Eclampsia overview: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
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.<ref name=lancet/> 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.<ref name=lancet>{{cite journal |journal=The Lancet 2001; 357:53-56 |title=Series, Pre-eclampsia trio. Pathogenesis and genetics of pre-eclampsia. |author=JM Roberts, DW Cooper}} </ref> Preclinical markers of the disease process are signs of increased platelet and endothelial activation.<ref name=lancet/> | 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.<ref name=lancet/> 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.<ref name=lancet>{{cite journal |journal=The Lancet 2001; 357:53-56 |title=Series, Pre-eclampsia trio. Pathogenesis and genetics of pre-eclampsia. |author=JM Roberts, DW Cooper}} </ref> Preclinical markers of the disease process are signs of increased platelet and endothelial activation.<ref name=lancet/> | ||
==Risk Factors== | |||
Eclampsia, like preeclampsia, tends to occur more commonly in first pregnancies and young mothers where it is thought that exposure to paternal [[antigen]]s still has been low. | |||
==References== | ==References== | ||
Revision as of 16:05, 11 February 2013
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Eclampsia Microchapters |
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Eclampsia overview On the Web |
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American Roentgen Ray Society Images of Eclampsia overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
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.
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.[1]
Historical Perspective
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]
Pathophysiology
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.[2] 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.[2] Preclinical markers of the disease process are signs of increased platelet and endothelial activation.[2]
Risk Factors
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.