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| '''For patient information, click [[Eclampsia (patient information)|here]]''' | | '''For patient information, click [[Eclampsia (patient information)|here]]''' |
| | {{Eclampsia}} |
| | {{CMG}} '''Assosciate Editor(s)-In-Chief:''' [[User: Navneet|Navneet Kaur M.B.,B.S.]] , [[User: Prashanthsaddala|Prashanth Saddala M.B.B.S]] |
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| | {{SK}} Toxemia with seizures, preeclampsia, toxemia with seizures, hypertensive disorders of pregnancy, HDP, Hypertensive disorders of pregnancy, seizures during pregnancy |
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| | ==[[Eclampsia overview|Overview]]== |
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| {{DiseaseDisorder infobox |
| | ==[[Eclampsia historical perspective|Historical Perspective]]== |
| Name = Eclampsia |
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| ICD10 = {{ICD10|O|15||o|10}} |
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| ICD9 = {{ICD9|642.6}} |
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| MedlinePlus = 000899 |
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| DiseasesDB = 4068 |
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| {{CMG}}
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| ==Overview==
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| '''Eclampsia''', an acute and life-threatening complication of [[pregnancy]], is characterized by the appearance of [[tonic-clonic seizure]]s 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.
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| ==Historical Perspective==
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| The term is derived from the Greek and refers to a flash, a term used by [[Hippocrates]] to designate a fever of sudden onset. <ref name=Chesley>{{cite book| author=Chesley LC| title=Hypertensive Disorders in Pregnancy, in Williams Obstetrics, 14th Edition| publisher=Appleton Century Crofts, New York (1971), page 700}}</ref>
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| ==Pathophysiology==
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| 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/>
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| Placental hypoperfusion is linked to abnormal modeling of the fetal-maternal interface that may be immunologically mediated<ref name=lancet/> The invasion of the trophoblast appears to be incomplete.<ref>{{cite journal |author=Zhou Y, Fisher SJ, Janatpour M, Gembacev O, Dejana E, Wheelock M, et al. | title=Human cytotrophoblasts adopt a vascular phenotype as they differentiate: a strategy for successful endovascular invasion? |journal=J Clin Invest 1997;99:2139-51}}</ref>
| | ==[[Eclampsia pathophysiology|Pathophysiology]]== |
| [[Adrenomedullin]], a potent vasodilator, is produced in diminished quantities by the placenta in preeclampsia (and thus eclampsia). <ref>{{cite journal| title=Adrenomedullin is decreased in preeclampsia because of failed response to epidermal growth factor and impaired syncytialization| author=Hongshi L., Dakour J, Kauman S, Guilbert LJ, Winkler-Lowen B, Morrish DW |journal=Hypertension 2003, vol. 42, no5, pp. 895-900}}</ref> Other vasoactive agents are at play including [[prostacyclin]], [[thromboxane]] A2, [[nitric oxide]], and [[endothelin]]s leading to vasoconstriction.<ref name=ACOG/> 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.<ref name="Sex Primes Women for Sperm">{{cite news | title=Sex Primes Women for Sperm | publisher=BBC News | date=[[2002-02-06]] | accessdate=2007-11-19 | http://news.bbc.co.uk/2/hi/health/1803978.stm}}</ref> | |
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| Eclampsia is seen as form of a [[hypertensive encephalopathy]] in the context of those pathological events that lead to preeclampsia. 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]].<ref name="Cipolla">{{cite journal | author=Cipolla MJ | title=Cerebrovascular function in pregnancy and eclampsia | journal=Hypertension | volume=50 | issue=1 | pages=14–24 | month=July | year=2007 | url=http://hyper.ahajournals.org/cgi/content/full/50/1/14 | pmid=17548723 | doi=10.1161/HYPERTENSIONAHA.106.079442 }}</ref> Typically an eclamptic seizure will not lead to lasting brain damage; however, intracranial hemorrhage may occur.<ref>{{cite journal |author=Richards A, Graham D, Bullock R. |title=Clinicopathological study of neurological complications due to hypertensive disorders of pregnancy. |journal=J Neurol Neurosurg Psychiatry 1988;51:416-21}}</ref>
| | ==[[Eclampsia differential diagnosis|Differentiating Eclampsia from other Diseases]]== |
| ===Histopathology===
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| {{#ev:youtube|ZluEUwp1oD4}}
| | ==[[Eclampsia epidemiology and demographics|Epidemiology and Demographics]]== |
| ==Epidemiology and Demographics== | |
| 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.<ref>{{cite journal |journal= Am J Obstet Gynecol. 1990 Aug;163(2): 460-5. | title=Epidemiology of preeclampsia and eclampsia in the United States, 1979-1986. |author=Saftlas AF, Olson DR, Franks AL, Atrash HK, Pokras R. |pmid=2396132}}</ref> While mortality can be kept low when antenatal care and [[maternal-fetal medicine| 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.<ref> {{cite journal |author= Swain S, Ojha KN, Prakash A, Bhatia BD.| title=Maternal and perinatal mortality due to eclampsia. |journal=Indian Pediatr. 1993 Jun;30(6):771-3}}</ref> | |
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| Eclamptic convulsions may appear in the last trimester (rarely before), during [[childbirth|labour]], and in the first two days [[postpartum]]; it would be highly unusual to see eclampsia later than 48 hours after delivery. <ref>Chesley, ibid p.701</ref>
| | ==[[Eclampsia risk factors|Risk Factors]]== |
| ==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. 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.<ref>{{cite journal| author=Chesley LC, Annitto JE, Cosgrove RA |title=The familial factor in toxemia of pregnancy.| journal=Obstet Gynecol 1968;32:303}}</ref> Patients with eclampsia are at increased risk for preeclampsia-eclampsia in a later pregnancy. | | ==[[Eclampsia natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
| ==Differential diagnosis== | | |
| Seizures during pregnancy that are unrelated to preeclampsia need to be distinguished from eclampsia. Such disorders include seizure disorders as well as brain tumor, aneurysm of the brain, medication- or drug-related seizures. Usually the presence of the signs of severe preeclampsia that precede and accompany eclampsia facilitate the diagnosis.
| | ==Diagnosis== |
| ==Signs and symptoms==
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| Typically patients show signs of [[pregnancy-induced hypertension]] and [[proteinuria]] prior to 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 have been already compromised by [[intrauterine growth retardation]], and with the toxemic changes during eclampsia may suffer [[fetal distress]]. Placental bleeding and [[placental abruption]] may occur.
| | [[Eclampsia history and symptoms|History and Symptoms]] | [[Eclampsia physical examination|Physical Examination]] | [[Eclampsia laboratory findings|Laboratory Findings]] |
| ===The eclamptic seizure===
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| Chesley distinguishes these four stages of an eclamptic event: In the ''stage of invasion'' facial twitching can be observed around the mouth. In the ''stage of contraction'' tonic contractions render the body rigid; this stage may last about 15 to 20 seconds. The next stage is the ''stage of convulsion'' when involuntary and forceful muscular movements occur, the tongue may be bitten, foam appears at the mouth. The patient stops breathing and becomes [[cyanosis|cyanotic]]; this stage lasts about one minute. The final stage is a more or less prolonged ''[[coma]]''. When the patient awakens, she is unlikely to remember the event.<ref>Chesley, ibid. page 702</ref> In some rare cases there are no convulsions and the patient falls directly into a coma. Some patients when they awake from the coma may have temporary blindness.
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| During a seizure, the fetus may experience [[bradycardia]].<ref name=ACOG/>
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| ==Treatment== | | ==Treatment== |
| The treatment of eclampsia requires prompt intervention and aims to prevent further convulsions, control the elevated blood pressure and deliver the fetus.
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| ===Prevention of convulsions===
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| Prevention of convulsion is usually done using [[magnesium sulfate]] (4-6 g loading dose in 100 ml iv fluid given over 15-20 minutes, then 2g per hour as a continuous infusion)<ref name=ACOG/> Evidence for the use of magnesium sulfate came from the international MAGPIE study.<ref>{{cite journal |author=Frayling, Frayling |title=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] |journal= |volume=4 |issue=1 |pages=5 |year=2004 |pmid=15113445}}</ref>
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| ===Antihypertensive management===
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| Antihypertensive management at this stage in pregnancy may consist of hydralazine (5-10 mg IV every 15-20 min until desired response is achieved) or labetalol (20 mg bolus iv followed by 40 mg if necessary in 10 minutes; the 80 mg every 10 up to maximum of 220 mg).<ref name=ACOG>{{cite journal |author=ACOG| title= Diagnosis and Management of Preeclampsia and Eclampsia |journal=ACOG Practice Bulletin # 33, 2002,}}</ref>
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| ===Delivery===
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| If the woman has not yet been delivered, steps need to be taken to stabilize the patient and deliver her speedily. This needs to be done even if the fetus is immature as the eclamptic condition is unsafe for fetus and mother. As eclampsia is a manifestation of a multiorgan failure, other organs (liver, kidney, clotting, lungs, and cardiovascular system) need to be assessed in preparation for a delivery, often a [[cesarean section]], unless the patient is already in advanced labor. Regional anesthesia for cesarean section is contraindicated when a [[coagulopathy]] has developed.
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| ===Invasive hemodynamic monitoring===
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| Invasive hemodynamic monitoring may be useful in eclamptic patients with severe cardiac disease, renal disease, refractory hypertensionpulmonary edema, and oliguria.<ref name=ACOG/>
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| ==Prevention==
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| Detection and management of preeclampsia is critical to reduce the risk of eclampsia. Appropriate management of patients with preeclampsia generally involves the use of magnesium sulfate as an agent to prevent convulsions, and thus preventing eclampsia.
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| ==References==
| | [[Eclampsia medical therapy|Medical Therapy]] | [[Eclampsia surgery|Surgery]] | [[Eclampsia primary prevention|Primary Prevention]] | [[Eclampsia cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Eclampsia future or investigational therapies|Future or Investigational Therapies]] |
| {{reflist|2}}
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| ==Bibliography== | | ==Case Studies== |
| * Mayes, M., Sweet, B. R. & Tiran, D. (1997). Mayes' Midwifery - A Textbook for Midwives 12th Edition, pp. 533–545. Baillière Tindall. ISBN 0-7020-1757-4
| | [[Eclampsia case study one|Case #1]] |
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| | ==Related Chapters== |
| | [[Preeclampsia]] |
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| {{Pathology of pregnancy, childbirth and the puerperium}} | | {{Pathology of pregnancy, childbirth and the puerperium}} |
| {{SIB}}
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| [[de:Eklampsie]] | | [[de:Eklampsie]] |
| [[es:Eclampsia]] | | [[es:Eclampsia]] |
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| [[Category:Disease]] | | [[Category:Disease]] |
| [[Category:Overview complete]]
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| [[Category:Obstetrics]] | | [[Category:Obstetrics]] |
| [[Category:Medical emergencies]] | | [[Category:Medical emergencies]] |
| [[Category:Emergency medicine]] | | [[Category:Emergency medicine]] |