Fulminant cerebral edema in the setting of acute dengue fever after mechanical thrombectomy in a patient with massive stroke and severe hypoalbuminemia: a case report.

Background: Malignant cerebral edema following mechanical thrombectomy for large vessel occlusion stroke carries high mortality. While reperfusion injury and metabolic factors are established contributors, the potential role of concurrent systemic inflammatory stressors remains underrecognized. Case presentation: We present the case of a 61-year-old male with a history of nephrotic syndrome and severe hypoalbuminemia (14.8 g/L), who developed an extensive left middle cerebral artery infarction. At approximately 20 h after onset, worsening neurological deficits (NIHSS 9 → 16) prompted mechanical thrombectomy. At 4 h postoperatively, the patient developed an abrupt high fever (39 °C), prompting immediate diagnostic reassessment, which confirmed acute dengue fever (NS1 antigen-positive) and concurrent bacterial pneumonia. Simultaneously, laboratory tests revealed a systemic inflammatory response, with procalcitonin (PCT) peaking at 1.18 ng/mL and markedly elevated interleukin-6 (IL-6). Within the following 20 h, cerebral edema progressed rapidly, with midline shift increasing from 4 mm to 11 mm, consistent with malignant cerebral edema and impending brain herniation. Despite aggressive medical management, the family declined further decompressive surgery and intensive treatment; the patient was discharged against medical advice, and death was confirmed on follow-up. Conclusion: This report suggests that the fulminant cerebral edema observed in this patient may have been related to blood-brain barrier (BBB) vulnerability following ischemia-reperfusion injury, together with superimposed systemic inflammatory stress and markedly reduced oncotic buffering capacity. Acute dengue infection may have acted as a systemic endothelial and inflammatory stressor during the post-reperfusion vulnerable period, rather than as an independent primary cause. Severe hypoalbuminemia may have represented a baseline physiological susceptibility condition that reduced tolerance to fluid shift once BBB integrity was compromised.