Acute hydrocephalus in carbon monoxide poisoning

Abstract

Carbon monoxide (CO) intoxication continues to be one of the most common causes of morbidity due to poisoning. The toxicity is caused by a combination of tissue hypoxia and direct CO‐mediated damage at the cellular level (1). Neurologic consequences of CO poisoning have been most often reported. Loss of consciousness, intermittent convulsions and respiratory failure may appear when carboxyhaemoglobin (COHb) concentrations of 60–80% are reached (2). However, it is important to recognize that COHb levels do not correlate with the severity of symptoms in a substantial number of cases (1). Pathological findings include necrosis and degeneration of the globus pallidus (3) and destructive lesions of the cerebral white matter (4). Computer tomography (CT) commonly shows bilateral low‐density areas in the globus pallidus (2–6) and low‐density lesions in the white matter (4). Magnetic resonance imaging (MRI) is more sensitive in detecting these lesions which appear as hyperintense signals in basal ganglia on T2 weighted images (4, 5). Neuropathological and radiological findings are well correlated (3).

Carbon Monoxide Brain Toxicity: Clinical, Magnetic Resonance Imaging, Magnetic Resonance Spectroscopy, and Neuropsychological Effects in 9 People

“…Although brain CT scans have shown evidence of brain swelling and/or hydrocephalus 19 subsequent to acute high-dose exposures, and brain MRI scans frequently show evidence of globus pallidus lesions as well as diffuse white matter lesions, these case studies indicate that such findings are not uniformly present. MRI scans are sometimes within normal limits despite clinical and neuropsychological evidence of intellectual impairment (eg, in SB and VB).…”