BackgroundBirth asphyxia is an insult to the fetus or newborn due to failure to breath or breathing poorly, leads to decrease oxygen perfusion to various organs. According to WHO, 4 million neonatal deaths occurred each year due to birth asphyxia. Our goal was to evaluate antepartum, intrapartum, and fetal risk factors of birth asphyxia.MethodsIt was a Retrospective Case control study, conducted at Neonatal Intensive Care Unit of pediatric ward (I, II, III) and in Gynecology wards (I, II, III) of Civil Hospital Karachi, Dow University of Health Sciences. Study was conducted from January 2011-November 2012. Neonates diagnosed with birth asphyxia were considered as “cases” while neonates born either with normal vaginal delivery or by cesarean section having no abnormality were considered as “control”. Demographics of both the mother and neonate were noted and Questions regarding possible risk factors were asked from mother. Ethical issues were confirmed from Institutional review board of Civil Hospital Karachi, Dow University of Health Sciences. All data was entered and analyzed through SPSS 19.ResultOut of total 240 neonates, 123 were “cases” and 117 were “control”. Mean maternal age in “case” group was 24.22 ± 3.38 while maternal age of control group was 24.30 ± 4.04. Significant antepartum risk factors were maternal age of 20–25 (OR 0.30 CI 95% 0.07-1.21), booking status (OR 0.20 CI 95% 0.11-0.37), pre-eclampsia (OR 0.94 CI 95% 0.90-0.98) and primigravidity (OR 2.64 CI 95% 1.56-4.46). Significant Intrapartum risk factors were breech presentation (OR 2.96 CI 95% 1.25-7.02), home delivery (OR 16.16 CI 95% 3.74-69.75) and maternal fever (OR 10.01 CI95% 3.78-26.52). Significant Fetal risk factors were resuscitation of child (OR 23 CI 95% 31.27-1720.74), pre-term babies(OR 0.34 CI 95% 0.19-0.58), fetal distress (OR 0.01 CI 95% 0.00-0.11) and baby weight (OR 0.13 CI 95% 0.05-0.32).ConclusionMeasures should be taken to prevent neonatal mortality with great emphasis on skilled attendance at birth and appropriate care of preterm and low birth weight neonates.

HEV generally causes a self-limited acute infection and treatment remains supportive. However, severe hepatitis or fulminant hepatic failure may occur, more so during pregnancy. It is an important cause of acute-on-chronic liver failure in endemic areas. Chronic HEV infection and progressive disease has been reported in recipients of solid organ transplants, haematological malignancies, HIV patients and those on haemodialysis. Clearance of HEV may occur after reducing immunosuppressive therapy, especially those targeting T-cells, in about one third of cases. Antiviral therapy should be considered for patients for whom immunosuppressive therapy cannot be reduced and for those who do not achieve viral clearance after reducing immunosuppression. For the patients with severe infection, fulminant hepatic failure and acute-on-chronic infection, ribavirin monotherapy should be considered to expedite the viral clearance and recovery. Although ribavirin therapy is contraindicated in pregnancy owing to teratogenicity, the risks of untreated HEV to the mother and fetus are high and treatment may be offered. A twelve-week course of pegylated interferon, ribavirin or a combination of the two agents leads to viral clearance in about two-thirds of patients with chronic hepatitis E. Three- to twelve-month treatment with pegylated interferon clears virus in liver transplant recipients and patients on haemodialysis. In kidney and heart transplant patients where interferon may lead to organ rejection, ribavirin may be given.

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