Mitochondrial toxicity and arterialization of venous blood

Abstract

Mitochondrial toxicity causes dysoxia, or abnormal tissue oxygen utilization. To maintain energy production, cells are forced to switch to the less efficient anaerobic metabolism that ultimately leads to cell death, multi-organ dysfunction, and death. Cyanide is one of the most common mitochondrial toxicants. Ingestion is usually oral in the form of salts, with autolytic intent, and diagnosis is difficult due to the low clinical suspicion and availability of diagnostic tests.

The clinical picture is highly variable depending on the amount ingested, although from a physiopathological point of view, it causes a hyperlactacidemic metabolic acidosis that can lead to multi-organ dysfunction. Treatment is merely supportive, although various antidotes can be administered.

We present a patient brought to the hospital for decreased level of consciousness and distributive shock of unclear etiology. As there were signs of poor oxygen consumption, the main diagnostic suspicion was poisoning by a mitochondrial toxicant, likely cyanide. After administration of hydroxocobalamin, oxygen consumption improved. However, multiorgan dysfunction could not be reversed and the patient ultimately died.