Abstract
Background
Aluminum phosphide poisoning is a highly lethal toxicologic emergency classically dominated by cardiovascular collapse. Delayed ischemic stroke after apparent clinical stabilization is exceptionally rare and mechanistically uncertain.Case presentation
A 21-year-old previously healthy Ethiopian woman intentionally ingested five aluminum phosphide tablets. After early gastric lavage, she remained hemodynamically stable during the initial 24 hours and was discharged. Ten days after ingestion, she developed sudden right facial weakness, right hemiparesis, and mild dysarthria. On day 11, her National Institutes of Health Stroke Scale score was 11. Contrast-enhanced brain computed tomography demonstrated acute-to-subacute hypodensity in the left lentiform nucleus, caudate head, and anterior limb of the internal capsule. Non-dedicated post-contrast computed tomography showed visual luminal asymmetry/narrowing of the left middle cerebral artery compared with the contralateral side. Evaluation with electrocardiography, 72-hour continuous inpatient telemetry, transthoracic echocardiography with agitated saline study, carotid/vertebral Doppler ultrasonography, cerebrospinal fluid analysis including acid-fast bacilli testing and GeneXpert, human immunodeficiency virus testing, tuberculosis screening, antiphospholipid antibodies repeated at 12 weeks, thrombophilia testing, and autoimmune markers did not identify an alternative cause within the limits of available investigations. Cerebrospinal fluid culture for tuberculosis and other bacteria, computed tomography angiography/magnetic resonance angiography, transcranial Doppler, serial vascular imaging, and prolonged outpatient Holter monitoring were unavailable. She received aspirin, venous thromboembolism prophylaxis, later atorvastatin 80 mg orally once daily, and structured rehabilitation. The modified Rankin Scale score improved from 4 at the 30-day functional assessment to 2 at three and six months.Conclusions
This case describes delayed deep MCA-territory ischemic stroke temporally associated with aluminum phosphide ingestion. The observed computed tomography (CT) luminal asymmetry is hypothesis-generating only and cannot distinguish toxin-associated vasospasm/arteriopathy from reversible cerebral vasoconstriction syndrome, inflammatory vasculopathy, dissection-related disease, or pseudostenosis artifact. Clinicians should maintain vigilance for delayed focal neurologic deficits after aluminum phosphide exposure and pursue neuroimaging and etiologic evaluation, including dedicated vascular studies and follow-up vascular imaging where available.Key clinical message
Delayed focal ischemic stroke may occur after apparent clinical stabilization following aluminum phosphide ingestion, even without early hemodynamic collapse or structural heart disease. New lateralizing neurologic deficits after phosphide exposure should prompt urgent neuroimaging and structured young-stroke evaluation. In this case, the association with aluminum phosphide remains temporal and biologically plausible but not causal or mechanistically proven, because dedicated vascular imaging, serial angiography, and follow-up vascular imaging were unavailable.