Inhalation Injury in the Burned Patient

Abstract

Inhalation injury causes a heterogeneous cascade of insults that increase morbidity and mortality among the burn population. Despite major advancements in burn care for the past several decades, there remains a significant burden of disease attributable to inhalation injury. For this reason, effort has been devoted to finding new therapeutic approaches to improve outcomes for patients who sustain inhalation injuries.The three major injury classes are the following: supraglottic, subglottic, and systemic. Treatment options for these three subtypes differ based on the pathophysiologic changes that each one elicits.Currently, no consensus exists for diagnosis or grading of the injury, and there are large variations in treatment worldwide, ranging from observation and conservative management to advanced therapies with nebulization of different pharmacologic agents.The main pathophysiologic change after a subglottic inhalation injury is an increase in the bronchial blood flow. An induced mucosal hyperemia leads to edema, increases mucus secretion and plasma transudation into the airways, disables the mucociliary escalator, and inactivates hypoxic vasocontriction. Collectively, these insults potentiate airway obstruction with casts formed from epithelial debris, fibrin clots, and inspissated mucus, resulting in impaired ventilation. Prompt bronchoscopic diagnosis and multimodal treatment improve outcomes. Despite the lack of globally accepted standard treatments, data exist to support the use of bronchoscopy and suctioning to remove debris, nebulized heparin for fibrin casts, nebulized N-acetylcysteine for mucus casts, and bronchodilators.Systemic effects of inhalation injury occur both indirectly from hypoxia or hypercapnia resulting from loss of pulmonary function and systemic effects of proinflammatory cytokines, as well as directly from metabolic poisons such as carbon monoxide and cyanide. Both present with nonspecific clinical symptoms including cardiovascular collapse. Carbon monoxide intoxication should be treated with oxygen and cyanide with hydroxocobalamin.Inhalation injury remains a great challenge for clinicians and an area of opportunity for scientists. Management of this concomitant injury lags behind other aspects of burn care. More clinical research is required to improve the outcome of inhalation injury.The goal of this review is to comprehensively summarize the diagnoses, treatment options, and current research.

Factors Associated with In-hospital Mortality in Severe Burn Patients in Songklanagarind Hospital: A Retrospective Study

“…Taken together with our finding that high serum creatinine was associated with unfavorable outcomes, the evidence suggests that management of circulatory failure and special attention to inhalation injuries should be priorities in improving the care process. As burns involving the facial area are associated with higher risk of inhalation injury [18][19][20] , airway and respiratory care should be promptly provided in patients with facial burns no matter how extensive the TBSA is. 21,22 Early bronchoscopy in order to grade the severity of inhalation injury is advised for cases with suggestive evidence such as signs of airway edema, respiratory failure, carboxyhemoglobinemia and adult respiratory distress syndrome.…”

Clinical Forensic Aspect of Burn Injury in Domestic Violence: A Case Report

“…Some deaths in burns occur due to laryngospasm due to the influence of hot air inhaled. (12)(13)(14) As mentioned before, the determination of the degree of burn is assesed by the depth of the burn, the extent of the burn and the injury that accompaniying the burn. In this case , it was found degree 2B burns as wide as 16% on the face, neck, chest, both hands and feet accompanied by inhalation injury.…”

Obstructive Tracheal Necrosis in a Dog Secondary to Smoke Inhalation Injury—Case Report

“…Fiber optic bronchoscopy has been advocated in people with suspected SII because it allows direct airway visualization and assessment of tissue damage such as erythema and epithelial sloughing that can occur from thermal damage or chemical inhalation (2,12). Additionally, during bronchoscopy the clinician can decide whether the patient is likely to require intubation to maintain airway patency (13).…”

“…Upper and lower airway damage and pulmonary parenchymal injury can occur associated with smoke exposure. Acute respiratory signs are often a consequence of direct thermal injury, and the derived soft tissue edema to the supraglottic structures with subsequent airway obstruction (2,3).…”

“…Upper and lower airway damage and pulmonary parenchymal injury can occur associated with smoke exposure. Acute respiratory signs are often a consequence of direct thermal injury, and the derived soft tissue edema to the supraglottic structures with subsequent airway obstruction ( 2 , 3 ). Delayed respiratory signs are generally attributed to pulmonary parenchymal injury leading to pulmonary edema or secondary bacterial infection.…”