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.

No abstract

Cuff measurements vary widely from those of intra-arterial lines, which have a low complication rate. Intra-arterial lines are advisable when tight control of the hemodynamic response is essential.

This pilot study was conducted to profile safety of nebulized racemic epinephrine when used as a therapy for smoke inhalation injury in severely burned children. We enrolled 16 patients who were 7 to 19 years of age ([mean ± SD] 12 ± 4 years) with burns covering over 30% of the total body surface area (55 ± 17%) and smoke inhalation injury, as diagnosed by bronchoscopy at burn center admission. Patients were randomized to receive either standard of care (SOC; n = 8), which consisted of nebulized acetylcysteine, nebulized heparin, and nebulized albuterol, or to receive SOC plus nebulized epinephrine (n = 8). Primary endpoints were death, chest pain, and adverse changes in cardiopulmonary hemodynamics (arrhythmia, arterial blood pressure, electrocardiographic [ST segment] changes, and peak inspiratory pressure). Additional endpoints included total days on ventilator, pulmonary function, and physiological cardiopulmonary measurements at ICU discharge. No adverse events were observed during or after the nebulization of epinephrine, and no deaths were reported that were attributable to the administration of nebulized epinephrine. The groups did not significantly differ with regard to age, sex, burn size, days on ventilator, pulmonary function, or cardiopulmonary fitness. Results of this pilot trial indicate epinephrine to be safe when administered to pediatric burn patients with smoke inhalation injury. Current data warrant future efficacy studies with a greater number of patients.

This information will be used to develop and help modify existing prevention campaigns.

Objective Electrical burns are a severe form of thermal injury extending deep into tissue. Here, we investigated the effect of electrical burns on metabolic rate, body composition, and aerobic capacity. Methods We prospectively studied a cohort of 24 severely burned children. Twelve patients had a combination of electrical and flame burns and 12 matched controls had only flame burns. Endpoints were cardiopulmonary fitness (maximal oxygen consumption [VO2]), muscle strength (peak torque per body weight), body mass index, lean body mass index, and days of myoglobinemia (≥ 500 mg/dL). Results Demographics of both groups were comparable. The electrical burn group had more days of myoglobinemia during acute hospitalization than the flame burn group (3.6 ± 1.8 days vs. 0.3 ± 0.5 days, p < 0.0001). Maximal VO2 was significantly lower in the electrical burn group than in the flame burn group at ICU discharge (27 ± 6 mL/kg/min vs. 34 ± 5 mL/kg/min, p < 0.0014). Conclusions Electrical burns are associated with myoglobinemia as well as decreased cardiopulmonary fitness.

Patients who participate in a community-based exercise program show significant improvements in cardiopulmonary fitness compared with SOC, supporting the use of a community-based exercise program as an alternative therapy to SOC in adults with severe burns.

Not applicable.