ABSTRACT
Perinatal hypoxia is a major risk factor for abnormal outcome in the neonatal period. Despite the potential severity and prevalence of this condition, the diagnosis is usually based on nonspecific clinical criteria. Identifying the extent of hypoxic insult is necessary to provide medical management that optimizes the medical and neurologic outcome. During hypoxia, reactive oxygen species cause lipid peroxidation of cell membrane, yielding oxidative products, the most abundant product being malondialdehyde [MDA]. The objective of this study was to investigate the concentration of malondialdehyde excreted in urine during the first day of life in term infants following acute hypoxia, and to demonstrate to what extent it would be correlated with other parameters of perinatal hypoxia. The study was conducted on twenty-four full term infants with acute perinatal hypoxia admitted to Neonatal Intensive Care Unit. Diagnosis of asphyxia was based on Apgar score < 5 at 5 minute and arterial cord blood pH < 7.2. Sixteen normal non-hypoxic full term infants were included as a control group. All newborns were subjected to detailed history and clinical examination, umbilical cord arterial bIood gases determination and cranial ultrasonographic examination. Urinary malondialdehyde was deterrminated in urine samples collected on the first day of life by measuring thiobarbituric acid-reacting substances levels using a spectrophotometric assay. The results proved that urinary MDA levels were significantly higher on hypoxic infants [8.11 +/- 3.92 ng/mg creatinine] compared to normal infants [5.53 +/- 2.97 ng/mg creatinine - P= 0.031]. Hypoxic infants with meconium in amniotic fluid, who needed resuscitation immediately after birth, those who developed hypoxic ischemic encephalopathy, and those with persistent cranial ultrasonographic findings had significantly higher urinary MDA levels than hypoxic infants without these risk factors [P= 0.028, 0.035, 0.01 and 0.015 respectively]. Significant correlations were found between urinary MDA levels and one-minute [r = 0.441] and five-minute Apgar scores [r = 0.537], but not with umbilical arterial blood pH [r = 0.332]
Conclusion: Determination of urinary malondialdehyde [by measuring thiobarbituric acid-reacting substances] in the first day of life provides a reliable, easy and early marker of the severity of acute perinatal hypoxia. Further studies are needed to show its value in prediction of the long-term outcome of birth asphyxia