Neonatal jaundice | causes, symptoms, diagnosis, treatment & pathology

Neonatal jaundice (hyperbilirubinemia) refers to the yellowish discoloration of a newborn's skin and sclera caused by elevated levels of serum bilirubin. It affects the majority of newborns in their first week of life as they transition from fetal to neonatal bilirubin metabolism. Pathophysiology Bilirubin is a byproduct of hemoglobin breakdown. Neonates produce more bilirubin than adults due to a higher red blood cell (RBC) mass and shorter RBC lifespan (approx. 90 days vs. 120 days). Unconjugated (indirect) bilirubin is lipid-soluble, bound to albumin, and transported to the liver, where the enzyme UGT1A1 conjugating it into a water-soluble form for excretion via bile and stool. Neonatal jaundice occurs when bilirubin production exceeds hepatic clearance, or when intestinal reabsorption increases via enteropathic circulation. Major Categories & Causes Physiological Jaundice: Appears between 24 to 72 hours of life, peaks around day 3 to 5, and resolves by 1 to 2 weeks. Caused by transiently low hepatic UGT1A1 activity, higher RBC turnover, and increased intestinal reabsorption. Pathological Jaundice: Any jaundice appearing within the first 24 hours of life, rising rapidly (greater than 5 mg/dL/day), reaching severe thresholds, or lasting beyond 14 days in term infants. Causes include: Hemolysis: ABO or Rh incompatibility, G6PD deficiency, or hereditary spherocytosis. Non-hemolytic: Cephalohematoma, polycythemia, or birth trauma. Decreased Conjugation: Crigler-Najjar or Gilbert syndrome. Breastfeeding vs. Breast Milk Jaundice: Breastfeeding (Suboptimal Intake) Jaundice: Occurs in the first week due to inadequate fluid intake, leading to dehydration, sluggish bowel motility, and increased enteropathic circulation. Breast Milk Jaundice: Onset after day 4 to 7, peaking at weeks 2 to 3. Factors in maternal milk inhibit bilirubin conjugation. Conjugated (Direct) Hyperbilirubinemia: Always pathological (direct bilirubin greater than 1.0 mg/dL or over 20% of total). Indicates cholestasis, biliary atresia, neonatal hepatitis, or metabolic conditions. Clinical Assessment & Cephalocaudal Progression Jaundice typically progresses in a dermal cephalocaudal direction—starting at the head and face, advancing down to the trunk, extremities, and finally the palms and soles as serum levels rise. Physical Exam: Evaluated by blanching the skin under bright light. Diagnostic Testing: Transcutaneous bilirubinometer (TcB) for non-invasive screening, followed by Total Serum Bilirubin (TSB) for definitive measurement. Further workup includes blood type, Direct Coombs test, complete blood count, and reticulocyte count if hemolysis is suspected. Complications Severe, untreated unconjugated hyperbilirubinemia can cross the blood-brain barrier: Acute Bilirubin Encephalopathy (ABE): Early signs include lethargy, poor feeding, and hypotonia; progresses to hypertonia, retrocollis, opisthotonos, and high-pitched crying. Kernicterus (Chronic Bilirubin Encephalopathy): Permanent neurological damage characterized by choreoathetoid cerebral palsy, sensorineural hearing loss, gaze abnormalities, and dental enamel hypoplasia. Management & Treatment Treatment decisions are guided by hour-specific bilirubin threshold charts (such as the Bhutani nomogram) accounting for gestational age and risk factors. Phototherapy: Blue-green light (wavelength 460-490 nm) converts unconjugated bilirubin into water-soluble photoisomers (lumirubin) that can be excreted in bile and urine without hepatic conjugation. Exchange Transfusion: Used when TSB reaches critically high levels or signs of ABE appear, manually replacing the infant's blood to rapidly remove bilirubin and maternal antibodies. Intravenous Immunoglobulin (IVIG): Administered in immune-mediated hemolysis (Rh or ABO incompatibility) to reduce RBC destruction. #viral #viralvideo #mbbs #mcq #bestmedicalcollegeinindia #neet #biology #mbbsabroad #mcqsseries