Preeclampsia is described as a pregnancy specific syndrome that can affect every organ system of the body. It is defined as new onset hypertension and either proteinuria or other signs of end organ damage after 20 weeks of gestation in a previously normotensive normoproteinuric woman. It involves multisystem disorder which includes thrombocytopenia, renal dysfunction, hepatocellular necrosis, central nervous system pertubations or pulmonary oedema. It is a syndrome where mother and fetus both are affected.

Maternal syndrome includes hypertension, intra uterine growth retardation, oliguria, HELLP syndrome, seizure, oedema, proteinuria, pleural effusion, pulmonary oedema, thrombocytopenia, disseminated intravascular coagulation and hemoconcentration.

Fetal syndrome includes preterm delivery, intra uterine fetal death.

Young and nulliparous are more vulnerable to develop preeclampsia while older women have a greater risk for developing chronic hypertension with superimposed preeclampsia. It is well proven that it is primarily a disorder of first pregnancy.

Gestational hypertension is a transient hypertension which develops after 20 weeks of gestation in a previously normotensive women with no proteinuria or no signs of endorgan damage.

Preeclampsia when complicated with Grand Mal Seizures (Generalized Tonic Clonic convulsions) and/or coma is called Eclampsia.

The American College of Obstetricians and Gynaecologists describes four types of hypertensive diseases:

1.     Preeclampsia and eclampsia syndrome

2.     Chronic hypertension due to other causes

3.     Preeclampsia superimposed on chronic hypertension

4.     Gestational hypertension

In normal pregnancy there is invasion of the endovascular trophoblasts into the wall of the spiral arterioles of the uteroplacental bed.Endovascular trophoblasts invades up to decidual segments in the first trimester(10-12 wks) and another wave of trophoblasts invades up to the myometrial segments in second trimester (16-18 wks), thus the endothelial lining and muscular arterial walls is replaced by fibrinoid formation as a result spiral arterioles becomes torturous,distended and funnel shaped which in turn transforms the spiral arterioles into a low resistance, low pressure, high flow system.In Preeclampsia there is a failure of second wave of endovascular trophoblast migration and reduction of blood supply to the fetoplacental unit.There are many theories which explain the pathophysiology of preeclampsia.One of the accepted hypothesis is abnormal placentation with incomplete secondary wave of trophoblastic invasion which leads to reduced uteroplacental blood flow, placental ischaemia and hypoxia.

Preeclampsia is seen in 5-8% of all pregnancies. It can virtually affect every organ system.It can be divided into early onset i.e., <34 wks; late onset i.e., >= 34 wks; Preterm onset i.e., <37 wks; Term onset i.e., >=37 wks.

Lactate Dehydrogenase is a marker which is raised in Preeclampsia. Its levels are several times higher inside the cell as compared to plasma. It is an intracellular enzyme belongs to 2-hydroxy acid oxidoreductase group which is responsible for interconversion of Pyruvate and Lactate in the cells during Glycolysis which is the major energy pathway in the placenta. In preeclampsia there is cell damage which results in leakage of enzyme into the circulation causing high serum levels.