Khaled Abdulqawi , Yousry Z. Al-Zohairy , Khaled Karam
Background: Neonatal brain injury due to intrapartum asphyxia is an important cause of cerebral palsy, mental retardation, and epilepsy. In developing countries, the incidence of post asphyxial neurological damage is particularly high. Despite advances in perinatal care over the past three decades, the incidence of cerebral palsy attributed to birth asphyxia has not changed.
Objectives: To predict the outcome of postasphyxial hypoxic ischemic encephalopathy early in the neonatal period, for proper counseling of the parents, to get benefit in clinical practice and to select patients who will benefit from recent management strategies.
Study Design: This study was conducted on 63 asphyxiated full term newborn infants who developed Hypoxic-Ischemic Encephalopathy (HIE) admitted at Neonatal Intensive Care Unit of Al-Jedaany Hospital, Jeddah, Kingdom Saudi Arabia in the period from May 2006 to January 2008. They were classified according to Sarnat and Sarrnat staging of HIE into the following: 16 with stage I, HIE (Group I), 19 with stage II, HIE (Group II) and 20 with stage III, HIE (Group III). Twenty full term healthy newborn infants, age and weight-matched, were served as a control. All infants were subjected to the following tests: cord blood gases at birth, and Urine sample for testing urinary lactate / creatinine ratio. Also a real-time cranial ultrasonography was done for infants who had HIE. Follow up of the cases was done by the followings: A neurodevelopmental clinical evaluation every three months till the age of one year of life was done for the cases and control infants. An Electroencephalogram (EEG) and auditory brainstem evoked response (ABR) were done at the age of three months and a second ABR at the age of six months for cases with abnormal previous ABR.
Results: Group III (stage III, HIE) has significantly increased initial, maximum and day 7 HIE scores (16.4 ± 3.1, 18.15 ± 2.79 and 13 ± 5.79) respectively compared with group I&II. Also HIE score significantly increased in group II (11.89 ± 2.09, 12.50 ± 2.29 and 5.05 ± 5.03) compared with group I (7.01 ± 1.3, 7.61 ±2.91 and 0). Cord blood metabolic acidemia and the increase of urinary lactate/ creatinine ratio are significantly present in all infants with HIE (groups III, II&I) compared with the control group. Also metabolic acidemia and the increased urinary lactate/ creatinine ratio significantly increase as HIE stages increase. HIE cases with abnormal neurodevelopmental clinical outcome has significant HIE scores [initial (14.51 ± 4.01), maximum (15.60± 4.21) &day 7(9.40± 6.51)], significant metabolic academia (7.04± 0.11) and significant increased lactate / creatinine ratio (3.6± 2.10), compared with HIE cases with normal outcome. Also HIE cases with abnormal ABR have statistically significant abnormal neurodevelopmental outcome while HIE cases with abnormal EEG have no abnormal outcome. Conclusion: Hypoxic ischemic encephalopathy score, capillary blood gases report, urinary lactate/creatinine ratio and cranial ultrasonographic findings are important early and easily predictors ofperinatal hypoxic ischemic encephalopathy outcome and provides a sliding scale of probabilities that could be used for prognostication and to design eligibility criteria for decision making including neuroprotective therapy.
