Not all bodies in a fire end up charred and disfigured. Some show no evidence of injury at all, while others demonstrate only searing burns. In the latter instance, the skin is a light brown color with a stiff leathery consistency
(Figure 13.2). Blisters may also be present. Blisters do not necessarily indicate that the deceased was alive at the time the burns were incurred, since they can be produced postmortem. A mistaken impression exists that an erythematous rim surrounding blisters or burns indicates that the individual was alive at the time they were incurred (Figure 13.7). This is incorrect. Blisters with a red rim have been produced on dead bodies. Heat applied to the skin causes contraction of dermal capillaries forcing liquid blood to the periphery of the blister or burn, simulating an antemortem hyperemic inflammatory response.
For the victim of a fire whose body shows no or minimum evidence of thermal injuries, the cause of death is often attributed to "smoke inhalation."
This is often used synonymously with carbon monoxide poisoning (intoxication). Examination of individuals overcome by smoke inhalation will usually reveal soot in the nostrils and mouth as well as coating the larynx, trachea, and bronchi (Figure 13.8). Absence of soot, however, does not necessarily mean that the individual was dead prior to the start of the fire. The authors have seen numerous cases in which there was no soot in the larynx or trachea, yet analysis of blood for carbon monoxide revealed lethal levels.
At autopsy, it is usually relatively easy to determine whether the individual died of carbon monoxide intoxication. The livor mortis, the muscles, and internal organs, as well as the blood, will have a cherry-red coloration. In spite of this coloration, a carbon monoxide determination on the blood is mandatory. The cherry-red coloration can be produced by other factors (e.g., cyanide). A cherry-red coloration to livor mortis is very common in bodies exposed to cold for long periods of time. In addition, an individual could have a fatal carbon monoxide level, yet a prominent cherry-red color be absent.
Attributing the cause of death in smoke inhalation cases to carbon monoxide intoxication is a simplification of a complicated process. The actual mechanism of death in individuals dying of smoke inhalation is not always clear. In individuals who die during fires, actual carbon monoxide levels, while toxic, are often insufficiently high to have caused death. These levels are characteristically 20% lower than in deaths caused by inhalation of carbon monoxide exhaust fumes. Thus, in the authors' experience, in individuals whose deaths are caused by inhalation of automobile exhaust, the average carbon monoxide level is 79%, with 82% of cases having levels of 70% or greater. In fires, the average carbon monoxide concentration is 57%, with carbon monoxide levels of 30 or 40% common, and with some levels in the 20% range. In some instances, this is aided by underlying disease. Thus, an individual with severe coronary atherosclerosis could die at lower carbon monoxide levels than a healthy individual. In other cases, drugs or alcohol can act as contributory factors.
A number of factors other than carbon monoxide have been suggested as causing death in smoke inhalation cases. These are oxygen deprivation, cyanide, free radicals, and nonspecified toxic substances. Oxygen deprivation caused by the fire's consumption of oxygen is not realistic as a causation of death in house fires. If there were insufficient oxygen to maintain life, the fire would go out.
Cyanide is produced in the burning of many common synthetic substances. It may, in a few rare instances, be a contributory cause of death, but to ascribe most or even many deaths to cyanide poisoning is a mistake. Cyanide as a cause of death in fires is a favorite theory of attorneys in cases of civil litigation. They picture the deceased as having been rapidly overcome and succumbing to a cloud of cyanide produced by burning synthetics. In fact, the amount of cyanide produced in fires is relatively small, with actual concentrations in real-life situations very low. Even in closed rooms with the introduction of pure gaseous cyanide in high concentrations, as occurred in the Nazi death chambers, incapacitation is not necessarily immediate and death may not occur for a number of minutes.
The detection and quantitation of cyanide in the blood is beset with difficulty. Cyanide can be produced postmortem in blood in both the body or a test tube, through the process of decomposition. In addition, if the method of analysis is not absolutely specific, other substances in the blood (sulfides) can react like cyanide, giving falsely elevated levels of cyanide.4 One extensively quoted study ascribing numerous deaths to cyanide is suspect because of its methodology.5 Free radicals have been proposed as one possibility in causing death, because they can inactivate surfactants, thus preventing oxygen from crossing the alveoli into the blood.6
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