Inhalation of Smoke in Fires

In fire situations, most people automatically relate deaths and injuries to fire burns. However, the main cause of death and need for hospitalization of individuals exposed to fires occurs due to the injuries caused by the inhalation of smoke. About 80% of deaths are by inhalation of vapors and chemicals, mainly carbon monoxide and cyanide.

Smoke emitted during fire
Smoke emitted during fire
 


Hazards from fire smoke

Smoke from combustion can cause death or serious injury by 3 basic mechanisms: respiratory tract injury from breathing air, asphyxiation from lack of oxygen, and direct irritation of the pulmonary tree from inhaled chemicals.

A. Thermal damage from smoke


The thermal lesions caused by smoke, that is, the burns caused by the heat of the smoke in the airways, are usually confined to the region of the oropharynx. The contact of the airways with very hot air stimulates the closure of the glottis, reducing the passage of heat into the lungs.

Another protective factor is the high heat dissipation in the upper respiratory tract, which helps reduce the temperature of the smoke before it reaches the lungs. Animal experiments show that inhaled smoke at 142°C cools to 38°C by the time it reaches the main bronchi, no longer being able to burn the lungs. An exception occurs in the case of aspiration of humid heat, such as vapors, which can keep warm to the lungs, and can cause serious thermal injuries in them. Hot humid air is more dangerous than hot dry air.

B. Asphyxiation


Heat injury can cause severe airway swelling (airway swelling), blocking the passage of air into the lungs, similar to severe allergy and glottal edema. Unable to breathe, the individual dies by suffocation.

Choking may also occur for reasons other than obstruction of the airways by swelling of the burns. As we all know, for combustion of any substance to occur, there must be oxygen consumption. Large fires indoors, with poor ventilation, consume a large amount of oxygen rapidly. In the ambient air we breathe, about 21% of the volume is composed of oxygen. In fires, the oxygen concentration drops by half, being insufficient for the oxygenation of blood and cells, leading patients to hypoxemia (lack of oxygen in the blood).

In addition to the drop in oxygen concentration in the air, aspiration of other substances into the smoke, such as carbon monoxide and/or cyanide can also cause choking. The mechanism is as follows:

Hemoglobins are proteins present in red blood cells, responsible for transporting oxygen through the blood. The hemoglobins go to the lungs, pick up on the oxygen breathed and take it towards the rest of the body, in order to oxygenate cells and tissues. Substances such as carbon monoxide or cyanide bind to hemoglobins and prevent them from receiving oxygen from the lungs. A molecule of carbon monoxide is 240 times more affinity for hemoglobin than the oxygen molecule, easily winning the contest for a place in these carrier proteins. In normal situations only 3% of hemoglobins are bound to carbon monoxide. Smokers usually have about 10% of their hemoglobins occupied. Already patients exposed to fires usually have more than 25% of their hemoglobins unable to carry oxygen.

Cyanide acts similarly to carbon monoxide, being considered one of the most poisonous substances we know. Cyanide gases are produced from the combustion of materials such as wool, silk, polyurethanes, polyacrylonitriles, nylon, melamine resins and plastics.

To sum up: the environment has oxygen, the patient can breathe it, but the lungs can not take it to the blood, cells and tissues of the body, because the hemoglobins are "occupied", filled with other substances.

C. Injury of the airways by inhaled chemicals


The smoke of a fire is a mixture of heated particles and gases, and it is impossible to know exactly what it is made of. The products being burned, the temperature of the fire and the amount of oxygen available for combustion can change the type of smoke produced.

In general, in the fumes there is a great amount of substances irritating to the mucosa of the respiratory system. Examples of chemical irritants found in fires include: sulfur dioxide, ammonia, hydrogen chloride and chlorine. These substances, when in contact with the mucous membranes of the respiratory tree, provoke an intense inflammatory reaction, leading to fluid leakage, edema formation, mucus production, epithelial desquamation, cell death and pulmonary tissue necrosis. All of these events contribute to a lower capacity for lung function and may cause acute respiratory failure.

Immediate treatment of the patient with inhalation of smoke

Every person exposed to a fire should receive the first medical attention at the scene of the accident. It is important to evaluate the respiratory pattern and conditions of the oropharynx. Because airway edema develops rapidly and can completely occlude air passage, clinicians must decide whether or not the patient needs to intubate in order to ensure airway permeability. It is paramount to prevent respiratory failure, as this is the leading cause of death in patients who are involved in fires.

Intubation is warranted if any of the following signs are present: stridor while breathing, severe use of the abdominal and thoracic muscles to breathe, difficulty breathing, hypoventilation, deep burns to the face and/or neck, blistering or oropharyngeal edema. All of these situations indicate a high risk of serious respiratory injury, with imminent respiratory failure.

Patients who are known to have been exposed to smoke but do not have these signs of severity should be observed for 24 hours, as edema of the airways may take a few hours to emerge. Anyone exposed to smoke for more than 10 minutes should be observed.

All individuals exposed to smoke should receive 100% oxygen supplementation (remember that the air we breathe is oxygen at 21%). This large volume of oxygen serves to reverse the hypoxemia caused by the low concentrations of oxygen in fires and to increase the competition for hemoglobin against carbon monoxide and cyanide.

Patients burned and exposed to smoke should preferably be treated in intensive care units specializing in large burnings. Rapid care by doctors accustomed to dealing with this type of injury is important in reducing the risk of death.

Follow-up for the patient with inhalation of smoke

In the first few hours airway edema and hypoxemia are the main causes of death. After 12 to 36 hours of exposure to smoke, patients begin to develop symptoms related to airway irritation by chemicals. Difficulty breathing, wheezing (wheezing), and cough with large mucus are signs of irritation and injury to the bronchi and pulmonary alveoli.

In patients with severe carbon monoxide poisoning, treatment with hyperbaric oxygen may be indicated. The administration of 100% oxygen at high pressures helps to displace the carbon monoxide from hemoglobins, improving the state of blood oxygenation. Hyperbaric oxygen accelerates up to 5x the elimination of carbon monoxide from hemoglobins.

Late treatment of the patient with inhalation of smoke

If a severe injury to the tracheobronchial tree has occurred, the necrotic tissues will begin to loosen in 3 or 4 days. Increased secretions and accumulation of dead tissue put the patient at increased risk of airway obstruction.

Infection of the lung by bacteria becomes propitious, with pneumonia being a common complication in these patients.

The secretions usually decrease within 7 to 10 days if there is no development of lung infection.

Acute Respiratory Distress Syndrome (ARDS) may occur several days after exposure to smoke. This is a picture that occurs due to intense inflammatory activity of the lungs, with great leakage of liquids into the respiratory tract and acute respiratory failure.

Sequelae from exposure to fire smoke

Most patients who survive do not suffer severe long-term sequelae. However, there are patients who present permanent lesions of the vocal chords, remaining hoarse; other patients complain of shortness of breath for prolonged time, especially during physical exertion. Patients with chemical lung injury are those most at risk for long-term sequelae.

People who have been delayed receiving appropriate treatment and have had prolonged hypoxemia may present neurological damage due to poor cerebral oxygenation. Early institution of hyperbaric oxygen (within the first 6 hours) appears to reduce the risk of neurological injury.
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