Frontiers in medicine · 2026
Acute severe carbon monoxide poisoning followed by recurrent cerebral infarction: a case report.
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Han Xinyuan, Liu Zehua
Аннотация
BACKGROUND: Carbon monoxide (CO) poisoning can lead to various neurological complications; however, recurrent cerebral infarction as a clinical manifestation is rarely reported.
CASE PRESENTATION: We report a case of a previously healthy 13-year-old girl who was admitted to the intensive care unit (ICU) with coma following acute severe CO poisoning (carboxyhemoglobin level 46%). She received multi-organ function monitoring and life support in the ICU. After hyperbaric oxygen therapy, her consciousness initially recovered. However, on day 5 post-intoxication, she acutely developed somnolence and right-sided hemiparesis and was readmitted to the ICU. Neuroimaging revealed acute cerebral infarction in the left basal ganglia region accompanied by severe stenosis of the left M1 segment of the middle cerebral artery (MCA). Although the affected vessel showed recanalization after comprehensive treatment, a follow-up MRI on day 19 unexpectedly identified a new acute infarction in the left cerebral peduncle. A systematic workup revealed no evidence of definite embolic sources. After 8 weeks of comprehensive treatment and rehabilitation, she was discharged with improved motor function (right limb strength graded 4/5 on the Medical Research Council [MRC] scale) but residual anterograde amnesia and personality changes.
CONCLUSION: This case presents a rare clinical course of recurrent cerebral infarction following acute severe CO poisoning, highlighting that even with early symptomatic improvement, vigilance for delayed cerebrovascular events and long-term neurofunctional and neuropsychological follow-up are essential.
CASE PRESENTATION: We report a case of a previously healthy 13-year-old girl who was admitted to the intensive care unit (ICU) with coma following acute severe CO poisoning (carboxyhemoglobin level 46%). She received multi-organ function monitoring and life support in the ICU. After hyperbaric oxygen therapy, her consciousness initially recovered. However, on day 5 post-intoxication, she acutely developed somnolence and right-sided hemiparesis and was readmitted to the ICU. Neuroimaging revealed acute cerebral infarction in the left basal ganglia region accompanied by severe stenosis of the left M1 segment of the middle cerebral artery (MCA). Although the affected vessel showed recanalization after comprehensive treatment, a follow-up MRI on day 19 unexpectedly identified a new acute infarction in the left cerebral peduncle. A systematic workup revealed no evidence of definite embolic sources. After 8 weeks of comprehensive treatment and rehabilitation, she was discharged with improved motor function (right limb strength graded 4/5 on the Medical Research Council [MRC] scale) but residual anterograde amnesia and personality changes.
CONCLUSION: This case presents a rare clinical course of recurrent cerebral infarction following acute severe CO poisoning, highlighting that even with early symptomatic improvement, vigilance for delayed cerebrovascular events and long-term neurofunctional and neuropsychological follow-up are essential.