B48-37 Malignant Right MCA Stroke With Refractory Cerebral Edema Despite Dual Hyperosmolar Therapy

Malignant MCA infarctions can cause rapid cerebral edema and increased intracranial pressure (ICP). While mannitol and hypertonic saline are both established ICP-lowering agents, current guidelines support the use of either agent alone. Evidence for combined (dual) hyperosmolar therapy remains limited, particularly in post-stroke patients. A 68-year-old male with uncontrolled type 2 diabetes mellitus, hypertension, and hyperlipidemia presented with acute left-sided weakness, dysarthria, and altered mentation. His NIH Stroke Scale score was 17. CT angiography showed a right MCA occlusion. He was outside the window for reperfusion therapy. He developed hypoxemic respiratory failure from aspiration pneumonia and was intubated and admitted to the ICU. Initial imaging showed no cerebral edema, but within 48 hours, repeat CT revealed a right-to-left midline shift of 3 mm. Hypertonic saline (3%) was initiated at 50 mL/hr with a target serum sodium of 150–160 mEq/L. After 24 hours, follow-up imaging showed progression of the midline shift to 8.5 mm. Mannitol 20% (1 g/kg every 6 hours) was added, with a goal osmolar gap < 15. This resulted in temporary improvement to a 6 mm midline shift. However, after an additional 24 hours, the shift increased again to 8 mm and remained stable for the rest of the hospital course. Despite radiographic worsening, the patient’s neurological exam remained stable and did not show signs of herniation. Given age and comorbidities, neurosurgery did not recommend decompressive hemicraniectomy. He was successfully extubated following pulmonary recovery; however, dysphagia remained, necessitated PEG placement. Given that patient had previously expressed that dependence on artificial feeding was not aligned with his goals of care, he was transitioned to comfort-focused management and passed away several days later. This case highlights the limited efficacy of dual hyperosmolar therapy in reversing cerebral edema in malignant MCA infarction. Despite radiographic progression, the absence of clinical deterioration raised complex decisions about aggressive intervention versus goal-concordant care. The case underscores the need for further research on ICP management strategies and the importance of integrating neurologic findings with patient values. This abstract is funded by: None