Vitality of the Body Was the Victim Dead Prior to or During the Fire

The lethality of fires involves different mechanisms: reduction of environmental O2, an increase in CO and other toxic gases, inhalational injury owing to smoke and heat, extreme heat and shock, burns, other types of trauma (e.g., blunt injuries sustained in an attempt at escape), and exacerbation of disease (32,37,52). In rare cases, impairment of breathing by tightening of the thorax or neck owing to heat effects has been proposed (52). Heat and toxic fumes are main causes of death during a fire (49).

Temperatures higher than 150°C (300°F) cause loss of consciousness or death within several minutes (32). Higher temperatures cause immediate death (32). A flashover or explosion can engulf a victim (4,32). Rapid death means that a victim inhales little, if any, combustion and pyrolysis products. Smoke- or heat-induced laryngospasm,

Fig. 15. Burn artifact. (A) Charred ends of bones (heat fractures). (B) Amputation of lower extremities due to heat fractures. (Courtesy of Dr. E. Tweedie, London Health Sciences Centre, London, Ontario, Canada.)

respiratory arrest, and/or a vagal reflex-caused cardiac arrest are proposed mechanisms of rapid death during a fire (42,52).

Within a minute, smoke causes incapacitation as a result of coughing, eye irritation, reduced visibility, and disorientation (4,33,37). An unimpaired individual usually attempts to extinguish the fire, warn others, and escape, but this is hindered by the effects of the smoke (4,33,37). Spreading smoke forms a hot layer at ceiling level and then descends rapidly (37). The smoke is relatively low in O2 and if the O2 level is below 7%, then incapacitation occurs rapidly (see Chapter 3, Subheading 3.10. and ref. 37). If

Fig. 16. Artifactual hole through calvarium of a charred skull. A radiograph showed no projectile. Internal examination did not reveal craniocerebral trauma.
Fig. 17. Charred bodies. (A) Epidural "hematoma" seen on removal of the calvarium. (Courtesy of the Office of the Chief Medical Examiner, Chapel Hill, NC.) (B) Bilateral epidural "hematoma" on undersurface of removed calvarium.

the individual crawls along the floor, the effects of smoke are delayed (37). Suffocation is expected when the O2 concentration falls to 10%, but levels in fires usually are not below 15%. At this point, a fire smolders (49,52). If there is flame evident, there is usually enough O2 for individuals to breathe (42).

Away from the fire, heat effects and O2 depletion are less important (37,53). The initial generation of carbon dioxide in a fire stimulates respiration, increasing the inhalation of other toxic gases (32). Inhalation of these gases, particularly CO, causes death (33,37). The amount of CO produced in a fire is variable, ranging from 0.1 to 10% in the fire atmosphere (see Chapter 3, Subheading 3.9.1., and refs 4 and 33). At high concentrations, death occurs quickly (33). At lower concentrations, victims can be active (33). CO can cause strange behavior (e.g., running back into the fire to save an imagined victim; hiding in a closet, under a bed; or in a bathtub [4]). Increased CO is inhaled when respiratory efforts increase during physical exertion (see Chapter 3, Subheading 3.9. and ref. 33). The higher O2 demands created by exertion can cause death at a lower carboxyhemoglobin (COHb) saturation than in subjects at rest (31). Mental and muscular performance deteriorate at a COHb of 30%, and fainting can occur (see Chapter 3, Table 4; and ref. 37). Victims can continue to inhale CO even when they are incapacitated (33).

Low levels of CO in victims away from the origin of the fire raises the possibility of inhalation of other toxic gases (37,54). COHb levels are generally higher in nonfire deaths, suggesting that other toxic factors play a role in fires (see Chapter 3, Subheading 3.9.4.; and ref. 37). Cyanide (CN) causes more rapid incapacitation than CO (33,37). Its rapid absorption and respiratory depressant effect may limit CO uptake (37). CN is generated from burning materials containing nitrogen compounds (e.g., polyurethane in vinyl, wool, nylon, urea formaldehyde [4,37]). Toxicity results from the inhibition of oxidation of reduced cytochrome a3 in the mitochondrial respiratory chain (55). CN stimulates breathing, which increases inhalation of other toxic gases (30). Various studies have shown no synergistic additive effects of CO and CN (30,37,55-58). In one study, there was no indication that certain cofactors—CO, alcohol, age, and heart disease—affect the level of CN reached in the blood of the victim (57). In many fire deaths, CO is in the fatal range and CN is not at toxic levels, indicating that CO poisoning is the more important cause in most fire deaths (58,59). CN causes incapacitation at blood concentrations in the range of 50 ¡imol/L (57). In certain situations (e.g., burning of nitrogen-containing plastics), CN in the range of 100 pmol/L is life-threatening and victims have relatively low COHb levels (57,58). Levels of CN ranging from 1 to 3 mmol/L (1000-3000 ¡imol/L) are lethal (37). If the burning materials contain fluorine, chlorine, or bromine (e.g., polyvinyl chloride, flame retardants), their respective hydrogen gases are released. The corrosive effects of these gases damage the respiratory mucosa and lead to delayed effects (37). Other irritants (formaldehyde, acrolein) are also generated (31). Generation of highly reactive free radicals leads to diffuse alveolar damage (33).

A victim's level of consciousness and ability to escape are affected by drugs and alcohol (4,37). Although intoxication by alcohol or drugs is thought by some to have a synergistic effect with CO, impairment of the ability to escape and to assist others is more likely (see Chapter 3, Subheading 3.9.4.; and refs. 4 and 59-62). In one study, victims found dead in bed and, presumably having made no attempt to escape, had a mean blood ethanol level of 268 mg/dL compared with an average of 88 mg/dL in victims found near an exit (59). Studies of fatal fires showed that one-third to one-half of deceased individuals have ingested alcohol (7,62-65).

The observations of increased CO (COHb > 10%) and other noxious gases in the blood, and soot in the mouth, upper respiratory ("smoke inhalation"), and gastrointestinal (GI) tracts are indicators that an individual was alive during the fire (Fig. 18; refs. 4 and 52).

Fig. 18. Victim alive during fire. (A) Soot in larynx and trachea (smoke inhalation). (B) Microscopic section, mainstem bronchus. Soot on sloughed respiratory epithelium (H&E, original magnification x100).

A COHb level of 50% or more is considered a cause of death, but an uncritical, rigid adherence to the requirement that fire victims have high COHb concentrations can be misleading (see Chapter 3, Subheading 3.9.4.; and refs. 37 and 66). The majority of fire victims who are dead at the scene show some combination of smoke inhalation, elevated COHb levels (>10%), and swallowing of soot. The latter tends to be less frequent (about one-third of cases in one study [42]). In another study, soot was found in the respiratory tract in about three-fourths of fire victims, in the upper GI tract in about half the cases, and COHb concentrations were above 10% in about two-thirds of deaths (52). Soot in the GI tract occurred in combination with soot aspiration (52). Many victims with elevated COHb also have aspirated soot; however, in some, these findings are not found in combination (42,52,67).

In one study, fire victims had a lethal level of COHb but no respiratory soot (65). Half these deaths were in smoldering fires and, in one, an accelerant had been used (65). Absence of smoke inhalation has been observed in some smoldering fires (42,68). Although soot can be absent and COHb levels low in some suicides by fire, the latter is elevated in most cases. Many are not "flash" fires which are associated with low COHb levels (69). Lower levels of COHb are seen in suicide victims found outdoors (17,18). Individuals found in vehicles tend to have higher COHb saturations (17,18). Soot is seen in cases having slightly elevated COHb (70). This pattern was observed in elderly, helpless individuals whose clothes caught fire (52).

Fig. 19. Motor vehicle collision and fire. Froth in mouth (arrow)—a sign of pulmonary edema and an antemortem reaction in this charred body. Cause of death: craniocerebral trauma, carboxyhemoglobin less than 10%.

Charring of the anterior dentition does not imply that the victim's lips were voluntarily open at the time of the fire (71). The presence of copious mucus in the airway indicates vitality during the fire, even in the absence of an increased COHb (49). Pulmonary edema, arising from irritation by smoke, causes foam to be expressed from the nostrils and mouth, indicating that the individual was breathing at the time of the fire (Fig. 19; ref. 47). In some fire deaths, aspiration of fire extinguisher material or foreign material occurs (72).

Other possible indicators of vitality during a fire include absence of burns and/or soot deposits in the corners of the eyes ("crow's feet") and incompletely singed eye-

Fig. 20. Inhalation injury. Red mucosa of epiglottis caused by congestion. Soot in airway. (See Companion CD for color version of this figure.)

lashes, suggestive of squinting or closing of the eyes owing to smoke irritation; detachment of the mucosa of the tracheobronchial tree, pharynx, epiglottis, or esophagus; and epiglottic swelling (see Subheading 4.5. and ref. 52). Air is a poor conductor of heat, and thermal injury is usually limited to the upper airways. Pulmonary damage arises from inhalation of smoke and fumes (49). In one review, heat damage to the upper airway or esophagus was present in about half of cases, some of which had soot deposition (Figs. 20 and 21; ref. 52). Conjunctival and neck muscle hemorrhages have been considered vital reactions in burn victims (73). Hemorrhage in the root of the tongue has been observed in fatal burns, particularly in victims with lower blood CoHb concentrations

Fig. 21. Inhalation injury. (A) Tongue erosions. (B) Unopened larynx-trachea. Erosion (arrow) of aryepiglottic folds owing to thermal injury. (Courtesy of Dr. C. Armstrong, London Health Sciences Centre, London, Ontario, Canada.)

(<30%), and the role of cranial congestion from thermal-induced neck or chest pressure has been raised (74). There is no relation between the degree of postmortem tongue protrusion and the amount of soot in the airway (74).

Fig. 22. Death prior to fire. No evidence of smoke inhalation and negligible carboxy-hemoglobin. Pinned during dismantling of boxcar. Collapsed boxcar wall lifted from body. Burning due to acetylene torch used by worker. Torn subclavian artery seen at autopsy.

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