Case Files of the University of Massachusetts Toxicology Fellowship: Does This Smoke Inhalation Victim Require Treatment with Cyanide Antidote?

Cyanide toxicity is common after significant smoke inhalation. Two cases are presented that provide framework for the discussion of epidemiology, pathogenesis, presenting signs and symptoms, and treatment options of inhalational cyanide poisoning. An evidence-based algorithm is proposed that utilizes point-of-care testing to help physicians identify patients who benefit most from antidotal therapy.

Disaster preparedness: Experience from a smoke inhalation mass casualty incident.

OBJECTIVE: We describe a modified triage system used in managing a smoke inhalation mass casualty incident that we recently encountered at our community hospital. MATERIALS AND METHODS: The patients were triaged as priority 1, 2 or 3 on the basis of their symptoms, signs and circumstances at scene. In addition, the use of fibre-optic examinations of the upper airway, chest radiography and carboxyhaemoglobin levels with arterial blood gas analyses were used to aid in disposal plans. RESULTS: Of the 22 patients evacuated, 15 were triaged as priority 2 and the remaining seven as priority 3. None of the patients was identified as priority 1. All the priority 2 patients underwent further investigations. Those with mild upper airway oedema (four patients) or raised carboxyhaemoglobin levels (two patients) were admitted. Only one patient had both. Another patient who was a known asthmatic developed bronchospasm and was admitted as well. All six were admitted to the general ward with subsequent good recovery and were discharged within 3 days. The remaining nine priority 2 and seven priority 3 patients were discharged from the emergency department. CONCLUSIONS: These modified triage criteria, with selective use of fibre-optic examinations, chest radiography and arterial blood gas analyses with carboxyhaemoglobin levels, are useful in smoke inhalation mass casualty incidents without dermal burns. Systemic injury and poisoning by toxic fumes often coexist with airway burns and should not be overlooked. Lastly, disaster planning and frequent drills at both local and national levels will optimize the response to future mass casualty incidents.

Assessment of erythrocyte cholinesterase activity in victims of smoke inhalation.

BACKGROUND: The nature of the toxic gases that cause death from smoke inhalation is incompletely understood, and the mechanisms leading to incapacitation remain to be determined. Thermal degradation products of various compounds, including phosphorous-based fire retardants, are suspected capable of impairing human cholinesterase activity. The aim of this study was to measure the erythrocyte cholinesterase activity in victims of smoke inhalation. METHODS: We prospectively measured the erythrocyte cholinesterase activity in blood samples obtained at the scene of residential fires from 49 fire victims. We compared the results with those in an unmatched group of 45 persons with acute drug poisoning. RESULTS: The median (25th-75th percentiles) erythrocyte cholinesterase activity in the 49 fire victims, 1968 IU/L (1660-2276), was significantly lower than in the 45 control subjects 2460 IU/mL (1968-2890), (p = 0.0004). There was no significant difference of the red blood cell counts or plasma protein levels between the 2 groups, while the hematocrit was significantly greater in the fire victims than in the drug-poisoned patients. There was a significant correlation between blood cyanide and carbon monoxide concentrations in the fire victims (r = 0.494, p = 0.002). There was no correlation between erythrocyte cholinesterase activity and either blood cyanide (r = 0.11, p = 0.44) or blood carbon monoxide concentrations (r = 0.04, p = 0.78). CONCLUSIONS: We found a significantly lower level of erythrocyte cholinesterase activity in victims of residential fires, when compared with a convenience sample of hospitalized poisoned patients. Despite the limitations of the study, investigations of the toxic gases potentially responsible for impairment of cholinesterase activity and the clinical significance of this lower enzymatic activity merit further investigation.