From the Guidelines
Smoke inhalation resulting in acute lung injury is a complex process involving direct thermal injury, chemical irritation, and systemic toxicity, ultimately leading to inflammation, increased capillary permeability, and potential progression to acute respiratory distress syndrome (ARDS). The pathophysiology of this condition is multifaceted, involving various damaging mechanisms. Initially, inhaled hot gases cause thermal injury to the upper airways, resulting in edema and potential obstruction. Simultaneously, toxic chemicals in smoke, such as aldehydes, nitrogen oxides, and sulfur dioxide, directly damage the bronchial epithelium, leading to increased capillary permeability, inflammation, and bronchospasm 1.
Key factors contributing to the development of acute lung injury include:
- Direct thermal injury to the upper airways
- Chemical irritation throughout the respiratory tract
- Systemic toxicity from absorbed compounds, such as carbon monoxide and cyanide
- Inflammatory mediators triggering neutrophil infiltration into lung tissue
- Surfactant dysfunction, alveolar collapse, pulmonary edema, and ventilation-perfusion mismatch
The severity of smoke inhalation-induced acute lung injury depends on various factors, including exposure duration, smoke composition, and pre-existing conditions. Treatment focuses on oxygenation support, airway management, and addressing specific toxicities like carbon monoxide and cyanide poisoning. The morbidity and mortality associated with acute lung injury may be declining slowly, although it is widely considered to remain in excess of 40%, with mortality most often due to unresolved sepsis or multisystem organ failure (MOF) as opposed to progressive respiratory failure 1.
From the Research
Pathophysiology of Acute Lung Injury due to Smoke Inhalation
- Acute lung injury (ALI) is characterized by acute pulmonary inflammation with disruption of the pulmonary vasculature endothelial and alveolar epithelial barriers 2
- Smoke inhalation injury can cause upper airway thermal burns, inflammation from lower airway irritants, and systemic effects of carbon monoxide and cyanide, contributing to ALI 3, 4
- The pathophysiology of ALI involves disruption of the alveolar-capillary membrane, leading to impaired gas exchange, and can progress to acute respiratory distress syndrome (ARDS) 5, 2
Clinical Presentation and Diagnosis
- Patients with smoke inhalation injury may present with hypoxemia, tachypnea, and cyanosis, and may require close monitoring for development of airway compromise 3, 4
- Diagnosis is mostly clinical, aided by bronchoscopy and other supplementary tests, and imaging findings may show bilateral pulmonary infiltrates without pulmonary edema 2
Treatment and Management
- Treatment for smoke inhalation injury includes airway and respiratory support, lung protective ventilation, 100% oxygen or hyperbaric oxygen therapy for carbon monoxide poisoning, and hydroxocobalamin for cyanide toxicity 3, 4
- Inhaled anticoagulation regimens may improve survival and decrease morbidity in patients with smoke inhalation-associated ALI, although further studies are needed to validate their use 6
- Clinical management of ALI is often supportive and may include corticosteroids, mechanical ventilation, and careful fluid management, with the goal of preserving and recovering lung function 2