Acute Eclampsia

Etiology

The etiology of the disorder remains elusive. The placenta seems to have a prime role in its etiology. An increase in placental mass, as in plural pregnancies, increases the risk for the preeclampsia-eclampsia spectrum, as does placental edema that occurs in pregnancies complicated by fetal hydrops. Molar pregnancies that impact placental architecture also have a higher risk of the complication.

Epidemiology

In developed countries, the incidence of preeclampsia has been described to be between 1.5 to 10 cases in 100,000 deliveries. The condition is more prevalent in developing countries. The risk factors of preeclampsia are similar to those of preeclampsia and include nulliparity, non-White race, low socioeconomic backgrounds, plural pregnancies, and extremes of maternal age. Additionally, it is associated with an array of maternal medical conditions such as chronic hypertension, chronic renal disease, and autoimmune disorders. Obesity and maternal diabetes are also recognized as increasingly important etiologies. Fetal conditions, such as fetal hydrops, have been associated with preeclampsia. 

Pathophysiology

Some have suggested hypertension causes breakdown of the autoregulatory mechanisms of cerebral circulation, inducing endothelial dysfunction that concludes in cytotoxic edema and expression of a generalized seizure. Inflammation of the cerebrum seems to play a role in the pathophysiology. In some scenarios, it may be associated with posterior reversible encephalopathy syndrome due to posterior circulation's inability to autoregulate itself in response to acute hypertension.[2]

Histopathology

In a 1973 report, autopsy findings included more than 50% of women who died within 2 days of seizures had evidence of cerebral hemorrhages. It also described brain histopathology. Occipital lobe petechial hemorrhages were a common finding. Cerebral venous thrombosis was also frequently observed. Since then, some studies have used free radical stains to demonstrate endothelial, histiocytic, and platelet markers suggestive of capillary injury in otherwise intact brain parenchyma.

History and Physical

There may be a history of worsening headaches with vision changes such as blurred vision or “spots.” Hypertension and proteinuria may be present or absent. Impending eclampsia may have clonus. Eclampsia is a clinical diagnosis described by the occurrence of new-onset generalized tonic-clonic seizures in a woman with preeclampsia; however, on occasion, it may be the first presentation of preeclampsia. Clinical findings may include posterior reversible encephalopathy syndrome (due to vasogenic edema predominantly localized in the posterior cerebral hemispheres), including headaches, confusion, visual symptoms, and seizure.

Evaluation

Women known to have preeclampsia may develop eclamptic, generalized, tonic-clonic seizures that conclude with no persistent neurologic deficit, meaning they do not deserve diagnostic evaluation beyond that performed for preeclampsia. A preeclampsia workup would include evaluating renal function, liver function, complete blood count, and imaging of the fetoplacental unit. Obstetric ultrasound imaging of the fetus includes an assessment of fetal growth as well as fetal health (biophysical profile and as indicated umbilical artery cord Doppler studies), including fetal heart rate strip.[3] Clinical monitoring for placental abruption is heightened, as is maternal monitoring for evolving complications such as pulmonary edema or renal dysfunction. Neuroimaging should be considered if:

• Persistent neurologic deficits
• Prolonged loss of consciousness
• The onset of seizures is 48 hours beyond delivery.
• An eclamptic seizure occurs before 20 weeks.
• Recurrent seizures despite adequate magnesium sulfate therapy

Treatment / Management

Acute care is prioritized to maintain the airway, prevent aspiration, and prevent maternal injury. The patient should be shifted onto her left side, and once the seizures have concluded, maternal oxygenation is optimized with the supplemental oxygen of 8 to 10 liters per minute administered via a nonrebreathing face mask to treat hypoxemia that occurs from hypoventilation during the seizure activity.[3]

Magnesium sulfate is a treatment of choice to prevent recurrent seizures; however, approximately 10% will have a repeat seizure despite magnesium sulfate therapy. Recurrent seizures require surveillance for rhabdomyolysis, metabolic acidosis, aspiration pneumonia, and neurogenic pulmonary edema. Magnesium sulfate remains superior for recurrent seizure activity (an additional 2 gm bolus can be considered in those already on magnesium sulfate therapy), but intravenous lorazepam 2mg intravenously over 3 to 5 minutes may also be considered. The initial loading bolus of magnesium sulfate is 4 gm to 6 gm intravenously over 15 to 20 minutes with a maintenance dose of 1 gm to 3 gm an hour, depending on renal function. Blood levels of magnesium are monitored every four hours and targeted at four mEq/L to -7 mEq/L or 5 mg/dl to 9 mg/dl. Urine output is closely monitored. Should magnesium sulfate toxicity occur calcium, gluconate 1 gm intravenously can be administered.

Management of severe hypertension is the next focus of patient care. A preferred agent for the treatment of severe hypertension is intravenous labetalol (initial dose of 20 mg and for recalcitrant severe hypertension follow-up dose of 40 mg and 80 mg every 15 minutes). Maintaining systolic blood pressure between 140 mm Hg to 160 mmHg and diastolic blood pressure between 90 mmHg to 105 mmHg are targeted treatment goals.

Fetal bradycardia lasting 3 to 5 minutes is a common finding during and immediately after the seizure and does not indicate emergency cesarean delivery. Stabilization of the mother by stabilizing the seizure activity and correction of maternal hypertension if present and oxygen to treat hypoxemia and hypercarbia is the mainstay of initial supportive therapies are part of fetal intrauterine fetal resuscitation.  However, if the fetal heart rate strip does not improve after 15 minutes of maternal and fetal resuscitative interventions, then a differential diagnosis of occult abruption should be considered, and emergent cesarean delivery may be indicated. Eclampsia represents an absolute contraindication to expectant management. Once the maternal-fetal condition is stabilized, delivery should be accomplished by labor induction. This is a particularly reasonable option after 32 weeks of gestation. It may be an option at early gestations with a favorable Bishop score; however, long induction-delivery intervals are best avoided with a clear end-point for delivery to be concluded within 24 hours.

Differential Diagnosis

• Adrenal insufficiency and adrenal crisis

• Cerebral hemorrhage

• Cerebral aneurysms

• Cerebral venous thrombosis

• Encephalopathy

• Encephalitis

• Gestational trophoblastic neoplasia

• Head trauma

• Hypertensive emergencies

• Hypoglycemia

Prognosis

Most females with mild preeclampsia have positive pregnancy outcomes. Eclampsia has an overall 2% mortality rate, so it is a serious condition. The recurrence risk for preeclampsia depends on the severity of the condition.

Patients with eclampsia may demonstrate an increased risk for cardiovascular disease later in life; this risk is increased in more severe cases or those with early-onset.

Complications

• Cortical blindness
• Neurological deficits
• Stroke
• Coronary event
• Renal failure
• Liver dysfunction
• DIC
• Death
• Intrauterine growth retardation