Tasers

The Taser is an electric control device (conducted energy weapon) using high voltage to the body to incapacitate people via neuromuscular disruption causing the incapacitation. Two darts or probes are discharged from the weapon, penetrating the skin of the target. There are wires attached to the darts extending out over 35 feet depending on the weapon. There is a pulsed current output delivered with the pressing of the weapon’s trigger. Skin lesions can be observed at the penetration site of the dart, and there are usually local burns at the contact sites. In studies done with Taser devices on canines, no cardiac arrhythmias were noted (Merck & Miller, 2013). In the author’s personal experience, usually one or both of the barbed darts are still in place when the animal is found, with focal areas of irritation or reddening.

Histology

Electric burns versus thermal burns can be differentiated. Electric burns have sharp borders with an abrupt transition from normal to injured tissue. There is a honeycomb vacuolization in the stratum corneum. There are subepidermal bullae due to the detachment of the epidermis from the dermis, denaturing of the dermal collagen and vaporized metal on the surface of the skin with high voltage. Computed tomography and light microscopy can assist with differentiating electric, flame burn, or abrasion type skin injuries (Merck & Miller, 2013).

Elevated creatinine kinase levels may be used as marker for cellular damage in humans, another indicator consistent with electrocution (Teodoreanu et al., 2014).

Smoke Inhalation

Acute pulmonary injury is caused by smoke inhalation. If asphyxia is not immediate, the combined chemical and heat effects cause widespread epithelial necrosis and exudation, and may result in death within a few days (Maxie, 2016; Wohlsein et al., 2016).

Smoke inhalation and internal thermal injury can result from a companion animal exposure to fire in either a structure or direct contact (set on fire). The cause of death when an animal is caught in a fire environment is carbon monoxide poisoning, smoke toxicity, thermal injury to the airways or the body, or any combination (Merck & Miller, 2013).

The oral cavity, nostrils, and upper and lower airways may contain soot in the event of smoke inhalation (Figure 12.6). The soot can be swallowed, resulting in the presence of flakes in the esophageal and stomach lining (Spitz, 2006). To avoid oral or laryngeal soot particles from descending into the lower airways and causing potential contamination, a ball of absorbent cotton can be used to obstruct (block) the upper airway and trachea while the pluck is removed for examination during a necropsy. Soot may be present in mucus and can be removed by using a scalpel or spatula and spread onto a clean white paper towel for documentation (Spitz, 2006). The absence of soot is not definitive for death prior to a fire related event (Maxie, 2016).

Microscopic findings in the lung parenchyma can assist in determining if the animal was alive or dead before and during a fire (Figure 12.7a-c). Histological signs in humans consist of bronchial dilation, ductal over-insufflation, alveolar insufflation, and alveolar hemorrhage (Merck & Miller, 2013). Additional thermal damage may be the result of an animal breathing in hot gases causing edema and/or burns discussed earlier. This results in destruction of tissue in the oral mucosa, nasopharynx, and generalized damage to the remaining respiratory tract (Merck & Miller, 2013).

Figures 12.6 (a) Mucosal lining of the vestibule (arrows) is multifocally discolored by deposited black pigmented material (soot), (b) The nasal turbinates are congested, (c) The dorsal tongue and entrance to the larynx is discolored with black pigmented material (soot), (d) Nearly diffusely, mucosal lining of the larynx, trachea, and bronchi are discolored by deposited black pigmented material (soot). Mild amounts of foam within the carina and the lungs, trachea, and laryngeal muscles are dark red. ([b-d] Photos courtesy Dr. J.D. Struthers.)

The resulting thermal injuries may cause laryngeal edema resulting in obstruction and suffocation (Saxon & Kirby, 1992; Wang et al., 2014). During the initial 24 hours post-injury, damage to the upper airway passages may cause an obstruction in this region (Tans, 1989). Severe laryngeal burns manifest as severe edema or atrophy, either or both of which may result in obstruction (Wang et al., 2014). The mucosal lining of the airways may slough into the lumen, potentiating more airway obstruction within 2-6 days of the initial injury (Saxon & Kirby, 1992) and hinder surfactant production (Juthowitz, 2005). The resulting luminal burn wounds may cause systemic inflammation or result in sepsis that can cause acute lung injury or acute respiratory distress syndrome (ARDS) (Juthowitz, 2005).

Smoke inhalation injury can occur alone or in combination with thermal or chemical injury. This can be most severe when the animal is discovered in an enclosed space or unconscious within a fire (Saxon & Kirby, 1992). Thermal injury is usually restricted to upper airways due to poor heat-carrying capacity of dry air and efficient heat dissipating capacity of an airway (Pope, 2003). Steam has exponentially higher heat carrying capacity of dry air and can cause severe destruction in the lower airways. Thermal damage in lower airways occurs in less than 5% of cases of inhalation injury (Pope, 2003).