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. 2023 Mar 21;103(3):439–451. doi: 10.1016/j.suc.2023.01.006

Acute Respiratory Distress Syndrome, Mechanical Ventilation, and Inhalation Injury in Burn Patients

Edward Bittner a,b, Robert Sheridan c,∗
PMCID: PMC10028407  PMID: 37149380

Abstract

Respiratory failure occurs with some frequency in seriously burned patients, driven by a combination of inflammatory and infection factors. Inhalation injury contributes to respiratory failure in some burn patients via direct mucosal injury and indirect inflammation. In burn patients, respiratory failure leading to acute respiratory distress syndrome, with or without inhalation injury, is effectively managed using principles evolved for non–burn critically ill patients.

Keywords: ARDS, Burn injury, Inhalation injury, Mechanical ventilation, Protective ventilation, Ventilator-induced lung injury

Key points

  • •

    Acute respiratory distress syndrome (ARDS) is common in seriously burned patients, driven by a combination of inflammatory and infection factors.

  • •

    Inhalation injury contributes to respiratory failure in some burn patients.

  • •

    In burn patients, ARDS with or without inhalation injury is effectively managed using principles evolved for non–burn patients.

Acute respiratory distress syndrome

Epidemiology and Pathophysiology

Burn patients are at risk of developing acute respiratory distress syndrome (ARDS) as a result of systemic inflammation, fluid resuscitation, protein loss, prolonged mechanical ventilation (MV), and multiorgan dysfunction (MODS) (Fig. 1 ). Inhalation injury---via direct cellular damage, disruption of mucociliary clearance, airway obstruction, and proinflammatory cytokines---further increases the risk.1 Between 20% and 50% of mechanically ventilated burn patients will develop ARDS. Onset is most commonly during the first week postburn, although it may be delayed.2 , 3 Pathologically, ARDS is acutely characterized by inflammation-mediated injury resulting in increased alveolar-capillary permeability, edema, alveolar collapse/derecruitment, reduced lung compliance, increased pulmonary vascular resistance, ventilation-perfusion (VQ) mismatch and shunting, and impaired gas exchange.4 Chronic changes are characterized by fibrosis, vascular smooth muscle hypertrophy, and capillary obliteration.4 ARDS contributes to mortality and morbidity in burn patients.5 Mortality in ARDS is caused primarily by the development of MODS.6

Fig. 1.

Fig. 1

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Postburn ARDS are often nonspecific, showing inhomogeneous consolidation and perihilar fullness.

The management of ARDS is largely supportive, and most approaches in burn patients have been translated from the non–burn population. Although MV is often essential, the process itself can inflict further damage to the lungs, referred to as ventilator-induced lung injury (VILI).7 Mechanisms of VILI include high inspiratory pressures (barotrauma), high tidal volumes (TV; volutrauma), repeated opening and closing of alveoli (atelectrauma), oxygen toxicity, and inflammatory cytokine release (biotrauma).8 , 9 Recently, additional mechanisms of injury have been implicated, including high mechanical power (ergotrauma), stress frequency, respiratory muscle overuse/underuse (myotrauma), and pulmonary capillary stress failure.10, 11, 12

Protective Ventilation

The standard approach to protective mechanical ventilation (PMV) includes small TVs to limit volutrauma, setting positive end-expiratory pressure (PEEP) to minimize atelectrauma, and recruitment maneuvers (RMs) to open collapsed regions of the lung. An individualized approach to MV based on lung pathophysiology and morphology, ARDS cause, and lung imaging and monitoring has been suggested to improve ventilation practice and outcome.13 In addition, PMV has been expanded beyond the lung itself to include right-heart-protective ventilation, diaphragmatic-protective ventilation, minimization of repetitive-stress injury, capillary-stress reduction, and consideration of patient self-inflicted lung injury (P-SILI).11

Tidal Volumes

A TV of 4 to 6 mL/kg predicted body weight is commonly used to maintain a plateau pressure (Pplat) < 30 cm h 2 o.14 Minimizing airway driving pressure (DP), calculated as Pplat minus PEEP, is another suggested strategy for selecting TV.15 Importantly, Pplat and DP are indirect measures for peak lung stress. When functional residual capacity is markedly reduced in severe ARDS, overdistention can occur in nondependent regions despite achieving target levels. Real-time bedside monitoring with pressure and imaging techniques, such as esophageal manometry, electrical impedance tomography, and lung ultrasound, are increasingly used to select TV to minimize overdistention.16, 17, 18

Unique characteristics of burn patients may affect the successful application of a low-TV approach. For example, low TV in a burn patient with poor chest compliance and/or inhalation injury with obstruction of the conducting airways can result in lung underinflation. A retrospective study in pediatric burn patients with inhalation injury found that a low-TV approach was associated with more atelectasis, longer duration of MV, and a higher incidence of ARDS than a higher-TV approach.19 A recent international cohort study found that low-TV ventilation was used in most burn patients, but was not associated with a reduction in days ventilator-free and alive at day 28.20 Strict application of low-TV ventilation in the setting of increased co 2 production from burn-associated hypermetabolism can result in “air hunger,” patient-ventilator dyssynchrony, and hypercapnia. Although hypercapnia may be tolerated to an extent (“permissive hypercapnia”), adjustments to the ventilator mode and increases in sedation are often needed.

Positive end-expiratory pressure

PEEP is used in ARDS to minimize atelectasis and reduce lung heterogeneity, thereby increasing the amount of aerated lung available for ventilation. PEEP may also shift edema fluid from the flooded alveoli into the interstitial space, decreasing shunt fraction and promoting more uniform alveolar mechanics.8 However, PEEP will only have benefit when alveolar recruitment surpasses overexpansion of patent alveoli. There is no simple method to assess the risk-to-benefit ratio of different PEEP levels. In ARDS, derecruitment is a continuous process in which the rate of collapse increases as PEEP decreases. With decreasing levels of PEEP, derecruitment ceases in the sternal lung zones at PEEP of 10 cm h 2 o, whereas it continues in dorsal regions down to 0 cm h 2 o.21 Consequently, a minimum PEEP of 10 to 12 cm h 2 o might reduce derecruitment during the acute phase of ARDS, and higher levels may be necessary in severe cases. Approaches to select an optimal PEEP level in ARDS include the use of tables that assign PEEP based on Fio 2, use of the highest PEEP that optimizes oxygenation while allowing an acceptable TV and Pplat, and bedside PEEP titration based on lung compliance and recruitability.22

Recruitment Maneuvers

Computed tomographic (CT) scans have indicated that tissue consolidation can account for up to 50% of the lung in ARDS.23 RMs apply a higher-than-normal inflation pressure (usually ≥35 cm h 2 o) to the lungs for 20 to 40 seconds to “open the lung” by recruiting atelectatic regions.24 Evidence to support their routine use in ARDS is lacking.25 However, RMs may be beneficial for improving oxygenation in patients with hypoxemia.25 The improvement in oxygenation from an RM is often greatest when followed by an increase in the level of PEEP.25 Repeated RMs during lung-protective ventilation can improve pulmonary compliance and oxygenation and do not appear to worsen lung injury in severe ARDS.26 Most alveolar recruitment occurs during the first 10 seconds of an RM; extended durations (eg, minutes) may be associated with worse outcomes.27 RMs appear to be most effective in improving oxygenation during early ARDS rather than during the fibroproliferative phase.28

Right-Heart-Protective Ventilation

Pulmonary hypertension (PH) in ARDS results from pulmonary vasoconstriction (caused by hypoxia or hypercarbia), microthrombosis, and ventilation with high DPs.29 Right-ventricular (RV) dysfunction develops with sustained elevations in PH, as the RV has no adaptive mechanism other than dilatation when its afterload is increased.30 In ARDS, RV dysfunction can lead to RV failure (acute cor pulmonale), and if left untreated, cardiogenic shock can develop. Elevated right-heart pressure can also worsen hypoxemia by right-to-left intracardiac shunting of deoxygenated blood through a patent foramen ovale. RV PMV has been suggested to reduce RV afterload to include the following: (1) minimizing lung stress by limiting Pplat and DP, (2) reducing pulmonary vasoconstriction by improving oxygenation and control of co 2, and (3) prone positioning (PP) to unload the RV.31 Optimization of RV-protective PEEP must balance alveolar recruitment and overdistention. If RV-protective measures are insufficient (or unfeasible), ancillary therapies, such as inhaled vasodilators or extracorporeal membrane oxygenation (ECMO), may be required.

Diaphragm

Respiratory-muscle weakness rapidly develops in critically ill, mechanically ventilated patients and carries a poorer prognosis.32 , 33 Exposure to excessive workloads even for brief periods can result in diaphragmatic inflammation referred to as use atrophy.11 Failing to allow full rest following the onset of acute respiratory failure or after a failed weaning trial can induce this injury and prolong MV.11 Furthermore, sepsis can incite and exacerbate diaphragmatic injury, through the effects of proinflammatory cytokines.34 Disuse atrophy can result from prolonged periods of MV and loss of electromyographic stimulation.35 Diaphragmatic PMV uses the following dual approach12: (1) early after the onset of acute respiratory failure, avoiding prolonged periods of high work of breathing (WOB) by providing adequate ventilatory support and sedation; (2) during recovery, limiting passive ventilation and targeting an inspiratory effort level similar to that of healthy subjects at rest to accelerate liberation from ventilation.33

Self-Induced Lung Injury

Increased respiratory drive and vigorous inspiratory efforts are often attempts to compensate for impairments in respiratory mechanics and gas exchange. These vigorous spontaneous breathing efforts may have injurious physiologic effects mediated by swings in transpulmonary pressure (TPP), increases in transvascular pressure resulting in edema, intratidal shift of gas between different lung zones (pendelluft), and diaphragmatic injury. This is referred to as P-SILI.36 In patients receiving MV, vigorous respiratory efforts may also result in patient-ventilator dyssynchrony and increased mechanical lung injury owing to high TPPs and/or cyclic atelectasis.37 , 38 Preventing P-SILI in clinical practice requires assessment of a patient’s inspiratory effort and the detection of potentially harmful patient-ventilator interactions. For some patients with vigorous spontaneous breathing and/or patient-ventilator dyssynchrony, sedation or paralysis may be protective treatment.

Stress Frequency and Permissive Hypercapnia

Higher ventilatory frequencies are often used with low-TV ventilation to reduce hypercapnia, but this may have detrimental effects on respiratory mechanics, gas exchange, and cumulative lung trauma.39 , 40 Higher ventilatory frequencies shorten inspiratory time, resulting in the need for higher peak-flow rates, which may augment parenchymal shear stress, worsen oxygenation, and contribute to greater pressure-related cyclic lung stress and strain. Shortened expiration times may have detrimental effects, including dynamic hyperinflation, reduced compliance, increased TPP, and diaphragmatic dysfunction. A reduction of the frequency of ventilation with resulting hypercapnia may be beneficial in ARDS by facilitating a reduction of the cumulative intensity of cyclic stress and strain. Hypercapnia itself may also have beneficial physiologic benefits, including improved VQ matching from pulmonary vasoconstriction, increased local alveolar ventilation from inhibition of airway tone, increased oxygen delivery from an increase in cardiac output, increased unloading of oxygen in the tissues, microvascular vasodilation, and anti-inflammatory effects.41 Some studies have reported benefit from permissive hypercapnia in ARDS, although they are confounded by the inability to dissect the effects of permissive hypercapnia from the effects of low TV.42 Because hypercapnia increases respiratory drive, deep sedation or neuromuscular blockade may be required.

Fluid Overload and Capillary Stress Reduction

Fluid-conservative approaches have been associated with improved outcomes in non–burn ARDS, but have the potential to compromise burn resuscitation.43 Consequently, application of a fluid-conservative approach in a burn patient with ARDS should be considered carefully, with close attention to administering the least amount of fluid that still achieves adequate organ perfusion.

Unconventional Mechanical Ventilation

A variety of unconventional modes of MV, including high-frequency percussive ventilation (HFPV), high-frequency oscillatory ventilation (HFOV), or airway-pressure-release ventilation (APRV), are used in some burn centers for patients with ARDS.44

HFPV delivers very small, high-frequency tidal breaths superimposed on a conventional pressure-controlled breath.45 HFPV improves oxygenation, improves ventilation, and lowers airway pressures compared with other modes of MV. HFPV also produces intrabronchial percussion, airway turbulence, and higher airflow, all of which enhance mobilization and clearance of airway debris and secretions. HFPV, although shown not to be superior to conventional ventilation in the general ARDS population, has a suggested role in inhalation injuries and burn-related ARDS.46 HFPV is routinely used in some burn centers, particularly in patients with inhalation injury or in those who fail conventional MV.

HFOV delivers small, sub-dead-space TVs at high frequency to maximize lung recruitment and avoid cyclic alveolar collapse.47 HFOV in burn-related ARDS has not been extensively studied. HFOV is sometimes used as a rescue approach for burn patients with refractory hypoxemia but is generally unsuccessful in improving oxygenation in inhalation injury, probably because effective lung recruitment is impaired by obstruction of the conducting airways.48

APRV is a mode of pressure-controlled ventilation that allows spontaneous breathing at regularly fluctuating high and low levels of continuous positive airway pressure.49 Proposed benefits include alveolar recruitment and stabilization, improved VQ matching, increased mean airway pressure, and minimization peak and Pplats.50 Spontaneous breathing in APRV reduces sedation requirements, thereby preserving airway reflexes and facilitating cough and pulmonary toilet. There is limited literature supporting the benefit of APRV for ARDS. Specific evidence in the burn population is lacking.

Noninvasive Ventilation

For patients with mild ARDS, noninvasive ventilation (NIV) may be beneficial, as it allows patients to communicate more easily, requires less sedation, allows more effective cough and expectoration of secretions, and avoids intubation-related complications. NIV appears safe and effective in mild to moderate hypoxemia, but it may delay intubation and increase mortality in more severe hypoxemia.51 In patients with inhalation injury or that have received large-volume fluid resuscitation, NIV may mask evidence of progressive airway obstruction.52 There is currently limited literature examining the impact of NIV in the burn population.53

High-Flow Nasal Cannula

High-flow nasal cannula (HFNC) is increasingly used in the management of respiratory failure, including mild ARDS.54 HFNC is capable of delivering up to 100% heated and humidified oxygen at flow rates of up to 60 L per minute. The benefits include a reduction in WOB, reduction of the anatomic dead space, generation of a small amount of PEEP, and improvement of mucociliary clearance.55 There are limited reports of HFNC use in patients with burns and/or inhalation injury.56

Strategies for refractory hypoxemia

Prone Positioning

When a patient with ARDS is turned from supine to prone, the atelectatic dorsal lung regions are freed from the weight of the more ventral lung, the heart, and the mediastinum, favoring expansion of dorsal regions. The net effect is more homogeneous aeration with a more uniform strain distribution leading to an improvement of gas exchange and a decreased risk of VILI.57 A systematic review of 9 randomized controlled trials (RCTs) concluded that patients with ARDS most likely to derive a survival benefit from PP were those with severe hypoxemia and in whom it was used more than 16 hours per day.58 Data on PP of burn patients are limited; it presents logistical and safety challenges.59 A case series reports improvements in oxygenation and a low rate of complications in patients with burn-related ARDS undergoing PP.60 PMV should continue to be used during PP, and reassessment of ventilatory parameters should be performed, as respiratory mechanics may change with proning.61 , 62 Increased sedation and neuromuscular blockade may be required.

Neuromuscular Blockade

Neuromuscular blocking agents (NMBAs) are sometimes used in patients with severe ARDS to enhance gas exchange and reduce Pplats, ventilator dyssynchrony, and VILI. A meta-analysis of 5 RCTs in moderate to severe ARDS concluded that early initiation (within 36–48 hours of ARDS diagnosis) of a 48-hour infusion of cisatracurium improved oxygenation and lowered barotrauma risk without increasing intensive care unit weakness.63 There is no specific evidence to guide the use of NMBAs in burn-injured patients with ARDS. It is reasonable to consider them in burn patients with severe ARDS.64

Inhaled Pulmonary Vasodilators

Inhaled pulmonary vasodilators, including nitric oxide (NO) and epoprostenol, selectively increase blood flow to ventilated lung regions, thereby improving VQ matching and improving oxygenation.65 They can also benefit ARDS patients with right-heart failure. A meta-analysis of 14 RCTs in adults with ARDS found that inhaled NO increased oxygenation but did not affect duration of MV or survival.66 Improvement in oxygenation with inhaled NO has been demonstrated in burn-injured patients with ARDS.67 Inhaled epoprostenol is a less-expensive agent that has similar effects.68

Extracorporeal Life Support

If other rescue strategies used in ARDS management fail to improve oxygenation, ECMO may be beneficial. A recent report concluded that mortality for burn-injured patients receiving ECMO was comparable that for non–burn ECMO patients.69 Considerations include the risks of anticoagulation, need for further operative care, and consideration of the goals or futility of care.70 Patients most likely to benefit from ECMO are those with severe ARDS within the first week of MV and without multiple organ failure.71 ECMO for burn patients should be provided only in centers experienced in both burn care and in the use of extracorporeal support for ARDS.

Inhalation injury

Usually sustained in structural or vehicular fires, inhalation injury occurs in about 5% of burn-unit admissions.72 , 73 Survival has improved with the evolution of supportive respiratory care, but inhalation injury remains a significant source of morbidity and mortality in burn patients. It increases mortality in patients with large cutaneous burns.74

Pathophysiology

The smoke generated during structural fires contains many incomplete combustion products, chemicals, and fine debris with varied particle size and weight. Gas temperatures can rise above floor level to several hundred degrees Fahrenheit. Exposure to such temperatures in inhaled gas can cause direct thermal damage to the supraglottic airway. Rarely, particularly with steam inhalation injury in enclosed spaces, thermal injury below the glottis can occur. Aerosolized irritants can cause inflammation, bronchospasm, increased bronchial blood flow, surfactant depletion, and mucosal slough. The local response to inhaled irritants attracts inflammatory cells, generates reactive oxygen species, and causes local release of proinflammatory molecules.75 These can induce variable degrees of alveolar flooding and bronchial exudate with secondary VQ mismatching. These inflammatory changes are thought to explain the significant resuscitation fluid volume required by burn patients with inhalation injury.76, 77, 78 Inhalation injury may be accompanied and complicated by carbon monoxide and/or cyanide poisoning.

Inhalation injury carries a strong risk of ARDS, and of pneumonia secondary to sloughing of the respiratory epithelium with resulting loss of ciliary clearance and accrual of obstructive endobronchial debris. This results in small-airway occlusion, atelectasis, and infection. Deaths owing to inhalation injury are often related to secondary ARDS and infection, with a classic report suggesting up to a 60% increase in expected burn mortality in the setting of coincident inhalation injury and pneumonia.79

Diagnosis

Tools to evaluate the presence and severity of inhalation injury include clinical evaluation, bronchoscopy, and radiography. Unfortunately, none of these tools reliably predict clinical course.80 Severity grading schemes have been proposed,81 but have not proven to be reliably useful for clinical care. History and clinical presentation are the most reliable methods of evaluation. Burns occurring in a closed space, burns around the nose and mouth, singed nasal hair, soot in the airway, carbonaceous sputum, hoarseness, wheezing, and stridor all suggest inhalation injury. Bronchoscopic examination will often reveal carbonaceous debris, ulceration, pallor, and mucosal slough, although patients inhaling fine-particle smoke or burning hydrocarbons may have deceptively unremarkable bronchoscopy. Those with overt bronchoscopic signs on initial evaluation seem to have more challenging clinical courses.82 Serial bronchoscopy for pulmonary toilet may have value later in the hospital course, but there is no demonstrated role for early bronchoscopic removal of visible soot. Early chest radiographs are usually normal. Radionuclide ventilation scanning with xenon-133, technetium-99 DTPA, or macroaggregated albumin may show inhomogeneous tracer clearance suggestive of small airway obstruction.83 CT scanning has been proposed for early diagnosis.89, 84, 85, 86, 87, 88

Management

During initial evaluation, intubation is indicated for usual reasons of obtunded mental state or respiratory distress. Inhalation injury alone does not mandate intubation unless airway patency is threatened, particularly if cutaneous burns are small. In patients with severe facial edema or stridor, rapid assessment is critical, and intubation is often required. Evolving upper airway edema may complicate reintubation, so tube security is essential. Routine use of prophylactic antibiotics or empiric steroids is not supported.

Inhalation injury is associated with mucosal slough and loss of ciliary clearance with compromised pulmonary toilet. Chest physiotherapy and suctioning or stimulated cough is front-line therapy. Uncommonly, repeated bronchoscopy for pulmonary toilet may be needed.89 Tracheobronchitis and pneumonia may occur and are addressed with targeted antibiotics and pulmonary toilet. Additional proposed therapies have included HFPV,90 high-volume ventilation,91 and nebulized heparin and N-acetylcysteine.92 Tracheostomy, weaning, and extubation follow standard critical-care indications. Rarely, patients will suffer tracheal injury requiring reconstruction93; most survivors have no long-term pulmonary sequalae.94

Summary

ARDS is common in patients with burn injury, and the need for large-volume fluid resuscitation, frequent surgery, presence of inhalation injury, superimposed sepsis, and burn-associated hypermetabolism all contribute to ventilation challenges.

Clinics care points

  • •

    Respiratory distress and failure are common occurences in burn patients driven by direct respiratory system injury, pulmonary and systemic infection, and systemic inflammation

  • •

    Inhalalation injury is caused by inhaled irritants and can result in multi-level iinvolvement of the respiratory system

Disclosure

The authors have nothing to disclose.

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