Smoke Inhalation
Smoke inhalational injury is the most prominent cause of death in patients involved in fire accidents. It has been said that prevalence of death due to inhalation of smoke and other noxious substances stands between 60 and 80% in the United States. (Lafferty, 2010). Smoke inhalational injury remains a serious threat to the health of victims of explosions, house fires and other forms of fire disaster. (Murakami & Traber, 2002)
In the Pathophysiology of acute and chronic Smoke Inhalational Injury, three mechanisms readily come into mind. They include thermal damage of the lung parenchyma, pulmonary irritation and asphyxiation. (Lafferty, 2010).
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Damage due to heat is usually found at the region of the oropharynx. This injury is said to be as a result of poor conduction of air and the amount of dissipation that occurs at the level of the upper part of the airways. The dissipation means that the temperature of the inhaled air or gas is rapidly reduced. As a result of this, the surrounding tissue of the upper part of the airway absorbs the heat generated. This results in direct thermal burns to this region, leading to rapid coagulative necrosis of the tissue of the upper airways. (Lafferty, 2010) Smoke is made up of gases and particles. The nasopharynx is responsible for clearing air to be inspired of the particles. However, during a fire, the nasopharynx may have been irritated by the irritant gases, leading the victims to breathe through the mouth. This leads to more particles being deposited in the airways. This leads to progressive injury to the tissues of the airways and lung injury. (Rehberg et al, 2009)
Another mechanism of acute smoke inhalational injury is asphyxiation. Asphyxiation can result from the reduction in the level of oxygen in the closed space that is the lung. This is as a result of the oxygen being used up in the combustion process. There is a significant reduction in the concentration of ambient Oxygen to as low as 10%. (Murakami & Traber, 2002) This leads to reduction in the proportion of oxygen that is inhaled from the air, which can lead to rapid tissue hypoxia. This is in the face of adequate circulation and oxygen-carrying capacity of the blood (Lafferty, 2010). Asphyxia can also be caused by Carbon monoxide which is a by-product of incomplete combustion. Carbon monoxide caused hypoxia by decreasing the oxygen-carrying capacity of the blood. The mechanism by which it does this is to bind with hemoglobin to form Carboxyhemoglobin. Hemoglobin has a higher affinity for carbon monoxide than Oxygen [the ratio is up to 200:1]. As a result, there is little of no chance of the carbon monoxide dissociating from hemoglobin as readily as oxygen would have done. This also has a direct effect on the myocardium which rapidly reduces myocardial contractility, thereby stopping the heartbeat after some time leading to cardiac arrest. Another mechanism of asphyxiation is by the gas Cyanide. Cyanide is a by-product of combustion of materials like different kinds of clothing, plastic, paper and polyurethane. The gas is even more toxic than carbon monoxide and causes immediate respiratory arrest. Cyanide binds to the ferric ion in Cytochrome a3.This action subsequently leads to stopping of cellular respiration (Murakami & Taylor 2003).. The effect is the cessation of the electron transport system, leading to rapid anaerobic metabolism and high lactic acidosis.
The mechanism of pulmonary irritation is such that irritants can cause direct injury to lung tissue. There can also be bronchospasm. The body’s inflammatory response system can also be activated.
The injury caused to the lung is a function of the size of the particles, the solubility of the particles in water and its acid-base status. Highly water soluble substances because more damage at the upper part of the airways. However, substances that is only partly soluble in water cause damage at both the upper and lower part of the airways. Substances that are not soluble in water, moreover, cause damage to the parenchyma of the lungs.
Pneumonia is a common cause of respiratory compromise in patients that have inhalational smoke injury. This is due to destruction of the ciliary mechanism for the removal of particles and microorganisms. This leads to infection of the lung parenchyma. Pneumonia can cause rapid respiratory compromise and even death if not treated promptly.
A long term sequelae is also chronic bronchitis due to continuous irritation of the airways. The individual usually presents with a chronic cough that persists a long time after the accident.
The mechanism of bronchial blood flow has also been implicated in smoke inhalational injury. Marakami and traber (2002) stated that the dual blood supply of the lungs [systemic and pulmonary] contributes to the pulmonary edema that results from increased in bronchial blood flow after smoke inhalational injury.
Nitrous oxide has also been implicated in lung injury following inhalation of smoke. Although Nitrous oxide has a role in regulating the microcirculation by vasodilatation, and also being a potent inhibitor of platelet aggregation. Production of excessive amount of nitrous oxide leads to it acting as a free radical which is highly reactive. It then mediates inflammation.
References
Denise, Serebrisky (2012). Inhalation Injury. Medscape Reference.
Kazunori, Murakami & Daniel, Traber (2003). Pathophysiological Basis of Smoke inhalation Injury. News Physiol Sci 18:125-129. 10.1152/nips 01427.2002
Keith, Lafferty (2010). Smoke Inhalation. Medscape Reference: Drugs, diseases & Procedures.
Robert, Demling (2008). Smoke Inhalation Lung Injury: An Update. Eplasty 2008; 8: e27
Sebastian, Rehberg et al (2009). Pathophysiology, Management and treatment of smoke inhalation injury. Expert Rev Respir Med. 2009 June 1; 3(3): 283–297. doi: 10.1586/ERS.09.21
