Inhalation injury: epidemiology, pathology, treatment strategies

Abstract

Lung injury resulting from inhalation of smoke or chemical products of combustion continues to be associated with significant morbidity and mortality. Combined with cutaneous burns, inhalation injury increases fluid resuscitation requirements, incidence of pulmonary complications and overall mortality of thermal injury. While many products and techniques have been developed to manage cutaneous thermal trauma, relatively few diagnosis-specific therapeutic options have been identified for patients with inhalation injury. Several factors explain slower progress for improvement in management of patients with inhalation injury. Inhalation injury is a more complex clinical problem. Burned cutaneous tissue may be excised and replaced with skin grafts. Injured pulmonary tissue must be protected from secondary injury due to resuscitation, mechanical ventilation and infection while host repair mechanisms receive appropriate support. Many of the consequences of smoke inhalation result from an inflammatory response involving mediators whose number and role remain incompletely understood despite improved tools for processing of clinical material. Improvements in mortality from inhalation injury are mostly due to widespread improvements in critical care rather than focused interventions for smoke inhalation.Morbidity associated with inhalation injury is produced by heat exposure and inhaled toxins. Management of toxin exposure in smoke inhalation remains controversial, particularly as related to carbon monoxide and cyanide. Hyperbaric oxygen treatment has been evaluated in multiple trials to manage neurologic sequelae of carbon monoxide exposure. Unfortunately, data to date do not support application of hyperbaric oxygen in this population outside the context of clinical trials. Cyanide is another toxin produced by combustion of natural or synthetic materials. A number of antidote strategies have been evaluated to address tissue hypoxia associated with cyanide exposure. Data from European centers supports application of specific antidotes for cyanide toxicity. Consistent international support for this therapy is lacking. Even diagnostic criteria are not consistently applied though bronchoscopy is one diagnostic and therapeutic tool. Medical strategies under investigation for specific treatment of smoke inhalation include beta-agonists, pulmonary blood flow modifiers, anticoagulants and antiinflammatory strategies. Until the value of these and other approaches is confirmed, however, the clinical approach to inhalation injury is supportive.

Figure 1

Relationship between burn size and incidence of inhalation injury illustrates the rise in occurrence of inhalation injury with increasing burn size [[5]].

Figure 2

Burn size as percentage of total body surface area on X axis, age on Y axis, and percent increment in mortality due to the presence of inhalation injury on Z axis are shown. Mortality, in the presence of inhalation injury alone, rose by a maximum of approximately 20% in patients in midrange of severity of injury as indexed by age and burn size [5].

Figure 3

Burn size as percentage of total body surface area on X axis, age on Y axis, and percent increment in mortality on Z axis are shown. Mortality rose by a maximum of approximately 60% in patients in midrange of age and burn size when both inhalation injury and pneumonia were present [5].

Figure 4

Hemoglobin is converted rapidly to carboxyhemoglobin in the presence of carbon monoxide [[3]].

Figure 5

Carboxyhemoglobin-induced changes in the oxygen-hemoglobin dissociation curve. Oxygen-carrying capacity is markedly diminished when carboxyhemoglobin values reach 40% to 50%. In addition, the leftward displacement of the oxygen-hemoglobin dissociation curve makes the oxygen that is bound to hemoglobin less available for delivery to tissues [3].