Delayed Neurocognitive Sequelae of Carbon Monoxide Poisoning: Recovery Following Late-Initiated Hyperbaric Oxygen Therapy

Authors : Hakan Şilek, Yunus Diler, Serdar Özdemir

Pages : 41-46

Doi:10.55994/ejcc.1816679

View : 35 | Download : 166

Publication Date : 2025-12-31

Article Type : Other Papers

Abstract :Background: Carbon monoxide (CO) poisoning is a leading cause of accidental intoxication worldwide, with delayed neurocognitive sequelae (DNS) occurring in up to one-third of survivors. While hyperbaric oxygen therapy (HBOT) is established for acute presentations, its role in delayed cases remains uncertain. Case Presentation: A 55-year-old male construction worker developed progressive cognitive decline, visuospatial dysfunction, and gait disturbance three weeks after CO exposure in an enclosed tent. Initial carboxyhemoglobin was 4.1% and troponin I was 252 ng/L. Despite normobaric oxygen during the acute phase, he deteriorated with severe cognitive impairment (MMSE 18/30). Brain MRI revealed bilateral subcortical white matter hyperintensities with sparing of the basal ganglia, while EEG showed diffuse slowing. HBOT was initiated 28 days post-exposure consisting of 20 sessions at 2.4 ATA for 120 minutes each. After HBOT, the patient showed marked improvement with MMSE rising to 27/30, normalization of clock drawing, resolution of behavioral symptoms, and restoration of normal gait. At three- and six-months follow-up, recovery was sustained and MRI demonstrated partial resolution of white matter lesions. The patient returned to full employment. Conclusion: HBOT may offer meaningful neurocognitive recovery even when initiated weeks after CO exposure in patients with DNS. Emergency physicians should consider referral to hyperbaric centers for patients presenting with delayed cognitive or behavioral decline following CO poisoning.
Keywords : karbon monoksit zehirlenmesi, gecikmiş nörobilişsel sekeller, hiperbarik oksijen tedavisi, beyaz cevher hasarı, acil tıp

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