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Smoke Inhalation

Author: Keith A Lafferty, MD, Adjunct Assistant Professor of Emergency Medicine, Temple University; Consulting Staff, Department of Emergency Medicine, South West Regional Medical Center
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Updated: Dec 9, 2009

Introduction

Background

Smoke inhalation (SI) was described as early as the first century AD, when Pliny reported the execution of prisoners by exposure to the smoke of greenwood fires.

Many victims of fire accidents have both smoke inhalation and thermal injury. Inhalation injury from smoke and the noxious products of combustion in fires may account for as many as 60-80% of fire-related deaths in the US, many of which are preventable. Even though the excellence of care rendered at today's burn centers has greatly reduced the mortality from surface burns, the mortality from pulmonary injury has been increasing. Diagnosis of inhalation injury is not always straightforward, sensitive screening tests are lacking, and symptoms may be delayed until 24-36 hours after injury.

Pathophysiology

The 3 primary mechanisms that lead to injury in smoke inhalation are thermal damage, asphyxiation, and pulmonary irritation.

Thermal damage

Thermal damage usually is limited to the oropharyngeal area. This is due to the poor conductivity of air and the high amount of dissipation that occurs in the upper airways. Animal experiments have shown that if air at 142°C is inhaled, then by the time it reaches the carina it will have cooled to 38°C. Steam, volatile gases, explosive gases, and the aspiration of hot liquids provide some exceptions, as moist air has a much greater heat-carrying capacity than dry air.

Asphyxiation

Tissue hypoxia can occur secondary to several mechanisms. Combustion utilizes oxygen, which in a closed space may be consumed, significantly decreasing the ambient concentration of oxygen to as low as 10-13%. The decrease in fraction of inspired oxygen (FIO₂) leads to hypoxia, despite adequate circulation and oxygen-carrying capacity.

Carbon monoxide (CO) causes tissue hypoxia by decreasing the oxygen-carrying capacity of the blood. Hemoglobin binds CO with an affinity more than 200 times greater than the affinity for oxygen. Even though this tissue hypoxia is the primary insult, other mechanisms attribute to its pathophysiology.

CO also causes a left shift in the oxyhemoglobin saturation dissociation curve. CO has been shown to bind to the cytochrome oxidase chain in vitro. Finally, since CO binds to virtually all heme molecules, myocardial myoglobin is affected and consequently myocardial contractility is decreased.

Combustion of plastics, polyurethane, wool, silk, nylon, nitriles, rubber, and paper products can lead to the production of cyanide (CN) gas. CN also takes the form of solid crystals bound to sodium and potassium salts. It is also found abound in foods such as cassava and in apple, pear, apricot, and peach seeds. Hydrogen CN is a colorless gas with a bitter almond odor to the 40% of the population who are able to detect it. It is 20 times more toxic than CO and can cause immediate respiratory arrest.

Consider CN toxicity in all patients with smoke inhalation who have CNS or cardiovascular findings. CN is a chemical asphyxiant that interferes with cellular metabolism by binding to the ferric ion on cytochrome a₃, subsequently halting cellular respiration. As a consequence of the cessation of the electron transport system, anaerobic metabolism ensues, with corresponding high lactate acidosis and decreased oxygen consumption.

Methemoglobinemia occurs in fire due to heat denaturation of hemoglobin, oxides produced in fire, and methemoglobin-forming materials such as nitrites. Occurrence of methemoglobinemia is a rarer phenomenon than CN and CO toxicity. The pathophysiologic consequences of methemoglobin formation are a decrease in the oxygen-carrying capacity of the blood and a shift of the oxyhemoglobin dissociation curve to the left, similar to carboxyhemoglobin (HbCO).

Pulmonary irritation

Irritants can cause direct tissue injury, acute bronchospasm, and activation of the body's inflammatory response system. Activated leukocytes and/or humoral mediators, such as prostanoids and leukotrienes, produce oxygen radicals and proteolytic enzymes. Supporting the importance of the inflammatory response to the mechanism of tissue destruction, some studies have shown that the administration of the cyclooxygenase inhibitor, ibuprofen, was found to reduce the lung lymph flow in animals with smoke inhalation. The direct injury is a consequence of the size of the particle, its solubility in water, and its acid-base status. Ammonia produces alkaline injury, while sulfur dioxide and chlorine gas lead to acid injuries. Other chemicals act via different mechanisms; for instance, acrolein causes free radical formation and protein denaturation.

The location of injury depends on the solubility of the substance in water. High-solubility substances such as acrolein, sulfur dioxide, ammonia, and hydrogen chloride cause injury to the upper airway. Substances with intermediate solubility, such as chlorine and isocyanates, cause upper and lower respiratory tract injury. Phosgene and oxides of nitrogen have low water solubility and cause diffuse parenchymal injury.

In a study evaluating survivors of the World Trade Center collapse, 44% had persistent lower respiratory symptoms after 19 months of follow up.¹ Hence the term, "World Trade Center cough."

Frequency

United States

Burns and fires are the third leading cause of accidental death in all age groups. They comprise the second leading cause of death in the home for all ages and the leading cause of death in the home for children and young adults. In 1998, approximately 381,500 residential fires occurred in the US, resulting in 3,250 nonfirefighter deaths, 17,175 injuries, and nearly $4.4 billion in property loss. These figures do not include the estimated 90% of fires not reported to fire departments. More than half of all fatal residential fires started between the hours of 11 pm and 7 am.

Incidence of smoke inhalation increases from less than 10% in patients with a mean total body surface area (TBSA) burn size of 5% to more than 80% in patients with a mean TBSA burn size of 85% or more. Smoke inhalation is present in one third of patients treated at burn centers. The magnitude of smoke inhalation is devastating, as the presence of an inhalation injury has a greater effect on mortality than either patient age or surface area burned.

International

The US has one of the highest fire fatality rates in the developed world, accounting for 2.3 deaths per 100,000 population. In fact, fire death rates in the US and Canada are twice as high as in Western Europe and Japan.

Mortality/Morbidity

Mortality is related to associated cutaneous burns.

• In patients with a burn and no associated SI or respiratory failure, the mortality rate is less than 2%. In patients with smoke inhalation alone and no burn or respiratory failure, the mortality rate is 7%.
• For patients with a burn and smoke inhalation, the mortality rate increases to 29%, suggesting that the burn wounds themselves put an additional stress on the compromised lung.
• Studies have shown shown that children with CO poisoning alone compared to those with combined smoke inhalation and CO toxicity had an increase in mortality rate from 0% to 22.6%.
• In rats and sheep models, cutaneous burns result in systemic complement activation with pulmonary sequestration of activated neutrophils, which in turn release toxic metabolites, further injuring the lung.

Race

One study in New Jersey reports on the demographics of fire fatalities and notes that victims who perished did not parallel the ethnic census of the time.²

• Whites accounted for 53% of fatalities and comprised 49% on the census.
• African Americans accounted for 38% of fatalities and 13% of the census.

Sex

The male-to-female ratio is about 3:2.

Age

The New Jersey study also showed that children and the elderly represented a disproportionate percentage of people injured by fire.² People younger than 11 years or older than 70 years constituted 22% of the population but accounted for 40% of all fire fatalities. These statistics closely match national figures.

A comprehensive study in Dallas looked at all house fires from 1991-1997.³ Many of the findings parallel those of the New Jersey study.

• Relative risk of injury was 1.8 for men, 1.4 for boys, 2.8 for blacks, and 2.6 for elderly persons.
• In addition, among the injured, the proportion of injuries that were fatal was higher in persons older than 65 years (53%) and in those younger than 10 years (67%) compared with those aged 10-64 years (30%).
• The lowest income tracts had the highest rate of injury. The rate of injury in households with a median income below $20,000 per year was 8 times that of tracts with a median income greater than $80,000 per year. In fact, tracts with extremely low incomes, less than $10,000 per year, had rates of injury 20 times that of the above.
• Houses built in the 1950s and 1960s were somewhat more likely to burn than houses built before this time. This may be a case of "selection of the fittest" houses, with those houses most prone to burn having already done so leaving the most structurally sound ones still standing.
• Fires caused by arson occurred predominately in census tracts with lower median incomes. Eighty percent of fires occurred in homes with median incomes of less than $40,000 per year.
• The cause of the house fires were arson (25.5%), electrical wiring/equipment (16.6%), heating equipment (15.8%), cooking (11.4%), smoking (5.5%), children playing with fire (4.5%), and unknown/other (20.6%).
• The rate of fire-related injury in houses in Dallas without a functioning smoke detector was 8.7 times that of homes with a functioning smoke detectors. Houses that are most likely to have fires were least likely to have functioning smoke detectors.
• As a result of this study, a program in Dallas now provides and installs smoke detectors in census tracts with the highest rates of injuries and deaths related to house fires.

Clinical

History

• Fires in closed spaces increase the risk of smoke inhalation significantly.
• Particular materials in fires may contain dangerous asphyxiants.
• Polyurethane, wool, and silk increase the patient's risk of CN toxicity.
• Conditions at the scene may yield critical information, such as loss of consciousness or deaths in the same environment.
• CO measurement at the scene correlates much better with toxicity than does the measurement in the ED.
• A history of respiratory illnesses, such as asthma or chronic obstructive pulmonary disease (COPD), predisposes patients to respiratory insufficiency.

Physical

Inhalation injury can range from an immediate threat to a patient's airway and respiratory status to only minor mucosal irritation. Follow a trauma management protocol.

• Primary survey
  • First, assess the airway. Maintain cervical immobilization in any patient who is obtunded, has distracting injuries, has been involved in a significant mechanism of injury, has bony tenderness, or complains of neck symptoms.
  • Assess breathing by respiratory rate, chest wall motion, and auscultation of air movement.
  • Assess circulation by level of consciousness, pulse rate, blood pressure, capillary refill, and by symmetry and strength of pulses.
  • A brief neurological evaluation should include a determination of the Glasgow Coma Scale, pupil size and reactivity, and any focal findings.
  • Remove all clothes to expose traumatic injuries/burns and to prevent ongoing thermal injury from smoldering clothes. Evaluate patient's back and perform a log roll if appropriate.
• Respiratory
  • Identification of impending respiratory failure is paramount.
  • As burns to the upper airway and smoke inhalation set off the inflammatory cascade with its associated vasodilation and capillary leak, treat any early sign or symptom of airway compromise aggressively and early before inevitable rapid progression to upper airway obstruction ensues.
  • Hoarseness, change in voice, complaints of throat pain, and odynophagia indicate an upper airway injury that may be severe.
  • Carbonaceous sputum should be regarded as a marker of exposure. Transportation to a burn center with such findings should lower one’s threshold for early endotracheal security.
  • Tachypnea may be present.
  • Wheezing, rales and rhonchi, and use of accessory respiratory muscles may be noted.
• Patients with facial burns should be carefully evaluated for smoke inhalation.
  • One study has shown a 59% incidence of respiratory injury with burns involving the nose, lips, brows, and neck area compared with a 22% incidence in patients with either peripheral or no facial burns.
  • Again, early airway security is paramount before edema and airway compromise develop.
  • Patients with facial burns showed an increased mortality and more of a need for ventilatory support.
• Large cutaneous burns indicate an inability to escape flame and a risk for smoke inhalation injury.
• The secondary survey continues in a complete head-to-toe examination as in any other trauma evaluation.

Causes

• Based on a study looking at the characteristics of survivors and casualties of fire fatalities, specific risk factors seem to elevate the rate of mortality.⁴
  • Age is an important predictor, with elderly persons (>64 y) and young persons (<10 y) being the most likely to die as a result of a fire.
  • Persons having a physical or cognitive disability have a higher mortality rate than matched controls, as do persons under the influence of alcohol or other drugs. For these vulnerable populations, if a nonvulnerable potential rescuer was present, the fatality rate dropped from 49% to 39%.
  • The absence of a functioning smoke detector increases the risk of death in a fire by about 60%.

• Search for CME/CE on This Topic »

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