Lactic acidosis, cyanide poisoning

Graham DL, Laman D, Theodore J, Robin ED Acute cyanide poisoning complicated by lactic acidosis and pulmonary edema. Arch Intern Med 137 1051-1055, 1977... 

Cellular hypoxia may occur in spite of adequate ventilation and oxygen administration when poisoning is due to cyanide, hydrogen sulfide, carbon monoxide, and other poisons that interfere with transport or utilization of oxygen. Such patients may not be cyanotic, but cellular hypoxia is evident by the development of tachycardia, hypotension, severe lactic acidosis, and signs of ischemia on the electrocardiogram. 

Baud FJ et al Value of lactic acidosis in the assessment of the severity of acute cyanide poisoning. Crit Care Med 2002 30(9) 2044-2050. [PMiD 12352039] (Ten-year retrospective anaiysis of 11 patients with CN poisoning. The median piasma iactate concentration was 168 mg/dL before antidotai therapy.)... 

A. Specific ieveis. Cyanide ieveis may be obtained but are not usually available rapidly enough to guide treatment when cyanide poisoning is suspected. Cyanide levels may not accurately reflect toxicity because of simultaneous production of methemoglobin, which binds some of the cyanide. Cyanide levels greater than 1 mg/L usually produce a demonstrable lactic acidosis. Thiocyanate levels higher than 50-100 mg/L may cause delirium and somnolence. 

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