [[sublingual]] routes, the recommended dose of [[misoprostol]] is 800 μg.<br />
**For oral administration, the recommended dose of [[misoprostol]] is 400 μg.<br />
**With gestations up to 7 weeks [[misoprostol]] may be administered by [[vaginal]], [[sublingual]] or oral routes. After 7 weeks of [[gestation]], oral administration of [[misoprostol]] should not be used.<br />
**With [[Gestation|gestations]] up to 9 weeks [[misoprostol]] can be administered by [[vaginal]], [[sublingual]] routes.<br />
|-<br />
|'''For [[pregnancies]] of [[gestational age]] between 9 and 12 weeks''' <br />
*The recommended method for medical abortion is 200 mg [[mifepristone]] administered orally followed 36 to 48 hours later by 800 μg [[misoprostol]] administered [[Vaginal|vaginally]].<br />
*Subsequent [[misoprostol]] doses should be 400 μg, administered either [[Vaginal|vaginally]] or [[Sublingual|sublingually]], every 3 hours up to four further doses, until expulsion of the products of [[conception]].<br />
|-<br />
|'''For [[pregnancies]] of [[gestational age]] over 12 weeks''' <br />
The recommended method for medical abortion is 200 mg [[mifepristone]] administered orally followed 36 to 48 hours later by repeated doses of [[misoprostol]]. <br />
<br />
*[[Gestation|Gestations]] between 12 and 24 weeks, the initial [[misoprostol]] dose following oral [[mifepristone]] administration may be either 800 μg administered [[Vaginal|vaginally]] or 400 μg administered orally. Subsequent [[misoprostol]] doses should be 400 μg, administered either [[Vaginal|vaginally]] or sublingually, every 3 hours up to four further doses.<br />
<br />
*For [[pregnancies]] beyond 24 weeks, the dose of [[misoprostol]] should be reduced, due to the greater [[sensitivity]] of the [[uterus]] to [[prostaglandins]], but the lack of [[clinical]] studies precludes specific dosing recommendations.<br />
|}<br />
<br /><br />
===Surgery===<br />
<br />
*[[Surgery]] evacuation with sharp [[curettage]] or [[suction curettage]] is not the first-line treatment option for [[patients]] with early [[pregnancy loss]].<br />
*[[Surgery]] is usually reserved for [[patients]] with either [[hemorrhage]], [[hemodynamic instability]], or [[signs]] of [[infection]].<ref name="pmid18053098">{{cite journal| author=Wen J, Cai QY, Deng F, Li YP| title=Manual versus electric vacuum aspiration for first-trimester abortion: a systematic review. | journal=BJOG | year= 2008 | volume= 115 | issue= 1 | pages= 5-13 | pmid=18053098 | doi=10.1111/j.1471-0528.2007.01572.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18053098 }}</ref><br />
*This is also the preferred method of treatment for women with comorbid [[conditions]] such as [[cardiovascular disease]], [[infection]], [[Anemia|severe anemia]], or [[bleeding]] disorders.<br />
<br />
{| class="wikitable"<br />
|+Guideline for safe abortion according to WHO<ref name="urlapps.who.int2">{{cite web |url=https://apps.who.int/iris/bitstream/handle/10665/70914/9789241548434_eng.pdf?sequence=1 |title=apps.who.int |format= |work= |accessdate=}}</ref><br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Recommended methods of abortion for [[pregnancies]] of [[gestational age]] over 12 to 14 weeks<br />
|-<br />
|[[Dilation and curettage|Dilatation and evacuation]] (D&E) and medical methods ([[mifepristone]] and [[misoprostol]]; [[misoprostol]] alone) are both recommended methods for abortion for gestation over 12 to 14 weeks. Facilities should offer at least one, and preferably both methods, if possible, depending on provider experience and the availability of training.<br />
|}<br />
<br />
*[[Antibiotic|Antibiotic prophylaxis]] should be given before surgical [[Evacuation of retained products of conception|evacuation]]<br />
<br />
{| class="wikitable"<br />
|+<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Guidelines for antibiotic prophylaxis prior uterine evacuation with vacuum aspiration<ref name="urlwww.rcog.org.uk">{{cite web |url=https://www.rcog.org.uk/globalassets/documents/guidelines/best-practice-papers/best-practice-paper-2.pdf |title=www.rcog.org.uk |format= |work= |accessdate=}}</ref><br />
|-<br />
|'''If there is no suspicion of [[infection]] and [[Uterine|uterine size]] is less than 14 weeks'''<br />
|-<br />
|Antibiotic prophylaxis should be given before [[surgical]] evacuation <br />
<br />
*200 mg [[doxycycline]] within 2 hours before the [[procedure]] or<br />
*A single dose of 500 mg [[azithromycin]] within 2 hours before the [[procedure]]<br />
<br />
(NB. If [[antibiotics]] are not available, the procedure should not be delayed.)<br />
|-<br />
|'''If there is no suspicion of [[infection]] and [[uterine]] size is 14 weeks or larger'''<br />
*[[Antibiotic]] prophylaxis should be given before [[surgical]] [[Evacuation of retained products of conception|evacuation]] <br />
**200 mg [[doxycycline]] within 2 hours before the [[procedure]] (with or without 200 mg [[doxycycline]] after the abortion) or<br />
**A single dose of 500 mg [[azithromycin]] within 2 hours before the [[procedure]]<br />
|}<br />
===Primary Prevention===<br />
Effective measures for the [[primary prevention]] of unsafe abortion include :<ref name="pmid22883917">{{cite journal| author=Faúndes A| title=Strategies for the prevention of unsafe abortion. | journal=Int J Gynaecol Obstet | year= 2012 | volume= 119 Suppl 1 | issue= | pages= S68-71 | pmid=22883917 | doi=10.1016/j.ijgo.2012.03.021 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22883917 }}</ref><br />
<br />
*Use of [[contraception]] has been shown an effective decrease in the abortion rate.<br />
*[[Sexual]] [[education]] programs.<br />
*Easy access to [[contraception]].<br />
*Social protection to reduce induced abortion among pregnant women who have been abandoned by their partners, rejected by their families.<br />
<br />
===Secondary Prevention===<br />
The only way to prevent an unsafe abortion is to provide safe services for [[termination of pregnancy]].<ref name="pmid22883917" /><br />
<br />
==References==<br />
{{reflist|2}}<br />
<br />
[[Category:Primary care]]<br />
[[Category:Obstetrics]]<br />
[[Category:Medicine]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Bruxism&diff=1694513Bruxism2021-03-15T18:12:28Z<p>Caroline Collis: </p>
<hr />
<div><div style="-webkit-user-select: none;"><br />
{| class="infobox" style="position: fixed; top: 65%; right: 10px; margin: 0 0 0 0; border: 0; float: right;"<br />
|-<br />
|{{#ev:youtube|https://https://www.youtube.com/watch?v=SsdM13B3PdI|350}}<br />
|-<br />
|}<br />
__NOTOC__<br />
<br />
'''For patient information click [[Bruxism (patient information)|here]]'''<br />
<br />
{{Infobox_Disease<br />
| Name = {{PAGENAME}}<br />
| Image = <br />
| Caption = <br />
| DiseasesDB = 29661<br />
| ICD10 = <br />
| ICD9 = <br />
| ICDO = <br />
| OMIM = <br />
| MedlinePlus = 001413<br />
| MeshID = <br />
}}<br />
{{SI}}<br />
{{CMG}} ; {{AE}} {{ADG}}<br />
<br />
==Overview==<br />
Bruxism is defined as repeated involuntary grinding and clenching of [[teeth]] which can occur either diurnal or nocturnally. In 1907, Marie Pielkiewics coined the French term 'La Bruxomanie" for bruxism. Bruxism can be classified into awake bruxism and sleep bruxism based on the [[physiological]] [[sleep]] status of the individual. The [[etiology]] of bruxism can be categorized into three groups:[[psychosocial]] factors, peripheral factors, and [[pathophysiological]] factors. Multifactorial [[etiology]] causes involving [[brain]] [[neurotransmitters]] or [[basal ganglia]]. Bruxism affects [[men]] and [[women]] equally. Factors associated with an increased risk of bruxism include [[obstructive sleep apnea]], [[alcohol abuse]], [[caffeine]] intake, [[smoking]], and [[anxiety]]. The [[symptoms]] of bruxism usually develop in the first decade of life, and start with the appearance of the first primary upper and lower anterior [[teeth]]. Common [[complications]] of bruxism are [[tooth]] wear, and [[tooth]] hypersensitivity. Bruxism is primarily diagnosed based on the [[clinical]] presentation. History of complaints of disturbance from the clicking or grating sound by the accompanied partners. The most common [[symptoms]] of bruxism include involuntary rhythmic contractions of the masticator [[muscle]]<nowiki/>s during [[sleep]]. Removal of any offending agent responsible for bruxism is the primary step in the management. [[Surgery]] is the mainstay of [[treatment]] in the management of bruxism.<br />
==Historical Perspective==<br />
<br />
*In 1907, Marie Pielkiewics coined the French term 'La Bruxomanie" for bruxism. <ref name="pmid21886404">{{cite journal |vauthors=Shetty S, Pitti V, Satish Babu CL, Surendra Kumar GP, Deepthi BC |title=Bruxism: a literature review |journal=J Indian Prosthodont Soc |volume=10 |issue=3 |pages=141–8 |date=September 2010 |pmid=21886404 |pmc=3081266 |doi=10.1007/s13191-011-0041-5 |url=}}</ref><br />
*In 1931, Frohman first coined the English term bruxism.<br />
<br />
==Classification==<br />
Bruxism can be classified into awake bruxism and [[sleep]] bruxism based on the [[physiological]] [[sleep]] status of the individual.<ref name="pmid22976557">{{cite journal |vauthors=Thorpy MJ |title=Classification of sleep disorders |journal=Neurotherapeutics |volume=9 |issue=4 |pages=687–701 |date=October 2012 |pmid=22976557 |pmc=3480567 |doi=10.1007/s13311-012-0145-6 |url=}}</ref><ref name="pmid12531159">{{cite journal |vauthors=Bader G, Lavigne G |title=Sleep bruxism; an overview of an oromandibular sleep movement disorder. REVIEW ARTICLE |journal=Sleep Med Rev |volume=4 |issue=1 |pages=27–43 |date=February 2000 |pmid=12531159 |doi=10.1053/smrv.1999.0070 |url=}}</ref><br />
{| class="wikitable"<br />
|+<br />
!Awake Bruxism/Diurnal Bruxism<br />
!Sleep Bruxism/Nocturnal Bruxism<br />
|-<br />
|Day Time /Awake<br />
|[[Sleep]]<br />
|-<br />
|Semi-Voluntary<br />
|Stereotyped<br />
|-<br />
|Clenching predominant<br />
|[[Teeth]] grinding<br />
|}<br />
{| class="wikitable"<br />
|+<br />
! colspan="2" |Definitions<br />
|-<br />
|American Academy of Orofacial Pain (2008)<br />
|[[Diurnal]] or [[nocturnal]] [[Parafunctional habit|parafunctional]] activity including clenching, bracing, gnashing, and grinding of the [[teeth]]. I<br />
|-<br />
|The Academy of Prosthodontics (2005)<br />
|<br />
*1. The [[Parafunctional habit|parafunctional]] grinding of [[teeth]].<br />
*2. An [[oral]] habit consisting of involuntary rhythmic or spasmodic non-functional gnashing, grinding or clenching of [[teeth]], in other than [[chewing]] movements of the [[mandible]], which may lead to occlusal [[trauma]] – called also [[tooth]] grinding, occlusal neurosis<br />
|-<br />
|The International Classification of Sleep Disorders (2005)<br />
|Sleep-related bruxism is an [[oral]] activity characterized by grinding or clenching of the [[teeth]] during [[sleep]], usually associated with sleep arousals.<br />
|}<br />
<br />
==Causes==<br />
The [[etiology]] of bruxism can be categorized into three groups: [[psychosocial]] factors, peripheral factors, and pathophysiological factors.<ref name="pmid12531159">{{cite journal |vauthors=Bader G, Lavigne G |title=Sleep bruxism; an overview of an oromandibular sleep movement disorder. REVIEW ARTICLE |journal=Sleep Med Rev |volume=4 |issue=1 |pages=27–43 |date=February 2000 |pmid=12531159 |doi=10.1053/smrv.1999.0070 |url=}}</ref><br />
<br />
{| class="wikitable"<br />
|+<br />
! colspan="2" |Etiology of Bruxism<br />
|-<br />
|[[Psychological]]<br />
|Common [[psychological]] factors responsible for bruxism include:<br />
<br />
*[[Stress]]-induced bruxism<br />
*[[Depression]]-associated bruxism<br />
*[[Anxiety]]-related bruxism<br />
|-<br />
|Peripheral<br />
|<br />
*[[Caffeine]] intake<br />
*[[Smoking]]<br />
*[[Alcohol consumption]]<br />
|-<br />
|[[Pathological]]<br />
|<br />
*Problem with arousal mechanism during [[sleep]]<br />
*Imbalance in the [[dopamine]] release in the [[basal ganglion]]<br />
*<br />
|}<br />
==Pathophysiology==<br />
<br />
*Bruxism is caused by the activation of [[reflex]]ive [[chewing]] activity<ref name="pmid18557915">{{cite journal |vauthors=Lavigne GJ, Khoury S, Abe S, Yamaguchi T, Raphael K |title=Bruxism physiology and pathology: an overview for clinicians |journal=J Oral Rehabil |volume=35 |issue=7 |pages=476–94 |date=July 2008 |pmid=18557915 |doi=10.1111/j.1365-2842.2008.01881.x |url=}}</ref><br />
*[[Mastication|Chewing]] is a [[neuromuscular]] activity that is controlled by the [[reflex]] [[nerve]] pathways.<br />
*During [[sleep]], the [[reflex]] part is active while the higher control is inactive, resulting in bruxism.<br />
*As stated, bruxism is considered to have multifactorial [[etiology]]. Multifactorial [[etiology]] causes involving [[brain]] [[neurotransmitters]] or [[basal ganglia]].<br />
*'''Pathophysiological Factors'''<br />
**As bruxism often occurs during [[sleep]], the [[physiology]] of [[sleep]] has been studied extensively, especially the ‘arousal response’, in search of possible [[causes]] of a disorder.<ref name="pmid18557915">{{cite journal |vauthors=Lavigne GJ, Khoury S, Abe S, Yamaguchi T, Raphael K |title=Bruxism physiology and pathology: an overview for clinicians |journal=J Oral Rehabil |volume=35 |issue=7 |pages=476–94 |date=July 2008 |pmid=18557915 |doi=10.1111/j.1365-2842.2008.01881.x |url=}}</ref><br />
**Arousal response is a sudden change in the depth of the [[sleep]] during which the individual either arrives in the lighter [[sleep]] stage or actually wakes up.<br />
**Such a response is accompanied by gross body movements, increased [[heart rate]], [[respiratory]] changes, and increased [[muscle]] activity.<br />
**It is derived that disturbances in the central [[neurotransmitter system]] may be involved in the [[etiology]] of bruxism.<br />
**It is hypothesized that the direct and indirect pathways of the [[basal ganglion]], a group of five subcortical nuclei that are involved in the coordination of movements, is disturbed in bruxer.<br />
**The direct output pathway goes directly from the stratum to the [[thalamus]] from where afferent signals project to the [[cerebral cortex]]. The indirect pathway, on the other hand, passes by several other nuclei before reaching it to the [[thalamus]].<br />
**If there is an imbalance between the pathways, movement disorder results like [[Parkinson’s disease]].<br />
**The imbalance occurs with the disturbances in the [[dopamine]]-mediated transmission of an [[action potential]]. In the case of bruxism there may be an imbalance in both pathways.<br />
**Acute use of [[dopamine]] precursors like [[L-dopa]] inhibits bruxism activity and chronic long-term use of [[l-dopa]] results in increased bruxism activity. SSRTs ([[serotonin reuptake inhibitors]]), which exert an indirect influence on the [[dopaminergic system]], may cause bruxism after long-term use.<br />
**[[Amphetamine]], which increases the [[dopamine]] concentration by facilitating its release has been observed to increase bruxism.<br />
**[[Nicotine]] stimulates central [[dopaminergic]] activities, which might explain the finding that [[Cigarette smoking|cigarette smokers]] report bruxism two times more than the nonsmokers.<br />
<br />
*'''Psychosocial Factors'''<br />
**There is no proper description of conclusive nature of [[psychological]] factors role in bruxism because of the absence of large scale longitudinal trials.<br />
<br />
===Associated Factors===<br />
<br />
*Disturbed [[sleep]] pattern/other [[sleep disorder]]s<ref name="Riskfactors-Stanford">Maurice M. Ohayon, MD, DSc, PhD; Kasey K. Li, DDS, MD and Christian Guilleminault, MD: "[http://www.chestjournal.org/cgi/content/full/119/1/53 Risk Factors for Sleep Bruxism in the General Population]";Stanford University School of Medicine, Sleep Disorders Center, Stanford, CA;</ref><ref>Y. Kobayashi, M. Yokoyama, H. Shiga, and N. Namba: [http://iadr.confex.com/iadr/2004Hawaii/techprogram/abstract_44562.htm 1198 Sleep Condition and Bruxism in Bruxist], Nippon Dental University, Tokyo, Japan</ref> ([[obstructive sleep apnea]],<ref>Oksenberg A, Arons E.: "[http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=14592147&itool=iconabstr&itool=pubmed_docsum&query_hl=2 Sleep bruxism related to obstructive sleep apnea: the effect of continuous positive airway pressure.]";Sleep Disorders Unit, Loewenstein Hospital-Rehabilitation Center, P.O. Box 3, Raanana, Israel</ref> [[snoring]],<ref>Ng DK, Kwok KL, Poon G, Chau KW "[http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=12683350&itool=iconabstr&itool=pubmed_docsum&query_hl=2 Habitual snoring and sleep bruxism in a paediatric outpatient population in Hong Kong.]" Department of Paediatrics, Kwong Wah Hospital, Waterloo Road, Hong Kong, SAR China.</ref> moderate daytime [[Somnolence|sleepiness]]<ref name="Riskfactors-Stanford" />)<br />
*[[Malocclusion]], in which the upper and lower [[teeth]] fit together in a dysfunctional way, typically through lateral asymmetry and dysocclusion of the front [[teeth]] through premature contact of back [[teeth]].<!--My text here needs to be reworded more technically--><br />
*Relatively high levels of consumption of caffeinated drinks and foods, such as [[coffee]], colas, and [[chocolate]]<ref name="Riskfactors-Stanford" /><br />
*High levels of [[alcohol consumption]]<ref name="Riskfactors-Stanford" /><br />
*[[Smoking]]<ref name="Riskfactors-Stanford" /><br />
*High levels of [[anxiety]] and/or [[Stress (medicine)|stress]]<ref name="Riskfactors-Stanford" /><br />
*[[SSRI]]s<br />
*[[Digestive]] problems<!--bit vague; reference?--><br />
*Hypersensitivity of the [[dopamine]] receptors in the [[brain]].<br />
*Consumption of stimulant drugs and medications, such as those of the [[amphetamine]]-based family, such as [[MDMA]]<ref name="Riskfactors-Drugs">Winocur E, Gavish A, Voikovitch M, Emodi-Perlman A, Eli I: "[http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=12836498&dopt=AbstractPlus Drugs and bruxism: a critical review.]";Department of Occlusion and Behavioral Sciences, Maurice and Gabriela Goldschleger, School of Dental Medicine, Tel Aviv University, Tel Aviv, Israel.</ref><br />
*Excessive use of (i.e., frequent redosing and dependency on) [[gamma-Hydroxybutyric acid|GHB]] and similar [[GABA]]-inducing analogues such as [[Phenibut]] <ref name="Riskfactors-Drugs" /><br />
*Disorders such as [[Huntington's disease|Huntington's]] and [[Parkinson's disease]]s <ref>[http://www.mayoclinic.com/health/bruxism/DS00337 Bruxism/Teeth grinding - MayoClinic.com<!-- Bot generated title -->]</ref><br />
<br />
<br /><br />
<br />
==Epidemiology and Demographics==<br />
Bruxism often occurs during [[sleep]] and can even occur during short naps. Bruxism is one of the most common [[Sleep disorders|sleep disorder]]<nowiki/>s: 30 to 40 million Americans grind their [[teeth]] during sleep.<br />
====Gender====<br />
<br />
*Bruxism affects [[men]] and [[women]] equally.<br />
<br />
====Age====<br />
<br />
*Bruxism commonly affects individuals younger than 6 years of [[age]] and its [[incidence]] declines as [[age]] increases.<br />
*<br />
<br />
==Screening==<br />
There is insufficient evidence to recommend routine [[screening]] for bruxism.<br />
==Risk Factors==<br />
Factors associated with an increased risk of bruxism include:<br />
<br />
*[https://www.wikidoc.org/index.php/Obstructive_sleep_apnea Obstructive sleep apnea]<br />
*[https://www.wikidoc.org/index.php/Alcohol_abuse Alcohol abuse]<br />
*[[Caffeine]] intake<br />
*[https://www.wikidoc.org/index.php/Smoking Smoking]<br />
*[https://www.wikidoc.org/index.php/Anxiety Anxiety]<br />
<br />
==Natural History, Complications and Prognosis==<br />
===Natural History===<br />
<br />
*The [[symptoms]] of bruxism, usually develop in the first decade of life, and start with [[symptoms]] such as appearance of the first primary upper and lower anterior [[teeth]].<br />
*The [[symptoms]] of bruxism typically develop in [[childhood]] and may persist into [[adult]] due to presence of other [[risk factors]].<br />
*Usually bruxism follows a [[benign]] course.<br />
*If left untreated, bruxism can lead to [[hypertrophy]] of [[masseter muscle]] accompanied by tenderness of [[TMJ]], which manifests as [[otalgia]].<br />
<br />
===Complications===<br />
Common [[complications]] of bruxism are:<br />
<br />
*Tooth wear<br />
*[[Tooth]] hypersensitivity<br />
*[[Tooth]] mobility<br />
*[[Pain]] in the [[temporomandibular joint]] (TMJ) or [[jaw]] musculature<br />
*Temporal [[headache]],<br />
*Poor [[sleep]]<br />
*Signs of this parafunctional habit<br />
**Indentation on the [[tongue]]<br />
**Presence of [[linea alba]] along the biting plane of the [[buccal mucosa]]<br />
**[[Gingival]] recessions<br />
<br />
==Diagnosis==<br />
===Diagnostic study of choice===<br />
Bruxism is primarily diagnosed based on the clinical presentation.<br />
<br />
*History of tooth grinding during [[sleep]]<br />
*Confirmation by parents or bed partners.<br />
<br />
<br /><br />
===History===<br />
<br />
*History of complaints of disturbance from the clicking or grating sound by the accompanied partners.<br />
<br />
===Symptoms===<br />
The most common [[symptoms]] of bruxism include:<ref name="MacedoMacedo2014">{{cite journal|last1=Macedo|first1=Cristiane R|last2=Macedo|first2=Elizeu C|last3=Torloni|first3=Maria R|last4=Silva|first4=Ademir B|last5=Prado|first5=Gilmar F|last6=Macedo|first6=Cristiane R|title=Pharmacotherapy for sleep bruxism|year=2014|doi=10.1002/14651858.CD005578.pub2}}</ref><br />
<br />
*Involuntary rhythmic contractions of the masticator muscles during [[sleep]].<br />
*Secondary [[symptoms]] may develop due to forceful grinding in some [[patients]] which include:<br />
**Morning [[headaches]]<br />
**[[Jaw pain]]<br />
**Clicking in the [[temporomandibular joint]]<nowiki/>s<br />
*[[Dental]] deformities may be seen, however not [[disease]] specific, and not limited to:<br />
**Thermal sensitivity in the [[teeth]]<br />
**Hypermobility<br />
**Need for [[dental]] restorations<br />
**[[Tooth]] wear on [[tooth]] surfaces that contact during biting or [[chewing]]<br />
**Lateral grinding forces in particular can be particularly destructive.<br />
*Severe cases of bruxism do present with:<br />
**Injury to soft tissues of the [[mouth]]<br />
**[[Dental fractures]]<br />
**Difficulty with [[chewing]]<br />
**[[Temporomandibular joint]] [[pain]] and dysfunction<br />
**[[Head]] and [[neck pain]]<br />
<br />
===Physical Examination===<br />
Patients with bruxism usually appear normal.<br />
<br />
===Laboratory Findings===<br />
There are no diagnostic [[laboratory]] findings associated with bruxism.<br />
<br />
===Electrocardiogram===<br />
There are no [[ECG]]findings associated with bruxism.<br />
<br />
===X-ray===<br />
There are no [[x-ray]] findings associated with bruxism.<br />
<br />
===Echocardiography or Ultrasound===<br />
There are no [[echocardiography]]/[[ultrasound]] findings associated with bruxism .<br />
<br />
===CT scan===<br />
There are no [[CT scan]] findings associated with bruxism.<br />
<br />
===MRI===<br />
There are no [[MRI]] findings associated with bruxism.<br />
<br />
===Other Imaging Findings===<br />
There are no other imaging findings associated with bruxism.<br />
<br />
===Other Diagnostic Studies===<br />
There are no other diagnostic studies associated with bruxism.<br />
<br />
==Treatment==<br />
===Medical Therapy===<br />
<br />
*Removal of any offending agent responsible for bruxism is the primary step in management.<ref name="MacedoMacedo2014">{{cite journal|last1=Macedo|first1=Cristiane R|last2=Macedo|first2=Elizeu C|last3=Torloni|first3=Maria R|last4=Silva|first4=Ademir B|last5=Prado|first5=Gilmar F|last6=Macedo|first6=Cristiane R|title=Pharmacotherapy for sleep bruxism|year=2014|doi=10.1002/14651858.CD005578.pub2}}</ref><ref name="pmid21356412">{{cite journal |vauthors=Ommerborn MA, Taghavi J, Singh P, Handschel J, Depprich RA, Raab WH |title=Therapies most frequently used for the management of bruxism by a sample of German dentists |journal=J Prosthet Dent |volume=105 |issue=3 |pages=194–202 |date=March 2011 |pmid=21356412 |doi=10.1016/S0022-3913(11)60029-2 |url=}}</ref><ref name="pmid17949541">{{cite journal |vauthors=Huynh N, Manzini C, Rompré PH, Lavigne GJ |title=Weighing the potential effectiveness of various treatments for sleep bruxism |journal=J Can Dent Assoc |volume=73 |issue=8 |pages=727–30 |date=October 2007 |pmid=17949541 |doi= |url=}}</ref><br />
<br />
*The wait-and-see approach is recommended in cases with medically induced bruxism, as spontaneous remission is ensured with the cessation of the offending agent.<br />
*[[Pharmacotherapy]] mainly concentrated to alleviate [[symptoms]]<br />
*[[Buspirone]] and [[Gabapentin]] are the two recommended medications to manage bruxism<br />
**Preferred regimen 1 : [https://www.wikidoc.org/index.php/Buspirone Buspirone] 15 to 20 mg/day PO q12.<br />
**Preferred regimen 2: [https://www.wikidoc.org/index.php/Gabapentin Gabapentin] 100 to 300 mg PO q24<br />
<br />
===Surgery===<br />
Surgery is the mainstay of treatment in the management of bruxism.<br />
====Indications====<br />
<br />
<br />
The treatment of bruxism is indicated when there are any of these possible consequences:<ref name="MacedoMacedo2014">{{cite journal|last1=Macedo|first1=Cristiane R|last2=Macedo|first2=Elizeu C|last3=Torloni|first3=Maria R|last4=Silva|first4=Ademir B|last5=Prado|first5=Gilmar F|last6=Macedo|first6=Cristiane R|title=Pharmacotherapy for sleep bruxism|year=2014|doi=10.1002/14651858.CD005578.pub2}}</ref><ref name="pmid21356412">{{cite journal |vauthors=Ommerborn MA, Taghavi J, Singh P, Handschel J, Depprich RA, Raab WH |title=Therapies most frequently used for the management of bruxism by a sample of German dentists |journal=J Prosthet Dent |volume=105 |issue=3 |pages=194–202 |date=March 2011 |pmid=21356412 |doi=10.1016/S0022-3913(11)60029-2 |url=}}</ref><br />
<br />
*Mechanical wear of the [[teeth]], which results in loss of occlusal morphology and flattening of the occlusal surfaces<br />
*Hypersensitive [[teeth]]<br />
*Loss of [[periodontal]] support<br />
*[[Tooth]] fractures<br />
*Restorations fractures, usually class I and class II restorations, fracture of [[crown]]s, and fixed partial [[prosthesis]]<br />
*Restorations or [[dental implant]]s failure<br />
*Hypertrophy of [[masticatory muscles]]<br />
*Tenderness and stiffness in [[jaw]] [[muscles]]<br />
*When bruxism leads to limited [[mouth]] opening<br />
*[[Temporomandibular]][[pain]]<br />
*[[Pain]] in the [[preauricular]] region<br />
<br />
<br /><br />
<br />
==References==<br />
{{reflist|2}}<br />
<br />
[[Category:Sleep disorders]]<br />
[[Category:Neurology]]<br />
[[Category:Psychiatry]]<br />
[[Category:Up-To-Date]]<br />
<br />
{{WikiDoc Help Menu}}<br />
{{WikiDoc Sources}}</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Vomiting_in_children&diff=1692160Vomiting in children2021-02-26T15:12:24Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{SI}} <br />
{{CMG}} {{AE}} [[Adenike Eketunde]]<br />
<br />
{{SK}} Vomiting in kids<br />
<br />
==Overview==<br />
Vomiting in children is common and can range from a [[benign]] condition to a life-threatening condition. Most cases of vomiting are [[gastrointestinal]] in origin, most commonly [[gastroesophageal reflux disease]] and [[gastroenteritis]].<br />
Vomiting, also known as [[emesis]], is the oral expulsion of [[gastrointestinal]] content from the mouth due to the [[gut]] and thoracoabdominal wall muscles' contraction. At the same time, [[nausea]] refers to the need to vomit. [[Retching]] is used to describe the muscular event of vomiting with the expulsion of [[vomitus]].<br />
<br />
==Historical Perspective==<br />
<br />
There is limited information about the historical perspective of vomiting in children.<br />
<br />
==Classification==<br />
Vomiting in children may be classified according to the content of vomitus, motion, and duration into:<br />
<br />
*Bloody and non-bloody<br />
*[[Bilious]] and non-bilious<br />
*Projectile and non-projectile<br />
*[[Acute]] and [[chronic]] <ref name="AndradeMarin2020">{{cite journal|last1=Andrade|first1=Gabriela Bonente Herculano de|last2=Marin|first2=Barbara Said|last3=Medeiros|first3=Daniela Nasu Monteiro|last4=Yamanari|first4=Mauricio Gustavo Ieiri|last5=Troster|first5=Eduardo Juan|title=Vomiting in newborns as a result of a duodenal membrane: two case reports|journal=Einstein (São Paulo)|volume=18|year=2020|issn=1679-4508|doi=10.31744/einstein_journal/2020RC4641}}</ref><ref name="pmid30567916">{{cite journal| author=Galea R, Said E| title=Infantile Hypertrophic Pyloric Stenosis: An Epidemiological Review. | journal=Neonatal Netw | year= 2018 | volume= 37 | issue= 4 | pages= 197-204 | pmid=30567916 | doi=10.1891/0730-0832.37.4.197 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30567916 }} </ref><ref name="pmid27401959">{{cite journal| author=Tomasik E, Ziółkowska E, Kołodziej M, Szajewska H| title=Systematic review with meta-analysis: ondansetron for vomiting in children with acute gastroenteritis. | journal=Aliment Pharmacol Ther | year= 2016 | volume= 44 | issue= 5 | pages= 438-46 | pmid=27401959 | doi=10.1111/apt.13728 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27401959 }} </ref><br />
<br />
==Pathophysiology==<br />
<br />
<br />
*The vomiting center can be triggered by the [[gastrointestinal]] (GI) tract, the [[vestibular system]], the [[chemoreceptor trigger zone]], and higher centers in the [[cortex]] and [[thalamus]].<br />
*The vomiting center is found in the [[medulla oblongata]]'s reticular formation with [[muscarinic]] type receptor, which activates the vomiting center. Signals are then sent out to the abdominal muscle via the efferent pathway with the [[trigeminal]] (CN V), [[facial]] (CN VII), [[glossopharyngeal]] (CN IX), [[vagus]] (CN X), and [[hypoglossal]] (CN XII) to the upper [[gastrointestinal tract]], within [[vagal]] and [[sympathetic]] nerves to the lower tract, and within [[spinal]] nerves to the [[diaphragm]] and abdominal muscles causing vomiting.<br />
*The [[chemoreceptor trigger zone]] (CTRZ), which contains the Dopamine 2 receptor, is located outside the [[blood-brain barrier]] and can be activated directly by an irritant.<ref name="pmid21174569">{{cite journal| author=Becker DE| title=Nausea, vomiting, and hiccups: a review of mechanisms and treatment. | journal=Anesth Prog | year= 2010 | volume= 57 | issue= 4 | pages= 150-6; quiz 157 | pmid=21174569 | doi=10.2344/0003-3006-57.4.150 | pmc=3006663 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21174569 }} </ref><br />
<br />
==Causes==<br />
<br />
Common causes of vomiting in children include:<br />
<br />
*[[Acute gastroenteritis]]<br />
*Obstruction of the GI tracts<br />
*[[Infantile hypertrophic pyloric stenosis]]<br />
*[[Intussusception]]<br />
*[[Indirect inguinal hernia]]<br />
*[[Appendicitis]]<br />
*[[Volvulus]]<br />
*[[Inflammation]] of the GI tract including [[esophagitis]], [[gastroenteritis]], [[peptic ulcer disease]], [[hepatitis]], [[pancreatitis]], [[cholecystitis]] or [[appendicitis]] may cause vomiting<br />
*[[Hepatitis]]<br />
*[[Gallbladder]] disease<br />
*[[Pancreatitis]]<br />
*CNS injury [[concussion]]/[[post-concussion syndrome]], [[increased intracranial pressure]] (ICP), [[migraine headache]] and [[viral meningitis]].<br />
*[[Renal]] disease<br />
*Drugs <ref name="pmid33263676">{{cite journal| author=Andrade GBH, Marin BS, Medeiros DNM, Yamanari MGI, Troster EJ| title=Vomiting in newborns as a result of a duodenal membrane: two case reports. | journal=Einstein (Sao Paulo) | year= 2020 | volume= 18 | issue= | pages= eRC4641 | pmid=33263676 | doi=10.31744/einstein_journal/2020RC4641 | pmc=7687917 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33263676 }} </ref><ref>https://www.merckmanuals.com/professional/pediatrics/symptoms-in-infants-and-children/nausea-and-vomiting-in-infants-and-children</ref><br />
<br />
==Differentiating [disease name] from other Diseases==<br />
<br />
Vomiting in children must be differentiated from other diseases that cause vomiting in children such as [[cyclic vomiting syndrome]] (CVS) <ref name="pmid33224097">{{cite journal| author=Raucci U, Borrelli O, Di Nardo G, Tambucci R, Pavone P, Salvatore S | display-authors=etal| title=Cyclic Vomiting Syndrome in Children. | journal=Front Neurol | year= 2020 | volume= 11 | issue= | pages= 583425 | pmid=33224097 | doi=10.3389/fneur.2020.583425 | pmc=7667239 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33224097 }} </ref>, [[gastrointestinal]] disease (obstructive and inflammatory) <ref name="pmid18646021">{{cite journal| author=Sullivan PB| title=Gastrointestinal disorders in children with neurodevelopmental disabilities. | journal=Dev Disabil Res Rev | year= 2008 | volume= 14 | issue= 2 | pages= 128-36 | pmid=18646021 | doi=10.1002/ddrr.18 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18646021 }} </ref>, [[central nervous system]] (CNS) disease, [[pulmonary]] disease, [[renal]] disease, [[endocrine]]/[[metabolic]] disorders, drugs (either as side effects or in [[Overdose]]), or [[psychiatric]] disorders.<br />
<br />
==Epidemiology and Demographics==<br />
<br />
Vomiting in children is very common and there are no racial, gender, age, or race predispstions to vomiting in children.<br />
<br />
==Risk Factors==<br />
There are no established risk factors for vomiting in children.<br />
==Natural History, Complications and Prognosis==<br />
<br />
*The majority of children with vomiting is mostly due to [[gastroenteritis]]. [[Gastroenteritis]] ranges from asymptomatic to [[dehydration]] to death, and usually starts with mild [[fever]] and vomiting, followed by 1-4 days of non-bloody, watery [[diarrhea]].<ref name="AndradeMarin2020">{{cite journal|last1=Andrade|first1=Gabriela Bonente Herculano de|last2=Marin|first2=Barbara Said|last3=Medeiros|first3=Daniela Nasu Monteiro|last4=Yamanari|first4=Mauricio Gustavo Ieiri|last5=Troster|first5=Eduardo Juan|title=Vomiting in newborns as a result of a duodenal membrane: two case reports|journal=Einstein (São Paulo)|volume=18|year=2020|issn=1679-4508|doi=10.31744/einstein_journal/2020RC4641}}</ref><br />
*Common complications of vomiting in children is [[dehydration]].<br />
*Prognosis ranges from excellent to poor depending on the etiology of the vomiting (include [[gastroenteritis]] to [[meningitis]] respectively)<br />
<br />
==Diagnosis==<br />
===Diagnostic Criteria===<br />
<br />
*The diagnosis of vomiting in children is made with both medical history and physical examination.<br />
<br />
===Symptoms===<br />
<br />
*Symptoms of vomiting in children include the following:<br />
<br />
:*[[Fever]]<br />
:*[[Lightheadedness]]<br />
:*[[Vertigo]]<br />
:*[[Rapid pulse]]<br />
:*[[Excessive sweating]]<br />
:*[[Dry mouth]]<br />
:*[[Decreased urination]]<br />
:*[[Chest pain]]<br />
:*[[Fainting]]<br />
:*[[Confusion]]<br />
:*Excessive [[sleepiness]] <ref name="pmid27175718">{{cite journal| author=Reust CE, Williams A| title=Acute Abdominal Pain in Children. | journal=Am Fam Physician | year= 2016 | volume= 93 | issue= 10 | pages= 830-6 | pmid=27175718 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27175718 }} </ref><br />
<br />
===Physical Examination===<br />
<br />
*Physical examination may be remarkable for signs of [[dehydration]]:<br />
<br />
:*[[Dry skin]]<br />
:*Cracked lips<br />
:*Dark-[[Color]] [[urine]]<br />
:*[[Dizziness]]<br />
:*[[Fatigue]]<br />
:*[[Sweating]]<br />
:*Frequent urination. <ref name="pmid25870468">{{cite journal| author=Hoxha T, Xhelili L, Azemi M, Avdiu M, Ismaili-Jaha V, Efendija-Beqa U | display-authors=etal| title=Performance of clinical signs in the diagnosis of dehydration in children with acute gastroenteritis. | journal=Med Arch | year= 2015 | volume= 69 | issue= 1 | pages= 10-2 | pmid=25870468 | doi=10.5455/medarh.2015.69.10-12 | pmc=4384849 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25870468 }} </ref><br />
<br />
===Laboratory Findings===<br />
<br />
*There are no specific laboratory findings associated with vomiting in children. However, blood and urine tests are helpful in diagnosis to check for [[infection]] and [[kidney function]].<br />
<br />
===Electrocardiogram===<br />
There are no [[ECG]] findings associated with vomiting in children.<br />
===X-ray===<br />
There are no [[x-ray]] findings associated with vomiting in children.<br />
===Echocardiography or Ultrasound===<br />
There are no [[echocardiography]]/[[ultrasound]] findings associated with vomiting in children.<br />
===CT scan===<br />
There are no [[CT scan]] findings associated with vomiting in children.<br />
===MRI===<br />
There are no [[MRI]] findings associated with vomiting in children.<br />
===Other Imaging Findings===<br />
There are no other [[imaging]] findings associated with vomiting in children.<br />
===Other Diagnostic Studies===<br />
<br />
*There are no other [[imaging]] findings associated with vomiting in children.<br />
<br />
==Treatment==<br />
===Medical Therapy===<br />
<br />
*The mainstay of therapy for vomiting in children is to treat underlying conditions and [[rehydration]]. [[Antiemetic]] can be used in the treatment of vomiting.<ref name="pmid22424648">{{cite journal| author=Carter B, Seupaul RA| title=Update: antiemetics for vomiting associated with acute gastroenteritis in children. | journal=Ann Emerg Med | year= 2012 | volume= 60 | issue= 3 | pages= e5-6 | pmid=22424648 | doi=10.1016/j.annemergmed.2012.01.031 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22424648 }} </ref><br />
*Hydration includes giving fluid in small amounts; [[electrolytes]] can be used in some situations as determined by the doctor to treat dehydration. Children with vomiting might stop oral intake and decompression of the stomach with a [[nasogastric tube]] necessary for a certain patient depending on the cause. Indications for [[nasogastric tube]] include [[duodenal atresia]], [[midgut malrotation]], [[volvulus]], [[jejunoileal atresia]], and [[meconium ileus]], [[necrotizing enterocolitis]], etc.<ref name="pmid23340985">{{cite journal| author=Singhi SC, Shah R, Bansal A, Jayashree M| title=Management of a child with vomiting. | journal=Indian J Pediatr | year= 2013 | volume= 80 | issue= 4 | pages= 318-25 | pmid=23340985 | doi=10.1007/s12098-012-0959-6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23340985 }} </ref><br />
*A study shows that [[Ondasteron]] reduces required intravenous hydration by 51% and increase oral rehydration therapy in children with [[acute gastritis]] and [[acute gastroenteritis]].<ref name="pmid18006189">{{cite journal| author=Roslund G, Hepps TS, McQuillen KK| title=The role of oral ondansetron in children with vomiting as a result of acute gastritis/gastroenteritis who have failed oral rehydration therapy: a randomized controlled trial. | journal=Ann Emerg Med | year= 2008 | volume= 52 | issue= 1 | pages= 22-29.e6 | pmid=18006189 | doi=10.1016/j.annemergmed.2007.09.010 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18006189 }} [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=&cmd=prlinks&id=19332600 Review in: Evid Based Med. 2009 Apr;14(2):44] </ref><br />
*Another [[antiemetic]]; [[metoclopramide]], often used in adults with refractory [[chemotherapy-induced nausea and vomiting]] (CIN V), is also used for CINV prevention in children. Regulatory bodies advised against its use in children aged <1 years and to caution against its use in children aged <5 years and its duration of service beyond five days.<ref name="pmid27003816">{{cite journal| author=Lau Moon Lin M, Robinson PD, Flank J, Sung L, Dupuis LL| title=The Safety of Metoclopramide in Children: A Systematic Review and Meta-Analysis. | journal=Drug Saf | year= 2016 | volume= 39 | issue= 7 | pages= 675-87 | pmid=27003816 | doi=10.1007/s40264-016-0418-9 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27003816 }} </ref><br />
<br />
===Surgery===<br />
<br />
*[[Surgical]] intervention is not recommended for the management of vomiting in children.<br />
<br />
===Prevention===<br />
<br />
*There are no primary preventive measures available for vomiting in children.<br />
<br />
==References==<br />
{{Reflist|2}}<br />
<br />
[[Category:Pediatrics]]<br />
[[Category:Primary care]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Orthostatic_hypotension&diff=1692158Orthostatic hypotension2021-02-26T15:07:32Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{SI}}<br />
<br />
{{CMG}}; {{AE}} {{Mitra}}; {{S.G.}}; {{Norina Usman}}<br />
<br />
{{SK}} Postural hypotension; orthostatic intolerance; head rush; dizzy spell<br />
<br />
<br />
==Overview==<br />
[[Orthostatic hypotension]] or [[postural hypotension]] is defined as a reduction of [[systolic blood pressure]] of at least 20 mm Hg or 10 mm Hg in [[diastolic blood pressure]] within 3 minutes of standing. A similar fall during [[head-up tilt test]] at 60 degrees also defines [[orthostatic hypotension]]. [[Orthostatic hypotension]] may be asymptomatic or may cause symptoms of [[lightheadedness]], [[dizziness]], [[blurred vision]] or [[cognitive impairment]]. It may have acute or chronic causes. Management of [[orthostatic hypotension]] may be challenging, in particular in patients with [[orthostatic hypotension]] and concomitant [[supine]] [[hypertension]]. <ref name="pmid14705758">{{cite journal| author=Bradley JG, Davis KA| title=Orthostatic hypotension. | journal=Am Fam Physician | year= 2003 | volume= 68 | issue= 12 | pages= 2393-8 | pmid=14705758 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14705758 }} </ref><ref name="pmid1592445">{{cite journal| author=Rutan GH, Hermanson B, Bild DE, Kittner SJ, LaBaw F, Tell GS| title=Orthostatic hypotension in older adults. The Cardiovascular Health Study. CHS Collaborative Research Group. | journal=Hypertension | year= 1992 | volume= 19 | issue= 6 Pt 1 | pages= 508-19 | pmid=1592445 | doi=10.1161/01.hyp.19.6.508 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1592445 }} </ref><ref name="pmid9109468">{{cite journal| author=Ooi WL, Barrett S, Hossain M, Kelley-Gagnon M, Lipsitz LA| title=Patterns of orthostatic blood pressure change and their clinical correlates in a frail, elderly population. | journal=JAMA | year= 1997 | volume= 277 | issue= 16 | pages= 1299-304 | pmid=9109468 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9109468 }} </ref><br />
<br />
==Classification==<br />
<br />
*Based on the underlying [[pathophysiology]] correlated to a postural drop in [[blood pressure]], orthostatic hypotension can be classified into:<br />
<br />
'''Initial orthostatic hypotension (iOH)'''<br />
<br />
*It is most common in healthy adolescents<br />
*It is demarcated as a brief BP decrease of >40 mmHg systolic or >20 mmHg diastolic with symptomatic [[cerebral hypoperfusion]] within five to fifteen seconds after standing, typically resolved by twenty seconds.<br />
<br />
'''Neurogenic orthostatic hypotension (nOH)'''<br />
<br />
*In [[Neurogenic orthostatic hypotension]], the [[sympathetic]] [[noradrenergic]] nerves continually fail to facilitate the reflexive cardiovascular responses essential to sustain blood pressure in response to orthostatic stress.<br />
*It is described as a constant [[BP]] decrease of >20 mmHg systolic or >10 mmHg diastolic, without or with symptoms, within three minutes of head-up tilt or standing.<br />
<br />
'''Delayed orthostatic hypotension (dOH)'''<br />
<br />
*[[Delayed orthostatic hypotension]] (dOH) is demarcated as a fall in blood pressure that accomplishes neurogenic orthostatic hypotension criteria but ensues after three minutes.<br />
<br />
'''Neurally mediated syncope (vOH)'''<br />
<br />
*It is also recognized as vasodepressor or [[vasovagal syncope]], it involves a [[paroxysmal]] extraction of [[sympathetic]] [[vasopressor]] tone, frequently during prolonged standing, in patients with an effective [[autonomic nervous system]].<br />
<br />
'''Cardiovascular orthostatic hypotension (cOH)'''<br />
<br />
*[[Cardiovascular orthostatic hypotension]] occurs from intravascular [[hypovolemia]] or reduced [[cardiac output]] along with compensatory [[tachycardia]].<br />
<br />
'''Orthostatic pseudohypotension (pOH)''' <br />
<br />
*It is stated as apparent [[orthostatic hypotension]] when baseline supine [[blood pressure]] is raised, which may be due to a short time at rest to create a valid baseline, related recumbent [[hypertension]], or fluctuation of baseline blood pressure with labile [[hypertension]] <ref name="pmidhttps://doi.org/10.1007/s10286-016-0382-6">{{cite journal| author=Schmoldt A, Benthe HF, Haberland G| title=Digitoxin metabolism by rat liver microsomes. | journal=Biochem Pharmacol | year= 1975 | volume= 24 | issue= 17 | pages= 1639-41 | pmid=https://doi.org/10.1007/s10286-016-0382-6 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10 }} </ref><ref name="pmid17199559">{{cite journal| author=Wieling W, Krediet CT, van Dijk N, Linzer M, Tschakovsky ME| title=Initial orthostatic hypotension: review of a forgotten condition. | journal=Clin Sci (Lond) | year= 2007 | volume= 112 | issue= 3 | pages= 157-65 | pmid=17199559 | doi=10.1042/CS20060091 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17199559 }} </ref><ref name="pmid21431947">{{cite journal| author=Freeman R, Wieling W, Axelrod FB, Benditt DG, Benarroch E, Biaggioni I | display-authors=etal| title=Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome. | journal=Clin Auton Res | year= 2011 | volume= 21 | issue= 2 | pages= 69-72 | pmid=21431947 | doi=10.1007/s10286-011-0119-5 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21431947 }} </ref><ref name="pmid19390349">{{cite journal| author=Wieling W, Schatz IJ| title=The consensus statement on the definition of orthostatic hypotension: a revisit after 13 years. | journal=J Hypertens | year= 2009 | volume= 27 | issue= 5 | pages= 935-8 | pmid=19390349 | doi=10.1097/HJH.0b013e32832b1145 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19390349 }} </ref><br />
<br />
==Pathophysiology==<br />
<br />
*In the standing position, 500 to 1000 mL of [[blood]] pools in the [[lower extremities]] and [[splanchnic circulation]], causing a rapid decline in [[venous return]] to the heart.<br />
*Decreased [[ventricular filling pressures]] lower [[cardiac output]] and systemic [[blood pressure]]. <ref name="pmid2674714">{{cite journal| author=Lipsitz LA| title=Orthostatic hypotension in the elderly. | journal=N Engl J Med | year= 1989 | volume= 321 | issue= 14 | pages= 952-7 | pmid=2674714 | doi=10.1056/NEJM198910053211407 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2674714 }} </ref><ref name="pmid7791382">{{cite journal| author=Low PA, Opfer-Gehrking TL, McPhee BR, Fealey RD, Benarroch EE, Willner CL | display-authors=etal| title=Prospective evaluation of clinical characteristics of orthostatic hypotension. | journal=Mayo Clin Proc | year= 1995 | volume= 70 | issue= 7 | pages= 617-22 | pmid=7791382 | doi=10.4065/70.7.617 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7791382 }} </ref><ref name="pmid11093411">{{cite journal| author=Zaqqa M, Massumi A| title=Neurally mediated syncope. | journal=Tex Heart Inst J | year= 2000 | volume= 27 | issue= 3 | pages= 268-72 | pmid=11093411 | doi= | pmc=101078 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11093411 }} </ref><ref name="pmid7746371">{{cite journal| author=Mathias CJ| title=Orthostatic hypotension: causes, mechanisms, and influencing factors. | journal=Neurology | year= 1995 | volume= 45 | issue= 4 Suppl 5 | pages= S6-11 | pmid=7746371 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7746371 }} </ref><ref name="pmid1475949">{{cite journal| author=Hollister AS| title=Orthostatic hypotension. Causes, evaluation, and management. | journal=West J Med | year= 1992 | volume= 157 | issue= 6 | pages= 652-7 | pmid=1475949 | doi= | pmc=1022100 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1475949 }} </ref><br />
*[[Baroreceptors]] located mainly in the [[aorta]] and [[carotid arteries]] are very sensitive to fluctuations in blood pressure. A fall in [[blood pressure]] decreases the stretching of [[baroreceptors]], thus decreasing their firing. The decreased firing of [[baroreceptors]] increases [[sympathetic]] and decreases [[parasympathetic]] outflow.<br />
*This compensatory reflex increases [[heart rate]], [[contractility]] and [[peripheral vascular resistance]] (i.e., both arteriolar and venous [[vasoconstriction]]). These changes result in increased [[venous return]] and increased [[cardiac output]], and limit the decline in [[blood pressure]]. This compensatory reflex is known as [[baroreflex]].<br />
<br />
*Any disruption in this pathway can cause a significant decline in [[blood pressure]] upon standing (i.e., [[orthostatic hypotension]]), causing symptoms of cerebral hypoperfusion including [[nausea]], [[dizziness]], [[headache]], [[lightheadedness]], [[blurred vision]], and impaired [[cognition]].<br />
<br />
*Although many pathologic causes may alter this normal physiologic response to standing, the most common pathophysiologic mechanisms include:<br />
**[[Autonomic dysfunction]] affecting the [[baroreflex]] (i.e. baroreflex dysfunction)<br />
**[[Volume depletion]]<br />
**Adverse effects of certain [[medications]]<br />
<br />
[[Image:barereflex.jpg|center|1000px|]]<br />
<br />
==Causes==<br />
<br />
Common causes of [[orthostsic hypotension]] include: <ref name="Jiang-2005">{{cite journal | author=Jiang W, Davidson JR. | title=Antidepressant therapy in patients with ischemic heart disease. | journal=Am Heart J | year=2005 | volume=150 | issue=5 | pages=871-81 | id=PMID 16290952}}</ref><ref name="Delini-Stula-1999">{{cite journal | author=Delini-Stula A, Baier D, Kohnen R, Laux G, Philipp M, Scholz HJ. | title=Undesirable blood pressure changes under naturalistic treatment with moclobemide, a reversible MAO-A inhibitor--results of the drug utilization observation studies. | journal=Pharmacopsychiatry | year=1999 | volume=32 | issue=2 | pages=61-7 | id=PMID 10333164}}</ref><ref name="Jones-2002">{{cite journal | author=Jones RT. | title=Cardiovascular system effcts of marijuana. | journal=J Clin Pharmacol | year=2002 | volume=42 | issue=11 Suppl | pages=58S-63S | id=PMID 12412837}}</ref><ref name="pmid1898124">{{cite journal |vauthors=Hohmann M, Künzel W |title=Orthostatic hypotension and birthweight |journal=Arch. Gynecol. Obstet. |volume=248 |issue=4 |pages=181–9 |date=1991 |pmid=1898124 |doi=10.1007/bf02390357 |url=}}</ref><br />
<br />
{| class="wikitable"<br />
|+<br />
|-<br />
| align="center" style="background: #4479BA; color: #FFFFFF " |'''Causes of [[orthostatic hypotension]]'''<br />
|-<br />
|'''[[Cardiac diseases]]'''<br />
|-<br />
|<br />
*[[Myocardial ischemia]]/[[Myocardial infarction]]<br />
|-<br />
|<br />
*[[Cardiac arrhythmias]]<br />
|-<br />
|<br />
*[[Congestive heart failure]]<br />
|-<br />
|<br />
*[[Myocarditis]]/[[pericarditis]]<br />
|-<br />
|<br />
*[[Valvular heart diseases]]<br />
|-<br />
|'''[[Intravascular volume depletion]]'''<br />
|-<br />
|<br />
*[[Anemia]]<br />
|-<br />
|<br />
*[[Blood loss]]<br />
|-<br />
|<br />
*[[Dehydration]]<br />
|-<br />
|<br />
*[[Diuretics]]<br />
|-<br />
|'''[[Venous pooling]]/[[venous vasodilation]]'''<br />
|-<br />
|<br />
*[[Prolonged bed rest]]<br />
|-<br />
|<br />
*[[Pregnancy]]<br />
|-<br />
|<br />
*[[Venous insufficiency]]/[[Varicosities]]<br />
|-<br />
|'''[[Autonomic nervous system disorders]]'''<br />
|-<br />
|<br />
*Primary:<br />
**Pure autonomic failure<br />
**[[Multiple system atrophy]]<br />
|-<br />
|<br />
*Secondary:<br />
**[[Diabetes]]<br />
**[[Amyloidosis]]<br />
**[[Sarcoidosis]]<br />
**[[Renal failure]]<br />
|-<br />
|'''Endocrine'''<br />
|-<br />
|<br />
*[[Adrenal insufficiency]]<br />
|-<br />
|<br />
*[[Diabetes insipidus]]<br />
|-<br />
|<br />
*[[Hyperglycemia]] (acute)<br />
|-<br />
|<br />
*[[Hypoaldosteronism]]<br />
|-<br />
|<br />
*[[Hypokalemia]]<br />
|-<br />
|<br />
*[[Hypothyroidism]]<br />
|-<br />
|<br />
*[[Pheochromocytoma]]<br />
|-<br />
|'''[[Medications]]'''<br />
|-<br />
|'''Miscellaneous'''<br />
|-<br />
|<br />
*[[AIDS]]<br />
|-<br />
|<br />
*[[Anxiety]] or [[panic disorder]]<br />
|-<br />
|<br />
*[[Eating disorders]]<br />
|-<br />
|<br />
*[[Postprandial hypotension]]<br />
|-<br />
|}<br />
{|<br />
|- <br />
|}<br />
<br />
<br />
{| class="wikitable"<br />
|+<br />
| colspan="2" rowspan="2" align="center" style="background: #4479BA; color: #FFFFFF " |'''Medication-induced [[Orthostatic Hypotension]]'''<br />
|+<br />
|+<br />
| colspan="1" rowspan="1" |'''[[Vasodilation]] through [[Alpha-1]] blockade'''<br />
| colspan="1" rowspan="1" |<br />
*[[Alpha-1 blockers]]: <br />
**[[Terazosin]]<br />
**[[Prazosin]]<br />
**[[Doxazosin]]<br />
*[[Antipsychotics]]:<br />
**[[Perphenazine oral|Perphenazine]]<br />
**[[Risperidone]]<br />
**[[Thioridazine hydrochloride]]<br />
**[[Clozapine]]<br />
**[[zotepine]]<br />
**[[Olanzapine]]<br />
**[[Fluphenazine (patient information)|Fluphenazine]]<br />
*[[Antihistamines]]<br />
*[[Antidepressants]]:<br />
**[[Trazodone]]<br />
**[[Tricyclic antidepressants]] ([[TCA]]s)<br />
**[[Serotonin norepinephrine reuptake inhibitors]] ([[SNRI]]s):<br />
***[[Venlafaxine]]<br />
***[[Duloxetine]]<br />
**[[Monoamine oxidase inhibitors]]<br />
|-<br />
| colspan="1" rowspan="1" |'''[[Vasodilation]] (Others)'''<br />
| colspan="1" rowspan="1" |<br />
*[[ACE Inhibitor]]s<br />
*[[ARBs]]<br />
*[[Dihydropyridine]] [[calcium channel blockers]]<br />
*[[Hydralazine]]<br />
*[[Nitrates]]<br />
*[[Phosphodiesterase inhibitors]]:<br />
**[[Sildenafil]]<br />
|-<br />
| colspan="1" rowspan="1" |'''Volume depletion'''<br />
| colspan="1" rowspan="1" |<br />
*[[Diuretics]]:<br />
**[[Ethacrynic acid (patient information)|Ethacrynic Acid]]<br />
**[[Hydrochlorothiazide (patient information)|Hydrochlorothiazide]]<br />
**[[Furosemide]]<br />
*[[SGLT-2 inhibitors]]<br />
|-<br />
| colspan="1" rowspan="1" |'''Sympathetic blockade'''<br />
| colspan="1" rowspan="1" |<br />
*[[Ganglionic blocking agents]]<br />
*[[Beta Blockers]]:<br />
**[[Propranolol]]<br />
*[[Clonidine]]<br />
|-<br />
| colspan="1" rowspan="1" |'''[[Dopamin agonists]] and other anti-Parkinsonian medications'''<br />
| colspan="1" rowspan="1" |<br />
*[[Dopamine agonists]]<br />
**[[Bromocriptine]]<br />
**[[Pramipexole]]<br />
**[[Ropinirole]]<br />
*[[Levodopa]]<br />
*[[Monoamine oxidase inhibitor]]s:<br />
**[[Selegiline]]<br />
**[[Rasagiline]]<br />
*[[COMT inhibitors]]:<br />
**[[Entacapone (patient information)|Entacapone]]<br />
|-<br />
| colspan="1" rowspan="1" |'''Others'''<br />
| colspan="1" rowspan="1" |<br />
*[[Alcohol]]<br />
*[[Apomorphine hydrochloride]]<br />
*[[Cidofovir]]<br />
*[[Iloperidone]]<br />
*[[Loxapine]]<br />
*[[Niacin]]<br />
*[[Pergolide]]<br />
*[[Ritonavir]]<br />
*[[Rotigotine]]<br />
*[[Narcotics]]:<br />
**[[Opiates]]: [[Morhine]]<br />
*[[Sedative-hypnotics]]:<br />
**[[Tempazepam]]<br />
*[[Muscle relaxants]]:<br />
**[[Tizanidine]]<br />
*[[Thiothixene]]<br />
*[[Tiagabine]]<br />
*Chemotherapeutic agents:<br />
*[[Vincristine]]<br />
*[[Vinblastine]]<br />
|-<br />
|}<br />
<br />
==Differentiating Orthostatic Hypotension from Other Diseases==<br />
Orthostatic hypotension must be differentiated from [[neurogenic syncope]], [[cardiogenic syncope]], [[situational syncope]], [[multiple system atrophy]] with orthostatic hypotension, [[neurally mediated hypotension]], [[postural orthostatic tachycardia syndrome]] (POTS) and [[vasovagal syncope]] <ref name="pmid25498732">{{cite journal| author=Poewe W, Seppi K, Fitzer-Attas CJ, Wenning GK, Gilman S, Low PA | display-authors=etal| title=Efficacy of rasagiline in patients with the parkinsonian variant of multiple system atrophy: a randomised, placebo-controlled trial. | journal=Lancet Neurol | year= 2015 | volume= 14 | issue= 2 | pages= 145-52 | pmid=25498732 | doi=10.1016/S1474-4422(14)70288-1 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25498732 }} </ref><ref name="pmid15875516">{{cite journal| author=Brignole M| title=Neurally-mediated syncope. | journal=Ital Heart J | year= 2005 | volume= 6 | issue= 3 | pages= 249-55 | pmid=15875516 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15875516 }} </ref><ref name="pmid24630686">{{cite journal| author=Trahair LG, Horowitz M, Jones KL| title=Postprandial hypotension: a systematic review. | journal=J Am Med Dir Assoc | year= 2014 | volume= 15 | issue= 6 | pages= 394-409 | pmid=24630686 | doi=10.1016/j.jamda.2014.01.011 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24630686 }} </ref><ref name="pmid26198889">{{cite journal| author=Garland EM, Celedonio JE, Raj SR| title=Postural Tachycardia Syndrome: Beyond Orthostatic Intolerance. | journal=Curr Neurol Neurosci Rep | year= 2015 | volume= 15 | issue= 9 | pages= 60 | pmid=26198889 | doi=10.1007/s11910-015-0583-8 | pmc=4664448 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26198889 }} </ref><ref name="pmid28375909">{{cite journal| author=Cheshire WP| title=Syncope. | journal=Continuum (Minneap Minn) | year= 2017 | volume= 23 | issue= 2, Selected Topics in Outpatient Neurology | pages= 335-358 | pmid=28375909 | doi=10.1212/CON.0000000000000444 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28375909 }} </ref><ref name="pmid3528810">{{cite journal| author=Dohrmann ML, Cheitlin MD| title=Cardiogenic syncope. Seizure versus syncope. | journal=Neurol Clin | year= 1986 | volume= 4 | issue= 3 | pages= 549-62 | pmid=3528810 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3528810 }} </ref><ref name="pmid21160608">{{cite journal| author=Aydin MA, Salukhe TV, Wilke I, Willems S| title=Management and therapy of vasovagal syncope: A review. | journal=World J Cardiol | year= 2010 | volume= 2 | issue= 10 | pages= 308-15 | pmid=21160608 | doi=10.4330/wjc.v2.i10.308 | pmc=2998831 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21160608 }} </ref><br />
<br />
{| class="wikitable"<br />
|+<br />
! rowspan="2" align="center" style="background: #4479BA; color: #FFFFFF " |Disease<br />
! colspan="12" align="center" style="background: #4479BA; color: #FFFFFF " |History and Physical Examination<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |<br />
! colspan="4" align="center" style="background: #4479BA; color: #FFFFFF " |Diagnostic approach<br />
|-<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Lightheadedness<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Fatigue<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Autonomic symptoms<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Fever<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Nausea/vomiting<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Diminished Vision<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Dizziness<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Slurred Speech<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Tachycardia<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Altered mentation<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Loss of Consciousness<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Weakness<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Neurological Deficit<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Labs and CSF findings<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |ECG<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |CT/MRI<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Gold standard test<br />
|-<br />
|'''Multiple system atrophy with orthostatic hypotension'''<br />
| +<br />
| +<br />
| +<br />
|<nowiki>-</nowiki><br />
| -<br />
| +<br />
| +<br />
|<nowiki>+</nowiki><br />
| -<br />
| +<br />
| -<br />
| +<br />
| +<br />
|<nowiki>-</nowiki><br />
| -<br />
|Atrophy of brain stem and cerebellum<br />
|<br />
*Clinical assessment<br />
|-<br />
|'''Neurally mediated hypotension'''<br />
|<nowiki>+</nowiki><br />
| +<br />
| +<br />
|<nowiki>-</nowiki><br />
| +<br />
| +<br />
| +<br />
| +<br />
| -<br />
| +<br />
| -<br />
| +<br />
| -<br />
|<nowiki>-</nowiki><br />
| -<br />
|<nowiki>-</nowiki><br />
|<br />
*Clinical assessment<br />
|-<br />
|''''Postural Orthostatic Tachycardia Syndrome (POTS)'''<br />
| +<br />
| +<br />
| +<br />
|<nowiki>-</nowiki><br />
|<nowiki>-</nowiki><br />
|<nowiki>-</nowiki><br />
|<nowiki>-</nowiki><br />
|<nowiki>-</nowiki><br />
| +<br />
|<nowiki>-</nowiki><br />
| -<br />
|<nowiki>-</nowiki><br />
| -<br />
|<nowiki>-</nowiki><br />
| +<br />
|<nowiki>-</nowiki><br />
|<br />
*Clinical assessment<br />
|-<br />
|'''Neurologic syncope'''<br />
|<nowiki>+</nowiki><br />
|<nowiki>-</nowiki><br />
| +<br />
|<nowiki>-</nowiki><br />
| +<br />
|<nowiki>+/-</nowiki><br />
|<nowiki>+</nowiki><br />
| -<br />
| -<br />
|<nowiki>-</nowiki><br />
| +<br />
|<nowiki>+/-</nowiki><br />
| -<br />
| -<br />
| -<br />
| -<br />
|<br />
*Clinical assessment<br />
|-<br />
|'''Cardiac syncope'''<br />
|<nowiki>+</nowiki><br />
| +<br />
| +<br />
|_<br />
| +<br />
| +<br />
| +<br />
| +<br />
| +<br />
|<nowiki>+/-</nowiki><br />
| +<br />
|<nowiki>+</nowiki><br />
| -<br />
| -<br />
| +<br />
| -<br />
|<br />
*[[ECG]]<br />
*[[Holter monitor]]<br />
*[[Echocardiography]]<br />
|-<br />
|'''Situational syncope'''<br />
|<nowiki>+</nowiki><br />
| +<br />
| +<br />
|<nowiki>-</nowiki><br />
| +<br />
| +<br />
| +<br />
| +/-<br />
| +/-<br />
|<nowiki>+/-</nowiki><br />
| +<br />
|<nowiki>+/-</nowiki><br />
| -<br />
| -<br />
| -<br />
| -<br />
|<br />
*Clinical assessment syncope occurs during defecation, micturition, or coughing<br />
|-<br />
|'''Vasovagal syncope (also known as cardio-neurogenic syncope)'''<br />
| +<br />
| +<br />
| +<br />
|<nowiki>-</nowiki><br />
| +<br />
|<nowiki>+/-</nowiki><br />
| +<br />
| +<br />
| -<br />
| +<br />
| +<br />
|<nowiki>+/-</nowiki><br />
| -<br />
| +<br />
| +<br />
| -<br />
|<br />
*[[ECG]]<br />
*[[Echocardiogram]]<br />
*[[Exercise stress testing|Exercise stress test]]<br />
|}<br />
<br />
==Epidemiology and Demographics==<br />
<br />
'''Incidence'''<br />
<br />
*The approximation of orthostatic hypotension‐associated hospitalization is 36 per 100,000 adults, and the rate can be as high as 233 per 100,000 patients >75 years of age. <ref name="pmid28713844">{{cite journal| author=Palma JA, Kaufmann H| title=Epidemiology, Diagnosis, and Management of [[Neurogenic Orthostatic Hypotension]]. | journal=Mov Disord Clin Pract | year= 2017 | volume= 4 | issue= 3 | pages= 298-308 | pmid=28713844 | doi=10.1002/mdc3.12478 | pmc=5506688 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28713844 }} </ref><br />
<br />
'''Prevalence'''<br />
<br />
*The overall prevalence of [[orthostatic hypotension]] depends on age as it increases with age in the general population.<br />
*The [[prevalence]] ranges from 5% in patients <50 years of age to 30% in those >70 years of age.<br />
*It is ~20% in >65-year-old patients. <ref name="pmid26271068">{{cite journal| author=Ricci F, De Caterina R, Fedorowski A| title=Orthostatic Hypotension: Epidemiology, Prognosis, and Treatment. | journal=J Am Coll Cardiol | year= 2015 | volume= 66 | issue= 7 | pages= 848-860 | pmid=26271068 | doi=10.1016/j.jacc.2015.06.1084 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26271068 }} </ref><ref name="pmid18368301">{{cite journal| author=Low PA| title=Prevalence of orthostatic hypotension. | journal=Clin Auton Res | year= 2008 | volume= 18 Suppl 1 | issue= | pages= 8-13 | pmid=18368301 | doi=10.1007/s10286-007-1001-3 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18368301 }} </ref><br />
<br />
'''Age'''<br />
<br />
*[[Orthostatic Hypotension]] is commonly seen in individuals older than 50 years of age.<br />
<br />
'''Gender''' <br />
<br />
*[[Orthostatic hypotension]] affects men and women equally.<br />
<br />
==Risk Factors==<br />
<br />
Common [[Risk factor|risk factors]] in the development of orthostatic hypotension include: <ref name="ArnoldShibao2013">{{cite journal|last1=Arnold|first1=Amy C.|last2=Shibao|first2=Cyndya|title=Current Concepts in Orthostatic Hypotension Management|journal=Current Hypertension Reports|volume=15|issue=4|year=2013|pages=304–312|issn=1522-6417|doi=10.1007/s11906-013-0362-3}}</ref><ref name="CanobbioWarnes2017">{{cite journal|last1=Canobbio|first1=Mary M.|last2=Warnes|first2=Carole A.|last3=Aboulhosn|first3=Jamil|last4=Connolly|first4=Heidi M.|last5=Khanna|first5=Amber|last6=Koos|first6=Brian J.|last7=Mital|first7=Seema|last8=Rose|first8=Carl|last9=Silversides|first9=Candice|last10=Stout|first10=Karen|title=Management of Pregnancy in Patients With Complex Congenital Heart Disease: A Scientific Statement for Healthcare Professionals From the American Heart Association|journal=Circulation|volume=135|issue=8|year=2017|issn=0009-7322|doi=10.1161/CIR.0000000000000458}}</ref><br />
<br />
*[[Age]] (>65)<br />
*[[Medication|Medications]]<br />
*[[Autonomic neuropathies]], such as[[Parkinson's Disease|Parkinson's disease]], [[diabetes]]<br />
*[[Volume depletion]]<br />
*[[Postpartum period]]<br />
*[[Prolong bedrest]].<br />
<br />
==Screening==<br />
<br />
*Orthostatic hypotension screening consists of [[blood pressure]] measurements in [[supine]] (or sitting) and [[standing position]] during clinical consultations. <ref name="pmid30418320">{{cite journal| author=Cremer A, Rousseau AL, Boulestreau R, Kuntz S, Tzourio C, Gosse P| title=Screening for orthostatic hypotension using home blood pressure measurements. | journal=J Hypertens | year= 2019 | volume= 37 | issue= 5 | pages= 923-927 | pmid=30418320 | doi=10.1097/HJH.0000000000001986 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30418320 }} </ref><br />
<br />
==Natural History, Complications, and Prognosis==<br />
====Natural History====<br />
<br />
*The symptoms of orthostatic hypotension mainly develop in the elderly, and start with generalized symptoms of [[dizziness]], [[lightheadedness]], or [[syncope]] and less frequently with [[headache]], [[leg buckling]], or [[chest pain]] <ref name="pmid28846238">{{cite journal| author=| title=StatPearls | journal= | year= 2020 | volume= | issue= | pages= | pmid=28846238 | doi= | pmc= | url= }} </ref><ref name="pmid14705758">{{cite journal| author=Bradley JG, Davis KA| title=Orthostatic hypotension. | journal=Am Fam Physician | year= 2003 | volume= 68 | issue= 12 | pages= 2393-8 | pmid=14705758 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14705758 }} </ref><br />
<br />
====Complications====<br />
Common [[Complication (medicine)|complications]] of orthostatic hypotension include: <ref name="pmid21438868">{{cite journal |vauthors=Romero-Ortuno R, Cogan L, Foran T, Kenny RA, Fan CW |title=Continuous noninvasive orthostatic blood pressure measurements and their relationship with orthostatic intolerance, falls, and frailty in older people |journal=J Am Geriatr Soc |volume=59 |issue=4 |pages=655–65 |date=April 2011 |pmid=21438868 |doi=10.1111/j.1532-5415.2011.03352.x |url=}}</ref><ref name="RicciFedorowski2015">{{cite journal|last1=Ricci|first1=Fabrizio|last2=Fedorowski|first2=Artur|last3=Radico|first3=Francesco|last4=Romanello|first4=Mattia|last5=Tatasciore|first5=Alfonso|last6=Di Nicola|first6=Marta|last7=Zimarino|first7=Marco|last8=De Caterina|first8=Raffaele|title=Cardiovascular morbidity and mortality related to orthostatic hypotension: a meta-analysis of prospective observational studies|journal=European Heart Journal|volume=36|issue=25|year=2015|pages=1609–1617|issn=0195-668X|doi=10.1093/eurheartj/ehv093}}</ref><br />
<br />
*Symptomatic orthostatic hypotension may cause falling. <ref name="pmid23265229">{{cite journal| author=van Hateren KJ, Kleefstra N, Blanker MH, Ubink-Veltmaat LJ, Groenier KH, Houweling ST | display-authors=etal| title=Orthostatic hypotension, diabetes, and falling in older patients: a cross-sectional study. | journal=Br J Gen Pract | year= 2012 | volume= 62 | issue= 603 | pages= e696-702 | pmid=23265229 | doi=10.3399/bjgp12X656838 | pmc=3459777 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23265229 }} </ref> <ref name="pmid21391928">{{cite journal| author=Gangavati A, Hajjar I, Quach L, Jones RN, Kiely DK, Gagnon P | display-authors=etal| title=Hypertension, orthostatic hypotension, and the risk of falls in a community-dwelling elderly population: the maintenance of balance, independent living, intellect, and zest in the elderly of Boston study. | journal=J Am Geriatr Soc | year= 2011 | volume= 59 | issue= 3 | pages= 383-9 | pmid=21391928 | doi=10.1111/j.1532-5415.2011.03317.x | pmc=3306056 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21391928 }} </ref><br />
**The risk of recurrent falls is particularly higher in frail, older adults.<br />
*According to various studies, [[orthostatic hypotension]] may be a [[risk factor]] for: <ref name="pmid20698925">{{cite journal| author=Fedorowski A, Hedblad B, Engström G, Gustav Smith J, Melander O| title=Orthostatic hypotension and long-term incidence of atrial fibrillation: the Malmö Preventive Project. | journal=J Intern Med | year= 2010 | volume= 268 | issue= 4 | pages= 383-9 | pmid=20698925 | doi=10.1111/j.1365-2796.2010.02261.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20698925 }} </ref> <ref name="pmid23675460">{{cite journal| author=Xin W, Lin Z, Li X| title=Orthostatic hypotension and the risk of congestive heart failure: a meta-analysis of prospective cohort studies. | journal=PLoS One | year= 2013 | volume= 8 | issue= 5 | pages= e63169 | pmid=23675460 | doi=10.1371/journal.pone.0063169 | pmc=3652866 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23675460 }} </ref> <ref name="pmid20651699">{{cite journal| author=Fedorowski A, Engström G, Hedblad B, Melander O| title=Orthostatic hypotension predicts incidence of heart failure: the Malmö preventive project. | journal=Am J Hypertens | year= 2010 | volume= 23 | issue= 11 | pages= 1209-15 | pmid=20651699 | doi=10.1038/ajh.2010.150 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20651699 }} </ref> <ref name="pmid20458003">{{cite journal| author=Fagard RH, De Cort P| title=Orthostatic hypotension is a more robust predictor of cardiovascular events than nighttime reverse dipping in elderly. | journal=Hypertension | year= 2010 | volume= 56 | issue= 1 | pages= 56-61 | pmid=20458003 | doi=10.1161/HYPERTENSIONAHA.110.151654 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20458003 }} </ref> <ref name="pmid23216860">{{cite journal| author=Fedorowski A, Melander O| title=Syndromes of orthostatic intolerance: a hidden danger. | journal=J Intern Med | year= 2013 | volume= 273 | issue= 4 | pages= 322-35 | pmid=23216860 | doi=10.1111/joim.12021 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23216860 }} </ref> <ref name="pmid9826316">{{cite journal| author=Masaki KH, Schatz IJ, Burchfiel CM, Sharp DS, Chiu D, Foley D | display-authors=etal| title=Orthostatic hypotension predicts mortality in elderly men: the Honolulu Heart Program. | journal=Circulation | year= 1998 | volume= 98 | issue= 21 | pages= 2290-5 | pmid=9826316 | doi=10.1161/01.cir.98.21.2290 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9826316 }} </ref><br />
**Cardiovascular and all-cause mortality<br />
**Cardiovascular events<br />
**[[Congestive heart failure]]<br />
**[[Atrial fibrillation]]<br />
**Cognitive decline or [[dementia]]<br />
**[[Anxiety]], [[depression]], and impaired quality of life<br />
<br />
====Prognosis====<br />
<br />
*Depending on the underlying cause of [[orthostatic hypotension]], the prognosis may vary.<br />
<br />
==Diagnosis==<br />
<br />
===Diagnostic study of choice===<br />
<br />
*[[Orthostatic vitals]] are the best diagnostic tests that are simple and easy to perform in a clinical setting. <nowiki></ref></nowiki><ref name="pmid21431947">{{cite journal| author=Freeman R, Wieling W, Axelrod FB, Benditt DG, Benarroch E, Biaggioni I | display-authors=etal| title=Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome. | journal=Clin Auton Res | year= 2011 | volume= 21 | issue= 2 | pages= 69-72 | pmid=21431947 | doi=10.1007/s10286-011-0119-5 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21431947 }} </ref><ref name="pmid19390349">{{cite journal| author=Wieling W, Schatz IJ| title=The consensus statement on the definition of orthostatic hypotension: a revisit after 13 years. | journal=J Hypertens | year= 2009 | volume= 27 | issue= 5 | pages= 935-8 | pmid=19390349 | doi=10.1097/HJH.0b013e32832b1145 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19390349 }} </ref><br />
*[[Blood pressure]] and [[heart rate]] should be measured within 2-5 minutes of standing after a 5-minute period of supine rest.<br />
*[[Orthostatic hypotension]] is diagnosed when there is:<br />
**At least a 20 mmHg decline in [[systolic blood pressure]]<br />
**At least 10 mmHg decline in [[diastolic blood pressure]]<br />
<br />
*The absence of the normal rise in [[heart rate]] on standing is a diagnostic clue to the presence of [[autonomic dysfunction]]; however, an increased [[heart rate]] cannot exclude autonomic failure.<br />
<br />
===History and Symptoms===<br />
<br />
*When evaluating a patient with [[orthostatic hypotension]], the following features in history may provide a clue to the diagnosis: <ref name="pmid17904451">{{cite journal| author=Gupta V, Lipsitz LA| title=Orthostatic hypotension in the elderly: diagnosis and treatment. | journal=Am J Med | year= 2007 | volume= 120 | issue= 10 | pages= 841-7 | pmid=17904451 | doi=10.1016/j.amjmed.2007.02.023 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17904451 }} </ref><br />
*Use of certain medications known to cause [[orthostatic hypotension]].<br />
*Recent history of [[volume depletion]] (such as [[fever]], [[fluid restriction]], [[vomiting]], [[diarrhea]], [[hemorrhage]])<br />
*Medical history of common diseases causing [[orthostatic hypotension]], such as [[congestive heart failure]], [[diabetes]], [[Parkinson's disease]], [[malignancie]]s.<br />
*History of [[alcohol]] consumption<br />
*Particular attention should be made to the presence of neurologic symptoms (e.g., [[parkinsonism]], [[ataxia]], [[peripheral neuropathy]]) or symptoms of [[autonomic dysfunction]] (e.g. abnormal [[pupillary response]], chronic [[constipation]], [[erectile dysfunction]], [[urinary incontinence]])<br />
<br />
*Symptoms of [[orthostatic hypotension]] are prominent immediately upon standing, might improve in sitting position, and disappear in the supine position (i.e., postural symptoms). <ref name="pmid26879239">{{cite journal| author=Palma JA, Norcliffe-Kaufmann L, Kaufmann H| title=An orthostatic hypotension mimic: The inebriation-like syndrome in Parkinson disease. | journal=Mov Disord | year= 2016 | volume= 31 | issue= 4 | pages= 598-600 | pmid=26879239 | doi=10.1002/mds.26516 | pmc=4833617 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26879239 }} </ref><ref name="pmid18256396">{{cite journal| author=Freeman R| title=Clinical practice. Neurogenic orthostatic hypotension. | journal=N Engl J Med | year= 2008 | volume= 358 | issue= 6 | pages= 615-24 | pmid=18256396 | doi=10.1056/NEJMcp074189 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18256396 }} </ref><br />
*Symptoms may also be seen in association with meals, exercise, and prolonged standing<br />
*Symptoms are due to cerebral [[hypoperfusion]]<br />
*Symptoms usually last for few minutes<br />
*The most common symptoms are [[lightheadedness]] and [[dizziness]] upon standing.<br />
*Other symptoms include:<br />
<br />
:*Generalized [[weakness]]<br />
:*[[Headache]]<br />
:*Blurred or dimmed [[eye|vision]] (possibly to the point of momentary [[blindness]])<br />
:*[[Fatigue]]<br />
:*[[Cognition|Cognitive]] impairment<br />
:*[[Loss of consciousness]] ([[syncope]]) may be seen in severe cases<br />
<br />
===Physical Examination===<br />
Common physical examination findings of orthostatic hypotension include checking the [[blood pressure]], pulse, and symptoms while having the [[patient]] in the standing and sitting position. <ref name="pmid23569093">{{cite journal |vauthors=Stewart JM |title=Common syndromes of orthostatic intolerance |journal=Pediatrics |volume=131 |issue=5 |pages=968–80 |date=May 2013 |pmid=23569093 |pmc=3639459 |doi=10.1542/peds.2012-2610 |url=}}</ref><br />
<br />
===Laboratory Findings===<br />
There are no diagnostic laboratory findings associated with orthostatic hypotension. While the definitive diagnosis of orthostatic hypotension is made clinically, other tests contribute to understanding the [[risks]] of disease and may provide clues to the selection of [[treatment]] options. <ref name="pmid17904451">{{cite journal| author=Gupta V, Lipsitz LA| title=Orthostatic hypotension in the elderly: diagnosis and treatment. | journal=Am J Med | year= 2007 | volume= 120 | issue= 10 | pages= 841-7 | pmid=17904451 | doi=10.1016/j.amjmed.2007.02.023 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17904451 }} </ref><br />
These tests include those that access the underlying [[cause]] that may be altered in patients suffering from [[orthostatic hypotension]]. <br />
<br />
*[[CBC]]<br />
*[[Basic metabolic panel]]<br />
*[[Serum electrolytes]]<br />
*Blood [[Glucose]]<br />
*[[Creatinine]]<br />
*[[TSH]]<br />
<br />
===Electrocardiogram===<br />
An [[ECG]] may be helpful in the diagnosis of cardiovascular causes of [[orthostatic hypotension]].<br />
<br />
===X-ray===<br />
<br />
There are no [[x-ray]] findings associated with orthostatic hypotension.<br />
<br />
===Echocardiography===<br />
<br />
Echocardiography may be helpful in the diagnosis of [[orthostatic hypotension]]. Findings on an [[echocardiography]] diagnostic of [[orthostatic hypotension]] include cardiac structural changes such as [[left ventricular hypertrophy]], development of [[diastolic dysfunction]], and decreased right chamber volume. <ref name="pmid26643688">{{cite journal| author=Magnusson M, Holm H, Bachus E, Nilsson P, Leosdottir M, Melander O | display-authors=etal| title=Orthostatic Hypotension and Cardiac Changes After Long-Term Follow-Up. | journal=Am J Hypertens | year= 2016 | volume= 29 | issue= 7 | pages= 847-52 | pmid=26643688 | doi=10.1093/ajh/hpv187 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26643688 }} </ref><br />
<br />
===CT scan===<br />
<br />
A CT scan may be helpful in the diagnosis of [[orthostatic hypotension]]. Findings on a CT scan diagnostic of [[orthostatic hypotension]] include the presence of a [[cerebral tumor]] or [[communicating hydrocephalus]]. <ref name="pmid23180176">{{cite journal| author=Metzler M, Duerr S, Granata R, Krismer F, Robertson D, Wenning GK| title=Neurogenic orthostatic hypotension: pathophysiology, evaluation, and management. | journal=J Neurol | year= 2013 | volume= 260 | issue= 9 | pages= 2212-9 | pmid=23180176 | doi=10.1007/s00415-012-6736-7 | pmc=3764319 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23180176 }} </ref><br />
<br />
===MRI===<br />
<br />
A brain [[MRI]] may be helpful in the diagnosis of [[orthostatic hypotension]]. Findings on a [[MRI]] suggestive of [[orthostatic hypotension]] include:<br />
<br />
*[[Neurodegenerative disorder]]<br />
*[[Stroke]]<br />
<br />
===Other Imaging Findings===<br />
<br />
There are no other diagnostic studies associated with [[orthostatic hypotension]].<br />
<br />
===Other Diagnostic Studies===<br />
<br />
There are no other diagnostic studies associated with [[orthostatic hypotension]].<br />
<br />
==Treatment==<br />
<br />
*Asymptomatic [[hypotension]] is a common finding in practice and does not require any treatment.<br />
*There is no specific target [[blood pressure]] goals in the management of orthostatic hypotension.<br />
*However, management is targeted to alleviate symptoms, prevention of future falls, and excessive [[supine hypertension]].<br />
*Management of orthostatic hypotension can be categorized into lifestyle modifications and medical therapy.<br />
*Education of the patient and non-pharmacological treatments are the cornerstone of treatment of orthostatic hypotension.<br />
{{familytree/start}}<br />
{{familytree | | | | | | | | | | | | | | | | A01 | | | | | |A01=Drop of systolic BP > 20 mmHg (30 for [[hypertensive]] [[patients]])}}<br />
{{familytree | | | | | | | | | | | | | | | | |!| | | | | | | | }}<br />
{{familytree | | | | | | | | | |,|-|-|-|-|-|-|^|-|-|-|-|-|-|.| }}<br />
{{familytree | | | | | | | | | C01 | | | | | | | | | | | |C02|C01=Symptomatic|C02=Asymptomatic}}<br />
{{familytree | | | | | | | | | |!| | | | | | | | | | | | | |!| }}<br />
{{familytree | | | | | | | | | D01 | | | | | | | | | | | |D02|D01=Non-pharmacological treatment|D02=Observation<br />
and follow-up}}<br />
{{familytree | | | | | | | | | |!| | | | | | | | | }}<br />
{{familytree | | | | | | | | | E01 | | | | | | | |E01=Persistence of symptoms}}<br />
{{familytree | | | | | | | | | |!| | | | | | | | | }}<br />
{{familytree | | | | | | | | | E01 | | | | | | | |E01=Pharmacological Treatment}}<br />
{{familytree | | | | | | | | | |!| | | | | | | | | }}<br />
{{familytree | | |,|-|-|-|-|-|-|^|-|-|-|-|-|-|.| | }}<br />
{{familytree | | |!| | | | | | | | | | | | | |!| | }}<br />
{{familytree | | E01 | | | | | | | | | | | | E02 | | |E01=No supine [[hypertension]] or chronic [[heart failure]]|E02=Supine hypertension or chronic [[heart failure]]: }}<br />
{{familytree | | |!| | | | | | | | | | | | | |!| | }}<br />
{{familytree | | E01 | | | | | | | | | | | | E02 | | E01= [[Fludrocortisone]]<br>[[Midodrine]]|E02=[[Midodrine]]}}<br />
{{familytree/end}}<br />
<br />
<br />
===Non-Pharmacological Therapy===<br />
<br />
*Education of the patient and non-pharmacological treatments are the cornerstone of treatment of orthostatic hypotension.<ref name="Singer-2003">{{cite journal | author=Singer W, Opfer-Gehrking TL, McPhee BR, Hilz MJ, Bharucha AE, Low PA. | title=Acetylcholinesterase inhibition: a novel approach in the treatment of neurogenic orthostatic hypotension. | journal=J Neurol Neurosurg Psychiatry | year=2003 | volume=74 | issue=9 | pages=1294-8 | id=PMID 12933939}}</ref><ref name="FigueroaBasford2010">{{cite journal|last1=Figueroa|first1=J. J.|last2=Basford|first2=J. R.|last3=Low|first3=P. A.|title=Preventing and treating orthostatic hypotension: As easy as A, B, C|journal=Cleveland Clinic Journal of Medicine|volume=77|issue=5|year=2010|pages=298–306|issn=0891-1150|doi=10.3949/ccjm.77a.09118}}</ref><ref name="FreemanAbuzinadah2018">{{cite journal|last1=Freeman|first1=Roy|last2=Abuzinadah|first2=Ahmad R.|last3=Gibbons|first3=Christopher|last4=Jones|first4=Pearl|last5=Miglis|first5=Mitchell G.|last6=Sinn|first6=Dong In|title=Orthostatic Hypotension|journal=Journal of the American College of Cardiology|volume=72|issue=11|year=2018|pages=1294–1309|issn=07351097|doi=10.1016/j.jacc.2018.05.079}}</ref><ref name="FreemanAbuzinadah20182">{{cite journal|last1=Freeman|first1=Roy|last2=Abuzinadah|first2=Ahmad R.|last3=Gibbons|first3=Christopher|last4=Jones|first4=Pearl|last5=Miglis|first5=Mitchell G.|last6=Sinn|first6=Dong In|title=Orthostatic Hypotension|journal=Journal of the American College of Cardiology|volume=72|issue=11|year=2018|pages=1294–1309|issn=07351097|doi=10.1016/j.jacc.2018.05.079}}</ref><ref name="pmid/10.1016/j.jacc.2015.06.1084">{{cite journal| author=Schmoldt A, Benthe HF, Haberland G| title=Digitoxin metabolism by rat liver microsomes. | journal=Biochem Pharmacol | year= 1975 | volume= 24 | issue= 17 | pages= 1639-41 | pmid=/10.1016/j.jacc.2015.06.1084 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10 }} </ref><ref name="pmid14705758">{{cite journal| author=Bradley JG, Davis KA| title=Orthostatic hypotension. | journal=Am Fam Physician | year= 2003 | volume= 68 | issue= 12 | pages= 2393-8 | pmid=14705758 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14705758 }} </ref><ref name="pmid10071663">{{cite journal| author=Carlson JE| title=Assessment of orthostatic blood pressure: measurement technique and clinical applications. | journal=South Med J | year= 1999 | volume= 92 | issue= 2 | pages= 167-73 | pmid=10071663 | doi=10.1097/00007611-199902000-00002 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10071663 }} </ref><br />
*Cessation of orthostatic hypotension inducing [[drugs]] such as [[anti-hypertensives]]s in patients with a mean [[blood pressure]] below target value is recommended.<br />
*Avoidance of certain factors that aggravate hypotension such as heat, and alcohol intake.<br />
*Consumption of large meals induces [[splanchnic]] [[vasodilation]] thereby resulting in hypotension [[postprandially]].<br />
**Fractionated meals are recommended in patients with postprandial symptoms.<br />
<br />
{| class="wikitable"<br />
|+<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Non-Pharmacological methods<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Mechanism of alleviating hypotension<br />
! align="center" style="background: #4479BA; color: #FFFFFF " |Recommendations<br />
|-<br />
|Elastic stockings<br />
|<br />
*Reduce [[venous pooling]] in the splanchnic and mesenteric circulations.<br />
|<br />
*Elastic stockings expanding up to the waist are recommended.<br />
*Leg compression alone is not considered effective.<br />
**Due to the minor venous capacitance of legs relative to the abdomen.<br />
*Separate abdominal and leg compression is recommended to avoid patient discomfort.<br />
|-<br />
|Physical Maneuvers<br />
|<br />
*Transiently increase venous return and peripheral vascular resistance<br />
|<br />
*Contraction of a group of muscles<br />
*Leg crossing<br />
*Toe raising<br />
*Bending at the waist<br />
|-<br />
|Head up tilt sleeping<br />
|<br />
*Enhance orthostatic tolerance upon the first morning rise<br />
|<br />
*Results in reduction in supine hypertension, pressure-natriuresis<br />
|-<br />
|Intravascular volume<br />
|<br />
*Tubular loss of salt and fluid<br />
*Decreased vascular tone creates relative hypovolemia<br />
|<br />
*Volume expansion can alleviate symptoms even in the presence of normal intravascular volume.<br />
**2 liters of water and 6 g of salt<br />
**Twenty-four-hour urine collection is helpful to guide treatment and follow-up<br />
|-<br />
|Intake of cold water<br />
|<br />
*Increase systolic orthostatic hypotension by more than 30 mmHg<br />
**Via gastropressor response<br />
|<br />
*Rapid drinking of approximatively 500 mL of cold water, independent of daily water intake<br />
|}<br />
<br />
===Medical Therapy===<br />
<br />
*Pharmacological: Some drugs that are used in the treatment of orthostatic hypotension include [[fludrocortisone]] (Florinef), [[erythropoietin]], [[midodrine]] and [[Pyridostigmine bromide]] (Mestinon) <ref name="pmid19422980">{{cite journal| author=Benditt DG, Nguyen JT| title=Syncope: therapeutic approaches. | journal=J Am Coll Cardiol | year= 2009 | volume= 53 | issue= 19 | pages= 1741-51 | pmid=19422980 | doi=10.1016/j.jacc.2008.12.065 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19422980 }} </ref><ref name="pmid24697914">{{cite journal| author=Wieling W, van Dijk N, Thijs RD, de Lange FJ, Krediet CT, Halliwill JR| title=Physical countermeasures to increase orthostatic tolerance. | journal=J Intern Med | year= 2015 | volume= 277 | issue= 1 | pages= 69-82 | pmid=24697914 | doi=10.1111/joim.12249 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24697914 }} </ref><ref name="pmid18420158">{{cite journal| author=Low PA, Singer W| title=Management of neurogenic orthostatic hypotension: an update. | journal=Lancet Neurol | year= 2008 | volume= 7 | issue= 5 | pages= 451-8 | pmid=18420158 | doi=10.1016/S1474-4422(08)70088-7 | pmc=2628163 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18420158 }} </ref><ref name="pmid17346129">{{cite journal| author=Maule S, Papotti G, Naso D, Magnino C, Testa E, Veglio F| title=Orthostatic hypotension: evaluation and treatment. | journal=Cardiovasc Hematol Disord Drug Targets | year= 2007 | volume= 7 | issue= 1 | pages= 63-70 | pmid=17346129 | doi=10.2174/187152907780059029 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17346129 }} </ref><br />
<br />
===Initial Therapy===<br />
<br />
*Preferred regimen (1): Fludrocortisone acetate at a dose of 0.1 mg per day, administered in the morning, which can eventually be increased up to 0.3 mg per day.<br />
**Considered first-line regimen for hypotension in the absence of [[heart failure]] and [[supine hypertension]]<br />
*Preferred regimen (2): Midodrine 2.5 to 10 mg three times a day.<br />
**Max dose should not exceed 40 mg/day.<br />
*Preferred regimen (2): Droxidopa starts at 100 mg and escalates to 600 mg three times per day. <br />
**Patients should not take droxidopa within four to five hours of bedtime in order to limit supine hypertension.<br />
<br />
===Second-line Therapy===<br />
<br />
*Preferred regimen (1): [[Erythropoietin]] is administered SC or IV at doses between 25 to 75 units/kg three times a week.<br />
*Preferred regimen (1): [[Methylxanthine]] caffeine 100 to 250 mg three times a day with meals.<br />
*Preferred regimen (1): [[Pyridostigmine]] initiated at a dose of 30 mg three times daily, up to a maximum dose of 90 mg three times daily.<br />
*Preferred regimen (1): [[Non-steroidal anti-inflammatory drug|Non-steroidal anti-inflammatory drugs]] are rarely effective as monotherapy<br />
**They can supplement treatment with fludrocortisone or a sympathomimetic agent.<br />
<br />
===Third-line Therapy===<br />
<br />
*Preferred regimen (1): [[Atomoxetine]]<br />
*Preferred regimen (1): [[Vasopressin]] analogs (desmopressin (DDAVP))<br />
*Preferred regimen (1): [[Yohimbine]] a single dose of yohimbine (5.4 mg). <br />
**[[Yohimbine]] has limited availability in the United States.<br />
*Preferred regimen (1): [[Somatostatin]] subcutaneous doses range from 25 to 200 mcg.<br />
*Preferred regimen (1): [[Ergotamine|Ergotamine-caffeine]] (1 mg/100 mg) up to twice-daily dosing in patients with orthostatic hypotension.<br />
*Preferred regimen (1): [[Metoclopramide]] and [[domperidone]]<br />
<br />
===Primary Prevention===<br />
Effective measures for the primary prevention of orthostatic hypotension include:<br />
<br />
ABCDEF method<br />
<br />
*A. Abdominal compression: Wear an abdominal binder when out of bed<br />
*B. A bolus of water/elevate bed: On bad days, drink two 8-ounce glasses of cold water prior to prolonged standing and sleep with the head of the bed raised about 4 inches<br />
*C. [[Counter-maneuvers]]: While standing, contract the lower abdominal muscles for about 30 seconds<br />
*D. [[Drugs]]: [[Midodrine]], [[Pyridostigmine]], or [[Fludrocortisone]] can be used to elevate [[blood pressure]] (acknowledge any [[medications]] currently taken that can lower [[blood pressure]])<br />
*E. Education & Exercise: Note any symptoms that indicate a fall in [[blood pressure]] while standing, recognize conditions that lower [[blood pressure]] (i.e. heavy metals, temperature changes, exercise, change in position)<br />
*F. Fluids: Stay hydrated<br />
<br />
==References==<br />
{{Reflist|2}}<br />
[[Category:Cardiology]]<br />
<br />
{{Circulatory system pathology}}<br />
<br />
<br />
[[nl:Orthostatische hypotensie]]<br />
[[es:Hipotensión ortostática]]<br />
[[fr:Hypotension orthostatique]]<br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Hematuria_resident_survival_guide&diff=1692151Hematuria resident survival guide2021-02-26T14:47:17Z<p>Caroline Collis: </p>
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<div><div style="width: 1px; height: 1px; background-color: #999999; position: fixed; top: 10px; left: 10px"></div><br />
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{| class="infobox" style="margin: 0 0 0 0; border: 0; float: right; width: 5%; background: #A8A8A8; position: fixed; top: 250px; right: 20px; border-radius: 10px 10px 10px 10px;" cellpadding="0" cellspacing="0" ;<br />
|-<br />
! style="padding: 0 5px; font-size: 80%; background: #A8A8A8;" align="center" |{{fontcolor|#2B3B44|Hematuria<BR>Resident Survival Guide}}<br />
|-<br />
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC; border-radius: 5px 5px 5px 5px;" align="left" |[[{{PAGENAME}}#Overview|Overview]]<br />
|-<br />
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC; border-radius: 5px 5px 5px 5px;" align="left" |[[{{PAGENAME}}#Causes|Causes]]<br />
|-<br />
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC; border-radius: 5px 5px 5px 5px;" align="left" |[[{{PAGENAME}}#Complete Diagnostic Approach|Diagnosis]]<br />
|-<br />
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC; border-radius: 5px 5px 5px 5px;" align="left" |[[{{PAGENAME}}#Treatment|Treatment]]<br />
|-<br />
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC; border-radius: 5px 5px 5px 5px;" align="left" |[[{{PAGENAME}}#Dos|Dos]]<br />
|-<br />
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC; border-radius: 5px 5px 5px 5px;" align="left" |[[{{PAGENAME}}#Don'ts|Don'ts]]<br />
|}<br />
__NOTOC__<br />
<br />
{{CMG}};{{AE}}{{TAM}} <br />
<br />
{{SK}} [[Hematuria resident survival guide|Blood in urine resident survival guide]]<br />
<br />
==Overview==<br />
Presence of >5 [[RBC|red blood cells (RBCs)]] per high-power [[Microscopic|microscopi]]<nowiki/>c field in the urine is called [[hematuria]]. It can have either [[benign]] or [[malignant]] [[etiology]]. [[Patients]] with [[hematuria]] can be [[asymptomatic]]. Therefore, all [[patients]] presenting with a single episode of [[hematuria]] require urgent investigation. [[Microscopic hematuria]], or microhematuria (MH), is defined as the presence of [[RBC]] on [[microscopic examination]] of the [[urine]] not evident on visual inspection of the [[urine]]. The prevalence of MH among healthy participants in screening studies is 6.5% (95% [[confidence interval]] [CI] 3.4 to 12.2), with higher rates in studies with a predominance of [[male]]<nowiki/>s, older [[patients]], and smokers.<br />
<br />
<br />
==Causes==<br />
===Life-Threatening Causes===<br />
Life-threatening causes include conditions that may result in death or permanent [[disability]] within 24 hours if left untreated.<ref name="pmid27261791">{{cite journal |vauthors=Avellino GJ, Bose S, Wang DS |title=Diagnosis and Management of Hematuria |journal=Surg. Clin. North Am. |volume=96 |issue=3 |pages=503–15 |date=June 2016 |pmid=27261791 |doi=10.1016/j.suc.2016.02.007 |url=}}</ref><ref name="pmid11554278">{{cite journal |vauthors=Sokolosky MC |title=Hematuria |journal=Emerg. Med. Clin. North Am. |volume=19 |issue=3 |pages=621–32 |date=August 2001 |pmid=11554278 |doi= |url=}}</ref><ref name="pmid27440856">{{cite journal |vauthors=Silverman JA, Patel K, Hotston M |title=Tuberculosis, a rare cause of haematuria |journal=BMJ Case Rep |volume=2016 |issue= |pages= |date=July 2016 |pmid=27440856 |doi=10.1136/bcr-2016-216428 |url=}}</ref><ref name="pmid21445110">{{cite journal |vauthors=Ogunjimi MA, Adetayo FO, Tijani KH, Jeje EA, Ogo CN, Osegbe DN |title=Gross haematuria among adult Nigerians: current trend |journal=Niger Postgrad Med J |volume=18 |issue=1 |pages=30–3 |date=March 2011 |pmid=21445110 |doi= |url=}}</ref><br />
<br />
*[[Bladder rupture|Intraperitoneal bladder rupture]]<br />
<br />
*[[Fistula|Ureteroarterial fistula]]<br />
<br />
*[[Hemorrhagic cystitis]]<br />
<br />
*[[Heart failure]]<br />
<br />
*[[Malignant hypertension]]<br />
<br />
*[[Shock]]<br />
<br />
===Common Causes===<br />
{| class="wikitable" border="1"<br />
! style="width: 300px;background:#4479BA" |{{fontcolor|#FFF| '''Children'''<ref name="AminZaritsky2011">{{cite journal|last1=Amin|first1=Nimisha|last2=Zaritsky|first2=Joshua J.|title=Hematuria|year=2011|pages=258–261|doi=10.1016/B978-0-323-05405-8.00069-3}}</ref>}}!! style="width: 300px;background:#4479BA" |{{fontcolor|#FFF| '''Age <50 years'''<ref name="Surgery (Oxford)">{{cite web |url=http://www.surgeryjournal.co.uk/article/S0263-9319(10)00199-7/abstract |title=www.surgeryjournal.co.uk |format= |work= |accessdate=}}</ref>}}!! style="width: 300px;background:#4479BA" |{{fontcolor|#FFF| '''Age >50 years'''<ref name="Surgery (Oxford)">{{cite web |url=http://www.surgeryjournal.co.uk/article/S0263-9319(10)00199-7/abstract |title=www.surgeryjournal.co.uk |format= |work= |accessdate=}}</ref>}}<br />
|-<br />
| valign="top" |<br />
*[[Urinary tract infection]]<br />
*[[Benign familial hematuria]] or [[Thin basement membrane disease]]<br />
*[[IgA nephropathy]]<br />
*[[hypercalciuria|Idiopathic hypercalciuria]]<br />
*Transient unexplained<br />
| valign="top" |<br />
*[[Urinary tract infection]]<br />
*Transient unexplained<br />
*[[Kidney stone|Stones]]<br />
*[[Exercise]]<br />
*[[Trauma]]<br />
*[[Polycystic kidney disease]]<br />
| valign="top" |<br />
*[[Urinary tract infection]]<br />
*Transient unexplained<br />
*[[Kidney stone|Stones]]<br />
*[[Benign prostatic hyperplasia]]<br />
*[[Bladder cancer]]<br />
*[[Renal carcinoma]]<br />
*[[Prostate cancer]]<br />
|}<br />
<br />
==Diagnosis==<br />
The approach to the diagnosis of [[hematuria]] is based on a step-wise testing strategy. Below is an algorithm summarizing the identification and laboratory diagnosis of [[hematuria]]. The algorithm was developed and modified according to the American Urological Evaluation (AUA) Guideline. <ref name="urlAUA Guidelines 2020: Microhematuria">{{cite web |url=https://www.urotoday.com/conference-highlights/aua-2020/aua-2020-bladder-health/122536-aua-guidelines-2020-microhematuria.html |title=AUA Guidelines 2020: Microhematuria |format= |work= |accessdate=}}</ref><ref name="pmid27261791">{{cite journal| author=Avellino GJ, Bose S, Wang DS| title=Diagnosis and Management of Hematuria. | journal=Surg Clin North Am | year= 2016 | volume= 96 | issue= 3 | pages= 503-15 | pmid=27261791 | doi=10.1016/j.suc.2016.02.007 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27261791 }}</ref><br />
{{familytree/start |summary=Hematuria.}}<br />
{{familytree | | | | | | | | | | | | | A01 | | | A01=<div style="float: left; text-align: left; width: 15em; padding:1em;">'''Seek proper history:'''<div class="mw-collapsible mw-collapsed"><br> ❑ Onset <br> ❑ Progression <br> ❑ Pain/burning on urination<br> ❑ [[Fever]]<br> ❑ Abdominal pain/flank pain<br> ❑ [[Polyuria]], frequency <br> ❑ Straining during urination <br> ❑ [[Nocturia]] <br> ❑ Weak stream <br> ❑ Dribbling </div> }}<br />
{{familytree | | | | | | | | | | | | | |!| | | | | | }}<br />
{{familytree | | | | | | | | | | | | | B01 | | | B01=<div style="float: left; text-align: left; width: 15em; padding:1em;">'''Examine the patient:'''<div class="mw-collapsible mw-collapsed"><BR>❑ [[Tachypnea]]<br>❑ Cold and clammy skin <br>❑ [[Hypotension]]<br>❑ HEENT signs:<br />
* Conjunctival [[pallor]]<br />
* [[Jaundice]]<br><br />
❑ Cardiovascular exam:<br />
* [[Tachycardia]]<br><br />
❑ Abdominal exam:<br />
* Costovertebral angle (CVA) tenderness<br> <br />
❑ skin exam:<br />
* Look for rash<br><br />
❑ Musculoskeletal exam:<br />
* Joint pain</div>}}<br />
{{familytree | | | | | | | | | | | | | |!| | | | | | | }}<br />
{{familytree | | | | | | | | | | | | | C01 | | | C01=<div style="float: left; text-align: left; width: 15em; padding:1em;">'''Initial workup for [[hematuria]]:'''<div class="mw-collapsible mw-collapsed"><br> ❑ [[Complete blood count]] (CBC) with differential <br>❑ [[Urinalysis]], urine strain, and culture <br>❑ [[BUN-to-creatinine ratio|Blood urea nitrogen:creatinine]] (BUN:Cr) <br>❑ [[Ultrasound]] (U/S) and [[CT Scan|CT abdomen]] <br>❑ [[Cystoscopy]]</div>}}<br />
{{familytree | | | | | | | | | | | | | |!| | | | | | | }}<br />
{{familytree | | | | | | | | | | | | | D01 | | | D01=<div style="float: left; text-align: center; width: 15em; padding:1em;">'''[[Dipsticks|Urine dipstick]] positive for heme:'''<br><br />
*Does microscopic urinalysis reveal >3 RBC/HPF?</div>}}<br />
{{familytree | | | | | | | | | | |,|-|-|^|-|-|.| | | | }}<br />
{{familytree | | | | | | | | | | M01 | | | | M02 | |M01=<div style="float: left; text-align: center; width: 10em; padding:1em;">'''Yes''' <br>❑ Consider [[hematuria]]|M02=<div style="float: left; text-align: left; width: 20em; padding:1em;">'''No''' <br> Causes include: <br>❑ Ingestion of certain foods: beets, blackberries, food coloring ❑ Ingestion of certain medications: [[Chloroquine]], [[Ibuprofen]], [[Iron]], [[Sorbitol]], [[Nitrofurantoin]], [[Phenazopyridine]], [[Urate|Urates]] or [[Rifampin]] (which often produces orange urine) ❑ [[Hemoglobinuria]]: often in the setting of [[hemolytic anemia]] ❑ [[Myoglobinuria]]'': related to muscle damage ([[rhabdomyolysis]]), often after vigorous exercise or trauma ❑ [[Urinary tract infection]]'': secondary to the action of [[Peroxidase|bacterial peroxidases]] on the [[Dipsticks|dipstick]] ❑ Delay in reading [[Dipsticks|urine dipstick]] after submersion in [[urine]] ❑ Presence of semen in [[urine]]<ref name="AminZaritsky2011">{{cite journal|last1=Amin|first1=Nimisha|last2=Zaritsky|first2=Joshua J.|title=Hematuria|year=2011|pages=258–261|doi=10.1016/B978-0-323-05405-8.00069-3}}</ref></div>}}<br />
{{familytree | | | | | | | | | | |!| | | | | | | }}<br />
{{familytree | | | | | | | | | | E01 | | | | | | | E01=<div style="float: left; text-align: center; width: 10em; padding:1em;">'''[[Hematuria]]'''</div>}}<br />
{{familytree | | | | | | | | | | |!| | | | | | | }}<br />
{{familytree | | | | | | | | | | F01 | | | | | | | F01=<div style="float: left; text-align: left; width: 10em; padding:1em;">'''Is acute onset unilateral flank pain present?'''</div>}}<br />
{{familytree | | | | | | | |,|-|-|^|-|-|.| | | | | }}<br />
{{familytree | | | | | | | G01 | | | | G02 | | | | G01=<div style="float: left; text-align: center; width: 10em; padding:1em;">'''Yes''' <br><br />
Evaluate [[Kidney stones|Nephrolithiasis]]|G02=<div style="float: left; text-align: center; width: 10em; padding:1em;">''' No''' <br><br />
Are any of the following present?<br>❑ Symptoms of [[urinary tract infection]] <br>❑ Urine WBCs<br>❑ Positive [[urine|urine nitrite]]</div>}}<br />
{{familytree | | | | | | | | | | |,|-|-|^|-|-|.| }} <br />
{{familytree | | | | | | | | | | H01 | | | | H02 |H01=<div style="float: left; text-align: center; width: 10em; padding:1em;">'''No'''|H02=<div style="float: left; text-align: center; width: 10em; padding:1em;">'''Yes'''</div>}} <br />
{{familytree | | | | | | | | | | |!| | | | | |!| | | | | | | }}<br />
{{familytree | | | | | | | | | | |!| | | | | I01 | I01=<div style="float: left; text-align: left; width: 10em; padding:1em;">'''[[Urine culture]] to exclude [[urinary tract infection]]'''</div>}} <br />
{{familytree | | | | | | | | | | |!| |,|-|-|-|^|-|-|.| }}<br />
{{familytree | | | | | | | | | | |!| J01 | | | | | J02 |J01=<div style="float: left; text-align: center; width: 10em; padding:1em;">'''Negative'''|J02=<div style="float: left; text-align: center; width: 10em; padding:1em;">'''Positive'''</div>}}<br />
{{familytree | | | | | | | | | | |!| |!| | | | | | |!| | | | | | | }}<br />
{{familytree | | | | | | | | | | | K01 | | | | | | K02 | K01=<div style="float: left; text-align: left; width: 10em; padding:1em;">'''Is [[hematuria]] visible <br> (pink, red, or brown urine color, or blood clots)?'''|K02=<div style="float: left; text-align: center; width: 10em; padding:1em;">'''Treat [[urinary tract infection]]'''<br>❑ Repeat [[urinalysis]] with microscopy in six weeks</div>}}<br />
{{familytree | | | | | | | | | |,|-|^|-|.| | | |,|-|^|-|.| | }}<br />
{{familytree | | | | | | | | | L01 | | L02 | | L03 | | L04 |L01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Yes'''<br> '''❑ [[Hematuria|Gross Hematuria]]'''|L02=<div style="float: left; text-align: center; width: 10em; padding:1em;">'''No'''<br>❑ '''[[Hematuria|Microscopic Hematuria]]'''|L03=<div style="float: left; text-align: center; width: 10em; padding:1em;">'''Persistent [[hematuria]]'''<br>❑ Refer to [[hematuria]] (above)|L04=<div style="float: left; text-align: center; width: 10em; padding:1em;">'''No [[hematuria]]'''<br>❑ No further evaluation required </div>}}<br />
{{Family tree/end}}<br />
<br />
<br />
===Gross Hematuria===<br />
<br />
{{familytree/start |summary=Gross Hematuria.}}<br />
{{familytree | | | | | | | | | | | | A01 | |A01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''[[Hematuria|Gross Hematuria]]'''</div>}}<br />
{{familytree | | | | | | | | | | | | |!| | | }}<br />
{{familytree | | | | | | | | | | | | B01 | | B01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Are blood clots present/visible in the urine?'''</div>}}<br />
{{familytree | | | | | | | | | |,|-|-|^|-|-|.| }} <br />
{{familytree | | | | | | | | | C01 | | | | C02 |C01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''No'''<br><br> '''Is there any evidence suggesting glomerular bleeding?'''<br>❑ [[Albuminuria]] (quantitative or semiquantitative)<br>❑ Acutely elevated serum [[creatinine]] <br>❑ [[Hypoalbuminemia]] <br>❑ Dysmorphic RBCs <br>❑ RBCs casts <br>❑ WBCs casts <br>❑ New or worsening [[hypertension]] <br>❑ New or worsening [[edema]]|C02=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Yes'''<br><br> '''Order the following:'''<br>❑ [[CT Scan|Abdominopelvic CT]] with and without contrast for urography<br>❑ Urgent urologic referral </div>}}<br />
{{familytree | | | | | | |,|-|-|^|-|.| }}<br />
{{familytree | | | | | | D01 | | | D02 |D01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Yes'''|D02=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''No'''</div>}}<br />
{{familytree | | | | | | |!| | | | |!| }}<br />
{{familytree | | | | | | E01 | | | |!| |E01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Refer patient to nephrology'''</div>}}<br />
{{familytree | | | |,|-|-|^|-|-|.| |!| }}<br />
{{familytree | | | F01 | | | | | F02 | | |F01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Cause identified'''<br>❑ Treatment of the specific cause|F02=<div style="float: left; text-align: center; width: 20em; " padding:1em;">'''Cause not identified'''<br>❑ Female of childbearing potential?</div>}}<br />
{{familytree | | | | | | | |,|-|-|^|-|.| | }}<br />
{{familytree | | | | | | | G01 | | | G02 | |G01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Yes'''<br>❑ Perform [[pregnancy test]]|G02=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''No'''</div>}}<br />
{{familytree | | | | |,|-|-|^|-|-|.| |!| |}}<br />
{{familytree | | | | H01 | | | | | H02 | | |H01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Positive'''<br><br>❑ Perform [[ultrasound]] of kidneys and bladder. Avoid further evaluation, if possible, until after delivery.|H02=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Negative'''<br><br>'''Order the following:'''<br>❑ [[Ct scan|Abdominopelvic CT]] with and without contrast for urography<br>❑ Urology referral for [[cystoscopy]]</div>}}<br />
{{familytree | | | | | | | | |,|-|-|^|-|.| | }}<br />
{{familytree | | | | | | | | I01 | | | I02 | | |I01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Cause identified'''<br><br>❑ Treatment of the specific cause|I02=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Cause not identified'''<br><br>❑ Has the patient already had a nephrology evaluation?</div>}}<br />
{{familytree | | | | | | | | | | |,|-|-|^|-|.| | }}<br />
{{familytree | | | | | | | | | | J01 | | | J02 | | |J01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''No'''<br><br>❑ Refer patient to nephrology|J02=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Yes'''<br><br> '''Annual [[urinalysis]]'''<br>❑ If negative for two years, stop<br>❑ If persistently positive for three years, repeat anatomic evaluation.</div>}}<br />
{{Family tree/end}}<br />
<br />
===Microscopic Hematuria===<br />
<br />
{{familytree/start |summary=Microscopic Hematuria.}}<br />
{{familytree | | | | | | | | | | | | A01 | |A01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''[[Hematuria|Microscopic Hematuria]]'''</div>}}<br />
{{familytree | | | | | | | | | | | | |!| | | }}<br />
{{familytree | | | | | | | | | | | | B01 | | B01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Do any of the following apply?'''<br>❑ [[Urine]] collected from a women during menses<br>❑ [[Urine]] collected shortly after vigorous exercise<br>❑ [[Urine]] collected shortly after acute trauma</div>}}<br />
{{familytree | | | | | | | | | |,|-|-|^|-|-|.| }} <br />
{{familytree | | | | | | | | | C01 | | | | C02 |C01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''No'''|C02=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Yes'''</div>}}<br />
{{familytree | | | | | | | | | |!| | | | | |!| | | | | }}<br />
{{familytree | | | | | | | | | |!| | | | | D02 |D02=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Repeat [[urinalysis]] with microscopy at least six weeks later and in the absence of menses, vigorous exercise, and trauma '''</div>}}<br />
{{familytree | | | | | | | | | |!| |,|-|-|-|^|-|-|-|-|-|.| | }}<br />
{{familytree | | | | | | | | | |!| E01 | | | | | | | | E02 |E01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Persistent [[hematuria]]'''|E02=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''No [[hematuria]]'''</div>}}<br />
{{familytree | | | | | | | | | |!| |!| | | | | | | | | |!| | }}<br />
{{familytree | | | | | | | | | | F01 | | | | | | | | | F02 | |F01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Is there any evidence suggesting glomerular bleeding?'''<br>❑ [[Albuminuria]] (quantitative or semi-quantitative)<br>❑ Acutely elevated serum [[creatinine]]<br>❑ [[Hypoalbuminemia]]<br>❑ Dysmorphic RBCs<br>❑ RBC casts<br>❑ WBC casts<br>❑ New or worsening [[hypertension]]<br>❑ New or worsening [[edema]]|F02=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''No further evaluation required'''</div>}}<br />
{{familytree | | | | | | | |,|-|-|^|-|-|.| }} <br />
{{familytree | | | | | | | G01 | | | | G02 |G01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''No'''|G02=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Yes'''<br>❑ Refer patient to nephrology</div>}}<br />
{{familytree | | | | | | | |!|,|-|-|-|-|^|-|-|.| }}<br />
{{familytree | | | | | | | |!|H01| | | | | | H02 |H01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Cause not identified'''|H02=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Cause identified'''<br>❑ Treatment of the specific cause</div>}}<br />
{{familytree | | | | | | | |!|!| | | }}<br />
{{familytree | | | | | | | |!|!| | | }}<br />
{{familytree | | | | | | | |!|!| | | }}<br />
{{familytree | | | | | | | I01 | | |I01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Any of the following risk factors present?'''<br>❑ Age >35 years<br>❑ History of smoking<br>❑ Prior [[hematuria|gross hematuria]]<br>❑ Occupational exposure to [[benzenes]] or [[Aromatic amine|aromatic amines]]<br>❑ History of heavy non-narcotic analgesic use<br>❑ History of urologic disorder or disease (e.g, [[Benign prostatic hyperplasia|BPH]], [[Kidney stones|nephrolithiasis]])<br>❑ History of painful, frequent, or urgent urination<br>❑ History of chronic, recurrent [[urinary tract infection]]<br>❑ History of pelvic irradiation<br>❑ Prior use of alkylating agents such as [[cyclophosphamide]]<br>❑ Prior use of aristolochic acid</div>}}<br />
{{familytree | | | |,|-|-|-|^|-|-|-|.| | }}<br />
{{familytree | | | J01 | | | | | | J02 |J01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Yes'''|J02=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''No'''</div>}}<br />
{{familytree | | | |!| | | | | | | |!| | | }}<br />
{{familytree | | | K01 | | | | | | K02 | |K01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Female of childbearing potential?'''|K02=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Female of childbearing potential?'''</div>}}<br />
{{familytree | |,|-|^|-|.| | | | |,|^|-|-|-|-|.| }}<br />
{{familytree | L01 | | L02 | | | L03 | | | | L04 | |L01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Yes'''<br>❑ Perform [[pregnancy test]]|L02=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''No'''|L03=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''No'''|L04=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Yes'''<br>❑ '''Order a [[pregnancy test]]'''</div>}}<br />
{{familytree | |!| | | |!| | | | |!| | | |,|-|^|-|-|.| }}<br />
{{familytree | M01 | | M02 | | | |)|-|-| N01 | | | N02 | |M01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Positive'''<br><br>❑ Perform [[ultrasound]] of kidneys and bladder. Avoid further evaluation, if possible, until after delivery|M02=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''No <br>and<br>Negative [[pregnancy test]]'''<br><br>'''Order the following:'''<br>❑ [[CT Scan|Abdominopelvic Ct]] with and without contrast for urography<br>❑ Urology referral for [[cystoscopy]]|N01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Negative'''<br>❑ Imaging exams and [[cystoscopy]] not required. However, some experts would perform [[ultrasound]] of kidneys and bladder or an alternate imaging exam with or without [[cystoscopy]] on such patients even in the absence of risk factors.|N02=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Positive'''<br>❑ Perform ultrasound of kidneys and bladder. Avoid further evaluation, if possible, until after delivery.</div>}}<br />
{{familytree | | | | | |!| | | | |!| | | | | }}<br />
{{familytree | |,|-|-|-|^|v|-|-|-|'| | | }}<br />
{{familytree | O01 | | |O02| | |O01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Cause identified'''<br><br>❑ Treatment of the specific cause|O02=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Cause not identified'''<br><br>❑ Has the patient already had a nephrology evaluation?</div>}}<br />
{{familytree | | | |,|-|-|^|.| | }}<br />
{{familytree | | | P01 | | P02 | | |P01=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''No'''<br><br>❑ Refer patient to nephrology|P02=<div style="float: left; text-align: center; width: 10em; " padding:1em;">'''Yes'''<br><br> '''Annual [[urinalysis]]'''<br>❑ If negative for two years, stop<br>❑ If persistently positive for three years, repeat anatomic evaluation.</div>}}<br />
{{Family tree/end}}<br />
<br />
<br />
{|<br />
! colspan="2" style="background:#DCDCDC;" align="center" + |This algorithm was developed and modified according to the American Urological Association (AUA) Guideline.<br />
|- <br />
|}<br />
<br />
==Treatment==<br />
The management of [[hematuria]] will depend on the underlying cause. Click on each disease shown below to see detail management for every cause of [[hematuria]]. <ref name="pmid27261791">{{cite journal| author=Avellino GJ, Bose S, Wang DS| title=Diagnosis and Management of Hematuria. | journal=Surg Clin North Am | year= 2016 | volume= 96 | issue= 3 | pages= 503-15 | pmid=27261791 | doi=10.1016/j.suc.2016.02.007 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27261791 }}</ref><br />
<br />
{| class="wikitable" border="1"<br />
! style="width: 300px;background:#4479BA" |{{fontcolor|#FFF| '''Initial hematuria:''' (Blood at beginning of micturition with subsequent clearing)}}!! style="width: 300px;background:#4479BA" |{{fontcolor|#FFF| '''Terminal hematuria:''' (Blood seen at end of micturition after initial voiding of clear urine)}}!! style="width: 300px;background:#4479BA" |{{fontcolor|#FFF| '''Total hematuria:''' (Blood visible throughout micturition)}}<br />
|-<br />
|❑ '''[[Urethritis]]'''<br> ❑ '''[[Catheterization|Trauma (e.g, catheterization)]]'''<br />
|❑ '''[[Urothelial cancer]]'''<br> ❑ '''[[Cystitis|Cystitis (Infectious/post radiation)]]'''<br> ❑ '''[[Kidney stones|Urotheliasis]]''' <br> ❑ '''[[Benign prostatic hypertrophy]]'''<br> ❑ '''[[Prostate cancer]]'''<br />
|❑ '''[[Renal cancer|Renal mass (benign/malignant)]]'''<br> ❑ '''[[Glomerulonephritis]]'''<br> ❑ '''[[Kidney stones|Urolithiasis]]'''<br> ❑ '''[[Polycystic kidney disease]]'''<br> ❑ '''[[Pyelonephritis]]'''<br> ❑ '''[[Urothelial cancer]]'''<br> ❑ '''Trauma'''<br />
|}<br />
<br />
==Dos==<br />
<br />
*The assessment of [[hematuria]] [[patient]] should include a careful [[History and Physical examination|history, physical examination]], and [[laboratory]] examination to rule out [[benign]] causes of [[hematuria]] such as [[infection]], [[menstruation]], vigorous [[exercise]], medical [[renal disease]], viral illness, [[trauma]], or recent [[urological]] procedures.<br />
*At the initial evaluation, an estimate of [[renal function]] should be obtained (may include calculated e[[GFR]], [[creatinine]], and [[BUN]]) because the intrinsic [[renal disease]] may have implications for [[renal]]-related risk during the evaluation and management of [[patients]] with [[asymptomatic]] [[microscopic hematuria]].<br />
*[[Microscopic hematuria|Microhematuria]] that occurs in [[patients]] who are taking [[Anticoagulants|anticoagulants]] requires [[Urological|urologic]] evaluation and nephrologic evaluation regardless of the type or level of [[Anticoagulants|anti-coagulation]] therapy.<br />
*A [[cystoscopy]] should be performed on all [[patients]] who present with [[risk factors]] for [[renal cancer|urinary tract malignancies]] (e.g., irritative voiding symptoms, current or past [[tobacco use]], chemical exposures) regardless of age.<br />
*For the [[Urologic|urologi]]<nowiki/>c evaluation of [[Microscopic hematuria|asymptomatic microhematuria]], a [[cystoscopy]] should be performed on all [[patients]] aged 35 years and older. <ref name="urlMicrohematuria: Asymptomatic - American Urological Association">{{cite web |url=https://www.auanet.org/guidelines/asymptomatic-microhematuria-(amh)-guideline |title=Microhematuria: Asymptomatic - American Urological Association |format= |work= |accessdate=}}</ref><br />
*Following an unrevealing workup for [[hematuria]], a [[urinalysis]] should be checked annually. If the [[patient]] has two consecutive annual [[urinalyses]] negative for [[blood]], then no further follow-up is required. [[Patients]] with persistent [[Asymptomatic|asymptomati]]<nowiki/>c [[hematuria]] after a negative initial evaluation warrant repeat evaluation in 3-5 years, especially in those with [[risk factors]] for [[urologic]] [[malignancy]]. <ref name="urlMedical Student Curriculum: Hematuria - American Urological Association">{{cite web |url=http://www.auanet.org/education/auauniversity/for-medical-students/medical-students-curriculum/medical-student-curriculum/hematuria |title=Medical Student Curriculum: Hematuria - American Urological Association |format= |work= |accessdate=}}</ref><br />
*If a [[patient]] has [[microscopic hematuria]] in the presence of [[pyuria]] or [[bacteriuria]], a [[urine culture]] should be obtained to rule out [[urinary tract infection]]. Culture-directed [[antibiotics]] should be administered, and a microscopic [[urinalysis]] should be repeated in six weeks to assess for the resolution of the [[hematuria]]. If the [[hematuria]] has resolved after the [[infection]] has cleared, no further workup is needed. If the [[hematuria]] persists, the [[diagnostic]] evaluation should commence. <ref name="pmid24364522">{{cite journal| author=Sharp VJ, Barnes KT, Erickson BA| title=Assessment of asymptomatic microscopic hematuria in adults. | journal=Am Fam Physician | year= 2013 | volume= 88 | issue= 11 | pages= 747-54 | pmid=24364522 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24364522 }} </ref><br />
<br />
==Don'ts==<br />
<br />
*A positive [[urine dipstick]] does not define [[Dipsticks|microscopic hematuria]], and evaluation should be based solely on findings from the [[microscopic]] examination of [[urinary sediment]] and not on a [[Dipsticks|urine dipstick]] reading. <ref name="urlMicrohematuria: Asymptomatic - American Urological Association">{{cite web |url=https://www.auanet.org/guidelines/asymptomatic-microhematuria-(amh)-guideline |title=Microhematuria: Asymptomatic - American Urological Association |format= |work= |accessdate=}}</ref><br />
*The presence of dysmorphic [[red blood cells]], [[proteinuria]], cellular casts, and/or [[renal insufficiency]], or any other clinical indicator suspicious for [[renal parenchymal disease]] warrants concurrent nephrologic workup but does not preclude the need for urologic evaluation.<br />
*The use of [[urine cytology]] and urine markers (NMP22, BTA-stat, and UroVysion FISH) is not recommended as a part of the routine evaluation of the [[hematuria|asymptomatic microhematuria]] patient.<br />
*Blue light [[cystoscopy]] should not be used in the evaluation of patients with [[asymptomatic]] [[microhematuria]].<br />
*If a [[patient]] with a history of persistent [[asymptomatic]] [[microhematuria]] has two consecutive negative annual [[urinalysis|urinalyses]] (one per year for two years from the time of initial evaluation or beyond), then no further [[urinalysis]] for the purpose of evaluation of [[asymptomatic]] microscopic [[hematuria]] is necessary. <ref name="urlMicrohematuria: Asymptomatic - American Urological Association">{{cite web |url=https://www.auanet.org/guidelines/asymptomatic-microhematuria-(amh)-guideline |title=Microhematuria: Asymptomatic - American Urological Association |format= |work= |accessdate=}}</ref><br />
<br />
==References==<br />
{{Reflist|2}}<br />
[[Category:Primary care]]<br />
[[Category:Resident survival guide]]<br />
[[Categort:Urology]]<br />
<br />
{{WikiDoc Help Menu}}<br />
{{WikiDoc Sources}}<br />
<references /><br />
[[Category:Up-To-Date]]</div>Caroline Collishttps://www.wikidoc.org/index.php?title=Boerhaave_syndrome_history_and_symptoms&diff=1692149Boerhaave syndrome history and symptoms2021-02-26T14:36:56Z<p>Caroline Collis: </p>
<hr />
<div>__NOTOC__<br />
{{Boerhaave syndrome}}<br />
{{CMG}} {{AE}} {{DM}}, {{Ajay}}, {{FT}}<br />
==Overview==<br />
The clinical manifestations of [[Boerhaave syndrome]] (BHS) depend on the location of the perforation. [[Boerhaave syndrome]] often presents with excruciating [[retrosternal]] [[chest pain]] due to an [[intrathoracic]] [[esophageal perforation]]. [[Boerhaave syndrome]] is classically associated with a history of severe [[retching]] and [[vomiting]]. However, 25 to 45 percent of patients have no history of [[vomiting]].<br />
<br />
==History and Symptoms==<br />
The history and symptoms are as follows:<ref name="pmid1994204">{{cite journal |vauthors=McGovern M, Egerton MJ |title=Spontaneous perforation of the cervical oesophagus |journal=Med. J. Aust. |volume=154 |issue=4 |pages=277–8 |year=1991 |pmid=1994204 |doi= |url=}}</ref><ref name="pmid5112482">{{cite journal |vauthors=Wilson RF, Sarver EJ, Arbulu A, Sukhnandan R |title=Spontaneous perforation of the esophagus |journal=Ann. Thorac. Surg. |volume=12 |issue=3 |pages=291–6 |year=1971 |pmid=5112482 |doi= |url=}}</ref><ref name="ER09">{{cite journal |author=Woo KM, Schneider JI |title=High-risk chief complaints I: chest pain--the big three |journal=Emerg. Med. Clin. North Am. |volume=27 |issue=4 |pages=685–712, x |year=2009 |month=November |pmid=19932401 |doi=10.1016/j.emc.2009.07.007 |url=}}</ref><ref name="pmid2730190">{{cite journal |vauthors=Pate JW, Walker WA, Cole FH, Owen EW, Johnson WH |title=Spontaneous rupture of the esophagus: a 30-year experience |journal=Ann. Thorac. Surg. |volume=47 |issue=5 |pages=689–92 |year=1989 |pmid=2730190 |doi= |url=}}</ref><ref name="pmid9079278">{{cite journal |vauthors=Brauer RB, Liebermann-Meffert D, Stein HJ, Bartels H, Siewert JR |title=Boerhaave's syndrome: analysis of the literature and report of 18 new cases |journal=Dis. Esophagus |volume=10 |issue=1 |pages=64–8 |year=1997 |pmid=9079278 |doi= |url=}}</ref><br />
===History===<br />
* Obtaining history gives important information in making a diagnosis of BHS. <br />
* It provides insight into the cause, precipitating factors, and associated [[Comorbidities|comorbid]] conditions. <br />
* A complete history will help determine the correct [[therapy]] and determining the [[prognosis]]. <br />
* The areas of focus should be on onset, duration, and progression of symptoms such as<br />
<br />
===Symptoms===<br />
*The clinical manifestations of [[Boerhaave syndrome]] depend on the:<br />
**Location of the perforation ([[cervical]], [[intrathoracic]], or intra-abdominal), <br />
**The time since the injury <br />
**The degree of leakage<br />
*[[Boerhaave syndrome]] often presents with excruciating [[retrosternal]] [[chest pain]] due to an [[intrathoracic]] [[Boerhaave syndrome|esophageal perforation.]] <br />
*[[Boerhaave syndrome]] is classically associated with a history of severe [[retching]] and [[vomiting]], however, 25 to 45 percent of patients have no history of [[vomiting]].<br />
*Soon after the [[perforation]], patients can have:<br />
**[[Odynophagia]]<br />
**[[Dyspnea]]<br />
**[[Fever]]<br />
**[[Tachypnea]]<br />
**[[Tachycardia]] <br />
**[[Cyanosis]], and [[hypotension]] on physical examination. <br />
**A [[pleural effusion]] may also occur.<br />
*Patients with [[cervical]] [[perforations]] can present with:<br />
**Neck pain<br />
**[[Dysphagia]] <br />
**[[Dysphonia]]<br />
*Patients with an intra-abdominal [[perforation]] have [[epigastric pain]] that may radiate to the shoulder causing physicians to confuse an [[esophageal perforation]] with a [[myocardial infarction]]. <br />
*These patients may also have back pain or present with an [[acute abdomen]].<br />
*'''Mackler's triad''' is only present in 14% of patients which includes:<br />
**[[Chest pain]]<br />
**[[Vomiting]]<br />
**[[Subcutaneous emphysema]]<br />
*It may also be audibly recognized as [[Hamman's sign]].<br />
*'''[[Hamman's sign]]''' is a crunching, rasping sound, synchronous with the heartbeat, heard over the [[precordium]] in spontaneous [[Mediastinum|mediastinal]] [[emphysema]] produced by the heart beating against air-filled [[tissues]].<br />
<br />
==References==<br />
{{reflist|2}}<br />
<br />
{{WH}}<br />
{{WS}}<br />
<br />
[[Category:Gastroenterology]]<br />
[[Category:Surgery]]<br />
[[Category:Up-To-Date]]</div>Caroline Collis