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Author: Charles Stewart, MD, FACEP, Emergency Medicine Physician, Colorado Springs, CO.
Peer Reviewer: Steven M. Winograd, MD, FACEP, Attending Emergency Medicine Physician, Jeannette District Memorial Hospital, Jeannette, PA; University of Pittsburgh Medical Center, PA.
Children with an inhalation injury are a challenging problem for the emergency department (ED) physician. Although children are far more likely to be burned by hot food, a stove top, grill, or scalding water than suffer an inhalation injury, inhalation injuries represent potentially lethal insults,1-3 and the importance of these toxic inhalations cannot be overstated. Between 8000 and 12,000 people die from fires in the United States each year.4 About 1000 of these deaths occur in children younger than age 15.5 Four out of five of these deaths result from smoke inhalation (not flames).6-9
Children may be nonverbal or have difficulty communicating an inhalational exposure; therefore, emergency physicians must be alert to environmental clues that suggest inhalation injury. Additionally, the ED physician must be aware of the potential toxic components of the inhalation injury, such as cyanide.
Early recognition and timely intervention remain the most important aspects of caring for a child with an inhalational injury.— The Editor
The lungs are critical for successful maintenance of oxygenation and ventilation. If the lung is unable to function, the remaining life span is measured in moments, and treatment options are limited. In addition, the lungs represent such a large surface area that they readily absorb toxic materials into the systemic circulation.
The airway and pulmonary problems that can occur from the inhalation of noxious agents can be broadly classified into four groups:
An inhalation injury may involve concurrent mechanisms. It is common, for example, for the fire to partly consume oxygen and produce carbon dioxide and monoxide, cyanide, soot, and superheated air. The concentration and composition of the toxins in smoke varies from fire to fire and even within the fire.10 The constituents of smoke can destroy lung surfactant, increase pulmonary vascular resistance, and contribute to edema of the lung and airway. The injury resulting from breathing such a mixture will be multifaceted.
Airflow limitation can result from bronchospasm, upper airway narrowing from edema, increased secretions, ciliary dysfunction, and inspissation of destroyed epithelial cells. Circumferential burns of the neck or chest can cause upper airway obstruction from an encircling eschar.
The pathology at the cellular level is extremely complex and represents a cascade of cellular and molecular events that can cause severe pulmonary dysfunction. Direct cellular injury to the respiratory epithelium and destruction of the pulmonary alveolar macrophages causes activation of the inflammatory cascade. Damaged epithelial cells release prostaglandins. Pulmonary alveolar macrophages release chemotactic factors that recruit inflammatory cells to the injured area. These inflammatory cells release vasoactive mediators that increase blood flow and increase vascular permeability. The resulting protein rich fluid leaks into the interstitial space and edema forms. The edema causes increased airway resistance, bronchospasm, and atelectasis. Lung compliance decreases.
Necrotic cellular debris accumulates in the small airways as the dead epithelial cells slough into the airway. This leads to formation of cellular casts in the airways, which obstructs the airways.
The result is a patient who requires increasing inspiratory pressures and oxygen concentrations to overcome hypoxemia, increased airway resistance, and poor lung compliance. As the airway pressures increase, particularly in the child, barotrauma may result. Progressive pulmonary failure may ultimately lead to death.
Types of Injury
Anoxia. When a fire consumes oxygen, ambient oxygen concentrations may drop from 21% to 10% or lower.11 Simply put, there isn’t enough oxygen present in this environment to support life. The low availability of oxygen in a fire may be intensified by the individual’s impaired oxygen-carrying capacity and tissue injury caused by other facets of the inhalation injury.
Ambient oxygen concentrations of 2% may lead to severe anoxic injury or even death in as little as one minute. Since children have a higher metabolic rate than adults, the hypoxic insult is more rapid in the pediatric patient.
In general, symptoms of hypoxia are produced when the oxygen content falls below 15% in an enclosed space. Unfortunately, if the oxygen content is less than 6-8%, the first symptom of hypoxia may be collapse.
Thermal Upper Airway Injury. Thermal injury of the upper airway may cause laryngeal and supraglottic edema. Marked edema may form within minutes to hours and may be exacerbated by aggressive fluid administration.12 Upper airway obstruction may develop from laryngeal edema, laryngospasm, accumulation of secretions, or extrinsic obstruction secondary to neck or facial burns. With the smaller airway caliber of the child’s airway, the emergency physician zealously must look for this edema.
It should be emphasized that the most common cause of death in the early phases of burn treatment is upper airway injury. The extent of this injury and the level of respiratory tract involvement depend upon the specific inhaled gases, the length of exposure, and the environment of the exposure. Emergency intubation or tracheostomy may be required to prevent rapid airway obstruction due to edema.
Children with suspected aspiration of hot liquids also have risk of respiratory obstruction. In these patients, there may be no signs of external burns. Symptoms of upper airway edema from hot liquid burns of the oropharynx may mimic acute epiglottitis. If inhalation injury is suspected from aspiration of hot liquids, the physician should consider early intubation.13
Thermal Pulmonary Injury. Thermal injury of the lung itself is rare. Gases have a relatively low specific heat; therefore, transfer of heat from gases to tissues occurs rapidly. As a hot gas passes through the respiratory tract, it loses most of its heat energy when it converts the liquid water normally found in the oropharynx and upper respiratory tract into water vapor. This heat transfer, even of superheated gases, usually occurs in the supraglottic and laryngeal areas, hence the propensity of burns in this area. Inhalation of superheated steam can produce a direct mucosal injury as far distal as the major bronchioles. The superheated water vapor has 4000 times the specific heat of hot air and is able to transfer more thermal energy to the distal lung.14 It also loses little of its energy when respiratory tract liquids are vaporized. Inhalation of steam may produce a true pulmonary parenchymal injury.
Toxic Airway Injury. Pulmonary parenchymal and tracheobronchial injuries also may result from toxic products of combustion or from direct inhalation of toxins. These irritants can cause direct tissue injury, bronchospasm, and an inflammatory response. The inflammatory response contributes to the tissue destruction. Activated leukocytes and/or humoral mediators such as leukotrienes and prostaglandins (prostanoids) produce oxygen radicals and proteolytic enzymes. In animal studies of smoke inhalation, ibuprofen has been found to decrease the damage to lung tissue. Other major complications from inhaling these toxic products include chemical pneumonitis and adult respiratory distress syndrome (ARDS). Late deaths may be due to pneumonia in damaged lung tissue.
There are several variables to be considered when a child is exposed to toxic agents:
1. The type or types of gases (or particulates) involved. Most fires release a large number of toxic gases, including acids, aldehydes, phosgene, chlorine, ammonia, hydrogen chloride, acroleins, nitrogen oxides, and cyanides. While these products may irritate the upper airway, they also can injure the lung. This lung damage may be manifested by mucosal and pulmonary edema, increased capillary permeability, and sloughing of the mucosal lining. Since these alveolar irritants may cause little irritation to the eyes, nose, or upper airway, the internal effects of these substances may not be felt until hours after initial exposure.
2. The duration of exposure.
3. The time elapsed between exposure and proper treatment.
4. The concentration of the gas or particles. If the toxin is present in high concentrations, it will act more quickly than a more diluted agent. If the child is exposed to a consistent concentration for a longer duration, the effects will be more profound.
5. The water solubility of the material. If the agent is water soluble, it may be absorbed more easily in the oral cavity and cause less life-threatening damage. Less soluble and particulate materials tend to pass into the lower airways and alveoli.
6. The underlying health of the subject. Cardiovascular and respiratory illnesses may increase the lethality of a specific toxin. Other toxins may affect those who are very young, very old, or pregnant. Use of cigarettes, industrial exposures, and licit or illicit drugs may alter the effects of a toxin.
Particulate Matter. Beside heat and irritating gases, smoke contains suspended particulates and liquid products of combustion. These aerosolized particles often are saturated with other products of combustion. The magnitude of the injury is dependent upon the size of the particles or drops, the degree and type of contamination with other toxins, and the extent of exposure. The extent of exposure depends upon the patient’s minute volume at the time of exposure, the concentration of the agents, and the duration of exposure to the smoke.
These superheated particles also may cause thermal injury in distant airways. As particle size increases, the heat carrying capacity also increases, but the particle settles out in the upper airway. As particle size decreases, the particles travel into the lower airway more easily. About 0.06 micron appears to be deposited best in the lower respiratory tract.
Inhalation of Toxic Gases. Some toxic gases are clinically undetectable because they may be both colorless and odorless. Tests to detect many gases can be difficult to perform, whether at the incident site or the hospital. The result of inhalation of most gases is poorly studied, and there are few diagnostic studies that confirm an exposure after the gas has been eliminated from the body. There are, of course, exceptions to this, such as carbon monoxide.
Diagnosis of the Inhalation Injury. Diagnosis of the inhalation injury is of paramount importance. Effective, early therapy often is life-saving. The injury may be obvious, with clinical signs including pharyngeal or laryngeal edema, wheezing, stridor, hoarseness, respiratory distress, and cough yielding carbonaceous sputum. Unfortunately, these signs often herald a fatal course. More often, the clinician makes the diagnosis from the history and physical examination.
In the absence of obvious injury, the clinician must have a high index of suspicion and respond accordingly. Certain mechanisms of injury place the victim in an extremely high-risk category, including:
The on-scene care providers often will give the best information available about the mechanism of injury in these cases and should be questioned carefully.
The diagnosis of inhalation injuries may be somewhat complicated. Facial burns, carbonaceous sputum, wheezing, and singed nasal hairs often are cited as classic hallmarks of inhalation injury. (See Table 1.)
Unfortunately, these signs are not diagnostic. Facial burns portend a possible inhalation injury, but 86% of patients without an inhalation injury have some degree of facial burns. A child who is within a smoke-filled space for even a few minutes can inhale significant amounts of smoke without incurring any burns to the skin or singed nasal hairs. Only 50% of victims of inhalation injuries having facial burns, and singed nasal hairs are an accurate indicator of pulmonary injury in only 13% of the patients.15-16 Only 50% of the burn victims with a proven inhalation injury had carbonaceous sputum or wheezing. Pediatric fire victims who have syncope and normal arterial blood gases also should be suspected of having an inhalation injury. Any alteration of consciousness at the scene of the fire should be treated as an inhalation injury until proven otherwise.
Some diagnostic tests may yield a definitive diagnosis, including flexible fiberoptic bronchoscopy, pulmonary function testing, and xenon lung scans.
Fiberoptic Bronchoscopy. Fiberoptic bronchoscopy is easily performed in the emergency department and will readily detect edema, swelling, and obstruction. If a significant inhalation injury is suspected, bronchoscopy can prove the presence of airway inflammation. Endoscopic criteria used to diagnose an inhalation injury include mucosal erythema, hemorrhage, necrosis, ulcerations, and the presence of carbonaceous deposits. Fiberoptic bronchoscopy will not help in the diagnosis of an injury that is limited to the lung parenchyma.
If upper airway burns are observed by fiberoptic bronchoscopy or laryngoscopy, the patient needs to be intubated immediately. If a fiberoptic laryngoscope is used for this examination, an appropriate endotracheal tube should be positioned over it for rapid intubation. A fiberoptic laryngoscope is useful in diagnosis of the pulmonary injury but its field of view is limited to the mainstem bronchi and trachea.
Pulmonary Function Testing. Pulmonary function testing will show increased work of breathing, increased airway resistance, decreased lung compliance, and decreased flow rates in the presence of a pulmonary injury. The presence of normal spirometry values probably excludes a significant injury to the lower respiratory tract.17 Unfortunately, pulmonary function tests often are not obtainable if the patient is a young child, unconscious, or not cooperative.
Xenon Lung Scan. Another test for diagnosis of an inhalation injury is a xenon lung scan. Xenon 133 is an inert, insoluble gas that is injected intravenously. After injection, the xenon is carried by the blood to the lungs, where it is cleared by exhalation within 90 to 180 seconds. Normally, if xenon is retained or unequal clearing of the radioactive tracer is found, an inhalation injury is suspected. Unfortunately, prior lung disease such as asthma or bronchitis may cause a false-positive result.
Carboxyhemoglobin Levels. Measurement of carboxyhemoglobin (COHb) is an important and useful screening test for inhalation injuries. It is more fully discussed in the section below on carbon monoxide poisoning.
Arterial Blood Gases. Arterial blood gas values may increase suspicion of an inhalation injury, but they do not provide a diagnosis. A distinct advantage to obtaining arterial blood gases is that they frequently return before other laboratory tests. If normal PaO2, PaCO2, and O2 saturations are found in the presence of an obviously dyspneic or apneic patient, the clinician should consider that the child may have inhaled toxins such as carbon monoxide or cyanide.
Unfortunately, the oxygen saturation is calculated from a measured oxygen tension in most laboratories. Since the oxygen tension of arterial blood is unchanged by carbon monoxide, calculated results will be higher than if it was actually measured. For best results, the laboratory should measure the saturation and not calculate it.
Chest X-ray. A chest x-ray should be obtained on all patients with a suspected inhalation injury. The chest x-ray may be normal for nearly 24 hours after the injury, and as such, is an unreliable screening tool.18 It will, however, serve as a good baseline for future changes. If positive, the pattern may be mixed, show an alveolar infiltrate, an interstitial infiltrate, or congestive heart failure. Infiltrates are more common in the upper lung fields. X-rays may show concomitant injuries such as fractured ribs or pneumothorax. A normal chest x-ray does not rule out inhalational injury.
The burned pediatric patient with a potential inhalation injury should never be sent to x-ray without a qualified attendant. Likewise, intubation should not be delayed to take an x-ray in a patient who requires stabilization of his or her airway.
Electrocardiogram. Since hypoxia is such a frequent concomitant of most inhalation injuries, an electrocardiogram (ECG) is indicated both as a baseline and to assess hypoxic insults to the myocardium. If the ECG is abnormal, the patient should be monitored for any dysrhythmia.
Urinalysis. Although urinalysis may not seem like a test of the respiratory tree, the inhaled toxic gas may have systemic effects. The urine should be checked for hematuria and proteinuria. For example, proteinuria could suggest exposure to carbon monoxide, hydrogen sulfide, halogens, or carbon disulfide. Hematuria may suggest hydrogen sulfide, halogens, or carbon disulfide inhalation.
Miscellaneous Laboratory Tests. Ethanol levels should be determined, particularly if the patient has any altered mental status. Likewise, toxicology screens may be appropriate for some patients.
Cyanide levels often are unavailable or greatly delayed. Suspicion must guide the practitioner who does not have this laboratory exam readily available.
The spectrum of inhalation injury can range from an immediate threat to the patient’s life because of airway obstruction to a minor mucosal irritation and cough. Any sign of airway compromise must be treated aggressively before rapid progression to upper airway obstruction occurs.
The progression of the inhalation injury is related to the extent and intensity of both the chemical and thermal components. In severe inhalation injuries, respiratory distress may begin within minutes to hours and may be seen in as many as 70% of patients who have inhalation injuries.19 In these cases, the problem is likely to be multifaceted. Mortality of patients with an inhalation injury and respiratory failure is as much as 50%.18-19
Airway. Hypoxia and anoxia or the direct toxic effects of rapidly acting toxins may incapacitate the pediatric patient within minutes. Bronchospasm and alveolar damage may cause rapid deterioration and high mortalities in these patients.20 Irritant effects may cause edema of the airway that may lead to respiratory obstruction. Absorbed acids, toxins, and irritants may cause an inflammatory response with release of histamine and other vasoactive substances or smooth muscle spasm.
Although concerns about the upper airway have focused on the first few hours after the burn, the maximum edema may peak 36-48 hours later. The patient may have no respiratory difficulties on admission, and gradually develop stridor, hoarseness, labored breathing, and retractions. Particularly in young patients, the early arterial blood gases may reflect only the tachypnea until the patient tires. Later intubations require maximum expertise because of the airway edema that may be encountered. Physicians should have a low threshold for intubation of a patient with inhalational injuries.
Airway Plugs. About 3-4 days after injury, soot, tars, resins, epithelial debris, and necrotic tissue may act as physical plugs to small airways. Plugging from debris and spasm may lead to atelectasis, air trapping, or emphysematous areas. This plugging also may set the stage for recurrent pneumonia, empyema, abscesses, and all of the myriad complications of the aspirated foreign body.
Clinically monitor the patient for a sudden deterioration in the PO2 or the PCO2 in a patient who has previously done well. These patients may have only nonspecific findings on chest x-ray, including both areas of hyperinflation and atelectasis. Increased secretions, wheezing, and increased difficulty ventilating the patient also may be found. These plugs often are easily removed with a fiberoptic bronchoscope.
Pulmonary Edema and ARDS. Pulmonary edema also may develop between 8 and 36 hours following the exposure to some inhaled toxins. It occurs somewhat earlier in patients with underlying pulmonary disease, congestive heart failure, or a past history of myocardial ischemia. Pulmonary edema also may be precipitated by an iatrogenic fluid load. This pulmonary edema is not uncommon about the third day after the injury, as the tissue edema is reabsorbed into the circulation. Sepsis also may trigger ARDS.
Pulmonary edema due to inhaled toxins responds poorly to diuretic therapy. Early use of positive end expiratory pressure (PEEP) should be considered in these cases. If the patient develops pulmonary edema after an inhalation injury, the administration of fluids should be guided by pulmonary artery pressures.
ARDS also may develop as a delayed complication. It may be a challenging diagnostic exercise to differentiate between the early appearance of ARDS and pulmonary edema. A normal or low pulmonary artery occlusion pressure "wedge" in the face of pulmonary edema will suggest the diagnosis of ARDS.
Pneumonia. The most delayed pulmonary complication to develop often is a bacterial bronchopneumonia. This pneumonia develops after the lung’s defenses have been destroyed by the toxin. This complication also may be partly due to the impaired clearance of secretions, plugging, and atelectasis. Ciliary impairment due to the toxins decreases the clearance of secretions and debris.
Cardiovascular. Cardiovascular collapse may result from hypoxia or from the direct action of a toxin such as freon. These toxins may precipitate arrhythmias, cardiac arrest, hypotension, conduction blocks, or pulmonary edema. The hypoxia may cause infarcts or ischemic ECG changes.
Central Nervous System. Early, general symptoms of toxic gas inhalation include restlessness, "intoxication," headache, dizziness, confusion, seizures, or coma. One question needs to be answered immediately: Are the symptoms due to the toxin or merely hypoxia? This question is best answered by removal of the person from the offending agent and applying 100% oxygen. Always remember to include trauma, alcohol, and drugs (licit and illicit) in the differential.
Hepatic and Renal Systems. It is difficult to separate hepatic or renal failure due to toxic damage from hypoxic injury. The inhaled toxin may cause hepatic necrosis, such as is found with the hydrocarbons. Acute tubular necrosis may result from toxic effects elsewhere, such as from the rhabdomyolysis or hemolysis that may be found with carbon monoxide and other inhaled toxins.
Gastrointestinal Systems. Nausea and vomiting are common symptoms that result from multiple inhaled toxins. The most prominent examples are the nausea and vomiting from carbon monoxide; or the salivation, urination, vomiting, and diarrhea seen with organophosphates.
Skin and Musculoskeletal Systems. The skin should be checked for cyanosis, cherry red color, or brownish tinge. The inhaled toxin may lead to necrosis, ulcers, or frank burns on exposed skin. Bullae formation on dependent parts is particularly common in carbon monoxide poisoning.
The musculoskeletal system may be damaged by the toxin or the hypoxic effects of the toxin. An example of this damage is rhabdomyolysis due to carbon monoxide.
General. Effective treatment of the inhalation injury depends first upon an accurate initial diagnosis and early recognition of complications. (See Table 2.)
|Table 2. Emergency Treatment of Inhalational Injuries|
|•||Humidification with cool mist (100% oxygen at first).|
|•||Consider intubation; airway swelling can be profound.|
|•||Consider cricothyrotomy if intubation is problematic.|
|•||Secure IV access (in unburned skin, if possible).|
|Emergency department care|
|•||Administer supplemental humidified oxygen (100%) to all patients.|
|•||Intubate if there is any sign of respiratory distress.|
|•||Consider intubation if the patient is high risk. (See Table 3.)|
|•||Consider intubation if the patient will be transported.|
|•||Positive end expiratory pressure if PaO2 is less than 50 despite supplemental oxygen.|
|•||Administer IV fluids per burn formula of choice.|
|•||Assume CO is present in all inhalation injuries, but get COHb level.|
|•||Consider presence of cyanide and consider use of cyanide kit in all patients who are intubated.|
|•||Consider bronchodilators [Ventolin (Tm) or albuterol aerosol therapy in usual doses].|
|•||Use antibiotics only when infection is documented.|
|•||Use of steroids is controversial.|
The appropriate airway treatment principles for both pre-hospital and ED care are to:
Monitoring and Admission. Cardiac toxicity and arrhythmias are common in the presence of hypoxia. In suspected inhalation injuries, cardiac monitoring should be instituted promptly. All patients with an inhalation injury should be monitored for at least 4-6 hours in the ED. The following patients should be strongly considered for hospitalization (see Table 3):
The following patients should be hospitalized in an intensive care environment:
|Table 3. Consideration for Hospitalization|
|The following patients should be strongly considered for hospitalization:|
|•||Patients who are coughing up carbonaceous sputum|
|•||A history of closed space exposure for 10 minutes or more|
|•||Patients with central facial burns|
|•||Patients with bronchospasm|
|Patients with the following should be hospitalized in an intensive care environment:|
|•||Arterial PO2 less than 60 mmHg|
|•||COHb levels above 15%|
Be aware that the child may be asymptomatic on arrival but may develop significant signs and symptoms for as long as 36 hours after exposure. The cogent physician will have a low threshold for bronchoscopy and for admission.
Be aware that a child may be asymptomatic on arrival but may develop significant signs and symptoms for as long as 36 hours after exposure. The cogent physician will have a low threshold for admission.
Airway Management. Intubation. The victim of an inhalation injury who is alert, awake, and conversant needs no airway protection but should be placed on 100% oxygen pending CO levels. To intubate, by rote, the child who has "classic" hallmarks of inhalation injury but who is in no respiratory distress, is phonating well, and has normal pulmonary functions is inappropriate. An alert and cooperative patient with "classic" findings of an inhalation injury deserves confirmatory flexible fiberoptic bronchoscopy and pulmonary function testing.
The patient who has stridor or severe dyspnea should be intubated rapidly, placed on 100% oxygen by endotracheal tube, and considered for bedside bronchoscopy.
The child who is unconscious following exposure to smoke also should be rapidly intubated. If the patient has an alteration of consciousness or loss of the gag reflex, intubation is indicated for airway protection and to provide 100% oxygen.
A pediatric flexible fiberoptic bronchoscope requires a 4-mm tube orifice to pass. Mucous plugging, soot, and debris in the airway may require repeat bronchoscopy for pulmonary toilet. Reintubation of an edematous airway is not a trivial task. The oral route may allow placement of a larger tube and subsequent bronchoscopy through the tube.
Tracheostomy. Early tracheostomy once was advocated for airway control. Now that low-pressure endotracheal tubes are available, routine tracheostomy no longer is recommended. Emergent tracheostomy has no advantage over intubation and many more complications, particularly when performed through burned skin. For facial trauma, severe respiratory distress, or massive facial burns, cricothyrotomy is preferred as the emergency surgical airway of choice.
Tracheostomy may be appropriate when it is required for pulmonary toilet in children who are sloughing large amounts of endobronchial debris.
Oxygenation. Once the child has been intubated, humidified oxygen at high flows should be maintained. As noted earlier, carbon monoxide toxicity is associated with smoke inhalation and is emergently treated by administration of high-flow oxygen. Even patients with chronic lung disease such as bronchopulmonary dysplasia should be given high-flow oxygen.
Ventilation. Ventilatory support may be enhanced by the use of high-frequency ventilation. Since the use of high-frequency ventilation, mortality has decreased from 41% to 29%.21 High-frequency ventilation decreases the barotrauma associated with conventional ventilators and mechanically mobilizes the secretions and casts in the tracheobronchial tree.22
Pulmonary Toilet. Management of patients with inhalation injury often requires aggressive pulmonary toilet. Frequent postural drainage, coughing, and encouragement of deep breathing all aid in clearing the airway of debris and secretions. Frequent airway suctioning often is needed to help remove this debris. Occasionally, fiberoptic or rigid bronchoscopy is effective for removal of debris. As noted previously, escharotomy of chest and abdominal burns may be required for circumferential burns.
Positive pressure ventilation facilitates the management of children with large intrapulmonary shunts or poor mechanics of breathing. High peak inspiratory pressures should be avoided because they are associated with barotrauma.
Bronchospasm. If the child has bronchospasm or wheezing, a trial of nebulized aerosol bronchodilators such as albuterol or terbutaline is indicated. Pulmonary edema from toxic gas exposure frequently does not resolve with diuretics. Positive pressure breathing such as PEEP and intubation often are required.
Later treatment includes prompt recognition and treatment of bacterial infections and reversal of ventilation-perfusion abnormalities. In many cases, these occur during the more prolonged hospital stays and are well covered in the many definitive texts upon the management of burns.
Antibiotics. Inhalation injuries clearly predispose the patient to pulmonary infection after several days.23 Poor macrophage function, decreased ciliary function, and localized cellular injury all contribute to increased rates of infection. Despite the increased incidence of pneumonia, prophylactic antibiotics should not be used. Studies have shown that organisms resistant to the antibiotics may result when prophylactic antibiotics are given.
Surfactant. Inhalation injuries decrease lung surfactant. In experimental induction of inhalation injury, instillation of artificial surfactant was helpful.24-27 Larger human studies may show improvement in survival with use of supplemental surfactant.
Steroids. Animal and prospective human studies have indicated that steroids are not beneficial.27 Indeed, steroids are associated with a significant increase in mortality even when used briefly.
Heparin/N-acetylcysteine. A recent pediatric study has shown that aerosolized heparin and N-acetylcysteine will decrease the incidence of atelectasis and mortality.28-29 Aerosolized deferoxamine also appears to decrease the lung injury caused by smoke inhalation.30
Extracorporeal Membrane Oxygenation (ECMO). With the use of conventional mechanical ventilation of the burned child, worsening compliance and increasing airway pressures often cause barotrauma. Early institution of ECMO may prevent this barotrauma by supporting the lung while it recovers.31-32 Currently ECMO use is limited because of the tremendous costs, scarcity of the units, and associated bleeding complications. As ECMO becomes more available, clinical studies of ventilatory support with ECMO in the child with severe inhalation injury are likely.
Description of Specific Toxic Gases
Treatment for exposure to irritant gases is mainly supportive, since few specific antidotes exist. All patients with toxic gas exposure (see Table 4) should be hospitalized for observation for 24 hours, since so many delayed symptoms may appear.
Carbon monoxide is an odorless, colorless, tasteless gas generated by burning carbon with a reduced level of oxygen. It can be found when burning gasoline, coal, charcoal, natural and synthetic polymers, and other carbon-containing materials.
The carbon monoxide blood level is determined by the carbon monoxide concentration, the ambient oxygen tension, the ventilatory rate, the hemoglobin, and the blood volume. Small amounts of carbon monoxide are produced by the body and COHb levels of 0.3-0.7% do not signify any exposure. COHb levels may be as high as 8% in smokers and higher in those exposed to urban air pollution who also smoke.7,33
Carbon monoxide intoxication causes an estimated 50% of deaths from fires. During the active burning phase of a fire, carbon monoxide levels can reach as much as 15,000 parts per million. (More than 1500 parts per million have been associated with significant morbidity and mortality.)
Carbon monoxide is a hematologic poison. It interferes with the transport of oxygen by binding with hemoglobin. Although this binding is reversible, the affinity for hemoglobin is about 230-270 times greater than that of oxygen. Carbon monoxide shifts the oxygen-hemoglobin curve to the "left," forcing hemoglobin to retain oxygen longer. Carbon monoxide also binds to myoglobin and impairs oxygen transport to the muscles.
Clinical Picture. Although many authors have felt that the blood level of carbon monoxide correlates closely with the symptoms of carbon monoxide poisoning, newer evidence shows that chronic lower levels may cause more tissue damage. The acute symptoms correlate poorly with the blood COHb levels.34-35 In fact, extensive animal studies with long-term administration of CO and subsequent complete exchange transfusion have shown little improvement in symptoms.
Carbon monoxide affects every body system. Although the entire body is affected by carbon monoxide poisoning, the heart and nervous system—the tissues most sensitive to hypoxia—account for the major toxic manifestations. The extent of the symptoms depends upon a total COHb concentration, duration of exposure, activity, and the underlying state of the individual. The signs of acute carbon monoxide poisoning include headache, dizziness, nausea, vomiting, drowsiness, tachypnea, chest pain, pallor, confusion, irritability, irrational behavior, and loss of consciousness.
There are few symptoms in those people who have an acute COHb level below 10%. In patients with coronary artery disease, or in young children or infants, these lower concentrations of carbon monoxide may cause symptoms. Infants have a higher susceptibility to carbon monoxide because of their increased ventilatory rates. They simply breathe in more CO per body weight. Exposure to CO during pregnancy poses an even higher risk to the fetus than to the mother.36 If the CO exposure occurs over a long period of time, there will be more symptomatology at lower levels.
At a COHb level of 10-20%, the patient may experience headache, nausea, and vomiting. The patient also may have some ataxia, loss of short-term memory, and loss of manual dexterity. More severe headache, weakness, dizziness, dimness of vision, nausea, and vomiting appear at blood levels of 20-30% carbon monoxide. Symptoms intensify during activity and may be accompanied by tachycardia, tachypnea, and syncope. Once the CO concentration passes 30%, the victim often becomes confused and lethargic. Frequently, ECG tracings will show some depression of the ST segment.
When the COHb level rises to between 40% and 60% , the patient becomes comatose. Death usually occurs once 60% of hemoglobin is bound to CO.
Diagnosis of CO Poisoning. An immediate concern about any victim of suspected smoke inhalation is whether they have carbon monoxide poisoning. Carbon monoxide levels will rapidly rise to lethal levels if the fire is in an enclosed area. The diagnosis of carbon monoxide poisoning is made by measuring the COHb level.
Absence of CO in the blood does not rule out carbon monoxide poisoning or effects. Carbon monoxide blood levels also may be used as a screening test to increase suspicion for other inhaled toxins.
A co-oximeter or transcutaneous PO2 meter is accurate in detecting a decreased oxyhemoglobin level in the presence of an increase in COHb. Co-oximeters measure absorption of light on at least six frequencies, including those for reduced hemoglobin, COHb, methemoglobin, sulfhemoglobin, and oxyhemoglobin.
Pulse oximetry is inadequate in determining whether a patient has carbon monoxide poisoning. A pulse oximeter measures the light absorbed at 660 and 940 nm. These values correspond to the reduced hemoglobin and oxygenated hemoglobin levels, respectively. The maximum and minimum absorption of light at these wavelengths generates the "pulse" signal. The ratio of the absorbed light is then used to determine the oxygen saturation. The oxygen saturation calculated by the pulse oximeter simply won’t change with an increased COHb level because the CO molecule has a different maximum absorption wavelength. Pulse oximeters should not be used to monitor patients with suspected CO poisoning.
An older colorimetric assay is useful but not as accurate. Differential spectrophotometry can be used to determine blood levels of COHb but is not as rapid as co-oximetry.
Routine arterial blood gases are not helpful in the diagnosis of carbon monoxide poisoning. The PaO2 reflects the dissolved oxygen concentration rather that the hemoglobin saturation and is, therefore, usually normal. A relatively normal PaO2 with a low PaCO2 may suggest hyperventilation to compensate for the tissue hypoxia. Remember that many blood gas machines calculate the percent saturation of hemoglobin rather than measuring it and can report falsely elevated oxygen saturations.
COHb levels do not require arterial blood samples. Since CO is not easily removed from the lung, arterial CO and venous CO levels are equivalent.
Treatment. CO is excreted by the lungs. The rate of excretion is related to the competition of oxygen for binding sites on the hemoglobin molecule. An increase in the ambient oxygen tension from room air to 100% oxygen changes the half-life from 3-4 hours to about 40 minutes.
It should be reemphasized that the CO level in the blood stream is not a definitive toxic index, if the patient has received 100% oxygen en route to the hospital. COHb in the blood is cleared in about 80 minutes (half-life x 2) with 100% oxygen and the blood level may be only modestly elevated after a prolonged transport. The tissue CO levels may take longer to change and are not reflected by blood CO measurements. Consequently, treatment decisions should be governed by signs and symptoms of CNS dysfunction rather than blood levels.
Hyperbaric oxygen therapy for carbon monoxide poisoning is controversial, and there may be no clear advantage over treatment with 100% oxygen in the vast majority of patients.37 Patients with severe alteration of consciousness, severe acidosis, pulmonary edema, or elevated levels of COHb (CO greater than 25% or greater than 15% in the pregnant patient) may be appropriate for hyperbaric oxygen. The major reason to use hyperbaric oxygenation is for the prevention of delayed neurologic sequelae.38
Generally prognosis is good when treatment is prompt. Most early deaths are due to cardiac dysrhythmias. Prognosis is worse in patients with coma and with concurrent cyanide and carbon monoxide poisoning.
Inhaled hydrogen cyanide is quite lethal. Exposure to 140 ppm for 60 minutes or 1500 ppm for 3 minutes has an estimated 50% mortality. Cyanide toxicity should be considered in all smoke inhalation victims with CNS or cardiovascular findings.39-40 Cyanide is found in the burning fumes of x-ray film, wool, silk, nylon, paper, nitriles, rubber, urethanes, polyurethane, and other plastics. As a product of combustion, cyanide is commonly mixed with isocyanates, which are intense respiratory irritants.
Many children suffering from severe smoke inhalation syndromes also have elevated cyanide levels.41 Those patients with high cyanide levels also often have an elevated carbon monoxide level. The close association of the two makes it difficult to separate their effects during inhalation injuries. Sublethal concentrations of CO and cyanide may prove lethal in synergy.
Cyanide appears to inhibit the cytochrome oxidase system and thus interrupt aerobic cellular metabolism. This leads to a profound metabolic acidosis as the body attempts to use the less efficient anaerobic metabolism. Subsequent CNS, respiratory, and myocardial depression complicate the picture.
Diagnosis is difficult without a history of cyanide exposure. Cyanide exposure may be diagnosed by history of probable exposure and an odor of bitter almonds. Only about 50% of people can detect the smell of cyanide.
In most institutions, there is no "real-time" assay for cyanide. A new semiquantitative assay that uses calorimetric test strips may improve the laboratory evaluation of hydrogen cyanide poisoning.42
There is no reliable correlation between blood cyanide levels and fatalities. Before the cyanide level is correlated with clinical appearance, the elapsed times since the exposure and since the specimen was obtained must be considered. This, again, may be due to the apparent synergistic combination of cyanide and CO.
Arterial blood gases often will show a metabolic acidosis with normal oxygenation and calculated hemoglobin saturation. Venous gases have the same pattern, because the oxygen is not used up. Venous blood often looks arterial in color. The measured arterial oxygen saturation will be decreased, while the calculated saturation is normal.43 Again, the laboratory must report both measured and calculated oxygen saturation for this "gap" to be useful.
This picture of an abnormal hemoglobin and less than adequate saturation is found commonly with only four poisons. The toxidrome may occur with cyanide, carbon monoxide, hydrogen sulfide, and methemoglobin. Methemoglobin and COHb are easily measured. Hydrogen sulfide and cyanide are treated in a similar manner. Cyanide levels should be obtained in all cases, even though they may not be available for clinical use.
Symptoms. The symptoms of inhalation of cyanide are nonspecific. Early symptoms may include dryness and burning of the throat and air hunger. In small doses, headache, confusion, anxiety, dizziness, nausea, palpitations, tachycardia, tachypnea, and combativeness all may be found. In large doses, bradycardia, bradypnea, coma, gasping respirations, apnea, and death all may be common manifestations. The examiner should be suspicious of cyanide intoxication if the victim of smoke inhalation has an abrupt collapse that does not respond to oxygen. An audible gasp is thought to be characteristic of extreme exposure to HCN.
Treatment. The mainstays of treatment are oxygen and ventilation. Therapy beyond the basics is controversial and includes the classic Lilly cyanide kit, hyperbaric oxygenation, and massive doses of vitamin B12. Contaminated clothing must be removed and the skin washed. If cyanide was ingested, gastric lavage should be done. Activated charcoal will not absorb cyanide.
Lilly Cyanide Kit. Methemoglobin will compete for binding of cytochrome oxidase system with cyanide.44 When cyanide binds, the cytochrome oxidase is permanently inactivated. Methemoglobin binding can be reversed and the cell salvaged. Chen and colleagues first proposed this technique in the 1930s.
Methemoglobinemia is produced by inhalation of amyl nitrite and intravenous administration of sodium nitrite. About 30% methemoglobinemia is considered optimum, and the levels should be kept below 40%. After the methemoglobin has relieved the symptoms, the cyanide is permanently converted to thiocyanate by sodium thiosulfate. The thiocyanate ion may be safely excreted by the kidney. A high-tissue oxygen markedly potentiates the effects of this treatment.
Therapy with nitrites is not innocuous and can cause a fatal methemoglobinemia, particularly in young children. In those with mixed gas exposure, production of methemoglobinemia may induce tissue hypoxia. If sodium nitrite is given too rapidly, then hypotension and vasodilation may occur. If methylene blue is given, all of the methemoglobin will be released with a relapse of symptoms. Instructions are on the cyanide kits and should be followed explicitly.
Pediatric Doses of the Compounds in the Lilly Cyanide Kit:
• Amyl nitrate: Not approved. Adult dose is 15 seconds inhalation followed by 15 seconds rest, repeat until IV is established and nitrite given.
• Sodium nitrite: 0.3 mL/kg of 3% solution IV over 2-4 minutes.
• Sodium thiosulfate: 7 g/m2 not to exceed 12.5 g/dose (height and weight are needed to calculate body surface area).
• Methylene blue: use same dose as for adults. This drug can cause profound anemia in patients with G-6-PD deficiency.
These doses also are located on the inside front cover of the cyanide kit.
Hydroxycobalamin (Vitamin B12). Hydroxycobalamin has been used to prevent cyanide toxicity associated with prolonged administration of sodium nitroprusside. It also is effective for the treatment of acute cyanide poisoning.45-47 B12 reacts directly with the cyanide and does not change hemoglobin. B12 appears to be a preferable antidote for patients with another concurrent gas exposure such as carbon monoxide. There is limited use in the United States to date, but more than 15 years of experience are documented in the French literature.48 Hydroxycobalamin is essentially devoid of complications but is not available as a cyanide antidote in the United States.
Dicobalt-EDTA. Another antidote available in Europe is dicobalt-EDTA, sold as Kelocyanor. This agent chelates cyanide as cobalticyanide. It does cause significant hypertension and may cause dysrhythmias if no cyanide is present. Kelocyanor and hydroxycobalamin may be given together for additive effect.49 Dicobalt-EDTA is thought to act more quickly than nitrites.
Hyperbaric Oxygenation. Hyperbaric oxygenation may be the ideal adjunct to both hydroxycobalamin and nitrite therapies. With hyperbaric oxygenation, the oxygen dissolved in the tissues can support metabolism. This means the methemoglobinemia formed by nitrite administration is of less consequence. Hyperbaric oxygen also displaces cyanide from the cytochrome oxidase. In the case of a mixed gas inhalation, carbon monoxide will be effectively displaced from hemoglobin and will allow higher levels of nitrite to be used. Hyperbaric oxygen therapy will not replace chemical treatment since administration of nitrites is quicker than getting to the dive chamber. Delay in treatment of this disease can be lethal.
Phosgene and Hydrogen Chloride (HCL)
These two gases are similar, and phosgene decomposes to HCL and CO. They are both colorless and somewhat heavier than air. In the pure form, both are reputed to have the smell of newly mown hay, but this would be absent when produced by fires. Unfortunately, combustion of plastics, polyvinyl chlorides, and chlorinated hydrocarbons can produce these gases in house fires. Use of carbon tetrachloride fire extinguishers also may yield phosgene.
Phosgene was used as a war gas in World War I and was responsible for 60-80% of the inhalation injury deaths of that war. It is a relatively slow-acting agent. Since symptoms develop slowly, the exposure may be lengthy with the subsequent development of extensive alveolar damage. This slow action is thought to be due to poor water solubility.
Phosgene causes vasoconstriction of the pulmonary venous circulation, which increases the incidence of pulmonary edema. The pulmonary edema of phosgene gas exposure has been associated with massive fluid loss from the lungs and may require fluid replacement.50
Field care consists of decontamination and high-flow oxygen. Skin surfaces and eyes should be copiously irrigated after exposure. The patient who has been exposed to phosgene must be hospitalized for observation. Meticulous pulmonary care is needed for treatment of victims.
Oxides of nitrogen include nitrogen dioxide (NO2), nitrous oxide (NO), and nitric acid (HNO3). Nitrogen dioxide is generated by incomplete combustion of nitrogen-containing synthetic materials. Pulmonary edema and extensive respiratory damage may occur as a result of exposure to these agents.
These toxins are poorly soluble in water and therefore injure the lower respiratory tract. When nitrogen dioxide reaches the lower airways, moisture converts it to nitric acid. Because there is little upper respiratory irritation, quite extensive exposure may occur before the delayed symptoms appear.
Metal Fume Fever
A metal fume is a suspension of microscopic oxidized particles of the metal. These particles range in size from 0.02 to 0.25 microns. Exposures to metal fumes are seen after welding or smelting brass, copper, tin, magnesium, or nickel. Smelting cadmium, cobalt, manganese, or chromium also may cause this disease. A similar picture is found with exposure to hot polymers in "polymer fume fever."
The symptoms are those of influenza: sudden onset of thirst, fever, chills, myalgia, nausea, vomiting, and headache. A characteristic course involves resolution of symptoms during the weekend (24-48 hours after exposure). Airway and lung parenchymal injury and acute renal injury are rare. With chronic exposure, a long-lasting tracheobronchitis or pneumonitis may be found.
The pathogenesis is uncertain. The most commonly accepted theory is an allergy mediated complex, but other theories propose direct toxic effects, an endotoxin-like effect, and anaphylaxis.51 Serum or urinary heavy metal levels do not correlate with symptoms.
Treatment is removal from the source. Therapy is supportive with bed rest, analgesics, and fever control for symptomatic relief. Milk often is recommended to relieve the nausea and vomiting associated with metal fume fever. In most cases, the symptoms will resolve within 48-72 hours, if exposure is terminated.
Most fatalities resulting from fires are due to smoke inhalation. Rapid evaluation with a high index of suspicion for toxic exposure is critical. (See Table 5.) Children who are trapped in an enclosed space or who lose consciousness during a fire are at increased risk for smoke inhalation. This evaluation should include chest x-ray, arterial blood gas analysis, and possible bronchoscopy. If a significant toxic gas inhalation is suspected, an aggressive response with airway support, pulmonary toilet, ventilation, and high-flow oxygenation should be instituted.
Table 5. Pitfalls in the Emergency Treatment of Inhalational Injuries
|•||Don’t wait for the patient to go into respiratory distress before you intubate. It is easier to intubate before the swelling is present.|
|•||Remember that patients may be asymptomatic on arrival and develop symptoms later. Have a low threshold for intubation and diagnostic evaluation with bronchoscopy.|
|•||Remember to look for pertinent risk factors in inhalation injuries. These include: entrapment in a closed space, carbonaceous sputum, elevation of COHb levels, alterations of consciousness, and central facial burns.|
|•||Don’t treat the burn first—inhalation injury is more lethal and progresses more quickly than the burn.|
|•||Don’t assume that the patient is fine after an inhalation injury simply because the chest x-ray is normal and the ABG is normal. Some inhalation agents produce pulmonary inflammation, which develops over 12-24 hours.|
|•||Don’t wait for a COHb level to give 100% oxygen. Begin therapy as soon as possible.|
|•||Don’t assume that the only possible injurious gas from combustion is carbon monoxide.|
|•||Remember that EMS personnel have given oxygen and depressed the COHb level. The CO level in the ED may not correlate with the patient’s condition.|
|•||Don’t assume that syncope is from a faint when the patient has been exposed to toxic gases.|
The prudent emergency provider will recognize that the diagnosis of a specific toxic gas inhalation is difficult. It depends upon historical data, "toxidromes," and suspicion. The variability of gas composition and effects, and of the body’s response to these agents, make the emergency department identification of the agent difficult. Aggressive therapy is indicated to improve outcome following exposure.
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