Airway Management in Burn Patients

Key Points

• The priorities and approaches to airway management in the burn patient are different in the acute, subacute, and chronic phases of burn injury.

• Airway edema results from thermal and inhalation injury, and rapidly increases with fluid resuscitation.

• Induction drugs that cause vasodilation or decreased cardiac output can result in hemodynamic instability in burn patients, even though the dose requirements may be augmented.

• Succinylcholine is contraindicated following the initial 48 to 72 hours after injury due to life-threatening hyperkalemia risk. Succinylcholine can be administered again once the patient’s wounds have healed, mobility and muscle tone have returned, and critical illness has resolved.

• Face burns, neck burns, and airway edema can make mask fit and mask ventilation very difficult.

• Postburn contractures can restrict mouth opening and limit neck flexion in patients during the chronic phase of burn injury. A thorough airway exam—particularly observing circumoral and pharyngeal tightness and wound contractures—is important in airway management.

• Cuffed endotracheal tubes (ETTs) are recommended in pediatric burn patients, as airway and ventilatory mechanics can quickly change during the acute phase of burn injury and exchanging the endotracheal tube to maintain adequate ventilation poses significant risk.

• Identification of burn patients at high risk for failed extubation and difficult reintubation is critical so that the appropriate personnel and equipment are present and an interdisciplinary care plan is in place, should extubation fail.

Introduction

Burn injury results in approximately 40,000 hospitalizations and over 3000 fire and smoke inhalation deaths each year in the United States. Airway evaluation of burn patients assesses the extent of both direct burn injury and inhalation airway injury, the latter of which can present insidiously. Airway management of burn patients presents unique complexity, because the burn patient’s airway is continuously evolving from the time of injury throughout the period of recovery, and the challenges faced during the acute, subacute, and chronic periods postinjury are uniquely different.

Burn Injury and the Airway

The severity and prognosis of burn injury are typically assessed by estimating the total body surface area (TBSA) burned, the depth of burn, and the presence or absence of inhalation injury. The classification of burns, based on depth, is shown in Table 35.1 . Generally, burns are considered severe when partial- and full-thickness burn TBSA is greater than 25%.

The extent of direct thermal injury to the airway depends on the type of inhaled air. Dry air has a low specific heat capacity and loses heat rapidly, limiting damage to the supraglottic airway (SGA). The efficiency of the nares and pharynx in thermoregulating inhaled gases as well as the the glottis’s protection of the lower airway also play a role in limiting thermal injury to the upper airway. In contrast, wet air (steam) has a larger heat capacity, fast thermal transmission, and slow heat elimination, characteristics that predispose to lower airway injury.

Common signs on physical examination suggesting inhalation injury include facial burns, singed facial and nasal hair ( Fig. 35.1 ), oropharyngeal ulceration, mucosal edema, and cough producing carbonaceous sputum. Studies have shown that the incidence of difficult intubation in patients with face and neck burns is more than twice that of the general population.

Phases of Burn Injury

Burn injuries and their care are typically described in three phases: acute, subacute, and chronic. The acute phase of burn injury describes the 48-hour postinjury period when a classic systemic inflammatory response is present and requires critical interventions, including airway management and aggressive fluid resuscitation. Inhalation injury may be present as a result of damage to both the upper and lower airway by steam, smoke, and/or toxic chemicals; its presence predicts increased incidence of respiratory failure and mortality. Cardinal features of upper airway injury during this phase include stridor, dysphonia, dysphagia, and glottic and periglottic edema. Upper airway narrowing is augmented by accumulation of extravascular fluid/edema with the rapid administration of resuscitation fluids.

Subglottic or lower airway inhalational injury during the acute phase results from a constellation of pathophysiologic changes. Tracheobronchial epithelial damage leads to impaired mucociliary function, mucosal edema and sloughing, and increased airway secretions, all of which lead to lower airway obstruction, atelectasis, and consequent ventilation/perfusion (V/Q) mismatch. Toxic inhalation products in smoke trigger increased bronchial blood flow that, in combination with fluid resuscitation and compromised capillary membrane integrity, leads to further bronchial edema. Nitric oxide is also released with inhalation injury and impairs hypoxic pulmonary vasoconstriction, further contributing to physiologic shunt and V/Q mismatch. Lower airway injury during the acute phase of injury generally presents as bronchospasm from the inhalation of aerosolized irritants. Therefore, bronchodilator therapy is often required, and administration of epinephrine may be necessary if bronchospasm is refractory to other treatments.

The presence of circumferential full-thickness thoracic burns can also produce oxygenation and ventilation difficulties in the acute phase of burn injury. Such injuries reduce thoracic compliance and create a restrictive lung defect. This defect is worsened with large volume burn resuscitation, and limits chest wall excursion with either spontaneous or positive-pressure ventilation. Treatment of this restrictive defect involves chest wall escharotomies.

The subacute phase of burn injury begins approximately 3 to 5 days after injury, when burn wound excision and grafting procedures typically begin. The subacute phase is often marked by worsening pulmonary function and respiratory distress due to further accumulation of mucosal debris and secretions, and infectious complications (e.g., wound infection, pneumonia). It is estimated that pneumonia and bronchitis occur in up to half of severely burned patients 1 week postinjury.

The chronic phase of burn injury occurs weeks to years after the initial insult. By this point, lower lung injury is generally resolved; however, new airway management issues can arise because of unpredictable fibrous tissue deposition and scarring that lead to skin contractures. Contractures of the neck and mouth can distort upper airway anatomy, cause severely constricted mouth opening, and limit neck movement, particularly neck extension. During this phase, patients can also develop tracheal stenosis as a consequence of prolonged tracheal intubation and/or tracheostomy placement. Chest wall contractures can result from spontaneously healed or grafted circumferential truncal burns and create a restrictive lung defect due to decreased chest wall compliance.