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Iranian Journal of Pediatrics
Tehran University of Medical Sciences Press
ISSN: 1018-4406 EISSN: 2008-2150
Vol. 20, Num. 2, 2010, pp. 244-245

Iran Journal of Pediatrics, Vol. 20, No. 2, April-June, 2010, pp. 244-245

Letter To Editor

Frequency of hypoxic-ischemic encephalopathy among hospitalized neonates in West Iran

Pediatric department, Hamadan University of Medical Sciences, Hamadan, IR Iran

Correspondence Address:Department of Pediatric, Besat Hospital. Hamadan, IR Iran

eghhalian_fa@yahoo.com

Date of Submission: 16-Apr-2009

Date of Acceptance: 14-Oct-2009

Code Number: pe10038

Keywords: Hypoxic-ischemic Encephalopathy; Neonate; Brain damage

Hypoxic-ischemic encephalopathy (HIE) is brain damage from a shortage of oxygen or blood flow to the tissues [1],[2] and is characterized by clinical and laboratory evidence of acute or subacute brain injury due to asphyxia [1],[2],[3],[4],[5],[6]. It is a major contributor to neonatal death and morbidity [4],[5],[6]. 15%-20% of HIE cases die during the neonatal period and 30% of those who survive suffer from neurodevelopmental disorders [1],[3],[6].

An estimated 23% of the 4 million neonatal deaths and 8% of all deaths at <5 years of age throughout the world each year are associated with signs of asphyxia at birth [1],[4]. Even at referral centers in developed countries, death or moderate to severe disability occurs for 53% to 61% of infants diagnosed as having moderate to severe HIE [1],[4],[6]. Children with moderate/severe neonatal encephalopathy are at risk for reduced school performance, whereas those with mild encephalopathy have school performance scores similar to those of their peers [1],[6]. 1-LIE is one of the most common causes of cerebral palsy and other severe neurologic deficits in children occurring in two to nine of every 1000 live births [1],[2],[3],[4],[5],[6]. The incidence of HIE reported in different studies varies widely [2],[3],[4],[5],[6] , which may be explained by the selection criteria for studies of HIE during the neonatal period [3],[4].

The aim of the present study was to evaluate the frequency of hypoxic-ischemic encephalo-pathy in hospitalized neonates with seizure in Hamedan (west Iran) in a two year period. This is a retrospective cross sectional study on 34 neonates from 2004 to 2006.

Inclusion criteria were: all neonates with seizures due to HIE asphyxia having pH below 7, 5 th minute Apgar score between 0 and 3, decreased muscle tone and consciousness, cortical atrophy in brain CT scan and multiple organ involvement (eg, kidney, lungs, liver, heart, intestines). Neonates with jitteriness were excluded from the study.

The study was based on the recorded files of the patients. CT scan findings, blood gas findings, Apgar score of 5 th minute, decreased muscle tone and consciousness, seizure, age, sex and birth weight were recorded and analyzed using SPSS 13. Management plan for evaluation of hypoxic-ischemic encephalopathy included: Profound metabolic or mixed acidemia (pH<7), persistence of Apgar score of 0-3 for longer than 5 minutes, neonatal neurologic sequelae (eg, seizures, coma, hypotonia), multiple organ involvement (eg, kidney, lungs, liver, heart, intestines) and cortical atrophy in brain CT scan.

From 34 neonates with seizure, 11 (32.4%) had HIE. The infants who developed HIE had significantly 5th minute Apgar score between 0 and 3, decreased muscle tone and consciousness, pH below 7 in blood gas, cortical atrophy in brain CT scan and multiple organ involvement. The mean age of the neonates was 14.03±10.05 days (range 1 to 29 days). 25 (73.5%) neonates were boys and 9 (26.5%) girls. 23 (67.6%) neonates had normal weight (2500 to 4000 gr), 6 (17.6%) low birth weight (1500 to 2500 gr) and 5 (14.7%) very low birth weight (less than 1500 gr).

In 1980, the term hypoxic ischemic encephalopathy (HIE) came into use for all phases of ischemic changes [1]. HIE is a potential cause of brain injury that can produce some alterations of the neurologic development of the newborn [4],[5],[6]. The incidence of HIE reported in different studies varies widely. The variability in the reported incidence of HIE may be explained by the selection criteria for studies of HIE during the neonatal period [2],[3],[4],[5],[6]. In our study the incidence rate of Hypoxic-ischemic encephalopathy was 32.4%, which is higher than rates reported from other countries [1],[2],[4],[5]. This difference may be due to evaluation of the incidence of HIE in newborns with seizure in our study. HIE occurs in two to nine per 1000 live births in developing countries [1],[2],[3],[4],[5],[6]. Thomberg et al from Sweden reported an incidence rate of five and seven per 1000 live births [4]. The incidence of birth asphyxia in Palsdottir study in Iceland was 9.4/1000 live term births [2]. In the other study of Palsdottir et al the incidence of HIE after birth asphyxia was 1.4/1000. In Gonzales study in Spain the incidence of HIE was 4.66 cases per 100 full-term newborns, this is higher than the rate reported in the present study [5].

In our study 67.6% of neonates had normal birth weight, 17.6% low birth weight and 14.7% very low birth weight. Neonates with normal birth weight were more than those with other birth weights. This finding is different from the results of other studies [1],[2],[3],[4],[5],[6].

The incidence of cortical atrophy in brain CT scan in our study was 32.4%. This is consistent with incidence rates reported in the literature [1],[3],[6].

Neuroimaging appearances and EEG results help to prognosticate outcomes for preterm and term infants; the overall prognosis is poor [1],[6]. Eghbalian and Monsef reported that brain CT scan appearance helps to prognosticate the outcome [3]. Supportive care includes maintenance of adequate ventilation, avoidance of hypotension, maintenance of normal metabolic status including blood glucose, fluids, nutritional status, control of seizures, and control of brain edema. Selective brain hypothermia may improve outcome in HIE infants [1].

This was a retrospective study with its limitations. We recommend similar prospective research documenting that improvement in antenatal care and intro-partum monitoring can decrease the incidence of HIE.

References

1.Stoll BJ, Kliegman RM. Hypoxic-ischemic. In: Behrman RE, Kliegman RM, Jenson HB (eds). Nelson Textbook of Pediatrics. 18th ed. Philadelphia; Sounders. 2007; Pp:566-8.  Back to cited text no. 1    
2.Palsdottir K, Dagbjartsson A. Thorkelsson T, et al. Birth asphyxia and hypoxic ischemic encephalopathy, incidence and obstetric risk factors, Laeknabladid. 2007;93(9):595-601.  Back to cited text no. 2    
3.Eghbalian F, Monsef A. Neonatal seizures; Etiology and frequency, Iran J Child Neurol. 2008;2(1):39-42.  Back to cited text no. 3    
4.Thornberg E, Thiringer K, Odeback A, et al. Birth asphyxia: incidence, clinical course and outcome in a Swedish population. Acta Paediatr. 1995;84(8):927-32.  Back to cited text no. 4    
5.Gonzalez de Dios J, Moya M. Perinatal asphyxia, hypoxic-ischemic encephalo-pathy and neurological sequelae in full-term newborns: an epidemiological study. Pediatr Neurol. 2006;13(1):61-4.  Back to cited text no. 5    
6.Eghbalian F. Diagnosis and management of neonatal seizures. 1't ed, Hamadan University of Medical Sciences. 2004; Pp 60-76. (In Persian).  Back to cited text no. 6    

Copyright 2010 - Iran Journal of Pediatrics

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