Inhalation Injury

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Fires cause burns and these injuries are obvious but injuries to the lungs and airways from smoke inhalation are often less apparent and may not present until 24-36 hours after exposure. In 2011-2012, being overcome by gas, smoke or toxic fumes was partly or wholly the cause of death in 53% of fatalities. A further 19% were due to a combination of burns and being overcome by gas or smoke.[1] 

A study from North West England found that the overall admission rate to hospital for smoke inhalation or burns was 0.29/1,000 population per year. Another found that 10-30% of all burns admissions had smoke inhalation injury. The groups most at risk are the under-5s and the over-75s, with a male-to-female preponderance of about 2:1. Mortality is highest in the elderly and risk increases with social deprivation.

Risk factors[4] 

Risks are increased by being in a confined space, by the duration of exposure, by substances being burned that may emit various poisons and by pre-existing respiratory disease.

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There are three basic ways that damage occurs. Heat causes thermal damage, gases cause asphyxiation and there may be irritation of the lungs or airways.

Generally, heat damage is limited to the oropharynx, as heat is soon dissipated but steam and explosions may carry it rather deeper.

Asphyxiation results in tissue hypoxia. The fire may take a significant amount of oxygen from the air leaving only 10-13% oxygen, giving a pO2 of barely half the normal value. Even small amounts of carbon monoxide (CO) will aggravate the situation, as the gas has 200 times the affinity of oxygen for haemoglobin so that an atmosphere of 21% oxygen and 0.1% CO will cause the blood to leave the lungs 50% saturated with oxyhaemoglobin and 50% saturated with carboxyhaemoglobin.[6] 

CO also binds to myocardial myoglobin and reduces the contractility of the heart. Combustion of plastics, polyurethane, wool, silk, nylon, nitriles, rubber and paper products can all lead to cyanide production. Only 20-40% of the population carry the gene needed to smell hydrogen cyanide. It has an almond-like odour. It is 20 times as toxic as CO and can cause immediate respiratory arrest.[7] If patients with smoke inhalation have cardiovascular complications then cyanide poisoning should be considered.

Irritation of the lungs and airways will incite an inflammatory response with bronchospasm and an outpouring of fluid. This seems very much like the inflammatory response in acute asthma. Aerolised steroids may be of benefit but further research is required.[5] Chlorine and oxides of sulphur and nitrogen cause acids, whilst ammonia is alkaline. Highly soluble substances tend to aggravate the upper airways but less soluble poisons like phosgene and nitrogen oxides reach the lungs. Airways can be blocked by soot particles along with bronchospasm and the outpouring of inflammatory exudate. Pulmonary oedema may take a while to develop and so observation after smoke injury is important.[8] 

  • Look at the patient. Check whether breathing is normal or laboured. Note whether there is cyanosis. Note whether the chest wall moves normally and symmetrically.
  • Assess the airway but, if there is any risk of cervical spine trauma, be careful with the neck.
  • Note respiratory rate. Listen to the chest.
  • Note level of consciousness, pulse rate, blood pressure and peripheral circulation.
  • If the patient is not fully conscious and alert the Glasgow Coma Scale should be employed.
  • Note any injuries and burns, undressing the patient as required and possibly removing smoldering clothes. Check the back too.
  • Respiratory assessment is required in anyone with possible smoke injury. It may form a baseline, as conditions can deteriorate after rescue.
  • Check for signs of deteriorating respiratory function and treat aggressively before the situation becomes desperate.
  • Hoarseness and change in the voice may herald serious problems and tachypnoea is a bad sign.
  • Black sputum suggests excessive exposure to soot .
  • Note rhonchi, rales, wheeze and use of accessory muscles of respiration.
  • Facial burns show nearness to the fire. Other burns demonstrate an inability to escape.
  • A baseline CXR may be useful for comparison if pulmonary oedema ensues. Early CXR is often normal and a normal film should not give too much reassurance. Later features can include atelectasis, pulmonary oedema and acute respiratory distress syndrome.
  • Blood gases should be performed, including carboxyhaemoglobin and acid/base balance.
  • A pulse oximeter may give false readings by interpreting carboxyhaemoglobin as oxyhaemoglobin. Co-oximetry, a 4-wavelength technique of light refractance to measure carboxyhaemoglobin and oxyhemoglobin accurately, gives a more accurate assessment.
  • U&E and creatinine as a baseline are also important if there are substantial burns or crush injuries.
  • ECG may show evidence of cardiac ischaemia, especially after cyanide exposure .
  • Bronchoscopy may be very useful in identifying erythema, oedema, ulceration, the presence of carbonaceous material and atelectasis.
  • Cyanide may be emitted in household fires. Diagnosis of cyanide poisoning may be difficult in the early stages.  An elevated plasma lactate may be found in asphyxiation, under-resuscitation, CO poisoning or associated traumatic injury.[5][11] However, a serum lactate level above 10 mmol/L is sensitive and specific for cyanide poisoning in fire victims without burns.[12] 
  • Immediate management at the scene involves extracting the patient as rapidly as is safe, bearing in mind other possible injuries and getting out into the fresh air. Then (and only once clear of the fire!) oxygen should be given at high flow rate and humidified. Establish venous access, assess briefly and then transport with the minimum of delay. The most experienced people at dealing with smoke injury are in a burns unit and there may well be burns too.
  • A patient who has suffered smoke inhalation should be assumed to have CO poisoning and be treated accordingly. High flow 100% O2 significantly reduces the half life of CO in the blood. CO poisoning is responsible for most of the deaths which occur before reaching hospital. If it causes cardiac arrest, the chance of resuscitation is extremely poor. A systematic review highlighted that further research is needed about the mode of delivery of hyperbaric oxygen and mooted the possibility of portable devices, especially in mild cases.[14] 
  • One study found that of 41 patients with smoke inhalation injury, 8 required intubation. Intubation was positively correlated with physical examination findings of soot in the oral cavity, facial burns and body burns.[15] If there is a significant risk of intubation being required it should be performed early or else oedema may make it technically more difficult or impossible. Damage to the mucosa of the trachea makes it more vulnerable and so the endotracheal tube cuff should not be over-inflated. Even allow a little leakage.
  • Once in hospital, intubation may need to be supported by mechanical ventilation. When instituting ventilation a balance has to be struck between providing sufficient oxygenation and causing as little collateral harm as possible.[5] Lower tidal volumes and plateau pressures with high positive end-expiratory pressure (PEEP) and permissive hypercapnia have become widely accepted management regimes for patients with acute lung injury resulting from smoke inhalation.[16] High-frequency ventilation has also been found helpful.[16] 
  • Inhalation injury is not always associated with an increased requirement for fluids unless other burns injuries are present. There is a danger that over-replacement of fluid can increase the risk of pulmonary oedema. Fluid resuscitation should be guided by urine output and hemodynamic parameters of the individual patient.[5] 
  • Inhaled anticoagulation regimens (eg, nebulised or aerosolised heparin, heparinoids, antithrombins, or fibrinolytics) are increasingly being used to manage smoke inhalation-associated acute lung injury.[17] 
  • Prophylactic antibiotics may help to reduce mortality.[18] 
  • The treatment of cyanide poisoning has traditionally been with amyl and sodium nitrite. These create methaemoglobinaemia which can be dangerous when there is CO poisoning too. Increasingly, they are being substituted with hydroxocobalamin, which is safe enough to be used in pre-hospital care.[5] 
  • Patients with acute asthma or chronic obstructive pulmonary disease may develop bronchospasm that needs treating in the usual way.

Admission policy[19]

Patients who have suffered smoke inhalation but are not definite candidates for admission should be monitored in A&E for 4-6 hours before discharge. The following point to the need for admission:

  • Exposure in a closed space for more than 10 minutes.
  • Thick, black sputum.
  • PaO2 below 8 kPa (60 mm Hg) or metabolic acidosis.
  • Carboxyhaemoglobin above 15%.
  • Arteriovenous oxygen difference (on 100% oxygen) greater than 13.33 kPa (100 mm Hg).
  • Bronchospasm.
  • Burns to the face.
  • One American study looking at children aged 10-18 years, admitted with inhalation injury over a 10-year period (a sample of 850), reported a mortality rate of 16.4%.[20] A study of elderly patients with burns showed that smoke injury increased mortality by 400%.[21] This may be in part because of more severe exposure but, the presence of burns with smoke injury, means that the patient has to be treated more seriously.
  • Subglottic stenosis, bronchiectasis, pulmonary oedema and atelectasis can occur.
  • It seems quite possible that smoke injury may trigger susceptibility to asthma.[22] Polyvinyl chloride (PVC) is a particular risk.[23] 
  • Do not rely on CO levels in A&E to assess severity of exposure. The level at the scene may have been more relevant but beware of complications taking many hours to arrive.
  • If a patient is discharged they must be given written instructions on the warning signs which would indicate the need to return immediately. Those with normal vital signs and examination and with short exposure may safely be discharged.[24] The experience from disaster triage involving smoke inhalation is that patients without dermal burns and with normal bronchoscopy, chest radiography and normal blood gases (including carboxyhaemoglobin levels) have a low risk of complications.[25]

Due to its relative rarity, information on prognosis is not abundant. However, in one series of 96 patients, 13 patients developed immediate respiratory failure resulting from ventilatory insufficiency, 4 patients died and vocal cord and tracheal stenosis were noted in 5 patients and 1 patient respectively. In patients with reduction in pulmonary function, improvement was seen after three months, with no further changes being observed within the subsequent three months.[26] An American review quoted an increased mortality by a maximum of 20% over that predicted by age and extent of cutaneous burn alone. Pneumonia in these patients further increased mortality by a maximum of 40%. One estimate suggested that 75% of deaths following burn injury could be accounted for by inhalation injury but more recent cohort studies have suggested a decreasing mortality attributable to this cause.[2] A study of 13 patients suffering from isolated inhalation injury who required mechanical ventilation were all independent with activities of daily living at eight months. All were back to work, except for two who continued to need artificial airways.[27] 

The prevention of smoke injury is largely the prevention of fire but, if it does occur, then early warning is necessary. Smoke detectors save lives. An American study showed an 80% drop in fire related morbidity and mortality in a high-risk area, However, alarms only work if an effective battery is in situ and many people are lax about checking this. Even those less likely to respond so swiftly to an alarm, like the very young, the elderly, the infirm and those intoxicated by drugs or alcohol, may benefit.[28] Programmes to give away smoke alarms have not been randomised and American experience suggests that the batteries are not kept in order.[29] One study suggests that the use of an alarm which plays a recording of the parent's voice is more likely to wake a child than a conventional residential tone smoke alarm.[30] Initiatives to increase the uptake of alarms, such as incorporating them into child surveillance programmes, require further evaluation. Alarms which have a low 'nuisance' level (eg, which do not sound unnecessarily) seem to provide the most effective prevention.[31]

Deaths in children aged under 5 are sometimes associated with fire play and these are not usually prevented by smoke alarms, due to the behaviour of the children. Interventions to prevent fire play in this age group may be more successful.[32] 

The choice of household furnishings is important in terms of risk of emission of toxic gases on burning as well as combustibility. There are relevant laws about materials that may be used in the manufacture of furniture.

Further reading & references

  1. Fire Statistics, Great Britain, 2011-2012; Department for Communities and Local Government
  2. Sterner JB, Zanders TB, Morris MJ, et al; Inflammatory mediators in smoke inhalation injury. Inflamm Allergy Drug Targets. 2009 Mar;8(1):63-9.
  3. Rajpura A; The epidemiology of burns and smoke inhalation in secondary care: a population-based study covering Lancashire and South Cumbria. Burns. 2002 Mar;28(2):121-30.
  4. El-Helbawy RH, Ghareeb FM; Inhalation injury as a prognostic factor for mortality in burn patients. Ann Burns Fire Disasters. 2011 Jun 30;24(2):82-8.
  5. Rehberg S, Maybauer MO, Enkhbaatar P, et al; Pathophysiology, management and treatment of smoke inhalation injury. Expert Rev Respir Med. 2009 Jun 1;3(3):283-297.
  6. Rhoades R et al; Medical Physiology: Principles of Clinical Medicine, 2012
  7. The facts about cyanides; New York State Department of Health, 2012
  8. Demling RH; Smoke inhalation lung injury: an update. Eplasty. 2008 May 16;8:e27.
  9. Bishop S et al; Anaesthesia and intensive care for major burns, Contin Educ Anaesth Crit Care Pain (2012)
  10. Megahed MA, Ghareeb F, Kishk T, et al; Blood gases as an indicator of inhalation injury and prognosis in burn patients. Ann Burns Fire Disasters. 2008 Dec 31;21(4):192-8.
  11. Anseeuw K, Delvau N, Burillo-Putze G, et al; Cyanide poisoning by fire smoke inhalation: a European expert consensus. Eur J Emerg Med. 2013 Feb;20(1):2-9. doi: 10.1097/MEJ.0b013e328357170b.
  12. Reade MC, Davies SR, Morley PT, et al; Review article: management of cyanide poisoning. Emerg Med Australas. 2012 Jun;24(3):225-38. doi: 10.1111/j.1742-6723.2012.01538.x. Epub 2012 Feb 21.
  13. Smoke Inhalation; Health Protection Agency, 2005
  14. Smollin C, Olson K; Carbon monoxide poisoning (acute). Clin Evid (Online). 2010 Oct 12;2010. pii: 2103.
  15. Madnani DD, Steele NP, de Vries E; Factors that predict the need for intubation in patients with smoke inhalation injury. Ear Nose Throat J. 2006 Apr;85(4):278-80.
  16. Mohta M; What's new in emergencies, trauma and shock? Mechanical ventilation in trauma patients: A tight-rope walk! J Emerg Trauma Shock. 2014 Jan;7(1):1-2. doi: 10.4103/0974-2700.125630.
  17. Miller AC, Elamin EM, Suffredini AF; Inhaled anticoagulation regimens for the treatment of smoke inhalation-associated acute lung injury: a systematic review. Crit Care Med. 2014 Feb;42(2):413-9. doi: 10.1097/CCM.0b013e3182a645e5.
  18. Liodaki E, Kalousis K, Schopp BE, et al; Prophylactic antibiotic therapy after inhalation injury. Burns. 2014 Mar 11. pii: S0305-4179(14)00036-9. doi: 10.1016/j.burns.2014.01.022.
  19. Lafferty KA et al; Smoke Inhalation Inury, Medscape, Aug 2013
  20. Palmieri TL, Warner P, Mlcak RP, et al; Inhalation injury in children: a 10 year experience at Shriners Hospitals for J Burn Care Res. 2009 Jan-Feb;30(1):206-8.
  21. Lionelli GT, Pickus EJ, Beckum OK, et al; A three decade analysis of factors affecting burn mortality in the elderly. Burns. 2005 Dec;31(8):958-63. Epub 2005 Nov 2.
  22. Park GY, Park JW, Jeong DH, et al; Prolonged airway and systemic inflammatory reactions after smoke inhalation. Chest. 2003 Feb;123(2):475-80.
  23. Jaakkola JJ, Knight TL; The role of exposure to phthalates from polyvinyl chloride products in the development of asthma and allergies: a systematic review and meta-analysis. Environ Health Perspect. 2008 Jul;116(7):845-53. doi: 10.1289/ehp.10846.
  24. Mushtaq F, Graham CA; Discharge from the accident and emergency department after smoke inhalation: influence of clinical factors and emergency investigations. Eur J Emerg Med. 2004 Jun;11(3):141-4.
  25. Goh SH, Tiah L, Lim HC, et al; Disaster preparedness: Experience from a smoke inhalation mass casualty incident. Eur J Emerg Med. 2006 Dec;13(6):330-4.
  26. Cha SI, Kim CH, Lee JH, et al; Isolated smoke inhalation injuries: acute respiratory dysfunction, clinical Burns. 2007 Mar;33(2):200-8. Epub 2006 Dec 13.
  27. Chacko J, Jahan N, Brar G, et al; Isolated inhalational injury: Clinical course and outcomes in a multidisciplinary intensive care unit. Indian J Crit Care Med. 2012 Apr;16(2):93-9. doi: 10.4103/0972-5229.99120.
  28. Local Fire and Rescue Plan for Renfrewshire; Scottish Fire and Rescue Service, 2014-2017
  29. Marshall SW, Runyan CW, Bangdiwala SI, et al; Fatal residential fires: who dies and who survives? JAMA. 1998 May 27;279(20):1633-7.
  30. Smith GA, Splaingard M, Hayes JR, et al; Comparison of a personalized parent voice smoke alarm with a conventional residential tone smoke alarm for awakening children. Pediatrics. 2006 Oct;118(4):1623-32.
  31. Mueller BA, Sidman EA, Alter H, et al; Randomized controlled trial of ionization and photoelectric smoke alarm Inj Prev. 2008 Apr;14(2):80-6.
  32. Dougherty J, Pucci P, Hemmila MR, et al; Survey of primary school educators regarding burn-risk behaviors and fire-safety education. Burns. 2007 Jun;33(4):472-6. Epub 2007 Apr 30.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Laurence Knott
Current Version:
Peer Reviewer:
Dr Adrian Bonsall
Document ID:
2325 (v25)
Last Checked:
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