Autopsy findings in CO deaths are fairly characteristic. In Caucasians, the first impression one gets on viewing the body is that the person looks very healthy. The pink complexion is caused by coloration of the tissue by car-boxyhemoglobin, which has a characteristic cherry-red or bright-pink appearance that can be seen in the tissue. Cherry-red livor mortis suggests the diagnosis even before autopsying the individual. It must be realized, however, that this color can be simulated by prolonged exposure of the body to a cold environment (either at the scene of death or in a morgue "cooler") or cyanide poisoning. With blacks, the discoloration is prominent in the conjunctivae, nailbeds, and mucosa of the lips.
Internally, the musculature and the internal viscera will have a bright cherry-red coloration. This coloration of the viscera will persist even if tissue is removed and placed in formaldehyde. Nor will embalming change the color of the viscera. Blood withdrawn from the vessels will also have this characteristic color. This is not invariable, however. One of the authors autopsied an individual with a carboxyhemoglobin level of 45% in whom the characteristic coloration was not present. He at first ascribed the cause of death to heart disease. The individual had such a "healthy complexion." However, the author's suspicions were aroused enough to order a carbon monoxide determination. Death had been caused by CO, produced by a defective heating unit in the residence.
While elevated CO levels are virtually the rule in house fires, there might be no elevation of CO in a death from a flash fire that occurs in an open environment. Individuals who die in motor vehicle accidents in which a gas tank explodes, theoretically might not show an elevated carbon monoxide. This latter occurrence is very rare, usually involving unusual circumstances.
In some individuals, death from carboxyhemoglobin poisoning is not immediate. In such cases, if production of the carbon monoxide ceases after the onset of irreversible coma, the individual will gradually eliminate the carbon monoxide from the body, even though irreversible injury has occurred. Thus, the authors have seen individuals who died from carboxy-hemoglobin poisoning register low or even negative carboxyhemoglobin levels at autopsy. Such a diagnosis is made on the basis of scene investigation. For example, a man is found dead in a parked car. The ignition is on and the gas tank is empty. An autopsy and complete toxicological analysis fail to reveal a cause of death. Examination of the car, however, reveals defects in the exhaust system such that high concentrations of CO built up in the car while it was running.
Carbon monoxide can pass from the maternal to the fetal blood. The carboxyhemoglobin (COHB) concentration of the fetus is dependent on the percent saturation of the mother's hemoglobin with CO. Saturation of fetal hemoglobin with CO lags behind saturation of the maternal hemoglobin because of the slow dissociation of maternal carboxyhemoglobin. After a time, however, equilibrium will be reached. The final COHB is 10% higher than maternal COHB.19 Carbon monoxide can produce intrauterine death of the infant even though the mother may survive.
The brain is the organ most sensitive to the actions of carbon monoxide. Brain damage is characteristically localized to certain selective areas. If death does not occur immediately, the injury to these areas may increase over hours and days. Carbon monoxide produces selective injury to the cerebral gray matter. Bilateral necrosis of the globus pallidus is the most characteristic lesion, though other affected areas include the cerebral cortex, hippocampus, cerebellum, and substantia nigra. The lesions in the globus pallidus, however, are nonspecific and can be seen in drug overdoses as well.
Neurological sequelae caused by CO poisoning can develop during the acute phase of poisoning or post exposure after a period ranging from days to weeks without overt symptoms.20-23 In this situation, after an asymptomatic interval, the patient can develop severe headache, fever, nuchal rigidity, and neuropsychiatric symptoms. Transitory cortical blindness and memory defects are common. In addition, there can be aphasia, apathy, disorientation, hallucinations, incontinence, slow movements, and muscular rigidity. The permanent sequelae of CO intoxication include dementia, amnestic syndromes, psychosis, paralysis, chorea, cortical blindness, peripheral neuropathy, and incontinence. In a study by Choi, 11.8% of individuals requiring hospitalization for carbon monoxide poisoning exhibited delayed neurological deterioration.22 Virtually all demonstrated mental deterioration, with the majority having incontinence and gait disturbances. The median age of the individuals showing delayed deterioration was older than that of the hospitalized group as a whole. A lucid interval of 2-4 weeks commonly preceded the onset of the neurological sequelae. Three-quarters of the patients recovered within a year, though some showed persistent mild neurological injury. There were no clinical signs at the time of admission that would permit the physician to deduce which patients would incur the delayed neurological injury.
It has been demonstrated that some cells, for example, CAI pyramidal cells in the hippocampus, may resume their functioning after exposure to the carbon monoxide only to die days later.23 It has been hypothesized that this delayed injury is caused by post ischemic re-perfusion injury and the effects of CO on vascular endothelium and oxygen radical mediated brain oxygen re-oxygenation.
The delayed neurological syndrome in carbon monoxide intoxication is associated with lesions of the cerebral white matter.21 These lesions are nonspecific, however, and are found in other conditions associated with hypoxia and hypotension. It appears that a combination of hypotension and hypoxia is necessary to produce these lesions.
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