Barotrauma and Mechanical Ventilation Clinical Presentation

Updated: Feb 11, 2022
  • Author: Guy W Soo Hoo, MD, MPH; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
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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.

This definition was subsequently modified by a consensus group; the result is often referred to as the Berlin definition. The Berlin definition eliminated the need to measure the PAWP but retained the need to eliminate cardiogenic pulmonary edema as the cause of hypoxemic respiratory failure. Thresholds were specified for PEEP requirements (≥10 cm H2O), minute ventilation (≥10 L/min), and respiratory system compliance (< 40 mL/cm H2O). Three mutually exclusive categories of hypoxemia were also defined, as follows [15] :

  • Mild (PaO 2/FIO 2 >200 but ≤ 300)
  • Moderate (PaO 2/FIO 2 >100 but ≤ 200)
  • Severe (PaO 2/FIO 2 ≤ 100)

Some differences in ARDS may be based on whether the inciting cause involves direct lung injury (eg, from pneumonia, gastric acid aspiration, or pulmonary contusion) or indirect lung injury (eg, from sepsis, trauma with shock, acute pancreatitis, or 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 vein or the subclavian vein.

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.


Physical Examination

The manifestations of barotrauma span the entire clinical spectrum, from total absence of symptoms 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 are unable to communicate as a consequence of intubation, signs of respiratory distress (eg, tachypnea, patient-ventilator discoordination, use of accessory muscles [eg, neck muscles], diaphoresis, or 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 two 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 first clinical manifestation to be 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 livedo reticularis.

Some speculate that other clinical findings (eg, 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. [16]

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.