Introduction
Eclampsia is a major cause of maternal and perinatal morbidity and mortality. Its incidence in the United Kingdom and America reaches four to five per 1000 pregnancies and is responsible for 10% of maternal deaths. Preeclampsia is a multi system disorder that manifest with proteinuria and hypertension usually after the 20th gestational week.1
The term eclampsia is applied to the occurrence of seizures during or after pregnancy in patients with signs and symptoms of preeclampsia that manifests as a wide range of signs from severe hypertension, massive proteinuria and generalized edema to mild hypertension without proteinuria and edema.2, 3 However, eclampsia can occur in the absence of a prodrome and is not always preventable.4, 5
Current management schemes designed to prevent eclampsia are based on early detection of preeclampsia and subsequent use of preventive therapy in such women.6
Magnesium sulfate is the drug of choice for the prophylaxis and treatment of eclamptic seizures. In refractory cases, sodium amobarbital and thiopenton can be used to control seizures.7
We hereby report a case of eclampsia without preeclamptic prodromi that manifested as recurrent seizures resistant to magnesium sulfate.
Case report
The patient was a 26-year-old primigravida woman with a 2.5-year history of primary infertility and oligomenorrhea who became pregnant with Clomid and human menopausal gonadotrophin (HMG) treatment. She was under regular prenatal care. Her weight before pregnancy was 72
kg. She had normal blood pressure with average 110/70mmHg and normal routine paraclinical studies (CBC, differential, BUN, creatinine, Hbs Ag, U/A, U/C and platelet count) during pregnancy. Screening for diabetes was negative. She underwent a total of 16 prenatal visits during which she repeatedly had normal blood pressure (110/70 and 120/80mmHg). On last prenatal visit her weight and blood pressure were 87kg and 110/70mmHg, respectively.
The patient underwent cesarean section at 38 weeks of gestation due to cephalopelvic disproportion and arrest at labor. On admission her blood pressure was 120/80mmHg, complete blood count with differentials and platelet counts were normal and there was no proteinuria in the urine analysis. The patient developed tonic clonic seizures in the ward, 4h postoperatively, while her blood pressure was normal during and after operation. She was given 10mg of diazepam initially followed by two IV injections of 4mg magnesium sulfate that could not control the seizure; eventually after 30min the patient's seizure was controlled with 250mg thiopenton. She was intubated and transferred to ICU. For the first time in the ICU, elevated blood pressure of 170/110mmHg was detected. She was repeatedly given intravenous hydralazine for control of high blood pressure. Paraclinical studies including U/A, CBC, differential, platelet count, brain CT scan and post-seizure EEG were normal.
Twenty-four hours after control of seizures with thiopenton she was extubated and transferred to the ward. She recovered consciousness after 48h. Her urine output was normal during this period. She was treated with methyldopa and Adalat for hypertension in the ward. The baby was in the newborn care section during this period. The woman began breastfeeding after 48h. She felt happy at having this beautiful baby although she was anxious about her own health. There was not any problem with breastfeeding. She was discharged after 6 days. The woman said that she felt very lucky to be alive. The patient's blood pressure returned to normal 1 month after parturition without any significant squeals.
Discussion
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We reported a case of eclampsia without preeclamptic prodromi manifested as status epilepticus. The mentioned patient had not shown any sign of elevated blood pressure either during regular prenatal care or on admission. Diagnosis of eclampsia is confirmed in the presence of hypertension, proteinuria and seizure with hypertension being the hallmark for diagnosis. Hypertension may be severe (systolic blood pressure ≥160mmHg or diastolic blood pressure ≥110mmHg) or moderate (systolic blood pressure ≥140mmHg or diastolic blood pressure ≥90mmHg). In 16% of cases hypertension may be absent. Nevertheless, severe hypertension is present in most patients with antepartum eclampsia. Eclampsia is usually associated with proteinuria.4 In a series of 399 women with eclampsia, proteinuria (≥3+ on dipstick) was present in only 48% and was absent in 16%.8
A number of symptoms may precede seizure including refractory frontal or occipital headache, visual disturbance, photophobia, and epigastric pain. Patients have at least one of these symptoms in 56–75% of cases. Our reported patient did not have any of the mentioned symptoms and her blood pressure was normal during the operation and in the recovery room.
Adie et al. reported 162 cases of eclampsia in a period of 2 years of which 8% (13) had features of atypical eclampsia with normal blood pressure and without preeclamptic prodromi. In their study, postpartum convulsion had been occurred in 31% of patients.3
In another study, Katz et al. reported 53 cases of eclampsia in the absence of preeclamptic signs. In their patients, seizure was the main manifestation of disease in 60% of cases.8
Magnesium sulfate is the drug of choice to treat and prevent convulsions in women with eclampsia. There are several randomized trials comparing the use of magnesium sulfate for the prevention of convulsions in patients with severe preeclampsia. In one such study comparing magnesium sulfate with phenytoin, magnesium sulfate was associated with an overall decreased recurrence rate.9
Approximately 10% of seizures are not controlled with the first dose of magnesium sulfate and need further doses. In refractory cases, one can use sodium amobarbital and thiopental.10, 11
We had to turn to sodium thiopental when diazepam and magnesium sulfate failed to control the patient's seizure. Although we knew that magnesium sulfate is the drug of choice for prevention and control of seizure in eclampsia, in this emergency state magnesium sulfate was not available immediately. Diazepam is a second line choice and in our case, as seizures were not predicted and diazepam was available it was used first in the emergency.
Eclampsia is associated with increased risk of maternal death in developing countries reaching 16%. The high maternal mortality reported from the developing countries was reported among patients who had seizures outside of hospital and those without prenatal care. In addition this high mortality rate could be attributed to the lack of recourse and intensive care facilities needed to manage maternal complications from eclampsia.3 In Adie's report of 13 cases of atypical eclampsia, no mother was deceased.2
Low incidence of eclampsia in developed countries is probably related to seizure prophylaxis in patients with classic presentation. The majority of cases of eclampsia reported from USA were atypical without prodromal signs or occurring 48h postpartum.3
We reported a case of eclampsia without preeclamptic prodromi that started with recurrent seizures and was associated with normal biochemical, renal and hepatic function tests. Patient's seizures were controlled with thiopental after failure of diazepam and magnesium sulfate to do so. The patient recovered without sequela despite recurrent seizures. Despite all research efforts, there is no reliable test to predict eclampsia and warning signs (headache, blurred vision) are not always present.
Current management schemes designed to prevent eclampsia are based on early detection of preeclampsia and subsequent use of preventive therapy in such women. This management schemes assume that the clinical course in the development of eclampsia is characterized by a gradual process that begins with progressive weight gain followed by hypertension and proteinuria, which is followed by the onset of premonitory symptoms, and ends with the onset of generalized convulsions or coma.6
Most women who develop eclampsia do have preceding preeclampsia. However, as this case report highlights and others have also noted, the onset of convulsions does not necessarily follow the presumed progression from preeclampsia to ecalmpsia.12
We conclude that onset postpartum eclampsia can manifest without a preceding preeclampsia phase. Therefore, eclampsia is not always preventable. Pregnancies complicated by eclampsia require a well-formulated management plan.
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