Smoke Inhalation Injury Treatment & Management
- Author: Keith A Lafferty, MD; Chief Editor: Joe Alcock, MD, MS more...
Beware that patients may appear asymptomatic on arrival but may develop significant signs and symptoms as long as 36 hours after exposure, especially in fires, which produce small particles with low water solubility. Be aware of pertinent historical risk factors when treating patients with potential smoke inhalation injury. These include closed-space fires, carbonaceous sputum, elevated carbon monoxide (CO) levels, and central facial burns.
Acute respiratory distress usually responds very well to aggressive initial management. Normal laboratory values and imaging studies, coupled with clinical improvement, can give the health care provider a false sense of security. The patient then may be discharged, only to deteriorate as delayed pulmonary edema ensues. Any patient with significant exposure to toxic smokes should be observed for 24-48 hours and imaged with serial chest radiographs. Difficulty arises in defining a significant exposure, since the clinical response is so varied.
Provide intravenous (IV) access, cardiac monitoring, and supplemental oxygen in the setting of hypoxia. A small subset of patients manifests bronchospasm and may benefit from the use of bronchodilators, although this is not well documented. This is especially true of patients with underlying chronic obstructive pulmonary disease (COPD) or asthma.
Treatment of inhalation injuries caused from toxic smokes is based on clinical presentation and involves primarily supportive care directed at the cardiopulmonary system. In some cases (eg, cyanide [CN] poisoning, methemoglobinemia), specific antidotes are available. Subcutaneous epinephrine has been used in zinc oxide (HC) exposures.
Corticosteroids are attractive for suppressing inflammation and reducing edema, but no direct data support their use in smoke inhalation. Because of the increased risk of pulmonary infection and delayed wound healing, prolonged use of steroids is discouraged. However, consider a brief course of steroids in those patients with otherwise unresponsive severe lower airway obstruction. In addition, patients receiving steroids prior to injury who may experience adrenal insufficiency should receive stress doses of steroids.
Although controlled studies assessing the effects of steroids on various forms of chemical pneumonitis are disappointing, steroids have been suggested as having some value in exposure to the following:
Oxides of nitrogen (NOx)
Zinc oxide (HC)
Red phosphorus (RP)
Sulfur trioxide (FS)
Titanium tetrachloride (FM)
Polytetrafluoroethylene (PTFE; Teflon)
In a case series by Huang et al, 25% of patients presented after HC exposure with acute lung injury requiring ventilatory support. All of these patients survived with glucocorticoids, antibiotics and lung-protective ventilatory management. However, there was no control group, so a causal link could not be made between survival and steroid treatment.[3, 45]
Smoke inhalation injuries predispose the airways to infection because of cellular injury, reduction of mucociliary clearance, and poor macrophage function. Acute bacterial colonization and invasion peaks at 2-3 days after smoke inhalation. Prophylactic antibiotics should not be used, as they are not only ineffective but increase the risk of emergence of resistant organisms.
Discerning secondary infection from the effects of inhalation injury can be very difficult because both may produce fever, elevated white blood cell counts, and abnormal radiography findings. Antimicrobial therapy should be reserved for patients with definitive microbiologic evidence of infection that is not responding to aggressive support therapy or when clinical deterioration occurs in the first 72 hours.
The most common organisms in secondary pneumonia after smoke inhalation injury are Staphylococcus aureus and Pseudomonas aeruginosa. Direct parenteral coverage with antibiotics to cover these bacteria if infection is suspected.
As always, prehospital care providers must do everything in their power to remove the patient from ongoing exposure without becoming casualties themselves. Although emergency department (ED) care is mostly supportive, prompt delivery to the ED should be a priority.
Secure the airway as needed, deliver high-flow oxygen by mask, and obtain IV access. Cardiac monitoring also is important for any patient with respiratory distress. Beta-agonists such as albuterol may be given as a nebulized treatment to those who demonstrate signs of bronchoconstriction.
If respiratory failure is present, the patient should have assisted ventilation and/or endotracheal intubation. Perform cricothyrotomy if airway obstruction is present or impending and an airway cannot be secured orally.
Obtain a CO level at the scene if possible. In a consecutive case series of 18 patients, cardiac arrest complicating CO toxicity was uniformly fatal, despite administration of hyperbaric oxygen (HBO) therapy after the initial resuscitation. The prognosis of this condition should be considered when making triage decisions for these patients.
Emergency Department Care
Presently, no specific treatment exists to ameliorate the tissue damage and reduce the vulnerability to infection induced by smoke inhalation. Administer 100% oxygen because of the likelihood of CO inhalation in fires. Once CO toxicity, cyanide (CN) toxicity, and methemoglobinemia have been addressed, subsequent treatment is predominantly supportive.
The most urgent concern in patients is the patency of the upper airway and adequacy of ventilation. 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. The proportion of patients with an inhalation injury who require endotracheal intubation is higher for those who also have a burn injury: 62% with a burn versus 12% without a thermal injury and the incidence of inhalation injury increases with the size of the burn. See the image below.
It is of vital importance that the magnitude of the swelling in the areas of the face and mandible be closely scrutinized when making decisions about the need for an artificial airway. The threshold for intubation should be lower than in other patients due to the potential of rapid development of airway edema. This is especially true of the pediatric patient. 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.
If systemic paralysis is necessary for intubation, succinylcholine can be used safely in the immediate post-burn phase and up to several days afterward, although one should be cognizant of the possibility of a rise in serum potassium. Inflate the tube cuff to minimal levels, even allowing a small leak, in order to prevent iatrogenic tracheal damage in patients with an already compromised tracheal mucosa.
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. Large-bore IV catheter access may be needed to facilitate fluid resuscitation.
Use formulas (eg, Parkland) to calculate fluid resuscitation if severe burns are present. Even minor errors in estimation of body surface area; burned surface area; and fluid, electrolyte, and protein requirements can produce profound hemodynamic and respiratory compromise. Frequent evaluation of heart rate, perfusion, and blood pressure are needed to determine stability and guide therapy.
In mass casualty scenarios, the use of fiberoptic bronchoscopy may be beneficial to rapidly triage patients to intensive care, ward, or observation status. Mobilization of otolaryngology and/or anesthesia resources may be necessary to accomplish this in a timely fashion.
Hospital Admission Criteria
Patients with smoke inhalation should be monitored for 4-6 hours in the ED. Those who are at low risk for injury and whose vital signs and physical examination findings remain normal can usually be discharged with close follow-up and instructions to return if symptoms develop.
While there are no definite criteria for admission, patients with any of the following should be strongly considered for hospitalization:
History of closed-space exposure for longer than 10 minutes
History of syncope
Carbonaceous sputum production
Arterial PO 2 less than 60 mm Hg
Carboxyhemoglobin levels above 15%
Arteriovenous oxygen difference (on 100% oxygen) greater than 100 mm Hg
Central facial burns
For patients with isolated smoke inhalation, treatment in an intensive care unit is appropriate. However, patients with significant cutaneous burns should be transferred to a burn center when stable, if they meet the criteria for transfer.
Carbon Monoxide Poisoning
Assume elevated levels of carboxyhemoglobin in all fire victims. CO is not only responsible for most prehospital deaths due to smoke inhalation, it is also the leading cause of injury/death from all poisons worldwide.
The half-life of CO is 320 minutes on room air, 90 minutes on 100% oxygen, and 23 minutes in a hyperbaric chamber at 3 atmospheres absolute (ATA). Elimination of CO depends primarily on the law of mass action, so alveolar PO2, rather than alveolar ventilation, is the critical factor in its removal.
Hyperbaric oxygen therapy
In patients with CO poisoning from smoke inhalation, the main reason for use of hyperbaric oxygen (HBO) therapy is to prevent delayed neurological sequelae. Carboxyhemoglobin levels are poor indicators of the severity of intoxication; patients with significant toxicity may have low levels. In fact, at the time of the initial HBO treatment, patients enrolled in most studies have normal or near-normal carboxyhemoglobin levels.
At this time, 6 prospective, randomized controlled trials have compared HBO with normobaric oxygen (NBO) therapy for CO poisoning. Four of these studies show a benefit for CO poisoning; two do not. The data and conclusions drawn from these studies are conflicting and highlight the controversy surrounding the utility of HBO.
In a prospective, double-blind study that compared HBO with NBO in patients with symptomatic acute CO poisoning, Weaver and colleagues found that 3 HBO treatments decreased the incidence of cognitive sequelae by 46% at 6 weeks. Furthermore, a benefit continued to be seen at 12-month follow-up. Essentially, for every 6 patients treated with HBO, one case of delayed neurologic sequelae could be avoided. The evidence of benefit with HBO was so strong that the study was halted before its scheduled completion.
Although there has been much debate regarding the accuracy of neuropsychometric testing, including the fact that patients who are depressed and who have attempted suicide with non-CO means perform as poorly as CO-exposed patients, such testing remains an objective means to evaluate cognitive function.
Neurologic abnormalities and a history of loss of consciousness are the primary clinical features used to define severe CO toxicity and are indications for HBO. In addition, HBO use is indicated in patients with any of the following:
Base excess lower than -2 mmol/L
CO level greater than 25% (or >15% in pregnancy, as fetal hemoglobin binds CO more tightly)
Signs of cerebellar dysfunction
Extremes of age
Note that the incidence of delayed neurologic sequelae increases with a more symptomatic initial clinical picture, in older patients, and in those with a prolonged exposure.
The American College of Emergency Physicians Clinical Policies Subcommittee recommended in 2008 continued use of HBO in CO poisoning, especially in children and pregnant women, due to the conflicting results of previous studies.
Individuals exposed to CN poisoning may present with a variety of symptoms ranging from headache and altered mental status to hypotension, arrhythmia, and cardiovascular collapse followed by shock. Management of CN toxicity has historically involved the creation of an alternate binding site for CN to compete with cytochrome oxidase and also to provide substrate necessary to convert CN to a nontoxic metabolite.
Although not universally available, hydroxocobalamin (Cyanokit) is the preferred treatment of CN toxicity. In fact, many prehospital personnel use this product before the patient arrives if there is a high index of suspicion. It has been used in France for more than 30 years and was approved by the US Food and Drug Administration (FDA) in 2006.
Hydroxocobalamin is a hemelike molecule with a complexed cobalt atom that binds directly to CN to form cyanocobalamin (vitamin B-12), which is excreted renally. In vitro studies indicate that hydroxocobalamin penetrates cells and can act intracellularly. Adverse effects are chromaturia and reddening of the skin. Empiric administration to patients subsequently confirmed to have CN poisoning has been shown to be associated with 67% survival.
Hydroxocobalamin has a rapid onset of action, is easy to administer, does not interfere with tissue oxygenation, is well tolerated, and is safe for smoke inhalation patients. Additionally, it is not associated with hypotension or the formation of a dyshemoglobinemia (as was found in previous antidote kits) and it improves hemodynamic stability.[5, 48, 49]
The traditional CN antidote kit contains amyl and sodium nitrite to create a methemoglobin level of 3% and 20-30%, respectively, which, in turn, has a higher affinity for CN than for cytochrome a3. Also included is sodium thiosulfate, which provides substrate for the enzyme rhodanese; this combines thiosulfate and CN to form a nontoxic compound, thiocyanate, which is excreted renally.
Induction of methemoglobinemia is theoretically dangerous in a patient with an elevated carboxyhemoglobin level because further reduces oxygen-carrying capacity, so the clinician should consider withholding the nitrite portion of the kit. Another drawback of this treatment is the delayed onset of thiosulfate. Note that there is limited information about the efficacy of sodium thiosulfate for CN poisoning, as there are no clinical trials of sodium thiosulfate available. Finally, this treatment may be more preventative rather than curative.
Though no prospective studies have conclusively demonstrated a decrease in mortality with the use of sodium thiosulfate alone, optimal treatment at this time is the combined use of hydroxocobalamin and thiosulfate. This is due to the fact that sodium thiosulfate has poor intracellular penetration and slow onset. The combination of treatments allows quick extraction of cyanide without the formation of other dyshemoglombinemias and offers a sulfur-donating drug that maximizes the function of rhodanese.
Methemoglobinemia in smoke inhalation is relatively rare and rarely requires treatment with methylene blue. This antidote is reduced by the nicotinamide adenine dinucleotide phosphate (NADPH) methemoglobin reductase enzyme and, in return, reduces methemoglobin to hemoglobin. Indications for treatment with methylene blue as follows:
Alteration in mental status
Electrocardiographic (ECG) changes
Ischemic chest pain
Methemoglobin levels lower than 30% may not require treatment, depending on the patient's cardiorespiratory reserve.
Since the pathophysiology of smoke inhalation involves irritants setting off the inflammatory response, many recent studies have investigated the benefit of anti-inflammatories and anticoagulants as treatment options for this underlying pathogenesis of injury. Treatment with heparin and pentoxifylline has been shown to improve lung function after smoke inhalation.
Aside from its known effect on thrombin, heparin has been recognized to have a protective effect on microvascular endothelium. Its anionic sulfate groups give the compound the ability to function as a cation exchanger, thereby limiting the endothelial permeability of cationic proteases released by polymorphonuclear leukocytes (PMLs). Pentoxifylline has not only been observed to improve microvascular circulation, but also suggested to play a role in down-regulating the production and release of inflammatory mediators.
Currently, both heparin and pentoxifylline are delivered systemically, but with limited success in penetrating the deep lung areas. However, a feasible delivery alternative allowing deeper penetration and a rapid local onset of action for the acceleration of healing may provide clinical benefits in the future.
A study of inhalable aerosol formulations of heparin and pentoxifylline in particles 5 µm or smaller demonstrated that co-spraying of heparin or pentoxifylline with leucine supplementation over a 24-hour period allowed for deep lung drug deposition and a possible efficient route to improve therapeutic outcomes for smoke inhalation.
In contrast, a systematic review of heparin use in burn injury (topically, subcutaneously, intravenously, or via aerosol) found no strong evidence that heparin can improve clinical outcomes. Oremus and colleagues suggested that poor methodologic quality in studies of heparin may have led to severe bias in reports of its benefit.
Studies on experimental induction of smoke inhalation confirm the presence of an acute surfactant deficiency. Instillation of artificial surfactant shortly after injury was beneficial. Larger studies are needed before instituting such therapy.
Oxidant injury eventually leads to cast formation of cellular debris in the airways, thus contributing to pulmonary failure. A pediatric study has shown that aerosolized heparin/N -acetylcysteine decreases the incidence of atelectasis, reintubation rates, and overall mortality.
Acetylcysteine and L-3,4 dehydroproline and a combined regimen of hydrocortisone and penicillamine have been used to treat ARDS induced by inhalation of smoke from smoke bombs. Positive outcomes were attributed to early treatment with penicillamine. In animal studies, acetylcysteine has also been found effective for PTFE exposure.
In an animal model, whole-body hypothermia has been shown to suppress oxidant bronchoalveolar damage and pulmonary inflammation. Mechanistically, this appears to halt the progression of bronchoalveolar-capillary permeability.
As with many respiratory conditions, the use of chest physiotherapy is widely accepted in inhalation injury 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 patients who are intubated, 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 may be necessary in patients with declining lung function, oxygenation levels, and ventilation. Use of positive pressure ventilation with low tidal volumes (3-5 mL/kg) and positive end-expiratory pressure (PEEP) and maintenance of plateau pressures below 30 cm water significantly increases short-term survival and is associated with decreased tracheobronchial cast formation. In fact, this treatment has been shown to increase the intensive care unit (ICU) survival rate from 29% to 62%.
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.
High-frequency percussive ventilation (HFPV), while not as commonly used in the ED, is considered standard therapy in many burn centers. HFPV generates pulsatile flow at up to 600 cycles per minute, which entrains the humidified gas by its effect on molecular diffusion. It can improve clearance of airway secretions and allow continued patency of the lower airways. In patients with inhalation injury and burns involving less than 40% of total body surface area, HFPV decreases both morbidity and mortality.[54, 55, 56]
The timing of tracheostomy continues to be controversial. Certainly, tracheostomy can be lifesaving for patients in whom endotracheal intubation is not possible, because of severe airway edema or burns. 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 with 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, however, tracheostomy may be desirable for patient comfort and is easy to maintain.
Patients should take nothing by mouth until it becomes clear that they will not require tracheal intubation because of significant respiratory or hemodynamic compromise.
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.
Primary prevention with functioning fire and smoke alarms and family education for fire hazards is critical to help avoid fire injuries. Fire prevention should be viewed as the primary means to avoid inhalation injury
Smoke detectors reduce the risk of death by about 60% in all subgroups of people. This finding stands in contrast to past data that suggested that these early warning devices may not be effective in populations that have difficulty responding to an alarm in a timely manner, such as children, older adults, persons with disabilities, or those impaired by alcohol or other drugs. These new data clearly reinforce the point that all homes should have a working smoke detector in every room.
Although smoke detectors have been widely adopted by the public— 93% of US households have one in place—it is estimated that 30-45% of these devices are not operational, usually because the battery has died or has been removed. DiGuiseppi et al have shown that merely giving out free smoke alarms in a deprived, multiethnic, urban community did not reduce injuries related to fire, because few of the alarms were installed or properly maintained.
In the military setting, the mission-oriented protective posture (MOPP) gear ensemble provides adequate protection against all smokes. In the industrial setting, guidelines have been established for the protection of the worker as well as any person who may come in contact with toxic smokes. Aim preventive efforts at decreasing the concentration of the smoke and the time of exposure and recognizing underlying health problems that may be exacerbated by exposure to toxic smokes.
Rorison DG, McPherson SJ. Acute toxic inhalations. Emerg Med Clin North Am. 1992 May. 10(2):409-35. [Medline].
de Lange DW, Meulenbelt J. Do corticosteroids have a role in preventing or reducing acute toxic lung injury caused by inhalation of chemical agents?. Clin Toxicol (Phila). 2011 Feb. 49(2):61-71. [Medline].
Bizovi KE, Leikin JD. Smoke inhalation among firefighters. Occup Med. 1995 Oct-Dec. 10(4):721-33. [Medline].
Hall AH, Dart R, Bogdan G. Sodium thiosulfate or hydroxocobalamin for the empiric treatment of cyanide poisoning?. Ann Emerg Med. 2007 Jun. 49(6):806-13. [Medline].
Buyantseva LV, Tulchinsky M, Kapalka GM, et al. Evolution of lower respiratory symptoms in New York police officers after 9/11: a prospective longitudinal study. J Occup Environ Med. 2007 Mar. 49(3):310-7. [Medline].
Thai A, Xiao J, Ammit AJ, Rohanizadeh R. Development of inhalable formulations of anti-inflammatory drugs to potentially treat smoke inhalation injury in burn victims. Int J Pharm. 2010 Apr 15. 389(1-2):41-52. [Medline].
Urbanetti JS. Toxic inhalational injury. Medical Aspects of Chemical and Biological Warfare. 1997. 260-267. [Full Text].
Belli S, Basaran O, Ozdemir BH, et al. Protective role of simvastatin on lung damage caused by burn and cotton smoke inhalation in rats. J Surg Res. 2011 May 15. 167(2):e283-90. [Medline].
Kao LW, Nanagas KA. Toxicity associated with carbon monoxide. Clin Lab Med. 2006 Mar. 26(1):99-125. [Medline].
Goldbaum LR, Ramirez RG, Absalon KB. What is the mechanism of carbon monoxide toxicity?. Aviat Space Environ Med. 1975 Oct. 46(10):1289-91. [Medline].
Lawson-Smith P, Jansen EC, Hyldegaard O. Cyanide intoxication as part of smoke inhalation--a review on diagnosis and treatment from the emergency perspective. Scand J Trauma Resusc Emerg Med. 2011 Mar 3. 19:14. [Medline]. [Full Text].
Stewart RJ, Yamaguchi KT, Knost PM, Mason SW, Roshdieh BB, Samadani S. Effects of ibuprofen on pulmonary oedema in an animal smoke inhalation model. Burns. 1990 Dec. 16(6):409-13. [Medline].
Kimura R, Traber L, Herndon D, Niehaus G, Flynn J, Traber DL. Ibuprofen reduces the lung lymph flow changes associated with inhalation injury. Circ Shock. 1988 Mar. 24(3):183-91. [Medline].
Hill IR. Particulate matter of smoke inhalation. Ann Acad Med Singapore. 1993 Jan. 22(1):119-23. [Medline].
Chian CF, Wu CP, Chen CW, et al. Acute respiratory distress syndrome after zinc chloride inhalation: survival after extracorporeal life support and corticosteroid treatment. Am J Crit Care. 2010 Jan. 19(1):86-90. [Medline].
Hsu HH, Tzao C, Chang WC, Wu CP, Tung HJ, Chen CY, et al. Zinc chloride (smoke bomb) inhalation lung injury: clinical presentations, high-resolution CT findings, and pulmonary function test results. Chest. 2005 Jun. 127(6):2064-71. [Medline].
Conner MW, Flood WH, Rogers AE, Amdur MO. Lung injury in guinea pigs caused by multiple exposures to ultrafine zinc oxide: changes in pulmonary lavage fluid. J Toxicol Environ Health. 1988. 25(1):57-69. [Medline].
Marrs TC, Colgrave HF, Edginton JA, Brown RF, Cross NL. The repeated dose toxicity of a zinc oxide/hexachloroethane smoke. Arch Toxicol. 1988. 62(2-3):123-32. [Medline].
Loh CH, Chang YW, Liou SH, Chang JH, Chen HI. Case report: hexachloroethane smoke inhalation: a rare cause of severe hepatic injuries. Environ Health Perspect. 2006 May. 114(5):763-5. [Medline]. [Full Text].
Keyes DC. Metal fume fever. Dart RC. Medical Toxicology. 3rd ed. Philadelphia, Pa: Lippincott, Williams & Wilkins; 2004. 88-89.
Kuschner WG, D'Alessandro A, Wong H, Blanc PD. Early pulmonary cytokine responses to zinc oxide fume inhalation. Environ Res. 1997 Oct. 75(1):7-11. [Medline].
Agency for Toxic Substances & Disease Registry. Sulfur Trioxide & Sulfuric Acid. Toxic Substances Portal. Available at http://www.atsdr.cdc.gov/toxprofiles/tp.asp?id=256&tid=47. Accessed: May 9, 2013.
Weiss SM, Lakshminarayan S. Acute inhalation injury. Clin Chest Med. 1994 Mar. 15(1):103-16. [Medline].
Harduar-Morano L, Watkins S. Review of unintentional non-fire-related carbon monoxide poisoning morbidity and mortality in Florida, 1999-2007. Public Health Rep. 2011 Mar-Apr. 126(2):240-50. [Medline]. [Full Text].
Duclos P, Sanderson LM, Lipsett M. The 1987 forest fire disaster in California: assessment of emergency room visits. Arch Environ Health. 1990 Jan-Feb. 45(1):53-8. [Medline].
US Fire Administration’s (USFA’s) National Fire Incident Reporting System (NFIRS). Fatal Fires in Residential Buildings. US Department of Homeland Security, US Fire Administration. August 2010. Available at http://www.usfa.fema.gov/downloads/pdf/statistics/v11i2.pdf.
Barillo DJ, Goode R. Fire fatality study: demographics of fire victims. Burns. 1996 Mar. 22(2):85-8. [Medline].
Karter MJ Jr. Fire Loss in the United States during 2011. National Fire Protection Association, September 2012. Pediatrics. Available at http://www.nfpa.org/assets/files/pdf/os.fireloss.pdf. Accessed: May 14, 2013.
Istre GR, McCoy MA, Osborn L, Barnard JJ, Bolton A. Deaths and injuries from house fires. N Engl J Med. 2001 Jun 21. 344(25):1911-6. [Medline].
Large AA, Owens GR, Hoffman LA. The short-term effects of smoke exposure on the pulmonary function of firefighters. Chest. 1990 Apr. 97(4):806-9. [Medline].
Hoyert DL, Xu. Deaths: Preliminary Data for 2011. National Vital Statistics Reports. Available at http://www.cdc.gov/nchs/data/nvsr/nvsr61/nvsr61_06.pdf. Accessed: May 14, 2013.
Marshall SW, Runyan CW, Bangdiwala SI, Linzer MA, Sacks JJ, Butts JD. Fatal residential fires: who dies and who survives?. JAMA. 1998 May 27. 279(20):1633-7. [Medline].
Muller MJ, Pegg SP, Rule MR. Determinants of death following burn injury. Br J Surg. 2001 Apr. 88(4):583-7. [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. 2000 Jun. 16(3):151-5. [Medline].
Whitelock-Jones L, Bass DH, Millar AJ, Rode H. Inhalation burns in children. Pediatr Surg Int. 1999. 15(1):50-5. [Medline].
Roney N, Smith CV, Williams M. Toxicological Profile for Zinc (Update). US Dept of Health & Human Services. 2007. Available at http://www.atsdr.cdc.gov/toxprofiles/tp60.html#bookmark07.
Baud FJ, Barriot P, Toffis V, et al. Elevated blood cyanide concentrations in victims of smoke inhalation. N Engl J Med. 1991 Dec 19. 325(25):1761-6. [Medline].
Lahn M, Sing W, Nazario S, Fosberg D, Bijur P, Gallagher EJ. Increased blood lead levels in severe smoke inhalation. Am J Emerg Med. 2003 Oct. 21(6):458-60. [Medline].
Chou CH, Kao TW, Liou SH, Chen HI, Ku HY, Chuang HJ, et al. Hematological abnormalities of acute exposure to hexachloroethane smoke inhalation. Inhal Toxicol. 2010 May. 22(6):486-92. [Medline].
Koljonen V, Maisniemi K, Virtanen K, Koivikko M. Multi-detector computed tomography demonstrates smoke inhalation injury at early stage. Emerg Radiol. 2007 Jun. 14(2):113-6. [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. 1976 Mar. 16(3):218-24. [Medline].
Carr JA, Phillips BD, Bowling WM. The utility of bronchoscopy after inhalation injury complicated by pneumonia in burn patients: results from the National Burn Repository. J Burn Care Res. 2009 Nov-Dec. 30(6):967-74. [Medline].
Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. 2002 Oct 3. 347(14):1057-67. [Medline].
Wolf SJ, Lavonas EJ, Sloan EP, Jagoda AS. Clinical policy: Critical issues in the management of adult patients presenting to the emergency department with acute carbon monoxide poisoning. Ann Emerg Med. 2008 Feb. 51(2):138-52. [Medline].
Kung SW, Chan YC, Lau FL. Hydroxocobalamin for acute cyanide poisoning in smoke inhalation. Ann Emerg Med. 2008 Jan. 51(1):108; author reply 108-9. [Medline].
Borron SW, Baud FJ, Barriot P, Imbert M, Bismuth C. Prospective study of hydroxocobalamin for acute cyanide poisoning in smoke inhalation. Ann Emerg Med. 2007 Jun. 49(6):794-801, 801.e1-2. [Medline].
Huzar TF, George T, Cross JM. Carbon monoxide and cyanide toxicity: etiology, pathophysiology and treatment in inhalation injury. Expert Rev Respir Med. 2013 Apr. 7(2):159-70. [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. 2007 Nov-Dec. 28(6):794-804. [Medline].
Desai MH, Mlcak R, Richardson J, Nichols R, Herndon DN. Reduction in mortality in pediatric patients with inhalation injury with aerosolized heparin/N-acetylcystine [correction of acetylcystine] therapy. J Burn Care Rehabil. 1998 May-Jun. 19(3):210-2. [Medline].
Huang PS, Tang GJ, Chen CH, Kou YR. Whole-body moderate hypothermia confers protection from wood smoke-induced acute lung injury in rats: the therapeutic window. Crit Care Med. 2006 Apr. 34(4):1160-7. [Medline].
Cancio LC. Airway management and smoke inhalation injury in the burn patient. Clin Plast Surg. 2009 Oct. 36(4):555-67. [Medline].
Nieman GF, Cigada M, Paskanik AM, et al. Comparison of high-frequency jet to conventional mechanical ventilation in the treatment of severe smoke inhalation injury. Burns. 1994 Apr. 20(2):157-62. [Medline].
Hall JJ, Hunt JL, Arnoldo BD, Purdue GF. Use of high-frequency percussive ventilation in inhalation injuries. J Burn Care Res. 2007 May-Jun. 28(3):396-400. [Medline].
DiGuiseppi C, Roberts I, Wade A, Sculpher M, Edwards P, Godward C, et al. Incidence of fires and related injuries after giving out free smoke alarms: cluster randomised controlled trial. BMJ. 2002 Nov 2. 325(7371):995. [Medline]. [Full Text].
Hall AH, Saiers J, Baud F. Which cyanide antidote?. Crit Rev Toxicol. 2009. 39(7):541-52. [Medline].
Shepherd G, Velez LI. Role of hydroxocobalamin in acute cyanide poisoning. Ann Pharmacother. 2008 May. 42(5):661-9. [Medline].
|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 (mitochondrial toxins)||Carbon monoxidea||Combustion of weeds, coal, gas, heaters||Competes for oxygen sites on hemoglobin, myoglobin, heme-containing intracellular proteins|
|Hydrogen cyanideb||Burning of polyurethane, nitrocellulose (silk, nylon, wool)||Tissue asphyxiation by inhibiting intracellular cytochrome oxidase activity, inhibits ATP production, leads to cellular anoxia|
|Hydrogen sulfidec||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|
|a Major component of smoke.
b Smells like almonds, component of smoke from fires.
c Smells like rotten eggs.