Neonatal jaundice overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]

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.

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.

Neonatal jaundice can be classified based on the etiology of the jaundice into pathological jaundice, physiological jaundice, breastfeeding jaundice, and hemolytic jaundice.

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.

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.

Neonatal jaundice must be differentiated from other causes of jaundice as hepatocellular jaundice and cholestatic jaundice.

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.

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.

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.

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.

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.

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.

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.

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.

There are no ECG findings associated with neonatal jaundice.

There are no X-ray findings associated with neonatal jaundice.

There are no CT scan findings associated with neonatal jaundice.

There are no MRI findings associated with neonatal jaundice.

Ultrasound can be useful for assessing hepatomegaly, or liver enlargement, which can sometimes be seen in hemolytic diseases causing jaundice.

There are no other imaging findings associated with neonatal jaundice.

There are no other diagnsotic studies associated with neonatal jaundice.

The mainstay of treatment of patients with neonatal jaundice is phototherapy, intravenous immunoglobulins and blood exchange.

Surgery is not recommended for the management of neonatal jaundice.

Effective measures for the primary prevention of neonatal jaundice include breastfeeding of the infants and avoidance of dextrose water supplementation of the breastfeeded infants.

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.

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