Jaundice in children: Difference between revisions

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*[[Infants]] usually [[Appearance|appear]] well.
*[[Infants]] usually [[Appearance|appear]] well.
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| align="center" style="background:#DCDCDC;" + |'''[[Pathological]] [[jaundice|jaundice<ref name="pmid30422525" />]]'''
| align="center" style="background:#DCDCDC;" + |'''[[Pathological]] [[jaundice|jaundice<ref name="pmid30422525" />]][[Jaundice in children#cite%20note-pmid30422525-1|<span class="mw-reflink-text">[1]</span>]]'''
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*Seen anytime from the first few hours of [[life]].
*Seen anytime from the first few hours of [[life]].
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==Pathophysiology==
==Pathophysiology==


*[[Jaundice]] is caused by high [[concentrations]] of [[bilirubin]] in the [[bloodstream]]. A condition known as [[Hyperbilirubinemia]].
*[[Jaundice]] is caused by high [[concentrations]] of [[bilirubin]] in the [[bloodstream]], a condition known as [[Hyperbilirubinemia]].
*[[Hyperbilirubinemia]] can result from abnormalities in the [[metabolism]] of [[bilirubin]] which could occur at any stage from its [[production]] which is as a result of the excessive [[breakdown]] of [[red blood cells]], defects in its [[hepatic]] [[metabolism]], and its post [[hepatic]] transport.
*[[Hyperbilirubinemia]] can [[result]] from [[abnormalities]] in the [[metabolism]] of [[bilirubin]] which could occur at any stage from its [[production]] which is as a [[result]] of the excessive [[breakdown]] of [[red blood cells]], [[Defect|defects]] in its [[hepatic]] [[metabolism]], and its post [[hepatic]] [[Transporter|transport]].
*[[Hemoglobin]] from the [[breakdown]] of effete [[red blood cells]] is composed of [[heme]] and [[globin]]. [[Globin]] is further dismantled into its component [[amino acids]] and [[recycled]] while [[heme]] is split into [[iron]] and [[biliverdin]] by the [[enzyme]], [[heme oxygenase]] in the [[reticuloendothelial]] [[system]]. [[Iron]] is transferred to [[ferritin]] and used again to make [[hemoglobin]] while [[biliverdin]] is converted to [[bilirubin]] by [[biliverdin reductase]]. <ref name="pmid30422525">{{cite journal| author=| title=StatPearls | journal= | year= 2020 | volume=  | issue=  | pages=  | pmid=30422525 | doi= | pmc= | url= }} </ref>
*[[Hemoglobin]] from the [[breakdown]] of effete [[red blood cells]] is composed of [[heme]] and [[globin]]. [[Globin]] is further dismantled into its component [[amino acids]] and [[recycled]] while [[heme]] is split into [[iron]] and [[biliverdin]] by the [[enzyme]], [[heme oxygenase]] in the [[reticuloendothelial]] [[system]]. [[Iron]] is transferred to [[ferritin]] and used again to make [[hemoglobin]] while [[biliverdin]] is converted to [[bilirubin]] by [[biliverdin reductase]]. <ref name="pmid30422525">{{cite journal| author=| title=StatPearls | journal= | year= 2020 | volume=  | issue=  | pages=  | pmid=30422525 | doi= | pmc= | url= }} </ref>
*[[Water]]-insoluble [[bilirubin]] becomes coupled to [[albumin]] and transported into [[hepatic]] [[cells]] for conjugation.
*[[Water]]-insoluble [[bilirubin]] becomes coupled to [[albumin]] and transported into [[hepatic]] [[cells]] for [[conjugation]].
*This [[albumin]]-[[bilirubin]] compound is broken down and the unconjugated [[bilirubin]] enters the [[cytosol]] of [[hepatocytes]]to be conjugated to [[glucuronic acid]] in the [[endoplasmic reticulum]] by the [[enzyme]], Uridine diphosphate glucuronosyltransferase (UDPGT). <ref name="pmid31334972">{{cite journal| author=| title=StatPearls | journal= | year= 2020 | volume=  | issue=  | pages=  | pmid=31334972 | doi= | pmc= | url= }} </ref>
*This [[albumin]]-[[bilirubin]] compound is broken down and the [[unconjugated bilirubin]] enters the [[cytosol]] of [[hepatocytes]] to be [[Conjugated bilirubin|conjugated]] to [[glucuronic acid]] in the [[endoplasmic reticulum]] by the [[enzyme]], [[Uridine diphosphate glucuronyltransferase|uridine diphosphate glucuronyltransferase (UDPGT)]].<ref name="pmid31334972">{{cite journal| author=| title=StatPearls | journal= | year= 2020 | volume=  | issue=  | pages=  | pmid=31334972 | doi= | pmc= | url= }} </ref>
*This conjugated form of [[bilirubin]] is secreted into [[bile]] and then into the [[small intestine]] after being stored in the [[gall bladder]]. Subsequently reaches the [[colon]] where it is acted upon by [[bacterial]] [[flora]] and deconjugated to [[urobilinogen]]. Most are [[excreted]] into [[feces]] as the brown pigment, [[stercobilin]], and the rest is [[reabsorbed]] into the [[blood]], converted to yellow [[urobilin]] which is eventually excreted into the [[urine]].
*This [[Conjugated bilirubin|conjugated]] form of [[bilirubin]] is [[Secretion|secreted]] into [[bile]] and then into the [[small intestine]] after being stored in the [[gall bladder]]. Subsequently reaches the [[colon]] where it is acted upon by [[bacterial]] [[flora]] and deconjugated to [[urobilinogen]]. Most are [[excreted]] into [[feces]] as the [[brown]] [[pigment]], [[stercobilin]], and the rest is [[reabsorbed]] into the [[blood]], converted to yellow [[urobilin]] which is eventually excreted into the [[urine]].
*[[Hyperbilirubinemia]] whether conjugated or unconjugated gives a clue as to the defective point in the [[metabolism]] of [[bilirubin]].
*[[Hyperbilirubinemia]] whether [[Conjugated bilirubin|conjugated]] or [[Unconjugated bilirubin|unconjugated]] gives a clue as to the [[Defect|defective]] point in the [[metabolism]] of [[bilirubin]].


==Causes==
==Causes==


*Causes of [[jaundice]] in [[children]] can be classified as follows:
*[[Causes]] of [[jaundice]] in [[children]] can be [[Classification|classified]] as follows:
{{familytree/start}}
{{familytree/start}}
{{familytree| | | | | | | A01 | | | | | | | | | | | | | | | | | | | | | | | | | | | | | |A01=Causes of [[jaundice]] in [[children]]}}
{{familytree| | | | | | | A01 | | | | | | | | | | | | | | | | | | | | | | | | | | | | | |A01=Causes of [[jaundice]] in [[children]]}}

Revision as of 22:09, 22 December 2020

Jaundice in children Microchapters

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differential Diagnosis

Epidemiology and Demographics

Risk factors

Natural History, Complications and Prognosis

Diagnosis

Treatment

Prevention

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ifeoma Anaya, M.D.[2]

Synonyms and keywords: Jaundice in kids, hyperbilirubinemia

Overview

The word 'Jaundice' was derived from the French word for yellow which is jaune. Jaundice may be classified into two broad categories based on its time of onset and cause such as physiologic and pathologic jaundice. Jaundice is caused by high concentrations of bilirubin in the bloodstream, a condition known as hyperbilirubinemia. Hyperbilirubinemia can result from abnormalities in the metabolism of bilirubin which could occur at any stage from its production which is a result of excessive breakdown of red blood cells, defects in its hepatic metabolism, and its post hepatic transport. Pathologic causes of jaundice can be classified into causes of conjugated and unconjugated hyperbilirubinemia. Differentials for jaundice are very limited however, some skin discolorations in healthy individuals can look like jaundice in certain circumstances. The prevalence of jaundice varies among patient populations. In infants born at term, 60% will develop jaundice in their first-week of life which rises to 80% in preterms. Common risk factors in the development of jaundice in children are a family history of jaundice, family history of a child born with jaundice, hyperthyroidism in mother, medication use by the mother etc. It is essential for every clinician to note that jaundice is not always a benign condition therefore, extensive investigation of a child with jaundice is necessary to prevent severe complications. Symptoms of jaundice in children may include the yellowish discoloration of skin, sclera, and mucous membrane. A useful technique in assessing the severity of jaundice is by using the principle of skin discoloration progressing in a cephalo-caudal direction in newborns. Laboratory findings include measuring the serum bilirubin from a blood sample. The total and conjugated portions are measured and the unconjugated fraction is measured by subtracting the conjugated fraction from the total. Echocardiography can detect cardiac abnormalities in patients with Alagille syndrome and biliary atresia. Ultrasonography of the abdomen is used to screen for biliary atresia, choledochal cysts, or cholestatic workup in the setting of conjugated hyperbilirubinemia. Treatment options include phototherapy, intravenous immunoglobulin (IVIG), and exchange transfusion. Pharmacological options are also there. Surgery is the mainstay of therapy or the definitive treatment for most obstructive causes of conjugated hyperbilirubinemia. Several etiologies may be generally difficult to prevent however, the prevention of complications from jaundice is equally crucial. Parents should be educated on how to recognize jaundice very early in a neonate so as to present promptly for the management.

Historical Perspective

Classification

Classification of Jaundice
Type of Jaundice Details
Physiologic jaundice
Pathological jaundice[1][1]

Pathophysiology

Causes

 
 
 
 
 
 
Causes of jaundice in children
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Physiologic
 
 
 
Pathologic
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Unconjugated hyperbilirubinemia
 
 
 
Conjugated hyperbilirubinemia
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hemolytic
 
 
 
Non-hemolytic
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
•Rh incompatibility
ABO incompatibility
Hemoglobinopathies (Thalassemia)
•Hematomas
Polycythemia
Sepsis
 
 
 
Crigler-Najjar syndrome I and II
Gilbert syndrome
Breast milk jaundice
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Infectious
 
Obstructive
 
Drugs
 
Genetic/Metabolic
 
Storage disorders
 
Endocirnopathies
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Viral
Bacterial
Parasitic
 
Biliary atresia
Choledochal cyst
•Inspissated bile syndrome
Neonatal sclerosing cholangitis
Congenital hepatic fibrosis
•Intrinsic/extrinsic mass
 
Ceftriaxone
Isoniazid
Erythromycin
Rifampin
Sulfa drugs
Parenteral nutrition
Methotrexate
 
Alpha 1 antitrypsin deficiency
Alagille syndrome
Cystic fibrosis
Tyrosinemia
Galactosemia
Rotor syndrome
Trisomy 18 and Trisomy 21
 
Gaucher's disease
•Niemann-pick disease
Glycogen storage diseases
Mucolipidoses
 
Hypopituitarism
Hypothyroidism
•McCune Albright syndrome
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

Differentiating Jaundice in children from other Diseases

Epidemiology and Demographics

Age

Gender

Race

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Prevention

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 "StatPearls". 2020. PMID 30422525.
  2. Mittendorf R, Williams MA (1991). "Rho(D) immunoglobulin (RhoGAM): how it came into being". Obstet Gynecol. 77 (2): 301–3. doi:10.1097/00006250-199102000-00029. PMID 1846439.
  3. Weiss EM, Zimmerman SS (2013). "A tale of two hospitals: the evolution of phototherapy treatment for neonatal jaundice". Pediatrics. 131 (6): 1032–4. doi:10.1542/peds.2012-3651. PMID 23650299.
  4. 4.0 4.1 4.2 4.3 4.4 4.5 4.6 "StatPearls". 2020. PMID 31334972.
  5. Mishra S, Agarwal R, Deorari AK, Paul VK (2008). "Jaundice in the newborns". Indian J Pediatr. 75 (2): 157–63. doi:10.1007/s12098-008-0024-7. PMID 18334797.
  6. 6.0 6.1 6.2 Chee YY, Chung PH, Wong RM, Wong KK (2018). "Jaundice in infants and children: causes, diagnosis, and management". Hong Kong Med J. 24 (3): 285–292. doi:10.12809/hkmj187245. PMID 29807950.
  7. Mojtahedi SY, Izadi A, Seirafi G, Khedmat L, Tavakolizadeh R (2018). "Risk Factors Associated with Neonatal Jaundice: A Cross-Sectional Study from Iran". Open Access Maced J Med Sci. 6 (8): 1387–1393. doi:10.3889/oamjms.2018.319. PMC 6108787. PMID 30159062.
  8. Kelly DA, Davenport M (2007). "Current management of biliary atresia". Arch Dis Child. 92 (12): 1132–5. doi:10.1136/adc.2006.101451. PMC 2066090. PMID 17878208.