Smoke inhalation

Smoke inhalation occurs when you breathe in harmful smoke particles and gases. Smoke inhalation is the leading cause of death due to fires. Smoke inhalation produces injury through several mechanisms, including thermal injury to the upper airway, irritation or chemical injury to the airways from soot, asphyxiation, and toxicity from carbon monoxide (CO) and other gases such as cyanide ¹. The chemical property of smoke combined with burn injury induces a complex pathophysiologic process that results in hypoxic insult, early airway edema, and bronchoconstriction ². Damage to the windpipe, breathing passages, or lungs can cause cough, wheezing and/or shortness of breath. These symptoms can occur right away or take up to 24 hours to develop.

Smoke usually causes no more than mild irritation, and little or no treatment is required, but occasionally it causes more serious problems. In addition, people with other medical problems, especially respiratory or heart disease, or pregnant women, often require more investigations, observation, or treatment. People who have inhaled smoke are often sent to an emergency department to be assessed, unless their symptoms are obviously mild.

• Symptoms of carbon monoxide (CO) poisoning include headache, nausea, drowsiness, confusion, and coma.
• Burns of the mouth and throat cause swelling that can make it difficult to breathe air in. People may have soot in the mouth or nose, singed nasal hairs, or burns around the mouth.

Smoke forms when wood or other organic matter burns. The smoke from wood burning is made up of a complex mixture of gases and fine particles also called particle pollution or particulate matter ³. In addition to particle pollution, wood smoke contains several toxic harmful air pollutants including:

• benzene,
• formaldehyde,
• acrolein, and
• polycyclic aromatic hydrocarbons (PAHs).

The biggest health threat from smoke is from fine particles, also called fine particulate matter or PM2.5 ³. These microscopic particles can get into your eyes and respiratory system, where they may cause burning eyes, runny nose, and illnesses, such as bronchitis.

Fine particles (fine particulate matter or PM2.5) can make asthma symptoms worse and trigger asthma attacks. Fine particles can also trigger heart attacks, stroke, irregular heart rhythms, and heart failure, especially in people who are already at risk for these conditions.

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 (e.g., carbon monoxide, cyanide).

Carbon monoxide poisoning must be considered in any person injured in a fire. Carbon monoxide (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 carbon monoxide 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 cyanide is an asphyxiant that is released during the incomplete combustion of products such as cellulose, nylon, wool, silk, asphalt, polyurethane, and plastics. Cyanide has a characteristic almond-like odor. Hydrogen cyanide is absorbed rapidly, producing an almost immediate effect if exposure is by inhalation. In contrast, cyanide salts (eg, potassium, sodium cyanide, and, particularly, silver and copper cyanide), which are typically ingested, must be converted to hydrogen cyanide 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 lung tissue 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.

Smoke 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 ⁴.

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 lung tissue thermal injury are common. Theoretically, continued combustion of inhaled particulate matter could possibly produce more distal airway injury.

Thermal injury to the lining of the upper airways produces burns and swelling 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.

Treatment of smoke inhalation injuries caused from toxic smokes is based on clinical presentation and involves primarily supportive care directed at the cardiopulmonary system. In some cases (eg, cyanide poisoning, methemoglobinemia), specific antidotes are available. Subcutaneous epinephrine has been used in zinc oxide exposures.

Corticosteroids are attractive for suppressing inflammation and reducing edema, but no direct data support their use in smoke inhalation. Because of the increased risk of pulmonary infection and delayed wound healing, prolonged use of steroids is discouraged. However, consider a brief course of steroids in those patients with otherwise unresponsive severe lower airway obstruction. In addition, patients receiving steroids prior to injury who may experience adrenal insufficiency should receive stress doses of steroids.

Smoke inhalation key points

• Smoke inhalation can cause problems in several ways:
  • Suffocating the body with carbon monoxide. Carbon monoxide is a gas produced in many fires. When inhaled, carbon monoxide prevents the blood from carrying oxygen so tissues do not get enough oxygen.
  • Poisoning the body with toxic chemicals.
    • Many household and industrial substances release cyanide when burned and cause cyanide poisoning.
    • Inhalation of chemicals released in the smoke, such as hydrogen chloride, phosgene, sulfur dioxide, toxic aldehyde chemicals, and ammonia, can cause swelling and damage to the windpipe (trachea) and even the lungs. Eventually, the small airways leading to the lungs narrow, further obstructing airflow.
  • Damaging the windpipe, breathing passages, and/or lungs from toxic chemicals
  • Burning the mouth and throat from hot gases. Hot smoke usually burns only the mouth and throat rather than the lungs because smoke cools quickly. However, an exception is steam, which carries much more heat energy than smoke and thus can also burn the airways in the lungs.
• Most cases of smoke inhalation are mild and don’t cause problems. However, most people with smoke inhalation should be assessed in an emergency department. This applies particularly to pregnant women and people with existing health problems.
• Most people make a full recovery without any long term adverse effects.
• Less commonly, smoke can cause serious medical problems. Blood tests or a chest x-ray may be taken to investigate whether this is happening.
• If you develop increasing shortness of breath after leaving hospital, come back to hospital, if necessary by ambulance.

Smoke inhalation causes

Smoke inhalation usually happens with fires in enclosed spaces, e.g. inside buildings, but can also happen with prolonged exposure (hours) to smoke from bushfires.

Airway burns

Hot smoke can burn the airway (throat and trachea). This is usually obvious, with throat pain, hoarse voice, and noisy breathing. People with airway burns almost always have burns to the face or head, or severe burns elsewhere on the body. It is more common for smoke to cause mild throat irritation, which is usually not a sign of a significant burn to the airway.

Poisoning

Smoke contains poisons which can affect people. This usually happens only to people who have spent a long time (5 minutes or more) in an enclosed space full of smoke, especially if they been close enough to a fire to be burnt.

Carbon monoxide poisoning

Carbon monoxide is a colorless, odorless gas produced by incomplete burning, especially in enclosed spaces. If enough of it is inhaled, it quickly produces neurological (nervous system) symptoms ranging from headache to mild confusion, nausea and vomiting, to collapse, coma and rarely death. More commonly, not enough carbon monoxide is inhaled to cause problems. In pregnant women, the unborn baby can be more affect-ed than the mother as the baby’s blood retains more carbon monoxide than the mother’s. A blood test may be taken to see if there has been exposure to carbon monoxide, but this is not always needed if symptoms are mild. The treatment for carbon monoxide inhalation is a period of time breathing high concentrations of oxygen through a mask. This hastens the removal of the carbon monoxide compound (carboxyhemoglobin) from the blood. In severe cases of poisoning, treatment is with high pressure oxygen in a hyperbaric (high pressure) chamber, but this situation is rare.

Lung irritation

Many different chemicals and particles in smoke can irritate the lungs. In severe cases, this makes fluid enter the lungs, causing severe shortness of breath and cough, sometime with pink frothy sputum. People with asthma, emphysema or other lung diseases can have an “attack” of their existing disease triggered by smoke. A chest x-ray and blood tests may be required to investigate. More commonly, people exposed to smoke may develop a mild cough, which does not indicate lung damage. Occasionally, however, people exposed to smoke can take up to 24—36 hours to develop signs of serious lung irritation. If you develop increasing cough and shortness of breath after leaving hospital, come back to hospital. If you develop severe shortness of breath, call an ambulance.

Smoke inhalation prevention

Primary prevention with functioning fire and smoke alarms and family education for fire hazards is critical to help avoid fire injuries. Fire prevention should be viewed as the primary means to avoid inhalation injury

Smoke detectors reduce the risk of death by about 60% in all subgroups of people ⁵. This finding stands in contrast to past data that suggested that these early warning devices may not be effective in populations that have difficulty responding to an alarm in a timely manner, such as children, older adults, persons with disabilities, or those impaired by alcohol or other drugs. These new data clearly reinforce the point that all homes should have a working smoke detector in every room.

Although smoke detectors have been widely adopted by the public— 93% of US households have one in place—it is estimated that 30-45% of these devices are not operational, usually because the battery has died or has been removed. DiGuiseppi et al have shown that merely giving out free smoke alarms in a deprived, multiethnic, urban community did not reduce injuries related to fire, because few of the alarms were installed or properly maintained ⁶.

In the military setting, the mission-oriented protective posture gear ensemble provides adequate protection against all smokes. In the industrial setting, guidelines have been established for the protection of the worker as well as any person who may come in contact with toxic smokes. Aim preventive efforts at decreasing the concentration of the smoke and the time of exposure and recognizing underlying health problems that may be exacerbated by exposure to toxic smokes.

Smoke inhalation symptoms

Signs and symptoms of smoke inhalation

Findings on physical examination may include the following:

• Facial burns
• Blistering or swelling of the oropharynx
• Hoarseness
• Stridor (a variable, high-pitched respiratory sound that can be assessed during breathing)
• Upper airway mucosal lesions
• Carbonaceous sputum

Symptoms of lower respiratory tract injury include the following:

• rapid breathing or fast breathing (tachypnea)
• shortness of breath (dyspnea)
• Cough
• Decreased breath sounds
• Wheezing
• Rales (small clicking, bubbling, or rattling sounds in the lungs)
• Rhonchi (continuous gurgling or bubbling sounds typically heard during both inhalation and exhalation)
• Retractions

Cyanosis may be present. However, cyanosis is an unreliable indicator of hypoxia because neither carbon monoxide nor cyanide cause cyanosis.

Findings in patients exposed to asphyxiants may include the following:

• Central nervous system (CNS) depression, lethargy, and obtundation (dulled or reduced level of alertness or consciousness)
• Irritability, severe temporal headache, and generalized muscle weakness
• Coma (nearly always from carbon monoxide poisoning)

Toxic smokes

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

• Oxides of nitrogen (NOx)
• Zinc oxide
• Red phosphorus
• Sulfur trioxide
• Titanium tetrachloride
• Oil fog

Oxides of nitrogen

Because of their insolubility in water, oxides of nitrogen (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 oxides of nitrogen (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 oxides of nitrogen (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.

1. 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.
2. 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.
3. 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, oxides of nitrogen (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 zinc oxide 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.

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 zinc oxide 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 zinc oxide 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 zinc oxide 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

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

Sulfur trioxide-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 titanium tetrachloride 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 titanium tetrachloride. He died from complications resulting from inhalation of titanium tetrachloride 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 Smoke Generator Fog 2 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.

Smoke inhalation diagnosis

In the workup of smoke inhalation injuries caused by toxic smoke, the primary investigation focuses on the pulmonary system. Other tests may be clinically indicated based on history, physical examination, and underlying health problems. Initial blood tests should include lactate and carbon monoxide (CO)-oximetry in addition to electrolytes and arterial blood gases. Carbon dioxide levels also may be monitored, since patients with prior lung disease such as asthma and chronic obstructive pulmonary disease may be affected more severely and are at greater risk to retain carbon dioxide.

Studies may include the following:

• Pulse oximetry and carbon monoxide (CO)-oximetry
• Arterial blood gases (ABGs)
• Carboxyhemoglobin level
• Lactate
• Complete blood cell count (CBC)
• Chest radiography (in patients with significant exposure or pulmonary symptoms)
• Electrocardiogram (ECG)
• Serial cardiac enzymes (in patients with chest pain)
• Pulmonary function testing
• Direct Laryngoscopy and fiberoptic bronchoscopy

Pulse Oximetry and carbon monoxide (CO)-oximetry

Pulse oximetry readings can be misleading in the setting of carbon monoxide (CO) exposure or methemoglobinemia because these devices use only 2 wavelengths of light (the red and the infrared spectrum), which detect oxygenated and deoxygenated hemoglobin only and not any other form of hemoglobin. Readings are falsely elevated by carbon monoxide-bound hemoglobin (carboxyhemoglobin).

In methemoglobinemia, light reflection is similar to that in reduced hemoglobin. Pulse oximetry may show a depressed oxygen saturation, but the decrease does not accurately reflect the level of methemoglobinemia. In fact, as methemoglobin levels reach 30% or higher, the pulse oximetry reading converges on approximately 85%.

CO-oximeters use 4 wavelengths of light and are capable of detecting carboxyhemoglobin and methemoglobin as well as hemoglobin and oxyhemoglobin. Some newer co-oximeters use 5 wavelengths and are also able to measure sulfhemoglobin. The percent of oxyhemoglobin measured by CO-oximetry is an accurate measure of the arterial oxygen saturation. The difference between saturations obtained by CO-oximetry and calculated figures is known as the saturation gap and is an indicator of dyshemoglobinemia.

Arterial Blood Gases (ABGs)

Arterial oxygen tension (partial pressure of arterial oxygen [PaO2]) does not accurately reflect the degree of carbon monoxide (CO) poisoning or cellular hypoxia. The partial pressure of arterial oxygen (PaO2) level reflects the oxygen dissolved in blood that is not altered by the hemoglobin-bound carbon monoxide (CO). Because dissolved oxygen makes up only a small fraction of arterial oxygen content, a PaO2 level within the reference range may lead to serious underestimation of the decrement in tissue oxygen delivery and the degree of hypoxia at the cellular level that occurs when carbon monoxide (CO) blocks the delivery of oxygen to the tissues.

With most blood gas machines, the oxygen saturation is calculated on the basis of the PaO2 level. Thus, such a reading does not give an accurate determination of oxygen saturation, which must come from CO-oximetry.

Arterial Blood Gas measurements are nonetheless useful to assess the adequacy of pulmonary gas exchange. Although the presence of a PaO2 level that is within the reference range may not exclude significant tissue hypoxia due to the effects of carbon monoxide (CO), the presence of a low PaO2 (< 60 mm Hg in room air) or hypercarbia (alveolar [arterial] carbon dioxide pressure [PaCO2] level of 55 mm Hg) indicate significant respiratory insufficiency. Metabolic acidosis suggests inadequate oxygen delivery to the tissues.

The difference between the partial pressure of oxygen in the alveolus and that measured on an Arterial Blood Gas is the alveolar-arterial (A-a) gradient. This value, usually less than 5-10 mm Hg, may be several hundred mm Hg in the setting of significant pulmonary injury and can be used to assess improvement or deterioration in lung function when measured at a stable fraction of inspired oxygen (FiO2).

The alveolar gas equation can be used to estimate the efficiency of pulmonary oxygen delivery to the arterial circulation in the presence of supplemental oxygen administration. This formula determines the alveolar oxygen pressure.

The formula is as follows: PaO2 = (FiO2)(PB – PH2O) – (PaCO2/RQ). PB represents barometric pressure, PH20 represents the partial pressure of water vapor (47 mm Hg at body temperature, ambient pressure), and RQ represents the respiratory quotient (estimated at 0.8).

Carboxyhemoglobin Level

Carboxyhemoglobin levels in the blood and the corresponding clinical manifestations are as follows ⁷:

• 0-10% – Usually no symptoms
• 10-20% – Mild headache, atypical dyspnea
• 20-30% – Throbbing headache, impaired concentration
• 30-40% – Severe headache, impaired thinking
• 40-50% – Confusion, lethargy, syncope
• 50-60% – Respiratory failure, seizures
• Greater than 70% – Coma, death

Blood carboxyhemoglobin levels may underestimate the degree of carbon monoxide (CO) intoxication because of oxygen administered to the patient before arrival to the hospital. Smokers may have baseline levels up to 5-10% and may experience more significant carbon monoxide (CO) poisoning for the same level of exposure as nonsmokers. Finally, correlation between carboxyhemoglobin levels and eventual neurologic outcome is poor. The use of nomograms to extrapolate levels to the time of rescue has been shown to have prognostic value.

Lactate and other blood studies

Elevated lactate levels may result from metabolic acidosis secondary to the following:

• Hypoxia
• Carbon monoxide (CO)
• Cyanide
• Methemoglobinemia
• Inadequate resuscitation
• Unrecognized trauma

Lactate levels associated with cyanide poisoning have been reported as being above 8 mmol/L ⁸. The concentration of lactate increases proportionally with the degree of cyanide poisoning, and lactate levels higher than 10 mmol/L are a sensitive indicator of cyanide levels higher than 1 mg/mg ⁹. Note that in most institutions, cyanide levels can take hours to days for results; therefore, one must rely on clinical and indirect laboratory data.

Cyanide Levels

Cyanide levels correlate closely with the level of exposure and toxicity, but these values may not be readily available. Many hospitals send out tests for cyanide levels, and results may not return for several days to a week. In a setting consistent with potential cyanide exposure, institute specific empiric therapy while waiting for laboratory confirmation of the diagnosis.

Findings indicative of cyanide intoxication include the following:

• Persistent neurologic dysfunction unresponsive to use of supplemental oxygen
• Cardiac dysfunction
• Severe lactic acidosis, particularly in the presence of high mixed venous oxygen saturation
• “Arterialization” of the venous blood gas, with PO2 values similar to arterial levels due to lack of oxygen utilization by tissues

Other Blood Studies

Electrolyte testing can identify an anion gap acidosis. In patients who require large-volume fluid resuscitation, measure electrolytes at regular and frequent intervals to monitor for the electrolyte abnormalities that may occur in these patients. Use results to adjust both fluid and electrolyte replacement.

Blood urea nitrogen (BUN) and creatinine levels should be obtained for baseline renal function determination in patients in shock or with rhabdomyolysis. Patients with large cutaneous burns, crush injuries, or prolonged immobilization should have their serum creatine kinase (CK) checked and, if appropriate, urine myoglobin.

Exposure to zinc oxide warrants baseline liver function tests on initial presentation. Liver function should be followed over the course of hospitalization if exposure is severe enough to warrant admission.

Thermal degradation products of various compounds, including phosphorus-based fire retardants, are capable of impairing cholinesterase activity. A prospective study measured serum erythrocyte cholinesterase activity at the scene of residential fires for 49 victims. A significant lower level of cholinesterase activity was noted in these patients as compared to controls. Obviously, further investigation into the clinical significance of this lower enzymatic activity is needed before it can be used clinically.

Lead-containing paint is common in structures built before 1977, and this element can become aerosolized and absorbed directly into the bloodstream from the lungs. While it is true that severe smoke inhalation has been shown to increase serum lead levels more than 2-fold, no evidence suggests that these elevations are clinically relevant ¹⁰.

Smoke inhalation treatment

When a patient presents with smoke inhalation, immediate assessment of the patient’s airway, breathing, and circulation should be done ¹¹. Provide intravenous (IV) access, cardiac monitoring, and supplemental oxygen in the setting of hypoxia. Some patients manifest bronchospasm and may benefit from the use of bronchodilators. When upper airway injury is suspected, elective intubation should be considered. Airway edema can progress over the next 24-48 hours and may make later intubation difficult if not impossible. Studies have shown that initial evaluation is not a good predictor of the airway obstruction that may ensue later secondary to rapidly progressing edema ¹¹.

Although controlled studies assessing the effects of steroids on various forms of chemical pneumonitis are disappointing, steroids have been suggested as having some value in exposure to the following ¹²:

• Oxides of nitrogen (NOx)
• Zinc oxide
• Red phosphorus
• Sulfur trioxide
• Titanium tetrachloride
• Polytetrafluoroethylene (PTFE; Teflon)

Patients with smoke inhalation should be monitored for 4-6 hours in the emergency department. Those who are at low risk for injury and whose vital signs and physical examination findings remain normal can usually be discharged with close follow-up and instructions to return if symptoms develop ¹. Patients with any of the following should be strongly considered for hospitalization:

• History of closed-space exposure for longer than 10 minutes
• Carbonaceous sputum production
• Arterial PO2 less than 60 mm Hg
• Metabolic acidosis
• Carboxyhemoglobin levels above 15%
• Arteriovenous oxygen difference (on 100% oxygen) greater than 100 mm Hg
• Bronchospasm
• Odynophagia
• Central facial burns

Mechanical ventilation may be necessary in patients with declining lung function, oxygenation levels, and ventilation. It is given as follows ¹:

• Positive pressure ventilation with low tidal volumes (3-5 mL/kg)
• Positive end-expiratory pressure (PEEP), with plateau pressures below 30 cm water

Neurologic abnormalities and a history of loss of consciousness are the primary clinical features used to define severe carbon monoxide (CO) toxicity and are indications for hyperbaric oxygen (HBO) therapy. In addition, hyperbaric oxygen use is indicated in patients with any of the following:

• Base excess lower than -2 mmol/L
• Carbon monoxide (CO) level greater than 25% (or >15% in pregnancy, as fetal hemoglobin binds carbon monoxide (CO) more tightly)
• Signs of cerebellar dysfunction
• Cardiovascular dysfunction
• Pulmonary edema
• Extremes of age

In a case series by Huang et al, 25% of patients presented after zinc oxide exposure with acute lung injury requiring ventilatory support. All of these patients survived with glucocorticoids, antibiotics and lung-protective ventilatory management. However, there was no control group, so a causal link could not be made between survival and steroid treatment ¹³.

Smoke inhalation injuries predispose the airways to infection because of cellular injury, reduction of mucociliary clearance, and poor macrophage function. Acute bacterial colonization and invasion peaks at 2-3 days after smoke inhalation. Prophylactic antibiotics should not be used, as they are not only ineffective but increase the risk of emergence of resistant organisms.

Discerning secondary infection from the effects of inhalation injury can be very difficult because both may produce fever, elevated white blood cell counts, and abnormal radiography findings. Antimicrobial therapy should be reserved for patients with definitive microbiologic evidence of infection that is not responding to aggressive support therapy or when clinical deterioration occurs in the first 72 hours.

The most common organisms in secondary pneumonia after smoke inhalation injury are Staphylococcus aureus and Pseudomonas aeruginosa. Direct parenteral coverage with antibiotics to cover these bacteria if infection is suspected.

References

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