Postpartum Focal Seizure associated With Severe Progressive Hypotonic Hyponatremia and Pituitary Enlargement: A Care Case Report

Abstract

Background: New-onset seizure in the postpartum period is a neurological emergency in which eclampsia must be considered promptly, but vascular, structural, infectious, endocrine, and metabolic causes may produce an indistinguishable presentation. Severe hypotonic hyponatremia is a reversible seizure precipitant, whereas syndrome of inappropriate antidiuresis (SIAD) remains a diagnosis of exclusion. To our knowledge, the co-occurrence of a first-ever postpartum seizure, severe progressive hypotonic hyponatremia, MRI-documented pituitary enlargement, and an adrenal axis that could not be adequately characterized has rarely been reported together, and this combination, rather than a confirmed endocrine diagnosis, is what makes the present case instructive.

Case presentation: A 24-year-old gravida 3 para 3 woman developed a first focal convulsive seizure on postpartum day 8 after vaginal delivery. Serial investigations documented progressive hyponatremia from 142 mmol/L before delivery to a nadir of 112 mmol/L on postpartum day 11, measured serum osmolality 256 mOsm/kg, urine sodium 212 mmol/L, hypocalcemia to 6.3 mg/dL, and preserved renal function. The exact serum sodium at the moment of seizure was not recoverable from the available record. CT brain showed no acute intracranial abnormality. MRI demonstrated multifocal small bilateral subcortical parietal T2/FLAIR hyperintense lesions without diffusion restriction or susceptibility blooming and reported pituitary enlargement of approximately 10 x 11 mm. Clinical teams considered symptomatic hypotonic euvolemic hyponatremia and SIAD; however, urine osmolality was not documented, the timing of urine sodium relative to therapy was unclear, and a morning cortisol of 5.05 lacked a recorded unit or confirmatory adrenal-axis testing. Management included close monitoring, electrolyte correction, calcium supplementation, fluid restriction, increased oral salt intake, sodium valproate, and multidisciplinary review. The patient improved clinically and was referred for dedicated endocrine and pituitary assessment. The nadir sodium concentration was documented three days after the convulsive episode, and no time-stamped peri-ictal sodium, calcium, or urine osmolality value was retrievable; the seizure is therefore reported as associated with, and not attributed to, a serum sodium of 112 mmol/L.

Conclusion: Severe progressive hypotonic hyponatremia was a clinically important and potentially reversible contributor to this postpartum seizure presentation, but definitive attribution to SIAD cannot be made from the available data. The coexistence of pituitary enlargement and incompletely characterized adrenal function strengthens the need for structured endocrine follow-up. Postpartum seizures should be evaluated with parallel obstetric, metabolic, cerebrovascular, and endocrine pathways rather than being attributed to a single diagnosis prematurely. SIAD is consequently retained as a provisional, criteria-incomplete diagnosis, and postpartum eclampsia, posterior reversible encephalopathy syndrome (PRES), and cerebral venous sinus thrombosis (CVST) could not be completely excluded on the basis of the available record.