Journal of the royal medical services brain anoxia

Birth asphyxia and its well-known sequalea, hypoxic ischemic encephalopathy is an important cause of permanent brain damage leading to neonatal death or manifested later as cerebral palsy or mental retardation. Cerebral palsy is one of the most costly neurological disabilities because of its frequency (2/1000 birth), and its persistence over life span.)1,2( the neonatal brain can be damaged very easily when the cause is profound hypoxia and ischemic insult. In these circumstances, which are potentially damaging, rapid recognition and appropriate response is essential.)3( multiorgan dysfunction becomes apparent in asphyxiated babies including renal failure, necrotizing enterocolitis, persistent pulmonary hypertension and different metabolic abnormalities.(4)brain damage is of most concern because it is the least likely to heal completely.Brain anoxia

cholestasis in infancy is a non specific response to several hepatic injury which includes hypoxia that results in ischemic hepatitis.(5) evaluation of some liver biochemical markers as CPK and LDH can help us to predict neonates with asphyxia early in order to initiate hypothermia therapy

A total of fifty seven patients (group A) were enrolled in this study, forty three males (43), and fourteen females (14). Their birth weights ranges from 1.35 kg to 4.77 kg, twenty six were delivered normally (45.6%), fourteen were delivered by caesarean section (24.5%), and seventeen patients were delivered by vacuum delivery (29.8%). According to sarnat and sarnat classification, most of the patients, 35 patients (61.5%) were grade one I, eighteen patients (31.5%) were grade two II and four patients were grade three III (7%).Brain anoxia among the biochemical parameters, CPK values in the asphyxiated babies were significantly higher than the control, see figures 1, 2 and 3 which reveal this significant difference. Same observation is noted in regard to LDH values, where values in the asphyxiated babies were significantly higher than the control; see figures 4,5,6,7. Statistical inference for two samples (T-test) was conducted for the CPK values of normal and asphyxiated new born and results are shown in table I (outliers values (6 values as revealed in figure 1) were removed : 6204, 5649,5432,4798,4638 and 4532 prior conducting this test): T-test of difference = 0 (vs not =): T-value = 8.47 P-value = 0.000. DF (degree of freedom) = 52.Brain anoxia at the 0.05 level (α= 0.05) p value is less than 0.05 (0.000 0.05), the null hypothesis is rejected and we conclude that we have strong evidence that CPK is significantly higher in patients with asphyxia than normal. T test was also conducted for LDH values as well and indicates that it was significantly higher in patients with asphyxia, where p value 0.05 (an outlier value revealed in figure 2 was removed : 4450 prior performing this test)see table II. T-test of difference = 0 (vs not =): T-value = 13.52 P-value = 0.000 DF (degree of freedom) = 55 at the 0.05 level (α= 0.05) p value is less than 0.05 (0.000 0.05), the null hypothesis is rejected and we conclude that we have strong evidence that LDH is significantly higher in patients with asphyxia than normal.Brain anoxia surprisingly, two patients of those who were grade three HIE showed normal CPK and LDH. Brain ultrasound was done to all patients routinely and all were normal. Brain CT was done to those who showed abnormal CNS examination. They were seven patients, two of them showed subgaleal hematoma in brain CT scan, and one showed occipital hematoma. Abdominal ultrasound as well was not done routinely to all patients. But was performed in 4 patients, who showed abdominal distension and increasing abdominal girth, and all were normal.

This could be justified by the fact that most of these studies considered more specific enzymes like ALT and AST than CPK and LDH to detect liver involvement. The aim of this study was accomplished by the fact that both enzymes were significantly elevated in asphyxiated infants.Brain anoxia LDH and CPK were higher in neonates with asphyxia than controlled neonates according to our laboratory reference points. This was statistically significant since both values had a p value 0,05, see the below charts. This is similar to various different studies showed the same results.(11-17) many reports suggested that elevation of these biochemical markers especially LDH, is going parallel with the severity of the asphyxia. The greater the degree of the asphyxia, the greater the value of the enzymes elevation.(6,11-13) this was not statistically studied in our data, but upon observational basis, we found two patients with severe form of HIE (grade 3) with normal CPK and LDH. Such result is not unique to our study, some other studies showed similar pattern of involvement.(14,15) regarding brain imaging , it is well-known that brain MRI is the best tool for evaluating hypoxic patients especially between 4th and 8th day after hypoxia.Brain anoxia brain ultrasound is not satisfactory and its specificity in children is unacceptably low.(17,18) nevertheless, ultrasound was the preferred tool in our institution due to its accuracy in detecting intravntricular bleeding rather than estimating the degree of birth asphyxia.