Eclampsia
1. What every clinician should know
Eclampsia is one of the most serious obstetric emergencies. Eclampsia refers to the development of convulsions and/or unexplained coma during pregnancy or postpartum in patients with signs and symptoms of preeclampsia. Its incidence ranges from 1 in 2000 to 1 in 3448 pregnancies. The incidence is, however, higher in tertiary referral centers, in multifetal gestation, and in populations with no prenatal care.
2. Diagnosis and differential diagnosis
The diagnosis of eclampsia remains clinical and is based on the presence of convulsions in the setting of signs and/or symptoms of preeclampsia, including generalized edema, hypertension, proteinuria, and hypertension. A number of antecedent symptoms may be helpful in establishing this diagnosis, and these include persistent occipital or frontal headaches, blurred vision, photophobia, epigastric and/or right upper quadrant pain, and altered mental status.
Although the most common cause of seizures in the setting of hypertension and proteinuria is eclampsia, other etiologies can mimic eclampsia. These should be particularly contemplated in the presence of focal neurologic deficits, prolonged coma, or atypical eclampsia. Efforts should be made to identify an accurate diagnosis, as management strategies may differ among these conditions. Consultation with a neurologist may be helpful in these instances.
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3. Management
The first priority in the management of eclampsia is to prevent maternal injury and to support respiratory and cardiovascular functions. During or immediately after the acute convulsive episode, supportive care should be given to prevent serious maternal injury and aspiration, assess and establish airway potency, and insure maternal oxygenation. During this time, the bed’s side rails should be elevated and padded, a padded tongue blade inserted between the teeth, and physical restraints used. To minimize the risk of aspiration, the patient should lie in lateral decubitus position, and vomitus and oral secretion should be suctioned, as needed.
Although the initial seizure lasts only a few minutes, it is important to maintain oxygenation by supplemental oxygen administration via a facemask with or without oxygen reservoir at 8-10L/min. It is reasonable to use transcutaneous pulse oximetry to monitor oxygenation in all eclamptic patients, and arterial blood gas analysis is required if the pulse oximetry results are abnormal (oxygen saturation at or below 92%).
The next step in the management of eclampsia is to prevent recurrent convulsions. Magnesium sulfate is the drug of choice to treat and prevent subsequent convulsions in women with eclampsia. The patient may be started on a loading dose of 6g over 15-20 minutes, followed by a maintenance dose of 2 g/h as a continuous intravenous infusion. Yet, about 10% of eclamptic women will have a second convulsion after receiving magnesium sulfate. In these women, another bolus of 2g magnesium sulfate can be given intravenously over 3-5 minutes.
Occasionally, the patient will have recurrent convulsions while receiving adequate doses of magnesium sulfate. This patient can be treated with sodium amobarbital 250mg intravenously over 3-5 minutes.
Next, optimal control of blood pressure is warranted. The objective of treating severe hypertension is to avoid loss of cerebral autoregulation and to prevent congestive heart failure without compromising cerebral perfusion or jeopardizing uteroplacental blood flow that is already reduced in many women with eclampsia. It is advisable to keep systolic blood pressure between 140 and 160 mmHg and diastolic blood pressure between 90 and 110 mmHg.
The rationale for keeping maternal blood pressures at these levels is to avoid potential reduction in either uteroplacental blood flow or cerebral perfusion pressure. This can be achieved with bolus of 5-10mg doses of hydralazine or labetalol (20-40mg intravenously) every 15 minutes, as needed, or 10-20mg of nifedipine orally every 30 minutes for a maximum dose of 50mg in 1 hour. Other potent antihypertensive medications such as sodium nitroprusside or nitroglycerine are rarely needed in eclampsia.
Maternal hypoxemia and hypercarbia cause fetal heart rate and uterine activity changes during and immediately following a convulsion. Fetal heart rate changes can include bradycardia, decreased variability, late decelerations, and compensatory tachycardia. Changes in uterine activity can include increased frequency and tone. These changes usually resolve spontaneously within 3-10 minutes after the termination of convulsions and the correction of maternal hypoxemia.
The patient should not be rushed for an emergency cesarean delivery based on these findings, especially if the maternal condition is not stable. However, if the bradycardia and/or recurrent late decelerations persist beyond 10-15 minutes despite all resuscitive efforts, then a diagnosis of abruptio placentae or nonreassuring fetal status should be considered.
Once delivery needs to be pursued, it is noteworthy that the presence of eclampsia is not an indication for cesarean delivery. The decision to perform cesarean delivery should be based on fetal gestational age, fetal condition, presence of labor, and cervical Bishop score. A cesarean delivery is advised in cases of eclampsia before 30 weeks of gestation who are not in labor and whose Bishop score is below 5. Patients having labor or rupture of membranes are allowed to deliver vaginally in the absence of obstetric complications. When labor is indicated, it is initiated with either oxytocin infusions or prostaglandins in all patients with a gestational age of 30 weeks or more, irrespective of the Bishop score. A similar approach is used for those before 30 weeks of gestation if the cervical Bishop score is at least 5.
Maternal pain relief during labor and delivery can be provided by either systemic opioids or epidural anesthesia as recommended for women with severe preeclampsia. Either epidural, spinal, or combined techniques of regional anesthesia can be used for cesarean delivery. Regional anesthesia is contraindicated in the presence of coagulopathy or severe thrombocytopenia (platelet count less than 50,000). In women with eclampsia, general anesthesia increases the risk of aspiration and failed intubation due to airway edema and is associated with marked increases in systemic and cerebral pressures during intubation and extubation.
Women with airway or laryngeal edema may require awake intubation under fiberoptic observation with the availability of immediate tracheostomy.
As for postpartum management, patients should receive close monitoring of vital signs, fluid intake and output, and symptoms for at least 48 hours. These women usually receive large amounts of intravenous fluids during labor, delivery, and postpartum. In addition, during the postpartum period there is mobilization of extracellular fluid leading to increased intravascular volume. As a result, women with eclampsia, particularly those with abnormal renal function, those with abruptio placentae, and those with preexisting chronic hypertension, are at increased risk for pulmonary edema and exacerbation of severe hypertension postpartum.
These women should receive frequent evaluation of the amount of intravenous fluids, oral intake, blood products, and urine output, as well as monitoring by pulse oximetry and pulmonary auscultation. Parenteral magnesium sulfate should be continued for at least 24 hours after delivery and/or for at least 24 hours after the last convulsion. If the patient has oliguria (less than 100 mL/4h), the rate of both fluid administration and the dose of magnesium sulfate should be reduced.
Once delivery has occurred, other oral antihypertensive agents such as labetalol or nifedipine can be used to keep systolic blood pressure below 155 mm Hg and diastolic blood pressure below 105 mm Hg. The recommended dose of oral labetalol is 200mg every 8 hours (maximum dose of 2400mg/d), and the recommended dose of nifedipine is 10mg orally every 6 hours (maximum dose of 120mg/d).
4. Complications of eclampsia and its management
Complications that may be seen in eclamptic women include abruptio placentae, disseminated intravascular coagulopathy, intracerebral hemorrhage, blindness, cardiorespiratory arrest, aspiration pneumonitis, pulmonary edema, acute renal failure, liver rupture, and postpartum hemorrhage.
The simultaneous use of short-acting nifedipine and magnesium sulfate was associated with profound neuromuscular blockade (cardiac depression, muscle weakness) in two case reports. However, no such blockade was reported in the Magpie trial in which 1469 women assigned to receive magnesium sulfate also received nifedipine. In addition, no neuromuscular blockade was reported in any of the trials comparing hydralazine with nifedipine, in which there was simultaneous use of magnesium sulfate. The development of excessive neuromuscular blockade can be reversed with the administration of 1g of 10% solution calcium gluconate.
5. Prognosis and outcome
Pregnancies complicated by eclampsia may be associated with life-threatening complications for both the mother and infant. Women with a history of eclampsia are at increased risk of preeclampsia in subsequent pregnancies, particularly if the onset of eclampsia was in the second trimester. The rate of recurrent eclampsia is approximately 2%, and there is no preventive therapy for recurrent antepartum eclampsia.
6. What is the evidence for specific management and treatment recommendations?
Sibai, BM. “Diagnosis, prevention, and management of eclampsia”. Obstet Gynecol. vol. 105. 2005. pp. 402-10.
Ben Ami, M, Giladi, Y, Shalev, E. “The combination of magnesium sulfate and nifedipine: a cause of neuromuscular blockade”. Br J Obstet Gynaecol. vol. 101. 1994. pp. 262-3.
Snyder, SW, Cardwell, MS. “Neuromuscular blockade with magnesium sulfate and nifedipine”. Am J Obstet Gynecol. vol. 161. 1989. pp. 35-6.
“The Magpie Trial Collaborative Group. Do women with preeclampsia, and their babies, benefit from magnesium sulfate? The Magpie Trial: a randomized placebo-controlled trial”. Lancet. vol. 359. 2002. pp. 1877-90.
Douglas, KA, Redman, CW. “Eclampsia in the United Kingdom”. BMJ. vol. 309. 1994. pp. 1395-400.
Pritchard, JA, Cunningham, FG, Pritchard, SA. “The Parkland Memorial Hospital protocol for treatment of eclampsia: evaluation of 245 cases”. Am J Obstet Gynecol. vol. 148. 1984. pp. 951
Sibai, BM, Gabbe, SG, Niebyl, JR, Simpson, JL. “Hypertension.”. Obstetrics: normal and problem pregnancies. 2002. pp. 945-1004.
Witlin, AG, Sibai, BM. “Magnesium sulfate in preeclampsia and eclampsia”. Obstet Gynecol. vol. 92. 1998. pp. 883-9.
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