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Hypoxic- Ischemic Encephalopathy : An Overview. Saba Merchant. Case : Baby P. Full term infant born to 37 yo G4 P1 by emerg. CS Initial VBAC, late decels, mat fx-ampicillin, fetal scalp gases 7.23 and 7.31 decels and brady - CS - uterine rupture - baby in abd
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Hypoxic- Ischemic Encephalopathy : An Overview Saba Merchant
Case : Baby P • Full term infant born to 37 yo G4 P1 by emerg. CS • Initial VBAC, late decels, mat fx-ampicillin, fetal scalp gases 7.23 and 7.31 • decels and brady - CS - uterine rupture - baby in abd • At birth no HR, RR, tone, poor color, no response to stimuli • dried, suctioned, bag + mask within 30sec, HR<60,some chest movt, again bag and mask HR<60 • Intubated at 1min 15sec, A/E good but HR<60, reintubated and chest compression + epi • Revisualise tube and reintubated - epi • Apgars 0 1 1 7 • 1st gas 6.99/33/146/8/-23 at 37 min
Case : contd • O/E no dysmorphisms, AGA, vented, neurologically compromised, hyperexcitable - clonus, hypotonia, poor suck/swallow, gag absent, DTR exagg., planter clonus • PB started, weaned from ventilator, extubated 4 days later to R/A, feeds started 7 days later • CT scan head, EEG, HUS, neurology consult • 14 days later transferred to level 2 • Secretions++, suction , longterm G tube • Rpt EEG and VEP pending • At present parents signed DNR
HIE Definition : It is the term used to designate the clinical and neuropathological findings of an encephalopathy that occurs in a full term infant who has experienced a significant episode of intrapartum asphyxia.
Incidence of Asphyxia • 2% in full term and 60% in LBW • 20-50% die in newborn period • Of survivors 25% have permanent handicap
Definitions • Hypoxia/anoxia : denotes a partial or complete lack of oxygen, respectively, in one or more tissues of the body, including the blood stream. • Asphyxia : is the state in which pulmonary or placental gas exchange is affected leading to progressive hypoxemia, which is severe enough to be associated with acidosis. • Ischemia : is a reduction in or cessation of blood flow that arises from either systemic hypotension, cardiac arrest, or occlusive vascular disease.
Pathology • Severity and distribution is dependent on several factors • certain vulnerable areas - cerebral cortex , hippocampus , basal ganglia, thalamus, brain stem, subcortical and periventricular white matter • In full term infants gray matter structures affected and in premature infants white matter • Four basic and clinically important lesions : Neuronal necrosis, status marmoratus, para-sagittal cerebral injury, periventricular leucomalacia
Status of infant at birth • Depressed on initial assessment • Generalized hypotonia • Apgars 3 or less @ 1min and 6 or less @ 5min • Major resuscitation required • Large base deficit by blood gas • Poor feeding to deep coma (ecephalopathic)
Prognosis based on apgars • Score at 1, 5 minutes does not give prognosis indicator • The longer the score remains lower, the greater its significance • 0-3 @ 1min has mortality of 5-10% • may be increased to 53% if at 20min apgars score 0-3 • 0-3 @ 5min , CP risk app. 1% • may be increased to 9%if for 15min • dramatic rise to 57% CP risk if for 20min
Newborn neurological assessment • Staging system of Sarnat and Sarnat • Means of recording severity of insult to brain, to initiate med management and to predict ultimate prognosis • Infants occasionally sustain insult to brain arising from complication of systemic disease • Seizures in 50-70%
Summary of staging (table no to memorize…just to know) • Mild : Hyperalertness, uninhibited reflexes, sympathetic overactivity , duration < 24 hrs • Moderate : Lethargy-stupor, hypotonia, suppressed primitive reflexes, seizures • Severe : Coma, flaccid tone, suppressed brainstem function, seizures, increased ICP
Prognosis based on Sarnat and Sarnat • Stage 1 invariably recover without neurological deficit • Stage 2 later develop normally if clinical and EEG abnormalities are fully reversed in 5 days of birth • Stage 3 encephalopathy is associated with a high mortality(50%) and universal neurological morbidity among the survivors.
Systemic Complications of Perinatal Asphyxia • Acute Tubular Necrosis • Hematurea, High BUN and creatinine • Hepatic necrosis or ischemic dammage • Elevated liver enzyme • Cardiomyopathy • Hypotension, weak heart muscle in Echo
Management • Prevention, prevention, prevention • Insure physiological oxygen and acid-base balance • Maintain environmental temp and humidity • Correct caloric, fluid and electrolyte disturbances • Maintain blood volume and hemostasis • Treat infection • Neuro-resus measures to reduce cerebral oedema ineffective • Sz treated with PB, dilantin or lorazepam • Newer modalities- excitatory amino antagonists, oxygen free radical inhibitors/scavengers, ca channel blockers, nitric oxide synthetase inhibitors • Hypothermia
Case presentation • Delivery of term baby after emergent C/S because of severe abdominal pain and at delivery fetus had prolonged and severe bradycardia. Placenta was found to be fully separated at delivery. Baby came out severely hypotonic, unresponsive, heart rate of 40/min.blue in color with no respiratory effort. 2 hours later on mechnical vetilator baby start to have seizure. After 20 days baby is not alert can not feed orally and hypertonia start to appeare
Question and Answers • Student should explain baby clinical finding at delivery based on history. • Should estimate apgars score and discuss what it means in term of resuscitation • Classify baby HIE to Sarnat stages including other component to examinE • Predict prognosis and outcome