Profile of hypoxic ischemic encephalopathy in newborns in a tertiary care centre of Bhilai, Chhattisgarh, India


  • C. Sudhakar Department of Paediatrics, CM Medical College and Hospital, Durg, Chhattisgarh, India
  • Pallavi Jindal Department of Paediatrics, CM Medical College and Hospital, Durg, Chhattisgarh, India



Cranial ultrasound, Hypoxic ischemic encephalopathy, Perinatal asphyxia


Background: Birth asphyxia is an important cause of static development and neurological handicap in both term and preterm infants. Birth asphyxia is found to be responsible for 28.7% deaths in hospital settings and 20% deaths in rural/tribal areas. Approximately the same number develops serious sequelae which cripples these children both physically and mentally. Children who have suffered moderate encephalopathy had varying rates of infant death and morbidity. Precise determination of the prognosis in the term new born, who sustains a hypoxic ischemic insult is hindered by difficulty in determining the severity of insult.

Methods: This was a prospective longitudinal, observational study was conducted in the Department of Paediatrics, CMC Bhilai with close association with the Department of Obstetrics and Gynecology, Department of Radio diagnosis and Department of Neurology. All deliveries taking place in the Department of Obstetrics and Gynecology of CMC Bhilai were enrolled for the study. Each enrolled infant underwent a detailed neurologic examination within the first 12 hours after birth. During the period of data collection 180 babies with birth asphyxia were admitted to NICU. Out of which 126 babies had fulfilled the inclusion criteria and completed one year follow up, hence as cases. Babies who lost follow up were not included in study. The neurological examination was performed 14 days after discharge, then at 1 month, 3-month, 6-month, 9 month and 12 months. Long term outcome in this study is defined as outcome at one year of age in terms of morbidity and mortality.

Results: The female and male ratio is 0.4:1. Most of the asphyxiated newborn, 81 (64%) were in 2500-3000gm. Among the study population, maximum number of cases 76 (60%) were suffering from HIE-I. Majority of study population, 87 (69%) were born by LSCS. Normal CUS in 93 babies and abnormal in 33 babies; with normal CUS, there were no death in study population and out of 33 abnormal CUS, 12 deaths occurred. Out of the different complications enlisted in the table convulsions (66.7%) is most common followed by Apnea (65.08%). Recurrent infections (45.24%) is the most common complication followed by seizure disorders (22.63%) and failure to thrive (20.63%).

Conclusions: Hypoxic ischemic encephalopathy is one of the major consequences of perinatal asphyxia. Despite of best care, some babies are likely to develop it.


Babu AB, Devi SS, Kumar KB. Birth asphyxia: incidence and immediate outcome in relation to risk factors and complications. Int J Res Hlth Sci. 2014;2(4):1064-71.

Volpe JJ. Neurology of the Newborn E-Book. Elsevier Health Sciences; 2008.

Cloherty JP, Eichenwald EC, Stark AR, eds. Manual of neonatal care. Lippincott Williams and Wilkins; 2008.

Lawn JE, Cousens S, Zupan J. million neonatal deaths: when? where? why? Lancet. 2004;365(9462):891-900.

Shetty J. Neonatal seizures in hypoxic–ischaemic encephalopathy–risks and benefits of anticonvulsant therapy. Developmental Medicine and Child Neurol. 2015;57(S3):40-3.

Basu P, Som S, Choudhuri N, Das H. Contribution of the blood glucose level in perinatal asphyxia. Eu J Pediatr. 2009;168(7):833-8.

Bang AT, Bang RA, Sanjay B, Mahesh D, Hanimi Reddy M. Burden of morbidities and the unmet need for health care in rural neonates - a prospective observational study in Gadchiroli, India observational. Indian Peditr. 2001;38:952-65.

McIntosh N. The Newborn. In: McIntosh N, Helms PJ, Smyth LR editors. Forfar and Arneil’s Textbook of Pediatrics. 7th edition. Newyork: Churchill Livingstone; 2008:177-392.

Dilenge ME, Majnemer A, Shevell MI. Topical review: Long-term developmental outcome of asphyxiated term neonates. J Child Neurol. 2001;16(11):781-92.

Nelson KB, Leviton A. How much of neonatal encephalopathy is due to birth asphyxia? Am J Dis Children. 1991;145(11):1325-31.

Badawi N, Felix JF, Kurinczuk JJ, Dixon G, Watson L, Keogh JM, et al. Cerebral palsy following term newborn encephalopathy: a population‐based study. Developmental Med Child Neurol. 2005;47(5):293-8.

Hankins GD, Speer M. Defining the pathogenesis and pathophysiology of neonatal encephalopathy and cerebral palsy. Obstet Gynecol. 2003;102(3):628-36.

Ilves P, Lintrop M, Metsvaht T, Vaher U, Talvik T. Cerebral blood‐flow velocities in predicting outcome of asphyxiated newborn infants. Acta paediatrica. 2004;93(4):523-8.

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

Hayes BC, Mc Garvey C, Mulvany S, Kennedy J, Geary MP, Matthews TG, et al. A case-control study of hypoxic-ischemic encephalopathy in newborn infants at >36 weeks gestation. Am J Obstet Gynecol. 2013;209(1):29-e1.

Babu AB, Devi SS, Kumar KB. Birth asphyxia: Incidence and immediate outcome in relation to risk factors and complications. Int J Res Health Sci. 2014;2(4):1064-71.

Carli G, Reiger I, Evans N. One‐year neurodevelopmental outcome after moderate newborn hypoxic ischaemic encephalopathy. J Paediatr Child Health. 2004;40(4):217-20.

Suwannachat B. Risk factors for birth asphyxia in Kalasin hospital. Srinagarind Med J. 2004;19(4):233-40.

Leijser LM, Vein AA, Liauw L, Strauss T, Veen S, Wezel-Meijler GV. Prediction of short-term neurological outcome in full-term neonates with hypoxic- ischaemic encephalopathy based on combined use of electroencephalogram and neuro-imaging. Neuropediatr. 2007;38(5):219-27.

Biagioni E, Mercuri E, Rutherford M, Cowan F, Azzopardi D, Frisone MF, et al. Combined use of electroencephalogram and magnetic resonance imaging in full-term neonates with acute encephalopathy. Pediatr. 2001;107(3):461-8.






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