Refers to the onset of seizures in the presence of preeclampsia syndrome.
Headache, blurred vision, abdominal pain, and mental status changes may herald the onset of preeclampsia/eclampsia.
Diagnosis should be considered in any peripartum woman with new onset seizures, proteinuria, or hypertension.
Risk factors include age over 35 years, first pregnancy, chronic hypertension, diabetes, renal disease, preeclampsia, multiparous pregnancy, and obesity.
Laboratory at the mileages include proteinuria.
Most cases occur after 28 weeks of geststation and within 48 hours of delivery, although cases may occur however outside this time frame.
Late postpartum eclampsia has been observed up to four weeks postpartum.
Posterior reversible encephalopathy syndrome in the setting of neurotoxicity strongly associated with eclampsia.
Posterior reversible encephalopathy syndrome associated with focal, symmetric distribution in watershed area bridal and occipital areas of the brain.
Posterior reversible encephalopathy syndrome can also affect frontal, brainstem, was cerebella zones.
Symptoms associated with posterior reversible enephalopathy syndrome include headaches, vision changes, focal neurological signs, mental status alterations, and seizures.
Magnesium sulfate mainstay of treatment to prevent recurrent convulsions.
In research trials magnesium infusion continued for 24 hours after delivery or the last after seizure was more efficacious than phenytoin, nimodipine, or benzodiazepines.
Elevated blood pressure is managed by antihypertensive agents.
Refers to the onset of seizures in a woman with pre-eclampsia.
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.
Onset may be before, during, or after delivery.
Most often its onset is during the second half of pregnancy.
The seizures are of the tonic–clonic type and typically last about a minute.
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.
Prevented measures include aspirin in high risk, calcium supplementation in areas with low intake, and treatment of prior hypertension with medications.
Exercise during pregnancy may also be useful.
The use of intravenous or intramuscular magnesium sulfate improves outcomes in those with eclampsia and is generally safe.
Other treatments may include blood pressure medications such as hydralazine and emergency delivery of the baby either vaginally or by cesarean section.
Pre-eclampsia is estimated to affect about 5% of deliveries while eclampsia affects about 1.4% of deliveries.
In the developed countries rates are about 1 in 2,000 deliveries.
Hypertensive disorders of pregnancy are one of the most common causes of death in pregnancy, resulting in 29,000 deaths in 2013.
Approximately one percent of women with eclampsia die.
Patients usually develops hypertension and proteinuria before the onset of a convulsion.
Eclampsia is preeclampsia and seizures.
Other cerebral signs may precede the convulsion, and include nausea, vomiting, headaches, and cortical blindness.
If multi-organ failure ensues, signs and symptoms of those failing organs will appear.
The fetus may develop intrauterine growth retardation, bradycardia, and fetal distress.
Placental bleeding, and placental abruption may also occur with eclampsia.
Eclampsia tends to occur more commonly in first pregnancies and young mothers where it is thought that novel exposure to paternal antigens is involved.
Women with pre-existing vascular diseases such as hypertension, diabetes, or nephropathy, or thrombophilic diseases such as the antiphospholipid syndrome are at higher risk
Having a large placenta due to multiple gestation also predisposes women to eclampsia.
A genetic component exists as a woman whose mother or sister had the condition is at higher risk.
Women who have experienced eclampsia are at increased risk for pre-eclampsia/eclampsia in a later pregnancy.
Pulmonary edema affects approximately 3% of the people with eclampsia, with most cases caused by too much intravenous fluid.
Eclampsia resolves when the placenta is removed.
Placental hypoperfusion 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.
Activation of the coagulation cascade may lead to microthrombi formation, which can further impair blood flow.
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.
The above events lead to hypertension; renal, pulmonary, and hepatic dysfunction, and cerebral edema with cerebral dysfunction and convulsions.
Decreased placental perfusion may be immunologically mediated.
The placenta produces a vasodilator adrenomedullin, which is reduced in pre-eclampsia and eclampsia, along with other diminished vasodilators prostacyclin, thromboxane A2, nitric oxide, and endothelins.
Reduced vasodilators lead to vasoconstriction.
It is a form of hypertensive encephalopathy.
With eclampsia cerebral vascular resistance is reduced, leading to increased blood flow to the brain, cerebral edema and resultant convulsions.
Convulsions associated with eclampsia usually does not cause chronic brain damage.
Convulsions during pregnancy unrelated to pre-eclampsia need to be distinguished from eclampsia and 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 of associated convulsions.
Lab evaluation includes: CBC, renal function test, liver function tests, coagulation screen, 24-hour urine creatinine and protein, and fetal/placental ultrasound.
Appropriate management with pre-eclampsia generally involves the use of magnesium sulphate to prevent convulsions.
The four goals of the treatment of eclampsia:
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.
Serum magnesium concentrations associated with maternal toxicity as well as neonatal depression, hypotonia, and low Apgar scores.
Serum magnesium concentrations of:
7.0–10.0 mEq/L, associated with loss of patellar reflex.
10.0–13.0 mEq/L: associated with respiratory depression.
15.0–25.0 mEq/L: associated with atrioventricular conduction and complete heart block abnormalities.
>25.0 mEq/L: associated with cardiac arrest.
With intravenous administration of magnesium sulfate the onset of anticonvulsant action is fast and lasts about 30 minutes.
Following intramuscular administration of magnesium sulfate the onset of action is about one hour and lasts for three to four hours.
Effective anticonvulsant serum levels of magnesium sulfate range from 2.5 to 7.5 mEq/liter.
Magnesium is excreted solely by the kidney.
As recurrent convulsions may occur additional dosage of magnesium may be needed.
Patients need to be monitored but with for respiratory, cardiac, and neurological depression.
If magnesium administration fails to control convulsions, other intravenous anticonvulsants may be used.
Blood pressure control is best achieved with hydralazine or labetalol,.
Patients with eclampsia should be delivered quickly, after stabilization.
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 eclampsia is unsafe for both baby and mother, delivery This needs to be done even if the baby is immature.
It is is a manifestation of a multiorgan failure, and many systems must be evaluated in preparation for a delivery, often by caesarean section.
If a coagulopathy is present regional anesthesia for caesarean section is contraindicated.
The term toxemia of pregnancy is no longer recommended, as placental toxins are not the cause of eclampsia.