Carbon Monoxide
Carbon monoxide (CO) is a poisonous, colorless, odorless gas that is lighter than air, arising from incomplete combustion of hydrogen carbon fuels (Carson, 1986). Due to its significant binding affinity for hemoglobin (210-240 times that of oxygen), CO displaces oxygen from hemoglobin,
Figure 12.7 (a) Photomicrograph of the trachea, 40x objective. Surface epithelium is overlaid by deposited granular black pigmented material (soot), (b) Photomicrograph 20x objective. The surface epithelium of a respiratory bronchiole and spilling into alveolar ducts contains deposited granular black pigmented material (soot) (arrows). The airway interstitium and vessel adventitia contain nodules of macrophage-associated inhaled and retained inorganic dusts (circled). Pneumoconiosis = inhalation and retention of inorganic dusts + anthracosis = inhalation and retention of carbon, (c) Photomicrograph 60x objective. An alveolus contains deposited granular black pigmented material (soot) that is intimately surrounded by intra-alveolar macrophages, some of which have intracytoplasmic phagocytose material (circled), ([a-c] Photos and interpretation, courtesy Dr. J.D. Struthers.)
causing tissue hypoxia (Pope, 2003). The carbon monoxide binds to hemoglobin (carboxyhemoglobin [COHb]), inhibiting its ability to carry oxygen. This shifts the oxygen-hemoglobin dissociation curve to the left, additionally reducing oxygen delivery to the tissue (Pope, 2003) (Merck & Miller, 2013). Increased COHb levels cause cherry-red or pink discoloration to the skin or in areas of lividity (Merck & Miller, 2013). Carbon monoxide levels as high as 8% have been measured experimentally in controlled house fires (Pope, 2003). COHb levels greater than 40% can cause irreversible nervous system damage. COHb levels greater than 60% may be fatal (Pope, 2003). In addition, the direct effects of CO may cause pulmonary injury, reducing normal reflex decrease in breathing when heated air is inhaled (Pope, 2003). Death can occur rapidly with sudden high levels. This may result from cardiac arrest due to cardiac dysfunction occurring before CNS effects (Merck & Miller, 2013). With CO toxicity, the necropsy exam findings may consist of dilated bronchi and distension of the major blood vessels. The ventricles of the heart can be dilated, specifically the right ventricle resulting from a sudden increase in central venous pressure sometimes observed with CO toxicity (Carson, 1986; Merck & Miller, 2013). Brain changes are observed related to anoxia consisting of necrosis in white matter of the cerebral hemispheres, globus pallidus, brain stem, and cortex. Edema, demyelination, and hemorrhage in the brain and necrosis in the hippocampus may occur (Carson, 1986; Merck & Miller, 2013).
Testing for levels of CO is important in corroborating antemortem versus postmortem findings. Venous blood should be obtained and transported immediately on ice (Merck & Miller, 2013). The COHb levels will need to be run at a human laboratory. In the event the animal is alive, COHb levels will decrease over time, further increasing the importance of testing levels of COHb as soon as possible for documentation (Merck & Miller, 2013).
Cyanide Poisoning in Fires
The most common cause of death in fires is the inhalation of noxious gasses rather than thermal injury. Hydrogen cyanide gas, potentially the most toxic of combustion gasses, is seldom recognized as an important hazard in smoke inhalation (Jones et al., 1987). Sources of cyanide toxicity are the use of synthetic polymers in building materials and furnishings (Jones et al., 1987). Cyanide disrupts the ability of the cells to use oxygen by binding with and inhibiting cellular respiratory enzyme mitochondrial cytochrome oxidase (Merck & Miller, 2013). It primarily affects the heart and the brain. An animal’s body may appear pink or cherry-red, corresponding to CO poisoning, caused by fully oxygenated blood due to the tissues’ inability to extract oxygen from the blood (Merck & Miller, 2013). The victim may become cyanotic. Diagnostic testing for cyanide gas poisoning may be difficult. Decomposition of the body causes cyanide production in the blood, falsely increasing the levels. Other substances in blood such as sulfides can react similarly to cyanide, falsely elevating levels (DiMaio & DiMaio, 2001; Merck & Miller, 2013). Consideration for cyanide levels should be given; however, there have been human cases where death occurred before COHb could be formed (Gerling et al., 2001).
Examining the Animal Fire Victim
Before examination of the patient, considerations should be given to the crime scene and what occurred there. The animal body should be photographed and examined in place if possible, to define the circumstances of the body as it relates to the crime scene. Evidence as to the origin of the fire may be found on the animal’s body, i.e., odors from an accelerant and the accelerant used. Evidence from the body should be collected. Consider discussing these considerations with a law enforcement crime scene analyst or local forensic laboratories. For example, samples of fur with an accelerant would need to be placed in an airtight paint can to be sent to a laboratory for analysis (Merck & Miller, 2013). Use whole-body radiographs to rule out antemortem trauma including fractures or projectiles. Extreme heat from a fire may cause fracturing of the bone (Merck & Miller, 2013).
A surviving animal victim’s fur will smell like smoke. In addition to any external thermal burns that may be observed, there may be burns within the oral cavity and the upper and lower airways. Evaluate the patient for laryngeal spasms. Injury to the airways can consist of edema, mucosal erythema, ulceration, hemorrhage, and soot particle accumulation (Merck & Miller, 2013). Carbon monoxide poisoning may be demonstrated as cherry-red skin and mucous membranes. Eye injuries, including corneal abrasions and conjunctivitis, may be observed. Tracheal aspirate cytological exams in moderate to severe cases can reveal burned ciliated cells, strands of mucus, and soot particles (Carson, 1986).
