Smoke Inhalation 

  • Author: Keith A Lafferty, MD; Chief Editor: Rick Kulkarni, MD   more...
 
Updated: Jun 30, 2010
 

Background

Smoke inhalation (SI) was described as early as the first century AD, when Pliny reported the execution of prisoners by exposure to the smoke of greenwood fires.

Many victims of fire accidents have both smoke inhalation and thermal injury. Inhalation injury from smoke and the noxious products of combustion in fires may account for as many as 60-80% of fire-related deaths in the United States, many of which are preventable.[1, 2] Excellent care rendered at today's burn centers has greatly reduced the mortality from surface burns, while the mortality from pulmonary injury has been increasing. In fact, respiratory failure is now the most common cause of death at burn centers.[3] Diagnosis of inhalation injury is not always straightforward, sensitive screening tests are lacking, and symptoms may be delayed until 24-36 hours after injury.

Next

Pathophysiology

The 3 primary mechanisms that lead to injury in smoke inhalation are thermal damage, asphyxiation, and pulmonary irritation.

Thermal damage

Thermal damage is usually limited to the oropharyngeal area, due to the poor conductivity of air and the high amount of dissipation that occurs in the upper airways. Animal experiments have shown that 142°C inhaled air cools to 38°C by the time it reaches the carina. Steam, volatile gases, explosive gases, and the aspiration of hot liquids provide some exceptions, as moist air has a much greater heat-carrying capacity than dry air.

Asphyxiation

Tissue hypoxia can occur secondary to several mechanisms. Combustion utilizes oxygen, which in a closed space may be consumed, significantly decreasing the ambient concentration of oxygen to as low as 10-13%. The decrease in fraction of inspired oxygen (FIO2) leads to hypoxia, despite adequate circulation and oxygen-carrying capacity.

Carbon monoxide (CO) causes tissue hypoxia by decreasing the oxygen-carrying capacity of the blood. Hemoglobin binds CO with an affinity more than 200 times greater than the affinity for oxygen. Even though this tissue hypoxia is the primary insult, other mechanisms contribute to its pathophysiology.[4]

CO also causes a left shift in the oxyhemoglobin saturation dissociation curve. CO has been shown to bind to the cytochrome oxidase chain in vitro. Finally, since CO binds to virtually all heme molecules, myocardial myoglobin is affected and consequently myocardial contractility is decreased.

Combustion of plastics, polyurethane, wool, silk, nylon, nitriles, rubber, and paper products can lead to the production of cyanide (CN) gas. CN also takes the form of solid crystals bound to sodium and potassium salts. It is also found abound in foods such as cassava and in apple, pear, apricot, and peach seeds. Hydrogen CN is a colorless gas with a bitter almond odor to the 40% of the population who are able to detect it. It is 20 times more toxic than CO and can cause immediate respiratory arrest.

Consider CN toxicity in all patients with smoke inhalation who have CNS or cardiovascular findings. CN is a chemical asphyxiant that interferes with cellular metabolism by binding to the ferric ion on cytochrome a3, subsequently halting cellular respiration. As a consequence of the cessation of the electron transport system, anaerobic metabolism ensues, with corresponding high lactate acidosis and decreased oxygen consumption.

Methemoglobinemia occurs in fire due to heat denaturation of hemoglobin, oxides produced in fire, and methemoglobin-forming materials such as nitrites. Occurrence of methemoglobinemia is a less common phenomenon than CN and CO toxicity. The pathophysiologic consequences of methemoglobin formation are a decrease in the oxygen-carrying capacity of the blood and a shift of the oxyhemoglobin dissociation curve to the left, similar to carboxyhemoglobin (HbCO).

Pulmonary irritation

Irritants can cause direct tissue injury, acute bronchospasm, and activation of the body's inflammatory response system. Activated leukocytes and/or humoral mediators, such as prostanoids and leukotrienes, produce oxygen radicals and proteolytic enzymes. Supporting the importance of the inflammatory response to the mechanism of tissue destruction, some studies have shown that the administration of the cyclooxygenase inhibitor, ibuprofen, was found to reduce the lung lymph flow in animals with smoke inhalation.[5, 6] The direct injury is a consequence of the size of the particle, its solubility in water, and its acid-base status. Ammonia produces alkaline injury, while sulfur dioxide and chlorine gas lead to acid injuries. Other chemicals act via different mechanisms; for instance, acrolein causes free radical formation and protein denaturation.[7]

The location of injury depends on the solubility of the substance in water. High-solubility substances such as acrolein, sulfur dioxide, ammonia, and hydrogen chloride cause injury to the upper airway. Substances with intermediate solubility, such as chlorine and isocyanates, cause both upper and lower respiratory tract injury. Phosgene and oxides of nitrogen have low water solubility and cause diffuse parenchymal injury.

In a study evaluating survivors of the 9/11 World Trade Center's collapse, 44% had persistent lower respiratory symptoms after 19 months of follow up[8] ; hence, the term "World Trade Center cough." A more recent study shows that 13% (1,720) of participants in the FDNY-WTC Monitoring Program referred for pulmonary evaluation, received either pulmonary function testing, methacholine challenge test, high-resolution chest CT scans, or a combination of these tests. Fifty-nine percent were found to have obstructive airway disease while few had evidence of interstitial disease.[9]

Previous
Next

Epidemiology

Frequency

United States

Burns and fires are the third leading cause of accidental death in all age groups. They comprise the second leading cause of death in the home for all ages and the leading cause of death in the home for children and young adults.[10] In 1998, approximately 381,500 residential fires occurred in the US, resulting in 3,250 nonfirefighter deaths, 17,175 injuries, and nearly $4.4 billion in property loss.[11] These figures do not include the estimated 90% of fires not reported to fire departments. More than half of all fatal residential fires started between the hours of 11 pm and 7 am.[10]

Incidence of smoke inhalation increases from less than 10% in patients with a mean total body surface area (TBSA) burn size of 5% to more than 80% in patients with a mean TBSA burn size of 85% or more. Smoke inhalation is present in one third of patients treated at burn centers. The magnitude of smoke inhalation is devastating, as the presence of an inhalation injury has a greater effect on mortality than either patient age or surface area burned.

International

The US has one of the highest fire fatality rates in the developed world, accounting for 2.3 deaths per 100,000 population.[12] In fact, fire death rates in the US and Canada are twice as high as in Western Europe and Japan.[10]

Mortality/Morbidity

Mortality is related to associated cutaneous burns.

  • In patients with a burn and no associated SI or respiratory failure, the mortality rate is less than 2%. In patients with smoke inhalation alone and no burn or respiratory failure, the mortality rate is 7%.
  • For patients with a burn and smoke inhalation, the mortality rate increases to 29%, suggesting that the burn wounds themselves put an additional stress on the compromised lung.[13]
  • Studies have shown that children with CO poisoning alone compared to those with combined smoke inhalation and CO toxicity had an increase in mortality rate from 0% to 22.6%.[14]
  • In rat and sheep models, cutaneous burns result in systemic complement activation with pulmonary sequestration of activated neutrophils, which, in turn, release toxic metabolites, further injuring the lung.

Race

One study in New Jersey reports on the demographics of fire fatalities and notes that victims who perished did not parallel the ethnic census of the time.[2, 10]

  • Whites accounted for 53% of fatalities and comprised 49% on the census.
  • African Americans accounted for 38% of fatalities and 13% of the census.

Sex

The male-to-female ratio is about 3:2.

Age

The New Jersey study also showed that children and the elderly represented a disproportionate percentage of people injured by fire.[10] People younger than 11 years or older than 70 years constituted 22% of the population but accounted for 40% of all fire fatalities. These statistics closely match national figures.

A comprehensive study in Dallas looked at all house fires from 1991-1997.[15] Many of the findings parallel those of the New Jersey study.

  • Relative risk of injury was 1.8 for men, 1.4 for boys, 2.8 for blacks, and 2.6 for elderly persons.
  • In addition, among the injured, the proportion of injuries that were fatal was higher in persons older than 65 years (53%) and in those younger than 10 years (67%) compared with those aged 10-64 years (30%).
  • The lowest income tracts had the highest rate of injury. The rate of injury in households with a median income below $20,000 per year was 8 times that of tracts with a median income greater than $80,000 per year. In fact, tracts with extremely low incomes, less than $10,000 per year, had rates of injury 20 times that of the above.
  • Houses built in the 1950s and 1960s were somewhat more likely to burn than houses built before this time. This may be a case of "selection of the fittest" houses, with those houses most prone to burn having already done so leaving the most structurally sound ones still standing.
  • Fires caused by arson occurred predominately in census tracts with lower median incomes. Eighty percent of fires occurred in homes with median incomes of less than $40,000 per year.
  • Causes of the house fires were arson (25.5%), electrical wiring/equipment (16.6%), heating equipment (15.8%), cooking (11.4%), smoking (5.5%), children playing with fire (4.5%), and unknown/other (20.6%).
  • The rate of fire-related injury in houses in Dallas without a functioning smoke detector was 8.7 times that of homes with functioning smoke detectors. Houses that are most likely to have fires were least likely to have functioning smoke detectors.
  • As a result of this study, a program in Dallas now provides and installs smoke detectors in census tracts with the highest rates of injuries and deaths related to house fires.
Previous
 
 
Contributor Information and Disclosures
Author

Keith A Lafferty, MD  Adjunct Assistant Professor of Emergency Medicine, Temple University School of Medicine; Medical Student Director, Department of Emergency Medicine, Gulf Coast Medical Center

Keith A Lafferty, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Association, and Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Harry J Goett, MD  Assistant Professor of Emergency Medicine, Department of Emergency Medicine, Temple University Hospital

Harry J Goett, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Daniel J Dire, MD, FACEP, FAAP, FAAEM  Clinical Professor, Department of Emergency Medicine, University of Texas Medical School at Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center San Antonio

Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

James Steven Walker, DO, MS  Clinical Professor of Surgery, Department of Surgery, University of Oklahoma College of Medicine

James Steven Walker, DO, MS is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, and American Osteopathic Association

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD  Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

References
  1. Bizovi KE, Leikin JD. Smoke inhalation among firefighters. Occup Med. Oct-Dec 1995;10(4):721-33. [Medline].

  2. Hall AH, Dart R, Bogdan G. Sodium thiosulfate or hydroxocobalamin for the empiric treatment of cyanide poisoning?. Ann Emerg Med. Jun 2007;49(6):806-13. [Medline].

  3. Demling RH. Smoke inhalation lung injury: an update. Eplasty. May 16 2008;8:e27. [Medline]. [Full Text].

  4. Kao LW, Nanagas KA. Toxicity associated with carbon monoxide. Clin Lab Med. Mar 2006;26(1):99-125. [Medline].

  5. 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. Dec 1990;16(6):409-13. [Medline].

  6. 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. Mar 1988;24(3):183-91. [Medline].

  7. Hill IR. Particulate matter of smoke inhalation. Ann Acad Med Singapore. Jan 1993;22(1):119-23. [Medline].

  8. 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. Mar 2007;49(3):310-7. [Medline].

  9. Weiden MD, Ferrier N, Nolan A, Rom WN, Comfort A, Gustave J. Obstructive airways disease with air trapping among firefighters exposed to World Trade Center dust. Chest. Mar 2010;137(3):566-74. [Medline].

  10. Barillo DJ, Goode R. Fire fatality study: demographics of fire victims. Burns. Mar 1996;22(2):85-8. [Medline].

  11. Reducing the number of deaths and injuries from residential fires. Pediatrics. Jun 2000;105(6):1355-7. [Medline].

  12. Marshall SW, Runyan CW, Bangdiwala SI, Linzer MA, Sacks JJ, Butts JD. Fatal residential fires: who dies and who survives?. JAMA. May 27 1998;279(20):1633-7. [Medline].

  13. Muller MJ, Pegg SP, Rule MR. Determinants of death following burn injury. Br J Surg. Apr 2001;88(4):583-7. [Medline].

  14. 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].

  15. Istre GR, McCoy MA, Osborn L, Barnard JJ, Bolton A. Deaths and injuries from house fires. N Engl J Med. Jun 21 2001;344(25):1911-6. [Medline].

  16. Baud FJ, Barriot P, Toffis V, et al. Elevated blood cyanide concentrations in victims of smoke inhalation. N Engl J Med. Dec 19 1991;325(25):1761-6. [Medline].

  17. Lahn M, Sing W, Nazario S, Fosberg D, Bijur P, Gallagher EJ. Increased blood lead levels in severe smoke inhalation. Am J Emerg Med. Oct 2003;21(6):458-60. [Medline].

  18. Koljonen V, Maisniemi K, Virtanen K, Koivikko M. Multi-detector computed tomography demonstrates smoke inhalation injury at early stage. Emerg Radiol. Jun 2007;14(2):113-6. [Medline].

  19. Cancio LC. Airway management and smoke inhalation injury in the burn patient. Clin Plast Surg. Oct 2009;36(4):555-67. [Medline].

  20. 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. Nov-Dec 2009;30(6):967-74. [Medline].

  21. 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. Apr 1994;20(2):157-62. [Medline].

  22. Hall JJ, Hunt JL, Arnoldo BD, Purdue GF. Use of high-frequency percussive ventilation in inhalation injuries. J Burn Care Res. May-Jun 2007;28(3):396-400. [Medline].

  23. Kao LW, Nanagas KA. Toxicity associated with carbon monoxide. Clin Lab Med. Mar 2006;26(1):99-125. [Medline].

  24. Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. Oct 3 2002;347(14):1057-67. [Medline].

  25. 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. Feb 2008;51(2):138-52. [Medline].

  26. Kung SW, Chan YC, Lau FL. Hydroxocobalamin for acute cyanide poisoning in smoke inhalation. Ann Emerg Med. Jan 2008;51(1):108; author reply 108-9. [Medline].

  27. Borron SW, Baud FJ, Barriot P, Imbert M, Bismuth C. Prospective study of hydroxocobalamin for acute cyanide poisoning in smoke inhalation. Ann Emerg Med. Jun 2007;49(6):794-801, 801.e1-2. [Medline].

  28. Sterner JB, Zanders TB, Morris MJ, Cancio LC. Inflammatory mediators in smoke inhalation injury. Inflamm Allergy Drug Targets. Mar 2009;8(1):63-9. [Medline].

  29. 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. May-Jun 1998;19(3):210-2. [Medline].

  30. 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. Apr 2006;34(4):1160-7. [Medline].

  31. Hall AH, Saiers J, Baud F. Which cyanide antidote?. Crit Rev Toxicol. 2009;39(7):541-52. [Medline].

  32. Shepherd G, Velez LI. Role of hydroxocobalamin in acute cyanide poisoning. Ann Pharmacother. May 2008;42(5):661-9. [Medline].

  33. 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. Nov 2 2002;325(7371):995. [Medline]. [Full Text].

  34. Hampson NB, Zmaeff JL. Outcome of patients experiencing cardiac arrest with carbon monoxide poisoning treated with hyperbaric oxygen. Ann Emerg Med. Jul 2001;38(1):36-41. [Medline].

Previous
Next
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.