CHAPTER 63
Inhalation Injury
(Smoke Inhalation)
Presentation
The patient was trapped in an enclosed space for some time with toxic gases or fumes (e.g., produced by a fire, a leak, evaporation of a solvent, a chemical reaction, or fermentation of silage) and comes to the emergency department complaining of some combination of coughing, wheezing, shortness of breath, irritated or runny eyes or nose, or skin irritation. More severe symptoms include confusion and narcosis, dizziness, headache, chest pain, nausea, vomiting, and rapidly evolving upper airway obstruction.
Symptoms may develop immediately or after a lag of as much as 1 day. On physical examination, the victim may smell of the agent or be covered with soot or burns. Inflammation of the eyes, nose, mouth, or upper airway may be visible, and pulmonary irritation may be evident as coughing, rhonchi, rales, or wheezing, although these signs may also take up to 1 day to develop.
What To Do:
Separate the victim from the toxic agent by having him remove his clothes, hose himself down, or wash with soap and water.
Make sure the victim is breathing adequately, and then add oxygen at 15 L/min through a nonrebreather mask with humidification. Oxygen helps treat most inhalation injuries and is essential in treating carbon monoxide (CO) poisoning.
Mild to moderate carbon monoxide poisoning is common. Patients often present with vague symptoms, such as headache, nausea, vomiting, dizziness, and confusion. The half-life of carboxyhemoglobin (HbCO) with the patient breathing room air is 4 to 6 hours. Breathing 90% to 100% oxygen at 1 atmosphere absolute pressure reduces the HbCO half-life to 60 to 90 minutes. Otherwise asymptomatic patients can be discharged when their CO levels are less than 5%. Hyperbaric oxygen (HBO) can reduce the HbCO half-life to 20 to 30 minutes. Current recommendations for the use of HBO are neurologic compromise (including transient loss of consciousness), metabolic acidosis, ECG evidence of myocardial ischemia or dysrhythmias, HbCO greater than 40%, pregnancy with HbCO greater than15%, or history of coronary artery disease with HbCO greater than 20%. Early consultation with a hyperbaric center is recommended.
Bronchodilators can be administered by aerosol inhalation when there is any evidence of bronchospasm.
The clinical course of inhalation injury is dependent on the agent inhaled and the intensity and duration of exposure. Look for evidence that may clarify the nature of the exposure: Was there a fire? What was burning? What was the estimated length of exposure? Was the patient in an open or a closed space? Was the patient disoriented or unconscious at the scene? What is the status of any other victims? Was there an associated blast?
Determine whether there are significant preexisting conditions, such as smoking, underlying allergies, cardiac or cerebrovascular disease, chronic obstructive pulmonary disease, asthma, or other chronic illness. Patients with underlying pulmonary disease are less able to compensate for inhalation injuries.
What material is on the victim? What does he smell of? What are his current signs and symptoms? Is there soot in the posterior pharynx, singed nasal hair, hoarseness, confusion, tachycardia, tachypnea, use of accessory respiratory muscles, wheezing, rales and rhonchi, or stridor to indicate significant injury to the respiratory tract? Note that the lack of physical findings does not reliably exclude airway injury.
There may be evidence of exposure to a specific toxin that calls for a specific antidote (e.g., muscle fasciculations, small pupils, and wet lungs may imply inhalation of organophosphates, which should be treated with atropine).
Unless the exposure is insignificant, obtain a chest radiograph, pulse oximetry, and arterial or venous blood gases. Record the percentage of oxygen being inhaled (FiO2 approximately 90% at 15 L/min). An increased alveolar-arterial partial pressure of oxygen (PO2) difference (A-a O2 gradient) may be the earliest sign of pulmonary injury, but even if the chest radiograph film and arterial blood gases are normal (as they often are), they can serve as a baseline for evaluation of possible later pulmonary problems. An abnormal initial chest radiograph is a poor prognostic factor.
With significant smoke inhalation, obtain a carboxyhemoglobin level, complete blood count (CBC) and electrolytes, and serial peak flow measurements, if available. With carbon monoxide poisoning, pulse oximetry (Spo2) is unreliable because of similar light absorption by carboxyhemoglobin and oxyhemoglobin. Carboxyhemoglobin (HbCO) saturation can be directly measured by co-oximetry. Blood and urine toxicology studies may be obtained to identify coexisting toxicity that may have contributed to the cause of the inhalation injury and also complicate its course.
Obtain an ECG if there is any loss of consciousness, a history of coronary artery disease, or any complaint of chest pain or palpitations. Inhalation injuries result in decrease oxygen delivery to the tissues, increasing the risk of cardiac ischemia.
Consider cyanide toxicity in any patient with smoke inhalation. Some burning plastics give off cyanide. An anion gap acidosis may be the result of elevated lactate levels secondary to cyanide, carbon monoxide, or hypoxia. A lactate level greater than 8 mmol/L is considered a surrogate marker of elevated cyanide levels and requires treatment. Treatment consists of sodium thiosulfate and/or hydroxocobalamin.
If the patient has difficulty breathing, hoarseness, change in voice, or throat pain—or if he has any abnormality evidenced by the radiography examination, arterial blood gas levels, or physical examination, suggesting acute pulmonary injury—administration of oxygen should be continued, and the patient should be admitted to the hospital or transferred to an appropriate tertiary center. Consider early, elective endotracheal intubation in patients at risk for developing airway compromise, particularly those with hoarseness, difficulty breathing, throat pain, drooling or difficulty swallowing.
If stridor or other physical evidence of upper airway edema is present or if there is impending respiratory failure, endotracheal intubation should be performed as soon as possible. Bronchoscopy may be useful in evaluating the extent of injury.
Wheezing and bronchospasm may be allergic reactions and may respond to conventional doses of aerosolized bronchodilators but, if not promptly reversible, are probably signs of pulmonary injury. The elderly (>64 years), the young (<5 years), and persons under the influence of alcohol or other drugs require a lower threshold for admission or transfer.
After minimal exposure, if no signs or symptoms of inhalation injury develop or if all have resolved in 3 to 4 hours, it may be safe to send the patient home with instructions to return for reevaluation the next day or sooner if any pulmonary signs or symptoms (e.g., stridor, coughing, wheezing, shortness of breath) occur.
With minimal to moderate exposure, the patient should be more closely observed for a period of at least 24 hours. Serial arterial blood gas levels, chest radiography, peak expiratory flow rate, airway and lung examination, and bedside spirometry, where available, help detect the evolution of delayed-onset distal airway and pulmonary parenchymal injury.
What Not To Do:
Do not assume that the patient has not suffered any inhalation injury simply because there are no symptoms or abnormalities evidenced by chest radiography or arterial blood gases in the first few hours after exposure. Some agents produce pulmonary inflammation that develops over 12 to 24 hours.
Do not wait until carboxyhemoglobin levels have been determined before giving 100% oxygen to treat suspected carbon monoxide poisoning. Begin oxygen administration as soon as possible.
Do not insist that the patient breathe room air for a long period before obtaining arterial blood gases. If oxygen administration is helping, its withdrawal is a disservice, and the alveolar-arterial PO2 gradient can still be estimated while the patient is being given supplemental oxygen.
Do not prescribe corticosteroids unless there is a history of asthma or allergy. Evidence of reduced clearance of lung bacteria and of increased incidence of bacterial pneumonia as a late complication of inhalation injury outweighs any potential anti-inflammatory effects.
Do not prescribe antibiotics unless there is a proven infection.
Discussion
One type of inhalation injury is caused by relatively inert gases, such as carbon dioxide and fuel gases (e.g., methane, ethane, propane, acetylene), which displace air and oxygen, producing asphyxia. Treatment consists of removing the victim from the gas, allowing him to breathe fresh air or oxygen, and attending to any damage (e.g., myocardial infarction, cerebral injury) caused by the period of hypoxia.
A second category of inhalation injury is caused by irritant gases, including ammonia (NH3), formaldehyde (HCHO), chloramine (NH2Cl), chlorine (Cl2), nitrogen dioxide (NO2), and phosgene (COCl2). When dissolved in the water lining the respiratory mucosa, irritant gases produce a chemical burn and an inflammatory response. The first three gases listed, which are more soluble in water, tend to produce more upper airway burns, irritating the eyes, nose, and mouth, whereas the latter two gases, being less water soluble, produce more pulmonary injury and respiratory distress. Phosgene can be found is household solvents and can cause delayed severe pulmonary edema, mandating prolonged observation if this agent is suspected. Chlorine is a gas of intermediate solubility and may exert irritant effects widely throughout the respiratory tract. Household bleach contains hypochlorite. Mixing hypochlorite bleach or cleaners with acids, such as hydrochloric acid, sulfuric acid, or phosphoric acid, generates chlorine. Mixing hypochlorite solutions with ammonium hydroxide-containing cleaners generates chloramine.
A third type of inhalation injury is caused by gases that are systemic toxins, such as carbon monoxide (CO), hydrogen cyanide (HCN), and hydrogen sulfide (H2S). All interfere with the delivery of oxygen for use in cellular energy production and with aromatic and halogenated hydrocarbons, which can result in later liver, kidney, brain, lung, and other organ damage.
A fourth cause of inhalation injury is allergic; inhaled gases, particles, or aerosols produce bronchospasm and edema similar to that caused by asthma or spasmodic croup.
A fifth cause of inhalation injury is direct thermal burns. They are usually limited to the upper airway and produce varying degrees of local edema. Inhalation of steam is far more injurious than heated air. (Steam has approximately 4000 times the heat-carrying capacity of heated air.) Consequently, steam can result in rapidly fatal obstructive glottic edema and lower airway destruction.
The diagnosis of inhalation injury is largely clinical, based on history (disorientation or unconsciousness at the scene, closed space exposure) and physical examination (singed nasal hairs and carbonaceous endobronchial secretions).
In general, treatment of inhalation injury is supportive only. There has been no demonstrated value to prophylactic steroids or antibiotics, but in cases in which the patient is experiencing an exacerbation of underlying COPD or asthma, routine use of steroids is appropriate. Inhaled β-adrenergics can be added if there is bronchospasm. There is promising research evaluating nebulized anticoagulants and N-acetylcysteine for treating inhalation injury.
Because symptoms of acute inhalation injury can be delayed in onset, a key decision that has to be made during the acute evaluation concerns how long to observe a patient for development of more severe respiratory involvement, and whether to admit the patient for hospital treatment. Current diagnostic tools cannot stratify inhalation injury by severity or accurately predict subsequent clinical course. Again, knowledge of the agent involved and the intensity and duration of exposure is critical.
Indicators of poor prognosis include a history of altered mental status at the scene, progressive respiratory difficulty, sputum production, rales, burns to the face, hypoxemia, and altered mental status at time of presentation.
▪ Although inhalation injuries are often self-limited events, even mild exposures require early follow-up with clear instructions to the patient to seek medical care immediately if symptoms worsen. At the follow-up appointments, serial spirometry can assess whether obstructive or restrictive disease is developing.
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
