Neonatal jaundice

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Assosciate Editor(s)-In-Chief: Prashanth Saddala M.B.B.S

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.

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.[1]

Neonatal jaundice can be physiological or pathological. Neonatal physiological jaundice is usually harmless: this condition is often seen in infants around the second day after birth, lasting until day 8 in normal births, or to around day 14 in premature births. Serum bilirubin normally drops to a low level without any intervention required: the jaundice is presumably a consequence of metabolic and physiological adjustments after birth. In extreme cases, a brain-damaging condition known as kernicterus can occur; there are concerns that this condition has been rising in recent years due to inadequate detection and treatment of neonatal hyperbilirubinemia. Neonatal jaundice is a risk factor for hearing loss.[2]

All jaundice should be medically evaluated before treatment can be given.

Epidemilogy and Demographics

This condition is common in newborns affecting over half (50 -60%) of all babies in the first week of life.[3]

Causes

In neonates, benign jaundice tends to develop because of two factors - the breakdown of fetal hemoglobin as it is replaced with adult hemoglobin and the relatively immature hepatic metabolic pathways which are unable to conjugate and so excrete bilirubin as fast as an adult. This causes an accumulation of bilirubin in the body (hyperbilirubinemia), leading to the symptoms of jaundice.

Severe neonatal jaundice may indicate the presence of other conditions contributing to the elevated bilirubin levels, of which there are a large variety of possibilities (see below). These should be detected or excluded as part of the differential diagnosis to prevent the development of complications. They can be grouped into the following categories:

 
 
 
 
 
 
 
 
 
 
 
 
Neonatal jaundice
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Unconjugated bilirubin
 
 
 
 
 
 
 
Conjugated bilirubin
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Pathologic
 
 
 
Physiologic
 
Hepatic
 
 
 
Post-hepatic
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hemolytic
 
 
 
Non-hemolytic
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Intrinsic causes
 
 
 
Extrinsic causes
 
 
 
 
 
 
 
 
 
 
 

Intrinsic causes of hemolysis

Extrinsic causes of hemolysis

Non-hemolytic causes

Hepatic causes

Post-hepatic

Breast feeding jaundice

"Breastfeeding jaundice" is caused by insufficient milk intake resulting in dehydration, and can be prevented by frequent breastfeeding sessions of sufficient duration to stimulate adequate milk production.

Breast milk jaundice

Whereas breast feeding jaundice is a mechanical problem, breast milk jaundice is more of a biochemical problem. The term applies to jaundice in a newborn baby.

Very rarely, "breast milk jaundice" occurs during the second or third week of life.

  • First, at birth, the gut is sterile, and normal gut flora takes time to establish. The bacteria in the adult gut convert conjugated bilirubin to stercobilinogen which is then oxidized to stercobilin and excreted in the stool. In the absence of sufficient bacteria, the bilirubin is de-conjugated by brush border β-glucuronidase and reabsorbed. This process of re-absorption is called enterohepatic circulation. It has been suggested that bilirubin uptake in the gut (enterohepatic circulation) is increased in breast fed babies, possibly as the result of increased levels of epidermal growth factor (EGF) in breast milk.[4]
  • Second, the breast-milk of some women contains a metabolite of progesterone called 3-alpha-20-beta pregnanediol. This substance inhibits the action of the enzyme uridine diphosphoglucuronic acid (UDPGA) glucuronyl transferase responsible for conjugation and subsequent excretion of bilirubin. In the newborn liver, activity of glucuronyl transferase is only at 0.1-1% of adult levels, so conjugation of bilirubin is already reduced. Further inhibition of bilirubin conjugation leads to increased levels of bilirubin in the blood [5][citation needed]. However, these results have not been supported by subsequent studies.[6]
  • Third, an enzyme in breast milk called lipoprotein lipase produces increased concentration of nonesterified free fatty acids that inhibit hepatic glucuronyl transferase, which again leads to decreased conjugation and subsequent excretion of bilirubin [7][citation needed].

Despite the advantages of breast feeding, there is a strong association of breast feeding with neonatal hyperbilirubinemia and thus risk of kernicterus, though this is uncommon. Serum bilirubin levels may reach as high as 30 mg/dL. Jaundice should be managed either with phototherapy or with exchange blood transfusion as is needed. Breast feeds however need not be discontinued. The child should be kept well hydrated and extra feeds given.

Neither condition is a reason to stop nursing, though caregivers may advise IV or other fluid administration to ensure the baby is not dehydrated.

Natural history, Complications and Prognosis

Complications

With high doses of bilirubin (severe hyperbilirubinemia) there can be a complication known as kernicterus. This is the chief condition that treatment of jaundice is aimed at preventing. The effects of kernicterus range from fever, seizures, and a high-pitched crying to mental retardation. This is due to a staining effect on the basal ganglia leading to neuronal damage. With aggressive treatment such as exchange transfusion to lower very high bilirubin levels, the neurological effects are almost always transient.

Diagnosis

Physical Examination

Notoriously inaccurate rules of thumb have been applied to the physical exam of the jaundiced infant. Some include estimation of serum bilirubin based on appearance. One such rule of thumb includes infants whose jaundice is restricted to the face and part of the trunk above the umbilicus, have the bilirubin less than 204 umol/l (12 mg/dL) (less dangerous level). Infants whose palms and soles are yellow, have serum bilirubin level over 255 umol/l (15 mg/dL) (more serious level)

Non-invasive measurements of jaundice

Ingram icterometer: In this method a piece of transparent plastic known as Ingram icterometer is used. Ingram icterometer is painted in five transverse strips of graded yellow lines. The instrument is pressed against the nose and the yellow colour of the blanched skin is matched with the graded yellow lines and biluribin level is assigned.

Transcutaneous bilirubinometer: This is hand held, portable and rechargeable but expensive and sophisticated. When pressure is applied to the photoprobe, a xenon tube generates a strobe light, and this light passes through the subcutaneous tissue. The reflected light returns through the second fiber optic bundle to the spectrophotometric module. The intensity of the yellow color in this light, after correcting for the hemoglobin, is measured and instantly displayed in arbitrary units.

Treatment

Infants with neonatal jaundice are often treated with bili lights, exposing them to high levels of colored light to break down the bilirubin. This works due to a photo oxidation process occurring on the bilirubin in the subcutaneous tissues of the neonate. Light energy creates isomerization of the bilirubin and consequently transformation into compounds that the new born can excrete via urine and stools. Blue light is typically used for this purpose. Green light is more effective at breaking down bilirubin, but is not commonly used because it makes the babies appear sickly, which is disturbing to observers.

The bilirubin levels for initiative of phototherapy varies depends on the age and health status of the newborn. However any newborn with a total serum bilirubin greater than 359 umol/l ( 21 mg/dL ) should receive phototherapy.[8]

Phototherapy

The use of phototherapy was first discovered, accidentally, at Rochford Hospital in Essex, England. The ward sister (Charge Nurse) of the premature baby unit, firmly believed that the infants under her care benefited from fresh air and sunlight in the courtyard. Although this led to the first noticing of jaundice being improved with sunlight, further studies only progressed when a vial of blood sent for bilirubin measurement sat on a windowsill in the lab for several hours. The results indicated a much lower level of bilirubin than expected based on the patient's visible jaundice. Further investigation lead to the determination that blue light, wavelength of 420-448 nm, oxidized the bilirubin to biliverdin, a soluble product that does not contribute to kernicterus. Although some pediatricians began using phototherapy in the United Kingdom following Dr. Cremer's publishing the above facts in the Lancet in 1958, most hospitals only began to regularly use phototherapy ten years later when an American group independently made the same discovery.[9][10]

Infants with neonatal jaundice are treated with colored light called phototherapy. Physicians randomly assigned 66 infants 35 weeks of gestation to receive phototherapy. After 15±5 the levels of bilirubin, a yellowish bile pigment that in excessive amounts causes jaundice, were decreased down to 0.27±0.25 mg/dl/h in the blue light. This suggests that blue light therapy helps reduce high bilirubin levels that cause neonatal jaundice.[11]

Exposing infants to high levels of colored light changes trans-bilirubin to the more water soluble cis-form which is excreted in the bile. Scientists studied 616 capillary blood samples from jaundiced newborn infants. These samples were randomly divided into three groups. One group contained 133 samples and would receive phototherapy with blue light. Another group contained 202 samples would receive room light, or white light. The final group contained 215 samples, and were left in a dark room. The total bilirubin levels were checked at 0, 2, 4, 6, 24, and 48 hours. There was a significant decrease in bilirubin in the first group exposed to phototherapy after two hours, but no change occurred in the white light and dark room group. After 6 hours, there was a significant change in bilirubin level in the white light group but not the dark room group. It took 48 hours to record a change in the dark room group’s bilirubin level. Phototherapy is the most effective way of breaking down a neonate’s bilirubin.[12]

Phototherapy works through a process of isomerization that changes trans-bilirubin into the water-soluble cis-bilirubin isomer.[13][14]

In phototherapy, blue light is typically used because it is more effective at breaking down bilirubin (Amato, Inaebnit, 1991). Two matched groups of newborn infants with jaundice were exposed to intensive green or blue light phototherapy. The efficiency of the treatment was measured by the rate of decline of serum bilirubin, which in excessive amounts causes jaundice, concentration after 6, 12 and 24 hours of light exposure. A more rapid response was obtained using the blue lamps than the green lamps. However, a shorter phototherapy recovery period was noticed in babies exposed to the green lamps. Green light is not commonly used because exposure time must be longer to see dramatic results.

Ultraviolet light therapy may increase the risk of or skin moles, in childhood. While an increased number of moles is related to an increased risk of skin cancer,[15][16][17] it is not ultraviolet light that is used for treating neonatal jaundice. Rather, it is simply a specific frequency of blue light that does not carry these risks.

Increased feedings help move bilirubin through the neonate’s metabolic system.[18]

The light can be applied with overhead lamps, which means that the baby's eyes need to be covered, or with a device called a Biliblanket, which sits under the baby's clothing close to its skin.

Brief exposure to indirect sunlight each day and increased feeding are also helpful. A newborn should not be exposed to direct sunlight because of the danger of sunburn, which is much more harmful to a newborn's thin skin than that of an adult.

If the neonatal jaundice does not clear up with simple phototherapy, other causes such as biliary atresia, PFIC, bile duct paucity, Alagille's syndrome, alpha 1 and other pediatric liver diseases should be considered. The evaluation for these will include blood work and a variety of diagnostic tests. Prolonged neonatal jaundice is serious and should be followed up promptly.

Exchange transfusions

Much like with phototherapy the level at which exchange transfusions should occur depends on the health status and age of the newborn. It should however be used for any newborn with a total serum bilirubin of greater than 428 umol/l ( 25 mg/dL ).[8]

See also

References

  1. Madlon-Kay, Diane J. Recognition of the Presence and Severity of Newborn Jaundice by Parents, Nurses, Physicians, and Icterometer Pediatrics 1997 100: e3
  2. [http://aapnews.aappublications.org/cgi/content/full/18/5/231 "Increased vigilance needed to prevent kernicterus in newborns --O�Keefe 18 (5): 231 -- AAP News"]. Retrieved 2007-06-27. replacement character in |title= at position 66 (help)
  3. "Neonatal Jaundice" (PDF). Intensive Care Nursery House Staff Manual. UCSF Children's Hospital. 2004. Retrieved 26 July 2011.
  4. Kumral, A (2009). "Breast milk jaundice correlates with high levels of epidermal growth factor". Pediatr Res. 66: 218–21. Unknown parameter |coauthors= ignored (help)
  5. Arias, IM (1964). "Prolonged neonatal unconjugated hyperbilirubinemia associated with breast feeding and a steroid, pregnane-3(alpha), 20(beta)-diol in maternal milk that inhibits glucuronide formation in vitro". J Clin Invest. 43: 2037–47. Unknown parameter |coauthors= ignored (help)
  6. Murphy, J F (1981). "Pregnanediols and breast-milk jaundice". Arch Dis Child. 56: 474–76. Unknown parameter |coauthors= ignored (help)
  7. Poland, R L (1980). "High milk lipase activity associated with breastmilk jaundice". Pediatr Res. 14: 1328–31. Unknown parameter |coauthors= ignored (help)
  8. 8.0 8.1 American Academy of Pediatrics Subcommittee on Hyperbilirubinemia (2004). "Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation". Pediatrics. 114 (1): 297–316. doi:10.1542/peds.114.1.297. PMID 15231951. Unknown parameter |month= ignored (help)
  9. Dobbs, R H (1975-11). "Phototherapy". Archives of Disease in Childhood. 50 (11): 833–836. doi:10.1136/adc.50.11.833. ISSN 0003-9888. PMC 1545706. PMID 1108807. Unknown parameter |coauthors= ignored (help); Check date values in: |date= (help)
  10. Cremer, R. J. (1958-05-24). "INFLUENCE OF LIGHT ON THE HYPERBILIRUBINÆMIA OF INFANTS". The Lancet. 271 (7030): 1094–1097. doi:10.1016/S0140-6736(58)91849-X. ISSN 0140-6736. Retrieved 2010-08-01. Unknown parameter |coauthors= ignored (help)
  11. Amato M, Inaebnit D (1991). "Clinical usefulness of high intensity green light phototherapy in the treatment of neonatal jaundice". Eur. J. Pediatr. 150 (4): 274–6. doi:10.1007/BF01955530. PMID 2029920. Unknown parameter |month= ignored (help)
  12. Leung C, Soong WJ, Chen SJ (1992). "[Effect of light on total micro-bilirubin values in vitro]". Zhonghua Yi Xue Za Zhi (Taipei) (in Chinese). 50 (1): 41–5. PMID 1326385. Unknown parameter |month= ignored (help)
  13. Stokowski LA (2006). "Fundamentals of phototherapy for neonatal jaundice". Adv Neonatal Care. 6 (6): 303–12. doi:10.1016/j.adnc.2006.08.004. PMID 17208161. Unknown parameter |month= ignored (help)
  14. Ennever JF, Sobel M, McDonagh AF, Speck WT (1984). "Phototherapy for neonatal jaundice: in vitro comparison of light sources". Pediatr. Res. 18 (7): 667–70. doi:10.1203/00006450-198407000-00021. PMID 6540860. Unknown parameter |month= ignored (help)
  15. Pullmann H, Theunissen A, Galosi A, Steigleder GK (1981). "[Effect of PUVA and SUP therapy on nevocellular nevi (author's transl)]". Z. Hautkr. (in German). 56 (21): 1412–7. PMID 7314762. Unknown parameter |month= ignored (help)
  16. Titus-Ernstoff L, Perry AE, Spencer SK, Gibson JJ, Cole BF, Ernstoff MS (2005). "Pigmentary characteristics and moles in relation to melanoma risk". Int. J. Cancer. 116 (1): 144–9. doi:10.1002/ijc.21001. PMID 15761869. Unknown parameter |month= ignored (help)
  17. Randi G, Naldi L, Gallus S, Di Landro A, La Vecchia C (2006). "Number of nevi at a specific anatomical site and its relation to cutaneous malignant melanoma". J. Invest. Dermatol. 126 (9): 2106–10. doi:10.1038/sj.jid.5700334. PMID 16645584. Unknown parameter |month= ignored (help)
  18. Wood, S. (2007, March). Fact or fable?. Baby Talk, 72(2).

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