Neonatal Jaundice Clinical Presentation

  • Author: Thor WR Hansen, MD, PhD, MHA, FAAP; Chief Editor: Ted Rosenkrantz, MD   more...
 
Updated: Feb 1, 2012
 

History

Presentation and duration of neonatal jaundice

  • Typically, presentation is on the second or third day of life.
  • Jaundice that is visible during the first 24 hours of life is likely to be nonphysiologic; further evaluation is suggested.
  • Infants who present with jaundice after 3-4 days of life may also require closer scrutiny and monitoring.
  • In infants with severe jaundice or jaundice that continues beyond the first 1-2 weeks of life, the results of the newborn metabolic screen should be checked for galactosemia and congenital hypothyroidism, further family history should be explored (see below), the infant's weight curve should be evaluated, the mother's impressions as far as adequacy of breastfeeding should be elicited, and the stool color should be assessed.

Family history

  • Previous sibling with jaundice in the neonatal period, particularly if the jaundice required treatment
  • Other family members with jaundice or known family history of Gilbert syndrome
  • Anemia, splenectomy, or bile stones in family members or known heredity for hemolytic disorders
  • Liver disease

History of pregnancy and delivery

  • Maternal illness suggestive of viral or other infection
  • Maternal drug intake
  • Delayed cord clamping
  • Birth trauma with bruising

Postnatal history

  • Loss of stool color
  • Breastfeeding
  • Greater than average weight loss
  • Symptoms or signs of hypothyroidism
  • Symptoms or signs of metabolic disease (eg, galactosemia)
  • Exposure to total parental nutrition
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Physical

Neonatal jaundice first becomes visible in the face and forehead. Identification is aided by pressure on the skin, since blanching reveals the underlying color. Jaundice then gradually becomes visible on the trunk and extremities. This cephalocaudal progression is well described, even in 19th-century medical texts. Jaundice disappears in the opposite direction. The explanation for this phenomenon is not well understood, but both changes in bilirubin-albumin binding related to pH and differences in skin temperature and blood flow have been proposed.[9, 10] This phenomenon is clinically useful because, independent of other factors, visible jaundice in the lower extremities strongly suggests the need to check the bilirubin level, either in the serum or noninvasively via transcutaneous bilirubinometry.

In most infants, yellow color is the only finding on physical examination. More intense jaundice may be associated with drowsiness. Brainstem auditory-evoked potentials performed at this time may reveal prolongation of latencies, decreased amplitudes, or both.

Overt neurologic findings, such as changes in muscle tone, seizures, or altered cry characteristics, in a significantly jaundiced infant are danger signs and require immediate attention to prevent kernicterus. In the presence of such symptoms or signs, effective phototherapy should commence immediately without waiting for the laboratory test results (see Laboratory Studies). The potential need for exchange transfusion should not preclude the immediate initiation of phototherapy.[11, 12]

Hepatosplenomegaly, petechiae, and microcephaly may be associated with hemolytic anemia, sepsis, and congenital infections and should trigger a diagnostic evaluation directed towards these diagnoses. Neonatal jaundice may be exacerbated in these situations.

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Causes

Physiologic jaundice is caused by a combination of increased bilirubin production secondary to accelerated destruction of erythrocytes, decreased excretory capacity secondary to low levels of ligandin in hepatocytes, and low activity of the bilirubin-conjugating enzyme uridine diphosphoglucuronyltransferase (UDPGT).

Pathologic neonatal jaundice occurs when additional factors accompany the basic mechanisms described above. Examples include immune or nonimmune hemolytic anemia, polycythemia, and the presence of bruising or other extravasation of blood.

Decreased clearance of bilirubin may play a role in breast feeding jaundice, breast milk jaundice, and in several metabolic and endocrine disorders.

Risk factors include the following:

  • Race: Incidence is higher in East Asians and American Indians and is lower in African Americans.
  • Geography: Incidence is higher in populations living at high altitudes. Greeks living in Greece have a higher incidence than those living outside of Greece.
  • Genetics and familial risk: Incidence is higher in infants with siblings who had significant neonatal jaundice and particularly in infants whose older siblings were treated for neonatal jaundice. Incidence is also higher in infants with mutations/polymorphisms in the genes that code for enzymes and proteins involved in bilirubin metabolism, and in infants with homozygous or heterozygous glucose-6-phosphatase dehydrogenase (G-6-PD) deficiency and other hereditary hemolytic anemias. Combinations of such genetic variants appear to exacerbate neonatal jaundice.[13, 5, 14, 6]
  • Nutrition: Incidence is higher in infants who are breastfed or who receive inadequate nutrition. The mechanism for this phenomenon may not be fully understood. However, when inadequate feeding volume is involved, increased enterohepatic circulation of bilirubin probably contributes to prolonged jaundice. Recent data have shown that breast milk jaundice correlates with higher levels of epidermal growth factor, both in breast milk and in infants' serum.[15] Data suggest that the difference between breastfed and formula-fed infants may be less pronounced with some modern formulas. However, formulas containing protein hydrolysates have been shown to promote bilirubin excretion.
  • Maternal factors: Infants of mothers with diabetes have higher incidence. Use of some drugs may increase the incidence, whereas others decrease the incidence.
  • Birthweight and gestational age: Incidence is higher in premature infants and in infants with low birthweight.
  • Congenital infection
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Contributor Information and Disclosures
Author

Thor WR Hansen, MD, PhD, MHA, FAAP  Professor, Department of Neonatology, Women and Children's Division, Chair, Clinical Ethics Committee, Oslo University Hospital HC, Rikshospitalet, Norway

Thor WR Hansen, MD, PhD, MHA, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Association for the History of Medicine, American Pediatric Society, European Society for Paediatric Research, New York Academy of Sciences, Perinatal Research Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Specialty Editor Board

Oussama Itani, MD, FAAP, FACN  Clinical Associate Professor of Pediatrics and Human Development, Michigan State University; Medical Director, Department of Neonatology, Borgess Medical Center

Oussama Itani, MD, FAAP, FACN is a member of the following medical societies: American Academy of Pediatrics, American College of Nutrition, American College of Physician Executives, and American Heart Association

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Brian S Carter, MD, FAAP  Professor of Pediatrics (Neonatology), Vanderbilt University School of Medicine; Director, Neonatal Follow-up Program, Monroe Carell Jr Children's Hospital at Vanderbilt

Brian S Carter, MD, FAAP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Society for Bioethics and Humanities, American Society of Law, Medicine & Ethics, National Hospice and Palliative Care Organization, Society for Pediatric Research, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Carol L Wagner, MD  Professor of Pediatrics, Medical University of South Carolina

Carol L Wagner, MD is a member of the following medical societies: American Academy of Pediatrics, American Chemical Society, American Medical Women's Association, American Public Health Association, American Society for Bone and Mineral Research, American Society for Clinical Nutrition, Massachusetts Medical Society, National Perinatal Association, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Ted Rosenkrantz, MD  Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine

Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Pediatric Society, Connecticut State Medical Society, Eastern Society for Pediatric Research, and Society for Pediatric Research

Disclosure: Nothing to disclose.

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The graph represents indications for phototherapy and exchange transfusion in infants (with a birthweight of 3500 g) in 108 neonatal ICUs. The left panel shows the range of indications for phototherapy, whereas the right panel shows the indications for exchange transfusion. Numbers on the vertical axes are serum bilirubin concentrations in mg/dL (lateral) and mmol/L (middle). In the left panel, the solid line refers to the current recommendation of the American Academy of Pediatrics (AAP) for low-risk infants, the line consisting of long dashes (- - - - -) represents the level at which the AAP recommends phototherapy for infants at intermediate risk, and the line with short dashes (-----) represents the suggested intervention level for infants at high risk. In the right panel, the dotted line (......) represents the AAP suggested intervention level for exchange transfusion in infants considered at low risk, the line consisting of dash-dot-dash (-.-.-.-.) represents the suggested intervention level for exchange transfusion in infants at intermediate risk, and the line consisting of dash-dot-dot-dash (-..-..-..-) represents the suggested intervention level for infants at high risk. Intensive phototherapy is always recommended while preparations for exchange transfusion are in progress. The box-and-whisker plots show the following values: lower error bar = 10th percentile; lower box margin = 25th percentile; line transecting box = median; upper box margin = 75th percentile; upper error bar = 90th percentile; and lower and upper diamonds = 5th and 95th percentiles, respectively.
Algorithm for the management of jaundice in the newborn nursery.
Guidelines for management of neonatal jaundice currently in use in most pediatric departments in Norway. The guidelines were based on previously used charts and were created through a consensus process in the Neonatal Subgroup of the Norwegian Pediatric Society. These guidelines were adopted as national at the fall meeting of the Norwegian Pediatric Society. The reverse side of the chart contains explanatory notes to help the user implement the guidelines. A separate information leaflet for parents was also created.
 
 
 
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