Eclampsia

Article Author:
Prabhcharan Gill
Article Editor:
James Van Hook MD
Updated:
11/18/2018 7:53:24 PM
PubMed Link:
Eclampsia

Introduction

Eclampsia is a uniquely pregnancy-related disorder that manifests as new onset of generalized tonic colonic seizures. It typically occurs after 20 weeks of concluded gestation, although it may occur sooner with plural gestations or molar pregnancies, and may additionally occur in the 6-week postpartum window. It represents the severe end of the preeclampsia spectrum. Preeclampsia spectrum includes symptoms of the central nervous system (CNS), for example, severe headaches or vision changes, and may involve hepatic abnormalities (such as elevated liver transaminases with right upper quadrant/epigastric discomfort), elevated blood pressures, and also may include thrombocytopenia, renal abnormalities, and pulmonary edema. In developed countries, resultant maternal mortality may be as high as 1.8%, and in the developing countries, it may be as high as 14%.[1]

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.[2][3]

Epidemiology

In the 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 the developing countries. The risk factors of preeclampsia are similar to those of preeclampsia and include nulliparity, non-white, low socioeconomic backgrounds, plural pregnancies, and extremes of maternal age. Additionally, it is associated with and 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. [4] [4]

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.[5][6]

Histopathology

In a 1973 report, findings at autopsy include 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 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 that is 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), which include a headache, 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 an evaluation of renal function, liver function, complete blood count, and imaging of 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. [7][8]Clinical monitoring for placental abruption is heightened and is maternal monitoring for evolving complications such as pulmonary edema or renal dysfunction. Neuroimaging should be considered if:

  • There are persistent neurologic deficits
  • The loss of consciousness is prolonged
  • The onset of seizures is 48 hours beyond delivery
  • An eclamptic seizure occurs before 20 weeks
  • Recurrent seizures in spite of 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.[1][9][10]

Magnesium sulfate is a treatment of choice to prevent recurrent seizures; however, approximately 10% of will have a repeat a 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 the addition of 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 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.

Complications

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

Pearls and Other Issues

As a point of caution, when an eclamptic seizure is diagnosed before 20 weeks, it deserves careful exclusion of non-obstetric etiologies such as brain tumor or ruptured aneurysm as does the diagnosis of delayed postpartum eclampsia. Approximately 60% of the cases occur antepartum, and 20% occur intrapartum, and finally, 20% of the cases occur postpartum. Approximately 90% of the postpartum seizures occur within one week of delivery.

Enhancing Healthcare Team Outcomes

Eclampsia is a serious disorder of pregnancy that can jeopardize the lives of both the mother and the fetus. Because the condition can affect many organ systems, a multidisciplinary approach to management is highly recommended. The nurse looking after a patient with eclampsia must be aware of the potential complications so that a prompt physician referral can be made. Over the past 3 decades, the outcomes of eclampsia have improved chiefly due to improvements in healthcare. However, morbidity from the disorder still occurs. At least 20% of women with eclampsia will go on to develop hypertension in subsequent pregnancies and another 2-5% will develop eclampsia in a future pregnancy. Overall, multiparous females are not only likely to develop hypertension but also have a higher mortality compared to primiparous women. Because there is no reliable test to predict who will develop pre-eclampsia, all high risk women are urged to take a low dose aspirin during pregnancy. Finally, all pregnant women should be educated about the signs and symptoms of preeclampsia and when to seek medical help.[3][10]