Mass Foodborne Poisoning Incidents: Clinical and Screening Laboratory Data May Differentiate Cyanide from Arsenic Poisoning
Alan H. Hall, MD, FACEP
Editor-in-Chief, Toxicology and Environmental Health, Micromedex, Inc., Englewood, Colorado USA
Senior Consultant, Rocky Mountain Poison and Drug Center, and Clinical Assistant Professor of Preventive Medicine and Biometrics, University of Colorado Health Sciences Center, Denver, Colorado USA

On 25 July 1998, 100 persons ate curry and rice at a festival in Wakayama, Japan. Four persons died and about 75 persons became ill. Cyanide poisoning originally was the suspected cause, but the final diagnosis was deliberate arsenic contamination. Acute arsenic and cyanide poisoning have similar non-specific, clinical effects, including mouth and throat irritation or burning, nausea, vomiting, central nervous system (CNS) depression, muscle spasms, and seizures. Diarrhea is common with arsenic, but rare with cyanide. Cyanide poisoning causes anxiety, agitation, hyperpnea, hyperventilation, giddiness, headache, and mild hypertension, which are rare with arsenic poisoning. Screening laboratory tests aid in suspicion of acute cyanide poisoning: serum electrolytes (anion gap >12-16 mmol/L), plasma lactate levels (>1 mmol/L), decreased arterial pH (often severe), relatively normal PaO2 and SaO2 saturation with elevated peripheral venous pO2 (>40 mmHg) or SaO2 saturation (>70%).

Arsenic ingestion produces a "garlic-like" breath odor that is easy to recognize. Cyanide produces a "musty" or "bitter almonds" breath odor that many persons cannot recognize. The cause of death in acute arsenic poisoning most often is hypovolemia from "third-spacing" of fluids and gastro-intestinal bleeding with hypotension and cardiovascular collapse. Administration of potent vasodilating amyl and sodium nitrite cyanide antidotes may be dangerous especially in this setting. Chelators are used to treat acute arsenic poisoning, but survival is determined mainly by supportive measures (volume repletion, transfusion). Late sequellae of arsenic poisoning include peripheral polyneuropathy and bone marrow depression with anemia, leukopenia, and pancytopenia, while a Parkinsonian-like condition is the major sequella of severe acute cyanide poisoning. Pancytopenia in the survivors from the Wakayama event led to the diagnosis of arsenic poisoning.

References:

1. Hall AH: Arsenic and arsine. In: Clinical Management of Poisoning and Drug Overdose, Haddad LM, Shannon MW, Winchester JF (Eds), 3rd ed. WB Saunders Company, Philadelphia, PA, 1998, pp 784-789.
2. Hall AH, Remake BH: Cyanide and related compounds, In: Clinical Management of Poisoning and Drug Overdose, Hatted LM, Shannon MW, Winchester JF (Eds), 3rd ed., WB Saunders Company, Philadelphia, PA, 1998, pp 899-905.
3. Hall AH: Systemic asphyxiants, In: Irwin & Rippe's Intensive Care Medicine, Irwin RS et al (Eds), 4th ed. Lippincott-Raven Publishers, Philadelphia, PA, 1999, pp 1797-1806.

Keywords: arsenic; cyanide; laboratory studies; poisoning; signs, clinical
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