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>There is some evidence that CO exposure also kills through direct brain >damage rather than simply converting carboxyhemoglobin. There is further >evidence that high CO exposure (at 1 ATA) can cause brain damage, >personality changes, long term confusion, onset of which symptoms can be >delayed up to about one month after exposure. This is true. It was neatly demonstrated by Goldbaum & co-workers in 1975 in experiments on dogs. They partially exsanguinated five dogs, removing 68% of their circulating volume and replacing it with packed cells from donors that had been exposed to CO and had 80% carboxyhaemoglobin levels. Following transfusion the recipient dogs had carboxyhaemoglobin levels between 52% and 64%, a level normally associated with severe symptoms of CO poisoning. None of the recipient dogs showed any ill effects, and further work suggested that CO is a cellular toxin possibly acting on the cytochrome enzyme system. Other research suggests that tissue hypoxia is an important contributor (CO is almost harmless under conditions of high tissue oxygenation) and time of exposure is also relevant (prolonged exposure to lower levels are relatively more damaging than short exposures to higher levels of CO). The delayed onset (also called a latent interval) of neurological symptoms of CO poisoning is classically 14-21 days; the patient, having been discharged from hospital, represents with neuropsychiatric symptoms. It is rare in persons under 30. Dr Andrew Pitkin apitkin@ci*.co*.co*.uk* "There's always slack somewhere" (Houdini)
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