Barotrauma and Mechanical Ventilation


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, 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, such as 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 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. However, now evident is 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.


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 heterogenous 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 distension 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 perivascular interstitial emphysema or 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.

Given the description above, alveolar overdistension is the key element in the development of barotrauma. In this sense, barotrauma is a misnomer because barotrauma 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 distension, 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, which describes the injury associated with repeated opening and closing (recruitment and collapse) of collapsed alveoli during mechanical ventilation. Biotrauma has been used to describe 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. The last 2 components 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 compared with persons with healthy lungs. These differences can be gleaned from the differences in barotrauma in a large cohort evaluated on the basis of underlying lung disease. Patients with chronic obstructive lung disease have the lowest incidence of barotrauma (2.9%). The incidence is highest in persons with chronic interstitial lung disease (10%), and patients with ARDS have an intermediate rate (6.5%). This observation underscores the heterogeneity of lung disease and regional differences in lung compliance.


United States

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, however, 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 in slightly more than 6% of persons with ARDS. As is discussed in subsequent sections, the change in the incidence of barotrauma 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 a reduction in plateau pressures.


No international or geographic influences are known to affect the incidence of barotrauma. Any differences are likely small and more a reflection of the underlying disease status of the patients and of differences in ventilator management in those locations than of any ethnic or environmental influence.

International multicenter trials involving patients with ARDS revealed a decrease in the incidence of barotrauma similar to that observed in the United States, to a range of 8-15%. This decline in the incidence of barotrauma is also associated with a decline in the mortality rate from ARDS, although not of the same magnitude as the decline in barotrauma.


The morbidity and mortality attributed to barotrauma is related to the severity of its manifestations in the patient.

  • PIE or air along tissue planes (eg, subcutaneous emphysema, pneumomediastinum) may be the only manifestation in some patients. This finding is more of 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 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.1 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 are used along with low plateau pressures, the incidence of barotrauma decreases. 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 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% (39% vs 51%).2

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 30-40%.


No ethnic predisposition to barotrauma is reported.


No sex differences are known regarding the development of 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.



The main historical consideration with respect to the risk of barotrauma in mechanically ventilated patients is their risk for developing ALI and ARDS. Patients are often intubated and unable to communicate, but historical data may be elicited from their medical records. The widely accepted definition of ALI and ARDS outlines a process characterized by an acute onset, bilateral infiltrates observed on chest radiographs, information that excludes cardiogenic pulmonary edema (pulmonary artery wedge pressure <18 mm Hg), and a low ratio of partial pressure of oxygen to fraction of inspired oxygen (PaO2/FIO2 ratio), which is defined as less than or equal to 300 for ALI and less than 200 for ARDS.

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, 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, 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 VILI, although 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.


As discussed in the Introduction, 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 (contralateral). 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, as follows:

  • 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.3
  • 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 overdistension may also activate cytotoxic and proinflammatory pathways. This is often referred to as biotrauma and 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, interleukin 6, and interleukin 8 with high tidal volumes, with a reduction in levels in subjects given low tidal volumes. These cytokines are the same as those implicated in systemic inflammatory response syndrome and sepsis; this observation provides insight into another possible benefit of low tidal volume ventilation.


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 overdistension 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 Acute Respiratory Distress Syndrome 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.

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 one due to mechanical ventilation may be difficult when it occurs.


Laboratory Studies

  • 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.

Imaging Studies

Chest radiography

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.

Image shows subtle manifestations of barotrauma, ...

Image shows subtle manifestations of barotrauma, pulmonary interstitial emphysema, and subcutaneous emphysema. This patient was being treated with noninvasive ventilation. Importantly, recognize that barotrauma can be associated with noninvasive ventilation.

Image shows subtle manifestations of barotrauma, ...

Image shows subtle manifestations of barotrauma, pulmonary interstitial emphysema, and subcutaneous emphysema. This patient was being treated with noninvasive ventilation. Importantly, recognize that barotrauma can be associated with noninvasive ventilation.

Findings such as nonbranching, fixed-caliber radiolucencies radiating from the hilum to the periphery or small collections of air in interlobular septa suggest PIE or subpleural air cysts. 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.

This patient was undergoing treatment for acute r...

This patient was undergoing treatment for acute respiratory distress syndrome when a new lucency was found on a routine portable chest radiograph. The lucency over the right midlung zone represents a subpleural air cyst. Such cysts can increase in size and eventually rupture, creating a pneumothorax.

This patient was undergoing treatment for acute r...

This patient was undergoing treatment for acute respiratory distress syndrome when a new lucency was found on a routine portable chest radiograph. The lucency over the right midlung zone represents a subpleural air cyst. Such cysts can increase in size and eventually rupture, creating a pneumothorax.

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.

This patient developed a left tension pneumothora...

This patient developed a left tension pneumothorax during treatment of a severe pneumonia. Note the marked shift of the mediastinal structures to the right, the partial collapse of the left lung, and the inversion and downward displacement of the left hemidiaphragm.

This patient developed a left tension pneumothora...

This patient developed a left tension pneumothorax during treatment of a severe pneumonia. Note the marked shift of the mediastinal structures to the right, the partial collapse of the left lung, and the inversion and downward displacement of the left hemidiaphragm.

This patient had a left pneumothorax with placeme...

This patient had a left pneumothorax with placement of a left thoracostomy tube. However, this portable chest radiograph shows a persistent retrocardiac lucency, which raised questions about a persistent pneumothorax.

This patient had a left pneumothorax with placeme...

This patient had a left pneumothorax with placement of a left thoracostomy tube. However, this portable chest radiograph shows a persistent retrocardiac lucency, which raised questions about a persistent pneumothorax.

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.

CT scanning

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 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. ChestCT scanning  is desirable, but patients must be in a sufficiently stable condition to tolerate transport to the CT scanner.

ChestCT 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. 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.

This chest CT scan was obtained on the same day a...

This chest CT scan was obtained on the same day as the chest radiograph of the patient in Media File 4. The image shows a loculated pneumothorax in the mid left lung. This image illustrates the information a chest CT scan can add and the difficulty in diagnosing a pneumothorax with the limited views provided by a portable chest radiograph.

This chest CT scan was obtained on the same day a...

This chest CT scan was obtained on the same day as the chest radiograph of the patient in Media File 4. The image shows a loculated pneumothorax in the mid left lung. This image illustrates the information a chest CT scan can add and the difficulty in diagnosing a pneumothorax with the limited views provided by a portable chest radiograph.

ChestCT scanning may help with the placement of tube thoracostomy tubes in patients in whom the pneumothorax may be confined or loculated. In some patients with large air leaks, more than 1 tube 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.

Other Tests

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 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 calculations 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.


No other procedures are needed to establish a diagnosis of barotrauma.

Histologic Findings

The diagnosis of barotraumas 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.4 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.


Medical Care

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 overdistension. It follows that avoiding or minimizing alveolar overdistension is key to preventing barotrauma.

Some controversy exists regarding whether this goal is best achieved by using low tidal volumes or by limiting the plateau pressure. Both 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 ARDS. However, clinicians have recognized the hazards of alveolar overdistension 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 Acute Respiratory Distress Syndrome Network trial, ventilation of patients with ARDS 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, but no lower than 4 mL/kg PBW) 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 between the low tidal volume group and 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 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 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 regarding focusing on increasing PEEP levels in conjunction with the low tidal volume and limited plateau pressure approach.5

Acknowledging differences in study protocols, the levels of PEEP used in the higher PEEP group averaged 13-15 cm water, compared with the lower PEEP, which was 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.6,7

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 therefore guide the use of PEEP, did result in improvements in oxygenation and respiratory compliance, but it 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 both groups.  Note that technical limitations and expertise may limit the use of this approach while awaiting results of larger trials.8

In summary, low tidal volumes and limiting plateau pressures remain the preferred approach in ventilator management, and this, in turn, reduces the risk for barotrauma. No mortality benefit is reported with higher PEEP, and the optimal approach to PEEP remains to be determined. See below for the ARDS Network mechanical ventilation protocol.

Acute Respiratory Distress Syndrome Network refer...

Acute Respiratory Distress Syndrome Network reference summarizing the mechanical ventilation protocol.

Acute Respiratory Distress Syndrome Network refer...

Acute Respiratory Distress Syndrome Network reference summarizing the mechanical ventilation protocol.

Aside from ventilator adjustments, other medical approaches may help reduce the risk for barotrauma. All these are supportive in nature and include 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. Early nutritional support facilitates recovery.

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.

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 sedation should be assessed on a daily basis.

Surgical Care

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, such 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 are reviewed below.

Emergency needle 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.

After the catheter is in, 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.

Large-bore thoracostomy

A large-bore thoracostomy tube requires some preparation and time. However, with an experienced operator, such tubes can be placed in an emergency situation. Enclosed kits are available to permit tube placement using a guidewire-through-a-needle technique (Seldinger) and by using progressive dilators; this may be used as a substitute for the traditional method, which is relatively invasive and requires blunt dissection.

Commercially available kits facilitate the placement of chest tubes by using the Seldinger technique. The location of tube placement and the preparation are the same as those used with the blunt dissection technique.

In the ideal situation, the patient is lying on his or her side in bed, although 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 muscle, the latissimus dorsi, the breast, and the axillary vessels.

After the site is localized, 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 tubes of 14-20F 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 guidewire is passed through the needle. The wire is marked at approximately its halfway point to indicate the limits of guidewire passage. The guidewire should be aimed apically, but the wire does not allow for its consistent placement. The guidewire 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, and each is passed over the wire to gradually enlarge the opening. 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 need to be advanced until they just pass the pleura.

The lumen of the thoracostomy tube has a tapered dilator. This is placed over the guidewire, 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 guidewire 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 and dressed with gauze. A chest radiograph is obtained to document its 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 stretch, and provides a natural soft tissue seal around the tube.

Placement of a chest tube using 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 produces 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 eventually passes over the fifth rib and into the pleural space. The tunnel 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.


Intensivists treat most patients in the ICU. These specialists are well versed in ventilator management and do not require additional consultation. In medical centers where the ICU is open and where these specialists are not primarily involved in the patients’ care, an intensivist or pulmonologist should be consulted for management. Rarely, a thoracic surgeon may need to be consulted to assist in the management of a persistent air leak in a patient with a long-standing chest tube.


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 about activity levels is not relevant in patient care. The ventilator limits the patient’s movement, as does the thoracostomy tube. However, after mechanical ventilation is discontinued, patients may be able to resume rehabilitative exercises and reconditioning, with limitations dictated by any tube attached to the patient’s chest.


No pharmacologic agents are effective in the prevention or treatment of ALI, ARDS, or barotrauma. Effective therapy has focused on ventilator management and general supportive care.

Medical therapy is aimed at sedation, bronchodilatation, reduction of extravascular lung water, and clearance of secretions. These therapies are part of the general supportive care of patients receiving mechanical ventilation, and they are not specific to the management of barotrauma.

In patients with ALI or ARDS, corticosteroids have been an intriguing option given their potential to reduce associated inflammation and lung destruction. However, results from prospective randomized trials of corticosteroids have generally been disappointing.9,10 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 one 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 treatment.


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.

Air leak and pneumothorax resolution

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 if the 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, determining that the air leak is from the pleural space and not from a break in the tubing apparatus to the pleural drainage is important. 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.

Tube removal

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 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 with thoracostomy tubes 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.

When to remove the thoracostomy tube is somewhat controversial with respect to the respiratory cycle. Removal of the tube at end inspiration of the lung 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 the end of expiration occurs when the differences between pleural and atmospheric pressures are minimal and pleural pressures are positive, minimizing air entry into the pleural space. A Valsalva maneuver is used in both circumstances. Some ask the patient to hum during the removal process. No data supports one method over the other, and personal preferences and experience may be the deciding factors.

Care must be taken in either circumstance to place occlusive gauze at the tube entry site during its 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, 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.

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.

Inpatient & Outpatient Medications

No specific medications are used in the treatment of ALI, ARDS or barotrauma. Early administration of corticosteroids may prove beneficial, but this remains a treatment strategy under investigation.

Medications used in the management of barotrauma are focused on symptomatic relief in patients who require mechanical ventilation or are focused on treating their underlying condition.


Transfer of patients at risk for barotrauma or with barotrauma to other facilities is not usually considered because they are often critically ill and cannot 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, as outlined in other sections, is required. Also needed is the ability to recognize a tension pneumothorax at the bedside without chest imaging and the knowledge 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.


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 overdistension, 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.

Of note, the average tidal volume used for mechanical ventilation has decreased over time. It is clearly not 6 mL/kg PBW, as indicated in the Acute Respiratory Distress Syndrome Network trial, but 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.


Complications of barotrauma range from asymptomatic 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.


Morbidity and mortality related to barotrauma are more a reflection of the underlying disease than of 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. 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.

Patient Education

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 therapist, who are involved in the care of mechanically ventilated patients.


Medicolegal Pitfalls

Improved understanding of the mechanisms underlying VILI and barotrauma makes it imperative for physicians adjust ventilator settings to prevent alveolar overdistension. Some controversy remains regarding the optimal low tidal volume for ventilation and the best parameter to monitor its effect (ie, plateau pressure). Although ventilation with low tidal volume is effective, clinicians have been slow to adopt this approach. The tidal volume used for mechanically ventilated patients had decreased over time, and current practice involves tidal volumes (8-10 mg/kg PBW) that are lower than those used in the past.  Limiting plateau pressures to less than 30 cm water may be another effective approach for all patients. With volume ventilators, this is best accomplished with low tidal volumes.

The failure to monitor patients for signs of barotrauma and the failure to diagnosis and treat a pneumothorax in a mechanically ventilated patient may subject a practitioner to medicolegal action. Unless limitations of care are established, drainage of a pneumothorax in a mechanically ventilated patient is imperative given its life-threatening potential and the lack of effective alternatives.

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