eMedicine Specialties > Pediatrics: General Medicine > Pulmonology
Inhalation Injury
Updated: Jun 6, 2008
Introduction
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 a child with burns and a coexistent inhalation injury requires a cohesive team of pediatric intensive care physicians, nurses, and burn specialists. Although children with burns 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 use 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 die from isolated pulmonary disease. However, the presence of multiorgan dysfunction, a common sequela of hypoxia, substantially raises morbidity and mortality.
Because CO does not directly injure the lung, 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-fold increased affinity for hemoglobin than oxygen but 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 use. Affected cells convert to anaerobic metabolism, and lactic acidosis ensues. The organs most sensitive to cellular hypoxia are the CNS and the heart. The CNS 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 significantly increases the morbidity and mortality of burns. 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.
Residual reactive airway disease, bronchiectasis, bronchiolitis obliterans, and interstitial fibrosis have been reported. However, the cause-and-effect relationships between toxic exposure and pulmonary sequelae remain controversial and unproven.
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 breath even after mild inhalation injury, 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 who arrive alive to the emergency department 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
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 the 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 4,451 children with thermal injuries over 10 years demonstrated that inhalation injury was often not recognized, manifested late, and usually had significant consequences, including parenchymal injury and secondary pneumonia.1
- 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 upon 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 CNS depression, lethargy, and obtundation. Hypoxia is caused by an asphyxiant and is usually evident upon presentation. Irritability, severe temporal headache, and generalized muscle weakness are also common findings.
- 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 below. Inhalants2,3
Open table in new window
[ CLOSE WINDOW ]Table
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 GI symptoms, peripheral neuropathy with weakness, coma, sudden death, chemical pneumonitis, CNS abnormalities, GI 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 Flulike symptoms, fever, myalgia, weakness * Major component of smokeType 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 GI symptoms, peripheral neuropathy with weakness, coma, sudden death, chemical pneumonitis, CNS abnormalities, GI 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 Flulike symptoms, fever, myalgia, weakness
† Smells like almonds, component of smoke from fires
‡ Smells like rotten eggs
More on Inhalation Injury |
 Overview: Inhalation Injury |
| Differential Diagnoses & Workup: Inhalation Injury |
| Treatment & Medication: Inhalation Injury |
| Follow-up: Inhalation Injury |
| References |
| Next Page » |
References
Whitelock-Jones L, Bass DH, Millar AJ, Rode H. Inhalation burns in children. Pediatr Surg Int. 1999;15(1):50-5. [Medline].
Rorison DG, McPherson SJ. Acute toxic inhalations. Emerg Med Clin North Am. May 1992;10(2):409-35. [Medline].
Weiss SM, Lakshminarayan S. Acute inhalation injury. Clin Chest Med. Mar 1994;15(1):103-16. [Medline].
Agee RN, Long JM 3rd, Hunt JL, Petroff PA, Lull RJ, Mason AD Jr, et al. Use of 133xenon in early diagnosis of inhalation injury. J Trauma. Mar 1976;16(3):218-24. [Medline].
Oremus M, Hanson MD, Whitlock R, Young E, Archer C, Dal Cin A, et al. A systematic review of heparin to treat burn injury. J Burn Care Res. Nov-Dec 2007;28(6):794-804. [Medline].
Jones WG, Madden M, Finkelstein J, Yurt RW, Goodwin CW. Tracheostomies in burn patients. Ann Surg. Apr 1989;209(4):471-4. [Medline]. [Full Text].
Bartlett RH. Critical Care Physiology. Little, Brown and Company: Boston, Mass; 1996:68-69.
Blanc PD, Galbo M, Hiatt P, Olson KR, Balmes JR. Symptoms, lung function, and airway responsiveness following irritant inhalation. Chest. Jun 1993;103(6):1699-705. [Medline].
Chou KJ, Fisher JL, Silver EJ. Characteristics and outcome of children with carbon monoxide poisoning with and without smoke exposure referred for hyperbaric oxygen therapy. Pediatr Emerg Care. Jun 2000;16(3):151-5. [Medline].
Clark CJ, Campbell D, Reid WH. Blood carboxyhaemoglobin and cyanide levels in fire survivors. Lancet. Jun 20 1981;1(8234):1332-5. [Medline].
Cohen MA, Guzzardi LJ. Inhalation of products of combustion. Ann Emerg Med. Oct 1983;12(10):628-32. [Medline].
Demarest GB, Hudson LD, Altman LC. Impaired alveolar macrophage chemotaxis in patients with acute smoke inhalation. Am Rev Respir Dis. Feb 1979;119(2):279-86. [Medline].
DiVincenti FC, Pruitt BA Jr, Reckler JM. Inhalation injuries. J Trauma. Feb 1971;11(2):109-17. [Medline].
Haponik EF, Crapo RO, Herndon DN, Traber DL, Hudson L, Moylan J. Smoke inhalation. Am Rev Respir Dis. Oct 1988;138(4):1060-3. [Medline].
Heimbach DM, Waeckerle JF. Inhalation injuries. Ann Emerg Med. Dec 1988;17(12):1316-20. [Medline].
Jackson MP, Philp B, Murdoch LJ, Powell BW. High frequency oscillatory ventilation successfully used to treat a severe paediatric inhalation injury. Burns. Aug 2002;28(5):509-11. [Medline].
Juurlink DN, Buckley NA, Stanbrook MB, Isbister GK, Bennett M, McGuigan MA. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev. Jan 25 2005;CD002041. [Medline].
Kipen HM, Rab S, Mohr S. Incidence of persistent symptoms and morbidity after inhalation exposure. American Review of Respiratory Disease. 1993;147:A113.
Madnani DD, Steele NP, de Vries E. Factors that predict the need for intubation in patients with smoke inhalation injury. Ear Nose Throat J. Apr 2006;85(4):278-80. [Medline].
Moritz AR, Henriques FC, McLean R. The effects of inhaled heat on the air passages and lungs: an experimental investigation. American Journal of Pathology. 1945;21:311-325.
Peterson JE, Stewart RD. Absorption and elimination of carbon monoxide by inactive young men. Arch Environ Health. Aug 1970;21(2):165-71. [Medline].
Pruitt BA Jr, Cioffi WG, Shimazu T, Ikeuchi H, Mason AD Jr. Evaluation and management of patients with inhalation injury. J Trauma. Dec 1990;30(12 Suppl):S63-8. [Medline].
Pruitt BA Jr, Erickson DR, Morris A. Progressive pulmonary insufficiency and other pulmonary complications of thermal injury. J Trauma. May 1975;15(5):369-79. [Medline].
Rossignol AM, Boyle CM, Locke JA, Burke JF. Hospitalized burn injuries in Massachusetts: an assessment of incidence and product involvement. Am J Public Health. Nov 1986;76(11):1341-3. [Medline].
Ruddy RM. Smoke inhalation injury. Pediatr Clin North Am. Apr 1994;41(2):317-36. [Medline].
Stone JP, Hazlett RN, Johnson JE. The transport of hydrogen chloride by soot from burning polyvinyl chloride. J of Fire Flammability. 1973;4:42.
Thom SR, Keim LW. Carbon monoxide poisoning: a review epidemiology, pathophysiology, clinical findings, and treatment options including hyperbaric oxygen therapy. J Toxicol Clin Toxicol. 1989;27(3):141-56. [Medline].
Vogel SN, Sultan TR, Ten Eyck RP. Cyanide poisoning. Clin Toxicol. Mar 1981;18(3):367-83. [Medline].
Weaver LK, Hopkins RO, Chan KJ, Churchill S, Elliott CG, Clemmer TP, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. Oct 3 2002;347(14):1057-67. [Medline].
Whitener DR, Whitener LM, Robertson KJ, Baxter CR, Pierce AK. Pulmonary function measurements in patients with thermal injury and smoke inhalation. Am Rev Respir Dis. Nov 1980;122(5):731-9. [Medline].
Witten ML, Quan SF, Sobonya RE, Lemen RJ. New developments in the pathogenesis of smoke inhalation-induced pulmonary edema. West J Med. Jan 1988;148(1):33-6. [Medline]. [Full Text].
Wright MJ, Murphy JT. Smoke inhalation enhances early alveolar leukocyte responsiveness to endotoxin. J Trauma. Jul 2005;59(1):64-70. [Medline].
Zikria BA, Weston GC, Chodoff M, Ferrer JM. Smoke and carbon monoxide poisoning in fire victims. J Trauma. Aug 1972;12(8):641-5. [Medline].
Further Reading
Keywords
inhalation injury, smoke inhalation, smoke, carbon monoxide, CO, hydrogen cyanide, reflex bronchoconstriction, hydrocarbon inhalation, hypoxemia, bacterial pneumonia, airway obstruction, residual reactive airway disease, bronchiectasis, bronchiolitis obliterans, interstitial fibrosis, asthma, respiratory distress, obtundation, hyperinflation, atelectasis, air trapping, lung injury, alveolar edema, ventilation-perfusion mismatch, hypoxia, lactic acidosis, hypotension, renal tubular acidosis, hepatitis, bone marrow insufficiency, thermal burns, conjunctivitis, corneal edema, rhinitis, pharyngitis, laryngitis, tracheitis, bronchitis, alveolitis, respiratory insufficiency
