Barotrauma is a well-recognized complication of mechanical ventilation. Although most frequently encountered in patients with the acute respiratory distress syndrome (ARDS), it can occur in any patient receiving mechanical ventilation.  In addition, barotrauma can occur in patients with a wide range of underlying pulmonary conditions (eg, asthma, chronic obstructive pulmonary disease [COPD], interstitial lung disease, Pneumocystis jiroveci [Pneumocystis carinii] pneumonia).
In clinical medicine, barotrauma is used to describe the manifestations of extra-alveolar air during mechanical ventilation. Early descriptions of barotrauma refer to rupture of the lung after forceful exhalation against a closed glottis—for example, pulmonary injury after a deep-sea dive (eg, breath-holding while pearl diving). Although nonmechanically ventilated patients may have barotrauma, most cases occur in patients receiving mechanical ventilation.
The clinical presentation can vary, ranging from absent symptoms with the subtle radiographic findings of pulmonary (or perivascular) interstitial emphysema (PIE) to respiratory distress or cardiac arrest due to a large tension pneumothorax.  Other manifestations include subcutaneous emphysema, pneumopericardium, pneumomediastinum, and even pneumoperitoneum, singly or in combination.
Barotrauma was once the most frequent and easily recognized complication of mechanical ventilation. It is now evident, however, that barotrauma represents only one of the mechanisms underlying the broad category of ventilator-induced lung injury (VILI). As the term suggests, the lung injury associated with barotrauma is mediated by increased alveolar pressures.
Other manifestations of VILI have been termed volutrauma, atelectotrauma, and biotrauma (cytokine and chemokine mediated) to reflect the major pathophysiologic events behind the injury.
Improved understanding of the mechanisms underlying VILI and barotrauma makes it imperative for physicians to adjust ventilator settings to prevent alveolar overdistention. Some controversy remains regarding the optimal approach for lung-protective ventilation, but there has been consistent benefit noted with low tidal volume for ventilation and no increased risk with varying levels of positive end-expiratory pressure (PEEP). While low tidal volume ventilation is strongly advocated, plateau pressure may be a more effective parameter to monitor and better reflects the risk of barotrauma in these patients.
Low tidal volume is an effective ventilation strategy, but clinicians have been somewhat slow to adopt this approach. With increasing evidence to support its use, the overall tidal volume used in mechanically ventilated patients had decreased over time, and current practice involves tidal volumes that are lower than those used in the past. Limiting plateau pressures to less than 30 cm water is an effective approach for all patients. With volume ventilators, this is best accomplished with low tidal volumes. It also appears that a pressure-limited approach is also effective.
An appreciation of the pathophysiology of barotrauma in mechanically ventilated patients improves the understanding of its clinical manifestations. It is important to recognize that lung involvement in persons with ARDS is heterogeneous and that some portions of the lungs are more adversely affected than others. This involvement can lead to maldistribution of mechanically delivered tidal volume, with some alveoli subjected to more distention than others.
Pressures between adjacent alveoli may initially equilibrate, but alveolar pressures eventually increase, creating a pressure gradient between the alveoli and adjacent perivascular sheath. This gradient may result in rupture of the alveoli adjacent to the perivascular sheath, with ensuing passage of air into the perivascular sheath, and proximal dissection into the mediastinum. This condition is often referred to as PIE.
In persons with PIE, alveolar air is further decompressed by dissecting along lines of least resistance. These pathways include subcutaneous tissues, where the air produces subcutaneous emphysema, or along tissue planes, resulting in pneumopericardium, pneumoperitoneum, or subpleural air cysts.
In the mediastinum, air can track along tissue planes, creating a pneumomediastinum, whereas increased pressures that rupture through the mediastinal pleura produce a pneumothorax. This is the most dreaded manifestation of barotrauma, and continued accumulation of air during mechanical ventilation can progress to a tension pneumothorax, sometimes with catastrophic consequences.
In many patients, radiographic evidence of barotrauma (eg, PIE, pneumomediastinum) can be noted before any clinical manifestations are evident and, certainly, before a pneumothorax occurs.
In view of the preceding description, alveolar overdistention is the key element in the development of barotrauma. In this sense, “barotrauma” is a misnomer, because the term suggests the presence of elevated pressures in its pathogenesis. Current concepts suggest that high tidal volume ventilation produces the alveolar disruption that triggers the aforementioned chain of events.
Therefore, VILI seen with high tidal volume is most accurately termed volutrauma, and it has been the basis for recent clinical trials that have established a low tidal volume approach to mechanical ventilation.
On the other hand, transalveolar pressure, a measure of alveolar distention, provides another indication of the risk of barotrauma. The concept is the same, with overdistended alveoli leading to disruption in the alveolar epithelium and decompression of air as previously outlined. The plateau pressure provides the best estimate of transalveolar pressure, and some have argued that this is the key risk factor for the development of barotrauma.
Other aspects of VILI include atelectotrauma and biotrauma. Atelectotrauma is the injury associated with repeated opening and closing (recruitment and collapse) of collapsed alveoli during mechanical ventilation. Biotrauma refers to the release of inflammatory cytokines and chemokines as a result of VILI. These cytokines have both pulmonary and systemic effects and may contribute to mortality.
These 2 aspects have not been implicated as direct causes of barotrauma, but they may contribute to the development of abnormal lung parenchyma and lung mechanics, which, in turn, may increase the risk of barotrauma.
Also important is to recognize that the effects of VILI are greater in patients with preexisting lung disease or those with acute lung injury (ALI) or ARDS than in persons with healthy lungs. These differences can be gleaned from differences in barotrauma evaluated on the basis of underlying lung disease.
In a large cohort, patients with COPD had the lowest incidence of barotrauma (2.9%). The incidence was highest in persons with chronic interstitial lung disease (10%); patients with ARDS had an intermediate rate (6.5%). These observations underscore the heterogeneity of lung disease and regional differences in lung compliance.
Barotrauma is one of the manifestations of VILI. In a multivariate analysis, the risk of barotrauma was increased in mechanically ventilated patients who had asthma, chronic interstitial lung disease, or ARDS and in those who developed ARDS during mechanical ventilation. Although barotrauma can occur in patients without ARDS, ARDS has always been the major risk factor for barotrauma in mechanically ventilated patients.
Because the current understanding of the pathophysiology underlying barotrauma is related to high tidal volumes that cause alveolar overdistention and alveolar rupture, it follows that barotrauma is related to the ventilator settings used in mechanical ventilation.
Barotrauma has been associated with high peak inspiratory airway pressures (>40 cm water) and plateau pressures (>35 cm water); however, its association with high tidal volumes has not been confirmed. The ARDS Network trial to compare high and low tidal volumes demonstrated a mortality benefit with low tidal volumes, but incidences of barotrauma did not differ between the groups. 
Plateau pressures provide an estimate of transalveolar pressure. Transalveolar pressure is a function of both the tidal volume and the underlying compliance of the lung. Therefore, plateau pressures can reasonably be used as another measure of the risk of barotrauma. Although the exact value of the optimal plateau pressure is debated, the general consensus is that a plateau pressure of less than 30 cm water is protective.
It follows that mechanical ventilation based on a pressure-limited approach using pressure-cycled ventilatory strategies such as pressure control ventilation should achieve outcomes similar to volume-based mechanical ventilation.  Data are limited, but reviews and meta-analyses using a pressure-limited strategy with a target plateau pressure less than 30 cm of water have shown reduced mortality without any increase in barotrauma.
Pneumothoraces can also occur in situations unrelated to mechanical ventilation. These include cases involving primary or secondary spontaneous pneumothoraces (underlying lung disease), pneumothoraces associated with invasive procedures, use of inhalational drugs, blunt or penetrating chest trauma, or menses (catamenial). Patients with these conditions may develop a pneumothorax that requires mechanical ventilation.
Although the events may be temporally separate, distinguishing a pneumothorax unrelated to mechanical ventilation from a pneumothorax due to mechanical ventilation may be difficult in practice.
The incidence of barotrauma in mechanically ventilated patients varies widely and is reported to be as low as 0.5% in postoperative patients and as high as 87% in patients with ARDS. The underlying condition of the lungs obviously plays a significant role in the development of barotrauma. Patients with ARDS have the highest incidence of barotrauma, at 40-60%, with the associated mortality rate in a similar range.
Notably, the incidence of barotrauma in persons with ARDS and all mechanically ventilated patients has decreased markedly over the past decade. In a retrospective analysis of more than 5000 patients, barotrauma was noted in approximately 3% of all mechanically ventilated patients and slightly more than 6% of ARDS patients.  This change in incidence is most likely related to changes in the approach to mechanical ventilation, specifically with respect to ventilator settings and the use of lower tidal volumes in conjunction with reduced plateau pressures.
Data from prospective ARDS trials also report a much lower incidence of barotrauma, in the 5-10% range in meta-analyses, and reports in the 5-6% range in focused research trials, strikingly lower that the nearly 50% figure noted in the past. [6, 7, 8]
No international or geographic influences are known to affect the incidence of barotrauma. Any differences are probably small and are more likely to be a reflection of the underlying disease status of the patients and local differences in ventilator management than of any ethnic or environmental influence.
International multicenter trials involving patients with ARDS revealed a decrease in the incidence of barotrauma to a range of 8-15%, a figure comparable to the incidence in the United States. This decline in barotrauma is also associated with a decline in the mortality rate from ARDS, although not of the same magnitude as the decline in barotrauma.
As a complication of mechanical ventilation, age is not expected to influence barotrauma. However, the incidence of ALI does increase with age, especially for individuals in whom sepsis is a risk factor for the development of ARDS. Additionally, note that lung compliance normally decreases with age, and this may be a factor in the risk for barotrauma in older patients.
No ethnic predisposition to barotrauma is reported. No sex differences are known regarding the development of barotrauma. 
The main historical consideration with respect to the risk of barotrauma in mechanically ventilated patients is the risk of developing acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Patients are often intubated and unable to communicate, but historical data may be elicited from their medical records.
A previous definition of ALI and ARDS outlined a process characterized by an acute onset, bilateral infiltrates observed on chest radiographs, information that excludes cardiogenic pulmonary edema (pulmonary artery wedge pressure [PAWP] < 18 mm Hg), and a low ratio of arterial partial pressure of oxygen (PaO2) to fraction of inspired oxygen (FIO2), which is defined as less than or equal to 300 for ALI and less than 200 for ARDS.
However, this definition has been modified by a consensus group, often referred to as the Berlin definition. This definition eliminated the need for measurement of the PAWP, but cardiogenic pulmonary edema must still be eliminated as the cause of hypoxemic respiratory failure. There are thresholds required for PEEP requirements (≥10 cm water), minute ventilation (≥10 L/min), and respiratory system compliance (< 40 mL/cm water). There were also three mutually exclusive categories of hypoxemia, defined as mild (200 < mm Hg PaO2/FIO2 ≤300 mm Hg), moderate (100 mm Hg < PaO2/FIOI2 ≤200 mm Hg), and severe (PaO2/FIO2 ≤100 mm Hg). 
Some differences in ARDS may be based on whether the inciting cause involves direct lung injury (eg, pneumonia, gastric acid aspiration, pulmonary contusion) or indirect lung injury (eg, sepsis, trauma with shock, acute pancreatitis, and multiple transfusions).
Although a mechanically ventilated patient with ARDS may be at risk for barotrauma, patients with blunt trauma, severe pneumonia, chronic obstructive pulmonary disease (COPD), or underlying interstitial lung disease may also be at risk. Iatrogenic pneumothoraces can occur in patients who undergo intravascular catheter placement into the internal jugular or subclavian.
Among patients receiving mechanical ventilation, the finding of barotrauma implies ventilator-induced lung injury (VILI), though barotrauma related to the underlying lung disease is possible, especially if it occurs early in the patient’s course.
In the isolated patient who may be able to communicate, reports of increased dyspnea, chest pain, discomfort, or subcutaneous air (in the chest or neck) may herald the development of barotrauma.
The manifestations of barotrauma span the entire clinical spectrum, from totally asymptomatic to full cardiac arrest. The severity of the presentation depends on the amount of extra-alveolar air present. In some individuals, the diagnosis is made only on the basis of chest radiographic findings.
Because patients usually cannot communicate because of intubation, signs of respiratory distress (eg, tachypnea, patient-ventilator discoordination, use of accessory muscles [eg, neck muscle], diaphoresis, tachycardia) may be the earliest indicators of barotrauma.
Subcutaneous emphysema may be palpable as crepitus under the skin. This crepitus can be unilateral and focal or bilateral, it can occur over the chest wall or supraclavicular area, and it can expand up to the neck and face and down to involve most of the body. In rare cases, auscultation reveals a systolic crunching sound over the precordium. This represents mediastinal air and is referred to as the Hamman crunch or Hamman sign.
A flail chest may be observed in patients with trauma. Flail chest appears as paradoxical movements during the respiratory cycle and is due to rib fractures or separation from the costal cartilages in at least 2 places. It may increase the suggestion of an underlying pneumothorax due to trauma, which may be indistinguishable from a pneumothorax due to the barotrauma of mechanical ventilation.
Barotrauma can manifest as a pneumothorax, with a tension pneumothorax being the most feared complication in mechanically ventilated patients. The continuous application of positive-pressure ventilation serves to perpetuate the passage of air into the extra-alveolar space, eventually causing a tension pneumothorax if untreated. In these patients, bedside detection of a pneumothorax can be difficult because of the noise from the equipment usually needed for mechanical ventilation.
Decreased breath sounds on the side of the pneumothorax is an initial finding. After tension develops, accumulating air displaces the mediastinum and associated structures away from the pneumothorax (contralaterally). This process includes contralateral displacement of the trachea. These findings may be detected by placing a finger in the space between the trachea and neck strap muscles just above the sternal notch. The space should be equivalent, and deviation decreases the amount of space palpable.
Chest-wall expansion on the side of the pneumothorax is preserved or hyperexpanded. A totally collapsed lung reveals decreased breath sounds on the side of the collapse, but chest-wall excursion is diminished, and the trachea is deviated to the side of the collapse. The distinction is important if tube thoracostomy is considered without the benefit of a confirmatory chest radiograph.
Cardiac arrest due to tension pneumothorax may be the clinical manifestation first recognized. Although any cardiac rhythm is possible, pulseless electrical activity in a mechanically ventilated patient should suggest tension pneumothorax. Evaluation for a possible tension pneumothorax can proceed as discussed above. Cyanosis reflecting profound hypoxemia may be another finding in this situation, but it may also reflect the patient’s underlying respiratory condition.
Although barotrauma focuses on the thorax, it can also adversely affect other organ systems. Systemic gas embolism is the most dramatic extrathoracic manifestation of barotrauma. This occurs in the context of the described thoracic manifestations, including lung cysts and pneumothoraces. Effects include cerebral air embolism with infarcts, myocardial injury, and livido reticularis.
Some speculate that other clinical findings, such changes in sensorium, seizures, and cardiac dysrhythmias without a clearly identified cause, may also be related to episodic systemic gas embolization. Fortunately, this complication is rare and preventable with a strategy of low tidal volume ventilation. 
The increased intrathoracic pressures that occur in mechanically ventilated patients may affect venous drainage of extrathoracic sites. This increase can affect venous return from the brain and abdomen, a change that may be of concern when the pressures in these areas are already elevated (eg, from cerebral edema or abdominal compartment syndrome). This process provides another impetus to adopt a ventilator strategy (ie, low tidal volume) that translates into lowered intrathoracic pressures.
Of course, barotrauma only worsens the pressures in the extrathoracic areas. If the pressures in these areas are monitored, a sudden increase may herald barotrauma as opposed to a problem in the area monitored.
VILI and alveolar overdistention may also activate cytotoxic and proinflammatory pathways. This event, often referred to as biotrauma, represents a mechanical transduction injury in which the injurious physical effects of mechanical ventilation lead to the release of a host of chemokines and cytokines.
Findings in both animal and human investigations have shown increases in leukocytes, tumor necrosis factor (TNF), interleukin (IL)-6, and IL-8 with high tidal volumes; levels are reduced in levels in subjects given low tidal volumes. The observation that these cytokines are the same as those implicated in systemic inflammatory response syndrome (SIRS) and sepsis provides insight into another possible benefit of low tidal volume ventilation.
Complications of barotrauma range from asymptomatic pulmonary interstitial emphysema (PIE) or subcutaneous emphysema to cardiac arrest due to tension pneumothorax. Prevention is key to management, which should focus on optimal ventilator management and treatment of the underlying condition .
The differential diagnosis includes the following:
No laboratory studies assist in the diagnosis of barotrauma. Arterial blood gas evaluations allow an assessment of acid-base status, oxygenation, and ventilation and, therefore, the consequences of barotrauma. However, arterial blood gas values do not help to establish the diagnosis.
The portable chest radiograph often provides the first indication of barotrauma, especially in an otherwise asymptomatic patient. Initial findings can be subtle because patients often have other pulmonary opacities that may obscure the appearance of extra-alveolar air (see the image below).
Findings such as nonbranching, fixed-caliber radiolucencies radiating from the hilum to the periphery or small collections of air in interlobular septa suggest pulmonary interstitial emphysema (PIE) or subpleural air cysts (see the image below). Pneumomediastinum causes outlining of the great vessels (superior vena cava and left subclavian, common carotid, and innominate arteries) with extension into the neck, whereas pneumopericardium causes outlining of the pericardium and contiguous diaphragm.
Pneumothoraces, especially small ones, may be difficult to detect on portable chest radiographs in mechanically ventilated patients. In most of these patients, studies are performed while they are supine, a position that changes the highest point in the hemithorax from an apical-lateral location to an anteromedial location, where air rises and accumulates. Air can also be subpulmonic and may be seen as a hyperlucent upper quadrant or a deep lucency in the lateral costophrenic angle; this is often referred to as the deep sulcus sign.
The obvious concern is that pneumothoraces may progress to a life-threatening tension pneumothorax. Although this is usually clinically evident, radiographic signs of structures under tension include displacement of mediastinal structures, collapsed lung, and flattening and inversion of the diaphragm (see the images below).
In patients with small collections of air, the diagnosis may be difficult with portable chest radiography. Alternative imaging studies in these situations include decubitus studies of the side in question and chest computed tomography (CT) scanning. The logistics of decubitus imaging in a critically ill, mechanically ventilated patient can be daunting, and the quality of the study results may make interpretation difficult. Chest CT scanning is desirable, but patients must be in a sufficiently stable condition to tolerate transport to the CT scanner.
Chest CT scanning is rarely indicated to establish the diagnosis of barotrauma, but it may be helpful in determining the size of a pneumothorax in mechanically ventilated patients (see the image below). Because the plain portable chest radiograph provides only a 2-dimensional view of the thorax, the size of pneumothoraces that span the hemithorax may be underestimated. Likewise, it may not be easy to appreciate pneumothoraces that are primarily anterior or basilar.
Chest CT scanning may help with the placement of thoracostomy tubes in patients in whom the pneumothorax may be confined or loculated. In some patients with large air leaks, more than 1 thoracostomy tube may be required, and the CT scan can assist with their placement.
The additional information a chest CT scan provides about the lung parenchyma, the pleural surfaces, and the vascular structures may also be useful in patient care.
Many ventilators currently in use also have a respiratory mechanics graphics package. This, along with the traditionally monitored airway pressures, may provide some insight into the care of patients at risk for barotrauma and into the diagnosis of barotrauma. However, these graphics packages should never be used in isolation to diagnose barotrauma. They provide complementary information and can lead the clinician to the diagnosis.
Chest radiography and the physical examination are essential to confirm suspected barotrauma, especially in a life-threatening situation in which tube thoracostomy is contemplated.
Airway pressures have traditionally been used to identify patients at risk for barotrauma. Because the vast majority of patients are ventilated with volume-cycle ventilators, airway pressures required to deliver set tidal volumes can provide insight into the state of the underlying lung.
High peak inspiratory pressure, plateau pressure, and positive end-expiratory pressure (PEEP) have all been implicated as risk factors for barotrauma. These, in turn, are proxy measures of the transalveolar pressure that may define the risk for barotrauma. Plateau pressure provides the best estimate of transalveolar pressure and has been used as both a threshold target and a monitoring tool to adjust ventilator settings to reduce the risk of barotrauma and to identify ventilated patients at risk.
The elliptical pressure-volume curve can provide information about the nature of the underlying lung. A line connecting the origin of the curve to the end of inspiration reflects lung compliance; the expected angle for a normal compliant lung is 45°.
Patients with acute respiratory distress syndrome (ARDS) can be expected to have decreased lung compliance, with a shift downward (to the right). In addition, patients with stiff lungs may reach a point at which increased airway pressure does not notably increase the delivered tidal volume. In these instances, the upper portion of the curve at the end of inspiration may become flattened and narrowed, simulating a bird’s beak or the appearance of a penguin.
Adjustments in ventilator settings, especially reduction of the tidal volume, may eliminate the terminal flattening, which should reduce the peak inspiratory pressures and plateau pressures transmitted to the lung. However, the pressure-volume curve is only a graphic display and a guide. It should never be used in lieu of plateau pressure measurements in the care of ventilated patients.
Some ventilator packages permit calculation of the static compliance of the lung. This compliance is calculated by dividing the tidal volume by the difference between the plateau pressure and PEEP values. It is decreased in patients with ARDS, but a sudden decrease in static compliance might herald the development of a pneumothorax. However, this finding is nonspecific, and any condition that decreases lung compliance is expected to have the same effect. Pulmonary edema is common and is encountered more frequently than pneumothorax.
Other changes in the ventilator parameters may suggest a pneumothorax. Patients at risk for barotrauma may have high peak inspiratory pressures. If a pneumothorax develops, peak pressures may initially decrease in association with a decrease in exhaled tidal volume as air escapes into the pleural space. However, if tension develops, inspiratory pressures may increase as the same tidal volume is being delivered to a shrinking anatomic surface area.
The diagnosis of barotrauma does not rely on histologic findings. If barotrauma is diagnosed only on the basis of histologic specimens, it usually represents an incidental finding or a finding noted during postmortem examination. As might be expected, histologic findings may demonstrate alveolar disruption with hemorrhage, edema, and inflammation. 
More importantly, the histologic findings of the lung surrounding the area of barotrauma provide insight into the severity of the lung disease and the patient’s risk for barotrauma. For example, a patient with ARDS is expected to have diffuse alveolar damage with hyaline membrane formation; exudative, proteinaceous alveolar fluid; neutrophils; macrophages; and disrupted alveolar epithelium.
Treatment & Management
Ventilator management and the adjustment of ventilator settings has been the focus of treatment in patients at risk for barotrauma. This approach is based on recognition of the deleterious effects of alveolar overdistention. It follows that avoiding or minimizing alveolar overdistention is key to preventing barotrauma.
Whether this goal is best achieved by using low tidal volumes or by limiting the plateau pressure is controversial. The 2 parameters are inexorably linked because in volume ventilation, peak pressures and therefore plateau pressures are dependent variables during mechanical ventilation. Both tidal volume and plateau pressures have been used to titrate ventilator settings, with low tidal volume as the primary variable under study.
The benefits of low tidal volume ventilation are demonstrated only in patients with acute respiratory distress syndrome (ARDS). However, clinicians have recognized the hazards of alveolar overdistention in all patients, and lower tidal volumes (in the range of 8-10 mL/kg) have generally been adopted for all patients. Other medical care is focused on treating the underlying condition.
In the ARDS Network trial, ventilation of ARDS patients with a low tidal volume was associated with a 9% absolute reduction in mortality. The low tidal volume was calculated on the basis of predicted body weight (PBW), which clinicians infrequently use. For men, PBW was calculated as 50 + 0.91 (height in centimeters – 152.4) or 50 + 2.3 (height in inches – 60). For women, PBW was calculated as 45.5 + 0.91 (height in centimeters – 152.4) or 45.5 + 2.3 (height in inches – 60).
Low tidal volume was also associated with improvements in ventilator-free days and in the incidence of nonpulmonary organ failure. However, the trial is somewhat controversial, not because of the results but because of the conduct of the trial and its comparison group. Some have argued that the plateau pressure may be the more appropriate target in adjusting ventilator settings.
Note that plateau pressures were limited to less than 30 cm water in the low tidal volume group, with further downward adjustment of the tidal volume (to < 6 mL/kg PBW, but no lower than 4 mL/kg) if plateau pressures exceeded that threshold. This area remains under investigation, but several analyses support the use of low tidal volumes. Also note that in this landmark study, the incidence of barotrauma was virtually the same in the low tidal volume group as in the high tidal volume group.
Post-hoc analyses of patients participating in combined trials of the ARDS Network have focused on the relationship of airway pressures and positive end-expiratory pressure (PEEP) to the development of barotrauma.
In more than 900 patients with a cumulative incidence of barotrauma of 13% over the first 4 study days, no relationship was detected between the peak airway pressure, plateau pressure, mean airway pressure, or driving pressure (plateau pressure – PEEP) to the development of barotrauma. However, higher concurrent PEEP was consistently associated with barotrauma with a relative hazard of 1.67 per 5-cm water increment.
PEEP also may provide a measure of protection against ventilator-induced lung injury (VILI). PEEP is well recognized to increase alveolar recruitment, and a strategy combining PEEP-induced alveolar recruitment with low tidal volumes may minimize this atelectotrauma and confer a clinical benefit in management. Several large, multicenter trials have been reported that focus on increasing PEEP levels in conjunction with the low tidal volume and limited plateau pressure approach. 
Across the differing study protocols, the levels of PEEP used in the higher PEEP group averaged 13-15 cm water, compared with those in the lower PEEP group, which averaged 6-8 cm water. No mortality benefit was found with any of the trials, but improvement was noted in secondary study endpoints in 2 of the 3 main trials, with improvement in hypoxemia, acidosis, use of rescue therapies, ventilator-free days, and organ failure–free days in the higher PEEP group. [13, 14]
Titrating based on plateau pressures, as opposed to oxygenation, may limit some of the adverse effects seen with higher levels of PEEP. No differences were noted in the incidence of barotrauma between the higher and lower PEEP groups, ranging from 5-11% in these trials.
In a single-center report of 61 patients, use of esophageal balloon catheters to measure transpulmonary pressure and thereby guide the use of PEEP yielded improvements in oxygenation and respiratory compliance but did not impact mortality. Of note, no barotrauma was noted in either group, with an average PEEP of 12 and 18 cm water administered in the 2 groups. Technical issues and limited availability of expertise may limit the use of this approach while the results of larger trials are being awaited. 
In summary, using low tidal volumes and limiting plateau pressures remain the preferred approach in ventilator management, and this, in turn, reduces the risk for barotrauma. It appears best to use the ARDS Network lung-protective thresholds in management, which are tidal volumes at 6 mL/kg PBW and plateau pressures less than 30 cm of water. No mortality benefit is reported with higher PEEP, and the optimal approach to PEEP remains to be determined. The ARDS Network has formulated a useful mechanical ventilation protocol (see the image below).
Clinicians should be aware that the low tidal volume approach may result in relative hypoventilation. This translates into hypercapnia, and patients may develop hypercapnic respiratory acidosis. Patients generally tolerate hypercapnia and respiratory acidosis well, and adjustments in the ventilator settings are not usually required. A respiratory acidosis with a pH in the range of 7.20-7.25 is not uncommon with low tidal volume ventilation, but lower pH levels have prompted some to increase the tidal volume or treat with bicarbonate.
During mechanical ventilation, most patients require some sedation, which may also contribute to hypercapnia. The need for and the dose of intravenous (IV) sedation should be assessed on a daily basis. Sedation is obviously essential for patient comfort, but also to minimize adverse effects that may occur with patient agitation and patient-ventilator dyssynchrony.
Along that line, neuromuscular blockade could virtually eliminate patient-ventilator dyssynchrony and its adverse effects, while maximizing efficient airflow and improving oxygenation. This, in turn, would be another method to reduce exposure to high airway pressures, whether in the form of peak airway pressures, plateau pressures, mean airway pressure, or driving pressures.
In a randomized investigation comparing neuromuscular blockage with 48 hours of cisatracurium compared with placebo, there was a statistically lower proportion with barotrauma (5% vs 11.7%; P = .03) in the neuromuscular blockade group.  The authors did not note an increase in plateau pressure readings prior to the episode of barotrauma (primarily pneumothoraces), but it was noted that the patients with barotrauma did have higher minute ventilation than the control group. Pneumothoraces also occurred earlier in the course of their study, which may provide further support for the barotrauma-protective effects with early use of cisatracurium as outlined in this study. A mortality benefit for cisatracurium was suggested, but statistical significance was not achieved. There was no increased in neuromuscular weakness associated with cisatracurium use.
While this study involved 340 patients, given the potential for adverse effects with neuromuscular blockade, there is uncertainty regarding the minimally effective duration of neuromuscular blockade and benefit concentrated to those with the most severe ARDS defined as a PaO2/FIO2 less than 120. A meta-analysis of 431 patients, all emanating from the same study group, also noted a reduction in barotrauma (5% vs 9.7%).  There remains a need for additional confirmatory investigations before neuromuscular blockade with cisatracurium can be endorsed for routine use.
Other medical approaches may help reduce the risk for barotrauma. Early nutritional support facilitates recovery. However, no pharmacologic agents are effective in the prevention or treatment of acute lung injury (ALI), ARDS, or barotrauma.
Pharmacotherapy includes diuretics to decrease lung water and pulmonary edema, sedatives to facilitate patient-ventilator synchrony, and bronchodilators to decrease airway resistance and possibly improve oxygenation and ventilation. These therapies are part of the general supportive care of patients receiving mechanical ventilation, and they are not specific to the management of barotrauma.
Medical therapies that were once promising but that failed to improve outcomes include surfactant replacement, nitric oxide, ketoconazole, and glucocorticosteroids. Therapies under investigation include beta-agonists to reduce alveolar fluid and anticoagulation with biologically engineered compounds.
In patients with ALI or ARDS, corticosteroids have been an intriguing option because of their potential to reduce associated inflammation and lung destruction. However, results from prospective randomized trials of corticosteroids have generally been disappointing. [17, 18] No mortality difference has been demonstrated, and the possibility of increased adverse events in patients treated with corticosteroids late (>14 d) into the course has been suggested.
Additionally, corticosteroids are known to adversely increase hyperglycemia and impair wound healing. However, patients treated within 7 days appear to have increased resolution of gas exchange abnormalities and quicker discontinuance of mechanical ventilation.
No data support that corticosteroid therapy reduces barotrauma. However, in a small study in which corticosteroids were administered 3 days after the onset of ALI or ARDS, a definite but nonsignificant decrease occurred in the incidence of pneumothorax (8% vs 21%) in the control group. Further studies are required to validate this potential benefit of corticosteroids.
Only rarely is surgical repair of the lung required for the management of barotrauma. However, effective management of barotrauma requires prompt evacuation of pleural air and placement of a device to permit the excess air to egress. The urgency and type of tube thoracostomy device depends on the patient's clinical status and the clinician’s experience. Fortunately, many leaks that occur in association with barotrauma are small, so that a tension pneumothorax will develop slowly.
In some patients, the air leak spontaneously closes and air accumulation ceases. These patients still require urgent placement of a tube thoracostomy, but this situation is not the same type of emergency as that seen in a patient with a tension pneumothorax.
Invasive approaches to the management of barotrauma include emergency needle thoracostomy and large-bore thoracostomy.
Emergency needle thoracostomy is indicated for patients with a tension pneumothorax that requires immediate decompression. Patients with a tension pneumothorax usually have hemodynamic compromise (eg, hypotension, tachycardia) because of the compressive effects of the air on the mediastinal vasculature.
In these mechanically ventilated patients, the amount of air that accumulates in their pleural space should be limited before needle decompression is performed. Therefore, the ventilator should be removed, and ventilatory support should be given with a bag-valve-mask device connected to oxygen. Relatively low tidal volumes should be delivered. In this way, the clinician can assess lung compliance and limit the volume of air delivered with each breath.
Because most patients are receiving PEEP, this method also eliminates PEEP from the system and further reduces the amount of air traversing the bronchopleural fistula. This effect, in turn, decreases the amount of air that accumulates in the pleural space and limits the hemodynamic consequences of the tension pneumothorax while allowing the staff to prepare for needle thoracostomy.
The actual decompression with needle thoracostomy does not require any specialized equipment. It can be performed with any angiocatheter needle, preferably 18 gauge or larger. A syringe with or without sterile sodium chloride solution or water can be attached to the end of the catheter. After the site is prepared, the needle assembly is placed over the second intercostal space in the midclavicular line, usually with the patient in a supine position. The needle can be felt traversing the pleura, and the syringe can be used to aspirate as the needle is passed into the pleural space. The aspiration of air or the appearance of air bubbles in the syringe fluid indicates a pneumothorax.
Once the catheter is in place, air can continue to be aspirated, or the catheter can be attached to a tube to allow air to drain. In the ideal case, a Heimlich drain is attached to allow air to drain but prevent inspiration into the chest. This is a temporary drain for use in emergency situations, and it must be replaced as soon as possible after the patient’s condition is stabilized.
Placement of a large-bore thoracostomy tube requires some preparation and time. However, an experienced operator can generally place such tubes in an emergency situation. Kits are available that permit tube placement by means of a guide wire-through-needle technique (Seldinger) and the use of progressive dilators; this method may be employed as a substitute for the traditional method, which is relatively invasive and requires blunt dissection. The tube placement site and preparation are the same for this technique as for the blunt dissection technique.
In the ideal situation, the patient is lying on his or her side in bed, though not necessarily in a lateral decubitus position. Some patients can only be positioned supine with a slight wedge. The arm on the side where the tube will be inserted should be placed under the patient’s head.
The tube should then be placed in the area of the anterior or posterior axillary lines at the level of the fourth or fifth intercostal space. This area has relatively little muscle, and placement here avoids potential injury to the pectoralis, the latissimus dorsi, the breast, and the axillary vessels.
After the site is chosen, the area should be prepared with a local antiseptic. Chlorhexidine is commonly used. The diagnosis of a pneumothorax is usually based on chest radiography or clinical findings, but bedside ultrasonography can be performed to confirm the pleural space air at the site of insertion. The area should be locally anesthetized with lidocaine with infiltration to the pleura. Aspiration during application of local anesthesia confirms the presence of air.
To drain air, small-bore (14-20 French) tubes are usually sufficient. After the site is draped, the introducer needle is placed into the pleural space, passing over the rib, with continuous aspiration once through the pleura.
Once air is aspirated, the syringe is removed and a soft, J-tipped guide wire is passed through the needle. The wire is marked at approximately its halfway point to indicate the limits of guide wire passage. The guide wire should be aimed apically, but the wire does not allow for its consistent placement. The guide wire should pass freely. After it is in place, the needle is removed.
A horizontal incision is made with a scalpel depth to the surface of the rib. The kit usually provides 3 dilators, which are passed over the wire 1 at a time to enlarge the opening gradually. Several passes with the dilators are made over the wire into the pleura. Resistance is felt at the pleural surface with the initial passage, and the resistance should decrease with each subsequent passage. The dilators must be advanced until they just pass the pleura.
The lumen of the thoracostomy tube has a tapered dilator. This is placed over the guide wire, past the pleura, and into the pleural space. The tube is scored to provide a gauge of the depth of insertion. After the tube is placed at the desired depth (≥10 cm deep and aimed toward the apex of the lung), the inner apparatus, which includes the guide wire and the last dilator, is removed, and the tube is attached to a pleural drainage device.
The tube is then sutured in place with 1-0 or 2-0 suture material and dressed with gauze. A chest radiograph is obtained to document tube placement and to assess the change in the pneumothorax. Progressive dilation of soft tissue limits the size of the incision, limits the amount of soft tissue subject to stretching, and provides a natural soft tissue seal around the tube.
Placement of a chest tube by means of the blunt dissection technique follows the same initial steps in preparation of the site. The choice of insertion method depends on the operator’s experience and skill. The blunt dissection technique typically causes more pain than the Seldinger technique.
After the site is prepared and anesthetized, a horizontal incision is made with a scalpel at the level of the fifth rib. A subcutaneous tunnel is created by means of blunt dissection with a hemostat, a Kelley clamp, or even a finger. This tunnel eventually passes over the fifth rib and into the pleural space. It is directed superiorly and obliquely to the incision before the pleural space is entered.
The pleural space is entered with the metal instrument. A considerable amount of force may be needed, and entry is usually associated with a sudden decrease in resistance as the instrument is pushed through. Once in, the instrument is opened to widen the opening. A finger is also passed through the ribs into the pleural space and swept around to loosen any adhesions or loculations that may be present.
The tube is then inserted into the pleura by passing it through the opening or by using the clamp to guide the tube in place. Some chest tubes are packaged with a trocar to assist with placement, but these pose a risk of damaging the underlying lung, and caution is advised with their use. After the tube is placed in the desired position, the tube is sutured and dressed, and a chest radiograph is obtained.
Most intensive care unit (ICU) patients are treated by intensivists, specialists well versed in ventilator management, and do not require additional consultation. In medical centers where the ICU is open and where intensivists are not primarily involved in the patients’ care, an intensivist or pulmonologist should be consulted for management of barotrauma.
On rare occasions, a thoracic surgeon may have to be consulted for assistance in the management of a persistent air leak in a patient with a long-standing chest tube.
Further inpatient care
The main issue in the subsequent management of pneumothoraces related to barotrauma involves the duration of placement of the thoracostomy tube and its removal.
Chest radiography provides information about the placement of the tube and the resolution of the pneumothorax. Serial (daily) chest radiographs can be obtained to confirm resolution of the pneumothorax. Recurrent air or persistent air may herald the need for another thoracostomy tube.
Bedside examination of the water-seal chamber for air is another method to determine whether an air leak has sealed or resolved. Closure of the air leak is obvious when the air leak is large because air would appear with every inspiratory cycle in a mechanically ventilated patient. Once the air leak has sealed, the large air leaks also disappear.
Positive intrathoracic pressure (usually created by asking the patient to cough) may be necessary to elicit passage of air in a patient who is not receiving mechanical ventilation. Small air leaks can be difficult to detect during bedside examination because air may not appear in the water-seal chamber for several respiratory cycles.
The use of suction in these patients is somewhat controversial. Some patients are treated with suction to facilitate evacuation of the pleural space air. However, continuous suction may also promote persistence of the bronchopleural fistula as the pressure gradients continue to favor flow from the airways (positive pressure) to the pleural space (negative pressure with suction).
The other approach is to leave the tube on water seal (no suction). This is intended to permit the air leaks to close and still allow pleural air to be evacuated. However, this is not a feasible option if the pleural space air is not completely evacuated and if a pneumothorax persists with the water seal.
Persistent air leaks pose particularly difficult management problems. The patient’s underlying lung disease and condition usually preclude any surgical closure. Surgery is difficult because the location of the leak is unlikely to be readily evident in reference to the barotrauma that occurs during mechanical ventilation. Surgical intervention may be possible in patients with penetrating chest injuries or other trauma.
Treatment of the underlying lung disease and use of a low tidal volume for ventilation may facilitate closure. Some concern may exist that higher levels of PEEP may delay or preclude closure of the bronchopleural fistula and PEEP is discontinued if persistent air leaks are detected. However, this may need to be balanced against goals of oxygenation.
Anecdotal reports mention the use of fibrin glue, instilled bronchoscopically or surgically, to close the air leaks. This therapy can be considered on a case-by-case basis. Its efficacy is variable, and no data support its application over general supportive care.
When air leaks persist, it is important to determine that the air leak is from the pleural space rather than from a break in the tubing apparatus to the pleural drainage. Clamping the tube at the site of exit from the chest wall can help in this determination. Air leaks that continue even with the tube clamped indicate a leak somewhere in the system.
After observations from the bedside examination of the water-seal chamber and after chest radiographs suggest resolution of the pneumothorax and closure of the air leak for approximately 24 hours, preparations can be made to remove the thoracostomy tube. The steps performed before the tube is removed can vary.
The tube is initially placed to water seal in the event that the patient has been receiving continuous suction. If the patient’s condition is stable with the water seal after 4-6 hours, a chest radiograph is obtained to determine if the pneumothorax is recurring. Some clinicians remove the thoracostomy tube at this time, but this strategy is best reserved for patients who have a pleural tube placed to drain pleural fluid.
In patients who have thoracostomy tubes in place because of a pneumothorax, the tube should be clamped at the chest wall with 2 clamps to absolutely block the passage of any air from the pleural space. After the tube is clamped, a repeat chest radiograph is obtained in 4-6 hours with the tube removed to assess for any recurrence of the pneumothorax. If no recurrence is found, the tube can be removed.
The timing of thoracostomy tube removal with respect to the respiratory cycle is somewhat controversial. Removal of the tube at end-inspiration is based on the rationale that the lung is maximally expanded and the pleural surfaces are opposed, an arrangement that minimizes the likelihood of air entering the pleural space. However, negative pleural pressures are at their greatest.
Removal at end-expiration occurs when the differences between pleural and atmospheric pressures are minimal and pleural pressures are positive; this minimizes air entry into the pleural space.
In both circumstances, a Valsalva maneuver is performed. Some ask the patient to hum during the removal process. No data support one method over the other; personal preferences and experience may be the deciding factors.
In either circumstance, care must be taken to place occlusive gauze at the entry site during tube removal and to remove the tube rapidly. A suture may be necessary to close the site. Although follow-up chest radiography is not a universal practice, most physicians obtain an image and often continue with serial imaging, especially if mechanical ventilation is continued.
Management of the other manifestations of barotrauma is usually symptom based and mainly consists of ventilator adjustments and serial imaging. Subcutaneous emphysema, pulmonary interstitial emphysema (PIE), pneumomediastinum, pneumopericardium, or air cysts may not progress to a pneumothorax, especially if the ventilator settings are adjusted to further minimize VILI.
In some patients with massive subcutaneous emphysema, incisions made in the skin over the anterior chest wall, or blowholes, may facilitate resolution of the subcutaneous air. Serial imaging should continue because it may help identify an early pneumothorax earlier, before signs that might permit bedside diagnosis appear and before it progresses to a tension pneumothorax.
Transfer of patients at risk for barotrauma or with barotrauma to other facilities is not usually considered, because these patients often are critically ill and unable to tolerate transfer.
In some patients and in some circumstances, the risks of barotrauma must be minimized en route to a facility, or the staff must be prepared to manage the life-threatening consequences of barotrauma (tension pneumothorax) if they occur. Proper management of ventilator settings is required. Also required is the ability to recognize a tension pneumothorax at the bedside without chest imaging and the capacity to proceed with needle thoracostomy or tube thoracostomy as the available equipment permits.
Transport of patients with thoracostomy tubes requires close attention to prevent dislodgement of the tube or kinking of the tubing and thereby prevent the egress of pleural air.
Further outpatient care
Once mechanical ventilation can be discontinued, the major risk for further barotrauma is removed. No specific outpatient management for barotrauma is described, but most patients have some underlying pulmonary condition that may limit the rapidity of their recovery.
Optimizing ventilator settings using low tidal volume and low plateau pressures provides a mortality benefit in patients with ARDS. Although the low tidal volume approach has not been validated in patients without ALI or ARDS, patients may develop evidence of ALI with high tidal volume ventilation.
Recognizing the deleterious effects of alveolar overdistention, limiting plateau pressures to less than 30 cm water while balancing other ventilator settings (tidal volume and PEEP) against oxygenation and metabolic parameters may be an effective approach for all patients, irrespective of the cause of their respiratory failure.
The average tidal volume used for mechanical ventilation has decreased over time. It is clearly not 6 mL/kg PBW, as indicated in the ARDS Network trial; it lies somewhere in the range of 8-10 mL/kg PBW and is certainly lower than the 12 mL/kg PBW volume applied to control patients in the aforementioned trial. This middle range of tidal volume may confer the same mortality benefit as the low tidal volume approach, but without the hypoventilation, hypercapnia, respiratory acidosis, and atelectasis noted with low tidal volumes.
Nutrition is important in the treatment of mechanically ventilated patients, but no specific dietary recommendations are known to affect the incidence of barotrauma or the course of ARDS.
Because this discussion of barotrauma is limited to mechanically ventilated patients, discussion of activity levels is not relevant here. The ventilator limits the patient’s movement, as does the thoracostomy tube.
After mechanical ventilation is discontinued, however, patients may be able to resume rehabilitative exercises and reconditioning, with limitations dictated by any tube attached to the patient’s chest.
The morbidity and mortality attributed to barotrauma are related to the severity of its manifestations in the patient, and these manifestations tend to reflect the underlying disease more than they do the barotrauma itself.
Given the spectrum of presentations, pneumothorax is the only manifestation expected to affect morbidity or mortality. Local complications (eg, bleeding, infection) can be related to the thoracostomy tube. If undetected, the pneumothorax can result in adverse consequences related to its cardiopulmonary effects (eg, hypotension, shock, hypoxemia, cardiac ischemia). Secondary effects, if corrected or eliminated, have little effect on the patient.
Pulmonary interstitial emphysema (PIE) or air along tissue planes (eg, subcutaneous emphysema, pneumomediastinum) may be the only manifestation in some patients. This finding is more a radiographic diagnosis than a clinical entity and is without clinical significance. However, it can be a harbinger of a pneumothorax. In one series, mediastinal emphysema led to a subsequent pneumothorax in 42% of patients.
Pneumothoraces can be life threatening, especially if they are not recognized and not treated. However, the effect of barotrauma on morbidity and mortality is mixed. In the 2000 Acute Respiratory Distress Syndrome (ARDS) Network trial of low versus high tidal volume, the incidence of barotrauma was similar between the groups, although the mortality rate was lower in the low tidal volume group.  Other series of patients with ARDS have not identified pneumothoraces as a cause of increased mortality in these patients.
Although a pneumothorax is a risk factor for mortality, it is more likely a reflection of the severity of the underlying lung disease than a cause of death. In one series of patients with ARDS, less than 2% of 66 deaths were directly attributable to a pneumothorax.
Early ventilator practices using high tidal volumes and resulting in high peak inspiratory pressures and plateau pressures may confound some of these data. In early series, the incidences of barotrauma and subsequent mortality were high and were associated with the barotrauma. When low tidal volumes were used along with low plateau pressures, the incidence of barotrauma decreased.
Although barotrauma did not appear to influence mortality in an interventional trial comparing low with high tidal volume, an observational study of more than 5000 intensive care unit (ICU) patients showed that barotrauma increased the median length of mechanical ventilation and ICU stay by 2 days and increased the mortality rate by 12% (from 39% to 51%). 
Overall, the prognosis for recovery from barotrauma is anticipated to be excellent; however, its effects at the time of the event and the patient’s underlying comorbidities and lung disease affect the prognosis. To provide perspective, the mortality rate from ARDS has been steadily decreasing over the past few decades, approaching or exceeding 70% in the early 1980s and declining to the 30-40% range and even lower (< 30%) in recent prospective trials. [8, 20]
Patient education does not affect the incidence of barotrauma, although education may improve a patient’s understanding of this complication and his or her underlying disease.
The use of optimal ventilator settings and prompt recognition of the signs of barotrauma and a tension pneumothorax are key to management and, therefore, are the areas of focus for educational efforts. These educational efforts should be directed at all health care providers—specifically, physicians, nurses, and respiratory therapists—who are involved in the care of mechanically ventilated patients.