Page 676 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Toxic Gases and Vapors Chapter | 48 641

VetBooks.ir matter (which may be superheated), and superheated air signs are related to progressive pulmonary decline and
acute respiratory distress.
(Lee-Chiong, 1999; Alarie, 2002; Enkhbaatar and Traber,
2004; Fitzgerald et al., 2006; Lee and Mellins, 2006;
Schnepp, 2006; Sicoutris and Holmes, 2006; Stefanidou
et al., 2008). Thus, the syndrome results from a combina- Diagnostic Testing
tion of thermal, gas, and particle effects. Smoke inhala- Bronchoscopy is the definitive diagnostic procedure. Clinical
tion always involves some degree of CO and cyanide chemistry may indicate metabolic acidosis resulting from a
poisoning. Combustion of plastics, polyurethane, wool, combination of hypoxia, CO poisoning, CN poisoning, and
silk, nylon, nitriles, rubber, and paper leads to the produc- methemoglobinemia. Elevated serum lactate is a relatively
tion of cyanide gas. Other combustion products may sensitive indication of cyanide poisoning. Patients may have
include acrolein and other reactive aldehydes (organic lowered blood cholinesterases because the pyrolysis products
combustion) and also chlorine, ammonia, ketones, hydro- of many phosphorus-based fire retardants are anticholines-
carbons, and various acids (combustion of rubber and terases. Pulse oximetry may provide misleading information
plastics). due to the presence of COHb and methemoglobinemia. If
available, pulse cooximetry is preferable.
Chest radiographs are common normal after smoke
Toxic Dose
inhalation, and the diagnostic accuracy of the technique is
The toxic dose depends on the source. low. Chest computerized tomography (CCT) is a prefera-
ble imaging technique. CCT abnormalities include
Pathophysiology ground-glass opacities in a peribronchial distribution and/
or patchy peribronchial consolidations. Such abnormal
Thermal damage primarily occurs in the upper respiratory
CCT findings may be present within a few hours follow-
tract, particularly in the oropharyngeal area, due to the poor
ing smoke inhalation. Pulmonary function tests are sensi-
heat conductivity of air and high dissipation of heat in the
tive indicators of smoke inhalation injury, but they are
upper airways (Clark et al., 1989, 1990; Clark, 1992; Lee-
rarely readily available in veterinary practice.
Chiong, 1999; Alarie, 2002; Enkhbaatar and Traber, 2004;
Fitzgerald et al., 2006; Lee and Mellins, 2006; Schnepp,
2006; Sicoutris and Holmes, 2006; Stefanidou et al., 2008). Treatment
Both pulmonary irritation and systemic effects occur.
The immediate treatment priority is the prompt removal
Systemic effects occur primarily due to direct and chemical
of the patient from the source of exposure. Rescuers need
asphyxiation. Chemical asphyxiation most commonly
to take great care not to become casualties in such cir-
occurs as a result of a combination of CO and cyanide (CN)
cumstances. The next treatment priority is the administra-
poisoning. Methemoglobinemia occurs due to direct heat
tion of 100% oxygen, resuscitation, and maintenance of
denaturation of hemoglobin, as well as the inhalation of
airway patency (Clark et al., 1989, 1990; Clark, 1992).
nitrites.
Unfortunately, there is no specific treatment for the
tissue damage and increased risk of infection associated
Vulnerable Populations with smoke inhalation. Studies in humans have indicated
Individuals with preexisting lung disease, reactive air- that positive pressure ventilation with low tidal volumes
way syndromes, and/or asthma are at significantly (3 5 mL/kg) and positive end-expiratory pressure may
greater risk. increase short-term survival (Cancio, 2009). High-
frequency percussive ventilation, whole-body hypother-
mia, and hyperbaric oxygen may also decrease mortality
Clinical Presentation (Reper et al., 1998; Thom et al., 2001). Unfortunately,
Any individual with facial burns is likely also to have none of these techniques are readily available in veteri-
concurrent smoke inhalation injury. Individuals who no nary medicine. Induction of methemoglobinemia for the
longer have eyelashes are very likely to have concurrent treatment of CN poisoning may be dangerous if signifi-
ocular injury. Common early clinical signs of respiratory cant CO poisoning is also present. However, the use of
tract injury include hoarseness and a change in voice, car- hydroxocobalamin (Cyanokit) in combination with low-
bonaceous nasal discharge or sputum, coughing, tachyp- dose sodium thiosulfate as a CN antidote may be consid-
nea, and use of accessory respiratory muscles (Clark ered (Borron et al., 2007a,b). Bronchodilator therapy is
et al., 1989, 1990; Clark, 1992; Lee-Chiong, 1999; Alarie, almost always indicated in cases of smoke inhalation.
2002; Enkhbaatar and Traber, 2004; Fitzgerald and Flood, Patients with significant smoke inhalation commonly
2006; Lee and Millens, 2006; Schnepp, 2006; Sicoutris require concurrent treatment for burns, a subject that is
and Holmes, 2006; Stefanidou et al., 2008). Later clinical beyond the scope of this chapter.