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:
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:
Particulate matter deposition
Systemic toxicity (including asphyxiation)
Any smoke inhalation injury could include aspects of these to different degrees.
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
In many cases the results can be impaired lung mechanics and V/Q matching.
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
Conversion of oxygen to CO2 by the process of combustion is a simple case of depletion of inspired oxygen that is required. 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.
Altogether, this results in an additive impairment of oxygen delivery from lungs to cellular utilisation, leading to tissue hypoxia.
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:
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:
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.
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:
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
Deaths at the scene
History of trauma e.g. fall trying to escape, RTC
Nature of fire
Signs/Symptoms With an A to E approach, a number of features will raise concern regarding smoke inhalation:
Voice change e.g. hoarseness (worrying)
Airway burns - nose, mouth
Soot in secretions and airway
Respiratory distress - work of breathing, RR, SpO2
Features of CO poisoning may include:
Depressed conscious level
Neurological signs e.g. increased muscle tone
Features of cyanide poisoning may include:
Depressed conscious level
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
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:
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
If a patient is being transferred e.g. to a burns centre, then the risk of deterioration during transfer should be factored in.
A number of options for intubation will be available including:
Rapid sequence induction
Awake fibreoptic intubation
The risk-benefit ratio of each will be affected by factors including:
Clinical urgency e.g. peri-arrest
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
Limiting peak inspiratory pressures
Evidence for this is minimal but sensible in the context of the pathophysiology.
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
Washout of the physical debris may reduce the inflammatory response and subsequent injury, as well as obstructive component. This is therefore done early.
Specific treatment of the inhalational injury is less evidence based, but may include:
These treatments theoretically work by reducing the development of airway casts (as an anticoagulant and mucolytic respectively) and therefore the respiratory complications/adverse features that arise as part of this. 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.