Sher Mohammad and authors look at smoke inhalation affecting airways, with a brief focus on carbon monoxide and hydrogen cyanide poisoning
Smoke inhalation injury is a major determinant of morbidity and mortality in a fire victim. It is a complex multifactorial injury affecting the airway, however in a short time it can become a complex life-threatening systemic disease affecting every organ in the body.
Up to 30% of all flame burns presentations may suffer with smoke inhalation injury and in higher proportions if facial burns are present. It carries a high mortality and is the most common cause of death at the incident of fire. Inhalation injury increases the risk of death from a burn many times. Respiratory complications are more than 70% and the risk of ARDS is 20%. Patients younger than 10 years and older than 65 are at risk. Likewise, physical or cognitive disability will contribute towards mortality.
In order to understand the pathophysiology, clinical presentation and the management of smoke inhalation injury, we will briefly mention the components of smoke first. For the sake of completion, we will briefly explain carbon monoxide and cyanide poisoning as well.
Components of smoke
Smoke is a product of combustion, which is composed of air borne solids, liquid particles and gases that are mixed with entrained air. The composition of smoke depends on materials present, the availability of O2 and the nature of combustion. The amount of smoke is less if the temperature generated is high and the O2 is in abundance. The products that are produced as a result of flame burn include chemicals that will cause chemical damage to the respiratory tract. Other products include CO and HCN, which results in systemic toxicity. Here is a list of chemicals/poisons produced as a result of flame burns.
- Aldehydes are produced from wood and paper.
- NO2 is produced from fabric.
- H2, Cl2, and SO2 are produced when rubber is burnt.
- N2 containing material will yield NH3.
- Synthetic materials such as furnishings, plastics and vinyl will produce hydrogen cyanide.
- NH3 will combine with H2O to form alkali e.g. NH4 OH
- H2, Cl2, and SO2 will combine with H2O to form acids e.g.HCl and H2SO4
Alkalis and acids will result in chemical burns of the throat, larynx and trachea. Hydrogen cyanide and CO are known asphyxiants and result in carbon monoxide and cyanide poisoning.
Smoke inhalation injury is caused by the inspiration of steam, superheated gases, or toxic, often incomplete products of combustion.
So smoke inhalation results in three physiological types of injury
- Thermal injury predominantly to the upper airway:
The heating capacity of steam is 4000 times that of hot dry air and thus causes tissue damage, even with momentary contact. Major pathophysiological change is the development of oedema in the respiratory tract. The upper airway including tongue, throat and glottis could be injured by superhot steam, of these the most fatal is the glottic oedema.
- Chemical injury to the upper and lower respiratory tract: Particles up to 10µm size will be entrained in nostrils and nasopharynx while particles of 1-2µm will reach up to alveoli.
The toxic chemicals can lead to chemical injury causing bronchoconstriction. Proteolytic elastases damage the lung parenchyma leading to the release of inflammatory mediators which increase the trans-vascular flux of fluids resulting in pulmonary oedema and atelectasis.
- Systemic effects of toxic gases such as CO and HCN: Early deaths in fire are predominantly due to hypoxia, which results from a lethal synergistic effect of low O2 levels (due to massive O2 consumption during combustion) and inhalation of high concentrations of CO and HCN (both result in inability of O2 consumption at mitochondrial level).
Systemic effects happen as a result of CO ad HCN poisoning leading to hypoxia.
Mechanism of systemic toxicity
If the victim of burns is in a closed space, the concentration of O2 could be as low as 10%. Products of incomplete combustion cause hypoxia, the main toxic compound in fire deaths is carbon monoxide (80% of fire deaths by fire gases). CO is a the main culprit which causes hypoxia by three mechanisms. Firstly, CO attaches itself to Hb more avidly(250 times) as compared to O2. Secondly, it shifts the Hb-O2 curve to the left decreasing unloading of O2 to the tissues. Thirdly, it inhibits the binding of O2 with cytochrome oxidase, mitochondrial enzyme needed in cellular utilization of O2.
Smoke inhalation is one of the most common cause of cyanide poisoning which is 20 times more toxic than CO. Hydrogen cyanide is a colourless gas with a bitter almond odour which cannot be detected by humans easily.
Hydrogen cyanide combines with Fe ion in cytochrome a-3 oxidase in mitochondria with high affinity, and so impairs cellular respiration by making structural changes in enzyme. That results in anaerobic metabolism and leads to high lactate levels (7-10mmols) and O2 consumption is seriously impaired. Both CO and cyanide have synergistic effect.
Clinical presentation of smoke inhalation injury
The clinical presentation of smoke inhalation injury could be remembered by referring to the acronym ”ASPHYXIATION”
|A Apparent burns on face, lips and tongue
S SOB and stridor
P Productive cough
H High pitched sound
Y Younger < 10 and older>65 are at high risk
X X-ray chest(normal does not exclude damage)
I Intoxication with acids and alkalis cause chemical burns
A ARDS 20%
T Thermal damage(superhot steam cause glottis oedema which is fatal)
I Increased work of breathing leads to respiratory failure
O O2 saturation<94% would be misleading(co-oximeter needed)
N Nasal endoscopy will assess the damage
Management of smoke inhalation injury
Airway management is important before glottic and laryngeal oedema happens. Mucus production and inactivation of surfactant leads to risk of sputum retention, atelectasis, infection and mechanical plugging. While managing the respiratory support, patients with smoke inhalation injury are susceptible to pulmonary barotrauma.
Acetyl cysteine and heparin are aerosolised regimens used in patients with inhalation injury. Acetyl cysteine is mucolytic and diminishes airway cast formation. Heparin is a potent activator of anti-thrombin Ⅲ and so leads to thrombus inactivation and decreases airway casts.
Hydoxocobalamine is probably the safest antidote for patients with concomitant inhalation and burn injury. It works by binding to HCN to form non-toxic cyanocobalamine, which is then excreted by the kidneys. Adult dose is 5gm over 15 minutes, may be repeated once given over 15 minutes. Paediatric dose is 70 mg Kg over 15 minutes, may be repeated once to 140mg.Kg given over 15 minutes.
Na-thiosulphate is another antidote that will convert cyanide to thiocyanates which are excreted by kidneys. Adult dose is 12.5gm to be given IVI over 10 minutes. Experts should be consulted for paediatric patients.
The management could be remembered with the acronym ”RE-OXYGENATION”
|R Resuscitate with standard monitors
RSI with ketamine+rocuronium, volatile induction or awake FOI
E ETT uncut(facial oedema develops later) and low pressure cuff
O O2 initially 100%(hyperbaric is controversial)
X X133 V/Q scan considered
Y Young victims managed by paediatricians
G Gravity dependant postural drainage(contraindicated in facial oedema)
E Exogenous surfactant is helpful
N Nebulised heparin 5000 iu/ml 0.9% NaCl 4 hourly for 5 days
Nebulised 20% acetylcysteine 3 ml 4 hourly
Nebulised salbutamol 2.5-5.0 mg 4 hourly
A Antidote e.g hydroxocobalamine
T Tracheostomy will increase infection risk
Trauma to lungs avoided(use protective ventilation strategies)
I Investigations: lactate> 7 mmol/L ,sensitive for HCN poisoning
CO and Met-Hb
O Optimise fluid status(Parkland or other formula)
N Nursing care and prevention of infection
Nutritional support as it is hypermetabolic state
Historically, cyanide has been used for mass suicide and by the Nazis for genocide. Chronic exposure can happen in those who eat almond, lima beans and seeds of apple and apricot. Eating improperly processed cassava can have similar effect. Chronic toxicity can also happen in those working in industries like metal polishing, textile and plastics. It can happen as a result of contact with chemicals used in photography. Exposure to certain insecticides, cigarette smoking and intake of sodium nitroprussides can cause chronic poisoning.
Low dose exposure can result in generalised weakness, dizziness, vertigo and confusion. Chronic low dose exposure can also cause hypothyroidism, miscarriages and mild hepato-renal derangements.
Inhaled HCN can result in coma, seizures, apnoea and cardiac arrest in a matter of a few seconds. Mild toxicity results in vomiting, tachycardia and hypertension. Severe toxicity will result in seizures, coma, bradycardia, hypotension and cardiac arrest.
The clinical presentation of acute ”CYANIDE” poisoning will be as follows
|C Cephalgia, confusion, convulsions
Y Yielding appropriate results: Blood cyanide levels
Mild toxicity0.5-1.0 mg/L
Moderate toxicity 1.0-2.0 mg/L
Severe toxicity 2.0-3.0 mg/L
A Acidosis( high anion gap)
N Nervous system(altered mental status)
I Increased lactate> 7 mmol/L sensitive for HCN poisoning
D Dysrhythmias leading to asystole
E Eyes(fixed dilated pupils)
Carbon monoxide Poisoning
Remember ”CARBON MONOXIDE”
|C Clinical toxicity 20 tissue effects
A Appearance is blush
R Red or cherry red (2-3%)
B Blisters on skin
O Ophthalmic: blurred vision
N Nausea and vomiting
M Malaise with no fever
O O2-Hb curve shifted left
N Nervous system: ataxia,confusion,dizziness,drowsiness
O Oedema of lungs
X X-ray/imaging(bilateral changes to Globus pallidus)
I Incontinence of faeces
D Dexterity diminished
E Elevated CO-Hb and coma are fatal
A Airway managed with an uncut ETT and FiO2 of 100%
B Bronchoscopic washout to remove casts and do microbiology of alveolar fluid
C Cyanide toxicity managed earlier.
D Drugs ( antidotes) considered
E Exogenous surfactants are useful
F Fluid management
G Gravity dependant postural drainage as appropriate
H Hyperbaric O2 to treat CO toxicity (controversial)
I IPPV →avoid barotrauma
Dr.Sher Mohammad1, Dr.Hasan Qayyum2, Dr. Rajeev Singh3, Dr.Noman Bin Yahya4
1.Consultant anaesthetist STH NHS FT,
2.Consultant Emergency Department, Sheikh Shakhbout Medical City, Abu Dhabi UAE
3. MTI Anaesthetics STH NHS FT
4. Junior Clinical fellow, Emergency Care Centre, Rotherham General Hospital
Correspondence Email: email@example.com
Fire statistics Great Britain 2010-2011,availabe from
Lafferty KA Bonhomme K Martenez CVet al.Smoke inhalation,2008.
Available from http://emedicine.medscape.com/article/771194-overview
Demling RH.Smoke inhalation lung injury.Eplasty 2008
Available from http://www.ncbi.nim.nih.gov/pubmed/18552974
Khan AA Rawlins J Shenton AF Sharp DT.The Bradford Burns Study
Emergency Med J;24:564-6
Toon MH Maybauer MO Greenwood JE Maybauer DM Fraser JF
Critical Care Resusc 2010;12:53-61
Ernest A Zibrank JD. Carbon monoxide poisoning N.Engl J Medicine 1998;339:1603-8