AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Although children are less likely than adults to experience significant smoke inhalation, it remains a serious and life-threatening problem in the pediatric population. Management of the burned child with a coexistent inhalation injury requires a cohesive team of pediatric intensive care physicians and nurses, along with burn specialists. Although burned children have traditionally been cared for in adult burn units, the increased availability of physicians, nurses, and ancillary staff trained in the care of severely ill pediatric patients make the pediatric intensive care unit a superior environment. Understanding that children are not merely small adults is critical to preventing therapeutic errors that can result in disastrous iatrogenic complications.

The heat generated during combustion can cause significant thermal injury to the upper airway. Particulate matter produced during combustion (soot) can mechanically clog and irritate the airways, causing reflex bronchoconstriction. Noxious asphyxiant gases released during thermal decomposition include carbon monoxide (CO) and hydrogen cyanide. Other byproducts produced by combustion of furniture and cotton (aldehydes) or rubber and plastics (chlorine gas, ammonia, hydrocarbons, various acids, ketones) produce injury. Exposure to metal fumes and fluorocarbons, systemic toxins typically released during industrial fires, is rare in the pediatric population. Children are less likely to be affected by systemic toxins than by toxins from household products and products of smoke, including CO and cyanide poisoning.

Routine use of smoke and CO detectors in the home is designed to decrease the risk of injury by permitting early escape. However, the risk for smoke inhalation remains high in the pediatric population, and ongoing prevention efforts are important.

Pathophysiology

Inhalation injury occurs in 3 ways: (1) by cell injury and pulmonary parenchymal damage by irritants, (2) hypoxemia by interruption of oxygen delivery by asphyxiants, and (3) end organ damage by systemic absorption through the respiratory tract.

Respiratory embarrassment can be broadly categorized as the result of thermal or chemical damage to the epithelial surfaces of the intrathoracic and extrathoracic airways. Secondary insult with bacterial pneumonia may occur days after inhalation, causing further cytotoxic damage. Ciliary function is impaired, leading to accumulation of airway debris. The inflammatory cascade initiates neutrophil infiltration. Macrophages within the alveoli are destroyed, allowing bacteria to proliferate. Lack of an intact epithelial barrier further facilitates the development of pneumonia.

Hypoxemia results from a decrease in inspired oxygen concentration at the scene of injury, a mechanical inability to exchange gas because of airway obstruction or parenchymal pulmonary disease, and inhibition of oxygen delivery and tissue utilization by toxins. With the advent of sophisticated intensive care support, patients who survive the acute injury and are successfully transported to an ICU now rarely expire from isolated pulmonary disease. However, the presence of multiorgan dysfunction, a common sequela of hypoxia substantially raises morbidity and mortality.

Because CO does not injure the lung directly, its toxic effect results from a displacement of oxygen from hemoglobin binding sites, thereby decreasing the oxygen-carrying capacity of the blood. It not only has a 250 times higher affinity for hemoglobin than oxygen but it also shifts the oxyhemoglobin dissociation curve to the left. The leftward shift of the oxyhemoglobin dissociation curve results in further tissue hypoxia because the hemoglobin is less able to unload oxygen. CO reacts with myoglobin to further impair oxygen uptake by decreasing facilitated diffusion of oxygen into muscle. CO also interacts with several heme-containing enzymes of the electron transport chain, further impairing tissue oxygen availability.

Cyanide causes tissue asphyxiation through the inhibition of intracellular cytochrome oxidase. It blocks the final step in oxidative phosphorylation and prevents mitochondrial oxygen utilization. Affected cells convert to anaerobic metabolism and lactic acidosis ensues. The organs most sensitive to cellular hypoxia are the central nervous system and the heart. The central nervous system reacts to low concentrations of cyanide through hyperventilation, thereby increasing exposure if the route is by inhalation.

Frequency

United States

Burns in children are 2.5 times more likely to occur by scalding rather than flame exposure. Hence, the percentage of children who experience respiratory symptoms after burns is less than that of adults who are more often exposed to smoke-producing flames. About 50% of all burn deaths are related to inhalation injuries. Early hypoxemia is a contributor to over 50% of smoke inhalation deaths, with CO intoxication accounting for as much as 80% of the fatalities.

Mortality/Morbidity

• Inhalation injury increases the morbidity and mortality of burns significantly. Small children are especially vulnerable because they are less likely to escape a confined space and also have a higher minute ventilation, which increases exposure to smoke and other toxins released during pyrolysis. In addition, their relatively smaller airways will be more severely affected by airway edema and obstructing material.
• Bacterial pneumonia often complicates inhalation injury within 4-5 days of presentation. This additional cellular damage can cause significant mortality days to weeks after the initial injury. Children with acute pulmonary injury secondary to toxic inhalations generally do well once supported through the initial inflammation and damage. Most of the pulmonary damage is self-limited and resolves within 2-3 days. The degree of recovery depends on the extent of the pulmonary parenchymal injury and subsequent hypoxic damage to the organs. Reports exist of residual reactive airway disease, bronchiectasis, bronchiolitis obliterans, and interstitial fibrosis. However, the cause-and-effect relationships between toxic exposure and pulmonary sequelae remain controversial and are not proven. Airway hyperreactivity generally improves over several months following inhalation injury. However, some authors documented long-term respiratory symptoms such as cough, wheeze, and shortness of breathevenaftermildinhalationinjury, indicating a more prolonged nature of the lung injury. The long-term effects of inhaled toxins on pulmonary function are not yet determined.
• CO intoxication is a particularly serious consequence of smoke inhalation and may account for as much as 80% of fatalities from inhalation injury. Most patients arriving alive to the emergency department nonetheless make a full recovery. However, up to one third of patients with significant CO exposure develop a secondary syndrome of long-term neurologic dysfunction within 1-3 weeks after exposure. Higher cortical functions seem most severely affected. Whether the use of hyperbaric oxygen (HBO) therapy alters the outcome of delayed-onset neurologic dysfunction due to CO poisoning remains controversial. Approximately one third of patients with smoke inhalation from domestic fires also have high blood cyanide levels.

CLINICAL

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• Underlying medical history: The presence of underlying lung disease, including asthma, makes a child more susceptible to airway irritation.
• Age at exposure
• • Children and adults are often exposed to smoke together.
  • The extent of disease can be notably different between children and adults, despite similar exposures.
  • Children have higher minute ventilation and smaller body size, which increase toxin exposure.
  • Children also have increased disorientation and delayed escape that may prolong exposure.
• Type of exposure
• • A history of patient exposure can help determine his or her risk for inhalation injury. The duration of exposure, the dose inhaled, and the actual toxins determine toxicity. Unfortunately, these details are often not known, although some information can be garnered from rescuers and other observers present at the scene.
  • 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.
  • Fires involving the combustion of cellulose, nylon, wool, silk, asphalt, and polyurethane increase the risk for hydrogen cyanide poisoning.
  • Damage varies with the chemical activity of the particular inhalants, their size, solubility, and the duration and concentration of exposure. Upper airway injuries tend to be caused by the more irritating, water-soluble, larger particles. Substances of smaller size and lower water solubility cause alveolar and parenchymal injury.
  • Gasoline self-extinguishes when oxygen concentrations in the surrounding gas fall below 15%. Other substances may continue to undergo thermal decomposition, further decreasing ambient oxygen tension.
• Thermal injury
  • Inhalation injuries occur without skin burns or other obvious external injury; hence, a high degree of suspicion must be maintained. A retrospective review of 4500 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.
• • Because of its vast heat capacitance, thermal injury is generally confined to the upper airway. Inhalation of steam is a notable exception, in which lower airway and pulmonary parenchymal thermal injury are common. Theoretically, continued combustion of inhaled particulate matter could possibly produce more distal airway injury.
  • Thermal injury to the mucosa produces burns and edema of the nose, mouth, pharynx, and larynx, much like the damage from burns. The loose tissues of the upper airway swell readily in response to injury. Fluid resuscitation and loss of colloid oncotic pressure can obstruct the airway.
  • 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.
• Simple carbon soot
• • This is not particularly toxic, although it may carry and deposit other toxins directly onto the airway surfaces, thereby increasing exposure.
  • Children frequently become disoriented 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
  • Pulmonary injury from smoke inhalation is characterized by both hyperinflation and atelectasis. Debris from cellular necrosis, inflammatory exudate, and shed epithelium combine with carbonaceous material to narrow airways that are already compromised by edema. Reflex bronchoconstriction further exacerbates the obstruction. Both inspiratory and expiratory resistance are increased, and the premature closure of small airways occurs, producing hyperinflation and air trapping. Surfactant production and activity are both impaired, leading to alveolar collapse and segmental atelectasis.
  • Low-pressure pulmonary edema plays an important role in the development of lung injury from smoke inhalation. Damage to the alveolar capillary membrane increases its permeability, and intravascular leakage into the pulmonary interstitium ensues. Eventually, increased lymphatic flow may be overwhelmed, resulting in alveolar edema. Alveoli fill with thick bloody fluid. Loss of compliance, further atelectasis, and increasing edema can result in severe ventilation-perfusion mismatch and hypoxia.
  • Pulmonary injury may also occur as a direct result of hypoxia. As with many pediatric illnesses and injuries, hypoxia itself may produce system dysfunction in many organs. The decrease in ambient oxygen tension that occurs during fires in closed spaces depends on the substances that are burned. Even small decrements in oxygen tension have a potentiating effect on inhaled asphyxiant gases such as CO and hydrogen cyanide, resulting in severe lactic acidosis and a high fatality rate.
• Carbon monoxide
• • CO is a colorless odorless gas produced by the incomplete combustion of carbon-containing compounds, such as wood, coal, and gasoline. It is a major component of the smoke produced in open fires. The combustion of wood, coal, gasoline, and other organic substances increases the risk of CO poisoning. CO is a major component of smoke produced in most open fires and must be considered in any person injured in a fire. Remember that significant CO exposure can occur in the absence of open flames with malfunctioning domestic equipment (eg, poorly ventilated space heaters, cooking gas) and exposure to automobile exhaust fumes either from a suicide attempt or accidentally from poor ventilation.
  • Significant toxicity occurs with the inhalation of asphyxiants, including CO, nitrogen, and methane. These asphyxiants cause injury by interrupting the delivery of oxygen to the tissues. Asphyxiants either displace oxygen from the air or interfere with tissue oxygen delivery by blocking the action of hemoglobin or cytochrome oxidase (eg, CO, cyanide).
• Cyanide
• • Hydrogen cyanide is an asphyxiant that is released during the incomplete combustion of products such as plastics and acrylics.
  • Cyanide has a characteristic almondlike 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.
  • At higher levels of exposure, obtundation, seizures, and apnea occur. Low levels of cyanide increase cardiac output. At higher levels, a wide variety of bradyarrhythmia and tachyarrhythmia occur.

Physical

Symptoms at clinical presentation range from mild to severe smoke inhalation with coexistent burns and toxic gas exposure. In most cases, the presentation of a person injured in a fire is obvious and usually witnesses and evidence of burns or smoke inhalation are present.

• Respiratory injury
• • Patients with respiratory injury present with many symptoms, ranging from minor eye irritation, cough, and uncomfortable breathing to acute respiratory failure. The full extent of respiratory tract injury may not be evident at initial presentation, although symptoms are usually present within 12-24 hours. Patients presenting with dyspnea, hemoptysis, cough, tachypnea, rales, rhonchi, wheezing, facial burns, carbonaceous sputum, pulmonary infiltration on radiography, and hypoxemia with or without acidosis should be closely observed because these findings increase the risk of progressive disease.
  • Burns on the face, soot marks, and singed eyebrows or facial hair are indicative of smoke inhalation. Inhalation injury can also occur without evidence of burns. Recognizing that upper airway swelling may take several hours to develop is imperative; thus, facial burns, hoarseness, stridor, upper airway injury with mucosal lesions identified on oral examination or bronchoscopy, and carbonaceous sputum are indications to promptly secure artificial airway access.
  • Symptoms of lower respiratory tract injury include tachypnea, dyspnea, cough, decreased breath sounds, wheezing, rales, rhonchi, and retractions. Cyanosis is an unreliable indicator of hypoxia because of the bright red color imparted to the skin when carboxyhemoglobin levels are elevated.
• Neurologic injury
• • This may take longer to appear than evidence of respiratory injury. Neurologic injury may be the result of hypoxia at the time of injury or may result from hypoxia secondary to pulmonary dysfunction. Fear, severe pain, and obtundation from inadequate perfusion may cloud the neurologic examination in the burned child. Serial examinations assessing the sensorium are extremely helpful in guiding the initial resuscitation and stabilization.
  • Patients exposed to asphyxiants, including CO and cyanide, present with hypoxic injury and subsequent central nervous system depression, lethargy, and obtundation. Hypoxia is caused by an asphyxiant and is usually evident upon presentation. Irritability, severe temporal headache, and generalized muscle weakness are also common findings.
  • The presence of coma following exposure to fire is nearly always indicative of CO poisoning and should be promptly treated with 100% oxygen. Suspect cyanide toxicity in the child whose sensorium remains clouded and who does not respond to oxygen therapy.
  • Red retinal veins resulting from elevated venous oxyhemoglobin saturation may be noted on funduscopic examination.
• Cardiovascular injury
• • Complex cardiovascular changes associated with surface burns may coexist with inhalation injury. Heart rate, capillary refill, warmth of unburned extremities, and blood pressure should be promptly evaluated at presentation and at frequent regular intervals during the initial stabilization.
  • Findings of acute ischemia on ECG in patients with young, otherwise healthy hearts are nearly always indicative of CO poisoning.
• Other injury
• • Pay careful attention to narrowed pulse pressure because this may indicate inadequate volume resuscitation. Hypotension is invariably a late finding of volume loss.
  • The respiratory, cardiovascular, and neurologic organ systems are commonly injured because of their direct exposure and exquisite sensitivity to hypoxia respectively. However, renal tubular acidosis, hepatitis, and bone marrow insufficiency are not uncommon, particularly when hypoxic injury is either severe or prolonged.
  • Organ system dysfunction is also common as a result of the complex hemodynamic and inflammatory reactions associated with significant burns. In the obtunded patient, assume coexistent spine injury. CO poisoning may produce cutaneous erythema, blisters, and edema that can easily be mistaken for thermal burns.

Causes

• Most often, inhalation injury results from direct damage to exposed epithelial surfaces and often causes conjunctivitis, corneal edema, rhinitis, pharyngitis, laryngitis, tracheitis, bronchitis, bronchiolitis, and alveolitis. Systemic absorption of toxins also occurs. Ascertaining if respiratory insufficiency is due to direct pulmonary injury or is the result of the extensive metabolic, hemodynamic, and subsequent infectious complications of surface burns is difficult.
• Inhalants are classified as irritant, asphyxiant, or systemic toxins. Irritants cause extensive cell injury within the respiratory tract. Asphyxiants interrupt the delivery of oxygen to the tissues. Systemic toxins are absorbed through the respiratory tract and go on to damage other organ systems. Toxic gases are liberated during the combustion of a variety of substances, as listed in Table 1.

  Table 1. Inhalants

  Type	Inhalant	Source	Injury/Mechanism
  Irritant gases	Ammonia	Fertilizer, refrigerant, manufacturing of dyes, plastics, nylon	Upper airway epithelial damage
  	Chlorine	Bleaching agent, sewage and water disinfectant, cleansing products	Lower airway epithelial damage
  	Sulfur dioxide	Combustion of coal, oil, cooking fuel, smelting	Upper airway epithelial damage
  	Nitrogen dioxide	Combustion of diesel, welding, manufacturing of dyes, lacquers, wall paper	Terminal airway epithelial damage
  Asphyxiants	Carbon monoxide*	Combustion of weeds, coal, gas, heaters	Competes for oxygen sites on hemoglobin, myoglobin, heme-containing intracellular proteins
  	Hydrogen cyanide†	Burning of polyurethane, nitrocellulose (silk, nylon, wool)	Tissue asphyxiation by inhibiting intracellular cytochrome oxidase activity, inhibits ATP production, leads to cellular anoxia
  	Hydrogen sulfide‡	Sewage treatment facility, volcanic gases, coal mines, natural hot springs	Similar to cyanide, tissue asphyxiant by inhibition of cytochrome oxidase, leads to disruption of electron transport chain, results in anaerobic metabolism
  Systemic toxins	Hydrocarbons	Inhalant abuse (toluene, benzene, Freon); aerosols; glue; gasoline; nail polish remover; typewriter correction fluid; ingestion of petroleum solvents, kerosene, liquid polishes	CNS narcosis, anesthetic stats, diffuse gastrointestinal symptoms, peripheral neuropathy with weakness, coma, sudden death, chemical pneumonitis, CNS abnormalities, gastrointestinal irritation, cardiomyopathy, renal toxicity
  	Organophosphates	Insecticides, nerve gases	Blocks acetylcholinesterase, cholinergic crisis with increased acetylcholine
  	Metal fumes	Metal oxides of zinc, copper, magnesium, jewelry making	Flu-like symptoms, fever, myalgia, weakness

  * Major component of smoke
  † Smells like almonds, component of smoke from fires
  ‡ Smells like rotten eggs
  (Adapted from Rorison, 1992; Weiss, 1994)

WORKUP

Section 4 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Pulse oximetry
• • Cutaneous pulse oximetry uses a 2-wavelength technique of light refractance to measure hemoglobin saturation that is falsely elevated by CO-bound hemoglobin. Obtain direct measures of carboxyhemoglobin and oxyhemoglobin.
  • To monitor oxygen saturation, recognizing that cutaneous pulse oximetry is falsely elevated by CO is imperative. One must not rely on pulse oximetry until the carboxyhemoglobin level has reached the reference range.
  • Cooximetry (arterial blood) uses a 4-wavelength technique of light refractance to accurately measure carboxyhemoglobin and oxyhemoglobin, in addition to deoxyhemoglobin and methemoglobin. The percent oxyhemoglobin measured by cooximetry is an accurate measure of the arterial oxygen saturation.
• Arterial blood gas
• • Arterial oxygen tension (PaO2) also does not accurately reflect the degree of CO poisoning or cellular hypoxia. The PaO₂ reflects the oxygen dissolved in blood that is not altered by the hemoglobin-bound CO. Because dissolved oxygen makes up only a small fraction of arterial oxygen content, a PaO₂ 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 CO blocks the delivery of oxygen to the tissues. With most blood gas machines, the oxygen saturation is calculated, based on the PaO₂. Thus, such a reading does not give an accurate determination of oxygen saturation, which must come from cooximatry.
  • Arterial blood gas measurements are nonetheless useful to assess the adequacy of pulmonary gas exchange. While the presence of a PaO₂ that is within the reference range may not exclude significant tissue hypoxia due to the effects of CO, the presence of a low PaO₂ ( <60 mm Hg in room air) or hypercarbia (PaCO₂ 55 mm Hg) are indicative of significant respiratory insufficiency. Metabolic acidosis suggests inadequate oxygen delivery to the tissues.
  • 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 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 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.

    PaO₂ = (FiO₂)(PB – PH₂O) – (PaCO₂/RQ)

    • PaO₂ = Partial pressure of oxygen in the alveolus
    • FiO₂ = Fraction of inspired oxygen
    • PB = Barometric pressure
    • PH₂O = Partial pressure of water vapor (47 mm Hg at body temperature, ambient pressure)
    • PaCO₂ = Alveolar (arterial) carbon dioxide pressure
    • RQ = Respiratory quotient (estimated at 0.8)
• Carboxyhemoglobin level
• • Provide supplemental oxygen therapy to all patients with suspected CO intoxication. Smokers may have baseline levels up to 5-10% and may experience more significant CO poisoning for the same level of exposure as nonsmokers.
  • Blood carboxyhemoglobin levels, however, may underestimate the degree of CO intoxication because of oxygen administration before arrival to the hospital. The use of nomograms to extrapolate levels to the time of rescue has been shown to have greater prognostic value. Symptoms vary with peak carboxyhemoglobin levels, but correlation between carboxyhemoglobin levels and eventual neurologic outcome is poor (see Table 2).

    Table 2. Patient Symptoms in Relation to Levels of Carboxyhemoglobin in the Blood

    Carboxyhemoglobin Level (% of Total)	Patient Symptoms
    0-10	Usually none
    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
    >70	Coma, rapidly fatal

    (From Rorison, 1992)
• Cyanide level
• • Levels correlate closely with the level of exposure and toxicity, but they may not be readily available.
  • Many hospitals send out tests for cyanide levels; therefore, laboratory confirmation may take several days to a week. Persistent neurologic dysfunction unresponsive to use of supplemental oxygen, cardiac dysfunction, and severe lactic acidosis, particularly in the presence of high mixed venous oxygen saturation, are indicative of cyanide intoxication. In a setting consistent with potential cyanide exposure, institute specific empiric therapy while waiting for laboratory confirmation of the diagnosis.
• Electrolytes
• • Obtain tests at regular and frequent intervals to monitor for electrolyte abnormalities that result from large-volume fluid resuscitation.
  • Use results to adjust both fluid and electrolyte replacement.
• Complete blood count, type, and cross
• • Hemoconcentration resulting from fluid losses is common immediately following injury.
  • Adequate restoration of intravascular volume results in a progressive fall in hematocrit.
  • Severe anemia may require blood replacement, particularly in the presence of significant hypoxia or hemodynamic instability.
  • A baseline white blood cell count can also be used for comparison when concerns arise about infection.

Imaging Studies

• C-spine radiography: Test for neck injury in all unconscious patients and in those in whom a potential mechanism of injury cannot be excluded (eg, jumped from window to escape fire, fell down stairs).
• Chest radiography
• • Roentgenographic abnormalities are frequently delayed and may not manifest on the initial chest radiograph.
  • Radiographic evidence of pulmonary injury typically appears 24-36 hours after the inhalation. Obtain a chest radiograph at the baseline examination for subsequent comparison in cases of significant injury. Radiographic studies are also useful to establish correct placement of the endotracheal tube and central venous catheters.

Other Tests

• Direct laryngoscopy and fiberoptic bronchoscopy
• • Both have diagnostic and therapeutic utility. Visualization of erythema, edema, ulceration, and soot deposition make bronchoscopy useful in evaluating the extent of injury to the tracheobronchial tree, although severe vasoconstriction from hypovolemia may mask significant injury.
  • Fiberoptic bronchoscopy can also be used to facilitate endotracheal tube placement, even in the technically difficult airway.
  • Bronchoscopy is more sensitive and accurate than clinical examination alone in diagnosing inhalation injury and is, therefore, particularly useful in cases where the decision to perform endotracheal intubation is unclear.
  • Serial bronchoscopy can help remove debris and necrotic cells in cases with aggressive pulmonary toilet or when suctioning and positive pressure ventilation are insufficient
  • Because of their small size, a child's airway can only accommodate a relatively small diameter bronchoscope. Extremely small diameter fiberoptic bronchoscopes with a suction port (capable of entering an endotracheal tube sized for a small toddler or infant) are only recently available and whether this will limit the ability to remove heavy particulate matter is unclear.
• Radionucleotide scintigraphy
• • Delayed or inhomogeneous clearance of xenon Xe 133 can be used to detect small airway parenchymal injury but adds little to the clinical management and it is not known to have any particular therapeutic advantage.
  • Likewise, increased clearance of aerosolized 99mTcDTPA (technetium Tc 99m–labeled diethylenetriaminepentaacetate) is a sensitive indicator of injury to the alveolar capillary membrane; however, its clinical utility is not yet established.
• Pulmonary function tests
• • With an inhalation injury, a decrease in pulmonary compliance, vital capacity, and functional residual capacity occurs. Airway obstruction causes a decrease in forced expiratory volume in one second (FEV₁) and peak flow. Although this helps determine lower airway disease and injury, similar to radionucleotide scintigraphy, it has little clinical utility in the initial stages of treatment.
  • In patients with cutaneous burns, the reduction in vital capacity and FEV₁ correlates closely with the extent of surface burns. Full resolution of pulmonary function test result abnormalities may take several months.
  • Some agents, particularly chlorine gas, may result in reactive airways syndrome, with subsequent development of airflow obstruction.

TREATMENT

Section 5 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

• Decision to admit
• • Evaluate patients presenting with inhalation injury for the extent of disease and degree of hypoxemia. The child who is at low risk for injury with no clinical symptoms can usually be observed for 4-12 hours and discharged with close follow-up and instructions to return if symptomatic.
  • Observe the high-risk child with only minimal symptoms for 4-12 hours and, if any symptoms or concerns arise, admit to the hospital for further observation and oxygenation monitoring.
  • The symptomatic child with any signs of airway obstruction, bronchospasm, respiratory distress, or concurrent burns is admitted to the hospital for appropriate monitoring because edema and obstruction typically worsen over the next 24-48 hours.
• Airways
• • Ensure patency and stability. Check for exposure to heat and thermal injury to the nose, mouth, face, and singed hair. Consider smoke involvement if soot is on the face and in sputum, although smoke inhalation is possible without evidence of soot.
  • Direct laryngoscopy and fiberoptic endoscopy are useful to evaluate the extent of airway edema and burns, although vasoconstriction from hypovolemia may result in underappreciation of the severity of injury. When upper airway injury is suspected, elective intubation should be considered because progression of edema over the next 24-48 hours may make later intubation difficult if not impossible.
• Breathing
• • Check for upper airway compromise, difficulty breathing, stridor, cough, retractions, and bilateral breath sounds. Administer 100% oxygen because of the likelihood of CO inhalation in fires.
  • The direct effects of inhalation injury are usually evident within 24 hours, although late pulmonary dysfunction may result from complex hemodynamic and infectious complications associated with surface burns.
• Circulation
• • Patients whose injury involves cutaneous burns have ongoing circulatory derangements. Fluid loss through burned areas from intense inflammation with vasodilatation and capillary leak or from the subsequent infectious complications necessitates large fluid volume resuscitation. Even minor errors in estimation of body surface area; burned surface area; and fluid, electrolyte, and protein requirements can produce profound hemodynamic and respiratory embarrassment.
  • Large-bore intravenous catheter access may be needed to facilitate fluid resuscitation. Frequent evaluation of heart rate, perfusion, and blood pressure are needed to determine stability and guide therapy.
• Neurology
• • Patient responsiveness helps determine his/her ability to protect the airway and is also an excellent indicator of adequacy of resuscitation success.
  • The neurologic examination is frequently clouded by hypoxic and toxic neurologic injury and the necessary use of potent analgesics.
• Burns
• • Check all body areas for additional injury and burns.
  • Wash unburned skin to remove any remaining toxic residues.
• Medications
• • Corticosteroids are attractive for suppressing inflammation and reducing edema. Controlled studies assessing their effects on various forms of chemical pneumonitis are disappointing and no direct data support their use in smoke inhalation. Because of the increased risk of infection and delayed wound healing, prolonged use of steroids is discouraged. Reports show increased incidence of pulmonary infection and mortality in steroid-treated patients. 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.
  • Patients with pulmonary damage from inhalation injury are at increased risk for secondary bacterial infection. The most common organisms are Staphylococcus aureus and Pseudomonas aeruginosa. Direct parenteral coverage with antibiotics to cover these bacteria if infection is suspected. 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, when infection is most likely to occur. Prophylactic antibiotics not only are not prophylactic, 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 radiographic abnormalities.
  • Although pulmonary damage includes inactivation of surfactant, the effectiveness of artificial surfactant administration has not been proven.
  • Cyanide is detoxified to thiocyanate (SCN-), predominately by rhodanese in the liver. Thiocyanate is excreted by the kidneys in the presence of normal renal function. Rhodanese is located around the mitochondria within the cells, placing it in close proximity to the major site of cyanide toxicity, the cytochrome oxidases. Sulfur is required for this enzymatic process to occur. Oxygen and sodium thiosulfate are the most widely accepted cyanide antidotes. Less accepted cyanide antidotes include hydroxocobalamin and dicobalt ethylenediaminetetraacetic acid (EDTA). The mechanism of action of oxygen as a cyanide antidote is unclear but it potentiates the effect of other antidotes. When used in the setting of smoke inhalation, it is also therapeutic for CO poisoning. Thus, high concentrations of oxygen should be delivered promptly.
  • Sodium thiosulfate increases the sulfur pool and dramatically favors conversion of cyanide to thiocyanate. In the presence of renal failure, thiocyanate is not eliminated and hemodialysis should be offered. Nitrites convert hemoglobin to methemoglobin. Cyanide becomes bound to methemoglobin because of its very high affinity for the ferric iron of methemoglobin. The induction of methemoglobinemia in the setting of smoke inhalation should be undertaken with caution because coexisting carboxyhemoglobinemia can seriously decrease oxygen carrying capacity and is potentially dangerous. Antidote kits (Lily Cyanide Antidote Kit) that include amyl nitrite, sodium nitrite, and sodium thiosulfate are commercially available.
  • Oxygen is used in cases with significant inhalation injury. See Medication for specific instructions.
  • Bronchodilators are used in those patients with bronchoconstriction. Intravenous bronchodilators may be needed in severe cases. See Medication for specific instructions.

Surgical Care

A team experienced in caring for burned children should evaluate children with significant cutaneous burns.

Consultations

• A pediatric pulmonologist, surgeon, or otolaryngologist should be consulted to perform direct laryngoscopy or bronchoscopy if needed.
• A pediatric pulmonologist is needed for children suspected of having residual pulmonary disease.

Diet

• Do not feed children by mouth until significant respiratory or hemodynamic compromise clearly does not require tracheal intubation.
• Even with extensive burns, most patients can tolerate enteral feedings at the end of the first 24 hours. Begin enteral feedings as soon as possible. As enteral intake increases, decrease intravenous fluids accordingly. Patients may demonstrate marked hypermetabolism. Therefore, providing adequate nutritional support is important.

Activity

Activity is performed as tolerated and as dictated by the extent of disease.

MEDICATION

Section 6 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Drug Category: Medical gases

Oxygen is used for any suspected significant inhalation injury. Treat with high concentrations of humidified oxygen en route to the hospital.

Drug Name	Hyperbaric oxygen therapy (HBO)
Description	This therapy also displaces CO from intracellular stores and may improve mitochondrial function. HBO requires special facilities that are not available at all centers, resulting in a delay in treatment while the patient is transported to facility with HBO. Hyperbaric therapy should be considered in those patients who have high carboxyhemoglobin levels >40%, who are unconsciousness, have other neurologic findings, or have severe metabolic acidosis (ph <7.1). Benefit of treating patients 12 h after CO exposure remains unproven.
Pediatric Dose	The half-life of carboxyhemoglobin can be further reduced to 15-30 min in 2-3 atm of HBO
Contraindications	None reported
Interactions	None reported
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	The potential benefits of preventing long-term neurologic sequelae from the secondary syndrome of CO poisoning should be weighed against the lack of patient access while undergoing HBO therapy; the anticipated use of hyperbaric therapy should never preclude the use of high concentrations of supplemental O2; complications include middle ear and sinus occlusion, air embolism, and seizures

Drug Category: Bronchodilators

These agents relieve reversible bronchospasm by relaxing smooth muscles of the bronchi. Increased resistance from airway edema and reflex bronchoconstriction from irritation of airway receptors contribute to airway obstruction.

Drug Name	Racemic epinephrine 2.25% (MicroNefrin, AsthmaNefrin, Racepinephrine)
Description	Alleviates airway edema and reflex bronchospasm. Although it has not been directly studied, inhaled racemic epinephrine can theoretically provide relief from both airway edema and reflex bronchospasm in this setting.
Adult Dose	Nebulizer: 0.25-0.5 mL (diluted in 3 mL of 0.9% NaCl) inhaled via nebulization q4-6h prn
Pediatric Dose	Administer as in adults
Contraindications	Documented hypersensitivity; cardiac arrhythmias; angle-closure glaucoma
Interactions	Increases toxicity of beta- and alpha-blocking agents and that of halogenated inhalational anesthetics
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency

Drug Name	Terbutaline (Brethine)
Description	Used for severe bronchoconstriction, especially in patients with underlying reactive airways disease. Acts directly on beta2-receptors to relax bronchial smooth muscle, relieving bronchospasm and reducing airway resistance.
Adult Dose	Loading dose: 0.25 mg IV Maintenance dose: 0.1-0.4 mcg/kg/min IV; titrate to effect
Pediatric Dose	Loading dose: 2-10 mcg/kg IV Maintenance dose: 0.08-0.4 mcg/kg/min IV; titrate to effect
Contraindications	Documented hypersensitivity; tachycardia resulting from cardiac arrhythmias
Interactions	Concomitant use with beta-blockers may inhibit bronchodilating, cardiac, and vasodilating effects of beta agonists; concomitant administration of MAOIs with beta sympathomimetics may result in severe hypertension, headache, and hyperpyrexia, which may result in a hypertensive crisis; MAOIs may potentiate activity of beta-adrenergic agonists on the vascular system; concurrent administration of oxytocic drugs such as ergonovine with terbutaline may result in severe hypotension
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Through intracellular shunting, terbutaline may decrease serum potassium levels, which can produce adverse cardiovascular effects; decrease is usually transient and may not require supplementation; paradoxical bronchoconstriction may occur with excessive use

Drug Name	Epinephrine (Adrenaline, EpiPen)
Description	Used for severe bronchoconstriction, especially in patients with underlying reactive airways disease. Alpha-agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta-agonist effects of epinephrine include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.
Adult Dose	0.1-0.5 mg (1:1000 concentration [1 mg/mL]) IM/SC q10-15min to 4 h; alternatively, 0.1-0.25 mg IV; single dose not to exceed 1 mg
Pediatric Dose	0.01 mg/kg/dose (0.01 mL/kg of the 1:1000 concentration [1 mg/mL]); not to exceed 0.5 mg/dose
Contraindications	Documented hypersensitivity; cardiac arrhythmias or angle-closure glaucoma; local anesthesia in areas such as fingers or toes because vasoconstriction may produce sloughing of tissue; use during labor (may delay second stage of labor)
Interactions	Increases toxicity of beta- and alpha-blocking agents and that of halogenated inhalational anesthetics
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in elderly persons and patients with prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias

FOLLOW-UP

Section 7 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Pulmonary toilet
• • As with many diseases, the utility of chest physiotherapy is widely accepted but remains unproven in controlled trials. The use of percutaneous cupping and postural drainage seem reasonable to clear airways of cellular debris and soot, thereby preventing atelectasis and obstruction. Obviously, care must be taken in attempting this in the presence of significant chest wall burns.
  • Encourage extubated patients to cough and deep breathe. In intubated patients, use gentle suctioning to remove mucus, debris, and sloughed epithelium. Fiberoptic bronchoscopy may be helpful in removing the debris and in facilitating pulmonary toilet.
• Mechanical ventilation with positive end expiratory pressure
• • With declining lung function, oxygenation, and ventilation, mechanical ventilation with positive end expiratory pressure (PEEP) may be necessary.
  • PEEP may assist in opening obstructed closed alveoli and help ventilation in those patients with poor compliance by increasing functional residual capacity. Ideally, PEEP stents alveoli open, preventing the atelectasis and alveolar flooding that can result from surfactant dysfunction, increasing interstitial fluid, and third-spacing.
• Tracheostomy
• • The timing of tracheostomy continues to be controversial. Certainly, in children in whom endotracheal intubation is not possible because of severe airway edema or burns, tracheostomy can be lifesaving. With early recognition of upper airway injury, this should be a rare occurrence.
  • Tracheostomy, especially through burned tissue, has an increased complication rate and risk of sepsis when compared to endotracheal intubation. Thus, most patients can be effectively managed with endotracheal intubation through the mouth or nose.
  • In patients expected to have a long period of convalescence because of severe neurologic or pulmonary injury, tracheostomy may be desirable for patient comfort, and it is easy to maintain.

Further Outpatient Care

• After recovery from the initial injury, closely monitor those patients with residual airway obstruction and pulmonary damage. Refer patients with ongoing symptoms to a pediatric pulmonologist.

Deterrence/Prevention

• Primary prevention with functioning fire and smoke alarms and family education for fire hazards is critical to help avoid fire injuries. View prevention as the primary means to avoid inhalation injury and the use of smoke and CO detectors should be encouraged community-wide.

Complications

• Severe pulmonary injury, edema, and the inability to oxygenate or ventilate can result in death. Concurrent CO poisoning and inhalation of other products of combustion can cause hypoxemia, end organ injury, and morbidity.

Prognosis

• Most inhalation injuries are self-limited and resolve within 48-72 hours. The severity of direct pulmonary parenchymal injury depends on the extent of exposure and the type of inhaled toxins produced during combustion. Most patients do not manifest spirometry changes. Rare long-term sequelae include tracheal stenosis, bronchiectasis, interstitial fibrosis, and bronchiolitis obliterans.

Patient Education

• Programs aimed at educating young children about the dangers of playing with lighters and matches and programs teaching families how to safely escape from burning buildings should be used to further limit the number of children experiencing inhalation and burn injury. Anticipatory guidance during well child visits should include fire safety instructions.
• For excellent patient education resources, visit eMedicine's Lung and Airway Center, Procedures Center and Poisoning Center. Also, see eMedicine's patient education articles Smoke Inhalation, Bronchoscopy and Carbon Monoxide Poisoning.

MISCELLANEOUS

Section 8 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Special Concerns

• Concomitant problems
• • Remember that significant inhalation injury can occur in the absence of cutaneous burns. The need to consider concomitant CO or cyanide poisoning remains paramount.
  • Inquire about exposure to industrial fumes that can generate specific toxins. Carefully investigate to identify coexistent injuries, including cutaneous burns and cervical spine injury in all obtunded patients and particularly in those who may have fallen or jumped. Some industrial toxins, particularly chlorine gas, may result in delayed development of airflow obstruction. This should be kept in mind if patients develop cough or wheeze 1-3 months after exposure.
• Suicide
• • Intentional inhalation of CO or cyanide gas as a suicide attempt may be more subtle. Global hypoxic injury may preclude the examiner from obtaining a history from the patient.
  • Careful interviews with friends, coworkers, family members, and rescuers at the scene may add insight to the possible mechanism of injury in the comatose child

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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Article Last Updated: Jul 24, 2006