Perinatal Asphyxia and Infection Flashcards
Hypoxia-Ischaemia at birth
Infants need resuscitations at birth
–> may have absent HR< infant not breathing
–> may require airway, respiratory and haemodynamic support
Infant subsequently encephalopathic
Hypoxia-ischaemia warnings
Decreased foetal warnings
Sentinel events- placental abruption, uterine rupture, cord prolapse
HI Preserved blood supply
CNS
Myocardium
Adrenals
HI Vulnerable blood supply
Kidneys
GI tract
Liver
Muscle
Encephalopathy in newborn
Abnormal neurologic function + consciousness level
Abnormalities of tone and reflexes
Autonomic dysfunction
Seizures
Sarnat study of perinatal asphyxia
Stage 1- less than 24 hrs, hyperalertness, uninhibited Moro and stretch reflexes, symp. effects and normal EEG
Stage 2- obtundation, hypotonia, multifocal seizures, EEG periodic pattern sometimes preceded by continuous delta activity
Stage 3- stuporous, flaccid and brain stem + autonomic functions suppressed
Foetal/perinatal hypoxia +/or ischaemic cerebral insult
Leads to primary neuronal injury Primary energy failure Derangement of cellular function Secondary energy failure Secondary neuronal injury, further necrosis and apoptosis
Energy consequences Hypoxia-Ischaemia
Phosphorus spectra normal first few hours after resuscitation
12-24 hours- progressive decline in PCr/Pi ratio
Delayed ATP decline
Secondary energy failure
Acute hypoxia ischaemia –> reperfusion (after resuscitation) –> secondary energy failure (several hours after reperfusion)
Cerebral Hypoxic-Ischaemic injury
Primary neuronal death
Resuscitation – Reperfusion, Oxygenation
Cerebrovascular dysfunction Glutamate release Free radicals Calcium entry Apoptosis
Secondary neuronal death
Mechanisms of brain injury in Hypoxia-Ischaemia
Glucose + O2 deprivation Energy depletion – decreased ATP Glutamate receptor activation Accumulation of intracellular Ca Free radicals – NO, superoxide, Fe, H2O2, Lipid peroxidation Oligodendroglial death Apoptosis
Neuroprotection targets
Decreased energy depletion
Glutamate
Inhibition of leukocyte/microglial/cytokine effects
Blockade of downstream intracellular events
Decreased energy depletion
Glucose
Hypothermia
Barbiturates
Glutamate
Inhibit glutamate release (Ca channel blockers, magnesium, adenosine, hypothermia)
Fix glutamate uptake impairment - hypothermia
Glutamate receptor blockade- magnesium
Blockade of downstream intracellular events
Hypothermia Free radical synthesis inhibitors (allopurinol, magnesium) Free radical scavengers (Vit E) NOS inhibitors Anti-apoptotic agents
Hypothermia
Decreased cerebral metabolism Decreased energy use Decreased accumulation of excitotoxic amino acids Decreased NO synthetase activity Decreased free radical activity
Early onset sepsis
Within 48 hours Microbes acquired from mother Before or during passage through birth canal 2-3 per 1000 live births Fulminating septicaemia --> meningitis, pneumonia PROM Maternal UTI Prematurity
Organisms causing early-onset sepsis
Group B Strep
E Coli
Early Onset GBS
Most cases sepsis develop within first few hours
May mimic perinatal hypoxia-ischaemia
–> apnoea, severe hypoxia, cardio-resp failure, hypotension, metabolic acidosis, tachycardia, poor perfusion
Early onset GBS predisposing factors
1% babies born vaginally to mothers who carry GBS become infected
Evidence chorioamnionitis including maternal fever
Prolonged labour
Prolonged rupture of membranes
Low birthweight
Prevention + treatment of GBS sepsis
Prevention vertical transmission- intrapartum antibiotic prophylaxis to women who show carriage during pregnancy screening
Treatment- Benzylpenicillin with amikacin or gentamicin
Late onset sepsis
More than 48 hours after birth From Postnatal environment Nosocomial 4-5 per 1000 live births Mostly preterm infants on neonatal units
Late onset sepsis organisms
Coagulase-negative staphylococci
Staph Aureus
Early onset GBS investigations
FBC- neutropenia CRP- rise may be delayed by 12 hours Blood cultures Lumbar puncture Chest X ray
