Case Presentation:

A 57 year old man with no significant medical or psychiatric history was admitted to our hospital after a suicide attempt. He was found unconscious in his car with the ignition running in a closed garage. His carboxyhemoglobin level was elevated at 13%. He regained consciousness within a few hours without requiring intubation or hyperbaric oxygen. After medical stabilization, he was no longer suicidal and discharged home.

About 2 weeks later, he developed severe memory impairment and strange behavior. Symptoms rapidly progressed and he became completely mute, unable to feed himself or follow any commands. His evaluation included electrolytes, TSH, B12 level, syphilis, drug screening, Carboxyhenoglobin level, MRI of the brain, EEG, CSF analysis, all of which were unremarkable. CT head showed diffuse periventricular white matter loss. After multiple subspecialist consultations, his symptoms were attributed to delayed sequelae of CO poisoning. Ultimately, this resulted in placement of a gastric tube prior to being discharged to a skilled facility.


Carbon Monoxide (CO) poisoning is the leading cause of unintentional poisoning deaths in the United States. Although most cases are unintentional, the incidence of CO-related suicide is rising. Among survivors of the initial exposure, up to 40% of patients may develop delayed neuropsychiatric syndrome (DNS), a disease entity characterized by variable degree of mental deterioration, mutism, and retropulsion. Morbidity from these symptoms can begin as early as 20 days and may last up to one year or longer.  Pathogenesis is unclear but oxidative stress from cellular uptake of CO, causing release of excitatory amino acid neurotransmitters is thought to play a role.

Due to the poor pathophysiologic understanding of DNS, treatment is not well established.  Some authors suggest using hyperbaric oxygen therapy (HBO) in all patients with CO intoxication to prevent development of DNS. If HBO is used, its benefit is greatest if treatment begins within six hours of initial CO exposure. Some case reports have also shown positive response from Ziprasidone therapy.  Results from these therapies however continue to be variable; and, lack of efficacious therapies have been associated with poor neurologic outcomes.


Despite being reversible, DNS remains a debilitating entity. All survivors of CO poisoning should be followed closely and monitored for development of DNS. More studies are needed to understand development of DNS. A better understanding of pathogenesis may lead to preventive and treatment modalities hence improving outcome.