Smoke inhalation

Signs and symptoms

After recent fire exposure, some of the signs and symptoms of smoke inhalation injury include cough, wheezing, stridor, confusion, difficulty breathing, low oxygen saturation, smoke debris (especially on the face or in saliva), burns (especially on the face), singed facial or nose hairs, or hoarse voice. A careful history can be helpful in determining where the fire occurred and what chemical fumes could have been inhaled as a result to determine what systemic toxicities may be present.

Smoke inhalation injury can lead to minor or major respiratory complications. Acute respiratory distress syndrome (ARDS) is a relatively delayed complication of smoke inhalation injury caused by chemical fumes inducing an inflammatory response in lung tissue, especially the small air sacs in the lungs where critical gas exchange occurs. Another potential complication is swelling of the upper airway from heat and chemical damage, which can become profound enough to obstruct breathing. The onset of airway swelling can be relatively delayed, making it difficult to intubate later on. Endotracheal intubation is considered early in certain situations for this reason. Other possible complications include pneumonia, vocal cord dysfunction and damage, and tracheal stenosis (usually delayed).

Mechanism

Inhalation of chemical toxins produced by combusting materials can cause damage to tissues of both the upper (above the larynx) and lower respiratory tract (below the larynx). Damage to the lower airways, air sacs, and lung tissue is due to an inflammatory cascade in response to the noxious chemicals which causes a variety of downstream effects such as increased secretions and exudative material that clogs the airways or air sacs, collapse of air sacs, vascular permeability that leads to fluid in the lungs, bronchoconstriction, activation of the coagulation cascade, and impaired function of the mucociliary escalator.

Inhalation of hot fumes can cause thermal damage to tissue, usually limited to the upper respiratory tract (above the larynx). Damage in this location can result in sloughing of the damaged tissue and swelling, both of which can cause obstruction of the respiratory tract, ulceration, increased secretions, and redness.

Systemic toxicity can occur from inhalation of chemical compounds produced as byproducts of combustion in a fire. Carbon monoxide poisoning is the most common systemic toxicity after smoke inhalation, and can cause organ failure from lack of oxygen (often heart attack). Carbon monoxide is a common byproduct of combusting substances in fires and is colorless and odorless. It has a much higher binding affinity for hemoglobin compared to oxygen and can block oxygen from binding to hemoglobin. Additionally, carbon monoxide also decreases the ability of oxygen to dissociate from hemoglobin to diffuse into tissue. Both of these lead to hypoxia.

According to a New York Times article from 2022, while smoke inhalation has not been proven to cause lung cancer, unlike cigarette smoke (including secondhand smoke), studies published around that time found a correlation between the two. A panel of experts from Stanford University compared the inhalation of wildfire smoke to smoking cigarettes, stating, "exposure to high levels of pollution from wildfire smoke is the equivalent of smoking seven cigarettes a day." Dr. Nadeau, one of the panel's experts, later stated that, "cigarettes at least have filters."

The article also mentioned a study published in 2019 which found that firefighters who worked an average of 7 weeks per year for 5 to 25 years increased their risk of lung cancer by 8 to 26 percent due to smoke inhalation.

Treatment

First responders often take the victim away from the fire and smoke, give 100% oxygen at high flow through a face mask (non-rebreather if available), assess level of consciousness, and check the victim for burns and/or injuries to the body for initial care. Upper respiratory tract injury due to heat exposure often results in swelling. Intubation should be considered early given that the swelling can have a slow, delayed onset but will make intubation very difficult once present.

Lower respiratory tract injury due to exposure to noxious fumes often consists of supportive measures such as intubation and ventilator support if indicated, suctioning of the airways, and other supportive measures. Intravenous fluids are a mainstay in treatment of fire victims with extensive burns to the body, however, there are differing perspectives on the risks and benefits of IV fluids in fire victims with both burns and smoke inhalation injury due to the potential worsening of pulmonary edema with large amounts of IV fluids typically given in burn victims.

Other treatments with differing perspectives and study findings on utility in smoke inhalation injury include nebulized bronchodilators (such as beta-2-agonists), IV corticosteroids, nebulized corticosteroids, nebulized epinephrine, nebulized heparin, and nebulized N-acetylcysteine.

Carbon monoxide poisoning is initially treated with high flow 100% oxygen. Hyperbaric oxygen therapy can be considered, but there are differing views on its clinical benefit in terms of outcomes.

Systemic poisonings

Products with systemic effects are mainly asphyxiating gases, such as carbon monoxide and cyanides.

Carbon monoxide

Carbon monoxide (СО), which is absorbed by the lungs, diffuses into the capillaries and dissolves in the plasma and erythrocytes, binding to hemoglobin. As its affinity is more than 200 times that of oxygen, the amount of oxygen bound to hemoglobin is reduced, leading to anoxia. In addition, carbon monoxide released at the tissue level binds to mitochondrial enzyme systems, resulting in the inability of cells to utilize oxygen. When exposed to excess CO, one of the body's natural reactions is to breathe faster. This further increases the CO level in the blood, eventually leading to cardiac arrest.

Cyanides

Once the cyanide ion (CN-) enters the bloodstream, it diffuses into body cells. It binds to the trivalent iron of mitochondrial cytochrome oxidase, causing its inhibition and hence tissue anoxia. The metabolism shifts towards anaerobic metabolism, leading to an increase in lactacidemia.