Inhalation injury

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 the year ending June 2024, there were 233 fire-related fatalities in 220 fatal fires in England, compared with 286 fire-related fatalities in 266 fatal fires in the previous year.¹

Systemic effects of inhalation injury occur both indirectly from hypoxia or hypercapnia resulting from loss of pulmonary function and systemic effects of proinflammatory cytokines, as well as directly from metabolic poisons such as carbon monoxide and cyanide. Both present with nonspecific clinical symptoms including cardiovascular collapse.²

How common are inhalation injuries? (Epidemiology)

US data from the Burns Registry suggests the percentage of patients with only smoke inhalation injury is 1.1% and with smoke inhalation injury plus burns almost 10%.³

Smoke inhalation injury markedly increases the morbidity and mortality after burns. The classic study of 1987 predicted mortality among patients with burns was 20% higher when inhalation injury was present, and if secondary pneumonia developed, mortality was 60% higher.⁴

Risk factors

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.

The increased use of electronic (e)-cigarettes has resulted in morbidity and mortality due to acute lung injury - e-cigarette or vaping use-associated lung injury (EVALI).⁵

Mechanism of injury

Smoke inhalation injury leads to airway lumen narrowing or blockage through bronchospasm, increased mucus production, formation of airway casts, and increased airway blood flow.

Augmented airway blood flow, in particular, plays a critical role in the pathogenesis of acute lung injury after smoke inhalation.⁶

A marked increase in bronchial blood flow occurs immediately following inhalation injury, resulting in lung oedema and pulmonary transvascular fluid movements. Moreover, increased plasma exudates in the airway play a role in the formation of obstructive casts, which diminish pulmonary function, and may cause atelectasis, pneumonia, and barotrauma respiratory distress.

General assessment⁷

• 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 smouldering 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.

Diagnosing inhalation injuries (investigations)⁸

• 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 oxyhaemoglobin accurately, gives a more accurate assessment. Smoke inhalation should be diagnosed by the presence of an elevated carboxyhaemoglobin level. A level greater than 10% of total haemoglobin is diagnostic.⁹

• Renal function tests 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 poisoning is not a common consequence of smoke inhalation but should be suspected if there is profound metabolic acidosis and no other explanation.⁹

Management of inhalation injuries¹⁰¹¹

• 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 and all patients with suspected or confirmed smoke inhalation should receive high-flow oxygen until the carboxyhaemoglobin is less than 10% of total haemoglobin.⁹ 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.

• If there is a significant risk of intubation being required it should be performed early or 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.

• Currently there are no consensus guidelines to guide decision making for inhalation injuries. Suggested guidelines can be found in the literature.⁶

• Inhalation injury is not always associated with an increased requirement for fluids unless other burn 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 haemodynamic parameters of the individual patient.

• All smoke inhalation victims should receive routine thromboprophylaxis according to local hospital protocols.⁹

• Carbon monoxide intoxication should be treated with oxygen, and cyanide with hydroxocobalamin.²

Admission policy¹¹

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.

Complications of inhalation injuries

Complications from inhalation injury can be categorised by anatomical levels and by the mechanism of injury - direct thermal injury to the upper airways or chemical injury to the subglottic region and tracheobronchial tree.¹²

People with inhalation injury are at increased risk for pneumonia (the leading cause of death) and multisystem organ failure.¹³ The associated complications vary with the level of injury and are also affected by intubation, infection and chronic inflammation. In addition, the complications from injury may be acute or delayed.

Pneumonia and airway obstruction are early complications of inhalation injury and have been well described in the literature.

Prognosis

Authors have reported an estimated 20% increase in mortality with burns and concomitant inhalation injury; mortality rate increases to 60% with the development of pneumonia.¹² They found inhalation injury and pneumonia to be independent risk factors for mortality.

Prevention of inhalation injuries¹⁴

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.

Programmes to give away smoke alarms have not been randomised and American experience suggests that the batteries are not kept in order. 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.

Deaths in children aged under 5 years 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.

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.