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

Year 2025, Volume: 7 Issue: 3, 41 - 46, 31.12.2025

Hakan Şilek , Yunus Diler , Serdar Özdemir

https://doi.org/10.55994/ejcc.1816679

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

References

• Sircar K, Clower J, Shin MK, et al. Carbon monoxide poisoning deaths in the United States, 1999-2012. Am J Emerg Med. 2015;33(9):1140-5. doi:10.1016/j.ajem.2015.05.034.
• Iqbal S, Clower JH, Hernandez SA, et al. A review of disaster-related carbon monoxide poisoning: surveillance, epidemiology, and opportunities for prevention. Am J Public Health. 2012;102(10):1957-63. doi:10.2105/AJPH.2012.300674.
• Prockop LD, Chichkova RI. Carbon monoxide intoxication: an updated review. J Neurol Sci. 2007;262(1-2):122-30. doi:10.1016/j.jns.2007.06.037.
• Thom SR. Carbon monoxide pathophysiology and treatment. Toxicol Lett. 2019;303:1-11. doi:10.1016/j.toxlet.2018.11.002.
• Özdemir S, Altunok İ, Eroğlu SE Relationship between carbon monoxide poisoning, lactate and cardiac marker. Van Med J. 2019;26(3):285-288. doi:10.5505/vtd.2019.24993.
• Choi IS. Delayed neurologic sequelae in carbon monoxide intoxication. Arch Neurol. 1983;40(7):433-5. doi:10.1001/archneur.1983.04050070051010.
• Sert ET, Kokulu K, Mutlu H. Clinical predictors of delayed neurological sequelae in charcoal-burning carbon monoxide poisoning. Am J Emerg Med. 2021 Oct;48:12-17. doi: 10.1016/j.ajem.2021.04.001.
• Yesildag K, Kokulu K, Mutlu H, et al. Argyrophilic nucleolar organizer regions as a promising biomarker for the detection of brain hypoxia levels caused by different doses of carbon monoxide poisoning. Gac Med Mex. 2021;157(6):610-617.
• Kokulu K, Mutlu H, Sert ET. Serum netrin-1 levels at presentation and delayed neurological sequelae in unintentional carbon monoxide poisoning. Clin Toxicol (Phila). 2020 Dec;58(12):1313-1319. doi: 10.1080/15563650.2020.1743302.
• Thom SR. Functional inhibition of leukocyte β2 integrins by hyperbaric oxygen in carbon monoxide-mediated brain injury in rats. Toxicol Appl Pharmacol. 1993;123(2):248-56. doi:10.1006/taap.1993.1241.
• Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. 2002;347(14):1057-67. doi:10.1056/NEJMoa013121.
• Raphael JC, Elkharrat D, Jars-Guincestre MC, et al. Trial of normobaric and hyperbaric oxygen for acute carbon monoxide intoxication. Lancet. 1989;2(8660):414-9. doi:10.1016/S0140-6736(89)90530-3.
• Scheinkestel CD, Bailey M, Myles PS, et al. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial. Med J Aust. 1999;170(5):203-10. doi:10.5694/j.1326-5377.1999.tb127996.x.
• Piantadosi CA. Diagnosis and treatment of carbon monoxide poisoning. Respir Care Clin N Am. 1999;5(2):183-202.
• Thom SR. Hyperbaric oxygen: its mechanisms and efficacy. Plast Reconstr Surg. 2011;127 Suppl 1:131S-41S. doi:10.1097/PRS.0b013e3181fbe2bf.
• O'Donnell P, Buxton PJ, Pitkin A, et al. The magnetic resonance imaging appearances of the brain in acute carbon monoxide poisoning. Clin Radiol. 2000;55(4):273-80. doi:10.1053/crad.1999.0353.
• Katafuchi T, Takehara S, Takahashi M, et al. MR imaging of carbon monoxide intoxication encephalopathy: relationship between clinical symptoms and MR findings. Radiat Med. 1991;9(6):225-9.
• Silverman CS, Brenner J, Murtagh FR. Hemorrhagic necrosis and vascular injury in carbon monoxide poisoning: MR demonstration. AJNR Am J Neuroradiol. 1993;14(1):168-70.
• Gorman D, Clayton D, Gilligan JE, et al. A longitudinal study of 100 consecutive admissions for carbon monoxide poisoning to the Royal Adelaide Hospital. Anaesth Intensive Care. 1992;20(3):311-6. doi:10.1177/0310057X9202000310.
• Annane D, Chadda K, Gajdos P, et al. Hyperbaric oxygen therapy for acute domestic carbon monoxide poisoning: two randomized controlled trials. Intensive Care Med. 2011;37(3):486-92. doi:10.1007/s00134-010-2086-9.
• Hopkins RO, Weaver LK. The cognitive effects of hyperbaric oxygen therapy in carbon monoxide poisoning. Neurosci Biobehav Rev. 2009;33(6):790-5. doi:10.1016/j.neubiorev.2009.01.006.
• Buckley NA, Juurlink DN, Isbister G, et al. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev. 2011;(4):CD002041. doi:10.1002/14651858.CD002041.pub3.
• Weaver LK. Hyperbaric oxygen therapy for carbon monoxide poisoning. Undersea Hyperb Med. 2014;41(4):339-54.
• Lin CH, Su WH, Chen YC, et al. Treatment with normobaric or hyperbaric oxygen and its effect on neuropsychometric dysfunction after carbon monoxide poisoning: a systematic review and meta-analysis. Medicine (Baltimore). 2018;97(39):e12456. doi:10.1097/MD.0000000000012456.
• Özdemir S, Akça HŞ. Evaluation of Clinical Symptoms in Carbon Monoxide Poisoning with Biochemical Parameters. Kocaeli Med J. 2022;11(2):35-37. doi:10.5505/ktd.2022.46656
• Jain KK. Textbook of Hyperbaric Medicine. 6th ed. New York: Springer; 2017.
• Özdemir S, Alper B, Alp H, et al. Carbon Monoxide Poisoning and Sequels of Cardiac Function. Phnx Med J. 2022;4(2):94-5.
• Gagnier JJ, Kienle G, Altman DG, et al. The CARE guidelines: consensus-based clinical case reporting guideline development. Glob Adv Health Med. 2013;2(5):38-43. doi:10.7453/gahmj.2013.008.
• Rose JJ, Wang L, Xu Q, et al. Carbon monoxide poisoning: pathogenesis, management, and future directions of therapy. Am J Respir Crit Care Med. 2017;195(5):596-606. doi:10.1164/rccm.201606-1275CI.