Management of Eclampsia






  • Video Clips on DVD


  • 10-1

    PowerPoint Discussion of Evaluation and Management of a Patient with Eclampsia


  • 10-2

    Discussion with Dr. Sibai on Emergent Management of a Woman Presenting with an Eclamptic Seizure


Eclampsia is defined as the onset of seizures and/or unexplained coma during pregnancy (usually not before 20 weeks of gestation) or postpartum in patients with signs and symptoms of preeclampsia. In the Western world, the incidence ranges from 1 in 2000 to 1 in 3448 pregnancies. Incidence is higher in tertiary referral centers, in the developing countries, and in patients with no prenatal care. Although most cases (90%) present in the third trimester or 48 hours following delivery, there have been rare cases (1.5%) at or before 20 weeks and as late as 23 days postpartum. Risk factors for eclampsia are described in Table 10-1 .



Table 10-1

Risk Factors for Eclampsia








  • First pregnancy



  • Previous eclampsia



  • Multifetal gestation



  • Chronic hypertension/renal disease



  • Collagen vascular disease



  • Molar pregnancy/partial mole



  • Gestational hypertension-preeclampsia plus




    • Severe headache



    • Persistent visual changes



    • Severe epigastric/right upper quadrant pain



    • Altered mental status






Case 1: Eclampsia with Eclamptic Seizure


An ambulance rushes Jessica, a 19-year-old G1P0 with an intrauterine pregnancy at 36 weeks’ gestation, to labor and delivery. She’s had no prenatal care. Her family says she has been complaining of headache and visual disturbance for the last few days. They’ve witnessed a 3-minute seizure during which she drooled saliva but had no urinary or fecal incontinence. Her medical/surgical and social history are completely negative.


On admission, her blood pressure is 170 mm Hg systolic over 110 mm Hg diastolic. She has 2+ protein on her urine dip. Bedside ultrasound confirms a singleton intrauterine pregnancy consistent with 36 weeks of gestation. Fetal heart rate tracing is reassuring, and cervical exam reveals a Bishop score of 7.


The 19-year-old patient underwent immediate suctioning of secretions and was placed in a lateral semirecumbent position and given oxygen by face mask. IV access was secured and laboratory tests were obtained for complete blood count (CBC), including platelet count, liver enzymes, and a metabolic profile. A loading dose of 6 g of magnesium sulfate was given over 20 minutes and that was followed by a maintenance dose of 2 g/hr. Because of her severe hypertension, a 10-mg bolus of IV hydralazine was administered. Blood pressures were monitored every 5 to 10 minutes, and after 30 minutes, the systolic was 150 mm Hg and diastolic was 105 mm Hg. Maternal urine output and reflexes were monitored every hour.


The results of the blood tests revealed a platelet count of 120,000/mm 3 , a hematocrit of 37%, and normal liver enzymes. Once maternal and fetal conditions were considered stable, IV oxytocin was started to initiate labor.


The patient subsequently spontaneously delivered vaginally an infant weighing 2700 g with Apgar scores of 7 and 9 at 1 and 5 minutes, respectively. Postpartum magnesium sulfate was continued for 24 hours. In addition, maternal vital signs, intake and urine output and patellar reflexes, were monitored every hour. She was started on oral nifedipine, 10 mg every 6 hours, because of elevated blood pressures and asked to return within 1 week for postpartum follow-up.


Discussion


This is a typical presentation of a patient with eclampsia in the absence of prenatal care. It’s terrifying to witness a life-threatening eclamptic convulsion develop. First the patient’s face becomes distorted and her eyes bulge; then she becomes red faced. Lasting usually 60 to 75 seconds, convulsions occur in two phase. The first—which lasts for 15 to 20 seconds—begins with facial twitching; then the body becomes rigid with generalized muscular contractions. During the 60-second second phase, the muscles of the body alternately contract and relax in rapid succession starting in the jaw muscles, then moving to the eyelids and the other facial muscles before spreading throughout the whole body. Apnea develops not just during but also immediately after the seizure. Coma sometimes follows seizures and the woman usually remembers nothing of the recent events. The woman often foams at the mouth and usually bites her tongue, unless it’s protected. A period of hyperventilation occurs after the tonic-clonic seizure to compensate for the respiratory acidosis that developed during the apneic period.


The majority of patients with eclampsia have hypertension (systolic blood pressure ≥140 and/or diastolic pressure ≥90 mm Hg), plus proteinuria (≥1+ on dipstick), and edema. In addition, as was the case in this patient, more than 50% will give a history of headaches, visual changes, and/or epigastric pain prior to seizures. Although hypertension is considered the hallmark for the diagnosis of eclampsia, it can be absent in 15% to 20% prior to seizures. In these cases, the patient will have proteinuria and associated central nervous system or epigastric pain with nausea and vomiting.


There is no single laboratory test that is diagnostic of eclampsia. The patient usually has hemoconcentration and elevated serum creatinine and uric acid, but normal platelet count and liver enzymes. Thrombocytopenia (platelet count <100 K/mm 3 ) is seen in approximately 20% of cases, and the full HELLP ( h emolysis, e levated l iver enzymes, and l ow p latelet count) syndrome in 10% to 15% of cases. Most patients demonstrate reduced oxygen saturation during and immediately after the seizure. If these persist, consider aspiration or pulmonary edema.


Although eclampsia is the most common cause of convulsions in association with hypertension in pregnancy and/or proteinuria, don’t overlook the other causes that—although rare—can produce convulsions in pregnancy or postpartum and can mimic eclampsia ( Table 10-2 ).



Table 10-2

Differential Diagnosis of Eclampsia








  • Cerebrovascular accidents




    • Hemorrhage



    • Ruptured aneurysm or malformation



    • Arterial embolism or thrombosis



    • Cerebral venous thrombosis



    • Hypoxic ischemic encephalopathy



    • Angiomas




  • Hypertensive encephalopathy



  • Seizure disorder



  • Amniotic fluid embolism



  • Metabolic diseases




    • Hypoglycemia, hyponatremia, thyroid storm




  • Reversible posterior leukoencephalopathy syndrome



  • Thrombophilia



  • Thrombotic thrombocytopenic purpura



  • Postdural puncture syndrome



  • Cerebral vasculitis



The basic goals of therapy are to support maternal condition, prevent maternal injury and aspiration, prevent recurrent convulsions, and control blood pressure and other associated maternal complications. Once maternal and fetal conditions are optimized, the next step is to initiate process of delivery ( Fig. 10-1 ). Specifics of detailed steps are described following.




Figure 10-1


Steps in managing an eclamptic seizure.




Step 1. Support Maternal Respiratory and Cardiovascular Functions to Prevent Hypoxia


Establish airway patency and maternal oxygenation during or immediately after the acute episode. Even if the initial seizure is short, it’s important to maintain oxygen levels by administering oxygen via face mask with or without reservoir at 8 to 10 L/min. The goal is to prevent the hypoxia and respiratory acidosis that often occur during the convulsions. I advise pulse oximetry to monitor oxygenation in these patients. Arterial blood gas analysis is required if the pulse oximetry is abnormal (oxygen saturation <92%), or aspiration or pulmonary edema is suspected. Sodium bicarbonate is not given unless the pH is less than 7.

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Mar 23, 2019 | Posted by in OBSTETRICS | Comments Off on Management of Eclampsia

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