From oxygen acquisition to cellular utilization, the final common pathophysiologic effect from smoke injury is hypoxia. Basic critical care strategies that optimize oxygen delivery and utilization are of primary importance in treatment. Once removed from the source of exposure and placed on oxygen, the primary problems that the clinician must treat are the effects of thermal injury and irritant gases on the airway, and systemic effects of cellular asphyxiants. High-flow oxygen, preferably humidified, should accompany initial resuscitation in symptomatic patients. In hypotensive patients insert two large-bore intravenous (IV) lines and provide aggressive fluid resuscitation to optimize perfusion and aid in oxygen delivery.
Critical airway compromise may be present upon initial hospital presentation or may develop in the ensuing hours.54,128 A major pitfall in the management of smoke inhalation is failing to appreciate the possibility of rapid deterioration. History and physical findings help to determine significant thermal injury or smoke exposure and the potential for clinical deterioration. The clinical effects of smoke exposure and their appropriate treatment are described in Fig. 128–2. Early airway intervention must always be considered as a seemingly patent airway may develop progressive obstruction that can make subsequent intubation difficult or impossible. For signs of current or impending airway compromise, upper airway patency must be rapidly established. When obvious oropharyngeal burns are observed, upper airway injury almost certainly is present. Singed hairs of the head, face, or nasal passages and soot in the oropharynx or nares may signify potential for airway edema.
The final common pathway from all pathophysiologic changes that occur in smoke inhalation is hypoxia. All treatments should be focused on improving oxygen delivery and oxygen utilization.
Even if overt injuries are not visualized, distal injury may be present and underestimated.54 Direct evaluation of the upper airway, preferably with fiberoptic endoscopy, is essential for assessing patients at high risk for inhalation airway injury.54,55,65 When evidence of upper airway injury exists, early endotracheal intubation should be performed under controlled circumstances, preferably with preparations for advanced or surgical airway interventions in the event that orotracheal intubation cannot be easily established. Other indications for early intubation include coma, stridor, and full-thickness circumferential neck burns.7,54,55,128 Edema of injured tissue, including that of the airway, is worsened with massive fluid resuscitation in burned patients; therefore, health care professionals should also consider early intubation for patients with any amount of inhalation injury and concomitant dermal burns undergoing aggressive fluid management.54,55,98,128
Pathophysiologic changes in the lung may result in progressive hypoxia over hours to days. Basic treatment of progressive respiratory failure includes continuous positive airway pressure, mechanical ventilation using lung protective strategies, positive end-expiratory pressure (PEEP), and vigorous clearing of pulmonary secretions.101 Decreased lung compliance is common secondary to cast formation, tissue damage, and atelectasis.90,101 Recommendations for limiting barotrauma in mechanically ventilated patients include using a low tidal volume (6–8 mL/kg), PEEP, and allowing permissive hypercapnia as necessary.81,90,100 Fraction of inspired oxygen (FiO2) should be weaned to below 0.4 as rapidly as tolerated to limit oxygen toxicity.90 Frequent airway suctioning, chest physiotherapy, and therapeutic bronchoscopy can clear inspissated secretions, plugs, and casts.30,90,97 As xenobiotics and soot can coat the airway in smoke inhalation victims, early bronchoscopy with bronchoalveolar lavage would intuitively be logical in an attempt to decontaminate the airway, similar to irrigation for dermal exposure. However, there are no data available regarding this modality in the care of smoke inhalation. High-frequency percussive ventilation (HFPV) may be considered as an alternative to conventional forms of ventilation in patients with inhalational injury. Several studies have investigated the use of HFPV in ventilated patients with inhalational injury. Although limited, some evidence suggests that HFPV may decrease peak pulmonary pressures, limit barotrauma, decrease the incidence of pneumonia, and improve mortality.22,28,50,90,124 A number of studies have examined experimental therapies such as percutaneous arteriovenous carbon dioxide removal, perfluorocarbons, inhaled nitric oxide, extracorporeal membrane oxygenation, instillation of natural surfactant into the lung, and deferoxamine–hetastarch complex for improving inhalation injury; however, none of these modalities have been definitively shown to improve outcome.29,35,57,73,96,105,108,109,122
Inhaled β2-adrenergic agonists are considered first-line therapy for acute reversible bronchoconstriction resulting from asthma or chronic obstructive pulmonary disease and can be used to improve oxygenation and ventilation in victims of smoke inhalation. Pathophysiologic changes induced by irritant toxins in smoke are similar to those found in asthma, suggesting that β2-adrenergic agonists would also improve airflow obstruction in smoke inhalation.69,86 β2-adrenergic agonists also possess antiinflammatory properties, partially through interaction with β-adrenergic receptors on immune cells.85,151 β2-adrenergic agonists may also enhance resolution of alveolar edema by modulating the flow of sodium and potassium across cell membranes.85,151 Limited data in an ovine model suggest that nebulized albuterol may improve pulmonary function after smoke inhalation and burn injury.114 Although human data on the efficacy of β2-adrenergic agonists in smoke inhalation injury are lacking, their role is well established in conditions with reversible bronchoconstriction; animal studies lend support for their use and the potential benefits greatly outweigh the risks.114,151
Corticosteroids have been used for smoke inhalation in an attempt to limit inflammation and improve outcome. One argument for their use is for the treatment of lung injury induced by oxides of nitrogen. Pulmonary sequelae, including bronchiolitis obliterans, are known to occur after significant exposure to oxides of nitrogen, which may be a prominent composition of smoke.64,76 Although data regarding efficacy are limited, corticosteroids are often used in treatment of nitrogen oxide exposure in relation to industrial exposure and silo filler’s disease to prevent bronchiolitis obliterans.64,134 The mixed xenobiotic exposure from smoke inhalation appears to further complicate the outcome. One early rat study showed a trend toward reduced mortality in animals given supraphysiologic doses (25–100 mg/kg) of methylprednisolone; however, other tested corticosteroids (hydrocortisone, dexamethasone, cortisone) failed to demonstrate similar improvement. Consequently, this study failed to effectively prove that corticosteroids reduce mortality after rat exposure to white pine smoke.38 Human studies have also failed to show an improvement in clinical outcome and may trend toward worsening outcome.20,77,102,129 Thus, the available literature does not support the use of corticosteroids for treatment of patients with smoke inhalation.
A significant amount of pulmonary injury after smoke inhalation is attributable to free radical damage. Smoke inhalation decreases systemic concentrations of the antioxidant vitamin E in sheep models and treatment with nebulized vitamin E (α- and γ-tocopherol) attenuates smoke inhalation induced pulmonary injury in animal models.51,93,144,155 Similarly, both nebulized heparin and N-acetylcysteine (NAC) are used by some centers to limit pulmonary damage.88 Heparin is a glycosaminoglycan with anticoagulant and antiinflammatory properties occasionally used both topically and intravenously in burn treatment. In an ovine model of combined cutaneous burn and smoke inhalation, nebulized heparin combined with recombinant human antithrombin reduced airway obstruction and improved gas exchange.39 The mechanism is likely attributable to decreased airway inflammation and decreased fibrin deposition and, consequently, decreased cast formation in the airway.39 Nebulized heparin combined with NAC appeared to attenuate lung injury in two small studies; however, other studies have failed to show benefit.37,63,88 Human data are currently limited regarding each of these modalities with little current evidence that each treatment improves outcomes. The initial treatment strategy for carbon monoxide poisoning focuses on optimizing oxygen delivery with supplemental oxygen administration.
Oxygen can be administered by a high-flow tight-fitting mask, endotracheal tube, or hyperbaric oxygen therapy (HBO). HBO can achieve very high arterial oxygen concentrations enhancing oxygen delivery to tissues and accelerating elimination of carbon monoxide from blood and tissues.56,119 HBO is recommended as a modality for treatment in certain situations involving carbon monoxide exposure; however, smoke inhalation injury is much more complex than poisoning with carbon monoxide alone (eg, a furnace leak).52 In victims of smoke inhalation, other clinical requirements, such as maintaining a secure airway and the need for additional resuscitative measures to treat ARDS, cardiovascular instability and metabolic derangements go beyond providing supplemental oxygen to treat CO poisoning. Optimal timing of HBO administration is often during the same period when intensive resuscitative efforts and focused ventilator management are required and could limit attention to these important therapies. In addition, it is known that pulmonary toxicity may result from elevated partial pressures of oxygen.135 Very little information is available to predict the effect of hyperoxygenation on pulmonary toxicity following smoke inhalation.141,154 Therefore, the decision to treat a smoke inhalation patient with HBO should take into account risks and other clinical requirements when determining the appropriate therapy17 (Chap. 125 and Antidotes in Depth: A37).
Cyanide is a common product of combustion, with toxic concentrations often measured in fire victims. Because no diagnostic test is readily available in the field or in the emergency department, cyanide poisoning should be suspected in seriously ill patients with smoke inhalation, particularly in the presence of metabolic acidosis with an elevated lactate concentration.44,126 Serum lactate concentrations at the time of hospital admission correlate closely with blood cyanide concentrations, with serum lactate concentrations of 10 μmol/L reported to be a sensitive indicator of cyanide toxicity.8 Baud demonstrated that carboxyhemoglobin levels of more than 10% also correlate with elevated cyanide concentrations. Additional clinical markers of potential cyanide poisoning include alteration of the central nervous system and cardiac function, although other factors of smoke inhalation injury can have similar effects. Specific treatment of cyanide toxicity should be implemented while other life support measures, including 100% oxygen therapy, are instituted.8,91,107 Treatment options include supportive care with or without empiric administration of a cyanide antidote. Systematic reviews of the human evidence regarding various cyanide antidotes conclude that it is possible to survive even cardiorespiratory arrest due to cyanide poisoning if given an appropriate antidote.48,123 In one review, 50% of cyanide poisoned victims (the majority due to smoke inhalation) had transient return of spontaneous circulation and 12% survived to hospital discharge; outcomes of treatment with hydroxocobalamin, thiosulfate, or a combination of sodium nitrite, amyl nitrite, and sodium thiosulfate were indistinguishable.48,123 The reviews found the onset of action of sodium thiosulfate slower when compared to hydroxocobalamin as the only clinically significant difference.48,123 Because definitive evidence of superiority is lacking, hydroxocobalamin (with or without sodium thiosulfate as an adjunct) or sodium thiosulfate alone are the antidotes of choice and should be considered for administration to smoke inhalation victims suspected of cyanide poisoning and exhibiting neurological impairment, cardiorespiratory collapse, or metabolic acidosis with elevated lactate123 (Chap. 126, Antidotes in Depth: A38 and A40).
Cyanide antidotes are intended as an adjunct to basic critical care strategies that optimize oxygen delivery and utilization. Therefore, the amyl nitrite and sodium nitrite components of the classic cyanide antidote kit should be avoided in victims of smoke inhalation. Amyl nitrite and sodium nitrite produce methemoglobinemia, which binds cyanide to form cyanmethemoglobin (Chap. 126 and Antidotes in Depth: A38). Unfortunately, methemoglobin is a dysfunctional type of hemoglobin that poorly utilizes oxygen, impairing delivery to the tissues.31 Impairing oxygen-carrying capacity and oxygen delivery to tissues with nitrite-induced methemoglobinemia is a valid concern in the presence of tissue hypoxia from carboxyhemoglobinemia, lung injury, or other factors. Furthermore, rapid infusion of sodium nitrite may cause hypotension secondary to vasodilation.49
Victims of fires may have respiratory compromise and other pathology not directly related to smoke inhalation, but rather from trauma or other underlying medical problems. Trauma from falls or explosions must be suspected and treatment started simultaneously with treatment of burns and inhalation injury. Comatose patients should be considered to have other causes for their status and should receive naloxone, thiamine, and hypertonic dextrose as indicated. Inhaled xenobiotics, such as carbon monoxide, may directly cause altered mental status, but drug and ethanol intoxication contribute significantly to fire fatalities and injuries. Blood ethanol concentrations correlate with elevated concentrations of carbon monoxide and cyanide, implying that intoxication impairs escape and prolongs toxic smoke exposure.5,11,99 Intracranial pathology should be considered and CT scans obtained as indicated.
Xenobiotics may injure the skin or mucous membranes in addition to the respiratory mucosa.27 The duration of contact of a xenobiotic with tissue is an important factor in determining the extent of chemical injury to the skin and eyes. Rapid removal of soot from the skin or eyes may prevent continued injury. The eyes should be evaluated for corneal burns caused by thermal or irritant chemical injury. Patients with signs of ophthalmic irritation should have their eyes irrigated, and dermal decontamination should be considered to prevent burns from toxin-laden soot adherent to the skin.