Smoke Inhalation Injury Clinical Presentation

Updated: Oct 15, 2021
  • Author: Keith A Lafferty, MD; Chief Editor: Joe Alcock, MD, MS  more...
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In patients exposed to smoke, details of the exposure—the duration, the amount of smoke inhaled, and the toxins contained in the smoke--can help determine the risk for inhalation injury. Unfortunately, these details are often not known, although some information can often be garnered from rescuers and other observers present at the scene.

Critical information regarding the scene includes the severity of injury to other victims, especially loss of consciousness or death. In addition, exposure to fire in a closed space, prolonged duration of entrapment, evidence of carbonaceous sputum, the requirement for cardiopulmonary resuscitation (CPR) at the scene, the presence of respiratory distress, and obtundation all increase the risk for significant pulmonary disease and hypoxic injury.

Simple carbon soot is not particularly toxic, although it may carry and deposit other toxins directly onto the airway surfaces, thereby increasing exposure. Significant toxicity occurs with the inhalation of asphyxiants, including carbon monoxide (CO), nitrogen, and methane. These asphyxiants cause injury by interrupting the delivery of oxygen to the tissues. Asphyxiants either displace oxygen from the air or interfere with tissue oxygen delivery by blocking the action of hemoglobin or cytochrome oxidase (eg, CO, cyanide [CN]).

CO poisoning must be considered in any person injured in a fire. CO is a major component of smoke produced in most open fires, particularly those involving wood, coal, gasoline, and other organic substances. In addition, significant CO exposure can occur in the absence of open flames, as a result of malfunctioning domestic equipment (eg, poorly ventilated space heaters, cooking gas) or exposure to automobile exhaust fumes either from a suicide attempt or accidentally from poor ventilation.

Hydrogen CN is an asphyxiant that is released during the incomplete combustion of products such as cellulose, nylon, wool, silk, asphalt, polyurethane, and plastics. CN has a characteristic almondlike odor. Hydrogen CN is absorbed rapidly, producing an almost immediate effect if exposure is by inhalation. In contrast, CN salts (eg, potassium, sodium CN, and, particularly, silver and copper CN), which are typically ingested, must be converted to hydrogen CN and are absorbed more slowly.

Damage varies with the chemical activity of the particular inhalants, their size, solubility, and the duration and concentration of exposure. Upper airway injuries tend to be caused by the more irritating, water-soluble, larger particles. Substances of smaller size and lower water solubility cause alveolar and parenchymal injury.

A history of respiratory illnesses, such as asthma or chronic obstructive pulmonary disease (COPD), predisposes patients to respiratory insufficiency.

The extent of illness from smoke inhalation can be notably different between children and adults, despite similar exposures. Children frequently become disoriented at fire scenes and may attempt to hide from flames and smoke, thereby prolonging their exposure to toxic inhalants. In addition, children have greater minute ventilation relative to body size than do adults, further increasing their exposure to toxic inhalants.

Inhalation injuries occur without skin burns or other obvious external injury; hence, a high degree of suspicion must be maintained. A retrospective review of 4,451 children with thermal injuries over 10 years demonstrated that inhalation injury was often not recognized, manifested late, and usually had significant consequences, including parenchymal injury and secondary pneumonia. [37]

Thermal injury is generally confined to the upper airway, because of its vast heat capacitance. Inhalation of steam is a notable exception, in which lower airway and pulmonary parenchymal thermal injury are common. Theoretically, continued combustion of inhaled particulate matter could possibly produce more distal airway injury.

Thermal injury to the mucosa produces burns and edema of the nose, mouth, pharynx, and larynx. The loose tissues of the upper airway swell readily in response to injury. Loss of colloid oncotic pressure can result in obstruction of the airway, particularly in patients receiving fluid resuscitation.

The full extent of airway compromise may not be evident until 12-24 hours after the initial injury. For patients with extensive surface burns, chest wall restriction may occur because of eschar formation, necessitating emergent escharotomy.

Toxic smokes

Different clinical presentations may result from exposure to smoke containing the following toxins:

  • Oxides of nitrogen (NOx)

  • Zinc oxide (HC)

  • Red phosphorus

  • Sulfur trioxide (FS)

  • Titanium tetrachloride (FM)

  • Oil fog

Oxides of nitrogen

Because of their insolubility in water, NOx tend not to cause immediate upper airway irritation. Unfortunately, this may allow a significant exposure to remain undetected for prolonged periods. As with most toxic inhalations, severity of illness and presentation are related to the concentration of the smoke or fumes, length of time of exposure, manner in which the exposure was delivered, and the health status of the exposed individual.

Mild exposure to NOx results in upper airway and ocular irritation such as itching or burning eyes. Cough, dyspnea, fatigue, chest tightness, throat tightness, nausea, vomiting, vertigo, somnolence, and loss of consciousness also may occur from mild exposure.

At weaker concentrations of NOx, the individual may experience very little discomfort, quickly accommodating to the cough, mild choking, or upper airway irritation. Because of this, symptoms may appear quickly or remain unnoticed for a few hours. Although the symptoms of mild exposure may become quite dramatic, complete recovery is expected within 24 hours, once the patient is removed from the exposure.

In more severe exposures, the clinical response may be described as triphasic. During phase 1, an intense respiratory symptom complex may occur. Severe cough, dyspnea, and pulmonary edema may arise suddenly. Physical exertion may be a precipitating factor, quickening the progression to pulmonary edema. If the patient survives this episode, spontaneous remission occurs within 48-72 hours postexposure.

Phase 2 lasts from 2-5 weeks and is relatively uneventful. A mild residual cough with malaise and perhaps dyspnea may linger, but the chest radiograph typically remains clear.

In phase 3, which occurs 3-6 weeks after the exposure, symptoms may recur. Severe cough, fever, dyspnea, and cyanosis may develop in the setting of rales and increasing carbon dioxide retention.

More acutely severe exposures can result in immediate death from bronchiolar spasm, laryngeal spasm, reflex respiratory arrest, or simple asphyxia. Some exposures can progress from mild upper airway irritation to pulmonary edema in 3-30 hours.

Even in individuals with asthma or chronic obstructive bronchitis, NOx concentrations of 0.5 ppm or less generally have no effect. levels from 0.5-1.5 ppm begin to bother patients with asthma, who notice minor airway irritation. With concentrations greater than 1.5 ppm, people with healthy lungs experience decreases on pulmonary function tests and decreased carbon monoxide diffusing capacity (DLCO), with widening of the alveolar-arterial gradient on arterial blood gas measurement.

Zinc oxide

Individuals exposed to HC smoke may complain of nose, throat, and chest irritation. They may experience cough and some nausea. Individuals with severe exposures may present in severe respiratory distress, and such exposures can be fatal. A thorough social history offers vital clues to exposure, since respiratory distress can mimic many different disease processes (see Etiology).

Patients with fume fever typically present in a delayed fashion 4-8 hours after exposure with a pattern of symptoms including dryness of the throat, coughing, substernal chest pain or tightness, and fever. Other symptoms include hoarseness, sore throat, retching, paroxysmal coughing, rapid pulse, malaise, shortness of breath, and abdominal cramps. Respiratory symptoms generally disappear in 1-2 days with supportive care.

Milder exposures are characterized by sensations of dyspnea without any auscultatory, radiologic, or blood gas abnormalities. A patient with moderate exposure to HC may demonstrate rapid clinical improvement within 6 hours. These patients usually are sent home, only to return in 24-36 hours with rapidly worsening dyspnea and dense infiltrative processes on chest radiography. The radiographic abnormalities usually clear, but significant hypoxia may persist during the time the chest radiograph is abnormal.

Prolonged exposures or exposures to very high doses of HC may result in sudden early collapse and death. This may be due to laryngeal edema or glottal spasm. If severe exposure does not kill the individual immediately, hemorrhagic ulceration of the upper airway may occur, with paroxysmal cough and bloody secretions. Death may occur within hours secondary to an acute tracheobronchitis.

Most individuals with HC inhalation injuries progress to complete recovery. Of exposed individuals, 10-20% develop fibrotic pulmonary changes. Distinguishing between those who will recover and those who will not is difficult, since both groups make an early clinical recovery.

Red phosphorus

Individuals with toxic inhalation usually have a history of exposure to the smoke either on the battlefield or in some other setting where phosphorus smokes are used. Complaints of eye, nose, and throat irritation are common. Severe exposure can be associated with an explosive, persistent cough. Most often, the cough and irritating symptoms resolve after the individual is removed from the exposure source. Contact with unoxidized phosphorus can produce painful, erythematous chemical burns to the skin.

Sulfur trioxide

FS smoke is extremely irritating. Consequently, people escape the smoke as soon as possible, and exposure tends to be brief.

FS-exposed individuals complain of cough; substernal ache or soreness; and a burning sensation in the eyes, nose, mouth, and throat. Blurry vision and photophobia also may be complaints. If inhalant injury is severe enough, explosive cough and shortness of breath may develop. The individual may complain of a prickling sensation of the exposed skin, which could be the prelude to pending chemical dermatitis.

Titanium tetrachloride

Several industrial exposures to FM liquid and smoke have been reported, but only 1 death. This was in a worker who accidentally was splashed over his entire body with liquid FM. He died from complications resulting from inhalation of FM fumes and overwhelming superinfection.

Oil fog

Individuals exposed to Smoke Generator Fog 2 (SGF2) or other oil mists may report mild irritation or slight cough, a sensation of shortness of breath, or headache. In persons with underlying pulmonary disease such as asthma or COPD, exposure to SGF2 may trigger symptoms of their disease.

Teflon particles

Exposure to smoke containing Teflon particles may result in influenzalike illness, with malaise, fever (at times to 104°F), chills, sore throat, sweating, and chest tightness 1-4 hours postexposure. These symptoms usually resolve 24-48 hours after the patient is removed from the source.

More intensely exposed individuals complain of dyspnea on exertion, orthopnea, and later, dyspnea at rest. Cough productive of bloody sputum occasionally is seen. Some animal studies have demonstrated disseminated intravascular coagulation and other organ involvement, but this may be due to global hypoxia, since this occurred only in animals with severe lung damage.

Cases of polymer fume fever from pyrolysis of Teflon have been reported in persons exposed to pyrolyzed hairspray and horse-rug waterproofing spray and in one individual smoking hand-rolled cigarettes after working with dry lubricant. [38]


Physical Examination

In the primary survey, assess patency of the airway, breathing, and circulation. 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.

Perform a brief neurological evaluation, including a determination of the Glasgow Coma Scale, pupil size and reactivity, and any focal findings. Remove all clothing 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.

Identification of signs or symptoms of airway compromise is important to permit early and aggressive treatment before rapid progression to upper airway obstruction and respiratory failure ensues.

The secondary survey continues in a complete head-to-toe examination as in any other trauma evaluation. Burns on the face, soot marks, and singed eyebrows or facial hair are indicative of smoke inhalation. Large cutaneous burns indicate an inability to escape flame and a risk for smoke inhalation injury. However, inhalation injury can occur without evidence of burns.

Recognizing that upper airway swelling may take several hours to develop is imperative. Thus, facial burns, hoarseness, stridor, upper airway injury with mucosal lesions identified upon oral examination or bronchoscopy, and carbonaceous sputum are indications to promptly secure artificial airway access.

Symptoms of lower respiratory tract injury include the following:

  • Tachypnea

  • Dyspnea

  • Cough

  • Decreased breath sounds

  • Wheezing

  • Rales

  • Rhonchi

  • Retractions

Neurologic injury

Signs of neurologic injury may take longer to appear than evidence of respiratory injury. Neurologic injury may result from hypoxia at the time of injury or hypoxia secondary to pulmonary dysfunction. Fear, severe pain, and obtundation from inadequate perfusion may cloud the neurologic examination. Serial examinations assessing the sensorium are extremely helpful in guiding the initial resuscitation and stabilization.

Patients exposed to asphyxiants, including CO and cyanide (CN), present with hypoxic injury and subsequent CNS depression, lethargy, and obtundation. Hypoxia is caused by an asphyxiant and is usually evident upon presentation. Irritability, severe temporal headache, and generalized muscle weakness are also common findings.

Coma following exposure to fire is nearly always indicative of CO poisoning and should be promptly treated with 100% oxygen. Suspect CN toxicity in the patient whose sensorium remains clouded and who does not respond to oxygen therapy.

Cardiovascular injury

Complex cardiovascular changes associated with surface burns may coexist with inhalation injury. Heart rate, capillary refill, warmth of unburned extremities, and blood pressure should be promptly evaluated at presentation and at frequent regular intervals during the initial stabilization.

Pay careful attention to narrowed pulse pressure because this may indicate inadequate volume resuscitation. Hypotension is invariably a late finding of volume loss.

Other injury

Renal tubular acidosis, hepatitis, and bone marrow insufficiency are not uncommon, particularly when hypoxic injury is either severe or prolonged. Organ system dysfunction is also common as a result of the complex hemodynamic and inflammatory reactions associated with significant burns. In the obtunded patient, assume coexistent spine injury.

Carbon monoxide

Altered vital signs in patients with CO toxicity may include tachycardia, hypertension or hypotension, and hypothermia or hyperthermia. Mild tachypnea may be present; rarely, patients with severe intoxication may have marked tachypnea. Noncardiogenic pulmonary edema may be present.

The skin may exhibit pallor; the classic sign of cherry-red skin occurs rarely and is generally a postmortem finding. Findings on ophthalmologic examination may show reveal bright red retinal veins, flame-shaped retinal hemorrhages, and papilledema.


CN stimulates nociceptors, leading to a sensation of burning and dryness in the throat and nose. Therefore, hoarseness, change in voice, complaints of throat pain, and/or odynophagia indicate an upper airway injury that may be severe. Tachypnea may be present. Wheezing, rales and rhonchi, and use of accessory respiratory muscles may be noted.

Low levels of CN increase cardiac output. At higher levels, a wide variety of bradyarrhythmias and tachyarrhythmias occurs. With progressively higher levels of exposure, obtundation, seizures, and apnea occur. In the most severe cases, death occurs immediately from respiratory arrest.

Oxides of nitrogen

The severity of physical examination findings depends on the severity of exposure. Mild exposure may result in injected conjunctivae and normal to mildly erythematous-appearing mucous membranes. After a more severe exposure, signs may range from mild respiratory distress (eg, tachypnea, accessory muscle use) to more severe signs of wheezes and rales, yellow frothy sputum, and yellow staining of the mucous membranes. This may be followed by cyanosis, lethargy, convulsions, coma, and death.

Zinc oxide

As with other inhalation injuries, physical examination findings in zinc oxide exposure depend on the time of exposure, concentration of the gas, method of gas distribution, and underlying general health of the exposed individual. Physical examination findings may range from slight dyspnea and increased work of breathing to severe respiratory distress, convulsions, coma, or death. Hoarseness and cough are common findings. Retching, fever, tachycardia, hypoxia, and cyanosis may be present, as well as pulmonary wheezes and rales.

Red phosphorus

Physical examination findings are those associated with irritation of mucosal surfaces. A cough or chemical burns to exposed skin surfaces from direct contact with unoxidized phosphorus may be present.

Sulfur trioxide and titanium tetrachloride

Physical examination findings vary due to length of exposure, concentration of FS smoke, environment of the exposure, and underlying health of the exposed individual. FS smoke exacerbates symptoms of asthma or COPD and can worsen pulmonary function test results in these patients.

Conjunctivitis, corneal erosion, lacrimation, erythema of exposed skin surfaces, and mucosal inflammation may be present. Intense salivation may follow. The individual may have a cough with bloody sputum, dyspnea, hypoxia, rales, or wheezes.

Teflon particles

Physical examination findings in patients exposed to Teflon fumes similar to that of patients with chemical inhalation injury, but fever often is present as well. Dyspnea, increased work of breathing, and rales are common. Pulmonary edema usually is mild and typically does not require oxygen supplementation.

More intense toxicity and hypoxia may be seen, requiring more invasive methods of oxygenation and ventilation. Pulmonary edema is also worse if the individual exercises after exposure.