Inhalation Injury

Definition

Inhalation injury is damage to the respiratory tract caused by breathing in heat, smoke particles, or chemical irritants. It is conventionally divided into three components, which can occur separately or together and which have different time courses and different treatments — the reason a single label is unhelpful without specifying which is present.

Pathophysiology

Why the upper airway swells late

The upper airway is efficient at absorbing heat, which protects the lungs but concentrates thermal injury in the pharynx and larynx. Oedema develops progressively as inflammatory fluid accumulates, and is compounded by the large-volume fluid resuscitation given for any associated skin burn. A patient whose voice is normal on arrival may have significant swelling hours later — and once the airway narrows, resistance rises steeply, so deterioration is abrupt rather than gradual.

What happens below the vocal cords

Smoke carries hundreds of chemical species adsorbed onto particles that carry them deep into the airways. They damage the epithelium and its cilia, so clearance fails at exactly the moment secretion increases. Sloughed lining, fibrin and mucus form casts that obstruct airways — a distinctive feature of this injury and the reason airway clearance matters so much. Surfactant is disrupted, permeability rises, and in severe cases the picture progresses to acute respiratory distress syndrome.¹

Carbon monoxide and cyanide

Carbon monoxide binds haemoglobin with far greater affinity than oxygen, so the blood carries less oxygen while pulse oximetry continues to read normally — a dangerous combination, because the number that would normally raise the alarm does not. Cyanide, released by burning synthetic materials, blocks cellular oxygen use and produces a profound metabolic acidosis. Both are treated at the scene and in the emergency department, and both are missed if not specifically considered.

Co-morbidities

• Cutaneous burns — frequently coexist, and the combination is considerably more dangerous than either alone; chest wall burns can also restrict breathing mechanically.
• Pre-existing lung disease — COPD and asthma both worsen the outcome and complicate the recovery.
• Smoking — impaired baseline clearance before the injury even begins.
• Pneumonia — a common secondary complication, particularly in the ventilated patient.
• ICU-acquired weakness — near-inevitable after a prolonged admission; see ICU-acquired weakness.
• Post-traumatic stress and anxiety — very common after fires, and a major determinant of how rehabilitation goes.
• Airway stenosis or tracheomalacia — late consequences of prolonged intubation or tracheostomy.

Prevalence

Inhalation injury complicates a substantial minority of major burn admissions, and it is the single strongest predictor of mortality in burns — its presence markedly increases the risk associated with any given burn size. It also occurs without any skin burn at all, in industrial chemical exposures, confined-space incidents and house fires where the person escaped the flames but not the smoke. Deaths from fire are more often caused by what was inhaled than by thermal injury to the skin.²

Causes

• House and building fires — particularly in an enclosed space, and especially where the person was unconscious, intoxicated or trapped.
• Steam — carries far more heat than dry air and can injure below the cords, unlike most dry heat.
• Industrial chemical exposure — chlorine, ammonia, oxides of nitrogen, hydrogen sulphide, phosgene.
• Confined-space incidents — silos, tanks, mines, where gases accumulate.
• Household chemical mixing — bleach with ammonia-containing products releases chloramine gas; a recurring domestic cause.
• Bushfire smoke — a significant exposure for firefighters and for people in affected communities, with different, lower-intensity but more prolonged characteristics.
• Explosions and blast injury — combining inhalation with direct pulmonary blast trauma.

Symptoms

Immediate features

• Hoarseness, a changed voice, or a barking cough — the most important early signs of laryngeal injury.
• Stridor, a harsh noise on breathing in — indicating significant narrowing and requiring immediate action.
• Sooty sputum, soot around the nose or mouth, and singed nasal hairs.
• Burns to the face or neck, particularly with a history of an enclosed fire.
• Cough, chest tightness, wheeze and breathlessness.
• Headache, confusion, drowsiness or collapse — suggesting carbon monoxide or cyanide.

The delayed picture

Deterioration over the following hours to days is the rule rather than the exception in significant injury: worsening breathlessness, rising oxygen requirement, productive cough with black or grey casts, and in severe cases progression to respiratory failure. This is why observation is mandatory after a meaningful exposure even when the initial assessment is reassuring.

Warning signs

Diagnosis

The history is the strongest indicator

Enclosed space, prolonged exposure, loss of consciousness, entrapment, and the presence of facial burns or soot all raise the probability substantially. There is no test that reliably rules the injury out early, so history and serial assessment do most of the work.

Assessment

• Bronchoscopy — the reference standard, allowing direct grading of mucosal injury below the cords, and used both diagnostically and therapeutically to remove casts.
• Carboxyhaemoglobin level — essential, because pulse oximetry is falsely reassuring in carbon monoxide poisoning.
• Arterial blood gas with lactate — a markedly raised lactate suggests cyanide toxicity.
• Chest imaging — usually normal at presentation; a normal film does not exclude significant injury.
• Serial airway assessment — voice, stridor, swallowing and work of breathing, repeated rather than recorded once.
• Lung function later — to characterise the residual obstructive or restrictive deficit during recovery.

Management

The acute phase

Early intubation is the decision that most often determines outcome, and it is made on the trajectory of swelling rather than on the current appearance — a threshold deliberately set low, because a delayed airway in this situation is extremely difficult to secure. High-flow oxygen is given to all patients with suspected carbon monoxide exposure, hydroxocobalamin where cyanide is suspected, and fluid resuscitation is titrated carefully because both under- and over-resuscitation worsen lung injury. Lung-protective ventilation is used where mechanical ventilation is required.

Airway clearance and nebulised therapy

Casts and sloughed mucosa are the specific problem of this injury, and clearing them is central to management. Humidification, regular suction and bronchoscopic removal are standard. Nebulised heparin combined with N-acetylcysteine is used in many burns centres on the reasoning that it reduces cast formation, though the evidence base is limited and the practice is not universal. Bronchodilators are used for the airway hyper-reactivity that commonly follows.³

The long recovery

Prolonged ventilation, tracheostomy, repeated surgery for associated burns, and a long period of immobility are common in severe injury. Rehabilitation runs alongside all of it rather than beginning afterwards.

Living with the aftermath

Breathing that takes months to settle

Persistent cough, wheeze, breathlessness on exertion and airway hyper-reactivity are common for months, and some patients are left with a permanent obstructive deficit or with bronchiectasis. Improvement continues over a longer period than most people expect, which is worth saying explicitly.

The psychological injury

Fires are traumatic events, and post-traumatic stress, nightmares, avoidance and anxiety are common — sometimes more limiting than the lung damage. Breathlessness and panic reinforce each other particularly strongly here, and the psychological component should be asked about routinely rather than waiting for it to be raised.

Returning to work

Where the exposure was occupational, return to work involves both physical capacity and the question of ongoing exposure risk. Firefighters, industrial workers and emergency responders need a specific assessment rather than a general clearance.

Prognosis

Mild injury usually resolves completely within weeks. Moderate to severe injury carries a considerably worse outlook, especially combined with a large cutaneous burn, and survivors may be left with fixed airflow obstruction, bronchiectasis, airway stenosis or reduced exercise capacity. Most functional recovery occurs over the first six to twelve months, but improvement continues beyond that with rehabilitation. Carbon monoxide poisoning can leave delayed neurological effects — memory, concentration and mood — that appear days to weeks later and are frequently attributed to something else.

Role of the physiotherapist

In the acute phase

Airway clearance is the priority, targeting the casts and retained secretions that define this injury: humidification, positioning, manual techniques where tolerated, suction, and assisted cough. Work closely with the medical team on timing around bronchoscopy. Where chest wall or facial burns restrict movement, positioning and early splinting matter for both respiratory function and later contracture. Early mobilisation, even in the ventilated patient, is the intervention with the most durable effect.

Assessment through recovery

Track exercise capacity with a field walking test, breathlessness on a validated scale, cough effectiveness, sputum volume and character, and the musculoskeletal consequences of burns and immobility. Reassess repeatedly — the trajectory over months is the useful information.

Rehabilitation

Combine aerobic and resistance training, progressing on symptoms and accounting for burn healing, graft sites, contractures and pain. Where a persistent obstructive deficit remains, pulmonary rehabilitation is appropriate. Expect deconditioning and ICU-acquired weakness to dominate the early picture rather than the lung injury itself.

Breathlessness, anxiety and trauma

Breathing pattern disorders are common after this injury, and the overlap with post-traumatic anxiety is substantial. Breathing control, pacing and graded exposure to activity all help; recognising when psychological input is needed, and saying so, is part of the role. See managing breathlessness.

Part 1 · References

1. Walker PF, Buehner MF, Wood LA, et al. Diagnosis and management of inhalation injury: an updated review. Crit Care 2015;19:351.
2. Colohan SM. Predicting prognosis in thermal burns with associated inhalational injury: a systematic review of prognostic factors in adult burn victims. J Burn Care Res 2010;31(4):529–539.
3. 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;42(2):413–419.

References are numbered in citation order (Vancouver/BMJ style) and were current at the time of writing. Guidelines are living documents — verify against the latest version before clinical use.