Chapter XXXVII - Carbon Monoxide Poisoning (excerpts)
"Devoid of Colour, smell, and taste, carbon monoxide (CO) is under ordinary circumstances found mixed with other gases; varying amounts are present in the fumes of blast furnaces, blasting discharges, charcoal stoves, coke ovens; a product of coal combustion, it forms one of the constituents of coal gas, illuminating gas, producer gas, water gas, and the dreaded after-damp of colliery explosions. It is no doubt responsible for much of the chronic ill-health of those whose work brings them into contact herewith when used for power, cooking, or heating purposes; as the source of danger from running exhausts in motor garages, it has achieved notoriety as a means of affecting a comfortable suicide.
On inspiration the gas displaces the oxygen of oxyhaemoglobin and quickly forms stable compound carboxyhaemoglobin, recognizable through the spectroscope by two absorption bands between the D and E lines (yellow and green). This imparts to the blood a bright pink or cherry-red colour, yet the fluid, incapable of yielding its oxygen to the tissues, becomes valueless for internal respiration and the subject dies in asphyxia. To this anoxaemia is commonly ascribed the extremely serious nature of the poisoning, but the pathogenesis is in reality more complex (see below).
Literature. - The distinctive features of coal gas poisoning have been known for many years. Klebs and Poelchen were among the first to investigate its pathology, and Haldane its physiology. The monograph of Sibelius (1906) has 200 references; a bibliography down to 1921 is given by Ruge. Cf. reviews by Sachs, Lewin, LeDosseur, etc.: additional references in text.
Symptomatology. - A general division into acute and chronic types has some clinical worth. Under the former are included cases in which exposure is followed by nausea, 'tightness' or 'fullness' in the head, neuralgia, vertigo, weakness, and - with continuing effect - faintness, somnolence, insensibility, and coma. Loss of sphincter control, twitching, and convulsions have been reported (Scott). According to McNally, the blood must be saturated to the amount of 30-50% for the more serious of the foregoing symptoms to appear, and to 50-60% for coma and fits. In garages where the air is contaminated to the extent of 0.2% almost all the workers suffer from headache (Krannenburg). Toxaemia of the more chronic kind induces this persistent headache, as well as giddiness, physical enfeeblement, impaired mental power and at times a psychosis. When sufficiently prolonged and severe, the intoxication damages neural structure and is followed by various symptoms - palsies, anaesthesias, choreiform movements, tremors, dysarthria, syndromes recalling multiple sclerosis, Landry's paralysis, neuritis, on the one hand; confusional states, mania, affective disturbance and hallucinations on the other. Almost any symptom from highest to lowest level may be expected; spastic quadriplegia, astasia-abasia, and speech disorder, catatonia, myositis, double personality, atrophic palsy, Korsakoff psychosis, may be chosen to exemplify the latitude of range. Recovery from the acute phase may be followed by days or weeks of seeming health ere one or other of these residua is observed; relapsing cases also occur. Despite frequent lesions of lenticular nuclei, however, it is curious how seldom a pure striatal syndrome is seen.
Pathology - Lesions have been recorded in almost every part of the nervous system, and are mostly diffuse. At an early stage nerve cells show acute swelling and eventual chromatolysis; some changes are ischaemic in character, others sclerotic. Local softening may ensue, or patches of 'bleaching'. Acute swelling of oligodendroglia is also found, and of microglia on occasion. Later, degeneration of parenchyma is more obvious, with irregular necrosis, and reaction on the part of microglia in the shape of macrophagic overgrowth. The endothelium of capillaries, precapillaries, and small vessels swells and may be shed, with a tendency to occlusion from endarteritis; perivascular and intramural infiltrates are frequently seen, but these are not 'inflammatory' so much as toxic or 'symptomatic'. Such lesions can develop locally or be spread more or less evenly over wide areas. Two special types of incidence should be noted.
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