Epidemiology

Fires are common events in the United States. It is estimated that fire departments respond to fire alarms every 20 seconds.¹ In 2007, more than 1 million fire incidents and nearly 3500 deaths were reported, with civilian fatalities occurring every 153 minutes on average.¹ An estimated 50% to 80% of fire-related deaths are the result of smoke inhalation. Incident after incident, most of the victims of fires in commercial buildings, such as clubs, escape burns but suffer from smoke inhalation

Smoke inhalation injuries related to fire result from the toxic gases generated. Deaths from smoke inhalation have increased in recent years because of the abundant use of newer synthetic material in building and furnishings.²

Pathophysiology

Deaths from fires are most often caused by smoke inhalation.^3,⁴ The injury from smoke inhalation is a result of direct thermal injury to the airway and lung parenchyma, as well as mucosal irritation, corrosive injuries, and asphyxiation from toxic gases. Toxic gases can be classified as irritant gases and asphyxiants. The danger from such toxic gases predominates in exposed fire victims. Smoke is composed of a complex mixture of suspended small particles, fumes, and gases. More than 400 toxic compounds have been demonstrated in the smoke of a typical house fire. Polyvinyl chloride, a component of many plastic goods, generates at least 75 different toxic products when burned. Of these toxic substances, carbon monoxide (CO) appears to be the most common fatal substance associated with fire victims.^5,⁶

Thermal inhalation injuries are usually localized to the upper airway. Irritant gases, depending on their water solubility, affect either the upper or lower airway. Highly water-soluble agents such as ammonia, hydrogen chloride, and sulfur dioxide predominantly affect the upper airway. Their solubility directly correlates with rapid adverse upper airway symptoms. Agents with lower water solubility, such as phosgene and nitrogen dioxide, which do not produce immediate irritation, will be inhaled deeper in the pulmonary system and result in injury to the alveoli; victims typically have delayed noncardiogenic pulmonary edema.

Asphyxiants further compound the injury in smoke inhalation victims. Simple asphyxiants, such as carbon dioxide and methane, will produce an oxygen-deprived environment. Systemic asphyxiants, such as CO, cyanide, and hydrogen sulfide (H₂S), will prevent utilization of oxygen by cells. Either mechanism will promote an anaerobic state and the development of lactic acidosis.

CO is a colorless, odorless, nonirritating gas produced by the incomplete combustion of hydrocarbons and petroleum distillates, whether from a fire, fuel source, or automobile exhaust or from the metabolism of methylene chloride, a solvent commonly used as a paint stripper. One of the major mechanisms of CO toxicity is its affinity to bind hemoglobin, with an affinity estimated to be approximately 250 times greater than that of oxygen, which results in reduction in oxyhemoglobin. The impairment in delivery of oxygen is exacerbated by displacement of the oxygen dissociation curve to the left. Furthermore, CO interferes with cellular respiration by binding to mitochondrial cytochrome oxidase and is involved in the formation of oxygen free radicals and subsequent lipid peroxidation. All the aforementioned mechanisms produce oxidative stress on the brain, the main organ affected by CO; excitatory amino acids such as glutamate are activated, which results in neuronal injury and cell death. Areas of the brain that are highly sensitive to hypoxemia, such as the basal ganglia, appear to sustain the most injury. CO is known to bind to myoglobin as well, a feature that contributes to impairment in myocardial contractility. Fetal hemoglobin is more sensitive to the binding of CO; levels are reported to be approximately 10% higher than maternal levels, with a half-life five times longer. Over time, carboxyhemoglobin will dissociate, with its half-life on room air being approximately 4 to 6 hours. With 100% oxygen, the half-life decreases to approximately 90 minutes, and in the setting of hyperbaric oxygen therapy, it is about 20 minutes.

Cyanide is a highly toxic chemical. Hydrogen cyanide is a common by-product of the pyrolysis of wool, silk, and plastics. Cyanogenic compounds such as nitriles are used in industry as solvents and adhesives and are metabolized by the body to cyanide. Acetonitrile, which in the past was commercially available as an artificial nail glue remover, has resulted in fatality when accidentally ingested.⁷ With increasing concern about terrorism, it is high on the potential lists of chemical agents. Its mechanism is binding of the cytochrome aa₃ site on the electron transport system of mitochondria. The result is an inability to use oxygen and subsequent cellular asphyxia.

H₂S is the by-product of certain industries, such as paper factories, petroleum refineries, and dehairing of hides. It is produced naturally from decay of organic matter and from sulfur hot springs. These products have the characteristic “rotten egg” odor. Like cyanide, it is a potent inhibitor of the cytochrome oxidase system. The human nose is exquisitely sensitive to the odor of H₂S, and it is easily detected at levels as low as 0.13 parts per million (ppm). Irritation of mucous membranes occurs at levels of approximately 50 to 100 ppm, and such levels are also capable of causing bronchospasm, blepharospasm, and laryngeal edema. At levels greater than 500 ppm, a phenomenon classically described as a “rapid knockdown” effect occurs, which includes immediate loss of consciousness with the potential for cardiovascular collapse and respiratory arrest. Sulfhemoglobin may result from exposure to H₂

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