Assessment and Management Of Airway Burns

The term “inhalational injury” has been used to describe the aspiration of toxic products of combustion, but also more generally any pulmonary insult associated with a burn injury. Patients with cutaneous burns are two to three times more likely to die if they also have lower airway burns. Death may be a direct result of lung injury but is usually due to the systemic consequences of such injury. It may be impossible to distinguish lung injury caused at the time of the burn directly to the lungs by a burn from injury due to the systemic consequences of the burn. Inhalation injury, age, and burn size are the three most commonly cited predictive factors for prolonged ventilator dependence, hospital stay, and death in burn patients. The injuries can generally be divided into three classes:
- thermal injury (restricted to upper airway structures except in cases of blast injury or steam inhalation),
- local chemical irritation throughout the respiratory tract, and
- systemic toxicity (eg, inhalation of toxins such as carbon monoxide or cyanide).

In the clinical setting, diagnosis of inhalation injury is usually a subjective decision based on a combination of history and physical exam, and confirmed by diagnostic studies (eg, fiberoptic bronchoscopy).
History includes -
mechanism of exposure, (eg, flame, electricity, blast injury, steam, or hot liquid)
quality of inhaled irritants (eg, house fire, industrial toxins), and
duration of exposure eg, trapped in an enclosed space or
conditions that limit avoidance behavior such as intoxication, loss of consciousness, or physical disability).

Physical exam can provide
an estimate of the intensity of exposure and includes findings such as
evidence of exposure of the respiratory tract to extreme heat (facial burns or singed facial or nasal hair),
soot deposited on the face or carbonaceous sputum,or
early manifestations of respiratory compromise such as airway obstruction by edema or parenchymal damage.

Defining diagnostic criteria for inhalation injuries is made difficult by the extreme heterogeneity of clinical presentation as evaluated therefore, diagnosis is with a high index of suspicion of airway burns in patients with one or more of the warning signs.

Warning signs of airway burns - Suspect airway burn if:
• Burns occurred in an enclosed space
• Stridor, hoarseness, or cough
• Burns to face, lips, mouth, pharynx, or nasal mucosa - Singed nasal hairs; red, tender oral membranes; or obvious intraoral or pharyngeal burns indicate likely airway burn.
• Soot in sputum, nose, or mouth
• Dyspnoea, decreased level of consciousness, or confusion
• Hypoxaemia (low SpO2 or PaO2) or increased carbon monoxide levels (>2%)
Onset of symptoms may be delayed

Mechanisms of pulmonary insult after lower airway burns
• Mucosal inflammation • Ciliary paralysis
• Mucosal burn • Reduced surfactant
• Bronchorrhoea • Obstruction by debris
• Bronchospasm • Systemic inflammatory response

The pathophysiology of airway burns is highly variable, depending on the environment of the burn and the incomplete products of combustion. The clinical manifestations are often delayed for the first few hours but are usually apparent by 24 hours. Airway debris—including secretions, mucosal slough, and smoke residue—can seriously compromise pulmonary function.

Management of Airway burns—key clinical points
• Restricting fluids increases mortality
• If in doubt, intubate
• Give 100% oxygen until carbon monoxide toxicity excluded
• Ventilatory strategies to avoid lung injury (low volume or pressure)
• Aggressive airway toilet
• Early surgical debridement of wounds
• Early enteral feeding

There is no specific treatment for airway burns other than ensuring adequate oxygenation and minimising iatrogenic lung insult. Prophylactic corticosteroids or antibiotics have no role in treatment. Studies on Beta 2 agonists, Nebulized Heparin,Tocopherol, Inhaled NO are also inconclusive or lack sufficient data.

Control of the airway, by endotracheal intubation, is essential before transporting any patient with suspected airway burn. Rapid fluid administration, with inevitable formation of oedema, may lead to life threatening airway compromise if control of the airway is delayed. Endotracheal intubation before oedema formation is far safer and simpler. Oxygen (100%) should be given until the risk of carbon monoxide toxicity has been excluded, since high concentrations of oxygen will clear carbon monoxide from the body more rapidly than atmospheric concentrations. Importantly, carbon monoxide toxicity may result in a falsely elevated pulse oximetry saturation.

Airway burns are associated with a substantially increased requirement for fluid resuscitation. Reducing the fluid volume administered, to avoid fluid accumulation in the lung, results in a worse outcome. Invasive monitoring may be required to guide fluid administration, especially with failure to respond to increasing volumes of fluid. Fluid administration should not be guided by calculated fluid requirements alone.Adequate oxygen delivery to all the tissues of the body is essential to prevent multi-organ failure.

Aggressive airway toilet is essential. Early surgical debridement, enteral feeding, mobilisation of the patient, and early extubation are desirable. Antibiotics should be reserved for established infections and guided by regular microbiological surveillance.

Several ventilatory strategies have been proposed to improve outcome following airway burns. Adequate systemic oxygenation and minimising further alveolar injury is the primary clinical objective. Prolonging survival will permit spontaneous lung recovery.