Abstracts

Rationale: Multiple complications with subdural grid electrode implantation have been reported in the literature including infection, subdural hematoma and cerebral edema.In the pediatric population this procedure is typically well tolerated and aggressive coverage is typically recommended to avoid repeated surgeries. Hyponatremia and the syndrome of inappropriate antidiuretic hormone (SIADH) alone or in combination with a transient neurological deficit have not been described in the literature as a complication of this procedure in the pediatric or adult population.Methods: We present a retrospective case series of pediatric patients who developed hyponatremia and transient focal neurologic deficits in the setting of subdural electrodes grid & strips implantation for epilepsy surgery.Results: We had 4 children (3 F, 1 M), ages 11-17 yo with focal onset refractory epilepsy. Pathology showed cortical dysplasia (2), tuberous sclerosis (1) & reactive astrocytosis (1). 3 patients had subdural grids & strips (128 electrodes in all cases) over the left hemisphere and one over the right. Three out of four patients developed hyponatremia with serum Na levels between 123-130mEq/L. Clinically 2 patients developed acute aphasia & 1 sudden dense left arm monoplegia. The fourth patient did not develop a true hyponatremia however did have a sudden drop in serum Na from 144 to 135mEq/L over 3.5 hours. This child developed dysarthria & right arm weakness & was found to have cerebral edema upon prompt grid removal. All patients experienced the hyponatremia and the focal deficits between days 2-4 postoperatively. All patients underwent head CT, 2 also had Brain MRI with no evidence of ischemia or hemorrhage. Hyponatremia fluctuated for 6-10 days in 3/4 patients requiring correction. The most common cause of the low sodium was SIADH. After removal of the subdural electrodes the various focal deficits resolved without sequela. Despite the perioperative complications all patients proceeded to resective surgery of the seizure focus and are currently doing well from an epilepsy standpoint.Conclusions: Hyponatremia has been described as a complication of intracranial disorders. In the setting of subdural grid and strips the presence of an acute focal neurological deficit would raise the concern for cerebral bleed, ischemia, focal status, infection or edema. Hyponatremia in this setting has not been well recognized. We present 4 cases in which focal neurological deficits are associated with low or rapid drop in serum Na levels. Based on this it may be beneficial to more frequently monitor serum Na levels on postop day 2-4. Typically hyponatremia results in a diffuse cerebral manifestation such as altered mental status. In our patients the focal manifestation of low Na were likely due to compression of the underlying swollen cerebral cortex by the subdural electrode itself. This is the first pediatric case series reported to describe the focal manisfestation of hyponatremia and the complete recovery in this setting.