Postpartum eclampsia of late onset

Introduction

Pre-eclampsia and eclampsia occur in 6% to 8% of all pregnancies.1 The British eclampsia study confirmed 383 cases of eclampsia during 1992 and warned of the severe consequences of the condition.2 In 1997 Leitch and colleagues showed that over a 60 year period the incidence of eclampsia had fallen from 74/10 000 to 7.4/10 000, although the incidence of postpartum eclampsia had increased.3

A US study identified 229 cases of postpartum preeclampsia or eclampsia between 1992 and 20024; 151 of these cases were diagnosed after readmission to hospital with new symptoms and signs after delivery, and 16% (24/151) of these had eclampsia. Other work from the United States identified 89 cases of eclampsia during 1996 to 20015; 29 cases (33%) presented in the postpartum period. In both these US studies most cases developed symptoms more than 48 hours post partum.

Most antenatal and intrapartum cases of eclampsia present to obstetricians, but postpartum cases are more likely to be encountered by non-obstetricians. We present a case of postpartum eclampsia.

Case report

A 27 year old woman in her second pregnancy delivered a healthy male baby weighing 3690 g at 38 weeks by elective caesarean section. Clinically significant proteinuria was present from 30 weeks onwards. In her first pregnancy she had had pre-eclampsia requiring delivery at 38 weeks. This second pregnancy was by a different partner. She was discharged on the third postpartum day with blood pressure of 130/68 mm Hg and no protein in her urine.

She visited her general practitioner on the ninth postpartum day because her baby was unwell with a rash, and she was seen in the accident and emergency department as the mother of a child requiring neonatal assessment. As the mother too looked ill, she was also examined. She was noted to have low grade fever, bradycardia, and hypotension. Her urine showed moderate proteinuria (2+) on dipstick examination. Chest radiography and blood and urine cultures were normal. She was admitted under the care of the general physicians and started on intravenous ceftriaxone for suspected infection. She received 500 ml of gelatin followed by 500 ml of normal saline. Overnight her blood pressure rose to 186/92, which was treated initially with nifedipine. Her blood pressure continued to rise—to a maximum of 200/112 mm Hg. She developed a headache and suddenly lost vision in both eyes. This was followed by a generalised tonic clonic convulsion. Blood analysis—including full blood count, urea and electrolytes, and glucose—was normal, as were her thyroid function tests, anticardiolipin, extractible nuclear antigens, double stranded DNA antibodies, and complement concentrations. Blood urate was not assessed. Urinary catecholamines were negative. Doppler examination of renal vasculature and renal ultrasonography were normal.

The consulting obstetricians diagnosed eclampsia, and the patient was started on intravenous hydralazine and later magnesium sulphate. A magnetic resonance scan of the brain showed small areas of high signal intensity on T2 weighted images, involving both cortical and subcortical white matter of the right posterior parietal and both occipital lobes (figure). There was no evidence of veno-occlusive disease. The scan suggested hypertensive posterior cerebral encephalopathy. The patient regained her vision within 24 hours after her blood pressure was controlled, and she was prescribed labetalol when she was discharged home 10 days later.

Axial FLAIR magnetic resonance image showing high T2 signal intensity abnormality involving bilateral parieto-occipital cortex and subcortical white matter (arrows)

Discussion

Eclampsia is a poorly understood multisystem complication of pregnancy that substantially contributes to maternal morbidity and mortality. The typical clinical picture is of generalised tonic clonic seizures during the third trimester, labour, or early puerperium in women who already have hypertension, proteinuria, and oedema.

The previously controversial existence of a delayed postpartum variant of eclampsia is now acknowledged by most experts.2^–8 Convulsions with initial presentation more than 48 hours but less than four weeks after delivery are commonly referred to as late postpartum eclampsia.6

Our patient had convulsions on the ninth postpartum day. Her response to magnesium sulphate, the magnetic resonance scan showing hypertensive posterior cerebral encephalopathy, the exclusion of metabolic and infectious causes strongly support the diagnosis of eclampsia.

Postpartum eclampsia can present with a variety of clinical and neurological symptoms and signs. Lubrasky6 and Chames5 reported that 44% and 79% of their respective patients with late onset postpartum eclampsia had not been identified as having preeclampsia before seizure onset. They reported that severe and persistent headache, visual symptoms, epigastric or right upper quadrant pain, and hypertension can present as prodromal symptoms before the onset of eclampsia.4^–6 Our patient had these symptoms.

Eclampsia should be considered in any postpartum woman who develops any of these prodromal symptoms. Further indicators include convulsions up to four weeks after delivery, hypertension, or proteinuria. This is important as eclampsia is amenable to treatment with magnesium sulphate.

The differential diagnosis includes epilepsy, cerebral venous thrombosis, intracerebral haemorrhage, phaeochromocytoma, space occupying lesions, and metabolic disorders.9 Neuroimaging, especially magnetic resonance imaging, shows micro-ischaemic injury patterns in parieto-occipital lobes.10 This form of posterior leukoencephalopathy syndrome can cause cortical blindness, which may be reversible with control of hypertension and magnesium sulphate therapy, as in our case. Lesions on a magnetic resonance scan cannot predict whether damage leading to cortical blindness is permanent or likely to be reversible.

Magnesium sulphate remains the drug of choice for preventing and treating eclamptic seizures. If such seizures are not treated appropriately, grave complications such as intracerebral haemorrhage and death can occur.

Late onset postpartum eclampsia can occur in normotensive uncomplicated postpartum women as well as in women with pre-eclampsia. The presence of prodromal symptoms should be thoroughly investigated, even in the absence of antecedent pre-eclampsia. We suggest that such patients seen in accident and emergency units within 14 days of delivery should be assessed by an experienced obstetrician.

Late onset postpartum eclampsia can occur in normotensive women with uncomplicated pregnancies, not just in women with pre-eclampsia