Neonatal Jaundice Learning Materials

Neonatal Jaundice Definition • Elevated levels of bilirubin in the blood - serum bilirubin concentration > 5 mg/dL or > 85.5 μmol/L Aetiology, pathophysiology, and pathogenesis Clinical Features • • physiological - asymptomatic expect for transient icterus ✓ A yellowish discoloration of the skin, sclerae, and mucous membranes due to the deposition of bilirubin. - Jaundice manifests after 1st day of life and usually resolves without treatment in 1 week (in term infants) or 2 weeks (in preterm infants). - Usually most serve on day 1 Pathological - Jaundice can appear less than 24 hours after birth and resists more than a week in term infants and more than 2 weeks in preterm infants Classification AMBOSS TABLE Diagnosis • • • Physical exam for icterus - Regular assessment for all neonates for jaundice (every 8-12 hrs) while in hospital Bilirubin test - Transcutaneous bilirubin measurement ✓ Bilirubin levels of more than 95th percentile on nomogram indicate neonates at high risk for developing neurological sequelae - Serum bilirubin measurement ✓ Total serum bilirubin measured ✓ Differentiation of direct (conjugated) and indirect (unconjugated) bilirubin ✓ Assessment of degree of jaundice based on nomogram -> infants more than 9th percentile must be evaluated for pathological jaundice Other lab tests - Complete blood account - Blood group - Direct and indirect coombs’ test ✓ Rh incompatibility - Markers of inflammation - Liver enzymes - Total serum protein and serum albumin - TSH and free T4 - G6PD deficiency Treatment and Management • Phototherapy - Primary treatment for babies with unconjugated hyperbilirubinemia - MOA: ✓ Blue-green light in the range of 460-490 nm is most effective for phototherapy. The absorption of light by the normal bilirubin (4Z,15Zbilirubin) generates configuration isomers, structural isomers, and photooxidation products. ✓ The 2 principal photoisomers formed in humans are shown. Configurational isomerization is reversible and much faster than structural isomerization. ✓ Structural isomerization is slow and irreversible. Photooxidation occurs more slowly than both configurational and structural isomerization. ✓ Photooxidation products are excreted mainly in urine. ✓ Excretion of water-soluble form in urine and/or bile ✓ Continued until total bilirubin levels are less than 15mg/dL - Side effects: ✓ ✓ ✓ ✓ ✓ ✓ • Diarrhoea Dehydration Changes in skin hue -> bronzing and skin rashes Separation of neonate from mother Increased risk of acute myelogenous leukaemia Bronze baby syndrome ➢ Rare ➢ Occurs in infants with elevated direct bilirubin (conjugated bilirubin more than 2mg/dL) following phototherapy ➢ Caused by abnormal accumulation of bronze-coloured pigments (photoisomers of bilirubin) within the skin ➢ Patients with reversible grey-brownish discolouration of skin, urine and serum ➢ Usually resolves slowly after cessation of phototherapy without complications Exchange transfusions - Indications: ✓ Threshold in a 24hr old term baby is a total serum bilirubin value of more than 20 mg/dL ✓ Inadequate response to phototherapy or a rapid rise in the total serum bilirubin level of more than 1 mg/dL hour in less than 6 hours ✓ Acute bilirubin encephalopathy: ➢ caused by increased levels of bilirubin and its neurotoxic effects. Clinical features include hypotonia, lethargy, apnea, and seizures. Can progress to chronic bilirubin encephalopathy (kernicterus) - Use ABO-matched and Rh-negative erythrocyte concentration - Exchange blood in quantities of 5-20 mL via an umbilical venous catheter until total serum bilirubin is less than 95th percentile on nomogram - Side effects ✓ Acidosis ✓ Thrombosis ✓ Electrolyte imbalances • ✓ Hypotension ✓ Electrolyte imbalance ✓ Higher mortality and morbidity from infections IV immunoglobulin - Indications: used in cases with immunologically mediated conditions or in in the presence of Rh, ABO or other blood group incompatibilities that cause significant neonatal jaundice - Dose range of IVIG: 500 – 1000 mg/kg Complications • • Acute bilirubin encephalopathy - Onset within first days of life - The unconjugated bilirubin can cross the blood-brain barrier - Lethargy, hypotonia (floppy infant syndrome), poor feeding - Fever and shrill cry - Stupor, apnea and seizures - Possibly fatal if neurotoxicity is severe Kernicterus (chronic bilirubin encephalopathy) - Develops over first years of life - MOA: deposition of unconjugated bilirubin (liposoluble) in the basal ganglia and/or brain stem nuclei - Clinical features: ✓ Cerebral paresis, hearing impairment, vertical gaze palsy ✓ Movement disorder (athetosis) ✓ Apparent intellectual and developmental disabilities ✓ Dental enamel hypoplasia