Neonatal Flashcards
Physiological causes of neonatal jaundice
Immature liver function, RBC breakdown
Forceps delivery, Cephalhaematoma
Presents 2-3 days post delivery
At what concentration does bilirubinaemia become symptomatic
> 200 micromol/L
Pathological causes of neonatal jaundice
<24 hrs - G6PD deficiency, congenital infection
Sepsis, polycythaemia, Crigler-Najjar, Gilbert’s syndrome
Causes of prolonged neonatal jaundice
breast milk
Hypothyroidism
GI - biliary atresia, choledochal cyst
Presentation of Kernicterus
Bilirubin encephalopathy:
change in tone and crying
Arched, stiff back
Seizures
Neonatal jaundice Investigations?
Transcutaneous - >205.2 measure serum
Measure serum immediately if visibly jaundiced
Management of jaundice
Physiological - reassure and observe
Pathological - phototherapy
Encephalopathy - exchange transfusion, hydration, IV immunoglobulin
Birth Asphyxia / Hypoxic Ischaemic Encephalopathy
Perinatal asphyxia –> neuronal death
Severe cases –> learning difficulties, HIE
If infant recovers by 2 weeks, then good prognosis
Name some vascular birthmarks
Haemangioma
Port wine stains
Macular stains (salmon patches)
name some pigmented birthmarks
Moles
Café au lait spots
Mongolian blue spots
Describe the features of Cephalhaematoma
Swelling, confined by skull sutures
most commonly affects parietal bone
will resolve by itself over time. May cause transient jaundice
Explain Rh sensitisation
Rh-ve mother, with Rh+ve first child –> sensitised
Her anti-Rh(D) antibodies attack and haemolyse fetal RBCs
Effects of Rh incompatibility on the child
Anaemia –> cardiomegaly and failure
Hepatosplenomegaly –> hypoalbuminaemia –> oedema
Haemolysis –> jaundice and kernicterus (severe)
Treatment of Rh incompatibility
Injection of Anti-D after 1st pregnancy
OR
Injections of Anti-D at 28 weeks and at birth
Anti-D mops up Rh+ve cells and removes them
Short term risk for premature babies
Hypothermia
Hypoglycaemia + hypocalcaemia –> convulsions
ARDS –> ventilation –> bronchopulmonary dysplasia
