Management of hypoxic ischemic encephalopathy (HIE) by Sunil Kumar Daha
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Transcript of Management of hypoxic ischemic encephalopathy (HIE) by Sunil Kumar Daha
Hypoxic-Ischemic Encephalopathy (HIE)
Sunil Kumar Daha
HYPOXIC ISCHEMIC ENCEPHALOPATHY
•Hypoxia: Decrease oxygenation to cells/ organs
• Ischemia: blood flow to cells or organs that is insufficient to maintain normal function
• Encephalopathy: a disease in which the functioning of the brain is affected by some agent or condition
- Important cause of permanent damage to CNS tissue that may result in neonatal death/ cerebral palsy/ developmental delay. (20-30% HIE die, ~33-50% survivors with permanent neurodevelopmental abnormalities)
ETIOLOGYBefore birth fetal hypoxia caused by:1. Inadequate oxygenation: hypoventilation during anesthesia,
respiratory failure, carbon monoxide poisoning2. low maternal blood pressure: Blood loss, spinal anesthesia,
compression of vena cava & aorta by gravid uterus3. inadequate relaxation of uterus: excessive oxytocin4. premature separation of placenta5. Knotting of the cord: 6. placental insufficiency from toxemia/post maturity
After birth hypoxemia caused by:1. Failure of oxygenation: due to cynotic heart disease, pulmonary
disease2. severe anemia: haemorrhage, hemolytic disease3. shock: sepsis, massive blood loss, intracranial haemorrhage
Pathophysiology
Clinical manifestation:• Intrauterine growth restriction with increased vascular resistance• Slow HR during labor• presence of meconium-stained amniotic fluid• depressed and may fail to breathe spontaneously• hypotonic/ hypertonic state• pallor, cyanosis, apnea, slow heart rate, unresponsive to
stimulation• seizure• Heart failure & cardiogenic shock, PPH, respiratory distress
syndrome, hematuria, ATN with perinatal asphyxia secondary to inadequate perfusion
SIGNS STAGE 1 STAGE 2 STAGE 3
Level of consciousness Hyperalert Lethargic Stuporous, coma
Muscle tone Normal Hypotonic Flaccid
Posture Normal Flexion Decerebrate
Tendon reflexes/clonus Hyperactive Hyperactive Absent
Myoclonus Present Present Absent
Moro reflex Strong Weak Absent
Pupils Mydriasis Miosis Unequal, poor light reflex
Seizures None Common Decerebration
Electroencephalographic findings Normal Low voltage changing to seizure activity Burst suppression to isoelectric
Duration<24 hr if progresses; otherwise, may remain normal 24 hr-14 days Days to weeks
Outcome Good Variable Death, severe deficits
Sarnat Classification of Hypoxic-ischemic Encephalopathy in Term Infants
Diagnosis• MRI is the preferred imaging modality in neonates with HIE
• CT scans : identifies focal hemorrhagic lesions, diffuse cortical injury, and
damage to the basal ganglia;
• CT has limited ability to identify cortical injury during the 1st few days of life.
• Ultrasonography has limited utility in evaluation of hypoxic injury in the term
infant; it is the preferred modality in evaluation of the preterm infant
• Apmlitude-integrated electroencephalography (aEEG) determine which
infant are at high risk for long term brain injury.
A- MRI showing focal neuronal injury; B- Diffuse weighted MRI showing HIE
Treatment
Hypothermia
Selective cerebral or whole body (systemic) therapeutic hypothermia
Decreases rate of apoptosis & suppress production of neurotoxic, glutamate,
free radical, NO, lactate
Reduces mortality or major neurodevelopmental impairment in term and near-
term infants with HIE. Effective if apply within 6 hrs. temperature should be 33.5C
Drug Therapy• Phenobarbital is drug of choice for seizure, IV loading dose (20mg/kg) +
additional 5-10mg/kg (up to 40-50mg/kg) may be needed
• Level should be monitored 24 hrs. after loading dose & maintenance therapy (5mg/kg/24hrs)
• Phenytoin (20mg/kg loading dose) or lorazepam (0.1mg/kg) for refractory seizure
Additional Therapy• Supportive care (management of organ system dysfunction) • Management of hyperthermia is important
• Ventilatory status & adequate oxygenation blood pressure, hemodynamic status acid- base balance & possible infection is important.
• Secondary hypoxia or hypotension due to complication of HIE must be prevented
• Aggressive treatment of seizure is critical and do with continuous EEG monitoring
Prognosis:• Depend up on timing & severity of the insult
• Ranging from complete recovery to death
• Infant with initial blood pH <6.7 have 90% risk of death/ severe neurological impairement
• Infant with apgar 0-3 at 5 minutes has high risk for death and impairement
• Severe encephalopathy:flaccid, coma, apnea, absence of oculocephalic reflexes & refractory seizure is poor prognosis
• Combined use of early EEG and MRI help to predicting outcomes in term infant with HIE
• Microcephaly/ poor head growth during 1st yrs of life is correlate with injury to basal ganglia & white matter & adverse developmental outcomes
• Brain death after neonatal HIE is diagnosed from clinical findings: coma, unresponsive to pain, auditory & visual stimuli, apnea with Pco2 from 40- >60 mmhg without ventilatory support and absence of brain stem reflexes.
Cont..
Refrence:• Nelson text book of paediatrics 19th edition• Ghai, Essential Paediatrics, 7th edition
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