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{{Cyanosis}}
{{Cyanosis}}
{{CMG}}; {{AE}}
{{CMG}}; {{AE}} {{Sara.Zand}} {{MAD}}


==Overview==
==Overview==
There is no treatment for [disease name]; the mainstay of therapy is supportive care.
In every neonate presented with cyanosis and shock, [[congenital heart disease]] dependent on [[patency ductus arteriosus]] should be considered. The physiologic constriction of [[ductus arteriosus]] after birth in a [[neonate]] whose [[pulmonary blood flow]] or [[aortic blood flow]] is dependent on [[PDA]] leads to [[shock]] and [[collapse]] in the [[neonate]]. Infusion of [[prostaglan]] in such a [[neonate]] is life-saving and keeps [[patency ductus arteriosus]]. Treatment of underlying causes of peripheral cyanosis such as tamponade or cardiogenic shock  due to [[low cardiac output state]] and [[peripheral vasoconstriction]] lead to disappearing of [[cyanosis]].


OR


Supportive therapy for [disease name] includes [therapy 1], [therapy 2], and [therapy 3].


OR
== Medical therapy ==


The majority of cases of [disease name] are self-limited and require only supportive care.


OR
*The mainstay of therapy for [[cyanosis]] is the treatment of underlying causes of [[cyanosis]].
* In cyanotic [[congenital heart disease ]] whether the flow is dependent on patency ductus arteriosus, infusion of  [[prostaglandin]] E1  is recommended.
* In the setting of pulmonary disease such as [[pneumonia]], [[pleural effusion]], treatment of underlying disease and [[oxygen]] therapy are advised.
* In the setting of low cardiac output state such as [[pulmonary thromboembolism]] and [[ cardiogenic shock]], management of thrombotic events and [[oxygen]] supplement therapy is recommended.
* In [[methemoglobinemia]] discontinuing the medications related disorder and administration of [[methylene blue]] is recommended.


[Disease name] is a medical emergency and requires prompt treatment.
== Medical therapy of [[Cyanosis]] ==
The mainstay of therapy is treatment of underlying causes of [[cyanosis]].<ref name="CucereaSimon2016">{{cite journal|last1=Cucerea|first1=Manuela|last2=Simon|first2=Marta|last3=Moldovan|first3=Elena|last4=Ungureanu|first4=Marcela|last5=Marian|first5=Raluca|last6=Suciu|first6=Laura|title=Congenital Heart Disease Requiring Maintenance of Ductus Arteriosus in Critically Ill Newborns Admitted at A Tertiary Neonatal Intensive Care Unit|journal=The Journal of Critical Care Medicine|volume=2|issue=4|year=2016|pages=185–191|issn=2393-1817|doi=10.1515/jccm-2016-0031}}</ref>
<ref name="HenretigGribetz2011">{{cite journal|last1=Henretig|first1=Fred M.|last2=Gribetz|first2=Bruce|last3=Kearney|first3=Thomas|last4=Lacouture|first4=Peter|last5=Loveiov|first5=Frederick H.|title=Interpretation of Color Change in Blood with Varying Degree of Methemoglobinemia|journal=Journal of Toxicology: Clinical Toxicology|volume=26|issue=5-6|year=2011|pages=293–301|issn=0731-3810|doi=10.1080/15563658809167094}}</ref><ref name="TisiWolfe1970">{{cite journal|last1=Tisi|first1=G M|last2=Wolfe|first2=W G|last3=Fallat|first3=R J|last4=Nadel|first4=J A|title=Effects of O2 and CO2 on airway smooth muscle following pulmonary vascular occlusion.|journal=Journal of Applied Physiology|volume=28|issue=5|year=1970|pages=570–573|issn=8750-7587|doi=10.1152/jappl.1970.28.5.570}}</ref><ref name="Austin1973">{{cite journal|last1=Austin|first1=John H. M.|title=Intrapulmonary Airway Narrowing after Pulmonary Thromboembolism in Dogs|journal=Investigative Radiology|volume=8|issue=5|year=1973|pages=315–321|issn=0020-9996|doi=10.1097/00004424-197309000-00003}}</ref><ref>{{cite journal|doi=10.1164/rccm.201503-0584OC.}}</ref><ref name="SmedleyGrocott2013">{{cite journal|last1=Smedley|first1=Tom|last2=Grocott|first2=Michael PW|title=Acute high-altitude illness: a clinically orientated review|journal=British Journal of Pain|volume=7|issue=2|year=2013|pages=85–94|issn=2049-4637|doi=10.1177/2049463713489539}}</ref>


OR
'''<span style="font-size:85%">'''Abbreviations:'''
'''d-TGA:''' [[ dextro-Transposition of great arteries]];
'''PDA:''' [[Patent ductus arteriosus]]  ;
'''ASD:''' [[Atrial septal defect]];
'''VSD:''' [[Ventricular septal defect]];
'''TOF:''' [[Tetralogy of fallot]];
'''CHD:''' [[Congenital heart disease]];
'''PS:''' [[Pulmonary stenosis]];
'''PTE:''' [[Pulmonary thromboembolism]];
'''AS:''' [[Aortic stenosis]];
'''ARDS:''' [[Acute respiratory distress syndrome]];
'''PFO:''' [[Patent foramen ovale]];
'''PVR:''' [[Pulmonary vascular resistance]];
'''SpO2:''' [[ Peripheral capillary oxygen saturation.]];
'''FiO2:''' [[Fraction of inspired oxygen]];
'''PEEP:''' [[Positive end-expiratory pressure]];
</span>
<br>
{| class="wikitable sortable"
|-
!Causes of [[cyanosis]]!![[CHD]]  with severe restriction of [[pulmonary blood flow]]!![[CHD]] with severe restriction of [[systemic blood flow]]!![[CHD]] due to bidirectional shunt!![[Methemoglobinemia]]!![[PTE]]!![[Cardiogenic shock]]!![[ARDS]]!![[Acute mountain sickness]]
|-


The mainstay of treatment for [disease name] is [therapy].
||'''Note'''||
*[[Pulmonary atresia]]
*[[Tricuspid atresia]]
*[[Tetralogy of Fallot]] with [[pulmonary atresia]]
||
*[[Severe AS]]
*[[Coarctation aorta]]
*[[Interrupted aortic arch]]
*[[Hypoplastic  left heart syndrome]]


OR
||
 
*[[TGA]]
The optimal therapy for [malignancy name] depends on the stage at diagnosis.
*[[Truncus arteriosus]]
*[[Double outlet right ventricle]]
|| Complication of exposue to some drugs such as [[nitrites]] and [[aniline]] leading to [[dizziness]] , [[coma]], chocolate-brown discoloration of [[blood]] samples, [[respiratory distress]] [[seizures]] and [[myocardial ischemia]] 
|| [[Hypoxia]] due to V/Q  mismatch, low [[cardiac out-put]] state, acute [[ right ventricular dilation]] and increased [[pulmonary vascular resistance]]
|| [[Cyanosis]], [[olyguria]], [[altered mental status]]  ||
*SpO2/FiO2 <315, No PEEP requirement
*Complication of [[pneumonia]], [[non cardiogenic shock]], [[drug overdose]], [[trauma]]
||Leakage of large molecules  into alveolar space  leading rich protein [[pulmonary edema]]
|-
| '''Mechanism of [[cyanosis]]''' || [[ Hypoxia]] and [[cyanosis]] due to constriction of the [[ductus arteriosus]] after birth and dependency of the [[Pulmonary circulation]] on the [[patency of the ductus arteriosus]]||[[Cyanosis]],[[systemic hypoperfusion]], [[circulatory collapse]], [[metabolic acidosis]], [[shock]] due to constriction ductus arteriosus and dependency systemic circulation on  [[PDA]] after birth  ||  Constriction of [[PDA]] after birth leading decreased systemic circulation due to mixing of [[pulmonary]] and [[systemic blood flow]] via [[PDA]]
||
*[[Oxidative sresss]] , [[methemoglobin]] level > 10 % total [[hemoglobin]]
* [[Cyanosis]] refractory to [[oxygen]] therapy,
||
*[[V/Q mismatches]]  due to small airway constriction in both nonperfused and nonembolized areas of [[lung]], reduced [[surfactant]] production, [[pulmonary edema]], [[atelectasis]]
*Right to left shunt via [[PFO]] leading [[central cyanosis]]
* Low [[cardiac output]] state due to [[right ventricular dilation]] and increased [[PVR]] leading to [[peripheral cyanosia]]
|| Low [[cardiac output]] state due to [[myocardial infarction]] and [[pump failure]] leading to  vasoconstriction and [[peripheral cyanosis]]||
*Increased alveolar vascular permeability
*Interstitial and alveolar [[pulmonary edema]]


OR
||  [[Central cyanosis]] due to alveolar [[hypoxia]] , [[pulmonary vasoconstriction]], [[ pulmonary hypertension]]
|-
|'''Treatment'''||[[Prostaglandin]] E1 ||[[Prostaglandin ]] E1||[[Prostaglandin]] E1||
*[[Methylenblue]] infusion
* Hyperbaric [[oxygen]] therapy
*[[Ascorbi:c acid]]
||
*[[Anticoagulant therapy]]
*[[Fibrinolytic]] therapy in case of [[ collapse]] and [[shock]]
*[[ Mechanical thrombectomy]]


[Therapy] is recommended among all patients who develop [disease name].
||[[Coronary revascularization ]]||
 
*[[Extracorporeal membrane oxygenation]]
OR
*[[High-frequency oscillatory ventilation]]
 
*[[Neuromuscular blocking agents]]
Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].
*Intravenous β-2 agonist ([[Salbutamol]])
 
||
OR
*Descent
 
*Supplement [[oxygen]] therapy
Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].
*Portable hyperbaric chamber
 
*[[Nifedipine]]
OR
|}
 
Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].
 
OR
 
Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].
 
==Medical Therapy==
 
* '''Conditions associated with decreased concentration of inspired oxygen:'''
** [[Smoke inhalation]] most commonly from house fires
** [[Carbon monoxide poisoning]]
** [[cyanide poisoning]]
** [[Pneumothorax]]
** [[Foreign body aspiration]]
*** [[Pertussis]] / [[Croup]]
*** [[Epiglottitis]]
*** [[Bacterial tracheitis]]
*** [[Choanal atresia]]
*** [[Laryngotracheomalacia]]
*** [[Myasthenia gravis]]
*** [[Asthma]]
*** [[Pneumonia]]
*** [[Bronchiolitis]]
*** [[Acute respiratory distress syndrome|Respiratory distress syndrome]]
*** [[Cardiac tamponade]]
 
**
** [[congestive heart failure]]
** [[Atrial septal defect]]
** [[Pulmonary hypertension]]
** [[Pulmonary edema]]
** [[Pulmonary hemorrhage]]
** [[Pulmonary embolism]]
** [[pulmonary arteriovenous malformation]]
** [[Shock]]
** [[Sepsis]]
** [[Amniotic fluid embolism]]
** [[Methemoglobinemia]]
** Severe [[hypoglycemia]]
 
==== [[Raynaud's phenomenon]] ====
==== [[Peripheral arterial disease|Peripheral vascular disease]] ====
 
== Initial management of neonantal cyanosis ==
Newborns with cyanosis require maintains adequate tissue perfusion and oxygenation.
 
Specific interventions for neonatal cyanotic congenital heart disease (CHD) include administration of prostaglandin E1 and cardiac catheter palliative or corrective procedures.
 
Initial management begins with general care that includes
 
cardiorespiratory support
 
monitoring to ensure sufficient organ/tissue perfusion and oxygenation
 
an adequate airway should be established immediately and supportive therapy (eg, supplemental oxygen and/or mechanical ventilation) instituted as needed.
 
Placement of secure intravenous and intraarterial catheters is most easily accomplished via the umbilical vessels.
 
This will enable efficient correction and monitoring of acid-base balance
 
metabolic derangements (eg, hypoglycemia, hypocalcemia), and blood pressure.
 
Inotropic agents such as dopamine or dobutamine may be necessary to correct hypotension.
 
In infants with severe polycythemia (>70 percent), an isovolumetric partial exchange transfusion should be performed with saline to reduce the hematocrit.
 
Hypoglycemia is common in critically
 
ill infants, therefore glucose levels should be monitored and glucose infusions provided to
 
maintain a blood glucose > 55 mg/dL. An airway and assisted ventilation should be considered
 
for infants with respiratory distress, but may be deferred for the comfortable infant.
 
Severe
 
acidosis should be corrected with infusions of sodium bicarbonate, but only after adequate gas
 
exchange has been established. If the infant is <10 days old and the umbilical stump is still
 
attached, umbilical venous and arterial lines can frequently be placed by experienced
 
Steinhorn
 
Hypocalcemia is often associated with cardiac disease
 
and critical illness, and should be corrected based on the ionized calcium.
 
Oxygen should be provided, although there are increasing concerns about the potential risks
 
associated with this therapy (6). Even brief (30 minute) exposures to extreme hyperoxia are
 
increasingly recognized to increase oxidative stress and potentially damage lung parenchymal
 
and vascular function, even in term infants (7. 8).
 
the use of 100% O2 should
 
generally be avoided at the outset. Initiating oxygen therapy with 40–60% O2 will allow the
 
caregiver to provide support, assess for improvement, and seek advice from a cardiologist.
 
This
 
point is particularly important if an infant has only a minimal response to oxygen, as this may
 
indicate potential cardiac disease and need for PGE1. In addition, it is important to remember
 
that oxygen may promote ductal closure. This may not be a major concern for lesions that limit
 
pulmonary blood flow, as the pulmonary venous PO2 would not be expected to rise.
 
However,
 
admixture lesions such as hypoplastic left heart syndrome may present with moderate cyanosis.
 
These conditions are dependent on a patent ductus to maintain systemic blood flow. Oxygen
 
may not only promote ductal closure, but may increase pulmonary and decrease systemic blood
 
flow.
 
In the infant who does not require assisted ventilation, oxygen may be delivered via a head
 
hood or nasal cannula (9). A head hood is the only method that allows the FiO2 to be determined
 
precisely.
 
The oxygen concentration should be measured by an oxygen analyser placed near
 
the baby’s mouth. Relatively high flows are needed achieve adequate concentrations of oxygen
 
and avoid carbon dioxide accumulation, although humidification is generally not necessary.
 
While head box oxygen is generally well tolerated, this method limits the infant’s mobility,
 
and oxygen concentrations fall quickly when the hood is lifted to provide care to the infant.
 
Oxygen is frequently delivered by a nasal cannula. The disadvantage of this method is that the
 
infant entrains variable amounts of room air around the nasal cannula. Therefore, it cannot
 
provide 100% oxygen, and the oxygen concentration in the hypopharynx (a good proxy for the
 
tracheal concentration) will be much lower than the concentration of oxygen at the cannula
 
inlet. Both the oxygen concentration and the cannula flow rate will be the major factors that
 
will determine the fraction of oxygen actually delivered. Therefore, it is generally better to
 
titrate delivery to achieve the desired oxygen saturation levels, generally 90% to 95% by pulse
 
oximetry.
 
Antibiotics
 
broad spectrum antibiotics should be initiated (ampicillin and gentamicin) after obtaining blood and urine cultures.
 
Specific CHD measures
 
An infant who fails the hyperoxia test and does not have persistent pulmonary hypertension of the newborn or a chest radiograph consistent with lung disease is likely to have a cyanotic CHD. In most cases, cyanotic CHD is dependent upon a patent ductus arteriosus (PDA) for pulmonary or systemic blood flow. Closure of the ductus arteriosus can precipitate rapid clinical deterioration with significant life-threatening changes (ie, severe metabolic acidosis, seizures, cardiogenic shock, cardiac arrest, or end-organ injury).
 
As a result, infants with ductal-dependent lesions are at increased risk for death and significant morbidity unless interventions are initiated to maintain patency of the ductus arteriosus for ductal-dependent lesions, ensure adequate mixing of deoxygenated and oxygenated blood, or relieve obstructed blood flow.
 
In infants with or who have a clinical suspicion for a ductal-dependent congenital heart defect, prostaglandin E1 (alprostadil) should be administered until a definitive diagnosis or treatment is established [7].
 
The initial dose is dependent on the clinical setting, as the risk of apnea, one of the major complications of prostaglandin E1 infusion, is dose dependent.
 
●If the ductus is known to be large in a patient with duct-dependent physiology, the initial dose is 0.01 mcg/kg per minute. This scenario typically is seen in patients with echocardiographic confirmation of a large PDA who are cared for in a tertiary center that provides treatment for neonates with cyanotic heart disease.
 
●If the ductus is restrictive or the status of the ductus is unknown, the initial dose is 0.05 mcg/kgper minute. This is the standard dose used in patients who require transport to a center with expertise in the care of neonates with cyanotic heart disease.
 
The dose of prostaglandin can be increased as needed to a maximum dose of 0.1 mcg/kg per minute.
 
Complications of prostaglandin E1 infusion include hypotension, tachycardia, and apnea [8]. As a result, a separate reliable intravenous catheter must be in place to provide fluids for resuscitation. Intubation equipment should be immediately available because apnea can occur at any time during infusion.
 
Deterioration of the clinical status after starting prostaglandin E1 usually indicates the presence of rare congenital cardiac defects associated with pulmonary venous or left atrial obstruction. These include obstructive (usually infradiaphragmatic) total anomalous pulmonary venous connection or various conditions associated with a restrictive atrial septum (eg, hypoplastic left heart syndrome, cor triatriatum, severe mitral stenosis or atresia, or D-transposition of the great arteries associated with restrictive atrial shunting). These patients require urgent echocardiography followed by interventional cardiac catheterization or surgery [9].
 
Cardiac catheterization
 
Cardiac catheter interventions can either be palliative by improving cyanosis or be corrective by relieving obstruction to flow.
 
●Balloon atrial septostomy can relieve marked cyanosis in patients with D-transposition of the great arteries associated with restrictive atrial shunting, and in patients with a restrictive atrial septum associated with left-sided obstructive disease. In patients with D-transposition of the great arteries, this procedure can be performed at the bedside under echocardiographic guidance. (See "Management and outcome of D-transposition of the great arteries", section on 'Balloon atrial septostomy' and "Hypoplastic left heart syndrome: Management and outcome", section on 'Initial medical management'.)
 
●Balloon valvuloplasty can be effective in patients with critical pulmonary stenosis or aortic stenosis. Selected patients with pulmonary atresia are also candidates for balloon valvuloplasty if the obstruction is membranous, the tricuspid annulus and right ventricular size are adequate to support a two ventricle repair, and the coronary circulation does not depend upon the right ventricle [10]. (See "Valvar aortic stenosis in children", section on 'First-line treatment'.)
 
●Transcatheter occlusion of pulmonary arteriovenous malformations can also be performed [11].
 
*** [[Tetralogy of Fallot|Tetralogy of fallot]]
 
*** [[Tricuspid atresia]]
*** [[Tricuspid stenosis]]
*** [[Ebstein's anomaly of the tricuspid valve|Ebstein's anomaly]]
** [[Pulmonary valve stenosis|Pulmonary stenosis]]
** [[Pulmonary atresia]] 
** [[TGA]]
** [[Truncus arteriosus]]
** [[Total anomalous pulmonary venous connection|TAPVC]]
** Left sided obstructive lesion
** [[Aortic coarctation|Coarctation of aorta]]
** Critical valvular [[aortic stenosis]]
** [[Eisenmenger's syndrome|Eisenmenger syndrome]]


==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
 
[[Category:Up-To-Date]]
{{WH}}
[[Category:Primary care]]
{{WS}}
[[Category: (name of the system)]]

Latest revision as of 20:12, 29 January 2021

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Mohammed Abdelwahed M.D[3]

Overview

In every neonate presented with cyanosis and shock, congenital heart disease dependent on patency ductus arteriosus should be considered. The physiologic constriction of ductus arteriosus after birth in a neonate whose pulmonary blood flow or aortic blood flow is dependent on PDA leads to shock and collapse in the neonate. Infusion of prostaglan in such a neonate is life-saving and keeps patency ductus arteriosus. Treatment of underlying causes of peripheral cyanosis such as tamponade or cardiogenic shock due to low cardiac output state and peripheral vasoconstriction lead to disappearing of cyanosis.


Medical therapy

Medical therapy of Cyanosis

The mainstay of therapy is treatment of underlying causes of cyanosis.[1] [2][3][4][5][6]

Abbreviations: d-TGA: dextro-Transposition of great arteries; PDA: Patent ductus arteriosus  ; ASD: Atrial septal defect; VSD: Ventricular septal defect; TOF: Tetralogy of fallot; CHD: Congenital heart disease; PS: Pulmonary stenosis; PTE: Pulmonary thromboembolism; AS: Aortic stenosis; ARDS: Acute respiratory distress syndrome; PFO: Patent foramen ovale; PVR: Pulmonary vascular resistance; SpO2: Peripheral capillary oxygen saturation.; FiO2: Fraction of inspired oxygen; PEEP: Positive end-expiratory pressure;

Causes of cyanosis CHD with severe restriction of pulmonary blood flow CHD with severe restriction of systemic blood flow CHD due to bidirectional shunt Methemoglobinemia PTE Cardiogenic shock ARDS Acute mountain sickness
Note Complication of exposue to some drugs such as nitrites and aniline leading to dizziness , coma, chocolate-brown discoloration of blood samples, respiratory distress seizures and myocardial ischemia Hypoxia due to V/Q mismatch, low cardiac out-put state, acute right ventricular dilation and increased pulmonary vascular resistance Cyanosis, olyguria, altered mental status Leakage of large molecules into alveolar space leading rich protein pulmonary edema
Mechanism of cyanosis Hypoxia and cyanosis due to constriction of the ductus arteriosus after birth and dependency of the Pulmonary circulation on the patency of the ductus arteriosus Cyanosis,systemic hypoperfusion, circulatory collapse, metabolic acidosis, shock due to constriction ductus arteriosus and dependency systemic circulation on PDA after birth Constriction of PDA after birth leading decreased systemic circulation due to mixing of pulmonary and systemic blood flow via PDA Low cardiac output state due to myocardial infarction and pump failure leading to vasoconstriction and peripheral cyanosis
  • Increased alveolar vascular permeability
  • Interstitial and alveolar pulmonary edema
 Central cyanosis due to alveolar hypoxia , pulmonary vasoconstriction, pulmonary hypertension
Treatment Prostaglandin E1 Prostaglandin E1 Prostaglandin E1 Coronary revascularization

References

  1. ↑ Cucerea, Manuela; Simon, Marta; Moldovan, Elena; Ungureanu, Marcela; Marian, Raluca; Suciu, Laura (2016). "Congenital Heart Disease Requiring Maintenance of Ductus Arteriosus in Critically Ill Newborns Admitted at A Tertiary Neonatal Intensive Care Unit". The Journal of Critical Care Medicine. 2 (4): 185–191. doi:10.1515/jccm-2016-0031. ISSN 2393-1817.
  2. ↑ Henretig, Fred M.; Gribetz, Bruce; Kearney, Thomas; Lacouture, Peter; Loveiov, Frederick H. (2011). "Interpretation of Color Change in Blood with Varying Degree of Methemoglobinemia". Journal of Toxicology: Clinical Toxicology. 26 (5–6): 293–301. doi:10.1080/15563658809167094. ISSN 0731-3810.
  3. ↑ Tisi, G M; Wolfe, W G; Fallat, R J; Nadel, J A (1970). "Effects of O2 and CO2 on airway smooth muscle following pulmonary vascular occlusion". Journal of Applied Physiology. 28 (5): 570–573. doi:10.1152/jappl.1970.28.5.570. ISSN 8750-7587.
  4. ↑ Austin, John H. M. (1973). "Intrapulmonary Airway Narrowing after Pulmonary Thromboembolism in Dogs". Investigative Radiology. 8 (5): 315–321. doi:10.1097/00004424-197309000-00003. ISSN 0020-9996.
  5. ↑ . doi:10.1164/rccm.201503-0584OC. Check |doi= value (help). Missing or empty |title= (help)
  6. ↑ Smedley, Tom; Grocott, Michael PW (2013). "Acute high-altitude illness: a clinically orientated review". British Journal of Pain. 7 (2): 85–94. doi:10.1177/2049463713489539. ISSN 2049-4637.
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