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

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

• carbon monoxide poisoning
• delayed neurocognitive sequelae
• hyperbaric oxygen therapy
• white matter injury
• emergency medicine

Karbon Monoksit Zehirlenmesine Bağlı Gecikmiş Nörobilişsel Sekeller: Geç Başlatılan Hiperbarik Oksijen Tedavisi Sonrası İyileşme

Abstract

Giriş: Karbon monoksit (CO) zehirlenmesi, dünya genelinde en sık görülen kaza kaynaklı intoksikasyon nedenlerinden biridir ve hastaların üçte birine kadarında gecikmiş nörobilişsel sekeller (DNS) gelişebilir. Hiperbarik oksijen tedavisi (HBOT), akut olgular için yerleşik bir tedavi seçeneği olmasına rağmen, gecikmiş olgulardaki etkinliği belirsizliğini korumaktadır. Olgu Sunumu: Elli beş yaşında erkek bir inşaat işçisi, kapalı bir çadırda CO maruziyetinden üç hafta sonra ilerleyici bilişsel gerileme, görsel-mekânsal işlev bozukluğu ve yürüme güçlüğü geliştirdi. İlk karboksihemoglobin düzeyi %4,1 ve troponin I düzeyi 252 ng/L idi. Akut dönemde normobarik oksijen tedavisi almasına rağmen bilişsel durumu kötüleşti (MMSE: 18/30). Beyin MRG’sinde bazal ganglionlar korunmuş olmakla birlikte bilateral subkortikal beyaz cevherde hiperintensiteler saptandı; EEG’de yaygın yavaşlama izlendi. CO maruziyetinden 28 gün sonra, her biri 120 dakika süren 20 seanslık 2.4 ATA basınçta HBOT başlatıldı. Tedavi sonrasında hastada belirgin iyileşme gözlendi; MMSE 27/30’a yükseldi, saat çizim testi normalleşti, davranışsal semptomlar düzeldi ve normal yürüyüş yeniden sağlandı. Üç ve altı aylık takiplerde iyileşmenin devam ettiği, MRG’de beyaz cevher lezyonlarında kısmi düzelme olduğu görüldü. Hasta işine tam olarak dönebildi. Sonuç: HBOT, CO maruziyetinden haftalar sonra başlatılsa dahi DNS gelişen hastalarda anlamlı nörobilişsel iyileşme sağlayabilir. Acil hekimleri, CO zehirlenmesi sonrası gecikmiş bilişsel veya davranışsal bozulma ile başvuran hastalarda hiperbarik tedavi merkezlerine yönlendirmeyi göz önünde bulundurmalıdır.

Keywords

• karbon monoksit zehirlenmesi
• gecikmiş nörobilişsel sekeller
• hiperbarik oksijen tedavisi
• beyaz cevher hasarı
• acil tıp

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