Neonatal jaundice overview: Difference between revisions
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==Overview== | ==Overview== | ||
''' Neonatal jaundice ''' is a yellowing of the [[skin]] and other tissues of a newborn [[infant]] caused by increased levels of [[bilirubin]]in the [[blood]]. | '''Neonatal jaundice ''' is a yellowing of the [[skin]] and other tissues of a newborn [[infant]] caused by increased levels of [[bilirubin]]in the [[blood]]. A [[bilirubin]] level of more than 85 umol/l (5 mg/dL) manifests clinical [[jaundice]] in [[neonates]] whereas in adults a level of 34 umol/l (2 mg/dL) would look [[icteric]]. In newborns jaundice is detected by blanching the skin with digital pressure so that it reveals underlying skin and subcutaneous tissue. Jaundice newborns have an apparent icteric [[sclera]], and yellowing of the face, extending down onto the chest. In neonates the dermal [[Icterus (medicine)|icterus]] is first noted in the face and as the bilirubin level rises proceeds caudal to the trunk and then to the extremities. | ||
A [[bilirubin]] level of more than 85 umol/l (5 mg/dL) manifests clinical [[jaundice]] in [[neonates]] whereas in adults a level of 34 umol/l (2 mg/dL) would look [[icteric]]. In newborns jaundice is detected by blanching the skin with digital pressure so that it reveals underlying skin and subcutaneous tissue. | |||
In neonates the dermal [[Icterus (medicine)|icterus]] is first noted in the face and as the bilirubin level rises proceeds caudal to the trunk and then to the extremities. | |||
==Historical Perspective== | ==Historical Perspective== | ||
Neonatal jaundice was first described by the authors of some | Neonatal [[jaundice]] was first described by the authors of some [[pediatrics]] texts in the 19th century. Some medical records showed several cases of icterum neonatorum in the period between 1885 and 1891. The [[Rh (D) disease|Rh body]] [[antigens]] were discovered in 1940. Through the 20th century, the description of the [[inherited]] neonatal jaundice syndromes were described. | ||
==Classification== | ==Classification== | ||
Neonatal jaundice can be classified based on the etiology of the jaundice into pathological jaundice, physiological jaundice, breastfeeding jaundice, and hemolytic jaundice. | Neonatal jaundice can be classified based on the etiology of the jaundice into [[pathological]] jaundice, [[physiological]] jaundice, [[breastfeeding]] [[jaundice]], and [[hemolytic]] jaundice. | ||
==Pathophysiology== | ==Pathophysiology== | ||
Bilirubin is the catabolic product of the heme which is the main component of the red blood cells. Bilirubin is formed in the liver and spleen then it passes through several process in order to be metabolized. Metabolism processes include hepatic uptake, conjugation, clearance and excretion of the bilirubin in the bile. Jaundice develops due to increase the level of bilirubin and deposition under the skin and cause the yellow discoloration of the skin. Pathogenesis of neonatal jaundice includes physiologic process of bilirubin accumulation or | [[Bilirubin]] is the [[catabolic]] product of the [[heme]] which is the main component of the [[red blood cells]]. Bilirubin is formed in [[Liver|the liver]] and [[spleen]] then it passes through several process in order to be metabolized. Metabolism processes include [[hepatic]] uptake, [[conjugation]], clearance and excretion of the [[bilirubin]] in [[Bile|the bile]]. Jaundice develops due to increase the level of [[bilirubin]] and deposition under the [[skin]] and cause the yellow discoloration of the skin. Pathogenesis of neonatal jaundice includes physiologic process of [[bilirubin]] accumulation or pathological mechanism. The pathological jaundice may be acquired or inherited. Acquired neonatal jaundice include Rh [[Hemolytic disease of the newborn|hemolytic disease]], [[ABO incompatibility (patient information)|ABO incompatibility disease]], and hemolytic disease due to [[Glucose-6-phosphate dehydrogenase deficiency|G6PD enzyme deficiency]]. Inherited neonatal jaundice is due to defect of one of the processes of [[bilirubin metabolism]] and it concludes some inherited syndromes. Inherited neonatal jaundice include [[Gilbert's syndrome]], [[Crigler-Najjar syndrome|Crigler-Najjar syndrome type I and II]], [[Lucey-Driscoll syndrome]], [[Dubin-Johnson syndrome]], and [[Rotor syndrome]]. | ||
==Causes== | ==Causes== | ||
Neonatal jaundice is caused | Neonatal jaundice is caused by [[hemolysis]] of the [[RBCs]] mainly due to either [[intravascular]] causes or extravascular causes. Other causes include non-hemolytic causes such as [[cephalosporin]] induced [[jaundice]], [[genetic mutations]] of the [[UGT1A1|UGT enzyme]], and [[Hepatic|hepatic causes]]. | ||
==Differentiating Neonatal jaundice from other Diseases== | ==Differentiating Neonatal jaundice from other Diseases== | ||
Neonatal jaundice must be differentiated from other causes | Neonatal jaundice must be differentiated from other causes of [[jaundice]] as [[hepatocellular jaundice]] and [[cholestatic jaundice]]. | ||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
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==Risk Factors== | ==Risk Factors== | ||
Common risk factors for neonatal jaundice | Common risk factors for neonatal jaundice include [[maternal]] risk factors and [[neonatal]] risk factors. Common maternal risk factors include mother of Asian race, usage of [[oxytocin]] during [[labor]], [[Breastfeeding|exclusive breastfeeding]], and prolonged labor. Neonatal risk factors include family history of siblings received [[phototherapy]], [[ABO blood group system|ABO blood group]] incompatiblity, preterm neonates, and [[cephalhematoma]]. Less common risk factors for neonatal jaundice include maternal age more than 25 years, siblings with [[jaundice]], male neonates, and black race neonates. | ||
==Screening== | ==Screening== | ||
According to the American Academy of Pediatrics, screening tests recommended for neonatal jaundice | According to the American Academy of Pediatrics, screening tests recommended for neonatal jaundice include [[blood typing]], clinical assessment of [[jaundice]] in the newborns, assessment of the total [[Serum bilirubin|serum bilirubin level]], measuring the level of [[Glucose-6-phosphate dehydrogenase|G6PD enzyme]]. Also, it is recommended for all hospitals to provide information to the parents on [[jaundice]] and its consequences. | ||
==Natural History, Complications, and Prognosis== | ==Natural History, Complications, and Prognosis== | ||
If left untreated, neonatal jaundice may lead to [[brain]] damage. Common complications of neonatal jaundice include acute [[bilirubin]] [[encephalopathy]] and [[kernicterus]]. Prognosis of neonatal jaundice is excellent with the proper treatment. | |||
== | ==Diagnosis== | ||
=== | === Diagnostic Study of Choice === | ||
Bilirubin plasma level is the [[Gold standard (test)|gold standard]] test for the diagnosis of jaundice. Usually the concentration of [[bilirubin]] in the [[blood]] must exceed 2–3 [[Milligram|mg]]/[[Decilitre|dL]] for the coloration to be easily visible. | |||
===History and Symptoms=== | ===History and Symptoms=== | ||
Family and maternal history obtaining is important for diagnosing | Family and maternal history obtaining is important for diagnosing of [[neonatal]] jaundice. Family history include the history of previous sibling who developed before neonatal jaundice, any other family member with [[Liver diseases|liver disease]], and family history of [[hemolytic anemia]]. Maternal history include obtaining the history of [[pregnancy]] and delivery, any maternal illnesses, [[breastfeeding]] history, and usage of any [[drugs]]. Symptoms of the neonatal jaundice include yellow color discoloration which is observed in the [[conjunctiva]], [[mucus membranes]], and [[skin]]. | ||
===Physical Examination=== | ===Physical Examination=== | ||
Patients with neoanatal jaundice usually appear drowsy in severe cases. Physical examination of patients with neonatal jaundice is usually remarkable for | Patients with neoanatal jaundice usually appear drowsy in severe cases. Physical examination of patients with neonatal jaundice is usually remarkable for yellow [[skin]], [[petichia]], yellow eye, [[hepatomegaly]], [[seizures]], and [[microcephaly]] in some cases. | ||
===Laboratory Findings=== | ===Laboratory Findings=== | ||
An elevated concentration | An elevated concentration of [[serum bilirubin]] in neonates in the first 24 hours of life is diagnostic of neonatal jaundice. [[Transcutaneous pacing|Transcutaneous]] [[bilirubin]] level measurement can be diagnostic in cases of mild [[jaundice]]. Other laboratory tests that can be performed include [[blood typing]] and [[Rh disease|Rh]][[antibodies]] determination, [[liver function tests]], [[direct Coombs test]], [[Serum albumin|serum albumin level]], and [[reticulocyte count]]. | ||
=== Electrocardiogram === | |||
There are no ECG findings associated with neonatal jaundice. | |||
=== X-ray === | |||
There are no X-ray findings associated with neonatal jaundice. | |||
=== CT scan === | |||
There are no CT scan findings associated with neonatal jaundice. | |||
=== MRI === | |||
There are no MRI findings associated with neonatal jaundice. | |||
=== Echocardiography or Ultrasound === | |||
Ultrasound can be useful for assessing [[hepatomegaly]], or liver enlargement, which can sometimes be seen in hemolytic diseases causing jaundice. | |||
===Other Imaging Findings=== | ===Other Imaging Findings=== | ||
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===Medical Therapy=== | ===Medical Therapy=== | ||
The mainstay of treatment of patients with neonatal jaundice | The mainstay of treatment of patients with neonatal jaundice is [[phototherapy]], [[intravenous]] [[immunoglobulins]] and [[Blood transfusion|blood exchange]]. | ||
===Surgery=== | ===Surgery=== | ||
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=== Secondary Prevention === | === Secondary Prevention === | ||
According to the American Academy of Pediatrics, secondary prevention of neonatal jaundice is achieved via proper screening tests which | According to the American Academy of Pediatrics, secondary prevention of neonatal jaundice is achieved via proper screening tests which include [[blood typing]], clinical assessment of [[jaundice]] in the newborns, assessment of the total [[Serum bilirubin|serum bilirubin level]], measuring the level of [[Glucose-6-phosphate dehydrogenase|G6PD enzyme]], and it is also recommended for all hospitals to provide information to the parents on [[jaundice]] and its consequences. | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
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{{WS}} | |||
[[Category:Medicine]] | |||
[[Category:Gastroenterology]] | |||
[[Category:Up-To-Date]] | |||
[[Category:Pediatrics]] | [[Category:Pediatrics]] | ||
[[Category:Hepatology]] | [[Category:Hepatology]] | ||
[[Category:Hematology]] | [[Category:Hematology]] | ||
Latest revision as of 22:57, 29 July 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]
Overview
Neonatal jaundice is a yellowing of the skin and other tissues of a newborn infant caused by increased levels of bilirubinin the blood. A bilirubin level of more than 85 umol/l (5 mg/dL) manifests clinical jaundice in neonates whereas in adults a level of 34 umol/l (2 mg/dL) would look icteric. In newborns jaundice is detected by blanching the skin with digital pressure so that it reveals underlying skin and subcutaneous tissue. Jaundice newborns have an apparent icteric sclera, and yellowing of the face, extending down onto the chest. In neonates the dermal icterus is first noted in the face and as the bilirubin level rises proceeds caudal to the trunk and then to the extremities.
Historical Perspective
Neonatal jaundice was first described by the authors of some pediatrics texts in the 19th century. Some medical records showed several cases of icterum neonatorum in the period between 1885 and 1891. The Rh body antigens were discovered in 1940. Through the 20th century, the description of the inherited neonatal jaundice syndromes were described.
Classification
Neonatal jaundice can be classified based on the etiology of the jaundice into pathological jaundice, physiological jaundice, breastfeeding jaundice, and hemolytic jaundice.
Pathophysiology
Bilirubin is the catabolic product of the heme which is the main component of the red blood cells. Bilirubin is formed in the liver and spleen then it passes through several process in order to be metabolized. Metabolism processes include hepatic uptake, conjugation, clearance and excretion of the bilirubin in the bile. Jaundice develops due to increase the level of bilirubin and deposition under the skin and cause the yellow discoloration of the skin. Pathogenesis of neonatal jaundice includes physiologic process of bilirubin accumulation or pathological mechanism. The pathological jaundice may be acquired or inherited. Acquired neonatal jaundice include Rh hemolytic disease, ABO incompatibility disease, and hemolytic disease due to G6PD enzyme deficiency. Inherited neonatal jaundice is due to defect of one of the processes of bilirubin metabolism and it concludes some inherited syndromes. Inherited neonatal jaundice include Gilbert's syndrome, Crigler-Najjar syndrome type I and II, Lucey-Driscoll syndrome, Dubin-Johnson syndrome, and Rotor syndrome.
Causes
Neonatal jaundice is caused by hemolysis of the RBCs mainly due to either intravascular causes or extravascular causes. Other causes include non-hemolytic causes such as cephalosporin induced jaundice, genetic mutations of the UGT enzyme, and hepatic causes.
Differentiating Neonatal jaundice from other Diseases
Neonatal jaundice must be differentiated from other causes of jaundice as hepatocellular jaundice and cholestatic jaundice.
Epidemiology and Demographics
The prevalence of neonatal jaundice ranges from a low of 60,000 to high of 70,000 per 100,000 neonates. The prevalence of the neonatal jaundice decreases by increasing the gestational age of the neonate. The prevalence of neonatal jaundice is more in the East Asian, American Indian, and Greek races.
Risk Factors
Common risk factors for neonatal jaundice include maternal risk factors and neonatal risk factors. Common maternal risk factors include mother of Asian race, usage of oxytocin during labor, exclusive breastfeeding, and prolonged labor. Neonatal risk factors include family history of siblings received phototherapy, ABO blood group incompatiblity, preterm neonates, and cephalhematoma. Less common risk factors for neonatal jaundice include maternal age more than 25 years, siblings with jaundice, male neonates, and black race neonates.
Screening
According to the American Academy of Pediatrics, screening tests recommended for neonatal jaundice include blood typing, clinical assessment of jaundice in the newborns, assessment of the total serum bilirubin level, measuring the level of G6PD enzyme. Also, it is recommended for all hospitals to provide information to the parents on jaundice and its consequences.
Natural History, Complications, and Prognosis
If left untreated, neonatal jaundice may lead to brain damage. Common complications of neonatal jaundice include acute bilirubin encephalopathy and kernicterus. Prognosis of neonatal jaundice is excellent with the proper treatment.
Diagnosis
Diagnostic Study of Choice
Bilirubin plasma level is the gold standard test for the diagnosis of jaundice. Usually the concentration of bilirubin in the blood must exceed 2–3 mg/dL for the coloration to be easily visible.
History and Symptoms
Family and maternal history obtaining is important for diagnosing of neonatal jaundice. Family history include the history of previous sibling who developed before neonatal jaundice, any other family member with liver disease, and family history of hemolytic anemia. Maternal history include obtaining the history of pregnancy and delivery, any maternal illnesses, breastfeeding history, and usage of any drugs. Symptoms of the neonatal jaundice include yellow color discoloration which is observed in the conjunctiva, mucus membranes, and skin.
Physical Examination
Patients with neoanatal jaundice usually appear drowsy in severe cases. Physical examination of patients with neonatal jaundice is usually remarkable for yellow skin, petichia, yellow eye, hepatomegaly, seizures, and microcephaly in some cases.
Laboratory Findings
An elevated concentration of serum bilirubin in neonates in the first 24 hours of life is diagnostic of neonatal jaundice. Transcutaneous bilirubin level measurement can be diagnostic in cases of mild jaundice. Other laboratory tests that can be performed include blood typing and Rhantibodies determination, liver function tests, direct Coombs test, serum albumin level, and reticulocyte count.
Electrocardiogram
There are no ECG findings associated with neonatal jaundice.
X-ray
There are no X-ray findings associated with neonatal jaundice.
CT scan
There are no CT scan findings associated with neonatal jaundice.
MRI
There are no MRI findings associated with neonatal jaundice.
Echocardiography or Ultrasound
Ultrasound can be useful for assessing hepatomegaly, or liver enlargement, which can sometimes be seen in hemolytic diseases causing jaundice.
Other Imaging Findings
There are no other imaging findings associated with neonatal jaundice.
Other Diagnostic Studies
There are no other diagnsotic studies associated with neonatal jaundice.
Treatment
Medical Therapy
The mainstay of treatment of patients with neonatal jaundice is phototherapy, intravenous immunoglobulins and blood exchange.
Surgery
Surgery is not recommended for the management of neonatal jaundice.
Primary Prevention
Effective measures for the primary prevention of neonatal jaundice include breastfeeding of the infants and avoidance of dextrose water supplementation of the breastfeeded infants.
Secondary Prevention
According to the American Academy of Pediatrics, secondary prevention of neonatal jaundice is achieved via proper screening tests which include blood typing, clinical assessment of jaundice in the newborns, assessment of the total serum bilirubin level, measuring the level of G6PD enzyme, and it is also recommended for all hospitals to provide information to the parents on jaundice and its consequences.
References
Template:WH Template:WS