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|Year : 2003 | Volume
| Issue : 4 | Page : 539-540
Late postpartum eclampsia without prodroma
Mathew R, Raj RS, Sudha P
Department of Neurology, Medical College Hospital, Trivandrum
Morning Star, Microwave Lane, Medical College PO, Trivandrum, Kerala 695011
Late postpartum eclampsia is an increasingly recognized entity. We describe a patient who developed postpartum eclampsia on the 6th day of delivery without any preceding pre-eclampsia. A high index of suspicion and close follow-up will help in the early detection of this condition. Awareness of this condition will also save the patient from unnecessary investigations. This may be all the more relevant in developing countries where eclampsia contributes to one-third of maternal mortality and the resources for patient investigation and management are limited.
|How to cite this article:|
Mathew R, Raj R S, Sudha P. Late postpartum eclampsia without prodroma. Neurol India 2003;51:539-40
Eclampsia continues to be a poorly understood neurological complication of pregnancy that substantially contributes to maternal morbidity and mortality. Traditionally, eclampsia is classified according to the time of onset of symptoms. Postpartum eclampsia denotes convulsions appearing within 7 days after delivery of the fetus and placenta in a patient who had pre-eclampsia. Most experts now acknowledge the existence of a late postpartum variant of eclampsia.,, Late postpartum eclampsia has been variably defined as seizures occurring 3 or 4 days to 4 weeks postpartum.,, Delayed postpartum eclampsia occurring without pre-eclampsia or other prodromal symptoms is rare and may pose a real diagnostic challenge. If not suspected clinically, it may also lead to unnecessary costly and invasive investigations. A case of delayed postpartum eclampsia occurring without pre-eclampsia is presented with a brief review of the relevant literature.
A 28-year-old healthy woman (gravida one, para one) gave birth to a healthy male baby by normal vaginal delivery. The postpartum period was uneventful until the 6th day, when she complained of headache and scotoma. The same day she developed 5 episodes of right focal seizures with secondary generalization, over a period of 3 hours and was referred to our hospital. Examination of the patient 2 hours after the last seizure revealed blood pressure of 210/140 mm Hg, pedal edema and normal temperature. She was stuporose and had bilateral papilloedema without any lateralizing deficits. She did not have any meningeal signs. Plain CT scan of the brain was normal. She had albuminuria and a uric acid level of 8.9mg%. Other renal parameters were normal. Baseline hematological investigations including platelet count and liver function tests were within normal limits. Cerebrospinal fluid study was not done, as we did not suspect infection or subarachnoid hemorrhage.
She was given a loading dose of intravenous diphenyl hydantoin and subsequently put on oral maintenance dose. She was initiated on nifedipine for control of blood pressure and subsequently switched over to amlodipine. She did not have any further episodes of seizures. She never had fever during the hospital stay. She was fully conscious and had no focal deficits 48 hours after the last seizure. She had mild headache and dimness of vision on and off, for the next 5 days. Magnetic resonance imaging with venography, done on the 5th day of seizure was within normal limits. An angiography was not done as suspicion of subarachnoid bleed was not high. At the time of discharge, 7 days after the onset of eclampsia, she did not have any symptoms or focal deficits and her blood pressure was controlled with amlodipine. Her papilloedema had started to resolve.
Pre-eclampsia is defined as the occurrence of hypertension along with proteinuria or edema or both, after 20 weeks of gestation. By definition, our patient had pre-eclampsia. The diagnosis of eclampsia was made in our case based on the clinical profile, biochemical findings, course of illness and negative radiographic findings. A CSF study would have further helped in ruling out infectious causes and subarachnoid hemorrhage, but was not done, as the clinical suspicion was not high. Her course in the hospital further supported this decision. A normal MRI scan with MR venography ruled out venous sinus thrombosis and other vascular/parenchymal structural causes (tumor, brain abscess, arteriovenous malformation). Biochemical investigations ruled out metabolic causes like hypoglycemia, hypocalcemia and water intoxication. By definition, she had late postpartum eclampsia as she developed the seizures on the 6th postpartum day.
Late postpartum eclampsia is a rare variant of eclampsia and has been recognized as a definite entity only recently.,,,, Late postpartum eclampsia occurring without preceding pre-eclampsia is even more rare. In the largest series published so far (54 patients over a period of 15 years), Lubarsky et al found that late postpartum eclampsia constitutes 56% of total postpartum eclampsia and 16% of all cases of eclampsia. Only 56% of patients had been identified as pre-eclamptic prior to the occurrence of seizures. One of the criticisms of this study is that the authors did not comment on whether signs of pre-eclampsia were truly absent or were not identified due to insufficient caretaker-attention during the postpartum period. There are also other case reports of late postpartum eclampsia occurring without any pre-eclampsia., Katz et al studied 53 pregnancies complicated by eclampsia and found that eclampsia was not a progression from severe pre-eclampsia. In his series, seizures were the first sign of pre-eclampsia in 60% of patients. In our case we are not clear of the time of onset of hypertension in the postpartum period as she was at home and was not regularly monitored.
The most important problem posed by this condition is the difficulty in diagnosing it at the right time. This being a rare entity, its awareness among treating physicians may be low. The patient may be subjected to unnecessary investigations, some of which may be costly and invasive, and proper treatment may get delayed.
At present there are no definite guidelines for early detection or prevention of late onset postpartum eclampsia in a patient without prior eclampsia. It has been found that these patients can have symptoms of brain edema (visual symptoms, headache) even when blood pressure remains normal. Atterbury et al, compared women who had no clinical evidence of pre-eclampsia at delivery, but who were later readmitted with postpartum severe pre-eclampsia or eclampsia with women who either remained normotensive or had severe pre-eclampsia or eclampsia at the time of delivery. They found that women in the study group had a significantly greater increase in the mean arterial pressure (MAP) after delivery than control subjects. Compared to women in the control group, mothers in the study group were significantly more likely to demonstrate an increase of more than 10 mm Hg in MAP between the intrapartum and postpartum periods. In another retrospective study, the same authors found that neurological complaints, malaise, nausea and vomiting were reported more often in women with postpartum pre-eclampsia than intrapartum pre-eclampsia. They also found that headaches were positively correlated with systolic, diastolic, and mean arterial blood pressures in women with postpartum pre-eclampsia although there was no relationship between blood pressure and headaches in the intrapartum pre-eclampsia group. In addition, multivariate analysis revealed that these patients were more likely to deliver at full term, have headaches and malaise, have normal platelet values, and develop seizures than mothers in the intrapartum group. Neurological complaints like visual symptoms and headache, which develop in the postpartum period have to be given due importance and followed up with frequent estimations of blood pressure and if necessary, with biochemical investigations, for early detection of pre-eclampsia, even in patients with uneventful pregnancy and delivery.
We conclude that late postpartum eclampsia is a definite clinical entity, which is increasingly detected. In many instances it can present without any pre-eclampsia. Since many of the patients develop neurological symptoms prior to the onset of pre-eclampsia/eclampsia, due attention to these symptoms and close follow-up can lead to early diagnosis. Lack of proper awareness and absence of a high degree of clinical suspicion may lead to unnecessary investigations and delay in proper management. This is particularly relevant in developing countries where eclampsia contributes to one-third of maternal mortality and the resources for extensive investigations and management are limited.
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