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BIRTH TRAUMA: Hypoxic-Ischemic Encephalopathy

INTRODUCTION
CNS disorders are important cause of neonatal mortality and short- and long-term morbidity
HYPOXIC-ISCHEMIC ENCEPHALOPATHY

Etiology - Perinatal

Pathophysiology
Pathophysiology • glutamate
o blood shunted to brain, heart and adrenals in • free radicals
preference to lung, liver, kidney and intestines • NO
o term infants: • lactate
o neuronal atrophy of the cortex, later – most effective when applied within 6 hours
cortical atrophy, and parasagittal ischemic of the event
injury 2. supportive care directed at management of organ
o preterm infants: system dysfunction
o PVL, later spastic diplegia, status – ventilation and adequate oxygenation
marmoratus of the basal ganglia, IVH – blood pressure and hemodynamic status
Clinical Manifestations – acid-base balance
• signs of hypoxia – infection control
– seizures
o in utero: IUGR with vascular resistance Prognosis
o labor: nonreactive fetal heart rate pattern; • outcome: timing and severity of insult
acidic fetal scalp blood • Poor outcome:
o delivery: – severe encephalopathy (stage 2 or 3)
 MSAF – low AS at 20 mins of age
 depressed, failure to – no spontaneous respirations at 20 mins of
spontaneously breath age
 tone: normal to hypo- or – persistent abnormal neurologic signs at 2
hypertonic wks
 pallor, cyanosis, apnea, slow – severe MRI and EEG abnormalities
heart rate, unresponsiveness to • Brain death:
stimulation, – coma unresponsive to pain, auditory or
visual stimuli
o 24 hours: cerebral edema ◊ profound – apnea with pCO2 rising from 40 to
brainstem depression ~ seizures >60mmHg without ventilatory support
o labor: nonreactive fetal heart rate pattern; – absent brainstem reflexes: pupil;
acidic fetal scalp blood oculocephalic; oculovestibular; corneal;
o delivery: gag; sucking
o MSAF – no hypothermia, hypotension and elevated
o depressed, failure to spontaneously breath levels of phenobarbital
o tone: normal to hypo- or hypertonic – persistent x 2 days (term) or 3 days
o pallor, cyanosis, apnea, slow heart rate, (preterm)
unresponsiveness to stimulation,
Hypoxic-Ischemic Encephalopathy in Term Infants
Diagnosis
o neuroimaging:
o ultrasound – preterm
o CTScan/MRI – term
o EEG
o detect seizure activity
o prognostication
Treatment
1. systemic or selective cerebral hypothermia
– decreases rate of apoptosis
– suppresses production of neurotoxic
mediators: