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Smoke Inhalation
PART XVIII ENVIRONMENTAL EMERGENCIES CHAPTER 147 SMOKE INHALATION Shailen Jasani,
MA, VetMB, MRCVS, DACVECC
KEY POINTS • The relative lack of clinical veterinary information on smoke inhalation likely reflects a very high incidence of preadmission mortality. Hypoxia from carbon monoxide poisoning is presumed to be the most common cause of immediate death. • Direct thermal injury to the upper respiratory tract can cause laryngeal obstruction. Lower respiratory tract injury from irritant gases and superheated particulate matter can result in atelectasis, pulmonary edema, decreased lung compliance, and acute respiratory distress syndrome. • Bacterial bronchopneumonia typically occurs later in the course of the condition and is usually secondary to therapeutic interventions or sepsis. • Acute neurologic dysfunction may be seen initially or as a delayed syndrome. • Significant dermal burn injury exacerbates morbidity and mortality. • Aggressive oxygen supplementation is the immediate priority to hasten carbon monoxide elimination. Supportive measures for respiratory and neurologic complications follow. • If carbon monoxide poisoning resolves, the prognosis is good in the absence of significant dermal burn injury, bronchopneumonia, or acute neurologic signs.
A significant number of dogs and cats are likely to be involved in residential fires each year, yet little information is available regarding actual clinical cases. This dearth of information is most likely due to a very high incidence of preadmission mortality. A recent case series describing 21 dogs trapped in a kennel fire has increased the available information to some extent.1
PATHOPHYSIOLOGY Carbon Monoxide Carbon monoxide is a nonirritant gas that competitively and reversibly binds to hemoglobin at the same sites as oxygen but with an affinity that is 230 to 270 times greater and results in marked anemic hypoxia.2,3 It is produced by incomplete combustion of carboncontaining materials and is therefore most significant in enclosed fires because there is increasingly less oxygen available.4 The resultant carboxyhemoglobin (COHb) also shifts the oxygen-hemoglobin dissociation curve to the left, which results in less offloading at the tissue level.2 There are three possible outcomes in pure, uncomplicated carbon monoxide poisoning: (1) complete recovery with possible transient hearing loss but no permanent effects, (2) recovery with
permanent central nervous system abnormalities, and (3) death.2,5-9 Carbon monoxide poisoning is the main cause of immediate death from smoke inhalation in humans, and death is due to cerebral and myocardial hypoxia.6,7
Hydrogen Cyanide Hydrogen cyanide (HCN) is most prevalent in fires involving wools, silks, and synthetic nitrogen-containing polymers (e.g., urethanes, nylon). It is a nonirritant gas that interferes with the utilization of oxygen by cellular cytochrome oxidase and thereby causes histotoxic hypoxia.3,6 The incidence and significance of cyanide toxicity in veterinary smoke inhalation victims remain undefined.4,10
Thermal Injury Direct thermal injury caused by hot, dry air is highly unusual distal to the larynx because heat is dissipated effectively by the thermal regulatory system of the nasal and oropharyngeal areas.6,11 Thermal injury can manifest as mucosal edema, erosions, and ulceration. Of greatest concern is the potential for laryngeal edema, which may result in fatal upper respiratory tract obstruction. Although these changes may not be apparent initially, they can be progressive. In one study, a tracheostomy was required because of laryngeal obstruction in 2 of 27 dogs with smoke exposure and was performed 24 and 72 hours after admission.8 Steam has a much greater heat capacity than dry air and is therefore likely to produce more extensive injury throughout the respiratory tract.6 Inhalation of superheated particulate matter (mainly soot) can result in thermal injury to the trachea and lower respiratory tract.
Irritant Gases and Superheated Particulate Matter A variety of irritant noxious gases can be inhaled during a fire, depending on the nature of the materials undergoing combustion. These include short-chain aldehydes, gases that are converted into acids in the respiratory tract (e.g., oxides of sulfur and nitrogen), highly water-soluble gases (e.g., ammonia, hydrogen chloride), and benzene (from plastics).6,11 Particulate matter acts as a vehicle by which these gases can be carried deep into the respiratory tract. The pathophysiologic consequences depend on the types of gases and particulate matter inhaled, the duration of exposure, and underlying host characteristics.6,12
Reduced lung compliance Lung compliance may be markedly reduced as a result of alveolar atelectasis due to impaired pulmonary surfactant activity, as well as pulmonary edema caused by increased permeability (see Chapter 21).3,6,13,14 Pulmonary edema can occur within minutes of smoke 785
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inhalation, although it typically develops over a period of up to 24 hours.6 Ventilation-perfusion alterations also occur, and acute lung injury and acute respiratory distress syndrome are potential sequelae (see Chapter 24). A recent case report described the successful management of a dog that developed acute respiratory distress syndrome following smoke inhalation.14a
Airway damage and obstruction The mucociliary escalator is significantly impaired following smoke inhalation. Progressive mucosal edema may be accompanied by mucosal sloughing over several hours, and the damaged epithelium gives rise to pseudomembranous casts.6,14 Marked tracheobronchitis, necrotizing bronchiolitis, alveolar hyaline membrane formation, and intraalveolar hemorrhage all may follow.6,14 Smoke inhalation induces a reflex bronchoconstriction, and airway obstruction is exacerbated by the copious secretions and edema fluid.6
Bacterial pneumonia Smoke inhalation may increase the likelihood of bacterial pneumonia by impairment of alveolar macrophage function. In addition, the stagnant luminal contents create a milieu conducive to bacterial colonization. Nevertheless, bacterial pneumonia is thought typically to occur as a secondary phenomenon following therapeutic interventions such as endotracheal intubation and tracheostomy, or due to sepsis associated with dermal burn injuries.12,15 Infection usually is not seen for at least 12 to 24 hours and is associated with a higher incidence of respiratory failure.6,12,15 Pseudomonas aeruginosa, Staphylococcus spp, and Streptococcus spp are most commonly involved in humans, but it is unknown if the same is true in dogs and cats.
Dermal Burn Injury The morbidity and mortality associated with smoke inhalation are much greater when significant concurrent dermal burn injury is present.8,10,11 This is due to both the pulmonary pathophysiology associated with dermal burns (pulmonary edema, bacterial pneumonia, acute lung injury, and acute respiratory distress syndrome) and to burn management requirements, including more aggressive fluid therapy and repeated general anesthesia (see Chapter 140).10,11
HISTORY If owner contact is possible, a full medical history should be obtained at the appropriate time. The current illness is usually related to being involved in an enclosed-space fire, and the duration of exposure and types of materials involved in the fire should be ascertained. The patient’s neurologic status at the scene predominantly reflects the degree of carbon monoxide poisoning. Paroxysmal or intractable coughing may suggest the inhalation of more irritating gases.
PHYSICAL EXAMINATION Physical examination findings depend on a number of factors, including the type, severity, and duration of smoke inhalation; the presence of dermal burn injuries; the use or nonuse of oxygen supplementation by human paramedics; the delay in arrival at the hospital; and the patient’s preexisting health status. Neurologic abnormalities on admission may include reduced mental status, from depression through coma, as well as anxiety, agitation, ataxia, and convulsions. In one case series dogs with altered mental status at the time of presentation had a significantly increased COHb concentration at presentation compared with normal dogs.1 New neurologic signs have been reported after 2 to 6 days in dogs that had neurologic dysfunction initially.16,17 Lethargy may be a common finding in cats.18
Respiratory signs may be absent initially and can take 24 hours or more to develop; however, two studies found that animals without respiratory abnormalities at admission typically did not go on to develop any significant problems.8,14,18 Clinical signs include tachypnea, panting (dogs), open-mouth breathing, dyspnea, inspiratory stridor, harsh lung sounds, expiratory wheezes, and crackles.1,6,8 In one report dogs with increased respiratory effort and abnormal auscultation findings had significantly greater carboxyhemoglobinemia than normal dogs.1 Cardiovascular findings may or may not be normal and depend on both the myocardial effects of carbon monoxide and HCN toxicity and the coexistence of significant dermal burn injury. Cardiovascular status tends to normalize quickly in uncomplicated cases, but complicated cases are more likely to show a range of cardiovascular abnormalities that persist for a longer period.6,12,18 The cherry red appearance of mucous membranes (and skin) attributed to carboxyhemoglobinemia is rarely witnessed in clinical cases. This probably reflects a high level of preadmission mortality in patients that would fall into this category.7 Individuals that live long enough to be treated are more likely to have either normal or hyperemic mucous membranes. Hyperemia may be due to carboxyhemoglobinemia, cyanide toxicosis, systemic vasodilation, and local vasodilation due to mucosal irritation, and this may mask both concurrent perfusion abnormalities and cyanosis.8 Rectal temperature may be normal, decreased, or increased.1,8 The animal’s coat is likely to smell of smoke. Ptyalism may be present and there may be evidence of soot in the oral cavity (or on microscopic examination of saliva). Mucosal edema and burns inside the oral cavity as well as on the face and lips may suggest smoke inhalation injury to the respiratory tract, but such findings are associated with a high incidence of false positives in humans.14 In two retrospective veterinary studies of smoke exposure, only 1 of the 27 dogs and none of the 22 cats had a major dermal burn injury; minor injuries such as singed hair and skin lacerations were more common in dogs.8,18 Evidence of ocular irritation and injury may be present.
CLINICAL EVALUATION Arterial Blood Gas Analysis Initially, when carbon monoxide (and HCN) poisoning is likely to be the predominant cause of morbidity, arterial partial pressure of oxygen (PaO2) may remain within normal limits.2,3,6 Oxygen saturation based on pulse oximetry may also appear normal because these devices do not differentiate between COHb and oxyhemoglobin.4 Co-oximetry allows direct measurement of oxyhemoglobin and COHb (see Chapter 186).10 A reduction in the arterial-venous oxygen gradient may be suggestive of significant HCN toxicity.10,19 Repeated arterial blood gas measurements are invaluable in detection and monitoring of the potentially progressive respiratory complications of smoke inhalation and may reveal impaired oxygenation and/or ventilation.
Acid-Base Status Acidemia is likely and may be of respiratory, metabolic, or mixed origin.6,11,12 Hyperlactatemia may be present as a result of tissue hypoxia, and excessively high plasma lactate levels at admission are a sensitive indicator of HCN intoxication (independent of hypoxemia) in humans.19
Thoracic Radiography Thoracic radiographic abnormalities may be absent initially when injury is confined to the airways but usually appear within the first 24 hours and can be expected in 70% to 80% of affected dogs and
CHAPTER 147 • Smoke Inhalation
cats.* Radiographic changes do not always correlate with either the severity of respiratory tract injury or patient morbidity; serial studies may be needed.6,8,18 An asymmetric radiographic pattern consistent with pulmonary edema is typical with alveolar, interstitial, and peribronchial changes.6,8,18,20 Diffuse coalescing consolidation, collapse of the right middle lung lobe, and pleural effusion (especially in cats) have all been reported.6,8,18 If bacterial pneumonia develops, a more pronounced alveolar pattern with air bronchograms can be expected.6 Computed tomography is likely to offer a more sensitive means of detecting lung injury earlier, but currently there is only limited published information on this topic for human patients and experimental animals.
Laryngoscopy, Bronchoscopy, and Transtracheal Aspiration Laryngoscopy is useful in sedated or unconscious animals to detect potentially progressive laryngeal obstruction. Fiberoptic bronchoscopy is used widely in humans to examine the lower airway. The presence of carbonaceous particulate matter in the airway confirms the diagnosis, and direct visualization of the anatomic level and extent of airway injury is possible along with sample collection.4 Serial examinations may need to be performed as respiratory changes progress.10 General anesthesia is required in veterinary patients in the absence of a tracheostomy, so a risk-benefit assessment must be made in considering this procedure. Transtracheal aspiration may be used in veterinary patients. Samples may reveal carbonaceous particulate matter as well as cytologic changes consistent with thermal injury affecting the ciliated epithelial cells in particular.21 This technique is also useful for the diagnosis of bacterial bronchopneumonia and for the procurement of samples for culture and susceptibility testing.
DIAGNOSIS Smoke inhalation is suspected in a patient with a history of involvement in an enclosed-space fire along with facial burns, especially if carbonaceous particulate matter is present in the oral cavity or on microscopic examination of saliva. The results of physical examination and clinical evaluation support the diagnosis. In animals with significant dermal burn injury, and in the absence of a COHb measurement, the use of a transtracheal wash or bronchoscopy may be necessary to diagnose smoke inhalation as the cause of respiratory abnormalities.
TREATMENT Smoke inhalation victims can be divided broadly into the following groups: (1) those that have no clinical signs and are assessed to be at low risk of progression, (2) those that have only mild signs but are assessed to be at high risk of progression, and (3) those that require intensive treatment from the outset.4 Treatment must be tailored to this initial assessment and adapted thereafter based on regular patient evaluation.
Oxygen Supplementation Oxygen supplementation is the immediate priority for presumed carbon monoxide toxicity and may cause significant clinical improvement within minutes.8,15,17 The half-life of carbon monoxide is approximately 250 minutes in patients with normal respiratory exchange breathing room air but is reduced to 26 to 148 minutes at a fraction of inspired oxygen (FiO2) of 100%.6,22 In one case series the change in COHb 24 hours following presentation was signifi-
*References 4, 6, 8, 10, 18, 20.
cantly greater in dogs that received oxygen therapy (78% reduction; range, 59% to 84%) than in dogs that did not (48% reduction; range, 32% to 68%).1 The use of hyperbaric oxygen therapy to potentially reduce the half-life of carbon monoxide still further has been reported in humans; other beneficial effects are also postulated. However, a recent Cochrane review evaluated seven randomized controlled trials that used hyperbaric oxygen therapy in carbon monoxide poisoning and concluded that there was insufficient evidence to support its use in human patients for this purpose.23 Providing an FiO2 of 100% via endotracheal tube is an effective, readily available alternative that allows access to the patient. Treatment periods ranging from 30 minutes to 6 hours have been described.6,24,25 Oxygen supplementation clearly has a crucial therapeutic role in treating the respiratory complications that may develop subsequently.
Cyanide Toxicity Usual treatment of cyanide toxicity involves administration of intravenous sodium nitrite followed by intravenous sodium thiosulfate. However, sodium nitrite may not be appropriate in smoke inhalation victims because it results in the formation of methemoglobin and further compromises oxygen-carrying capacity.6 Sodium thiosulfate should therefore be used alone.
Airway Management A tracheostomy may be required to treat laryngeal obstruction; strict aseptic technique must be maintained during the procedure, with regular suctioning and humidification thereafter, because secondary infection may be life-threatening. The empiric use of bronchodilators is indicated, especially in patients with wheezes on auscultation. Options include terbutaline (0.01 mg/kg intravenously [IV] or intramuscularly in both dogs and cats), aminophylline (dogs: 10 mg/kg slowly IV, diluted; cats: 4 mg/kg slowly IV, diluted), and inhaled albuterol. Supplemental oxygen must be humidified, and regular saline nebulization followed by coupage should also be performed. Human clinical studies have suggested that coupage is contraindicated in the presence of bacterial pneumonia (see Chapter 22). Gentle activity is to be encouraged if possible, and mucolytics such as bromhexine and acetylcysteine may also be helpful. Antitussives are best avoided because they reduce airway clearance.
Sedation Animals that are agitated at initial contact may be exhibiting neurologic symptoms associated with carbon monoxide (and HCN) toxicity. Use of appropriate chemical restraint to allow more aggressive oxygen supplementation is empirically justified in such cases. Thereafter, sedation may be required to minimize anxiety associated with dyspnea. Low-dosage opioids may be adequate, and additional sedation (e.g., acepromazine) may be necessary, especially in patients with upper respiratory tract compromise (see Chapter 142).
Mechanical Ventilation Assisted ventilation may be required due to either inadequate spontaneous ventilation or respiratory failure (see Chapter 30).10 A lungprotective strategy is warranted. Continuous positive airway pressure, provided to spontaneously breathing patients, may be an alternative in the absence of hypoventilation, but this usually necessitates orotracheal intubation or tracheostomy.26,27
Intravenous Fluid Therapy Fluid requirements are significantly increased in patients with dermal burns (see Chapter 140), but this is not necessarily the case in isolated smoke inhalation injury. Moreover, overresuscitation may increase pulmonary microvascular pressures and edema formation under the high-permeability conditions in early lung injury. Both overzealous
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fluid administration and excessive fluid restriction may potentially be harmful in patients with isolated smoke inhalation injury.10,14,28,29
Additional Therapies Prophylactic antibiotics are not recommended due to the risk of selecting for resistant organisms. In animals with suspected bacterial pneumonia, antibiotic selection should be based on culture and susceptibility testing of samples collected by transtracheal wash or bronchoscopy. Gram stain examination of these samples can guide drug selection while results are awaited. Otherwise, broad-spectrum coverage for both gram-negative and gram-positive infections should be instituted and then amended if necessary once test results are obtained. Blood cultures are recommended in animals that are thought to have developed bacterial pneumonia due to sepsis.4 The use of glucocorticoids following smoke inhalation has been widely investigated. Experimental studies report variable effects associated with this treatment, but the vast majority of clinical reports point to an increased incidence of bacterial pneumonia with no clear clinical benefit.4,8,11,14,30 The use of glucocorticoids is therefore not recommended in these patients.4,10,14 The permeability edema following smoke inhalation was said to be less responsive to standard diuretic therapy than high-pressure edema. However, there is more recent evidence in support of multimodal beneficial effects of judicious furosemide administration in such cases in the absence of hypovolemia or dehydration (see Chapter 21). A variety of inhaled drugs are under investigation in human patients and/or experimental animals. Nebulized heparin and N-acetylcysteine have been used in some human patients; topical antiinflammatory drugs, nitric oxide inhibitors, and antioxidants are other agents being explored.31
PROGNOSIS Mortality rates in people following admission for smoke inhalation have been reported to be less than 10% without and 25% to 65% with dermal burn injury.10 Of the 27 dogs with smoke exposure in one retrospective canine study, 4 died and a further 4 were euthanized. In uncomplicated cases, dogs recovering from the initial carbon monoxide poisoning had a favorable prognosis, with improvements in respiratory signs over 24 hours. However, dogs that were clinically worse the following day were more likely to die, to be euthanized, or to require prolonged hospitalization.8 In one retrospective case series of 21 dogs trapped in a kennel fire, 5 dogs had worsening of respiratory or neurologic signs following admission, but only 1 of the dogs failed to survive to discharge (euthanized after developing pneumonia).1 In another study, smoke-exposed dogs admitted with acute neurologic signs had an overall mortality rate of 46%.16 Despite initial improvement, acute, delayed neurologic signs developed in 46% of the dogs within 2 to 6 days. Mortality rate for this group was 60%.16 In a retrospective feline study, none of the 22 cats with smoke exposure died, but 2 were euthanized due to severe respiratory or neurologic signs.18 Animals with concurrent dermal burn injury should be given a more guarded prognosis from the outset. Although smoke inhalation can result in permanent changes to lung structure, any long-term effects on lung function are unlikely to be clinically significant.4,6,8,10
REFERENCES 1. Ashbaugh EA, Mazzaferro EM, McKierman BC, et al: The association of physical examination abnormalities and carboxyhemoglobin concentra-
tions in 21 dogs trapped in a kennel fire, J Vet Emerg Crit Care (San Antonio) 22:361, 2012. 2. Winter PM, Miller JN: Carbon monoxide poisoning, JAMA 236:1502, 1976. 3. West JB: Respiratory physiology: the essentials, ed 9, Baltimore, 2012, Lippincott Williams & Wilkins. 4. Ruddy RM: Smoke inhalation injury, Pediatr Clin North Am 41:317, 1994. 5. Berent AC, Todd J, Sergeeff J, et al: Carbon monoxide toxicity: a case series, J Vet Emerg Crit Care (San Antonio) 15:128, 2005. 6. Fitzgerald KT, Flood AA: Smoke inhalation, Clin Tech Small Anim Pract 21:205, 2006. 7. Thom SR: Smoke inhalation, Emerg Med Clin North Am 7:371, 1989. 8. Drobatz KJ, Walker LM, Hendricks JC: Smoke exposure in dogs: 27 cases (1988-1997), J Am Vet Med Assoc 215:1306, 1999. 9. Rozanski E: Acute lung injury: near-drowning and smoke inhalation. In Proceedings of 10th International Veterinary Emergency and Critical Care Symposium, San Diego, Calif, September 2004. 10. Clark WR: Smoke inhalation: diagnosis and treatment, World J Surg 16:24, 1992. 11. Trunkey DD: Inhalation injury, Surg Clin North Am 58:1133, 1978. 12. Stephenson SF, Esrig BC, Polk HC Jr, et al: The pathophysiology of smoke inhalation injury, Ann Surg 182:652, 1975. 13. Nieman GF, Clark WR Jr, Wax SD, et al: The effect of smoke inhalation on pulmonary surfactant, Ann Surg 191:171, 1980. 14. Herndon DN, Langner F, Thompson P, et al: Pulmonary injury in burned patients, Surg Clin North Am 67:31, 1987. 14a. Guillaumin J, Hopper K: Successful outcome in a dog with neurological and respiratory signs following smoke inhalation, J Vet Emerg Crit Care 33(3):328-334, 2013. 15. Zikria BA, Weston GC, Chodoff M, et al: Smoke and carbon monoxide poisoning in fire victims, J Trauma 12:641, 1972. 16. Jackson CB, Drobatz KJ: Neurologic dysfunction associated with smoke exposure in dogs, J Vet Emerg Crit Care (San Antonio) 12:193, 2002. 17. Mariani CL: Full recovery following delayed neurologic signs after smoke inhalation in a dog, J Vet Emerg Crit Care (San Antonio) 13:235, 2003. 18. Drobatz KJ, Walker LM, Hendricks JC: Smoke exposure in cats: 22 cases (1986-1997), J Am Vet Med Assoc 215:1312, 1999. 19. Band FJ, Bairiot P, Toffis V, et al: Elevated blood cyanide concentrations in victims of smoke inhalation, N Engl J Med 325:1761, 1991. 20. Teixidor HS, Rubin E, Novick G, et al: Smoke inhalation: radiologic manifestations, Radiology 149:383, 1983. 21. Tams TR: Aspiration pneumonia and complications of inhalation of smoke and toxic gases, Vet Clin North Am Small Anim Pract 15:971, 1985. 22. Weaver LK, Howe S, Hopkins R, et al: Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure, Chest 117:801, 2000. 23. Buckley NA, Juurlink DN, Isbister G, et al: Hyperbaric oxygen for carbon monoxide poisoning, Cochrane Database Syst Rev (4):CD002041, 2011. 24. Piantadosi CA: Hyperbaric oxygen for acute carbon monoxide poisoning, N Engl J Med 347:1053, 2002. 25. Hart GB, Strauss MB, Lennon PA, et al: Treatment of smoke inhalation by hyperbaric oxygen, J Emerg Med 3:211, 1985. 26. American Association for Respiratory Care: Application of continuous positive airway pressure to neonates via nasal prongs, nasopharyngeal tube, or nasal mask: 2004 revision and update, Respir Care 49:1100, 2004. 27. Orton CE, Wheeler SL: Continuous positive airway pressure therapy for aspiration pneumonia in a dog, J Am Vet Med Assoc 188:1437, 1986. 28. Clark WR, Nieman GF, Goyette D, et al: Effects of crystalloids on lung fluid balance after smoke inhalation, Ann Surg 208:56, 1988. 29. Hughes D: Fluid therapy with lung disease: is wetter better or drier desired? In Proceedings of the 9th International Veterinary Emergency and Critical Care Symposium, 2003. 30. Nieman GF, Clark WR, Hakim T: Methylprednisolone does not protect the lung from inhalation injury, Burns 17:384, 1991. 31. Toon MH, Maybauer MO, Greenwood JE, et al: Management of acute smoke inhalation injury, Crit Care Resusc 12:53, 2010.
MA, VetMB, MRCVS, DACVECC
KEY POINTS • The relative lack of clinical veterinary information on smoke inhalation likely reflects a very high incidence of preadmission mortality. Hypoxia from carbon monoxide poisoning is presumed to be the most common cause of immediate death. • Direct thermal injury to the upper respiratory tract can cause laryngeal obstruction. Lower respiratory tract injury from irritant gases and superheated particulate matter can result in atelectasis, pulmonary edema, decreased lung compliance, and acute respiratory distress syndrome. • Bacterial bronchopneumonia typically occurs later in the course of the condition and is usually secondary to therapeutic interventions or sepsis. • Acute neurologic dysfunction may be seen initially or as a delayed syndrome. • Significant dermal burn injury exacerbates morbidity and mortality. • Aggressive oxygen supplementation is the immediate priority to hasten carbon monoxide elimination. Supportive measures for respiratory and neurologic complications follow. • If carbon monoxide poisoning resolves, the prognosis is good in the absence of significant dermal burn injury, bronchopneumonia, or acute neurologic signs.
A significant number of dogs and cats are likely to be involved in residential fires each year, yet little information is available regarding actual clinical cases. This dearth of information is most likely due to a very high incidence of preadmission mortality. A recent case series describing 21 dogs trapped in a kennel fire has increased the available information to some extent.1
PATHOPHYSIOLOGY Carbon Monoxide Carbon monoxide is a nonirritant gas that competitively and reversibly binds to hemoglobin at the same sites as oxygen but with an affinity that is 230 to 270 times greater and results in marked anemic hypoxia.2,3 It is produced by incomplete combustion of carboncontaining materials and is therefore most significant in enclosed fires because there is increasingly less oxygen available.4 The resultant carboxyhemoglobin (COHb) also shifts the oxygen-hemoglobin dissociation curve to the left, which results in less offloading at the tissue level.2 There are three possible outcomes in pure, uncomplicated carbon monoxide poisoning: (1) complete recovery with possible transient hearing loss but no permanent effects, (2) recovery with
permanent central nervous system abnormalities, and (3) death.2,5-9 Carbon monoxide poisoning is the main cause of immediate death from smoke inhalation in humans, and death is due to cerebral and myocardial hypoxia.6,7
Hydrogen Cyanide Hydrogen cyanide (HCN) is most prevalent in fires involving wools, silks, and synthetic nitrogen-containing polymers (e.g., urethanes, nylon). It is a nonirritant gas that interferes with the utilization of oxygen by cellular cytochrome oxidase and thereby causes histotoxic hypoxia.3,6 The incidence and significance of cyanide toxicity in veterinary smoke inhalation victims remain undefined.4,10
Thermal Injury Direct thermal injury caused by hot, dry air is highly unusual distal to the larynx because heat is dissipated effectively by the thermal regulatory system of the nasal and oropharyngeal areas.6,11 Thermal injury can manifest as mucosal edema, erosions, and ulceration. Of greatest concern is the potential for laryngeal edema, which may result in fatal upper respiratory tract obstruction. Although these changes may not be apparent initially, they can be progressive. In one study, a tracheostomy was required because of laryngeal obstruction in 2 of 27 dogs with smoke exposure and was performed 24 and 72 hours after admission.8 Steam has a much greater heat capacity than dry air and is therefore likely to produce more extensive injury throughout the respiratory tract.6 Inhalation of superheated particulate matter (mainly soot) can result in thermal injury to the trachea and lower respiratory tract.
Irritant Gases and Superheated Particulate Matter A variety of irritant noxious gases can be inhaled during a fire, depending on the nature of the materials undergoing combustion. These include short-chain aldehydes, gases that are converted into acids in the respiratory tract (e.g., oxides of sulfur and nitrogen), highly water-soluble gases (e.g., ammonia, hydrogen chloride), and benzene (from plastics).6,11 Particulate matter acts as a vehicle by which these gases can be carried deep into the respiratory tract. The pathophysiologic consequences depend on the types of gases and particulate matter inhaled, the duration of exposure, and underlying host characteristics.6,12
Reduced lung compliance Lung compliance may be markedly reduced as a result of alveolar atelectasis due to impaired pulmonary surfactant activity, as well as pulmonary edema caused by increased permeability (see Chapter 21).3,6,13,14 Pulmonary edema can occur within minutes of smoke 785
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inhalation, although it typically develops over a period of up to 24 hours.6 Ventilation-perfusion alterations also occur, and acute lung injury and acute respiratory distress syndrome are potential sequelae (see Chapter 24). A recent case report described the successful management of a dog that developed acute respiratory distress syndrome following smoke inhalation.14a
Airway damage and obstruction The mucociliary escalator is significantly impaired following smoke inhalation. Progressive mucosal edema may be accompanied by mucosal sloughing over several hours, and the damaged epithelium gives rise to pseudomembranous casts.6,14 Marked tracheobronchitis, necrotizing bronchiolitis, alveolar hyaline membrane formation, and intraalveolar hemorrhage all may follow.6,14 Smoke inhalation induces a reflex bronchoconstriction, and airway obstruction is exacerbated by the copious secretions and edema fluid.6
Bacterial pneumonia Smoke inhalation may increase the likelihood of bacterial pneumonia by impairment of alveolar macrophage function. In addition, the stagnant luminal contents create a milieu conducive to bacterial colonization. Nevertheless, bacterial pneumonia is thought typically to occur as a secondary phenomenon following therapeutic interventions such as endotracheal intubation and tracheostomy, or due to sepsis associated with dermal burn injuries.12,15 Infection usually is not seen for at least 12 to 24 hours and is associated with a higher incidence of respiratory failure.6,12,15 Pseudomonas aeruginosa, Staphylococcus spp, and Streptococcus spp are most commonly involved in humans, but it is unknown if the same is true in dogs and cats.
Dermal Burn Injury The morbidity and mortality associated with smoke inhalation are much greater when significant concurrent dermal burn injury is present.8,10,11 This is due to both the pulmonary pathophysiology associated with dermal burns (pulmonary edema, bacterial pneumonia, acute lung injury, and acute respiratory distress syndrome) and to burn management requirements, including more aggressive fluid therapy and repeated general anesthesia (see Chapter 140).10,11
HISTORY If owner contact is possible, a full medical history should be obtained at the appropriate time. The current illness is usually related to being involved in an enclosed-space fire, and the duration of exposure and types of materials involved in the fire should be ascertained. The patient’s neurologic status at the scene predominantly reflects the degree of carbon monoxide poisoning. Paroxysmal or intractable coughing may suggest the inhalation of more irritating gases.
PHYSICAL EXAMINATION Physical examination findings depend on a number of factors, including the type, severity, and duration of smoke inhalation; the presence of dermal burn injuries; the use or nonuse of oxygen supplementation by human paramedics; the delay in arrival at the hospital; and the patient’s preexisting health status. Neurologic abnormalities on admission may include reduced mental status, from depression through coma, as well as anxiety, agitation, ataxia, and convulsions. In one case series dogs with altered mental status at the time of presentation had a significantly increased COHb concentration at presentation compared with normal dogs.1 New neurologic signs have been reported after 2 to 6 days in dogs that had neurologic dysfunction initially.16,17 Lethargy may be a common finding in cats.18
Respiratory signs may be absent initially and can take 24 hours or more to develop; however, two studies found that animals without respiratory abnormalities at admission typically did not go on to develop any significant problems.8,14,18 Clinical signs include tachypnea, panting (dogs), open-mouth breathing, dyspnea, inspiratory stridor, harsh lung sounds, expiratory wheezes, and crackles.1,6,8 In one report dogs with increased respiratory effort and abnormal auscultation findings had significantly greater carboxyhemoglobinemia than normal dogs.1 Cardiovascular findings may or may not be normal and depend on both the myocardial effects of carbon monoxide and HCN toxicity and the coexistence of significant dermal burn injury. Cardiovascular status tends to normalize quickly in uncomplicated cases, but complicated cases are more likely to show a range of cardiovascular abnormalities that persist for a longer period.6,12,18 The cherry red appearance of mucous membranes (and skin) attributed to carboxyhemoglobinemia is rarely witnessed in clinical cases. This probably reflects a high level of preadmission mortality in patients that would fall into this category.7 Individuals that live long enough to be treated are more likely to have either normal or hyperemic mucous membranes. Hyperemia may be due to carboxyhemoglobinemia, cyanide toxicosis, systemic vasodilation, and local vasodilation due to mucosal irritation, and this may mask both concurrent perfusion abnormalities and cyanosis.8 Rectal temperature may be normal, decreased, or increased.1,8 The animal’s coat is likely to smell of smoke. Ptyalism may be present and there may be evidence of soot in the oral cavity (or on microscopic examination of saliva). Mucosal edema and burns inside the oral cavity as well as on the face and lips may suggest smoke inhalation injury to the respiratory tract, but such findings are associated with a high incidence of false positives in humans.14 In two retrospective veterinary studies of smoke exposure, only 1 of the 27 dogs and none of the 22 cats had a major dermal burn injury; minor injuries such as singed hair and skin lacerations were more common in dogs.8,18 Evidence of ocular irritation and injury may be present.
CLINICAL EVALUATION Arterial Blood Gas Analysis Initially, when carbon monoxide (and HCN) poisoning is likely to be the predominant cause of morbidity, arterial partial pressure of oxygen (PaO2) may remain within normal limits.2,3,6 Oxygen saturation based on pulse oximetry may also appear normal because these devices do not differentiate between COHb and oxyhemoglobin.4 Co-oximetry allows direct measurement of oxyhemoglobin and COHb (see Chapter 186).10 A reduction in the arterial-venous oxygen gradient may be suggestive of significant HCN toxicity.10,19 Repeated arterial blood gas measurements are invaluable in detection and monitoring of the potentially progressive respiratory complications of smoke inhalation and may reveal impaired oxygenation and/or ventilation.
Acid-Base Status Acidemia is likely and may be of respiratory, metabolic, or mixed origin.6,11,12 Hyperlactatemia may be present as a result of tissue hypoxia, and excessively high plasma lactate levels at admission are a sensitive indicator of HCN intoxication (independent of hypoxemia) in humans.19
Thoracic Radiography Thoracic radiographic abnormalities may be absent initially when injury is confined to the airways but usually appear within the first 24 hours and can be expected in 70% to 80% of affected dogs and
CHAPTER 147 • Smoke Inhalation
cats.* Radiographic changes do not always correlate with either the severity of respiratory tract injury or patient morbidity; serial studies may be needed.6,8,18 An asymmetric radiographic pattern consistent with pulmonary edema is typical with alveolar, interstitial, and peribronchial changes.6,8,18,20 Diffuse coalescing consolidation, collapse of the right middle lung lobe, and pleural effusion (especially in cats) have all been reported.6,8,18 If bacterial pneumonia develops, a more pronounced alveolar pattern with air bronchograms can be expected.6 Computed tomography is likely to offer a more sensitive means of detecting lung injury earlier, but currently there is only limited published information on this topic for human patients and experimental animals.
Laryngoscopy, Bronchoscopy, and Transtracheal Aspiration Laryngoscopy is useful in sedated or unconscious animals to detect potentially progressive laryngeal obstruction. Fiberoptic bronchoscopy is used widely in humans to examine the lower airway. The presence of carbonaceous particulate matter in the airway confirms the diagnosis, and direct visualization of the anatomic level and extent of airway injury is possible along with sample collection.4 Serial examinations may need to be performed as respiratory changes progress.10 General anesthesia is required in veterinary patients in the absence of a tracheostomy, so a risk-benefit assessment must be made in considering this procedure. Transtracheal aspiration may be used in veterinary patients. Samples may reveal carbonaceous particulate matter as well as cytologic changes consistent with thermal injury affecting the ciliated epithelial cells in particular.21 This technique is also useful for the diagnosis of bacterial bronchopneumonia and for the procurement of samples for culture and susceptibility testing.
DIAGNOSIS Smoke inhalation is suspected in a patient with a history of involvement in an enclosed-space fire along with facial burns, especially if carbonaceous particulate matter is present in the oral cavity or on microscopic examination of saliva. The results of physical examination and clinical evaluation support the diagnosis. In animals with significant dermal burn injury, and in the absence of a COHb measurement, the use of a transtracheal wash or bronchoscopy may be necessary to diagnose smoke inhalation as the cause of respiratory abnormalities.
TREATMENT Smoke inhalation victims can be divided broadly into the following groups: (1) those that have no clinical signs and are assessed to be at low risk of progression, (2) those that have only mild signs but are assessed to be at high risk of progression, and (3) those that require intensive treatment from the outset.4 Treatment must be tailored to this initial assessment and adapted thereafter based on regular patient evaluation.
Oxygen Supplementation Oxygen supplementation is the immediate priority for presumed carbon monoxide toxicity and may cause significant clinical improvement within minutes.8,15,17 The half-life of carbon monoxide is approximately 250 minutes in patients with normal respiratory exchange breathing room air but is reduced to 26 to 148 minutes at a fraction of inspired oxygen (FiO2) of 100%.6,22 In one case series the change in COHb 24 hours following presentation was signifi-
*References 4, 6, 8, 10, 18, 20.
cantly greater in dogs that received oxygen therapy (78% reduction; range, 59% to 84%) than in dogs that did not (48% reduction; range, 32% to 68%).1 The use of hyperbaric oxygen therapy to potentially reduce the half-life of carbon monoxide still further has been reported in humans; other beneficial effects are also postulated. However, a recent Cochrane review evaluated seven randomized controlled trials that used hyperbaric oxygen therapy in carbon monoxide poisoning and concluded that there was insufficient evidence to support its use in human patients for this purpose.23 Providing an FiO2 of 100% via endotracheal tube is an effective, readily available alternative that allows access to the patient. Treatment periods ranging from 30 minutes to 6 hours have been described.6,24,25 Oxygen supplementation clearly has a crucial therapeutic role in treating the respiratory complications that may develop subsequently.
Cyanide Toxicity Usual treatment of cyanide toxicity involves administration of intravenous sodium nitrite followed by intravenous sodium thiosulfate. However, sodium nitrite may not be appropriate in smoke inhalation victims because it results in the formation of methemoglobin and further compromises oxygen-carrying capacity.6 Sodium thiosulfate should therefore be used alone.
Airway Management A tracheostomy may be required to treat laryngeal obstruction; strict aseptic technique must be maintained during the procedure, with regular suctioning and humidification thereafter, because secondary infection may be life-threatening. The empiric use of bronchodilators is indicated, especially in patients with wheezes on auscultation. Options include terbutaline (0.01 mg/kg intravenously [IV] or intramuscularly in both dogs and cats), aminophylline (dogs: 10 mg/kg slowly IV, diluted; cats: 4 mg/kg slowly IV, diluted), and inhaled albuterol. Supplemental oxygen must be humidified, and regular saline nebulization followed by coupage should also be performed. Human clinical studies have suggested that coupage is contraindicated in the presence of bacterial pneumonia (see Chapter 22). Gentle activity is to be encouraged if possible, and mucolytics such as bromhexine and acetylcysteine may also be helpful. Antitussives are best avoided because they reduce airway clearance.
Sedation Animals that are agitated at initial contact may be exhibiting neurologic symptoms associated with carbon monoxide (and HCN) toxicity. Use of appropriate chemical restraint to allow more aggressive oxygen supplementation is empirically justified in such cases. Thereafter, sedation may be required to minimize anxiety associated with dyspnea. Low-dosage opioids may be adequate, and additional sedation (e.g., acepromazine) may be necessary, especially in patients with upper respiratory tract compromise (see Chapter 142).
Mechanical Ventilation Assisted ventilation may be required due to either inadequate spontaneous ventilation or respiratory failure (see Chapter 30).10 A lungprotective strategy is warranted. Continuous positive airway pressure, provided to spontaneously breathing patients, may be an alternative in the absence of hypoventilation, but this usually necessitates orotracheal intubation or tracheostomy.26,27
Intravenous Fluid Therapy Fluid requirements are significantly increased in patients with dermal burns (see Chapter 140), but this is not necessarily the case in isolated smoke inhalation injury. Moreover, overresuscitation may increase pulmonary microvascular pressures and edema formation under the high-permeability conditions in early lung injury. Both overzealous
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PART XVIII • ENVIRONMENTAL EMERGENCIES
fluid administration and excessive fluid restriction may potentially be harmful in patients with isolated smoke inhalation injury.10,14,28,29
Additional Therapies Prophylactic antibiotics are not recommended due to the risk of selecting for resistant organisms. In animals with suspected bacterial pneumonia, antibiotic selection should be based on culture and susceptibility testing of samples collected by transtracheal wash or bronchoscopy. Gram stain examination of these samples can guide drug selection while results are awaited. Otherwise, broad-spectrum coverage for both gram-negative and gram-positive infections should be instituted and then amended if necessary once test results are obtained. Blood cultures are recommended in animals that are thought to have developed bacterial pneumonia due to sepsis.4 The use of glucocorticoids following smoke inhalation has been widely investigated. Experimental studies report variable effects associated with this treatment, but the vast majority of clinical reports point to an increased incidence of bacterial pneumonia with no clear clinical benefit.4,8,11,14,30 The use of glucocorticoids is therefore not recommended in these patients.4,10,14 The permeability edema following smoke inhalation was said to be less responsive to standard diuretic therapy than high-pressure edema. However, there is more recent evidence in support of multimodal beneficial effects of judicious furosemide administration in such cases in the absence of hypovolemia or dehydration (see Chapter 21). A variety of inhaled drugs are under investigation in human patients and/or experimental animals. Nebulized heparin and N-acetylcysteine have been used in some human patients; topical antiinflammatory drugs, nitric oxide inhibitors, and antioxidants are other agents being explored.31
PROGNOSIS Mortality rates in people following admission for smoke inhalation have been reported to be less than 10% without and 25% to 65% with dermal burn injury.10 Of the 27 dogs with smoke exposure in one retrospective canine study, 4 died and a further 4 were euthanized. In uncomplicated cases, dogs recovering from the initial carbon monoxide poisoning had a favorable prognosis, with improvements in respiratory signs over 24 hours. However, dogs that were clinically worse the following day were more likely to die, to be euthanized, or to require prolonged hospitalization.8 In one retrospective case series of 21 dogs trapped in a kennel fire, 5 dogs had worsening of respiratory or neurologic signs following admission, but only 1 of the dogs failed to survive to discharge (euthanized after developing pneumonia).1 In another study, smoke-exposed dogs admitted with acute neurologic signs had an overall mortality rate of 46%.16 Despite initial improvement, acute, delayed neurologic signs developed in 46% of the dogs within 2 to 6 days. Mortality rate for this group was 60%.16 In a retrospective feline study, none of the 22 cats with smoke exposure died, but 2 were euthanized due to severe respiratory or neurologic signs.18 Animals with concurrent dermal burn injury should be given a more guarded prognosis from the outset. Although smoke inhalation can result in permanent changes to lung structure, any long-term effects on lung function are unlikely to be clinically significant.4,6,8,10
REFERENCES 1. Ashbaugh EA, Mazzaferro EM, McKierman BC, et al: The association of physical examination abnormalities and carboxyhemoglobin concentra-
tions in 21 dogs trapped in a kennel fire, J Vet Emerg Crit Care (San Antonio) 22:361, 2012. 2. Winter PM, Miller JN: Carbon monoxide poisoning, JAMA 236:1502, 1976. 3. West JB: Respiratory physiology: the essentials, ed 9, Baltimore, 2012, Lippincott Williams & Wilkins. 4. Ruddy RM: Smoke inhalation injury, Pediatr Clin North Am 41:317, 1994. 5. Berent AC, Todd J, Sergeeff J, et al: Carbon monoxide toxicity: a case series, J Vet Emerg Crit Care (San Antonio) 15:128, 2005. 6. Fitzgerald KT, Flood AA: Smoke inhalation, Clin Tech Small Anim Pract 21:205, 2006. 7. Thom SR: Smoke inhalation, Emerg Med Clin North Am 7:371, 1989. 8. Drobatz KJ, Walker LM, Hendricks JC: Smoke exposure in dogs: 27 cases (1988-1997), J Am Vet Med Assoc 215:1306, 1999. 9. Rozanski E: Acute lung injury: near-drowning and smoke inhalation. In Proceedings of 10th International Veterinary Emergency and Critical Care Symposium, San Diego, Calif, September 2004. 10. Clark WR: Smoke inhalation: diagnosis and treatment, World J Surg 16:24, 1992. 11. Trunkey DD: Inhalation injury, Surg Clin North Am 58:1133, 1978. 12. Stephenson SF, Esrig BC, Polk HC Jr, et al: The pathophysiology of smoke inhalation injury, Ann Surg 182:652, 1975. 13. Nieman GF, Clark WR Jr, Wax SD, et al: The effect of smoke inhalation on pulmonary surfactant, Ann Surg 191:171, 1980. 14. Herndon DN, Langner F, Thompson P, et al: Pulmonary injury in burned patients, Surg Clin North Am 67:31, 1987. 14a. Guillaumin J, Hopper K: Successful outcome in a dog with neurological and respiratory signs following smoke inhalation, J Vet Emerg Crit Care 33(3):328-334, 2013. 15. Zikria BA, Weston GC, Chodoff M, et al: Smoke and carbon monoxide poisoning in fire victims, J Trauma 12:641, 1972. 16. Jackson CB, Drobatz KJ: Neurologic dysfunction associated with smoke exposure in dogs, J Vet Emerg Crit Care (San Antonio) 12:193, 2002. 17. Mariani CL: Full recovery following delayed neurologic signs after smoke inhalation in a dog, J Vet Emerg Crit Care (San Antonio) 13:235, 2003. 18. Drobatz KJ, Walker LM, Hendricks JC: Smoke exposure in cats: 22 cases (1986-1997), J Am Vet Med Assoc 215:1312, 1999. 19. Band FJ, Bairiot P, Toffis V, et al: Elevated blood cyanide concentrations in victims of smoke inhalation, N Engl J Med 325:1761, 1991. 20. Teixidor HS, Rubin E, Novick G, et al: Smoke inhalation: radiologic manifestations, Radiology 149:383, 1983. 21. Tams TR: Aspiration pneumonia and complications of inhalation of smoke and toxic gases, Vet Clin North Am Small Anim Pract 15:971, 1985. 22. Weaver LK, Howe S, Hopkins R, et al: Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure, Chest 117:801, 2000. 23. Buckley NA, Juurlink DN, Isbister G, et al: Hyperbaric oxygen for carbon monoxide poisoning, Cochrane Database Syst Rev (4):CD002041, 2011. 24. Piantadosi CA: Hyperbaric oxygen for acute carbon monoxide poisoning, N Engl J Med 347:1053, 2002. 25. Hart GB, Strauss MB, Lennon PA, et al: Treatment of smoke inhalation by hyperbaric oxygen, J Emerg Med 3:211, 1985. 26. American Association for Respiratory Care: Application of continuous positive airway pressure to neonates via nasal prongs, nasopharyngeal tube, or nasal mask: 2004 revision and update, Respir Care 49:1100, 2004. 27. Orton CE, Wheeler SL: Continuous positive airway pressure therapy for aspiration pneumonia in a dog, J Am Vet Med Assoc 188:1437, 1986. 28. Clark WR, Nieman GF, Goyette D, et al: Effects of crystalloids on lung fluid balance after smoke inhalation, Ann Surg 208:56, 1988. 29. Hughes D: Fluid therapy with lung disease: is wetter better or drier desired? In Proceedings of the 9th International Veterinary Emergency and Critical Care Symposium, 2003. 30. Nieman GF, Clark WR, Hakim T: Methylprednisolone does not protect the lung from inhalation injury, Burns 17:384, 1991. 31. Toon MH, Maybauer MO, Greenwood JE, et al: Management of acute smoke inhalation injury, Crit Care Resusc 12:53, 2010.