37. Perinatal Asphyxia and Infection Flashcards
How do newborns present with hypoxia-ischaemia?
Describe the redistribution of blood supply in hypoxia-ischaemia - what is prioritised?
What does ‘encephalopathy’ in the newborn refer to?
What is Sarnat grading for?
Need resuscitation at birth. may have absent HR and not breathing -> need support. Warnings: decreased movements, sentinel events (placental abruption, uterine rupture, cord prolapse).
Preserved: CNS, myocardium, adrenals. Vulnerable: kidneys, GI tract, liver, muscle.
Abnormal neurologic function and consciousness level, abnormalities of tone and reflexes, autonomic dysfunction, seizures.
A scale for HIE of the newborn, based on infant’s clinical presentation, examination findings, presence of seizures and duration of illness.
What disorder can HIE of the newborn result in?
What are the energy consequences of hypoxia-ischaemia?
What are the mechanisms of brain injury in hypoxia-ischaemia?
Cerebal palsy.
Acute hypoxic ischaemic, primary neuronal death -> Primary energy failure -> resus -> phosphorous spectra returns to normal in first few hours + reperfusion -> cerebrovascular dysfunction, glutamate release, free radicals, calcium entry, apoptosis -> secondary neuronal death -> progressive decline in PCr:Pi in the following 12-24hrs -> secondary energy failure. Delayed decline in ATP.
Glucose and O2 deprivation, energy depletion (decreased ATP), glutamate receptor activation, accumulation of intracellular Ca, free radicals (NO, superoxide, Fe, H2O2), lipid peroxidation, oligodendroglial death, apoptosis.
What are some potential targets for neuroprotection?
How is hypothermia (total body/selective head cooling) neuroprotective?
Decrease energy depletion (glucose, hypothermia, barbiturates), glutamate (inhibit glutamate release, fix glutamate uptake impairment, glutamate receptor blockade), inhibit leukocyte/microglial/cytokine effects, blockade of downstream intracellular events (hypothermia, free radical synthesis inhibitors, free radical scavengers, NOS inhibitors/scavengers, anti-apoptotic agents).
Decreases: cerebral metabolism, energy use, accumulation of excitotoxic amino acids, NO synthetase and free radical activity.
Why is it useful to make the differentiation between early or late onset neonatal sepsis?
Define early onset sepsis. What are the most common organisms causing it?
What are some symptoms of early onset sepsis?
What investgations should be done?
Difference in how infection may have been acquired, different organisms.
Sepsis within 48hrs, may mimic hypoxia-ischaemia, microbes acquired from mum before or during passage through birth canal, vertical/perinatal transmission. Group B streptococcus, E.coli most common, also H. influenzae, G-ve anaerobes, fungi and chyamydia.
Apnea, severe hypoxia, cardio-respiratory failure, hypotension, metabolic acidosis, tachycardia, poor perfusion.
FBC - neutropenia, CRP, blood cultures, lumbar puncture, CXR.
What are some predisposing factors to early onset GBS?
How is GBS prevented and treated?
What is late-onset sepsis in the newborn?
What are the most common organisms causing late-onset sepsis?
Chrorioamnionitis incl. maternal fever, prolonged labour or rupture of membranes, low birthweight.
Prevention: intrapartum antibiotic prophylaxis given to women who show carriage during screening in pregnancy. Tx: benzylpenicillin with amikacin or gentamicin.
>48h after birth, nosocomial, acquired from environment, mostly preterm infants.
Coagulase -ve staphylococci, staph aureus.
