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Abstract
Introduction. Fenpyroximate is a potent inhibitor of the mitochondrial proton-translocating NADH-quinone oxidoreductase (complex I). Although it is widely used as an acaricide, data on the acute toxicity of fenpyroximate in humans are very limited. Case detail. A 44-year-old woman was brought to our hospital with a reduced level of consciousness, hypotension, and severe lactic acidosis after deliberate ingestion of 5% fenpyroximate solution. The acidosis progressively deteriorated despite maximal supportive treatment, and cardiac arrest refractory to standard cardiopulmonary resuscitation developed. The patient was successfully resuscitated with percutaneous cardiopulmonary support, therapeutic hypothermia, and intravenous acetylcysteine. Blood gases of simultaneously obtained arterial and central venous blood revealed decreased arteriovenous oxygen difference. Discussion. The present case, along with previous cases of fatal complex I inhibitor poisoning, indicates that impaired oxygen utilization at the tissue level is the major mechanism underlying the fatality of this condition. Percutaneous cardiopulmonary support may help restore vital organ perfusion by increasing oxygen delivery even in the presence of decreased oxygen consumption, thereby allowing additional time for recovery and drug metabolism. Therapeutic hypothermia also may be beneficial in treating severe complex I inhibitor poisoning, since hypothermia itself attenuates oxidative processes and decreases the metabolic rate.