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Neonatal jaundice

 
Medical Encyclopedia: Neonatal Jaundice
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Definition

Neonatal jaundice (or hyperbilirubinemia) is a higher-than-normal level of bilirubin in the blood. Bilirubin is a by-product of the breakdown of red blood cells. This condition can cause a yellow discoloration of the skin and the whites of the eyes called jaundice.

Description

Bilirubin, a by-product of the breakdown of hemoglobin (the oxygen-carrying substance in red blood cells), is produced when the body breaks down old red blood cells. Normally, the liver processes the bilirubin and excretes it in the stool. Hyperbilirubinemia means there is a high level of bilirubin in the blood. This condition is particularly common in newborn infants. Before birth, an infant gets rid of bilirubin through the mother's blood and liver systems. After birth, the baby's liver has to take over processing bilirubin on its own. Almost all newborns have higher than normal levels of bilirubin. In most cases, the baby's systems continue to develop and can soon process bilirubin. However, some infants may need medical treatment to prevent serious complications which can occur due to the accumulation of bilirubin.

— Altha Roberts Edgren


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Children's Health Encyclopedia: Neonatal Jaundice
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Home > Library > Health > Children's Health Encyclopedia

Definition

Neonatal jaundice is the term used when a newborn has an excessive amount of bilirubin in the blood. Bilirubin is a yellowish-red pigment that is formed and released into the bloodstream when red blood cells are broken down. Jaundice comes from the French word jaune, which means yellow; thus a jaundiced baby is one whose skin color appears yellow due to bilirubin.

Description

Normally, small amounts of bilirubin are found in everyone's blood. It is formed and released into the bloodstream when red blood cells are broken down. It is then carried to the liver where it is processed and eventually excreted from the body. When too much bilirubin is made, the excess is discarded into the bloodstream and deposited in tissues for temporary storage. In the neonate, however, there is more bilirubin than can be handled due to immature liver functioning and extra red blood cells that break down. Thus, the extra bilirubin remains in the tissues. Neonatal jaundice affects 60 percent of full-term infants and 80 percent of preterm infants in the first three days after birth.

Demographics

Infants of East Asian and Native American descent have higher levels of bilirubin than white infants, who in turn have higher bilirubin levels than infants of African descent. There is an enzyme, glucose-6-phosphate dehydrogenase (G6PD), deficiency that is more prevalent in infants of East Asian, Greek, and African descent which causes neonatal jaundice to appear at approximately the same time as physiological jaundice. Sickle cell anemia does not predispose newborn infants to jaundice.

Causes and Symptoms

Typically, neonatal jaundice occurs in otherwise healthy infants for two reasons. First, infants have too many red blood cells and it is a natural process for the body to break down these excess red blood cells to form a large amount of bilirubin. It is this bilirubin that causes the skin to take on a yellowish color. Second, the newborn's liver is immature and cannot process bilirubin as quickly as the infant will be able to when older. This slow processing of bilirubin has nothing to do with liver disease. It merely means that the baby's liver is not as fully developed as it will be; thus, there is some delay in eliminating the bilirubin.

Breastfeeding is an important risk factor for hyperbilirubinemia in healthy infants and is related to inadequate maternal milk supply in the first few days, decreased caloric intake and delayed passage of meconium. Nonetheless, this is not a reason to give formula or stop breastfeeding. The breastfeeding mother just needs to nurse the baby more frequently and for longer periods of time to enhance the production of breastmilk. Other factors that cause neonatal jaundice are ABO incompatibility and Rh incompatibility. Both of these conditions result in a very fast breakdown of red blood cells. It is also possible for jaundice to appear in infants with physical defects in the organs that work to eliminate bilirubin from the body. An abnormal increase in red blood cells is frequently seen in infants who are large or small for their gestational age, as well as in trisomy syndromes, twin-to-twin transfusion syndrome, maternal-fetal transfusion, use of oxytocin in labor, Asian male babies, presence of bruising and cephalohematoma, and a family history of neonatal jaundice.

As the excess bilirubin builds up in the newborn, jaundice appears first in the face and upper body and progresses downward toward the toes. Most babies with jaundice have physiologic jaundice, which is the type caused by the natural process of breaking down red blood cells. If the baby's jaundice is caused by any other conditions, however, the healthcare giver will provide the parents with additional information for caring for the baby.

When to Call the Doctor

With short neonatal hospital stays, jaundice will not have peaked or become apparent at the time of hospital discharge. Therefore, infants at risk for severe hyperbilirubinemia should be identified so they can be observed closely both while in the hospital and after discharge. The parents need to be instructed on how to evaluate the infant for jaundice. They should look for it first in the face and upper body and if it progresses downward this means the concentration is getting too high and it is time to call the pediatrician. If there is an area of their living quarters that gets sunlight, it helps to let the baby lie there in only a diaper for a short period of time each day.

Diagnosis

Jaundice can be observed with the naked eye, but it is too difficult to estimate the variation in levels of bilirubin in that manner. Thus, if an infant begins to appear jaundiced, bilirubin levels will be ordered to determine the severity. Jaundice usually becomes apparent when total bilirubin levels exceed 5 mg/dL; however, the clinical significance of bilirubin levels depends on postnatal age in hours. A bilirubin level of 12 mg/dL may be pathologic in an infant younger than 48 hours but is benign in an infant older than 72 hours. In the determination of cause, it is suggested that laboratory testing be reserved for infants with nonphysiologic jaundice. In up to 50 percent of infants with severe jaundice, breastfeeding and lower gestational age were the only causes identified despite extensive workups.

Treatment

The mainstay in treatment of hyperbilirubinemia is phototherapy, which is safe and widely available. Its effectiveness was demonstrated in a study by the National Institute of Child Health and Human Development. Multiple factors can influence the effectiveness of phototherapy, including the type and intensity of the light and the extent of skin surface exposure. Special blue fluorescent light has been shown to be most effective, although many nurseries use a combination of daylight, white, and blue lamps. In the early 2000s, fiberoptic blankets have been developed that emit light in the blue-green spectrum, which is light at a wavelength of 425–475 nm. Light at this wavelength converts bilirubin to a water-soluble form that can be excreted in the bile or urine. The intensity of light delivered is inversely related to the distance between the light source and the skin surface. Since phototherapy acts by altering the bilirubin that is deposited in the tissue, the area of the skin exposed to phototherapy should be maximized. This has been made more practical with the development of fiberoptic phototherapy blankets that can be wrapped around an infant.

Home-based care for neonatal jaundice has become more prevalent than hospital care, and the availability of fiberoptic blankets has made it possible. Infants receiving home phototherapy need daily visits by a nurse, who performs a physical examination and measures the total serum bilirubin level. If bilirubin levels continue to rise, hospital readmission should be considered. Discontinuation of home phototherapy is safe once the total serum bilirubin level has decreased to less than 15 mg/dL in healthy full-term infants older than four days. Office evaluation within two to three days of discontinuing home phototherapy is recommended.

Potential side effects of phototherapy used for elevated bilirubin levels, include watery diarrhea, increased water loss, skin rash, and transient bronzing of the skin. Many infants who are readmitted to the hospital because of hyperbilirubinemia are mildly to moderately dehydrated. Breastfeeding should be increased to every two to two and a half hours. Increased feedings can increase peristalsis and meconium passage, decreasing bilirubin resorption into circulation.

Full-term infants rarely require an exchange transfusion if intense phototherapy is initiated in a timely manner. It should be considered if the total serum bilirubin level is approaching 20 mg/dL and continues to rise despite intense in-hospital phototherapy. Exchange transfusion corrects anemia associated with the destruction of red blood cells and is effective in removing sensitized red blood cells before they are destroyed. It also removes about 60 percent of bilirubin from the plasma, resulting in a clearance of about 30 percent to 40 percent of the total bilirubin. If a transfusion is not performed and bilirubin levels get higher, the infant progresses through three phases. In the first two to three days the infant is lethargic, has muscle weakness, and sucks weakly. Progression is marked by a tensing of the muscles, arching, fever, seizures, and high-pitched crying. In the final phase, the patient is hypotonic for several years.

Prognosis

The prognosis for physiological neonatal jaundice is generally very good. Very few infants ever have bilirubin levels greater than 20 mg/dL, which is the level that is correlated with kernicterus (an abnormal accumulation of bile pigment in the brain and other nerve tissue that causes yellow staining and tissue damage). It rarely occurs with bilirubin levels lower than 20 mg/dL but typically occurs when levels exceed 30 mg/dL. Levels between 20 and 30 mg/dL associated with prematurity and hemolytic disease may increase the risk of kernicterus. There are long-term neurological problems when this occurs. Affected children have marked developmental and motor delays in the form of cerebral palsy and mental retardation may also be present.

Prevention

Elevated bilirubin in the neonate is the most common reason for hospital readmission in the first two weeks of life. Kernicterus is still relatively uncommon but has been on the rise with the mandated early postnatal discharge policies. Bilirubin-induced complications can be prevented by introducing a neonatal jaundice protocol to identify infants at risk for significant bilirubin increases, by ensuring adequate parental education and providing for follow-up care.

Parental Concerns

Parents of a newborn need to be vigilant in monitoring changes in their infant. If the mother is breastfeeding, she should nurse the baby at least once every three hours to ensure the onset of milk production and to maintain hydration, which can also be evaluated by the number of wet diapers. Many pediatricians recommend seeing the infant at two weeks but if the parents feel it should be sooner due to alterations in the newborn's physical status, they should take the infant in for a visit.

Resources

Books

Klaus, M. H., and A. A. Fanaroff. Care of the High-Risk Neonate, 5th ed. Philadelphia, PA: Saunders Company, 2001.

Olds, Sally, et al. Maternal-Newborn Nursing and Women's Health Care, 7th ed. Saddle River, NJ: Prentice Hall, 2004.

Seidel, H. M., et al. Primary Care of the Newborn. St. Louis, MO: Mosby, 2001.

Periodicals

Morantz, C., and B. Torrey. "AHRQ report on neonatal jaundice: Agency for Healthcare Research and Quality." American Family Physician (June 1, 2003).

Organizations

Association of Women's Health, Obstetric and Neonatal Nursing. 2000 L Street, NW, Suite 740, Washington, DC 20036. Web site: www.awhonn.org.

American Academy of Pediatrics. 141 Northwest Point Blvd., Elk Grove Village, IL, 60007. Web site: www.aap.org.

American College of Obstetricians and Gynecologists. 409 12th Street, SW, PO Box 96920, Washington, DC 20090. Web site: www.acog.org.

[Article by: Linda K. Bennington, MSN, CNS]


Wikipedia: Neonatal jaundice
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Neonatal jaundice
Classification and external resources
ICD-10 P58., P59.
ICD-9 773, 774
DiseasesDB 8881
MedlinePlus 001559
eMedicine ped/1061
MeSH D007567

Neonatal jaundice is a yellowing of the skin and other tissues of a newborn infant. A bilirubin level of more than 85 umol/l (5 mg/dL) manifests clinical jaundice in neonates whereas in adults 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. This condition is common in upwards of 70% of newborns.

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].

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).

However, studies have shown that even trained examiners (physicians and nurses) make poor estimations based on physical appearance [1]

In infants jaundice can be measured using invasive or non-invasive methods. In non invasive method Ingram icterometer and Transcutaneous bilirubinometer are used.

Contents

Physiological jaundice

Most infants develop visible jaundice due to elevation of unconjugated bilirubin concentration during their first week. This common condition is called physiological jaundice. This pattern of hyperbilirubinemia has been classified into two functionally distinct periods.

Phase one
  1. Term infants - jaundice lasts for about 5 days with a rapid rise of serum bilirubin up to 204 umol/l (12 mg/dL).
  2. Preterm infants: For preterm infants jaundice lasts for about a week, with a rapid rise of serum bilirubin up to 255 umol/l (15 mg/dL).
Phase two - bilirubin levels decline about 34 umol/l (2 mg/dL) for 2 weeks, eventually mimicking adult values.
  1. Preterm infants - phase two can last more than 1 month.
  2. In babies who receive exclusive breast feedings, phase two can last more than 1 month.

Causes

Possible mechanisms involved in physiological jaundice

Increase bilirubin load on liver cells
  1. Increased red blood cell (RBC) volume
  2. Increased labeled bilirubin
  3. Increased circulation of bilirubin in the liver
  4. Decreased RBC survival
Defective hepatic uptake of bilirubin from blood plasma
  1. Decreased ligadin (Y protein)
  2. Increased binding of Y proteins by other anions
  3. Decreased liver uptake especially in phase two
Defective billirubin conjugation
  1. Decreased UDPG activity
Defective bilirubin excretion

Pathological Jaundice of Neonates

(syn. Unconjugated pathological hyberbilirubinemia)

Any of the following features characterizes pathological jaundice:

  1. Clinical jaundice appearing in the first 24 hours.
  2. Increases in the level of total bilirubin by more than 8.5 umol/l (0.5 mg/dL) per hour or (85 umol/l) 5 mg/dL per 24 hours.
  3. Total bilirubin more than 331.5 umol/l (19.5 mg/dL) (hyperbilirubinemia).
  4. Direct bilirubin more than 34 umol/l (2.0 mg/dL).

Causes of Pathological Jaundice of Neonates

  1. Increased production
    1. Fetomaternal blood group incompatibility: Rh, ABO
    2. Hereditary spherocytosis.
    3. Non-spherocytic hemolytic anemia: G-6-PD deficiency, a-thalassemia, Vitamin K3 induced hemolysis, pyruvate kinase deficiency.
    4. Sepsis.
    5. Increased enterohepatic circulation: Pyloric stenosis, or large bowel obstruction.
  2. Decreased clearance
    1. Inborn errors of metabolism: Criggler-Najjar syndrome type I and II
    2. Drugs and Hormones: Hypothyroidism, breast milk jaundice.

Differentiation between Physiological and Pathological jaundice

The aim of clinical assessment is to distinguish physiological from pathological jaundice. The sign which helps to differentiate pathological jaundice of neonates from physiological jaundice of neonates are presence of intrauterine retardation, stigma of intrauterine infections (e.g. cataracts, microcephaly, hepatosplenomegaly etc), cephalhematoma, bruising, signs of intra ventricular hemorrhage etc. History of illness is noteworthy. Family history of jaundice and anemia, family history of neonatal or early infant death due to liver disease, maternal illness suggestive of viral infection (fever, rash or lymphadenopathy), Maternal drugs (e.g. Sulphonamides, anti-malarials causing hemolysis in G-6-PD deficiency) are suggestive of pathological jaundice in neonates.

Causes of jaundice

In neonates, 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 quickly as an adult. This causes an accumulation of bilirubin in the blood (hyperbilirubinemia), leading to the symptoms of jaundice.

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.

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
 
 
 
 Physiological jaundice of Neonates
 
 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

Non-organic causes

Breast feeding jaundice

"Breastfeeding jaundice" or "lack of breastfeeding jaundice," is caused by insufficient breast milk intake, resulting in inadequate quantities of bowel movements to remove bilirubin from the body. This can usually be ameliorated by frequent breastfeeding sessions of sufficient duration to stimulate adequate milk production. Passage of the baby through the vagina during birth helps stimulate milk production in the mother's body, so infants born by cesarean section are at higher risk for this condition.

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 who is exclusively breastfed and in whom other causes of jaundice have been ruled out. The jaundice appears at the end of the first week of life and hence overlaps physiological jaundice. It can last for up to two months. Several factors are thought to be responsible for this condition.

First, in exclusively breastfed babies the establishment of normal gut flora is delayed. 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 and reabsorbed. This process of re-absorption is called entero-hepatic circulation.

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. Reduced conjugation of bilirubin leads to increased level of bilirubin in the blood[citation needed].

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[citation needed].

Breast-milk is now known to cause 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.

Maternal diet and breast milk jaundice

Wiki letter w.svg This section requires expansion.

Non-invasive measurement of jaundice

This method is more accurate and less subjective in estimating 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 rechargable 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

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.[3]

Phototherapy

newborn infant undergoing (white light) phototherapy to treat neonatal jaundice

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 shows that blue light therapy helps reduce high bilirubin levels that cause neonatal jaundice.[4]

Exposing infants to high levels of colored light breaks down the bilirubin. 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.[5]

Phototherapy works through a process of isomerization that changes the bilirubin into water-soluble isomers that can be passed without getting stuck in the liver.[6][7]

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(1). Green light is not commonly used because exposure time must be longer to see dramatic results(1).

Light therapy may increase the risk of nevi, or skin moles, in childhood. Randomly, 36 nevi, or moles, received ultraviolet phototherapy. After exposure, the moles' average size increased from 4.7 mm2 to 5.3 mm2. This was observed in 28 of the 36 moles. Going further, an autoradiograph proved that each mole had an increase in melanocytes, keratinocytes and dermal cells (all skin cells) in comparison with the unexposed nevi, which in turn also increased the risk of melanoma (skin cancer) [8][9][10].

Increased feedings help move bilirubin through the neonate’s metabolic system [11].

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.

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 ).[3]

Complications

Prolonged hyperbilirubinemia (severe jaundice) can result into chronic bilirubin encephalopathy (kernicterus).[12][13] Quick and accurate treatment of neonatal jaundice helps to reduce the risk of neonates developing kernicterus.[14]

An effect of kernicterus is a fever. A male full term neonate had hyperbilirubinemia (kernicterus) and jaundice at the age of 4 days old. He displayed symptoms of increased lethargy, refusal to eat, and had a fever. The neonate who was diagnosed with kernicterus displayed symptoms of a fever.[15]

Another effect of kernicterus is seizures. The Neonatal Unit at Allied Hospital Faisalabad studied 200 neonates of either gender who presented seizures during their hospital stay from April 2003 to June 2004. The seizures were evaluated and one cause of the seizures was kernicterus. 4.5%, or 9 neonates, displayed seizures caused by kernicterus.[16]

High pitched crying is an effect of kernicterus. Scientists used a computer to record and measure cranial nerves 8, 9 and 12 in 50 infants who were divided into two groups equally depending upon bilirubin concentrations. Of the 50 infants, 43 had tracings of high pitched crying.[17]

Exchange transfusions performed to lower high bilirubin levels are an aggressive treatment.[18][19]

Guidelines

American Academy of Pediatrics has issued guidelines for managing this disease, which can be obtained for free [20].

References

  1. ^ a b Madlon-Kay, Diane J. Recognition of the Presence and Severity of Newborn Jaundice by Parents, Nurses, Physicians, and Icterometer Pediatrics 1997 100: e3
  2. ^ "ABO Incompatibility". http://pediatrics.about.com/od/weeklyquestion/a/04_abo_incmplty.htm. Retrieved 2007-06-30.  at About.com
  3. ^ a b "Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation". Pediatrics 114 (1): 297–316. July 2004. doi:10.1542/peds.114.1.297. PMID 15231951. http://pediatrics.aappublications.org/cgi/pmidlookup?view=long&pmid=15231951. 
  4. ^ Amato M, Inaebnit D (February 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. 
  5. ^ Leung C, Soong WJ, Chen SJ (July 1992). "[Effect of light on total micro-bilirubin values in vitro]" (in Chinese). Zhonghua Yi Xue Za Zhi (Taipei) 50 (1): 41–5. PMID 1326385. 
  6. ^ Stokowski LA (December 2006). "Fundamentals of phototherapy for neonatal jaundice". Adv Neonatal Care 6 (6): 303–12. doi:10.1016/j.adnc.2006.08.004. PMID 17208161. 
  7. ^ Ennever JF, Sobel M, McDonagh AF, Speck WT (July 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. 
  8. ^ Pullmann H, Theunissen A, Galosi A, Steigleder GK (November 1981). "[Effect of PUVA and SUP therapy on nevocellular nevi (author's transl)]" (in German). Z. Hautkr. 56 (21): 1412–7. PMID 7314762. 
  9. ^ Titus-Ernstoff L, Perry AE, Spencer SK, Gibson JJ, Cole BF, Ernstoff MS (August 2005). "Pigmentary characteristics and moles in relation to melanoma risk". Int. J. Cancer 116 (1): 144–9. doi:10.1002/ijc.21001. PMID 15761869. 
  10. ^ Randi G, Naldi L, Gallus S, Di Landro A, La Vecchia C (September 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. 
  11. ^ Wood, S. (2007, March). Fact or fable?. Baby Talk, 72(2).
  12. ^ Juetschke, L.J. (2005, Mar/Apr). Kernicterus: still a concern. Neonatal Network, 24(2), 7-19, 59-62
  13. ^ Colletti JE, Kothari S, Kothori S, Jackson DM, Kilgore KP, Barringer K (November 2007). "An emergency medicine approach to neonatal hyperbilirubinemia". Emerg. Med. Clin. North Am. 25 (4): 1117–35, vii. doi:10.1016/j.emc.2007.07.007. PMID 17950138. 
  14. ^ Watchko JF (December 2006). "Hyperbilirubinemia and bilirubin toxicity in the late preterm infant". Clin Perinatol 33 (4): 839–52; abstract ix. doi:10.1016/j.clp.2006.09.002. PMID 17148008. 
  15. ^ Shah Z, Chawla A, Patkar D, Pungaonkar S (March 2003). "MRI in kernicterus". Australas Radiol 47 (1): 55–7. doi:10.1046/j.1440-1673.2003.00973.x. PMID 12581055. 
  16. ^ Malik BA, Butt MA, Shamoon M, Tehseen Z, Fatima A, Hashmat N (December 2005). "Seizures etiology in the newborn period". J Coll Physicians Surg Pak 15 (12): 786–90. doi:12.2005/JCPSP.786790. PMID 16398972. 
  17. ^ Vohr BR, Lester B, Rapisardi G, et al. (August 1989). "Abnormal brain-stem function (brain-stem auditory evoked response) correlates with acoustic cry features in term infants with hyperbilirubinemia". J. Pediatr. 115 (2): 303–8. doi:10.1016/S0022-3476(89)80090-3. PMID 2754560. 
  18. ^ Gómez M, Bielza C, Fernández del Pozo JA, Ríos-Insua S (2007). "A graphical decision-theoretic model for neonatal jaundice". Med Decis Making 27 (3): 250–65. doi:10.1177/0272989X07300605. PMID 17545496. 
  19. ^ Rothberg AD, Thomson PD, Andronikou S, Cohen DF (July 1982). "Transient neonatal hyperammonaemia. A case report". S. Afr. Med. J. 62 (6): 175–6. PMID 7089816. 
  20. ^ American Academy of Pediatrics. "AAP Issues New Guidelines for Identifying and Managing Newborn Jaundice". http://www.aap.org/family/jaundicefeature.htm. Retrieved 4 July 2009. 

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Certain conditions originating in the perinatal period / fetal disease (P, 760-779)
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