Smoke Inhalation Injury
Last updated 14th March 2018 - Tom Heaton
This is defined as “damage caused by breathing in the harmful gases, vapours and particulate matter contained in smoke”
This is a nice introductory video on the topic: https://www.youtube.com/watch?v=CB10airH5Sg
This is a nice introductory video on the topic: https://www.youtube.com/watch?v=CB10airH5Sg
Pathophysiology
Smoke is a product of combustion and thus is very variable in nature depending on the substance that is burning, and the conditions of the combustion.
It is a colloid formed by airborne solids, liquids and gases, mixed with entrained air.
Important components include:
Smoke inhalation injury has three main pathophysiological aspects to it:
Thermal Injury
Much of the upper airway has been evolved to allow effective humidification and warming of inspired gases, and thus is well designed for thermal transfer.
As such, the upper airways (nasal and oropharyngeal components) have a relatively high incidence of thermal injury, whilst thermal injury below the level of the vocal cords is rare.
Particulate matter deposition
This is the main mechanism of pulmonary injury in inhalational injury.
Particulate matter in the smoke, particular soot, can pass through the upper airway and enter the respiratory tract.
Part of the problem arises from the mechanical effects of particulate matter.
They can provide obstruction to airflow in the smaller airways leading to increased airway resistance.
Although the chemical nature of the molecules vary significantly, a wide number are very irritant and toxic to the airways.
This leads to an inflammatory response that involves leukocyte activation and the resulting local physiological disturbance and tissue injury.
The effects can include:
Systemic Toxicity
Asphyxiation can be a significant issue with smoke inhalation, though this will commonly lead to death at the scene.
Key mechanisms of asphyxiation are:
The mechanisms of carbon monoxide and hydrogen cyanide are slightly more complex.
Carbon monoxide exerts its toxicity through three main effects:
Hydrogen cyanide binds potently with the ferric ion in mitochondrial cytochrome a3 oxidase, structurally changing it and thus leading to cytotoxic hypoxia, with cells unable to respire aerobically.
Again, these effects can be seen to be synergistic with the other pathophysiological effects of smoke inhalation, particularly those of CO.
The physiological result of this will be a switch to anaerobic metabolism, which may manifest clinically as:
It is a colloid formed by airborne solids, liquids and gases, mixed with entrained air.
Important components include:
- Carbon (soot) - the visible part of smoke
- Carbon monoxide - formed from incomplete combustion of carbon (i.e. at lower oxygen levels)
- Hydrogen cyanide - formed from incomplete combustion of nitrogen-containing substances (e.g. synthetic materials - plastics, vinyls)
- Ammonia - formed from incomplete combustion of nitrogen-containing substances (i.e. at lower oxygen levels)
- Nitrogen oxides - form at high temperatures
- Carbon dioxide - can be asphyxiant in quantity
Smoke inhalation injury has three main pathophysiological aspects to it:
- Thermal injury
- Particulate matter deposition
- Mechanical obstruction
- Irritation/immune response
- Systemic toxicity (including asphyxiation)
Thermal Injury
Much of the upper airway has been evolved to allow effective humidification and warming of inspired gases, and thus is well designed for thermal transfer.
As such, the upper airways (nasal and oropharyngeal components) have a relatively high incidence of thermal injury, whilst thermal injury below the level of the vocal cords is rare.
Particulate matter deposition
This is the main mechanism of pulmonary injury in inhalational injury.
Particulate matter in the smoke, particular soot, can pass through the upper airway and enter the respiratory tract.
Part of the problem arises from the mechanical effects of particulate matter.
They can provide obstruction to airflow in the smaller airways leading to increased airway resistance.
Although the chemical nature of the molecules vary significantly, a wide number are very irritant and toxic to the airways.
This leads to an inflammatory response that involves leukocyte activation and the resulting local physiological disturbance and tissue injury.
The effects can include:
- Free oxygen radicals causing cellular injury
- Deposition of inflammatory casts in the airways
- Increased vascular permeability and oedema
- Impaired hypoxic pulmonary vasoconstriction
Systemic Toxicity
Asphyxiation can be a significant issue with smoke inhalation, though this will commonly lead to death at the scene.
Key mechanisms of asphyxiation are:
- Consumption of oxygen by the fire
- CO2
- Carbon monoxide
- Hydrogen cyanide
The mechanisms of carbon monoxide and hydrogen cyanide are slightly more complex.
Carbon monoxide exerts its toxicity through three main effects:
- Competition with O2 for transport on haemoglobin (Hb) - CO binds with 250 times greater affinity with Hb resulting in significantly impaired oxygen carrying capacity.
- Shift of the oxygen-haemoglobin dissociation curve to the left - the physicochemical impact on haemoglobin also affects the affinity of Hb for O2, increasing it and thus moving the curve to the left and impairing offloading of O2 at tissues.
- Competitive with O2 for binding at mitochondrial cytochrome oxidase - this impairs cellular utilisation of oxygen as well.
Hydrogen cyanide binds potently with the ferric ion in mitochondrial cytochrome a3 oxidase, structurally changing it and thus leading to cytotoxic hypoxia, with cells unable to respire aerobically.
Again, these effects can be seen to be synergistic with the other pathophysiological effects of smoke inhalation, particularly those of CO.
The physiological result of this will be a switch to anaerobic metabolism, which may manifest clinically as:
- Elevated lactate levels
- Reduced oxygen extraction (reduced arterio-venous difference)
- Metabolic acidosis (raised anion gap)
Epidemiology
Smoke inhalation is not necessarily a part of all burns, affecting around 2-30% of all flame burns, which only make up around 16% of all burn presentations.
Risk factors for smoke inhalation include:
The presence of a smoke inhalation injury increases the mortality of the burn by 3.6 times.
ARDS occurs in 20% of cases, but 76% will have some form of respiratory complication.
Risk factors for smoke inhalation include:
- Facial burns
- Enclosed space (they do not occur outdoors)
- Another death at the scene
- Loss of consciousness at the scene
The presence of a smoke inhalation injury increases the mortality of the burn by 3.6 times.
ARDS occurs in 20% of cases, but 76% will have some form of respiratory complication.
Assessment
Due to the emergency nature of these presentations, assessment will form part of an appropriate medical emergency approach e.g. A to E assessment as part of a ATLS response.
This will entail simultaneous treatment and assessment of potential life threatening problems, which will not be specifically described here.
In these presentations, other competing demands of urgency may include the burns or concomitant trauma.
Much of the concerns specific to he smoke inhalation relate to:
History
A focused history will gain details of the events surrounding the presentation.
This will provide information on the risk of smoke inhalation, as well as possible consequences e.g. the risk of hydrogen cyanide exposure.
Including:
Signs/Symptoms
With an A to E approach, a number of features will raise concern regarding smoke inhalation:
Features of CO poisoning may include:
Features of cyanide poisoning may include:
Investigations
Cyanide poisoning can be difficult to detect, partly because many of the other problems with smoke exposure can overlap e.g. CO poisoning.
Features on assessment may include:
This will entail simultaneous treatment and assessment of potential life threatening problems, which will not be specifically described here.
In these presentations, other competing demands of urgency may include the burns or concomitant trauma.
Much of the concerns specific to he smoke inhalation relate to:
- Airway - swelling and airway loss
- Breathing - insult to lungs impairing function
- Breathing - toxicity to oxygen delivery system (CO and cyanide)
History
A focused history will gain details of the events surrounding the presentation.
This will provide information on the risk of smoke inhalation, as well as possible consequences e.g. the risk of hydrogen cyanide exposure.
Including:
- Any loss of consciousness
- Drugs/alcohol?
- Deaths at the scene
- History of trauma e.g. fall trying to escape, RTC
- Nature of fire
- Residential/industrial
- Enclosed space/outdoors
Signs/Symptoms
With an A to E approach, a number of features will raise concern regarding smoke inhalation:
- Voice change e.g. hoarseness (worrying)
- Stridor (worrying)
- Cough
- Airway burns - nose, mouth
- Soot in secretions and airway
- Respiratory distress - work of breathing, RR, SpO2
- Chest signs
- Wheeze
- Crepitations
Features of CO poisoning may include:
- Depressed conscious level
- Neurological signs e.g. increased muscle tone
Features of cyanide poisoning may include:
- Neurological signs
- Confusion
- Seizures
- Depressed conscious level
- Cardiovascular signs
- Ischaemia
- Arrhythmia
- Cardiac arrest
Investigations
- Routine bloods - FBC, U&Es
- Arterial blood gas
- pO2 - assessing a-A gradient
- Lactate - can demonstrate aerobic respiration failure e.g. cyanide - severe poisoning can have levels >7mmol/l
- COHb levels - levels above 30% are severe poisoning
- Cyanide levels - can be taken but are analysed in limited locations and results will be too late to guide management.
- CXR - may be normal early in the presentation.
- ECG - may show ischaemia in CO poisoning
- Bronchoscopy - will require intubation and can form part of management as well as assessment (see below) but is considered goal standard for assessing smoke inhalation injury
Cyanide poisoning can be difficult to detect, partly because many of the other problems with smoke exposure can overlap e.g. CO poisoning.
Features on assessment may include:
- Elevated lactate - >7mmol/L
- Reduced arterio-venous oxygen difference
- Raised anion gap metabolic acidosis
Management
Again, the management of other problems (most commonly burns) will run alongside these specific inhalation consideration.
Airway
Airway loss can be very rapid in these patients, with oedema leading to rapid loss of airway calibre and adequate airflow.
Management here is supportive, with protection and maintenance of the airway whilst the oedema resolves.
This requires intubation and mechanical ventilation, and should be undertaken early to minimise the risks of difficulty posed by the increasing oedema.
However, not all patients will require this, and so assessment and risk analysis should be undertaken.
I&V is strongly indicated in:
Identifying those who are at risk of progressing to one of these complications is difficult, as patients may be seen very early in the pathophysiological process, and thus have no signs of compromise.
Nasendoscopy can provide additional information on the risk of developing complications, but must be done in an appropriate environment in case of complications e.g. airway deterioration.
Factors which correlate with a need for intubation include:
A number of options for intubation will be available including:
Specific considerations for technique include:
Breathing
High flow oxygen at as high an FiO2 as possible should be given.
This is the treatment of CO poisoning and will combat asphyxia.
Once intubated, lung protective ventilation strategies should be employed.
Bronchoscopy is the gold standard for diagnosing smoke inhalation injury (86% accurate).
It is therefore use to aid diagnosis and deliver treatment.
Finding on inspection of inhalation injury include:
Specific treatment of the inhalational injury is less evidence based, but may include:
The clinical evidence base is currently very small.
Carbon Monoxide
This should be considered in all patients.
SpO2 readings will be inaccurate in the presence of CO poisoning as it cannot distinguish between Hb carrying CO or O2.
Treatment involves optimising the displacement of CO from Hb.
Because of its high affinity, a high partial pressure of O2 is needed to compete - the highest FiO2 deliverable should be used.
Hyperbaric oxygen therapy, although theoretically advantage, is not clinically indicated.
Hydrogen Cyanide
The problems with treatment include the difficulty in diagnosis and the relative toxicity of some of the antidotes.
As such, if strongly suspected, treatment with the least toxic antidote is recommended in addition to optimal supportive care.
Airway
Airway loss can be very rapid in these patients, with oedema leading to rapid loss of airway calibre and adequate airflow.
Management here is supportive, with protection and maintenance of the airway whilst the oedema resolves.
This requires intubation and mechanical ventilation, and should be undertaken early to minimise the risks of difficulty posed by the increasing oedema.
However, not all patients will require this, and so assessment and risk analysis should be undertaken.
I&V is strongly indicated in:
- Cardiac arrest
- Respiratory arrest/compromise
- Depressed conscious level
- Impending or complete airway obstruction
Identifying those who are at risk of progressing to one of these complications is difficult, as patients may be seen very early in the pathophysiological process, and thus have no signs of compromise.
Nasendoscopy can provide additional information on the risk of developing complications, but must be done in an appropriate environment in case of complications e.g. airway deterioration.
Factors which correlate with a need for intubation include:
- Vocal cord (true or false) oedema on nasendoscopy - highly predictive
- Soot in the oral cavity
- Facial burns
- Body burns
A number of options for intubation will be available including:
- Rapid sequence induction
- Gas induction
- Awake fibreoptic intubation
- Clinical urgency e.g. peri-arrest
- Fasting status
- Features or difficult intubation (in addition to acute factors)
- Degree of cooperation
Specific considerations for technique include:
- Use of an uncut tube - significant facial swelling can occur after intubation, engulfing small tube.
- Need for smaller tubes
- Low pressure cuffs
- Suxamethonium - can be used as relaxant if under 24 hours after burn
- Plans for difficult airway
- Stated plans A, B, C etc
- Use of algorithm support e.g. DAS
- Anticipate the worst and be prepared!
Breathing
High flow oxygen at as high an FiO2 as possible should be given.
This is the treatment of CO poisoning and will combat asphyxia.
Once intubated, lung protective ventilation strategies should be employed.
- 6ml/kg tidal volumes
- PEEP
- Limiting peak inspiratory pressures
- Permissive hypercapnia
Bronchoscopy is the gold standard for diagnosing smoke inhalation injury (86% accurate).
It is therefore use to aid diagnosis and deliver treatment.
Finding on inspection of inhalation injury include:
- Soot in airways
- Erythema
- Ulceration
Specific treatment of the inhalational injury is less evidence based, but may include:
- Aerosolized heparin
- Aerosolized acetylcholine
The clinical evidence base is currently very small.
Carbon Monoxide
This should be considered in all patients.
SpO2 readings will be inaccurate in the presence of CO poisoning as it cannot distinguish between Hb carrying CO or O2.
Treatment involves optimising the displacement of CO from Hb.
Because of its high affinity, a high partial pressure of O2 is needed to compete - the highest FiO2 deliverable should be used.
Hyperbaric oxygen therapy, although theoretically advantage, is not clinically indicated.
Hydrogen Cyanide
The problems with treatment include the difficulty in diagnosis and the relative toxicity of some of the antidotes.
As such, if strongly suspected, treatment with the least toxic antidote is recommended in addition to optimal supportive care.
- Hydroxocobalamin - least toxic. 5g over 15 min.
- Sodium thiosulphate
Links & References
- Gill, P. Martin, R. Smoke inhalation injury. BJA Education. 2015. 15(3):143-148 https://academic.oup.com/bjaed/article/15/3/143/279223
- Nickson, C. Smoke inhalation. LITFL. 2014. https://lifeinthefastlane.com/ccc/smoke-inhalation/
- Lafferty, K. Smoke inhalation injury. Medscape. 2014. https://emedicine.medscape.com/article/771194-overview
