What are approach considerations in the treatment of smoke inhalation injury?

Updated: Oct 15, 2021
  • Author: Keith A Lafferty, MD; Chief Editor: Joe Alcock, MD, MS  more...
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Answer

Beware that patients may appear asymptomatic on arrival but may develop significant signs and symptoms as long as 36 hours after exposure, especially in fires, which produce small particles with low water solubility. Be aware of pertinent historical risk factors when treating patients with potential smoke inhalation injury. These include closed-space fires, carbonaceous sputum, elevated carbon monoxide (CO) levels, and central facial burns.

Acute respiratory distress usually responds very well to aggressive initial management. Normal laboratory values and imaging studies, coupled with clinical improvement, can give the health care provider a false sense of security. The patient then may be discharged, only to deteriorate as delayed pulmonary edema ensues. Any patient with significant exposure to toxic smokes should be observed for 24-48 hours and imaged with serial chest radiographs. Difficulty arises in defining a significant exposure, since the clinical response is so varied.

Provide intravenous (IV) access, cardiac monitoring, and supplemental oxygen in the setting of hypoxia. A small subset of patients manifests bronchospasm and may benefit from the use of bronchodilators, although this is not well documented. This is especially true of patients with underlying chronic obstructive pulmonary disease (COPD) or asthma.

Treatment of inhalation injuries caused from toxic smokes is based on clinical presentation and involves primarily supportive care directed at the cardiopulmonary system. In some cases (eg, cyanide [CN] poisoning, methemoglobinemia), specific antidotes are available. Subcutaneous epinephrine has been used in zinc oxide (HC) exposures.

Corticosteroids are attractive for suppressing inflammation and reducing edema, but no direct data support their use in smoke inhalation. Because of the increased risk of pulmonary infection and delayed wound healing, prolonged use of steroids is discouraged. However, consider a brief course of steroids in those patients with otherwise unresponsive severe lower airway obstruction. In addition, patients receiving steroids prior to injury who may experience adrenal insufficiency should receive stress doses of steroids.

In a case series by Huang et al, 25% of patients presented after HC exposure with acute lung injury requiring ventilatory support. All of these patients survived with glucocorticoids, antibiotics and lung-protective ventilatory management. However, there was no control group, so a causal link could not be made between survival and steroid treatment. [3, 46]

Smoke inhalation injuries predispose the airways to infection because of cellular injury, reduction of mucociliary clearance, and poor macrophage function. Acute bacterial colonization and invasion peaks at 2-3 days after smoke inhalation. Prophylactic antibiotics should not be used, as they are not only ineffective but increase the risk of emergence of resistant organisms.

Discerning secondary infection from the effects of inhalation injury can be very difficult because both may produce fever, elevated white blood cell counts, and abnormal radiography findings. Antimicrobial therapy should be reserved for patients with definitive microbiologic evidence of infection that is not responding to aggressive support therapy or when clinical deterioration occurs in the first 72 hours.

The most common organisms in secondary pneumonia after smoke inhalation injury are Staphylococcus aureus and Pseudomonas aeruginosa. Direct parenteral coverage with antibiotics to cover these bacteria if infection is suspected.


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