|Classification and external resources|
Eclampsia (Greek for "shining forth") is an acute and life-threatening complication of pregnancy characterized by the appearance of tonic–clonic seizures, usually in a woman who has developed pre-eclampsia.   (Pre-eclampsia and eclampsia are collectively called "hypertensive disorder of pregnancy" and "toxemia of pregnancy".)
Eclampsia includes seizures and coma that happen during pregnancy but are not due to pre-existing or organic brain disorders.
Signs and symptoms
Typically a woman shows signs of pregnancy-induced hypertension and proteinuria before the onset of the hallmark of eclampsia, the eclamptic convulsion.  Other cerebral signs may precede the convulsion such as nausea, vomiting, headaches, and cortical blindness. In addition, with the advancement of the pathophysiological process, other organ symptoms may be present including abdominal pain, liver failure, signs of the HELLP syndrome, pulmonary edema, and oliguria. The fetus may already have been compromised by intrauterine growth retardation, and with the toxemic changes during eclampsia may suffer fetal distress. Placental bleeding and placental abruption may occur.
In some rare cases there are no convulsions and the woman falls directly into a coma. Some women with eclampsia may experience temporary blindness upon waking from the coma.
Eclampsia, like pre-eclampsia, tends to occur more commonly in first pregnancies and young mothers where it is thought that novel exposure to paternal antigens is involved. Furthermore, women with pre-existing vascular diseases (hypertension, diabetes, and nephropathy) or thrombophilic diseases such as the antiphospholipid syndrome are at higher risk to develop pre-eclampsia and eclampsia. Having a large placenta (multiple gestation, hydatidiform mole) also predisposes women to eclampsia. In addition, there is a genetic component: a woman whose mother or sister had the condition are at higher risk. Women who have experienced eclampsia are at increased risk for preeclampsia/eclampsia in a later pregnancy. Pulmonary edema is a rather common complication of severe eclampsia affecting approximately 3% of the people with eclampsia. Most cases result of aggressive use of crystalloid solutions for intravascular volume expansion.
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. Placental hypoperfusion is a key feature of the process. It is accompanied by increased sensitivity of the maternal vasculature to pressor agents leading to vasospasm and hypoperfusion of multiple organs. Further, an activation of the coagulation cascade leads to microthrombi 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. Preclinical markers of the disease process are signs of increased platelet and endothelial activation.
Placental hypoperfusion is linked to abnormal modelling of the fetal–maternal interface that may be immunologically mediated. The invasion of the trophoblast appears to be incomplete. Adrenomedullin, a potent vasodilator, is produced in diminished quantities by the placenta in pre-eclampsia (and thus eclampsia). Other vasoactive agents are at play including prostacyclin, thromboxane A2, nitric oxide, and endothelins leading to vasoconstriction. 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.
Eclampsia is seen as a form of hypertensive encephalopathy in the context of those pathological events that lead to pre-eclampsia. It is thought that cerebral vascular resistance is reduced, leading to increased blood flow to the brain. In addition to abnormal function of the endothelium, this leads to cerebral edema. Typically an eclamptic seizure will not lead to lasting brain damage; however, intracranial haemorrhage may occur.
Seizures during pregnancy that are unrelated to pre-eclampsia need to be distinguished from eclampsia. Such disorders include seizure disorders as well as brain tumor, aneurysm of the brain, and medication- or drug-related seizures. Usually the presence of the signs of severe pre-eclampsia precede and accompany eclampsia, facilitating the diagnosis.
Detection and management of pre-eclampsia is critical to reduce the risk of eclampsia. Appropriate management of women with pre-eclampsia generally involves the use of magnesium sulphate as an agent to prevent convulsions, and thus preventing eclampsia.
Prevention of convulsion is usually done using magnesium sulphate. The idea to use Mg2+
for the management of eclamptogenic toxemia[disambiguation needed] dates from before 1955 when it was tested and published—the serum The international MAGPIE study, of 2004, evaluated the long-term implications of the magnesium sulphate therapies.
The treatment of eclampsia requires prompt intervention and aims to prevent further convulsions, control the elevated blood pressure, and immediately deliver the baby if possible.
If the baby has not yet been delivered, steps need to be taken to stabilize the woman and deliver her speedily. This needs to be done even if the baby is immature, as the eclamptic condition is unsafe for both baby and mother. As eclampsia is a manifestation of a multiorgan failure, other organs (liver, kidney, lungs, cardiovascular system, and coagulation system) need to be assessed in preparation for a delivery (often a caesarean section), unless the woman is already in advanced labor. Regional anesthesia for caesarean section is contraindicated when a coagulopathy has developed.
Invasive haemodynamic monitoring
Invasive haemodynamic monitoring may be useful in an eclamptic woman with severe cardiac disease, renal disease, refractory hypertension, pulmonary edema, and oliguria.
- Ghulmiyyah L, Sibai B (February 2012). "Maternal mortality from preeclampsia/eclampsia". Seminars in Perinatology 36 (1): 56–9. doi:10.1053/j.semperi.2011.09.011. PMID 22280867.
- Smith JM, Lowe RF, Fullerton J, Currie SM, Harris L, Felker-Kantor E (2013). "An integrative review of the side effects related to the use of magnesium sulfate for pre-eclampsia and eclampsia management". BMC Pregnancy and Childbirth 13: 34. doi:10.1186/1471-2393-13-34. PMC 3570392. PMID 23383864. Retrieved 2014-03-06.
- Chesley LC (1971). "Hypertensive Disorders in Pregnancy". Williams Obstetrics (14th ed.). New York: Appleton Century Crofts. p. 700.
- Kane SC, Dennis A, da Silva Costa F, Kornman L, Brennecke S (2013). "Contemporary Clinical Management of the Cerebral Complications of Preeclampsia". Obstetrics and Gynecology International 2013: 985606. doi:10.1155/2013/985606. PMC 3893864. PMID 24489551. Retrieved 2014-03-06.
- "ACOG practice bulletin. Diagnosis and management of preeclampsia and eclampsia. Number 33, January 2002". Obstet Gynecol 99 (1): 159–67. January 2002. PMID 16175681.
- Chesley LC, Annitto JE, Cosgrove RA (September 1968). "The familial factor in toxemia of pregnancy". Obstet Gynecol 32 (3): 303–11. PMID 5742111.
- Roberts JM, Cooper DW (January 2001). "Pathogenesis and genetics of pre-eclampsia". Lancet 357 (9249): 53–6. doi:10.1016/S0140-6736(00)03577-7. PMID 11197372.
- Zhou Y, Fisher SJ, Janatpour M, et al. (May 1997). "Human cytotrophoblasts adopt a vascular phenotype as they differentiate. A strategy for successful endovascular invasion?". J. Clin. Invest. 99 (9): 2139–51. doi:10.1172/JCI119387. PMC 508044. PMID 9151786.
- Li H, Dakour J, Kaufman S, Guilbert LJ, Winkler-Lowen B, Morrish DW (November 2003). "Adrenomedullin is decreased in preeclampsia because of failed response to epidermal growth factor and impaired syncytialization". Hypertension 42 (5): 895–900. doi:10.1161/01.HYP.0000095613.41961.6E. PMID 14517225.
- "Sex Primes Women for Sperm". BBC News. 6 February 2002. Retrieved 2007-11-19.
- Cipolla MJ (July 2007). "Cerebrovascular function in pregnancy and eclampsia". Hypertension 50 (1): 14–24. doi:10.1161/HYPERTENSIONAHA.106.079442. PMID 17548723.
- Richards A, Graham D, Bullock R (March 1988). "Clinicopathological study of neurological complications due to hypertensive disorders of pregnancy". J. Neurol. Neurosurg. Psychiatr. 51 (3): 416–21. PMC 1032870. PMID 3361333.
- Rozenberg, P. (Jan 2006). "[Magnesium sulphate for the management of preeclampsia]". Gynecol Obstet Fertil 34 (1): 54–9. doi:10.1016/j.gyobfe.2005.06.025. PMID 16406662.
- Frayling, Frayling; The Magpie Trial Follow Up Study Collaborative Group (2004). "The Magpie Trial follow up study: outcome after discharge from hospital for women and children recruited to a trial comparing magnesium sulphate with placebo for pre-eclampsia [ISRCTN86938761]". BMC pregnancy and childbirth 4 (1): 5. doi:10.1186/1471-2393-4-5. PMC 416479. PMID 15113445.