From Wikipedia, the free encyclopedia
Jump to: navigation, search
Classification and external resources
Specialty Obstetrics
ICD-10 O15
ICD-9-CM 642.6
DiseasesDB 4068
MedlinePlus 000899
eMedicine med/1905 emerg/796
Patient UK Eclampsia
MeSH D004461

Eclampsia is the onset of seizures (convulsions) in a woman with pre-eclampsia.[1] Pre-eclampsia is a disorder of pregnancy in which there is high blood pressure and either large amounts of protein in the urine or other organ dysfunction.[2][3] Onset may be before, during, or after delivery. Most often it is during the second half of pregnancy. The seizures are of the tonic–clonic type and typically last about a minute. Following the seizure there is typically either a period of confusion or coma. Complications include: aspiration pneumonia, cerebral hemorrhage, kidney failure, and cardiac arrest. Preeclampsia and eclampsia are part of a larger group of conditions known as hypertensive disorders of pregnancy.[1]

Recommendations for prevention include: aspirin in those at high risk, calcium supplementation in areas with low intake, and treatment of prior hypertension with medications.[4][5] Exercise during pregnancy may also be useful.[1] The use of intravenous or intramuscular magnesium sulfate improves outcomes in those with eclampsia and is generally safe.[6][7] This is true in both the developed and developing world.[6] Breathing may need to be supported. Other treatments may include blood pressure medications such as hydralazine and emergency delivery of the baby either vaginally or by cesarean section.[1]

Pre-eclampsia is estimated to affect about 5% of deliveries while eclampsia affects about 1.4% of deliveries.[8] In the developed world rates are about 1 in 2,000 deliveries due to improved medical care.[1] Hypertensive disorders of pregnancy are one of the most common causes of death in pregnancy.[9] They resulted in 29,000 deaths in 2013 – down from 37,000 deaths in 1990.[10] Around one percent of women with eclampsia die.[1] The word eclampsia is from the Greek term for lightning. The first known description of the condition was by Hippocrates in the 5th century BCE.[11]

Signs and symptoms[edit]

Typically the pregnant woman develops hypertension and proteinuria before the onset of a convulsion, the hallmark of eclampsia.[12] Eclampsia is preeclampsia and seizures. Other cerebral signs may immediately precede the convulsion, such as nausea, vomiting, headaches, and cortical blindness. If the complication of multi-organ failure ensues, signs and symptoms of those failing organs will appear, such as abdominal pain, jaundice, shortness of breath, and diminished urine output.

The fetus may develop intrauterine growth retardation, and with maternal convulsions, bradycardia,[13] and fetal distress. Placental bleeding, and placental abruption may also occur.

Sometimes the pregnant woman becomes comatose without preceding convulsions. Upon awakening from the coma, some experience amaurosis fugax: a "dark" and "fleeting" unilateral temporary blindness.[14]

Risk factors[edit]

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 is at higher risk than otherwise.[15] Women who have experienced eclampsia are at increased risk for pre-eclampsia/eclampsia in a later pregnancy. Pulmonary edema is a rather common complication of severe eclampsia affecting approximately 3% of the people with eclampsia: most is caused by too much intravenous fluid.


The presence of a placenta is required, and eclampsia resolves if it is removed.[16] Reduced blood flow to the placenta (placental hypoperfusion) is a key feature of the process. It is accompanied by increased sensitivity of the maternal vasculature to agents which cause constriction of the small arteries, leading to reduced blood flow to multiple organs. Also, an activation of the coagulation cascade may lead to microthrombi formation, which can further impair blood flow. Thirdly, increased vascular permeability results in the shift of extracellular fluid from the blood to the interstitial space, with further reduction in blood flow, and edema. These events lead to hypertension; renal, pulmonary, and hepatic dysfunction; and cerebral edema with cerebral dysfunction and convulsions.[16] Before symptoms appear, increased platelet and endothelial activation[16] may be detected.

Placental hypoperfusion is linked to abnormal modelling of the fetal–maternal placental interface that may be immunologically mediated.[16] The invasion of the trophoblast appears to be incomplete.[17] The placenta produces the potent vasodilator adrenomedullin: it is reduced in pre-eclampsia and eclampsia.[18] Other vasodilators are also reduced, including prostacyclin, thromboxane A2, nitric oxide, and endothelins, also leading to vasoconstriction.[13] Many studies have suggested the importance of a woman's reduced immunological tolerance to her baby's father, whose genes are present in the young fetus and the placenta.[19]

Eclampsia is a form of hypertensive encephalopathy: cerebral vascular resistance is reduced, leading to increased blood flow to the brain, cerebral edema and resultant convulsions.[20] An eclamptic convulsion usually does not cause chronic brain damage unless intracranial haemorrhage occurs.[21]

Differential diagnosis[edit]

Convulsions 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.

Investigations include: CBC, renal function test (RFT), liver function tests (LFT), coagulation screen, 24-hour urine creatinine and protein, and fetal/placental ultrasound.


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 to prevent convulsions.


The four goals of the treatment of eclampsia are to stop and prevent further convulsions, to control the elevated blood pressure, to deliver the baby as promptly as possible, and to monitor closely for the onset of multi-organ failure.


Convulsions are prevented and treated using magnesium sulfate.[22] The study demonstrating the effectiveness of magnesium sulfate for the management of eclampsia was first published in 1955.[23] Serum magnesium concentrations associated with maternal toxicity as well as neonatal depression, hypotonia, and low Apgar scores)[24] are:

  • 7.0–10.0 mEq/L: loss of patellar reflex
  • 10.0–13.0 mEq/L: respiratory depression
  • 15.0–25.0 mEq/L: altered atrioventricular conduction and (further) complete heart block
  • >25.0 mEq/L: cardiac arrest

With intravenous administration the onset of anticonvulsant action is fast and lasts about 30 minutes. Following intramuscular administration the onset of action is about one hour and lasts for three to four hours. Effective anticonvulsant serum levels range from 2.5 to 7.5 mEq/liter. Magnesium is excreted solely by the kidneys at a rate proportional to the plasma concentration and glomerular filtration.[25]

Even with therapeutic serum magnesium concentrations, recurrent convulsions may occur, and additional magnesium may be needed, but with close monitoring for respiratory, cardiac, and neurological depression. If magnesium administration with resultant high serum concentrations fail to control convulsions, the addition of other intravenous anticonvulsants may be used, facilitate intubation and mechanical ventilation, and to avoid magnesium toxicity including maternal thoracic muscle paralysis.

Magnesium sulfate results in better outcomes than diazepam, phenytoin or a combination of chlorpromazine, promethazine and pethidine.[26][27][28]

Blood pressure management[edit]

The agents of choice for blood pressure control during eclampsia are hydralazine and/or labetalol.[13] This is because of their effectiveness, lack of negative effects on the fetus, and mechanism of action.


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 may be elected in an eclamptic woman at risk for or with cardiac disease, renal disease, refractory hypertension, pulmonary edema, or poor urine output.[13]


The Greek noun "ἐκλαμψία", eklampsía, denotes a "light burst"; metaphorically, in this context, "sudden occurrence."[29] The New Latin term first appeared in Johannes Varandaeus’ 1620 treatise on gynaecology Tractatus de affectibus Renum et Vesicae.[30] The term toxemia of pregnancy is no longer recommended: placental toxins are not the cause of eclampsia occurrences, as previously believed.[31]


  1. ^ a b c d e f "40". Williams obstetrics (24th ed.). McGraw-Hill Professional. 2014. ISBN 9780071798938. 
  2. ^ Lambert, G; Brichant, JF; Hartstein, G; Bonhomme, V; Dewandre, PY (2014). "Preeclampsia: an update.". Acta anaesthesiologica Belgica 65 (4): 137–49. PMID 25622379. 
  3. ^ "Hypertension in pregnancy. Report of the American College of Obstetricians and Gynecologists’ Task Force on Hypertension in Pregnancy." (PDF). Obstet Gynecol. 122 (5): 1122–31. Nov 2013. doi:10.1097/01.AOG.0000437382.03963.88. PMID 24150027. 
  4. ^ WHO recommendations for prevention and treatment of pre-eclampsia and eclampsia. (PDF). 2011. ISBN 978-92-4-154833-5. 
  5. ^ Henderson, JT; Whitlock, EP; O'Connor, E; Senger, CA; Thompson, JH; Rowland, MG (May 20, 2014). "Low-dose aspirin for prevention of morbidity and mortality from preeclampsia: a systematic evidence review for the U.S. Preventive Services Task Force.". Annals of internal medicine 160 (10): 695–703. doi:10.7326/M13-2844. PMID 24711050. 
  6. ^ a b Smith, JM; Lowe, RF; Fullerton, J; Currie, SM; Harris, L; Felker-Kantor, E (5 February 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. PMID 23383864. 
  7. ^ McDonald, SD; Lutsiv, O; Dzaja, N; Duley, L (August 2012). "A systematic review of maternal and infant outcomes following magnesium sulfate for pre-eclampsia/eclampsia in real-world use.". International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics 118 (2): 90–6. doi:10.1016/j.ijgo.2012.01.028. PMID 22703834. 
  8. ^ Abalos, E; Cuesta, C; Grosso, AL; Chou, D; Say, L (September 2013). "Global and regional estimates of preeclampsia and eclampsia: a systematic review.". European journal of obstetrics, gynecology, and reproductive biology 170 (1): 1–7. doi:10.1016/j.ejogrb.2013.05.005. PMID 23746796. 
  9. ^ Arulkumaran, N.; Lightstone, L. (December 2013). "Severe pre-eclampsia and hypertensive crises". Best Practice & Research Clinical Obstetrics & Gynaecology 27 (6): 877–884. doi:10.1016/j.bpobgyn.2013.07.003. 
  10. ^ GBD 2013 Mortality and Causes of Death, Collaborators (17 December 2014). "Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013.". Lancet. doi:10.1016/S0140-6736(14)61682-2. PMID 25530442. 
  11. ^ Emile R. Mohler (2006). Advanced Therapy in Hypertension and Vascular Disease. PMPH-USA. pp. 407–408. ISBN 9781550093186. 
  12. ^ 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. 
  13. ^ a b c d "ACOG practice bulletin. Diagnosis and management of preeclampsia and eclampsia. Number 33, January 2002". Obstet Gynecol 99 (1): 159–67. January 2002. doi:10.1016/s0029-7844(01)01747-1. PMID 16175681. 
  14. ^ Cunningham FG, Fernandez CO, Hernandez C (Apr 1995). "Blindness associated with preeclampsia and eclampsia". American journal of obstetrics and gynecology 172 (4 Pt 1): 1291–8. doi:10.1016/0002-9378(95)91495-1. PMID 7726272. 
  15. ^ Chesley LC, Annitto JE, Cosgrove RA (September 1968). "The familial factor in toxemia of pregnancy". Obstet Gynecol 32 (3): 303–11. PMID 5742111. 
  16. ^ a b c d 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. 
  17. ^ 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. 
  18. ^ 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. 
  19. ^ "Sex Primes Women for Sperm". BBC News. 6 February 2002. Retrieved 2007-11-19. 
  20. ^ Cipolla MJ (July 2007). "Cerebrovascular function in pregnancy and eclampsia". Hypertension 50 (1): 14–24. doi:10.1161/HYPERTENSIONAHA.106.079442. PMID 17548723. 
  21. ^ 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. doi:10.1136/jnnp.51.3.416. PMC 1032870. PMID 3361333. 
  22. ^ 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. 
  23. ^ Pritchard JA (February 1955). "The use of the magnesium ion in the management of eclamptogenic toxemias". Surg Gynecol Obstet 100 (2): 131–40. PMID 13238166. 
  24. ^ Lu JF, Nightingale CH (April 2000). "Magnesium sulfate in eclampsia and pre-eclampsia: pharmacokinetic principles". Clin Pharmacokinet 38 (4): 305–14. doi:10.2165/00003088-200038040-00002. PMID 10803454. 
  25. ^
  26. ^ Duley, L; Henderson-Smart, DJ; Walker, GJ; Chou, D (Dec 8, 2010). "Magnesium sulphate versus diazepam for eclampsia.". The Cochrane database of systematic reviews (12): CD000127. doi:10.1002/14651858.CD000127.pub2. PMID 21154341. 
  27. ^ Duley, L; Henderson-Smart, DJ; Chou, D (Oct 6, 2010). "Magnesium sulphate versus phenytoin for eclampsia.". The Cochrane database of systematic reviews (10): CD000128. doi:10.1002/14651858.CD000128.pub2. PMID 20927719. 
  28. ^ Duley, L; Gülmezoglu, AM; Chou, D (Sep 8, 2010). "Magnesium sulphate versus lytic cocktail for eclampsia.". The Cochrane database of systematic reviews (9): CD002960. doi:10.1002/14651858.CD002960.pub2. PMID 20824833. 
  29. ^ Wictionary entry
  30. ^ Ong S. "Pre-eclampsia: A historical perspective", in Baker PN, Kingdom JCP, editors. Pr-eclampsia: Current perspectives on management; The Parthenon Publishing Group; New York, USA; 2004; pp. 15–24.
  31. ^ FAQ: Toxemia at the Pre-Eclampsia Foundation website

External links[edit]