Neonatal Flashcards
What counts as a stillbirth
foetus born with no sight of life ≥24w of pregnancy
Perinatal mortality vs neonatal mortality
perinatal: stillbirtths +deaths in 1st week per 1000 live&still
neonatal: deaths of liveborns within 1st 4 weeks per 100 live birth
Neonate/neonatal period
infant ≥28 days old
Pre-term, term and post-term
Pre-term: <37w
Term: 37-41w
Post-term: ≥42
Low, very low and extremely low birth weight
low <2500g
very low <1500g
extremely low <1000g
Small/Large gestational age
small: birthweight <10th centile for gestational age
large: birthweight >90th centile for gestational age
What is Hypoxic ischaemic encephalopathy
Perinatal asphyxia -> cardioresp depression in the neonatal condition/stage
(cerebral palsy is the post-neonatal condition if severe HIE is not treated)
Causes of hypoxic ischaemic encephalopathy
Failure of placental gas exchange (e.g. abruption)
Interruption of umbilical; blood flow (e.g. shoulder dystocia -> cord compression)
Inadequate matyernal placental perfusion )i.e. mater hypotension)
Compromised foetus (i.e IUGR)
Failure to breathe at birth
Signs and symptoms of hypoxic ishcaemic encephalopathy at diff severities.
Response within 1st 48hrs grades level
Mild = infant irritable, responds excessively to stimulation, staring eyes, hyperventilation, hypertonia. Recovery expected.
Moderate = abnormalities of movement, hypotonic, cannot feed, seizures. Resolved by 2w- good prognosis; persistent past 2w- bad.
Severe = no normal movements or response to pain, tone in limbs fluctuates hypo- to hyper-tonic, prolonged seizures/refractory to Tx, multi-organ failure. 30-40% mortality. >80% neurodisability -> cerebral palsy.
Management of hypoxic ischaemic encephalopathy
Supportive:
Resp support
Anticonvulsants for seizures
Fluid restriction (transient renal impairment)
Inotropes (for hypotension)
Electrolytes and glucose (hypoglycaemia and electrolytre imbalance)
Therapeutic hypothermia (>36w, mild hypothermia can reduce morbidity; requires NICU)
What is cerebral palsy
Abnormality of movement and posture, causing activity limitation to non-progressive disturbances that occurred in the developing foetal or infant brain.
Most common cause of motor impairment.
Clinical manifestations can emerge over time.
If brain injury occurs after 2 year olds, it is diagnosed at acquired brain injury (not CP)
Risk factors and causes for cerebral palsy
Risk factors:
Antenatal- preterm birth, chorioamnionitis, maternal infection
Perinatal- LBW, HIE, neonatal sepsis
Postnatal- meningitis
Causes:
Antenatal - vascular occlusion, cortical migration disorders, structural maldevelopment, genetic syndromes, congenital infection
HIE during delivery - cord compression -> dyskinetic CP
Postnatal - Periventricular leukomalacia (PVL) 2nd to ischaemia ±severe intraventricular haemorrhage
Signs and symptoms of cerebral palsy
Delayed milestones ± persistent primitive reflexes.
(Non-progressive condition, so shouldn’t be loss of previously attained milestones)
Abnormal limb or trunk posture and tone in infancy: stiff legs, scissoring of legs, unable to lift head, unable to weight bear, rounded back when sitting, hypotonia (floppy), spasticity (stiff), fisted hands
Feeding difficulties (slow, gagging, vomit), oro-motoe miscoordination
Abnormal gait once walking
Hand preference before 1y old (esp spastic unilateral CP)
GMFCS - gross motor function classification system (level 1-5)
Level 1 - Walks no limitations
Level 2 - Walks some limitations
Level 3 - Walks with handheld mobility device
Level 4 - Self-mobility with limitations; may use powered mobility
Level 5 - Manual wheelchair
What are the types/categorisation of CP
Spastic (90%) - spasticity - Damage to pyramidal/corticospinal tract
Dyskinetic - uncontrolled movement - Damage to basal ganglia
Ataxic (hypotonic) - Damage to cerebellum
