Letters to the Editor

Postpartum Eclampsia

to the editor: Preeclampsia is a disorder of pregnancy, and those patients who progress to eclamptic seizures do so prenatally, peripartum, and postpartum with equal frequency. Postpartum seizures generally occur within 24 hours of delivery. Prepartum, the disease is definitively treated by delivery with subsequent diuresis and resolution of proteinuria and hypertension.

A 37-year-old woman (gravida 5, para 3, spontaneous abortion 1) had an uneventful pregnancy with good prenatal care, documented normal blood pressures, and trace to zero proteinuria at all visits, culminating in a term repeat cesarean section and bilateral tubal ligation. The patient had an uneventful postoperative course and was discharged. Eleven days postoperatively the patient presented to the emergency department complaining of gradually worsening headache for the past three days with onset of blurred vision that morning. In the emergency room the patient had a witnessed generalized seizure and received lorazepam (Ativan) and magnesium sulfate.

On physical examination, the patient had a blood pressure of 185/91 mm Hg, 2+ generalized pitting edema of the arms and legs, and one to two beat clonus bilaterally of the ankle reflexes. Mental status remained oriented, with no focal neurologic signs and absent Babinski signs bilaterally.

Laboratory findings were significant: 3⁺ proteinuria; hemoconcentration with hemoglobin 15.5 g per dL (155 g per L) and a platelet count of 568,000 per mm³ (568.0 3 10⁹ per L); uric acid level of 8.1 mg per dL (486 mmol per L); and white blood cell (WBC) count, 15,400 per mm³ (15.4 3 10⁹ per L), with 84 percent polymorphonuclear cells and 4 percent band cells. Lumbar puncture following normal funduscopic examination revealed 822 red blood cells, 7 WBCs, normal blood glucose of 52 mg per dL (2.9 mmol per L) and an elevated protein of 152 g per dL (1.52 g per L). Gram stain of cerebrospinal fluid revealed no organisms.

The patient received a 4-g magnesium sulfate loading dose followed by a 2 g per hour drip, in addition to a loading dose of phenytoin (Dilantin). Neurologic consultation was obtained as well as consultation with the patient's obstetrician. Computed tomographic imaging revealed an area of decreased attenuation in the right posterior frontal lobe suspicious for edema. Magnetic resonance imaging (MRI) revealed diffuse confluent cortically based signal alteration within the posterior parietal lobes and occipital lobes bilaterally, suspicious for sequelae of preeclampsia/eclampsia. MRI was negative for venous sinus thrombosis. An electroencephalogram was read as normal.

Clinically, the patient responded to intravenous magnesium sulfate and labetalol, with more than 5 L of fluid diuresis in the first 24 hours and resolution of headache and visual symptoms by 48 hours. The patient remained on labetalol and phenytoin at the time of discharge and was completely asymptomatic.

Eclampsia in a patient 11 days postpartum is relatively rare, although a brief literature search did reveal case reports of eclampsia in two patients nine days postpartum and one patient 16 days postpartum.^1,2 The differential diagnosis includes meningitis, new-onset seizures, venous sinus thrombosis, intracranial hemorrhage, or tumor, all of which were excluded by diagnostic testing. Physicians should be aware of the possibility of remote eclampsia, which can be effectively treated with magnesium sulfate and antihypertensives. This clinical entity should be considered in the differential diagnosis of patients presenting with seizure up to two weeks or longer postpartum.

SAMANTHA NEWBOULD, M.D.
University of Nevada-Reno
Brigham Building/316
Reno, NV 89557-0046

REFERENCES

1. Veltkamp R, Kupsch A, Polasek J, Yousry TA, Pfister HW. Late onset postpartum eclampsia without pre-eclamptic prodromi: clinical and neuroradiological presentation in two patients. J Neurol Neurosurg Psychiatry 2000;69:824-7.
2. Felz MW, Barnes DB, Figueroa RE. Late postpartum eclampsia 16 days after delivery: case report with clinical, radiologic, and pathophysiologic correlations. J Am Board Fam Pract 2000;13:39-46.

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