General description

Carbon monoxide (CO) poisoning, also known as CO intoxication, results from exposure to CO, primarily produced by the incomplete combustion of carbon-containing substances. CO binds to hemoglobin with an affinity 230-300 times greater than oxygen, forming carboxyhemoglobin (COHb) and obstructing oxygen transport, leading to anemic hypoxia. This binding also shifts the oxyhemoglobin dissociation curve to the left, reducing both oxygen transport capacity and release to peripheral tissues. CO further binds to other heme-containing proteins, such as myoglobin in the heart and skeletal muscles, which, along with differences in elimination rates between blood and tissue, can cause delayed tissue injury.

In the brain, CO exhibits tissue toxicity by binding to iron-rich areas, particularly in regions like the globus pallidus and substantia nigra. Acute CO poisoning can present with symptoms ranging from mild headaches, dizziness, and nausea to severe outcomes like loss of consciousness, seizures, respiratory muscle paralysis, and even death. Symptoms vary based on CO concentration and exposure duration, with higher exposures leading to rapid progression to coma and potentially fatal outcomes. Chronic exposure may present with mild symptoms resembling influenza, such as headache, dizziness, weakness, and confusion, which complicates timely diagnosis.

CO poisoning is categorized into two clinical courses: non-intermittent and intermittent. In the non-intermittent type, after recovery from the initial consciousness disturbance, patients may continue to exhibit neuropsychiatric symptoms, including delirium, amnesia, apathy, parkinsonian symptoms, aphasia, agnosia, apraxia, and Gerstmann syndrome. The intermittent type, also called delayed neuropsychiatric sequelae, is characterized by an asymptomatic period lasting days to weeks after recovery from acute symptoms, followed by a sudden onset of disorientation, memory loss, and consciousness disturbances.

Radiographic features

Acute phase

MRI shows bilateral T2WI and FLAIR hyperintensity in the globus pallidus and substantia nigra, often accompanied by diffusion restriction. MRI also shows diffuse T2WI and FLAIR hyperintensity in the cerebral white matter.

Delayed phase

MRI shows bilateral T2WI and FLAIR hyperintensity in the semiovale and periventricular white matter.