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Neonatal Health

Neonatal Health. Assoc Prof Zsuzsoka Kecskes Dept of Neonatology The Canberra Hospital. Topics covered. Jaundice Hips Cardiac/Oxygen Saturation Monitoring. Neonatal jaundice. What is jaundice?. What is jaundice?.

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Neonatal Health

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  1. Neonatal Health Assoc Prof Zsuzsoka KecskesDept of NeonatologyThe Canberra Hospital

  2. Topics covered • Jaundice • Hips • Cardiac/Oxygen Saturation Monitoring

  3. Neonatal jaundice What is jaundice?

  4. What is jaundice? Jaundice is bilirubin that is deposited in the skin and mucous membranes. It is the end product of haem breakdown. Lysis of red blood cells releases haem from haemoglobin, haem is then converted to bilirubin and excreted.

  5. Bilirubin metabolism Uridine diphosphate glucuronyl transferase (UDPGT) Enterohepatic circulation

  6. Prevalence of neonataljaundice • 65% of term newborns develop clinical jaundice in first week • 80% of preterm infants

  7. Types of neonataljaundice Bilirubin exists in two main forms in serum Unconjugated bilirubin reversibly bound to albumin Conjugated bilirubin readily excretable via the renal and biliary systems

  8. Causes of neonatal jaundice Best classified by age of onset and duration: • Early:within 24 hrs of life • Intermediate:2 days to 2 weeks • Late:persists for >2 weeks

  9. Causes of neonatal jaundice

  10. Causes of neonatal jaundice

  11. Early jaundice • Apparent before 24 hours of age • Always pathological • The main cause for early jaundice is haemolysis such as: • Rhesus isoimmunisation • ABO incompatibility • G6PD deficiency

  12. Investigations for early jaundice • Serum bilirubin level • FBC and film • Blood group • Maternal blood group • Direct coombs test • Consider G6PD level

  13. Causes of neonatal jaundice

  14. Physiological jaundice • Physiological jaundice is jaundice that is present between day 2 and day 10

  15. Physiological jaundice • Physiological jaundice is due to: • High bilirubin production (fetalHb, high Hb) • Reduced bilirubin excretion (UDPGT concentrations at term are 1% of adult concentrations)

  16. What are the factors that exacerbate ‘physiological jaundice’?

  17. Factors that can increase the severity of physiological jaundice • Prematurity • Sepsis • Bruising • Cephalohematoma • Polycythaemia • Delayed passage of meconium • Breast feeding • Certain ethnic groups, esp Chinese

  18. Causes of neonatal jaundice

  19. Prolonged Jaundice Jaundice persisting after 14 days in the term infants Or Jaundice persisting after 21days in the preterm infant

  20. When to start phototherapy?

  21. Serum bilirubin level Conjugated fraction of bilirubin Liver function test (GGT, ALT, AST, Albumin) Coagulation profile (PT, PTT, INR) Abdominal ultrasound (gallbladder) DISIDA / HIDA scan (with follow through) Thyroid function test (TSH, free T4) Metabolic screen (urine for reducing substance) Hepatitis screen (TORCH) Liver biopsy (bile duct proliferation) FBC and film Blood group Maternal blood group Direct coombs test Investigations for prolonged jaundice

  22. Kernicterus • Also called bilirubin encephalopathy • Neurological syndrome resulting from neurotoxic affects of unconjugated bilirubin on basal ganglia and brainstem nuclei • Though infrequent, has at least 10% mortality and 70% morbidity

  23. Mechanism of neurotoxicity in kernicterus • Unbound (unconjugated) bilirubin is: • neurotoxic at high levels • lipophilic and can cross the blood-brain-barrier Bilirubin accumulates at nerve terminals Binds to cell components Impairs mitochondrial functions neurotransmitter synthesis Dysfunction and death of neurons Bilirubin staining of affected areas Long term clinical sequelae

  24. Kernicterus: signs and symptoms (first 24 hours) • Phase 1: • Poor suck, hypotonia and lethargy • Phase 2: • Hypertonia and opisthotonos • Phase 3: • Less hypertonia, high pitched cry, hearing and visual loss, poor feeding and athetosis

  25. Kernicterus: signs and symptoms (long term) • Choreoathetoid cerebral palsy • Upward gaze palsy • Sensorineural hearing loss • Intellectual delay (less common)

  26. Treatment of Neonatal Jaundice • Depends on the cause and level and type of bilirubin • Unconjugated hyperbilirubinaemia: • Ensure adequate fluid intake • Phototherapy • IV immunoglobulin • Exchange transfusion • Conjugated hyperbilirubinaemia: • Ensure adequate nutrition • Treat underlying problem

  27. Phototherapy • Biliblanket • Phototherapy lights

  28. Phototherapy • Phototherapy is NOT: • Ultraviolet light • Infrared light Ultraviolet light (10 – 400 nm) Infrared light (400 – 700 nm) Spectrum of light Blue is most effective (460 - 490 nm) Bilirubin absorbance Bilirubin absorbance and transmittance Maisels MJ et al. N Engl J Med 2008;358:920-8

  29. When to start phototherapy? Decision is based on: • Level of bilirubin • Rate of rise of bilirubin • Gestational age • Chronological age • Wellness of the baby

  30. When to start phototherapy?

  31. Take home message Jaundice before 24 hours is always pathological Kernicterus is rare but serious complication of Unconjugated hyperbilirubin Early diagnosis of biliary atresia impacts on long-term outcome

  32. Examination of the hips - Recommendations • All newborns are to be screened by physical examination (AAP) • properly trained health care provider with regular re-assessment of skills • evidence is good, expert consensus is strong • pre term babies at d/c health check or when acute needs have settled • Examination at 2-4 days, 1, 2, 4, 6, 9 & 12 months - (CTFPHC) • fair evidence

  33. Examination of the hips • Be aware of changes of physical exam with age • by 8-12 weeks Barlow & Ortolani tests are negative regardless of the status of the femoral head • at 3 months limitation of abduction is the most reliable sign associated with DDH (AAP). Asymmetry of thigh folds, leg length discrepancy & Galeazzi sign are also signs. • Hips continue to dislocate through out the first year of life • 1/5000 children have a dislocated hip detected at 18 months

  34. Examination of the hips – High Risk • Family history • Breech presentation • Foot deformities • Oligohydramnios • Primiparity • Females

  35. Examination of the hips - Incidence • White neonates: 1% CDH • Varies with Race:Blacks/Koreans/Chinese • F:M 4:1 • LHS 60% • RHS 20% • Bilat 20%

  36. Examination of the hips Identify at Risk infants: Examine the Hips for Dislocation and/or dislocatibility • If hips are stable and there are no risk factors  no further action • If there is a strong family history (parents or siblings) of CDH, delivery was as breech, or other deformities are present:  hip ultrasound at 6 weeks and appointment at the post-natal clinic even if hips are stable during the immediate postnatal period. • All babies with clicky hips MUST be reviewed by the Neonatal Registrar and NOT simply referred for U/S and follow-up. Clicky but stable hips are quite common in the first 48 hours of life!

  37. Heart Examination • Congenital heart disease (CHD) commonest congenital malformation (9 in 1000 live births) • Contributes significantly to infant mortality and morbidity. • Current post-natal screening CHD: physical examination after birth and repeat examination at 6-8weeks of age. • Can miss up to 25% of infants with critical CHD • Delayed or missed diagnosis associated with significant morbidity, the most significant being hypoxic / ischaemic brain injury.

  38. Heart Examination • Observational studies suggest that there may be some benefit in screening with pulse oximetry • To date no randomised controlled trials • Rarity of undiagnosed cyanotic CHD and large number of patients required for studies a randomised controlled trial may not be feasible.

  39. Heart Examination • Systematic reviews found overall sensitivity of 63% and specificity of 99.8% for pulse oximetry in diagnosing congenital heart disease in asymptomatic newborns • False positives 0.2-0.9% • Sensitivity of pulse oximetry screening 72% compared to 58% for clinical examination.

  40. Heart Examination • 2 other studies found that in asymptomatic babies a significantly higher number of babies with duct dependent heart disease were detected during screening by physical examination and pulse oximetry (86.2%) compared with those regions not using pulse oximetry screening (72%).  benefit of screening with pulse oximetry in addition to clinical examination. False positives for congenital heart disease will occur but may be expected to detect some other important medical problems, such as sepsis or RDS

  41. Heart Examination PULSE OXIMETRY SCREENING • Within 4-24 hours of life on PNW or DS If SaO2 < 90% • Medical review • If asymptomatic, repeat pulse oximetry in 2-3 hours • If symptomatic further investigations (bloods, CXR, ECG and echocardiography), consider admission)

  42. Heart Examination • Screening introduced to TCH 12 months ago • Audit after 4 months (976 neonates)

  43. Heart Examination • 40 (4%) of infants were missed • 15 (1.5%) were found to have saturations<90% • 3 (0.3%) incorrect assignment • 7 (0.7%) -passed on screen 2 • 1 (0.1%) other diagnosis (Pierre Robin sequence) • 4 (0.41%) failed both screens • 3 (0.31%) had sepsis with normal sats on discharge • 1 (0.1%) had PPHN and non critical congenital heart defect (ASD)

  44. Take home messages • Nutrition (weight, urine output) • Jaundice • Physical exam (heart, hips) • We are just at the end of the phone!!!!!

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