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Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults

Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults
Literature review current through: Jan 2024.
This topic last updated: Jan 16, 2024.

INTRODUCTION — Pulmonary barotrauma can complicate mechanical ventilation. It is most often due to alveolar rupture resulting in the release of air into extra-alveolar locations [1]. Pulmonary barotrauma may be associated with increased mortality and in some circumstances it may be life-threatening. Thus, it is important that clinicians prevent, recognize, and promptly manage barotrauma in this population.

The prevention, diagnostic evaluation, and management of pulmonary barotrauma are discussed in this topic review. Additional complications of mechanical ventilation are described separately. (See "Clinical and physiologic complications of mechanical ventilation: Overview".)

DEFINITION — Barotrauma is physical damage to body tissues caused by a difference in pressure between a gas space inside the body and its surrounding external environment. Pulmonary barotrauma from invasive mechanical ventilation refers to alveolar rupture due to elevated transalveolar pressure (the alveolar pressure minus the pressure in the adjacent interstitial space); air leaks into extra-alveolar tissue resulting in conditions including pneumothorax, pneumomediastinum, pneumoperitoneum, and subcutaneous emphysema. (See 'Alveolar rupture' below and 'Diagnostic evaluation and management' below.)

Although not true barotrauma, direct injury to the alveolar or pleural space (eg, from chest trauma or biopsy) results in conditions that present and are managed similarly. Thus, they will be included in this topic for the purposes of discussion. (See 'Direct injury' below.)

EPIDEMIOLOGY — The incidence of barotrauma during mechanical ventilation varies with the underlying indication for mechanical ventilation but ranges from 0 to 50 percent [2-7]. Since the application of low tidal volume ventilation in the mid-2000s, the rate may now be on the lower end of this range (approximately 10 percent or less).

In two randomized trials of low tidal volume ventilation for patients with acute respiratory distress syndrome (ARDS), the rate of barotrauma was approximately 10 percent in all study groups [3,4]. (See "Acute respiratory distress syndrome: Ventilator management strategies for adults".)

In a multicenter prospective cohort study of 5183 mechanically ventilated patients, the incidence of pulmonary barotrauma was 3 percent [2]. The incidence varied according to the reason for mechanical ventilation: chronic obstructive pulmonary disease (3 percent), asthma (6 percent); chronic interstitial lung disease (ILD; 10 percent), ARDS (7 percent), and pneumonia (4 percent).

In another meta-analysis of 14 trials of patients with ARDS (2270 patients), the incidence of barotrauma ranged from 0 to 49 percent, but was 12 percent in one prospective cohort included in the analysis [5].

The prevalence of barotrauma in patients with COVID-19-related ARDS is discussed separately. (See "COVID-19: Epidemiology, clinical features, and prognosis of the critically ill adult", section on 'Pneumothorax and barotrauma'.)

PATHOGENESIS AND RISK FACTORS — The possible mechanisms and etiologies associated with barotrauma are listed in the table (table 1). Mechanisms involve spontaneous rupture of alveoli and direct injury (figure 1).

Alveolar rupture — Processes that underlie alveolar rupture are ventilator-related and/or disease-related.

Ventilator-related

Positive pressure ventilation — All patients on mechanical ventilation are at risk of barotrauma. The normal respiratory cycle during spontaneous breathing is dependent upon negative pressure. In contrast, invasive mechanical ventilation involves the delivery of positive pressure. Positive pressure ventilation causes barotrauma by increasing transalveolar pressure (ie, alveolar pressure minus the pressure in the adjacent interstitial space), which results in alveolar rupture [8]. Alveolar rupture allows air from the alveolus to enter the pulmonary interstitium. The interstitial air can then dissect along the perivascular sheaths toward the pleural space, mediastinum, peritoneum, and/or skin, leading to pneumothorax, pneumomediastinum, pneumoperitoneum, and/or subcutaneous emphysema, respectively (figure 2 and image 1) [9,10].

The mechanism of barotrauma in patients who receive noninvasive ventilation (NIV), which also delivers positive pressure, is likely similar [11-15]. However, such instances are rare probably because airway pressures associated with NIV are lower when compared with invasive mechanical ventilation. (See "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications".)

Elevated pressures — Barotrauma refers to trauma induced by high pressures, while volutrauma refers to injury induced by overdistension of the lung during mechanical ventilation. These phenomena are interrelated when one considers tidal volume in relation to functional residual capacity (strain) and airway pressure in relation to pleural pressure (stress). However, limiting alveolar pressure appears to be the most effective way of preventing barotrauma suggesting that high alveolar pressures play a dominant role in alveolar rupture.

Ventilator pressures that increase the risk of barotrauma include:

Elevated plateau pressure – The plateau pressure (Pplat) represents the pressure applied to the small airways and alveoli. There is no absolute Pplat above or below which barotrauma does or does not occur but, in general, the higher the Pplat, the greater the risk of barotrauma with the highest rates occurring in those with a Pplat >35 cm H2O. Data to support this threshold are derived from a meta-analysis of 14 clinical trials (2270 patients with acute respiratory distress syndrome [ARDS]) and demonstrated a strong relationship between pulmonary barotrauma and a Pplat >35 cm H2O or a static compliance <30 mL per cm H2O [5]. Conversely, the lower the Pplat, the lower the risk of barotrauma [16].

Pplat is not routinely displayed. To determine Pplat, the clinician must apply an inspiratory breath hold (usually 0.5 to 1 second) to the ventilated patient and measure the airway pressure during the breath hold. In our practice, we follow the Pplat daily and also intermittently measure it when peak pressures are elevated. Targeting the ideal Pplat during mechanical ventilation to prevent barotrauma is discussed below. (See 'Prevention' below.)

Elevated peak pressure – Similar to Pplat, there is no absolute threshold for the peak pressure (Ppeak; also known as peak inspiratory pressure [PIP]), above which barotrauma occurs and in general, the lower the better.

Ppeak is routinely displayed on most ventilators and is the highest airway pressure measured during each respiratory cycle. It represents the total pressure needed to overcome the inspiratory flow resistance, elastic recoil of the lung and chest wall, and the alveolar pressure that exists at the beginning of each breath. Thus, Ppeak is partly determined by Pplat, such that when the Ppeak is >35 cm H2O and largely due to an elevated Pplat, the risk of barotrauma is likely elevated. Similarly, when Pplat is elevated to the same degree as Ppeak, then patients are at risk of alveolar overdistension and, therefore, barotrauma [17]. Ppeak is higher than the Pplat, with the difference between the two values being related to airway resistance. Larger differences indicate more airway resistance (eg, asthma exacerbation). Determining the contributions of airway resistance and plateau pressure to Ppeak is discussed separately. (See "Invasive mechanical ventilation in adults with acute exacerbations of asthma", section on 'Differentiating airway and lung parenchymal causes of high pressures'.)

Conflicting data on the value of Ppeak as a predictor of barotrauma suggest that Ppeak is probably a less reliable predictor than Pplat of pulmonary barotrauma [18]. Several studies found that Ppeak did not predict pulmonary barotrauma in mechanically ventilated patients due to a variety of etiologies [19-22]. In contrast, one study found that the Ppeak is often elevated prior to the development of pulmonary barotrauma and another study found that pulmonary barotrauma did not occur in patients whose peak airway pressures were less than 50 cm H2O [6,23].

High levels of positive end expiratory pressure (PEEP) – In the past, most experts traditionally considered high levels of PEEP as a potential risk factor for barotrauma based upon the rationale that in ARDS, high levels can result in overdistension in regions of the lung not involved with ARDS. However, several studies have reported that open lung ventilation strategies using high levels of PEEP or recruitment maneuvers, have not been shown to increase the risk of barotrauma [4,24-30]. This is probably because most open lung approaches also concomitantly use lung protection strategies (ie, low tidal volume with a target plateau pressure ≤30 cm H2O) and perhaps because the application of PEEP appropriately recruited involved atelectatic lung, thereby improving lung compliance. Thus, we believe that high levels of PEEP may increase the risk of barotrauma only when this strategy is ineffective in recruiting ARDS-affected atelectatic lung, or not performed together with lung protective ventilation. These ventilatory approaches and determining the optimal level of PEEP are discussed separately. (See "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Further titration/increase in PEEP (high PEEP)' and "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Recruitment maneuvers' and "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Open lung ventilation' and "Acute respiratory distress syndrome: Ventilator management strategies for adults".)

Other — The mode of ventilation (ie, pressure-versus volume-controlled ventilation) does not appear to influence the development of barotrauma, particularly when approaches that limit pressure (ie, Pplat ≤30 cm H2O) and volume-limited approaches are used (eg, tidal volume 6 mL/kg ideal body weight) [31,32]. (See 'Low plateau pressure' below and 'Low tidal volume ventilation' below.)

Disease-related — Asthma, chronic obstructive pulmonary disease (COPD), chronic interstitial lung disease, and ARDS have all been identified as independent risk factors for barotrauma [2,23,33]. The increased risk likely relates to increased alveolar pressure. Those with dynamic hyperinflation (eg, acute exacerbation of COPD or asthma), or low lung compliance (end-stage pulmonary fibrosis, severe ARDS) appear to be at highest risk.

Others include patients who develop prolonged increases in plateau pressure from central airway obstruction, mainstem bronchus intubation, or bronchoscopy during mechanical ventilation, patients with overdistended lung due to overventilation (eg, aggressive bag-mask ventilation during resuscitation or over ventilating pneumonectomized patients), those with cavitating lung disease (eg, from bacterial or pneumocystis pneumonia), or those with underlying cystic lung disease (eg, Langerhans cell histiocytosis).

Patients with COVID-19 pneumonia are at an increased risk of pneumomediastinum even when not receiving invasive mechanical ventilation [34-36]. The incidence of barotrauma in patients with COVID-19 is discussed separately. (See "COVID-19: Epidemiology, clinical features, and prognosis of the critically ill adult", section on 'Pneumothorax and barotrauma'.)

Direct injury — Although not true barotrauma, direct injury to the alveolar or pleural space in some mechanically ventilated patients may result in the escape of air to surrounding tissue resulting in conditions that present and are managed similarly. Populations at risk include postoperative thoracic surgery patients (eg, post lung resection or biopsy), patients with penetrating or blunt injury to the chest (including bronchial fracture or airway laceration during intubation), patients with recent spontaneous pneumothorax prior to mechanical ventilation, and patients who undergo interventions including thoracentesis, central line placement, or transbronchial or percutaneous transthoracic needle lung biopsy.

PREVENTION — The data to support a ventilatory approach that reduces the risk of barotrauma in mechanically ventilated patients are extrapolated from patients with asthma, chronic obstructive pulmonary disease (COPD), and acute respiratory distress syndrome (ARDS). Although no single strategy prevents barotrauma, we typically use lung protective ventilatory approaches by limiting plateau pressure (Pplat) ≤30 cm H2O and using low tidal volume ventilation (6 to 8 mL/kg ideal body weight [IBW]). Additional principles of prevention include the avoidance of overventilation, adopting measures to avoid or treat dynamic hyperinflation (auto-positive end expiratory pressure [PEEP]), and the cautious use of high levels of PEEP. The risk of barotrauma is not eliminated until the underlying predisposing condition is resolved and the patient is weaned from mechanical ventilation (table 2). (See 'Pathogenesis and risk factors' above.)

Low plateau pressure — While no absolute threshold exists, a Pplat ≤30 cm H2O is chosen by most intensivists and a Pplat >35 cm H2O should be avoided. Data to support these thresholds are derived from patients with ARDS where maintaining a Pplat ≤30 cm H2O (together with low tidal volume ventilation) is associated with improved mortality [3]. Noteworthy, is that although this strategy has not been shown to reduce the rate of barotrauma (approximately 10 percent) [3], lower pressures in other studies have been associated with a lower incidence of pulmonary barotrauma such that targeting Pplat as low as is feasible is appropriate [16]. Conversely, the incidence of pulmonary barotrauma increases significantly in patients with a Pplat >35 cm H2O and should be avoided, when feasible [5]. Occasionally, a Pplat between 31 and 35 cm H2O is used by experts, when necessary, acknowledging that the risk of barotrauma is increased in this setting.

Low tidal volume ventilation — This approach is based upon the rationale that overventilation is a risk factor for barotrauma and that this strategy reduces mortality in patients with ARDS (table 3) [3,37]. While low tidal volumes can induce hypercapnia, this is often an accepted consequence and is well tolerated when the pH is acceptable. In general, we use tidal volumes of 6 mL/kg IBW in high risk patients particularly those with ARDS, but also in those with COPD, asthma, and chronic interstitial lung disease (ILD) (see 'Disease-related' above). In other patients (eg, those mechanically ventilated for airway protection without underlying lung disease), ventilatory tidal volumes may be more liberal (eg, 6 to 8 mL/kg IBW). These data are discussed separately. (See "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Low tidal volume ventilation: Initial settings' and "Ventilator-induced lung injury".)

Avoidance or treatment of dynamic hyperinflation — This strategy is based upon data derived from patients with dynamic hyperinflation (DHI) from asthma and COPD. DHI is characterized by increased levels of intrinsic positive end-expiratory pressure (PEEPi or "auto-PEEP"). The hyperinflation is progressive (dynamic) because air accumulates in the lung with each breath as a result of a failure to achieve complete exhalation before the onset of the next breath (figure 3). The prevention and treatment of DHI are primarily achieved through a reduction in respiratory rate and/or tidal volume (ie, reducing minute ventilation) and shortening inspiratory time (both prolonging expiratory time), as well as treating the underlying airflow obstruction when present. Further details are discussed separately. (See "Invasive mechanical ventilation in acute respiratory failure complicating chronic obstructive pulmonary disease".)

Other strategies — Other preventative measures include:

Appropriate application of PEEP – We typically avoid the initial application of high levels of PEEP and use the recommended protocol listed in the table (table 3). Using this strategy high levels are usually only necessary in patients with moderate to severe ARDS. The application of extrinsic PEEP may be necessary in those with auto-PEEP to decrease the work of breathing and improve ventilator synchrony. (See "Invasive mechanical ventilation in acute respiratory failure complicating chronic obstructive pulmonary disease", section on 'Prevention and treatment' and "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Further titration/increase in PEEP (high PEEP)' and "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Open lung ventilation' and "Acute respiratory distress syndrome: Ventilator management strategies for adults".)

Judicious use of neuromuscular blockade – Although one large randomized trial and a meta-analysis have shown that the early use of neuromuscular blockers in patients with ARDS is associated with a lower incidence of barotrauma [38,39], they are not routinely used as a preventative measure due to unrelated serious adverse effects (eg, hypotension and critical care myopathy). Indications for their use are discussed separately. (See "Neuromuscular blocking agents in critically ill patients: Use, agent selection, administration, and adverse effects", section on 'Clinical use' and "Acute respiratory distress syndrome: Fluid management, pharmacotherapy, and supportive care in adults", section on 'Paralysis (neuromuscular blockade)'.)

DIAGNOSTIC EVALUATION AND MANAGEMENT — Common manifestations of barotrauma include pneumothorax, pneumomediastinum, pneumoperitoneum, subcutaneous emphysema, or combinations thereof (figure 1). Less common manifestations include pneumopericardium, bronchopleural fistula, tension lung cyst, subpleural air cyst, and air embolism [40]. Signs and symptoms range from an asymptomatic or atypical finding on routine chest radiography to tachypnea, tachycardia, acute respiratory distress, and profound hypoxemia, and rarely, hemodynamic collapse, obstructive shock, or death. Ventilator data may also reveal asynchrony, an acute elevation of peak and plateau pressures and/or an acute reduction in the expired tidal volume.

Pulmonary barotrauma is typically diagnosed radiographically. Critical to diagnosis is a high suspicion particularly in those who are at risk (eg, patients with a high plateau pressure and acute respiratory distress syndrome [ARDS]) such that daily physical examinations and surveillance of ventilator and chest radiography data is important for its early detection. (See 'Pathogenesis and risk factors' above.)

The principles of management involve concomitantly performing the following:

Managing the specific consequence of the barotrauma (eg, chest tube for pneumothorax) (see 'Barotrauma diagnosis and management' below)

Lowering the plateau pressure by lowering the tidal volume and positive end expiratory pressure as well as increasing sedation (including neuromuscular blockade) (see 'Ventilator management' below)

Managing the underlying disorder (see 'Management of underlying disorder' below)

Barotrauma diagnosis and management — The clinical features, diagnostic evaluation, and management of patients with specific forms of pulmonary barotrauma are discussed in this section.

Pneumothorax

Clinical features – Due to sedation some patients may not complain of symptoms but in those who can communicate, patients may complain of dyspnea or chest pain. Physical findings may include tachycardia, tachypnea, respiratory distress, hypertension, or hypoxemia accompanied by a new unilateral reduction of breath sounds. Ventilator asynchrony, acute elevation of peak and plateau pressures, and an acute reduction in expired tidal volume may be noted. Tension pneumothorax should be suspected in those who also have distended neck veins, tracheal deviation away from the affected side, and hypotension or shock. Although iatrogenic-induced pneumothorax is not ventilator-induced, the presenting features and management principles are often the same. (See "Treatment of secondary spontaneous pneumothorax in adults".)

The differential diagnosis and assessment of mechanically ventilated patients who develop respiratory distress are discussed separately. (See "Assessment of respiratory distress in the mechanically ventilated patient".)

Diagnosis – Pneumothorax is typically a radiographic diagnosis. Unless tension pneumothorax is suspected, a portable chest radiograph should be performed, although computed tomography is sometimes required. When available, ultrasonography is particularly useful when rapid diagnosis and/or treatment with tube thoracostomy is needed.

Chest radiography – Chest radiography for the diagnosis of pneumothorax in ventilated patients poses certain challenges. Pneumothorax on an upright chest radiograph in a spontaneously breathing patient most often reveals an apical white visceral pleural line which is separated from the parietal pleura by a collection of gas (ie, a radiolucent space with no lung markings). However, in ventilated patients, portable chest radiographs are obtained with the patient semirecumbent or supine, such that free air collects anteriorly or in a subpulmonic location, resulting in atypical findings (free air will rise superiorly and follow the path of least resistance) [41]. Gas in the subpulmonic location outlines the anterior pleural reflection, the anterolateral border of the mediastinum, and the costophrenic sulcus creating the "deep sulcus" sign or the "double diaphragm" sign (image 2 and image 3). On rare occasions, pneumothoraces are bilateral and may have evidence of gas in other locations (eg, subcutaneous, or mediastinal). Post-processing image enhancement can aid in the detection of pneumothorax on portable chest radiograph [42].

Computed tomography – CT of the chest may be necessary when more subtle or atypical presentations are suspected including a pneumothorax that is small (eg, <500 cc), loculated (eg, due to complex pleural pathology), obscured by overlying subcutaneous emphysema, or is in an unusual location (eg, posteriorly).

Ultrasonography – Bedside ultrasonography, when available, can be helpful when a rapid diagnosis of pneumothorax is needed (eg, those who present with shock or suspected tension pneumothorax). Utilizing the M-mode, the absence of "lung sliding" is indicative of the presence of a pneumothorax [43]. Ultrasonography may also be useful to guide chest tube placement. Identifying a pneumothorax via ultrasound is discussed in greater detail separately. (See "Bedside pleural ultrasonography: Equipment, technique, and the identification of pleural effusion and pneumothorax" and "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock", section on 'Tension pneumothorax' and "Indications for bedside ultrasonography in the critically ill adult patient", section on 'Evaluation for pneumothorax' and "Clinical presentation and diagnosis of pneumothorax", section on 'Diagnostic imaging'.)

When tension pneumothorax is suspected immediate intervention with tube thoracostomy or needle decompression followed by tube thoracostomy is typically indicated; thus, there is seldom time for radiographic evaluation, although ultrasonography may be useful diagnostically and therapeutically in such circumstances. Rapid clinical improvement following empiric aspiration of a suspected tension pneumothorax is considered by most experts as diagnostic. (See "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock", section on 'Tension pneumothorax'.)

Management – Patients with evidence of barotrauma-associated pneumothorax are managed with an immediate reduction in ventilatory pressures and most additionally undergo chest tube drainage. Although increased levels of supplemental oxygen are often administered, this strategy has no proven value, particularly for those already receiving high fractions of inspired oxygen.

Ventilator management – Management of ventilator settings is discussed separately. (See 'Ventilator management' below.)

Tube thoracostomy – There is a paucity of evidence to help guide the clinician regarding the decision to place a chest tube for the drainage of pleural air in mechanically ventilated patients. In general, we have a low threshold for thoracostomy tube placement based upon our observation that more than 30 percent of pneumothoraces in mechanically ventilated patients progress to tension pneumothoraces. Immediate insertion of a chest tube is indicated for suspected tension pneumothorax. Tube thoracostomy is also appropriate if the pneumothorax is symptomatic, impairs gas exchange or is large, persistent, or progressive. Further details regarding chest tube management (placement, duration, location, size, ultrasonography assistance), and management of persistent air leaks and bronchopleural fistulas are described separately. (See 'Follow-up' below and "Thoracostomy tubes and catheters: Indications and tube selection in adults and children" and "Management of persistent air leaks in patients on mechanical ventilation" and "Treatment of secondary spontaneous pneumothorax in adults".)

Pneumomediastinum

Clinical features – Patients may complain of dyspnea, chest pain, or neck pain. Physical findings may include tachycardia, tachypnea, or hypertension. A crunching sound is occasionally heard during cardiac auscultation. Hypotension due to decreased venous return and cardiac output may occur if tension pneumomediastinum develops, although this is rare [44].

Pneumomediastinum may be found incidentally, in isolation, or in conjunction with pneumothorax on chest radiography.

Diagnosis – Pneumomediastinum is commonly diagnosed on a chest radiograph. It appears as radiolucent streaks in the mediastinum (image 4). Free air tracking along normal anatomic structures (eg, trachea, heart) may outline those structures. When extensive, it may result in a linear lucency above the diaphragm including the central portion which is not normally visualized on the chest radiograph, a finding known as the continuous diaphragm sign (image 5). Although this finding may also be seen with pneumopericardium it is much more common with pneumomediastinum. However, if accumulations are small, pneumomediastinum may only be detected by CT chest.

Increased intramediastinal pressure results in collapse of the cardiac chambers, restriction of cardiac filling, and reduction of stroke volume and cardiac output. A flattened cardiac silhouette, known as the earth-heart sign (image 6), is suggestive of tension pneumomediastinum (ie, a larger transverse cardiac diameter and a smaller vertical cardiac diameter than usual). In the appropriate clinical context, the presence of the earth-heart sign together with classical radiologic features of pneumomediastinum strongly support the diagnosis of tension pneumomediastinum [45].

When found radiographically, other etiologies should be considered including a ruptured esophagus (eg, previous vomiting, nasogastric tube placement), trauma, endobronchial fracture, or mediastinitis from gas-producing organisms. The presence of the Naclerio V sign (image 7) on plain chest radiography films in patients with a pneumomediastinum suggests esophageal rupture. This appears as a V-shaped air collection, with one limb of the V produced by mediastinal gas outlining the left lower lateral mediastinal border and the other limb produced by gas between the parietal pleura and medial left hemidiaphragm. However, the Naclerio V sign is not specific to esophageal rupture.

Management – Pneumomediastinum due to pulmonary barotrauma is generally self-limited and typically resolves with a reduction in ventilatory pressures, and close monitoring (clinically and radiographic). (See 'Ventilator management' below and 'Pneumothorax' above.)

A notable exception is the rare patient who develops tension pneumomediastinum, in whom a mediastinotomy with drainage of air should be performed [44]. A mediastinal drain is often left in position following mediastinotomy.

Pneumoperitoneum

Clinical features – Patients may complain of abdominal pain. Examination findings may be subtle and may include abdominal distension, tenderness, or tympany. Abdominal compartment syndrome may develop if the pneumoperitoneum progresses to a tension pneumoperitoneum, but this is rare [46]. Retroperitoneal air can also cause back pain. (See "Abdominal compartment syndrome in adults".)

Diagnosis – Although pneumoperitoneum may be diagnosed by upright abdominal or chest radiography, the diagnosis is often missed such that when suspected, it is best evaluated by CT [47]. When feasible, the patient should remain in position for approximately 5 to 10 minutes before the CT is performed to allow the air to collect in sufficient volume to be detected radiographically. When plain film abdominal radiography is used, free air accumulates superiorly (ie, underneath the diaphragm) when the patient is upright, and anteriorly when the patient is supine; anterior accumulation of air appears as gas on both sides of the bowel wall (Rigler sign), gas outlining the falciform ligament, gas outlining the peritoneal cavity (Football sign), gas outlining the medial umbilical folds (inverted V sign), or gas localized in the right upper quadrant [48].

Since pulmonary barotrauma is a rare cause of pneumoperitoneum, other etiologies should be considered for which CT may also be useful. These include a ruptured viscus, abdominal trauma, recent abdominal laparoscopy or surgery, peritoneal dialysis, paracentesis, vaginal procedures, bacterial peritonitis, pneumatosis cystoides intestinalis, and bowel malignancy.

Management – Pneumoperitoneum due to pulmonary barotrauma is usually self-limited and often resolves spontaneously with a reduction in ventilatory pressures, monitoring, and supportive measures. An exception is the rare patient who develops abdominal compartment syndrome due to tension pneumoperitoneum. In case reports, most patients were managed with surgical decompression because this approach relieved the abdominal compartment syndrome and excluded gastrointestinal perforation as the etiology. Management of abdominal compartment syndrome due to tension pneumoperitoneum is similar to the management of abdominal compartment syndrome due to other causes, which is discussed separately. (See "Abdominal compartment syndrome in adults", section on 'Supportive care and temporizing measures'.)

Subcutaneous emphysema

Clinical features – Subcutaneous emphysema generally presents as sudden, painless soft tissue swelling, with a predilection for the upper chest, neck, and face (eg, periorbital) (figure 2). Compartment syndrome is a rare consequence of severe subcutaneous emphysema (ie, compression of blood supply such that life-threatening ischemia may occur) [49,50].

Diagnosis – Subcutaneous emphysema is often identified by finding crepitus during physical examination. It can also be seen on a plain radiograph. It appears as radiolucent streaks throughout the subcutaneous tissue and muscle and often obscures imaging of the underlying lung and mediastinal structures (image 8 and image 9 and image 10).

Management – Similar to pneumomediastinum and pneumoperitoneum, subcutaneous emphysema due to pulmonary barotrauma is usually self-limited and managed with a reduction in ventilatory pressures, monitoring, and supportive measures. (See 'Ventilator management' below and 'Pneumothorax' above.)

Compartment syndrome due to severe subcutaneous emphysema may require surgical decompression as a life-saving maneuver in those with hypotension or who are unstable. Surgical decompression involves creating one or more sterile surgical incisions ("blowhole incision"), usually 1 to 2 inches long through the dermis of the anterior chest wall to allow air to escape; air may be heard escaping through the skin and occasionally gentle massage of air through subcutaneous tissue can encourage decompression. Incisions may be left loosely covered with sterile gauze until healing has occurred. Subcutaneous drain placement and blow hole incisions with negative pressure wound therapy have also been reported for severe cases or for palliation of symptoms, although none of these techniques are validated [51-54].

Others — Rare manifestations of barotrauma include the following:

Pulmonary interstitial emphysema – Pulmonary interstitial emphysema can be detected in ARDS patients or explanted lung specimens, particularly when usual interstitial pneumonia from idiopathic pulmonary fibrosis is present. Air dissects through the alveolar walls into adjacent interstitial tissues to form an inflammatory reaction. While often asymptomatic, pulmonary interstitial emphysema can result in the development of air cysts within the lung parenchyma and air embolism, as well as other forms of barotrauma such as pneumothorax, which should be treated accordingly [55]. (See "Air embolism".)

Pneumopericardium – Pneumopericardium may be asymptomatic but may also present with cardiogenic shock due to pericardial tamponade, in which case drainage of air is necessary. (See "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock", section on 'Pericardial tamponade'.)

Air embolism – Air embolism is a rare manifestation of barotrauma that occurs when pulmonary vascular integrity is disrupted concomitantly with alveolar rupture from overdistention of the airspaces. Presentation and management of this phenomenon are discussed separately. (See "Air embolism".)

Ventilator management — When any type of pulmonary barotrauma is detected, immediate attempts should be made at the bedside to lower the plateau airway pressure [1].

Measures typically taken to lower plateau pressure (Pplat) and reduce lung distension involve performing one or more of the following (table 4):

Lower the tidal volume and/or positive end expiratory pressure (PEEP) – Although there is no ideal target tidal volume or PEEP setting, they should be readjusted to levels as low as is tolerated while simultaneously achieving acceptable gas exchange assuring that at minimum, Pplat is <30 cm H2O and tidal volume is ≤6 mL/kg ideal body weight (IBW). As an example, we typically initially lower the tidal volume until the Pplat is ≤30 cm H2O. PEEP may then be reduced by 3 to 5 cm, sometimes more, recognizing the need to increase the fraction of inspired oxygen to maintain adequate oxygenation, regardless of the risk of oxygen toxicity.

What is considered acceptable gas exchange is variable. At minimum, respiratory alkalosis should be avoided (or treated) and in some cases, patients may be underventilated by decreasing both the tidal volume and the respiratory rate to allow the arterial PCO2 to rise (ie, permissive hypercapnia). Targeting a peripheral arterial oxygen saturation ≥88 percent, preferably ≥93 percent is appropriate. (See "Permissive hypercapnia during mechanical ventilation in adults" and "Positive end-expiratory pressure (PEEP)".)

When auto-PEEP is suspected (eg, patients with acute asthma), it can be managed by reducing minute ventilation (ie, decrease tidal volume and respiratory rate). Inspiratory time may be shortened by increasing the flow rate when volume-controlled modes are used and lowering inspiratory:expiratory (I:E) ratio of 0.33 if pressure-controlled modes are being used. Inverse ratio ventilation (ie, inspiratory time exceeds expiratory time) should be avoided. (See "Invasive mechanical ventilation in adults with acute exacerbations of asthma", section on 'Troubleshooting high peak pressures' and "Invasive mechanical ventilation in acute respiratory failure complicating chronic obstructive pulmonary disease", section on 'Dynamic hyperinflation'.)

Increase sedation (including the administration of neuromuscular blockade) – This is particularly useful when patient-ventilator asynchrony and patient distress is contributing to elevated airway pressures. In addition, sedation can be used to suppress respiratory drive in order to reduce minute ventilation or induce permissive hypercapnia. (See "Sedative-analgesia in ventilated adults: Management strategies, agent selection, monitoring, and withdrawal" and "Sedative-analgesia in ventilated adults: Medication properties, dose regimens, and adverse effects" and "Neuromuscular blocking agents in critically ill patients: Use, agent selection, administration, and adverse effects".)

Additional strategies include:

Switch the mode of ventilatory support – Additional strategies used by some experts include switching the mode of mechanical ventilation, if feasible, to partial ventilatory support (eg, low-rate synchronous intermittent mandatory ventilation [SIMV] or pressure support ventilation [PSV]) rather than total ventilatory support (eg, assist-control, high-rate SIMV, pressure control ventilation, or pressure-regulated volume control [PRVC, also known as volume control plus or VC+]). (See "Modes of mechanical ventilation".)

Wean off mechanical ventilation – Ultimately, patients should be weaned off of mechanical ventilation, which may be hours or days for some and longer for others. However, this is often not immediately practical. (See "Weaning from mechanical ventilation: Readiness testing" and "Initial weaning strategy in mechanically ventilated adults".)

Management of underlying disorder — Treatment of the underlying medical condition is indicated in all patients. As an example, for those with an asthma or chronic obstructive pulmonary disease (COPD) exacerbation, aggressive bronchodilation with beta agonists may result in significant and immediate reduction in airway pressures. There is no contraindication to the use of steroids particularly when indicated for managing the underlying lung disease. Medical treatment of asthma, COPD, ARDS, and interstitial lung disease are discussed separately. (See "Acute exacerbations of asthma in adults: Home and office management" and "COPD exacerbations: Management" and "Treatment of idiopathic pulmonary fibrosis" and "Acute respiratory distress syndrome: Fluid management, pharmacotherapy, and supportive care in adults".)

For other rare cases, reversal of the offending cause is appropriate including treatment of central airway obstruction, repositioning the endotracheal tube when malpositioned in the mainstem bronchus, ventilating at lower than usual tidal volumes for those with pneumonectomy (eg, one-third to one-half), and antimicrobials for cavitating pneumonia. (See "Clinical presentation, diagnostic evaluation, and management of malignant central airway obstruction in adults", section on 'Diagnostic evaluation and initial management' and "Direct laryngoscopy and endotracheal intubation in adults", section on 'Excluding mainstem bronchus intubation' and "One lung ventilation: General principles" and "Complications of the endotracheal tube following initial placement: Prevention and management in adult intensive care unit patients".)

FOLLOW-UP — Once ventilator changes have been made and specific therapies have been administered (eg, bronchodilators, chest tube placement), follow up within one hour with an arterial blood gas is advised so that further ventilator adjustments can be made, if necessary. All patients must be monitored closely by routine clinical examination and assessment of vital signs and ventilator settings. While some physicians perform serial chest radiography (eg, every 8 to 12 hours until the patient is stable or has no signs of progression), we generally perform routine daily imaging and imaging that is symptom-directed. When air is not drained, it resorbs slowly and evidence of barotrauma may remain on radiographs for days to weeks.

For those in whom a thoracostomy tube is placed, some require tube repositioning or replacement, or additional tubes if followup imaging reveals an incomplete response or no response. Using the least amount or no chest tube suction to maintain lung inflation is typically preferred in order to reduce the risk of developing a persistent leak or bronchopleural fistula. The management of persistent air leaks and bronchopleural fistula are discussed separately. (See "Management of persistent air leaks in patients on mechanical ventilation" and "Treatment of secondary spontaneous pneumothorax in adults".)

The decision to remove thoracostomy tubes in ventilated patients is challenging and individualized, especially if they remain mechanically ventilated and the underlying disorder remains acutely active. We generally only remove them when the pneumothorax has completely resolved, the patient is clinically stable, and is successfully weaning (eg, low plateau pressure, minimal ventilator settings, on tracheostomy and ready for a long term care facility) or has weaned from mechanical ventilation (ie, extubated). Additional indications to remove chest tubes also include difficulty weaning due to pleural pain or infection from the chest tube itself or in those with direct injury to the pleural space (eg, pneumothorax due to central line placement). (See "Thoracostomy tubes and catheters: Indications and tube selection in adults and children" and "Management of persistent air leaks in patients on mechanical ventilation".)

We also avoid bronchoscopy and central line placement on the ipsilateral side, when feasible, until barotrauma has resolved. (See "Central venous catheters: Overview of complications and prevention in adults".)

PROGNOSIS — Pulmonary barotrauma may be associated with increased mortality [2,21,23,47,56,57]. However, barotrauma is not the direct cause of death in most patients; it is possible that it is a marker for more severe illness such that sicker patients may have a higher plateau airway pressure and are therefore more likely to develop pulmonary barotrauma as a result [23].

Mixed populations – In a multicenter, prospective cohort study of a mixed population of mechanically ventilated patients, those with barotrauma had a significantly higher mortality (51 versus 39 percent), longer length of intensive care unit stay (median nine versus seven days), and longer duration of mechanical ventilation (median six versus four days) than patients without barotrauma [2]. In one retrospective cohort study of 1700 mechanically ventilated patients, mortality approached 100 percent when pulmonary barotrauma caused a large (>500 mL per breath) bronchopleural fistula or when barotrauma was a later manifestation during the patients illness (eg, at 14 days as opposed to within first 24 hours) [56].

ARDS – In patients with acute respiratory distress syndrome (ARDS), the impact of barotrauma on outcome is less certain due to conflicting data. In a retrospective cohort study of 84 patients with severe ARDS, mortality was significantly higher among patients with pneumothorax than among those without pneumothorax (66 versus 46 percent) [57]. In contrast, a retrospective analysis of data collected during a randomized trial of 725 patients with ARDS found no significant difference in mortality among patients with pneumothorax, compared to patients without pneumothorax (46 versus 39 percent) [21]. In another retrospective study, patients with pneumomediastinum due to barotrauma were found to have a risk of mortality greater than those with pneumomediastinum due to other causes, such as blunt trauma [47].

SUMMARY AND RECOMMENDATIONS

Definition and epidemiology – Pulmonary barotrauma from invasive mechanical ventilation refers to alveolar rupture due to elevated transalveolar pressure. Estimates suggest that the incidence of barotrauma is approximately 10 percent or less. While direct injury to the alveolar or pleural space is not true barotrauma, the resulting conditions (eg, pneumothorax and pneumomediastinum) present and are managed similarly. (See 'Definition' above and 'Epidemiology' above.)

Pathogenesis and risk factors – All patients on mechanical ventilation are at risk of barotrauma, particularly those with elevated plateau pressures >35 cm H2O. Asthma, chronic obstructive pulmonary disease, chronic interstitial lung disease, and acute respiratory distress syndrome (ARDS) are independent risk factors for pulmonary barotrauma. These and other causes are listed in the table (table 1). (See 'Pathogenesis and risk factors' above.)

Prevention – No single strategy prevents barotrauma. We typically use lung protective ventilatory strategies by limiting plateau pressure (Pplat) ≤30 cm H2O and using low tidal volume ventilation (eg, 6 to 8 mL/kg ideal body weight [IBW]). We also use measures to avoid or treat dynamic hyperinflation (eg, lower minute ventilation, shorten inspiratory time, treat obstruction). These and other measures are listed in the table (table 2). (See 'Prevention' above.)

Diagnostic evaluation and management – The following is appropriate:

Manifestations – Common manifestations include pneumothorax, pneumomediastinum, pneumoperitoneum, and subcutaneous emphysema, or combinations thereof. Signs and symptoms range from an asymptomatic finding on routine chest radiography to tachypnea, tachycardia, acute respiratory distress, profound hypoxemia, and hemodynamic collapse. Ventilator asynchrony, acute elevation of peak and plateau pressures and an acute reduction in the expired tidal volume may also be noted. Pulmonary barotrauma is typically diagnosed radiographically, but physical examination is also appropriate. (See 'Barotrauma diagnosis and management' above.)

Management – For mechanically ventilated patients who develop pulmonary barotrauma, we suggest that the Pplat be immediately lowered (Grade 2C). An appropriate goal is a Pplat ≤30 cm H2O. This may require lowering the tidal volume and positive end-expiratory pressure as well as increasing sedation (including neuromuscular blockade). Additional therapies may involve managing the specific consequence of the barotrauma (eg, tube thoracostomy) and treating the underlying medical condition (eg, bronchodilators for asthma). (See 'Ventilator management' above and 'Management of underlying disorder' above.)

Follow-up – Once therapies have been instituted, patients should have an arterial blood gas within one hour so that further ventilator adjustments can be made, if necessary. All patients must be monitored closely by routine clinical examination, and regular assessment of vital signs, ventilator settings, and radiography data. (See 'Follow-up' above.)

Prognosis – Pulmonary barotrauma may be associated with increased mortality but is not the direct cause of death in most patients. (See 'Prognosis' above.)

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References

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