Smoke poisoning

Systemic and local effect: Smoke inhalation causes systemic and local, main ly respiratory, toxicity due to the asphyxiant and irritant properties of t oxic gases. Oxygen deprivation and intoxication: The syndrome of oxygen deprivation and intoxication by asphyxiant gases is caused by combustion-induced oxygen de privation and exposure to carbon monoxide (CO) and cyanide (CN), but also t o other toxic gases. A loss of consciousness is a good sign of systemic tox icity; however, the respective role of CO, CN and other toxic gases cannot be determined. The presence of apnea, lactic acidosis, and severe cardiovas cular disturbances is consistent with CN poisoning. A correlation exists be tween blood CO concentration determined on a sample obtained at the site of the fire, and the occurrence and severity of the clinical disorders. Irritant gases intoxication: This syndrome explains the mucosal injury affe cting the eyes and the lungs. These complications are better diagnosed by c linical examination rather than by various investigations such as chest X-r ay of fiberoptic bronchoscopy. Dysphonia is always a sign of severe poisoni ng. Clinical course: In non-burned victims, delayed neurological and respirator y complications can be observed. Oxygen administration is the cornerstone s upportive therapy. Hyperbaric oxygen should be discussed according to the s everity of the syndrome of oxygen deprivation and intoxication by asphyxian t gases. In case of cyanide poisoning, a safe and effective antidote should be given; hydroxocobalamine seems to be the drug of choice. Supportive tre atment is efficient to treat respiratory failure. Endotracheal intubation s hould be considered in patients exhibiting early dysphonia associated with dyspnea.