Neonatal problems Neonatal jaundice Pathophysiology and epidemiology Visible at >85 μmol/L of bilirubin (BR). The BR is usually unconjugated, which is fat-soluble thus can enter tissue (and cross the blood-brain barrier), causing damage. Common: affects 60% of term babies, and 80% of preterm. Usually physiological: onset after the first 24h, with BR not exceeding 200 μmol/L. Due to liver immaturity and replacement of fetal Hb. Early jaundice (onset <24h) Causes: Hemolytic disease: Rh incompatibility, ABO incompatibility (usually mild), G6PD deficiency, or spherocytosis. Make sure to ask about blood group and family history of hemolytic anaemia. Congenital infection: Group B Strep, TORCH (Toxoplasmosis, Rubella, CMV, HSV).

1. NEONATAL PROBLEMS
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2. NEONATAL JAUNDICE

3. PATHOPHYSIOLOGY AND EPIDEMIOLOGY
Visible at >85 μmol/L of bilirubin (BR). The BR is usually
unconjugated, which is fat-soluble thus can enter tissue
(and cross the blood-brain barrier), causing damage.
Common: affects 60% of term babies, and 80% of preterm.
Usually physiological: onset after the first 24h, with BR
not exceeding 200 μmol/L. Due to liver immaturity and
replacement of fetal Hb.

4. EARLY JAUNDICE (ONSET <24H)
Causes:
Hemolytic disease: Rh incompatibility, ABO
incompatibility (usually mild), G6PD deficiency, or
spherocytosis. Make sure to ask about blood group and
family history of hemolytic anaemia.
Congenital infection: Group B Strep, TORCH
(Toxoplasmosis, Rubella, CMV, HSV).

5. HIGH OR PROLONGED JAUNDICE (>2 WEEKS)
Causes:
Breast feeding (failure) jaundice: poor feeding leads to ↓gut motility, allowing more
conjugated BR to revert to unconjugated and re-enter the blood as part of the
enterohepatic circulation. Presents in first few days.
Breast milk jaundice: an enzyme in maternal breast milk unconjugates BR, thus
increasing enterohepatic circulation. Presents as prolonged jaundice.
Sepsis, most commonly from a UTI.

6. CAUSES:
Cephalohematoma: cranial hematoma due to birth trauma,
forming pool of blood which eventually breaks down leading to
↑haemolysis. Instrumentation increases the risk.
Biliary atresia: elevated conjugated BR (fraction >20%),
presenting with pale poo and dark pee. Leads to liver failure and
death if not treated surgically. Phototherapy is of no use.
Specific diseases: hypothyroidism, CF, galactosaemia.

7. SIGNS AND SYMPTOMS

8. SIGNS AND SYMPTOMS
Starts at head, spreads down.
Spread below the umbilicus suggests non-
physiological jaundice.
In non-white kids, check in eyes and by
pressing on nose tip.

9. INVESTIGATIONS
Basics tests:
Serum BR and conjugated fraction. Re-check every 6-8 hours after starting
phototherapy.
FBC
Blood film: may show evidence of haemolysis.
Reticulocyte count. Increased in haemolysis.
Blood group.
Direct antiglobulin (Coombs') test. +ve in Rh or ABO hemolytic anaemia.

10. FURTHER TESTS FOR PROLONGED
JAUNDICE:
 LFT. Increased in infection.
 Urine culture.
 Reducing substance in urine. +ve in galactosaemia.
 TFT
Phototherapy
 Admit and give phototherapy if onset 2 weeks, or BR above treatment line.
 Goal is to prevent kernicterus.
 Treatment line is age and gestation-specific.

11. PHOTOTHERAPY
Phototherapy isomerizes the BR, making it water soluble (like
conjugated BR) and thus easily excretable.
Ideally use lamp and biliblanket to ensure continuous exposure. Do
feed and nappy changes at same time – every 3-4 hours – to reduce
time out from lamp.
Continue phototherapy until BR is 50 μmol/L below the treatment
line, as there will often be a rebound after stopping treatment.
Side effects: eye damage (so protect eyes), hypothermia if uncovered,
dehydration (if it interferes with feeding).

12. COMPLICATION: KERNICTERUS
Unconjugated BR >360 μmol/L, which deposits in brain.
Signs and symptoms: sleepiness, reduced feeding, irritability, seizure, comas.
Long-term complications include cerebral palsy and deafness.
Neonatal respiratory distress
Signs and symptoms
RR >60
Chest wall recession.
Grunting, an expiratory groan caused by attempt to maintain positive end
expiratory pressure.
Cyanosis

13. CAUSES
Respiratory distress syndrome (RDS)
Due to surfactant deficiency. Occurs in pre-term babies as although surfactant
production starts at 20 weeks, it is not sufficient until about 34 weeks.
Presents within minutes or hours of birth. CXR shows widespread atelectasis
with ground glass appearance, and air bronchograms.
Prevention: maternal IM corticosteroids for deliveries
Management if RDS develops: nasal CPAP → if remains in distress, intubate
and give surfactant via endotracheal tube.

14. TRANSIENT TACHYPNOEA OF THE
NEWBORN
Delay in resorption of lung liquid. C-section and
maternal diabetes is a risk factor, the former because
the squeeze of vaginal delivery is missed.
Presents at birth, and usually resolves in 24-48 hours.
Management: O2 if needed.

15. MECONIUM ASPIRATION
SYNDROME (MAS)
Occurs when meconium is passed in utero (meconium in liquor)
or during birth and is inhaled. Can happen due to fetal
maturation (post-term baby) or in response to acute hypoxia.
Can lead to pneumonitis and obstruction, with the latter leading
to collapse or pneumothorax.
CXR may show patchy atelectasis or consolidation.
Management: intubate for suction.
Can be complex and lead to pulmonary hypertension.

16. BRONCHOPULMONARY
DYSPLASIA (BPD)
Chronic long disease resulting from disruption of normal lung development in
preterm infants with respiratory problems.
Clinically defined as need for supplemental O2 beyond 28 days postnatal or 36
weeks postmenstrual age in absence of other diagnosis requiring this (e.g. heart
disease, pneumonia).
Risk factors: preterm, low birth weight, prolonged/early ventilation, RDS, PDA,
male.
Prevention: prevent and treat RDS, minimize ventilation, caffeine IV if born
consider dexamethasone if premature and still ventilated at 8 days (though
possible risk of neurodevelopmental problems).
Management: O2 ± mechanical ventilation, fluid restriction ± furosemide,
dexamethasone if refractory.

17. OTHER CAUSES
Milk aspiration.
Apnea of prematurity: treat with caffeine IV.
Persistent pulmonary hypertension of the newborn: often
follows early complication such as MAS, sepsis, or pulmonary
hypoplasia.
Pneumonia: commonly Group B Strep.
Pneumothorax: may be spontaneous, follow trauma, or be due
to RDS, MAS, or congenital anomalies.

18. NEONATAL HYPOGLYCAEMIA
Normal for slightly low glucose
postpartum due to drop off of maternal
glucose, but glucose

19. CAUSES
Maternal diabetes: ↑glucose during pregnancy leads to
compensatory fetal ↑insulin, which remains postpartum while
maternal glucose stops.
Premature or SGA: limited glycogen stores.
Infection: ↑glucose use.
Hypothyroidism
Congenital hyperinsulinism: maternal diabetes, pancreatic islet
cell hyperplasia.

20. SIGNS AND SYMPTOMS
Lethargy and altered level of consciousness.
Seizures
Vomiting
Respiratory distress.
Cyanosis

21. INVESTIGATIONS
Check glucose in all at-risk newborns.
Check pre-feed levels in those with hypoglycaemia.
Management
Prevent through adequate feeding soon after birth
and then 3-hourly.
If asymptomatic, ensure feeding is adequate.
Consider NG tube if there are problems.
If symptomatic or severe (glucose

22. FLOPPY BABY

23. DEFINITION AND PRESENTATION
Persistent hypotonia which is especially apparent on being held up
when prone.
Frog-like posture.
Head lag when lifted up by hands.
In utero, there may be polyhydramnios due to poor swallow.
With CNS causes, baby often floppy but strong, with preserved
truncal tone.
With peripheral causes, baby may have lower motor neuron signs:
weakness ('floppy weak'), hyporeflexia, fasciculations.

24. CNS CAUSES
Hypoxic-ischaemic encephalopathy.
Genetic syndromes – e.g. Down's, Prader-Willi – which
often include dysmorphic features.
Cerebral palsy: hypotonia may occur before spasticity.
Metabolic and endocrine: hypoglycaemia, hypocalcaemia,
hypothyroidism.
Sepsis

25. LOWER MOTOR NEURON CAUSES
Spinal muscular atrophy. Accompanied by tongue fasciculations.
Congenital myopathy.
Congenital myotonic dystrophy.
Myasthenia gravis.
Management
Treat acute causes e.g. sepsis, electrolyte imbalances.
Respiratory support if needed.
Consider genetic testing.

26. ACUTE NEONATAL
NEUROLOGICAL PROBLEMS

27. NEONATAL SEIZURES
Causes:
 Hypoglycaemia
 Electrolytes abnormalities: ↓/↑Na+, ↓Ca2+, ↓Mg2+.
 CNS infection.
 Vascular: HIE, IVH.
 Kernicterus
Management:
 ABC
 Phenobarbital IV if >5 minutes.

28. HYPOXIC-ISCHAEMIC
ENCEPHALOPATHY (HIE)
Background
Due to perinatal asphyxia, defined as progressive hypoxia
with hypercapnia and acidosis.
Causes: prolonged uterine contractions, placental
abruption, cord compression, poor maternal perfusion,
respiratory failure.

29. SIGNS AND SYMPTOMS
Perinatal features: continued need for resuscitation at 10 mins,
Apgar score ≤5 at 10 mins, cord/arterial/capillary pH <7.
Signs within 24h: irritable if mild, otherwise lethargy/coma,
seizures, hypotonia, poor reflexes, multi-organ failure including
heart, lungs, kidney, and liver.
Investigations
Amplitude-integrated EEG (aka cerebral function analysis
monitoring).
Cranial USS. Easily available, but less sensitive than MRI for
long-term prognostication.

30. MANAGEMENT
Stabilize inc. airway management if needed.
Check glucose and exclude other causes.
Therapeutic hypothermia if moderate or severe. Start within 6 hrs of
birth, 34°C for 72 hrs.
Control seizures.
Complications
Death
Cerebral palsy.
Learning disabilities.

31. INTRA-VENTRICULAR HAEMORRHAGE
(IVH)
Occurs in premature (
Can lead to lifelong neurological deficits.
Signs: lethargy, seizures, apnoea, bulging
fontanelle.
Signs may be minimal, so premature and VLBW (

32. ACUTE NEONATAL GI PROBLEMS
Necrotising enterocolitis (NEC)
Bowel necrosis from unknown cause, typically in premature and/or
LBW babies.
Presents with abdominal distention or mass, bloody mucous stool,
bilious vomit, ↓bowel sounds, shock, and DIC.
X-ray may show pneumatosis intestinalis (gas in bowel wall), gas-
filled bowel loops, or pneumoperitoneum.
Management: stop feeds, insert NG for decompression, and give IV
antibiotics.

33. GASTROSCHISIS AND OMPHALOCELE
Pathophysiology and anatomy:
Congenital defects involving protrusion of abdominal contents
through anterior wall.
Gastroschisis: uncovered intestine (it can see the 'schi' (sky))
protrudes through defect to the right of the umbilicus.
Omphalocele: central protruding sac 'celed' (sealed) within the
mesentry, containing stomach, intestine, and sometimes liver, with
umbilical cord inserting into it.
Associated with other congenital defects such as Fallot, trisomy 13
and 18, and Beckwith-Wiedemann syndrome.

34. MANAGEMENT:
In gastroschisis, check for ischemia from torsion, and
rotate if needed.
Cover with warmed saline gauze, bandage, and plastic
wrap.
Fluids to compensate for loss, and prophylactic
antibiotics.
Definitive treatment is surgery. 90% survival in
gastroschisis, slightly less for omphalocele.

35. COMPLICATIONS OF PREMATURITY
AND LOW BIRTH WEIGHT
Respiratory:
Respiratory distress syndrome.
Meconium aspiration syndrome.
Transient tachypnoea of the newborn.
Metabolic:
Hypoglycaemia
Hypocalcaemia

36. CARDIOVASCULAR:
PDA
CNS:
IVH
Cerebral palsy.
Poor brain growth due to immaturity and inadequate
feeding.

37. RETINOPATHY OF PREMATURITY:
Abnormal vascular growth in retina due to arrest of normal
vascular growth.
Causes: premature birth (
Can lead to retinal detachment and blindness.
Treat with laser therapy.
Other:
Necrotising enterocolitis.
Hypothermia
Immunosuppression
Increased risk of SIDS.

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