1.1 Background to the study

Eclampsia is a Greek; means "shining forth" is an acute and life-threatening complication of pregnancy, characterized by the appearance oftonic–clonic seizures, usually in a patient who has developed pre-eclampsia. Pre-eclampsia and eclampsia are collectively calledhypertensive disorderof pregnancy and toxemia of pregnancy. Eclampsia includes seizures and coma that happen during pregnancy but are not due to preexisting or organic brain disorders (Chesley, 1971).

Eclampsia refers to the occurrence of one or more generalized convulsions and/or coma in the setting of pre-eclampsia and in the absence of other neurologic conditions. The clinical manifestations can appear anytime from the second trimester to the puerperium. In the past, eclampsia was thought to be the end result of preeclampsia, however; it is now clear that seizures should be considered merely one of several clinical manifestations of severe pre-eclampsia, rather than a separate disease. Despite advances in detection and management, pre- eclampsia/eclampsia remains a common cause of maternal death (Douglas and Redman, 1994).

An eclamptic seizure occurs in 2 to 3 percent of severely pre-eclamptic women not receiving anti-seizure prophylaxis; the seizure rate is estimated to be between 0  and 0.6 percent in women with mild pre-eclampsia (Sibai, 2004). The incidence of eclampsia has been relatively stable at 1.6 to 10 cases per 10,000 deliveries in developed countries (Douglas and Redman, 1994; Tan et al, 2006). In developing countries, however, the incidence varies widely: from 6 to 157 cases per 10,000 deliveries (Miguilet al, 2008).

Pre-eclampsia is a medical condition characterized by high blood pressure and significant amounts of protein in the urine of a pregnant woman. If left untreated, it can develop into eclampsia, the life-threatening occurrence of seizures during pregnancy (Chesley, 1971).

There are many different causes for the condition. It appears likely that there are substances from the placenta that can cause endothelial dysfunction in the maternal blood vessels of susceptible women. While blood pressure elevation is the most visible sign of the disease, it involves generalized damage to the maternal endothelium, kidneys, and liver, with the release of vasoconstrictive factors being a consequence of the original damage. An outdated medical term for pre-eclampsia is toxemia of pregnancy, since it was thought that the condition was caused by toxins (Sibai, 2004).The pathophysiologic processes underlying this disorder are described as occurring in two stages (Roberts and Hubel, 1999).

The first stage ischaracterized by reduced placental perfusion, possibly related to abnormal placentation, with impaired trophoblast invasion and inadequate remodeling of the uterine spiral arteries. The second stage refers to the maternal systemic manifestations characterized by inflammatory, metabolic, and thrombotic responses that converge to alter vascular function, which can result in multiorgan damage (Roberts and Gammill 2005; Steegerset al, 2010).

Many factors have been associated with an increased risk of developing preeclampsia including prior history or family history of preeclampsia, nulliparity, multigestational pregnancy, long time interval between pregnancies, obesity, age>40 years, diabetes mellitus, and preexisting history of other medical conditions such as chronic hypertension and renal disease, among others(Duckitt and Harrington 2005; Van Rijn et al, 2006).

Pre-eclampsia may develop from 20th week of gestation (it is considered early onset before 32 weeks, which is associated with an increased morbidity). Its progress differs among patients; most cases are diagnosed before labor typically would begin. Pre-eclampsia may also occur up to six weeks after delivery. Apart from Caesarean section and induction of labor (and therefore delivery of the placenta), there is no known cure. It is the most common of the dangerous pregnancy complications; it may affect both the mother and fetus (Sibai, 2004).

The hypertensive disorders during pregnancy affect up to 8.0% of all pregnancies (Sullivan and Martin, 1995).

Over the years, a lot of interest has been directed at studies on the role of serum uric acid, urea and creatinine in the pathogenesis of pregnancy induced hypertension (Egwuatu, 1986;Mustaphi, et al, 1996). At the same time hypertensive disorders account for 21% (Mustaphiet al, 1999) of cases of thrombocytopenia in pregnancy and the risk of anemia may also increase with the severity of hypertensive disorders(MustaphiandAnanth, 2009). Thus; though the roles of serum urea, uric acid and creatinine have been studied by many researchers, there is a constant ongoing search for better predictors and prognostic factors to assess the progress and severity of the disease, hematological parameters being one among them (Mustaphi and Nanda, 2013 ;Sivakumaret al, 2007).