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Neurological Rehabilitation

Late Onset Neuropsychiatric Encephalopathy Despite Hyperbaric Oxygen Treatment in Carbon Monoxide Poisoning: A Couple’s Case Report

Friday, October 24, 2025
12:00 PM - 1:30 PM MT
Location: Kiosk 7
Has Audio

    Primary Author(s)

  • Michael Reimer, MD

    Resident Physician
    University of Michigan Health System PM&R Program
    Ann Arbor, Michigan

    • Poster Presenter(s)

  • William Naber, DO

    Resident Physician
    University of Michigan Health System PM&R Program
    Ann Arbor, Michigan

    • Co-Author(s)

  • SK

    Sabrina Kasha, Other

    Fellow
    University of Michigan Health System PM&R Program
    Ann Arbor, Michigan

Disclosure(s):
Michael Reimer, MD: No financial relationships to disclose
William Naber, DO: No financial relationships to disclose
Case Diagnosis: An 83-year-old male and 74-year-old female with history of carbon monoxide (CO) poisoning

Case Description or Program Description: Two geriatric patients were found by emergency services after unintentional CO exposure. Upon emergency room arrival, carboxyhemoglobin (COHb) levels were confirmed at toxic saturation levels of 35% (male) and 30% (female) saturation. Both required intubation and received emergent hyperbaric oxygen treatment. Subsequently, both patients were admitted to inpatient rehabilitation (IPR) for non-traumatic brain injury secondary to CO poisoning. On admission to IPR, both patients were fully oriented and making significant cognitive improvements. During the second week of IPR the female experienced a precipitous cognitive decline followed by the male 2 months post-IPR with the development of neuropsychiatric symptoms including psychosis, movement disorders and dementia. Thorough workup for both patients deemed CO poisoning sequelae as the most likely cause. Neither patient has recovered to prior cognitive baseline.

Setting: Community Hospital and Inpatient Rehabilitation Hospital

Assessment/Results: Despite early and aggressive hyperbaric oxygen treatment, both patients experienced late onset neuropsychiatric encephalopathy secondary to CO poisoning.

Discussion (relevance): CO poisoning occurs from the accumulation of carbon monoxide in the blood with associated disruption of oxygen molecules binding capacity to hemoglobin due to CO’s higher binding affinity. The lack of oxygen binding and subsequent transport to tissues can damage organs and be fatal. To address CO poisoning and associated cognitive effects, standard treatment is aggressive hyperbaric oxygen to displace CO from the bloodstream. Delayed neuropsychiatric symptoms are uncommon and may occur weeks to months later; its mechanism is incompletely understood.

Conclusions: Early and aggressive hyperbaric oxygen administration can yield short term cognitive improvements but did not prevent remote neuropsychiatric sequelae for these patients. This case raises awareness of the possible delayed cognitive complications of carbon monoxide poisoning despite standard of care treatment.