विवरण
Neonatal jaundice, characterized by yellowing of a newborn's skin and eyes, is a common occurrence in the first days of life. It occurs due to the accumulation of bilirubin, a yellow pigment produced from the breakdown of red blood cells. In most cases, neonatal jaundice is physiological, resulting from the immature liver's inability to process bilirubin efficiently. Physiological jaundice typically appears within the first two to three days after birth and usually resolves within a week. Insufficient breast milk intake can lead to breastfeeding jaundice, where bilirubin levels rise due to fewer bowel movements and less bilirubin elimination. This occurs later, usually after the first week, and is associated with certain components in breast milk that interfere with bilirubin metabolism. Sometimes, elevated bilirubin levels can indicate an underlying issue, such as blood type incompatibility, genetic disorders, or infections.
सारांश
- Neonatal jaundice, or hyperbilirubinemia, is a common condition characterized by elevated bilirubin levels in newborns, resulting in yellowing of the skin, mucous membranes, and sclera. It's defined as a total serum bilirubin level exceeding the 95th percentile for age. Jaundice can stem from hepatic, extra-hepatic (obstructive), or hemolytic causes, but the focus here is on disorders of bilirubin metabolism where liver diseases are absent.
- Bilirubin metabolism involves the catabolism of heme, primarily from hemoglobin (80%), into bilirubin. This unconjugated bilirubin binds to albumin for transport. In the liver, it's taken up by hepatocytes, conjugated with UDP glucuronosyltransferase (UGT1A1), and excreted into bile. Infants have lower intestinal microbiota and increased beta-glucuronidase activity, leading to deconjugation and reabsorption of bilirubin, contributing to jaundice.
- Physiological jaundice appears 24-72 hours after birth, peaking at 3-5 days, and resolving by 2-3 weeks. Pathological jaundice, conversely, presents within the first 24 hours, with rapid bilirubin increases or direct bilirubin levels above 1 mg/dL. Pathological jaundice can arise from increased bilirubin production (hemolytic disorders), increased enterohepatic circulation, or decreased conjugation (enzyme deficiencies like Crigler-Najjar syndrome).
- Diagnosis involves a thorough history (onset of jaundice, stool/urine color), physical examination (skin discoloration, signs of dehydration), and lab evaluations. Lab tests include total and direct bilirubin, CBC, peripheral smear, reticulocyte count, Coombs test, G6PD analysis, and liver function tests. An algorithmic approach helps differentiate between physiological and pathological causes.
- Management includes phototherapy and exchange transfusion, guided by age-specific nomograms. Phototherapy uses blue light to convert bilirubin into a water-soluble form for excretion. Exchange transfusion is reserved for severe hyperbilirubinemia to remove bilirubin and antibodies. IVIG may be used in cases of isoimmune hemolytic disease. Gilbert syndrome is a common cause of unconjugated hyperbilirubinemia.
- Specific cases highlight the practical application of these principles. A late preterm baby with jaundice but adequate weight gain exemplifies physiological jaundice requiring reassurance and follow-up. An infant with significant weight loss and elevated bilirubin necessitates phototherapy and addressing the feeding issues. Management depends on plotting serum billirubin.
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