Neonatal jaundice

موضوع: Neonatal jaundice الثلاثاء أغسطس 10, 2010 4:31 pm

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).

Studies have shown that trained examiners assessment of levels of jaundice show moderate agreement with icterometer bilirubin measurements.[1]

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

Classification

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
Term infants - jaundice lasts for about 5 days with a rapid rise of serum bilirubin up to 204 umol/l (12 mg/dL).
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.
Preterm infants - phase two can last more than 1 month.
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:
Increased red blood cell (RBC) volume
Increased labeled bilirubin
Increased circulation of bilirubin in the liver
Decreased RBC survival

Defective hepatic uptake of bilirubin from blood plasma:
Decreased ligadin (Y protein)
Increased binding of Y proteins by other anions
Decreased liver uptake especially in phase two

Defective billirubin conjugation:
Decreased UDPG activity

Defective bilirubin excretion

Pathological Jaundice of Neonates

(syn. Unconjugated pathological hyberbilirubinemia)

Any of the following features characterizes pathological jaundice:
Clinical jaundice appearing in the first 24 hours.
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.
Total bilirubin more than 331.5 umol/l (19.5 mg/dL) (hyperbilirubinemia).
Direct bilirubin more than 34 umol/l (2.0 mg/dL).

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.

Hemolytic

Intrinsic causes of hemolysis
Membrane conditions
Spherocytosis
Hereditary ellipsoidosis
Systemic conditions
Sepsis
Arteriovenous malformation
Enzyme conditions
Glucose-6-phosphate dehydrogenase deficiency (also called G6PD deficiency)
Pyruvate kinase deficiency
Globin synthesis defect
sickle cell disease
Alpha-thalassemia

Extrinsic causes of hemolysis
Alloimmunity (The neonatal or cord blood gives a positive direct Coombs test and the maternal blood gives a positive indirect Coombs test)
Hemolytic disease of the newborn (ABO)[2]
Rh disease
Hemolytic disease of the newborn (anti-Kell)
Hemolytic disease of the newborn (anti-Rhc)
Other blood type mismatches causing hemolytic disease of the newborn
Breast milk feeding.

Non-hemolytic causes
Cephalohematoma
Polycythemia
Sepsis
Hypothyroidism
Gilbert's syndrome
Crigler-Najjar syndrome

Conjugated

Hepatic causes
Infections
Sepsis
Hepatitis B
TORCH infections
Metabolic
Galactosemia
Alpha-1-antitrypsin deficiency
Cystic fibrosis
Drugs
Total parenteral nutrition
Idiopathic

Post-hepatic
Biliary atresia
Bile duct obstruction

Non-organic causes

Breast feeding jaundice

"Breastfeeding jaundice" or "lack of breastfeeding jaundice," is caused by insufficient breast milk intake,[3] 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, 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.
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[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].

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.

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 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

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.

موضوع: رد: Neonatal jaundice الخميس أغسطس 12, 2010 1:46 pm

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موضوع: رد: Neonatal jaundice الجمعة أغسطس 13, 2010 8:09 am

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