IX Международная студенческая научная конференция Студенческий научный форум - 2017

Carbon monoxide (CO) is a tasteless and odourless gas produced by incomplete combustion. Poisoning may occur from car exhausts, fi res and faulty gas heaters. CO is also produced by metabolism of methylene chloride (used in paint strippers and as an industrial solvent). CO the O2-carrying capacity of the blood by binding haemoglobin (Hb) to form carboxyhaemoglobin (COHb). This impairs O2 delivery from blood to the tissues and inhibits cytochrome oxidase, blocking O2 utilization. These effects combine to cause severe tissue hypoxia. The elimination half-life of CO is about 4hr on breathing air, 1hr on 100 % O2, and 23min on O2 at 3 atmospheres pressure. Clinical features: Early features are headache, malaise, nausea and vomiting (sometimes misdiagnosed as a viral illness or gastroenteritis, especially if several members of a family are affected). In severe poisoning, there is coma with hyperventilation, hypotension, muscle tone, reflexes, extensor plantars and convulsions. Cherry-red colouring of the skin may be seen in fatal CO poisoning, but is rare in live patients. Skin blisters and rhabdomyolysis may occur after prolonged immobility. Pulmonary oedema, MI and cerebral oedema can occur. Neurological and psychiatric problems sometimes develop some weeks after CO poisoning, but usually improve over the following year. Management: Remove from exposure. Clear the airway and maintain ventilation with as high a concentration of O2 as possible. For a conscious patient use a tight-fitting mask with an O2 reservoir, but if unconscious intubate and provide IPPV on 100 %O 2. Record ECG and monitor heart rhythm: look for arrhythmias and signs of acute MI. Check ABG — SpO2 measurements are misleading in CO poisoning, as are paO2 values, but acidosis indicates tissue hypoxia. Check COHb levels (in blood or with a special pulse oximeter): although these correlate poorly with clinical features, COHb > 15 % after arrival at hospital suggests serious poisoning. COHb may be up to 8 %in smokers without CO poisoning. A nomogram can help to estimate COHb at the time of exposure. Correct metabolic acidosis by ventilation and O2: try to avoid bicarbonate, which may worsen tissue hypoxia. Consider mannitol if cerebral oedema is suspected. Hyperbaric O2 therapy is logical, but of no proven benefit for CO poisoning. Transfer to a hyperbaric chamber and pressurization may take hours and so hyperbaric treatment may be no more effective than ventilation on 100 % normobaric O2. Caring for a critically ill patient in a small pressure chamber may be impracticable. Discuss with a Poisons Information Service and consider hyperbaric treatment if a patient has been unconscious at any time, has COHb > 20 %, is pregnant, or has cardiac complications or neurological or psychiatric features. The Poisons Information Service can advise on the location and telephone numbers of hyperbaric chambers.

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