bilirubemia

8/8/2019 bilirubemia

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(JAUNDICE IN NEONATES)


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In breast-fed babies, mild jaundice sometimes lasts until 10 to 14 days after birth. Insome breast-fed babies, it goes away and then comes back. Jaundice may last

throughout breast-feeding. This isn't usually a problem as long as the baby gets

enough milk by being fed at regular times.

Jaundice is a condition that makes a newborns skin and the white

part of the eyes look yellow.

It happens because there is too much bilirubin in the babys

blood (hyperbilirubinemia).Bilirubin is a substance that is made when the

body breaks down old red blood cells.Jaundice usually is not a problem. But in rare cases, too much

bilirubin in the blood can cause brain damage (kernicterus).

This can lead to hearing loss, mental retardation, and

behavior problems.

In healthy babies, some jaundice almost always appears by 2 to 4 days of

age. It usually gets better or goes away on its own within a week or two

without causing problems.

WHAT IS JAUNDICE??


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y When serum bilirubin concentration is markedly elevated

y When serum albumin concentration is markedly low (eg, in preterm infants)

y When bilirubin is displaced from albumin by competitive binders

Kernicterus

Is the major consequence of neonatalhyperbilirubinemia.Although it is now rare, kernicterus still occurs and can nearly always beprevented.

Kernicterus is brain damage caused by unconjugated bilirubin

deposition in basal ganglia and brain stem nuclei, caused by

either acute or chronic hyperbilirubinemia. Normally, bilirubin

bound to serum albumin stays in the intravascular space.

However, bilirubin can cross the blood-brain barrier and cause kernicterus in

certain situations:


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PathophysiologyPathophysiology

Neonates, however, have sterile digestive tracts. They do have theenzyme -glucuronidase, which deconjugates the conjugated

bilirubin, which is then reabsorbed by the intestines and recycled

into the circulation. This is called enterohepatic circulation of

bilirubin

In adults, conjugated bilirubin is reduced by gut bacteria to

urobilin and excreted.

The majority of bilirubin is produced from the breakdown of Hb

into unconjugated bilirubin (and other substances).

Unconjugated bilirubin binds to albumin in the blood for

transport to the liver, where it is taken up by hepatocytes and

conjugated with glucuronic acid by the enzyme uridine

diphosphogluconurate glucuronosyltransferase (UGT) to makeit water-soluble. The conjugated bilirubin is excreted in bile into

the duodenum.


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Mechanisms ofMechanisms of

hyperbilirubinemiahyperbilirubinemia:Hyperbilirubinemia can be caused by one or more of

the following processes:

Increased production

Decreased hepatic uptake

Decreased conjugation

Impaired excretionImpaired bile flow (cholestasis)

Increased enterohepatic

circulation


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HyperbilirubinemiaHyperbilirubinemia

yPhysiologic hyperbilirubinemia

y Breastfeeding jaundice

y Breast milk jaundice

yPathologic hyperbilirubinemia due to

hemolytic disease


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PhysiologicPhysiologic hyperbilirubinemiahyperbilirubinemia

y This occurs in almost all neonates. Shorter

neonatal RBC life span increases bilirubin

production; deficient conjugation due to thedeficiency of UGT decreases clearance; and low

bacterial levels in the intestine combined with

increased hydrolysis of conjugated bilirubin

increase enterohepatic circulation. Bilirubinlevels can rise up to 18 mg/dL by 3 to 4 days of

life (7 days in Asian infants) and fall thereafter.


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Breastfeeding jaundiceBreastfeeding jaundice

y develops in one sixth of breastfed infants in the

first week of life. Breastfeeding increases

enterohepatic circulation of bilirubin in some

infants who have decreased milk intake andwho also have dehydration or low caloric intake.

The increased enterohepatic circulation also

may result from reduced intestinal bacteria that

convert bilirubin to nonresorbed metabolites.


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Breast milk jaundiceBreast milk jaundice

y is different from breastfeeding jaundice. It

develops after the first 5 to 7 days of life and

peaks at about 2 wk. It is thought to be caused

by an increased concentration of -glucuronidase in breast milk, causing an

increase in the deconjugation and reabsorption

of bilirubin.


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PathologicPathologic hyperbilirubinemiahyperbilirubinemia

in term infants is diagnosed ify Jaundice appears in the first 24 h, after the first week of

life, or lasts > 2 wk

y Total serum bilirubin (TSB) rises by > 5 mg/dL/day

y

TSB is > 18 mg/dLy Infant shows symptoms or signs of a serious illness

Some of the most common pathologic causes are

Immune and nonimmune hemolytic anemia

G6PD deficiency

Hematoma resorptionSepsis

Hypothyroidism


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Liver dysfunction (eg, caused by parenteral

alimentation causing cholestasis, neonatal

sepsis, neonatal hepatitis) may cause a

conjugated or mixed hyperbilirubinemia.


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Causes of NeonatalCauses of Neonatal HyperbilirubinemiaHyperbilirubinemiaMechanism Causes

Increased enterohepaticcirculation

Breast milk (breast milk jaundice)Breastfeeding failure (breastfeeding jaundice)Drug-induced paralytic ileus (Mg sulfate or morphine)

Fasting or other cause for hypoperistalsisHirschsprung's diseaseIntestinal atresia or stenosis, including annular pancreasMeconium ileus or meconium plug syndrome

Overproduction Swallowed bloodBreakdown of extravascular blood (eg, hematomas; petechiae; pulmonary, cerebral, or occult

hemorrhage)Polycythemia due to maternofetal or fetofetal transfusion or delayed umbilical cord clamping

Overproduction due to hemolyticanemia

Certain drugs and agents in neonates with G6PD deficiency (eg, acetaminophen, alcohol,

antimalarials, aspirin, bupivacaine, corticosteroids, diazepam, nitrofurantoin, oxytocin, penicillin,phenothiazine, sulfonamides)Maternofetal blood group incompatibility (eg, Rh, ABO)RBC enzyme deficiencies (eg, of G6PD or pyruvate kinase)SpherocytosisThalassemias (, )

Undersecretion due to biliaryobstruction

1-Antitrypsin deficiency Biliary atresiaCholedochal cyst Cystic fibrosisDubin-Johnson syndrome and Rotor's syndrome Parenteral nutritionTumor or band

Undersecretion due tometabolic-endocrine conditions

Crigler-Najjar syndrome Drugs and hormonesGilbert syndrome Hypermethioninemia

Hypopituitarism and anencephaly HypothyroidismLucey-Driscoll syndrome Maternal diabetesPrematurity Tyrosinosis

Mixed overproduction and

undersecretion

Asphyxia Intrauterine infections

Maternal diabetes Respiratory distress syndromeSepsis Severe erythroblastosis fetalis

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