Neonatology Flashcards
When should the NIPE be performed?
Within 72h of birth
Repeated at 6-8w by GP
Brief overview of NIPE (9)
1) Head: circumference, fontanelles, symmetry of skull
2) Face: dysmorphic features, check palate, ears
3) Eyes: jaundice, red reflex
4) Arms: digits, palmar crease, movement
5) Chest: murmur
6) Abdomen: organomegaly, distension, masses
7) Genitalia & anus: external genitalia, hypospadias, observe anus is present and adequately patent
8) Hips: femoral pulses, Barlow’s & Ortolani’s
9) Legs: digits, talipes, movement
10) Back & reflexes: scoliosis, dimples, hair tufts, Moro reflex
Extras: birthmarks
3 key risk factors for congenital hip dysplasia?
1) Breech
2) Female
3) FH
Cause of unilateral vs bilateral absemt red reflex?
Unilateral - retinoblastoma
Bilateral - congenital cataracts
What % of babies present with jaundice within the first week of life?
60%
Lifespan of newborn RBCs: term & preterm?
Term neonate: 60-90 days
Preterm neonate: 35-50 days
Describe how bilirubin is formed
1) RBC breakdown into haem & globin
2) Haem breakdown into iron & protoporphyrin
3) Protoporphyrin breakdown into unconjugated bilirubin (+ albumin)
4) Conjugated by the liver (UGT enzyme) into conjugated bilirubin
5) Transported to gall bladder via bile duct
Is physiological jaundice normally unconjugated or conjugated hyperbilirubinaemia?
ALWAYS unconjugated hyperbilirubinaemia
When does physiological jaundice resolve?
Term: <14 days
Preterm: <21 days
Cause of physiological jaundice?
Short lifespan of newborn RBCs & insufficient hepatic bilirubin metabolism due to immature liver enzymes (UGT).
Results in increased enterohepatic circulation of bilirubin.
What blood tests are indicated for all infants <28 days presenting with jaundice?
1) LFTs (includes total bilirubin)
2) Bilirubin profile - unconjugated & conjugated levels
3) FBC
4) Clotting screen
5) G&S
6) Direct Coombs test
7) Blood cultures
What is kernicterus?
Bilirubin-induced neurological damage, creates cerebral palsy type picture.
UNconjugated bilirubin (as can cross BBB)
What is the commonest cause of prolonged jaundice (>2 weeks)?
Breast milk jaundice
When does breast milk jaundice ALWAYS resolve by?
Typically resolves by 1 month, ALWAYS resolves by 2 months.
2 key red flags for pathological jaundice?
1) Onset <24h (sepsis, HDN)
2) Onset after >2 weeks of life
2 causes of HDN?
1) Rhesus incompatibility: less common, more severe
2) ABO incompatibility: more common, less severe
Hepatosplenomegaly in ABO vs rhesus incompatibility?
ABO - rare
Rhesus - hepatosplenomegaly prominent due to increased demand on immature hepatocytes
What test should be done in all cases of jaundice <24h?
Coombs test
Coombs test result in Rhesus vs ABO incompatibility?
Rhesus - strongly positive
ABO - weakly positive
What does the Coombs test involve?
Detects autoantibodies against RBCs:
- direct assesses antibodies on surface of RBC
- indirect detects unbound antibodies to RBCs in serum
Agglutination = positive test
Why is jaundice present so soon after birth in HDN?
As haemolysis has been occurring in utero
What is the only examinable cause of conjugated hyperbilirubinaemia?
Biliary atresia
When does jaundice caused by biliary atresia typically present?
AFTER 14 days of life
Pathophysiology in biliary atresia?
1) Obstruction in bile flow, due to obstructed or absent lumen (‘atresia’)
2) Bile starts to accumulate in biliary tree
3) Pressure increases until bile escapes through tight junctions lining biliary tree
4) Escapes into systemic circulation
Classic presentation of biliary atresia?
1) Jaundice onset >14 days of life
2) Pale stools
3) Dark urine
4) Distended abdo & hepatosplenomegaly
What procedure is indicated in biliary atresia?
Kasai hepatoportoenterostomy –> best outcome if performed <2 months of life
Note - many will go on to require a liver transplant later (by 2 years old)
What is surfactant produced by?
Type 2 pneumocytes
Role of surfactant?
Acts to reduce surface tension and prevent airway collapse
When does surfactant production begin?
24-28w gestation
Mx of RDS?
CPAP +/- artificial surfactant (in NICU)
Classic presentation of RDS?
- preterm <1 hour old
- increased work of breathing - grunting, tachypnoea
- cyanosis
- tachycardia
- high O2 requirement
What is the key risk factor for NEC?
Prematurity (rarely ever seen in term babies)
What is NEC?
Inflammation of intestinal wall.
Progression to bowel ischaemia, inflammation, necrosis and perforation.
Classic presentation of NEC?
- preterm
- 2nd to 3rd week of life
- poor feeding
- abdo distension & tenderness
- bloody stools
- perforation: fever, rigid abdomen, vomiting, shocked
1st line investigation in NEC?
AXR
What will AXR show in NEC?
1) Pneumatosis intestinalis (air in intestinal wall)
2) +/- pneumoperitoneum and free gas (if perforation)
Mx of NEC?
1) ABCDE
2) Bowel rest: NBM, TPN
3) IV Abx
4) If perforation –> emergency resection
