Cyanide Poisoning
Cyanide is a highly lethal poison that may be ingested, inhaled or absorbed through the skin. Although it is quite rare to have significant cyanide exposure, it may found in common settings, including but not limited to: workplace exposure, mining, jewelry production, combustion of wool, silk, plastics, household products, vehicles, and cigarettes among others. Cyanide prevents oxygen utilization by blocking the cytochrome oxidase a3 enzyme, which is needed to perform aerobic respiration; ultimately, this leads to a functional hypoxia where the body has adequate levels of oxygen that it is unable to use, and consequently a metabolic acidosis. Not only does cyanide cause brain damage by the anoxic-ischemic encephalopathy, but it increases oxygen free radicals, apoptosis, and may increase the risk of seizures.
The timing and severity of symptoms vary based on route of administration, the dose of cyanide and the length of exposure. Symptoms may include: headache, anxiety, confusion, coma, seizures, cardiac arrhythmias, cardiac arrest, respiratory arrest, vomiting, abdominal pain and red venous blood among others. Individuals that survive a significant dose of cyanide poising may go on to develop movement disorders like parkinsonism, or other neurologic symptoms. Chronic cyanide exposure may result in headache, taste abnormalities, vomiting, chest pain and anxiety among others.
On imaging, acute cyanide poisoning will most commonly show a bilateral involvement of the basal ganglia, namely the striatum and the cerebral cortex, as they have a high oxygen demand. In this setting, hemorrhagic necrosis of the basal ganglia and pseudolaminar necrosis along the cerebral cortex may be seen. On T1-weighted MRI, a high signal intensity is expected in the cortex due to pseudolaminar necrosis, but may also be due to presence of a hemorrhage. Contrast enhancement is typically seen on T1 C+ (Gd), and on diffusion-weighted imaging, an increased diffusion signal may be seen in the affected areas. On T2/FLAIR imaging, hyperintensities are seen in the affected areas, and become increasingly apparent in the subsequent weeks. It should be noted in severe cases, that the damage may be more generalized, and edema may be present. Chronically, it may take months to years for the signal hyperintensities to decrease in the affected areas.
References:
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