Primary outcome of babies with hypoxic ischemic encephalopathy

Anil Kumar Rawat, Rupali Praveen Shirke, Vipan Chandar


Background: Intrapartum fetal hypoxia followed by hypoxic ischemic encephalopathy (HIE) is a common cause of potentially avoidable brain injury in term infants.This study was conducted in a tertiary care centre and included 119 babies of hypoxic ischemic encephalopathy born in hospital as well as referred from neighbouring areas.

Methods: Babies with history of intrapartum hypoxia, delayed cry who required resuscitation at birth and in stage II or III of modified sarnat encephalopathy grade (MSEG) and those who had abnormal intrapartum course were included. After performing clinical neurological assessment further data collection included perinatal maternal characteristics- ante partum and intrapartum complications; morbidity pattern in baby including type of resuscitation, onset of seizure, antiepileptic drug, other co morbidity and short term outcome.

Results:Out of 119 babies 19% were born low birth and 6% were IUGR. 47% mother were primi gravida whereas 53% were multigravida, 32% pregnancy were unbooked. Ante partum risk factor was found in 3 cases and Intrapartum risk factor was found in 45 (38%) cases. According to MSEG stage II and III babies were enrolled overall 92% babies had seizure and 60% had on day one only. Single antiepileptic drug controlled seizure in 60% of babies who had seizure additional two and more antiepileptic drug were required in fewer no of cases. During stay most common complication was sepsis, observed in 26% cases followed by DIC in 11% cases and AKI in 7% cases. Majority 59% of babies were discharged, mortality was observed in 12.6% cases and 27% left against medical advice.    

Conclusions:Maternal perinatal risk factors and effective neonatal intervention may improve outcome in babies with hypoxic ischemic encephalopathy. 


Asphyxia, Hypoxic ischemic encephalopathy, Modified sarnat encephalopathy grade, Perinatal risk factors

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Amiel TC. Cerebral damage in full-term new-born. Aetiological factors, neonatal status and long-term follow-up. Biol Neonat. 1969;14(3):234-50.

Cowan F, Rutherford M, Groenendaal F, Eken P, Mercuri E, Bydder GM, et al. Origin and timing of brain lesions in term infants with neonatal encephalopathy. Lancet. 2003;361(9359):736-42.

Sarnat HB, Sarnat MS. Neonatal encephalopathy following fetal distress a clinical and electroencephalographic study. Arch Neurol. 1976;33(10):696-705.

Shalak LF, Laptook AR, Velaphi SC, Perlman JM. Amplitude-integrated electroencephalography coupled with an early neurologic examination enhances prediction of term infants at risk for persistent encephalopathy. Pediatrics. 2003;111(2):351-7.

Badawi N, Kurinczuk JJ, Keogh JM, Alessandri LM, Sullivan F, Burton PR, et al. Intrapartum risk factors for newborn encephalopathy: the Western Australia case–control study. Br Med J. 1998;317:1554-8.

Ellis M, Manandhar N, Manandhar DS, Costello AM. Risk factors for neonatal encephalopathy in Kathmandu, Nepal, a developing country:unmatched case-control study. Br Med J. 2000;320:1229-36.

Horn AR, Swingler GH, Myer L. Early clinical signs in neonates with hypoxic ischemic encephalopathy predict an abnormal amplitude-integrated electroencephalogram at age 6 hours. BMC Pediatrics. 2013;13:52.

Mizrahi EM, Kellaway P. Characterization and classification of neonatal seizures. Neurology. 1987;37:1837-44.

Painter MJ, Scher MS, Stein AD, Armatti S, Wang Z, Gardiner JC, et al. Phenobarbital compared with phenytoin for the treatment of neonatal seizures. N Engl J Med.1999;341:485-9.

Nouri S, Mahdhaoui N, Beizig S, Zakhama R, Salem N, Ben Dhafer S, , et al. Acute renal failure in full term neonates with perinatal asphyxia prospective study of 87 cases. Arch Pediatr. 2008;15(3):229-35.

Stoll BJ, Kliegman RM. Hypoxia-ischemia. In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed. Phidelphia: WB Saunders, 2004;566-568.