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==Risk factors==
==Risk factors==
Eclampsia, like preeclampsia, tends to occur more commonly in first pregnancies and young mothers where it is thought that novel exposure to paternal [[antigen]]s is involved. 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. Having a large placenta ([[multiple gestation]], [[hydatiform mole]]) also predisposes women to 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, like preeclampsia, tends to occur more commonly in first pregnancies and young mothers where it is thought that novel exposure to paternal [[antigen]]s is involved. 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. Having a large placenta ([[multiple gestation]], [[hydatiform mole]]) also predisposes women to 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 who've experienced eclampsia are at increased risk for preeclampsia/eclampsia in a later pregnancy.


==Pathophysiology==
==Pathophysiology==

Revision as of 05:11, 15 July 2011

Eclampsia
SpecialtyObstetrics Edit this on Wikidata

Eclampsia (Greek, "shining forth"), an acute and life-threatening complication of pregnancy, is characterized by the appearance of tonic-clonic seizures, usually in a patient who had developed pre-eclampsia. (Preeclampsia 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 preexisting or organic brain disorders.[1]

Signs and symptoms

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 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.

The eclamptic seizure

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 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.[2] In some rare cases there are no convulsions and the patient falls directly into a coma. Some patients may experience temporary blindness upon waking from the coma .

During a seizure, the fetus may experience bradycardia.[3]

Risk factors

Eclampsia, like preeclampsia, tends to occur more commonly in first pregnancies and young mothers where it is thought that novel exposure to paternal antigens is involved. 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. Having a large placenta (multiple gestation, hydatiform mole) also predisposes women to toxemia. Further, there is a genetic component; patients whose mother or sister had the condition are at higher risk.[4] Patients who've experienced eclampsia are at increased risk for preeclampsia/eclampsia in a later pregnancy.

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.[5] Dr.Mayank suggested that 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.[5] Preclinical markers of the disease process are signs of increased platelet and endothelial activation[5]

Placental hypoperfusion is linked to abnormal modeling of the fetal-maternal interface that may be immunologically mediated[5] The invasion of the trophoblast appears to be incomplete.[6] Adrenomedullin, a potent vasodilator, is produced in diminished quantities by the placenta in preeclampsia (and thus eclampsia).[7] Other vasoactive agents are at play including prostacyclin, thromboxane A2, nitric oxide, and endothelins leading to vasoconstriction.[3] 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.[8]

Eclampsia is seen as a form of 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.[9] Typically an eclamptic seizure will not lead to lasting brain damage; however, intracranial hemorrhage may occur.[10]

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.


Investigations

CBC, RFT (Renal Function test), LFT (Liver Function test), coagulation profile, plasma rate concentration, 24 hour urine analysis, ultrasound

Prevention

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.

Treatment

The treatment of eclampsia requires prompt intervention and aims to prevent further convulsions, control the elevated blood pressure and deliver the fetus.

Prevention of convulsions

Prevention of seizure convulsion is usually done using magnesium sulfate.[11] The idea to use Mg2+ for the management of eclamptogenic toxemia dates from before 1955 when it was tested and published—the serum Mg2+ therapeutic range for the prevention of the eclampsic uterine contractions is still considered: 4.0-7.0 mEq/L.[12] As per Lu and Nightingale,[13] serum Mg2+ concentrations associated with maternal toxicity (also neonate depression or hypotonia and low Apgar scores) 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

Even with therapeutic serum Mg2+ concentrations, recurrent convulsions and seizures may occur—patients would receive additional MgSO4 but under close monitoring for respiratory, cardiac and neurological depression: 4–6 g loading dose in 100 mL IV fluid over 15–20 min., then 2 g/hr as a continuous infusion.[3] If high Mg2+ concentrations fail to take effect, IV anticonvulsants will ease patient intubation and mechanical ventilation as adjuvants against the eclamptic convulsions (plus the hypermagnesemic thoracic muscle paralysis). Recently the long-term implications of the magnesium sulfate therapies were evaluated by the international MAGPIE study.[14]

Antihypertensive management

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; then 80 mg every 10 up to maximum of 220 mg).[3]

Delivery

If the baby 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.

Invasive hemodynamic monitoring

Invasive hemodynamic monitoring may be useful in eclamptic patients with severe cardiac disease, renal disease, refractory hypertension, pulmonary edema, and oliguria.[3]

References

  1. ^ Chesley LC. Hypertensive Disorders in Pregnancy, in Williams Obstetrics, 14th Edition. Appleton Century Crofts, New York (1971), page 700.
  2. ^ Chesley, ibid. page 702
  3. ^ a b c d e ACOG (2002). "Diagnosis and Management of Preeclampsia and Eclampsia". ACOG Practice Bulletin. 33.
  4. ^ Chesley LC, Annitto JE, Cosgrove RA. "The familial factor in toxemia of pregnancy". Obstet Gynecol 1968;32:303.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  5. ^ a b c d JM Roberts, DW Cooper. "Series, Pre-eclampsia trio. Pathogenesis and genetics of pre-eclampsia". The Lancet 2001; 357:53-56.
  6. ^ Zhou Y, Fisher SJ, Janatpour M, Gembacev O, Dejana E, Wheelock M; et al. "Human cytotrophoblasts adopt a vascular phenotype as they differentiate: a strategy for successful endovascular invasion?". J Clin Invest 1997;99:2139-51. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  7. ^ Hongshi L., Dakour J, Kauman S, Guilbert LJ, Winkler-Lowen B, Morrish DW. "Adrenomedullin is decreased in preeclampsia because of failed response to epidermal growth factor and impaired syncytialization". Hypertension 2003, vol. 42, no5, pp. 895-900.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  8. ^ "Sex Primes Women for Sperm". BBC News. 6 February 2002. Retrieved 2007-11-19.
  9. ^ Cipolla MJ (2007). "Cerebrovascular function in pregnancy and eclampsia". Hypertension. 50 (1): 14–24. doi:10.1161/HYPERTENSIONAHA.106.079442. PMID 17548723. {{cite journal}}: Unknown parameter |month= ignored (help)
  10. ^ Richards A, Graham D, Bullock R. "Clinicopathological study of neurological complications due to hypertensive disorders of pregnancy". J Neurol Neurosurg Psychiatry 1988;51:416-21.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  11. ^ Rozenberg, P. (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. {{cite journal}}: Unknown parameter |month= ignored (help)
  12. ^ Pritchard, JA. The use of the magnesium ion in the management of eclamptogenic toxemias. Surg Gynecol Obstet. 1955; 100:131–140
  13. ^ Lu JF,Nightingale CH. Magnesium sulfate in eclampsia and pre-eclampsia. Clin Pharmacokinet. 2000; 38:305–314
  14. ^ 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: 5. doi:10.1186/1471-2393-4-5. PMC 416479. PMID 15113445.{{cite journal}}: CS1 maint: unflagged free DOI (link)
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