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Eclampsia, an acute and life-threatening complication of pregnancy, is characterized by the appearance of tonic-clonic seizures in a patient who had developed preeclampsia; rarely does eclampsia occur without preceding preeclamptic symptoms. Hypertensive disorder of pregnancy and toxemia of pregnancy are terms used to encompass both preeclampsia and eclampsia. Seizures and coma that happen during pregnancy but are due to preexisting or organic brain disorders are not eclampsia.
The term is derived from the Greek and refers to a flash, a term used by Hippocrates to designate a fever of sudden onset. [1]
Eclampsia is a leading cause of maternal and perinatal mortality. The prevalence of eclampsia is reported to be 0.56 per 1,000 births (US data from 1979-86) versus 26 per 1,000 births for pre-eclampsia.[2] While mortality can be kept low when antenatal care and maternal-fetal services are provided, mortality rates are substantial in challenging settings. Thus in a setting in India , maternal mortality and perinatal mortality were reported to be 32% and 39%, respectively, in 1993.[3]
Eclamptic convulsions may appear in the last trimester (rarely before), during labour, and in the first two days postpartum; it would be highly unusual to see eclampsia later than 48 hours after delivery. [4]
Eclampsia, like preeclampsia, tends to occur more commonly in first pregnancies and young mothers where it is thought that exposure to paternal antigens still has been low. Further, women with preexisting vascular diseases (hypertension, diabetes, and nephropathy) or thrombophilic diseases such as the antiphospholipid syndrome are at higher risk to develop preeclampsia and eclampsia. Conditions with a large placenta (multiple gestation, hydatiform mole) also predispose for toxemia. Further, there is a genetic component; patients whose mother or sister had the condition are at higher risk.[5] Patients with eclampsia are at increased risk for preeclampsia-eclampsia in a later pregnancy.
While multiple theories have been proposed to explain preeclampsia and eclampsia, it occurs only in the presence of a placenta and is resolved by its removal.[6] E. W. Page suggested that placental hypoperfusion is a key feature of the process. It is accompanied by increased sensitivity of the maternal vasculature to pressure agents leading to vasospasm and hypoperfusion of multiple organs. Further, an activation of the coagulation cascade leads to microthombi formation and aggravates the perfusion problem. Loss of plasma from the vascular tree with the resulting edema additionally compromises the situation. These events lead to signs and symptoms of toxemia including hypertension, renal, pulmonary, and hepatic dysfunction, and – in eclampsia specifically – cerebral dysfunction.[6] Preclinical markers of the disease process are signs of increased platelet and endothelial activation[6]
Placental hypoperfusion is linked to abnormal modeling of the fetal-maternal interface that may be immunologically mediated[6] The invasion of the trophoblast appears to be incomplete.[7] Adrenomedullin, a potent vasodilator, is produced in diminished quantities by the placenta in preeclampsia (and thus eclampsia). [8] Other vasoactive agents are at play including prostacyclin, thromboxane A2, nitric oxide, and endothelins leading to vasoconstriction.[9] Many studies have suggested the importance of a woman’s immunological tolerance to her baby’s father, whose genes are present in the young fetus and its placenta and which may pose a challenge to her immune system.[10]
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