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cheobronchial injury, compared to pure upper airway injury [25]. Several studies have shown that patients with inhalation injury require increased fluids during resuscitation [3, 24], and this correlates with a decreased PaO2/FiO2 ratio and lon­ger MV times [25, 43]. Ventilation goals for inhalation injury are similar to lung-protective strategies derived from National Heart, Lung, and Blood Institute ARDS Network data (www.
ardsnet.org). Most conventional ventilator modes may be
used to achieve tidal volumes 6 mL/kg, plateau pressures <30cm water, and initial higher positive end-expiratory pres­sure [8, 44].
Poor oxygenation and ventilation may occur in those with extensive cutaneous injuries, higher grades of inhalation injury, fibrin casts, and mucous plugs. Alternative or advanced ventilator modes may be required to optimize airway patency, reduce ventilation-perfusion mismatching, and prevent the development of pneumonia [45]. Higher tidal volumes can be considered transiently in the pediatric population [7, 46]. High-frequency percussive ventilation and airway [47] pres­sure release ventilation have both been used to enhance oxygenation in inhalation injury, but no mortality benefit has been noted. High-frequency oscillatory ventilation is not rec­ommended [7, 45, 46].
Medical Therapy
Treatment for inhalation injury is currently supportive, although many pharmacologic agents and respiratory mea­sures have been used extensively by burn centers with vary­ing degrees of success. Therapeutic nebulized agents may be classified as mucolytic agents, bronchodilators, or anti­coagulants. Respiratory management includes intensive bronchial hygiene, oral care, incentive spirometry, and early ambulation. The potential role of steroids and other inflam­matory agents is an active area of research [8]. The empiri­cal use of corticosteroids is not recommended [46, 48] in all patients; however, corticosteroid therapy may decrease
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post- extubation stridor (and possible need for reintuba­tion) in patients with airway edema. In a subset of patients with upper airway edema, heliox (a mixture of helium and oxygen) has been used in our institution to avoid intuba­tion or as adjunct for early extubation [49]. Personnel with burn airway expertise are present when we use this gas mixture to improve laminar flow in small airways. Evidence­based guidelines for treatment of inhalation injury are sum­marized in Table5.3.
T . Guidelines for treatment of inhalation injury
Respiratory care→
Humidified high-flow oxygen to maintain SpO2 >90%
Cough, deep breathing every 2h, incentive spirometry exercises
Turn patient side to side every 2h
Chest physiotherapy and nasotracheal suctioning
Early ambulation
Sputum cultures and antibiotics if indicated
Repeat bronchoscopy for lavage and/or surveillance
Oxygenation→ Lung-protective mechanical ventilation
Alternative: high-flow percussive ventilation
Prone position, neuromuscular blockade
Pulmonary vasodilators, extracorporeal membrane oxygenation
Medications→ Nebulized 20% N-acetylcysteine (3mL)
every 4h
Nebulized bronchodilator (albuterol) every 4h (as needed for wheezing or scheduled)
(continued)
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T . (continued)
Alternate aerosolized heparin 5000–10,000 units (in 3mL normal saline) every 4h
Airway edema→
Other→ Pulmonary function tests at hospital discharge
Sources for this table [1, 13, 15, 18, 37, 40, 45, 46, 50]
Elevated head of bead
Corticosteroids
Heliox
Patient and family education
Scheduled follow-up appointments
Mucolytic agents address the issue of inspissated mucus and hypersecretion after severe inhalation injuries [45]. N-acetylcysteine (NAC), commonly used, enhances airway clearance and possesses anti-inflammatory properties. It may act as an airway irritant and should be used with bronchodila­tors to reduce bronchospasm. Beta-2 agonists, such as alb­uterol or salbutamol, relax bronchiole smooth muscle, inhibit bronchospasm, and may improve PaO2/FiO2 ratio [7]. Some patients may also benefit from the muscarinic receptor antag­onists, ipratropium or tiotropium; these inhaled anticholiner­gic medications function as bronchodilators. Nebulized heparin is added to aid the breakdown of fibrin casts. These nebulized medications can be continued for 7 days or until extubated [7, 45].
Complications
In addition to airway edema and obstruction, the most common early complication is respiratory tract infection [2]. Prophylactic antimicrobial therapy is not recommended in inhalation injury, but it should be initiated once the diagnosis of pneumonia occurs and sputum cultures are available [2,
46]. Bronchoscopy can be used for the initial diagnosis and
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for bronchoalveolar lavage (BAL); pneumonia is a complica­tion of prolonged intubation, and sequential bronchoscopy may reduce intubation times and hospital stay [24, 51, 52].
The degree of injury diagnosed by bronchoscopy (AIS) correlates with oxygen perturbations, development of acute respiratory distress syndrome (ARDS), prolonged mechani­cal ventilation, and increased fluid resuscitation needs [24]. In severe burn patients, multiple mechanisms contribute to ARDS: severe inhalation injury, sepsis, ventilator-induced lung injury, systemic inflammatory response to the burn [53]. Patients with inhalation injury may develop poor oxygen­ation and ARDS earlier than cutaneous burn patients with­out inhalation injury [54]. The Berlin definition should be used to diagnosis ARDS in burn patients [44, 55] (see Table5.4). Treatment for ARDS in the burn center is patient­dependent and involves lung-protective mechanical ventila­tion strategy, side or prone positioning, echocardiography to
T . Berlin denition for Acute Respiratory Distress Syndrome
Onset→
Chest imaging→
Pulmonary edema→
Classification→ Mild: 200mmHg<PaO2/FiO2≤300mmHg
Sources for this table [44, 55]
a
Based on oxygenation measured with a minimum of 5 cmH2O PEEP; for mild classification, oxygenation may also be assessed with noninvasive ventilation; for moderate or severe classification, the patient must be mechanically ventilated
a
Within 7days of a known risk factor (example: acute burn with inhalation injury)
Bilateral opacities consistent with pulmonary edema (chest radiograph or computed tomography)
Non-hydrostatic edema, not fully explained by heart failure or fluid overload; echocardiography may be required to clarify cardiogenic versus non-cardiogenic pulmonary edema
Moderate: 100mmHg<PaO2/FiO2≤200mmHg
Severe: PaO2/FiO2≤100mmHg
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clarify cardiogenic versus non-cardiogenic pulmonary edema, nebulized medications for inhalation injury, neuromuscular blockade if needed, and the nutritional and antioxidant enteral support required for the cutaneous burn [46]. A small percentage of patients will not respond to these interventions to improve oxygenation and ventilation, and this population may require the use of pulmonary vasodilators and/or extra­corporeal membrane oxygenation [56]. Pulmonary vasodilators include inhaled therapies, such as epoprostenol (synthetic prostacyclin) and nitric oxide.
Long-term sequelae in inhalation injury may be avoided with early extubation and treatment. Mild complications include vocal cord dysfunction with voice changes, endo­bronchial or vocal cord polyps, and persistent symptoms consistent with asthma or obstructive lung disease [6, 39] . Severe complications are rare and can be diagnosed rapidly with bronchoscopy. These include tracheal stenosis (seen more commonly in children with prolonged intubation), tracheoesophageal fistula, and tracheal rupture. Other complications are bronchiectasis, bronchiolitis obliterans, and vocal cord fusion. Many of these complications may have a delayed presentation; therefore, long-term follow-up is necessary [2]. Delayed airway obstruction may also occur due to severe scar contracture in facial burns with or with­out inhalation injury.
Conclusion
It is recommended that both adults and children with inhalation injury be observed in the acute setting with continuous monitoring, allowing for prompt treatment of airway edema and intervention prior to airway obstruction [40]. Inhalation injury is a complex medical problem requiring a multidisciplinary team and preventative therapies. Optimal management may require the collaboration of several medical providers: emergency physicians, intensivists, anesthesiologists, burn surgeons,
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otolaryngologists, plastic surgeons, speech pathologists, and physiotherapists [6].
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