Asphyxia triggers a cascade of cellular biochemical events that lead to tissue hypoxia and ischemia(1). Much of our current under- standing concerning the pathophysiology of perinatal brain disorders has evolved from animal studies(2). The relationship of severity of hypoxic injury to the brain and neurological outcome needs to be assessed carefully(3-5). Apgar score undoubtedly serves to predict neurologic outcome. However, fallacies in its ability to predict prognosis compelled the use of other diagnostic strategies like EEG, transfontanellar sonography and cranial CT in conjunction with neurological examination(6- 9). A ,CT evaluation of term asphyxiated neonates born in Government Rajaji Hospital, Madurai was undertaken to find out the pat- tern of intracranial changes and to correlate them with the type of obstetric intervention, Apgar score and clinical staging of Sarnat.

Subjects and Methods

Twenty three term neonates admitted with evidence of Hypoxia Ischemic Encephalopathy (HIE) formed, the subjects for the present study. Only those neonates who satisfied at least two of the following criteria were included in the study: (a) Evidence of perinatal asphyxia (peripartum asphyxia/birth asphyxia) defined as fetal bradycardia, meconium staining of the fetus, fetal heart irregularities (as assessed by intermittent auscultation); (b) Apgar scroe less than 7 at one minute; (c) Need for resuscitation; (d) Abnormal neurological signs such as seizures, altered muscle tone and abnormal neurological reflexes; and (e) Free from any associated neurological, cardiac, respiratory or other malformations, metabolic disorders, bleeding diathesis and shock. The cases were grouped under standard Apgar score and also classified into Sarnat stages I, II and III. Details, of antenatal history, drug therapy, previous registration, regular follow up; place and mode of delivery, and drugs used during delivery were recorded in the proforma. All the 23 term newborns were subjected to Computerised. Tomography (CT) within 48 hours after delivery using HITACHI model CT W 4 lOA. Ten transverse sections were taken. No contrast scan was made. All the cranial CT scans were analyzed and reviewed in an unbiased manner by the Radiologist without the clinical details and later the authors discussed them with the case details and the results were recorded and interpreted. Areas of hyperdensity were considered to represent hemorrhage and the density was measured by computerised inbuilt technique., Hemorrhages were classified according to its location. In addition areas of hypodensity and calcification were looked into. Ventricular size was also measured in all patients(10). Clinical data and outcome were subjected to statistical analysis using Chi square test.

Results

There were 16 males and 7 females in the study group. Nine males and 'one female in the study group expired. One of the four babies whose weight was below 2500 grams and 9 of the 19 above 2500 grams expired. The mean 1 minute Apgar was 4.2 among 10 deaths and 4.7 among 13 alive. The mean 5 minute Apgar was 6.7 among the 10 deaths and 7 among the 13 alive. The correlation between 1 minute Apgar and CT findings among the 10 deaths was not significant. However, 5 minute Apgar and CT findings had a significant statistical correlation (p <0.05). Eight out of 15 (53.3%) of babies who had compressed ventricles expired and 2 out of 8 (25%) of babies with normal ventricles died. Six of the 12 neonates (50%) without convulsions and four of II with convulsions died in the present study.

Of 23 neonates, 8 had stage I HIE, 5 had stage II HIE, and 10 had stage III HIE. On CT scan (Table 1) cerebral edema was seen in 21, while intracranial hemorrhage was seen in.12. All 3 babies in Stage III HIE with severe cerebral edema died (1 delivered by Caesarean and 2 were delivered normally). There was no death with cerebral edema in stage I and stage II HIE. Of 2 neonates in stage I with cerebral hemorrhage, I child had retrobulbar hemorrhage (forceps delivery) and the other had subdural hemorrhage (Breech delivery) and both of them survived. Of 3 neonates in stage II with cerebral hemorrhage, 2 babies had' straight sinus bleed and 1 had intra cerebellar bleed, and there was no death. Of 7 babies in stage III, 3 had subgaleal bleed, 3 had intraparenchymal bleeds and 1 neonate had subdural bleed and all these 7 delivered by forceps succumbed.
 

TABLE I

Correlation Between Sarnat Staging and CT Findings