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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 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 preexisting or organic brain disorders.
Signs and symptomsEdit
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 oedema, 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 seizureEdit
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. 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 .
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. Furthermore, 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, hydatidiform mole) also predisposes women to toxemia. In addition, there is a genetic component: patients whose mother or sister had the condition are at higher risk. Patients who've experienced eclampsia are at increased risk for preeclampsia/eclampsia in a later pregnancy.
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 preeclampsia (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 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 oedema. Typically an eclamptic seizure will not lead to lasting brain damage; however, intracranial haemorrhage may occur.
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, and medication- or drug-related seizures. Usually the presence of the signs of severe preeclampsia precede and accompany eclampsia, facilitating the diagnosis.
CBC, RFT (Renal Function test), LFT (Liver Function test), coagulation profile, plasma rate concentration, 24 hour urine analysis, ultrasound
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 sulphate as an agent to prevent convulsions, and thus preventing eclampsia.
The treatment of eclampsia requires prompt intervention and aims to prevent further convulsions, control the elevated blood pressure, and immediately terminate the pregnancy --via delivery of the newborn if possible.
Prevention of convulsionsEdit
Prevention of seizure convulsion is usually done using magnesium sulphate. 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. As per Lu and Nightingale, 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 should receive additional MgSO4 but with close monitoring for respiratory, cardiac, and neurological depression. The treat dosage is 4–6 g loading dose in 100 mL IV fluid over 15–20 min. then 2 g/hr as a continuous infusion. 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 sulphate therapies were evaluated by the international MAGPIE study.
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 minutes up to a maximum of 220 mg).
If the baby has not yet been delivered, steps need to be taken to stabilise the patient and deliver her speedily. This needs to be done even if the fetus is immature, as the eclamptic condition is unsafe for both fetus 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 patient is already in advanced labour. Regional anaesthesia for caesarean section is contraindicated when a coagulopathy has developed. according to Chestergtreat14
Invasive haemodynamic monitoringEdit
Invasive haemodynamic monitoring may be useful in eclamptic patients with severe cardiac disease, renal disease, refractory hypertension, pulmonary oedema, and oliguria.
- ↑ Chesley LC. Hypertensive Disorders in Pregnancy, in Williams Obstetrics, 14th Edition, Appleton Century Crofts, New York (1971), page 700.
- ↑ Chesley, ibid. page 702
- ↑ 3.0 3.1 3.2 3.3 3.4 ACOG (2002). Diagnosis and Management of Preeclampsia and Eclampsia. ACOG Practice Bulletin 33.
- ↑ Chesley LC, Annitto JE, Cosgrove RA. The familial factor in toxemia of pregnancy.. Obstet Gynecol 1968;32:303.
- ↑ 5.0 5.1 5.2 5.3 JM Roberts, DW Cooper. Series, Pre-eclampsia trio. Pathogenesis and genetics of pre-eclampsia.. The Lancet 2001; 357:53-56.
- ↑ 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.
- ↑ 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.
- ↑ includeonly>"Sex Primes Women for Sperm", BBC News, 6 February 2002. Retrieved on 2007-11-19.
- ↑ Cipolla MJ (July 2007). Cerebrovascular function in pregnancy and eclampsia. Hypertension 50 (1): 14–24.
- ↑ 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.
- ↑ (Jan 2006). [Magnesium sulphate for the management of preeclampsia]. Gynecol Obstet Fertil 34 (1): 54–9.
- ↑ Pritchard, JA. The use of the magnesium ion in the management of eclamptogenic toxemias. Surg Gynecol Obstet. 1955; 100:131–140
- ↑ Lu JF,Nightingale CH. Magnesium sulphate in eclampsia and pre-eclampsia. Clin Pharmacokinet. 2000; 38:305–314
- ↑ Frayling, Frayling (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.
Pathology of pregnancy, childbirth and the puerperium (O, 630-676)
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