Barotrauma and Mechanical Ventilation 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 has been controversial. The two parameters are inextricably 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 [cm] – 152.4) or 50 + 2.3 (height [in.] – 60). For women, PBW was calculated as 45.5 + 0.91 (height [cm] – 152.4) or 45.5 + 2.3 (height [in.] – 60).

Low tidal volume was also associated with improvements in ventilator-free days and in the incidence of nonpulmonary organ failure. However, the ARDS Network trial has been 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.

In this trial, plateau pressures were limited to less than 30 cm H₂O 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 have supported the use of low tidal volumes. It is also worth noting 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 relation was detected between peak airway pressure, plateau pressure, mean airway pressure, or driving pressure (plateau pressure – PEEP) and the development of barotrauma. However, higher concurrent PEEP was consistently associated with barotrauma, with a relative hazard of 1.67 for every increment of 5 cm H₂O.

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 focused on increasing PEEP levels in conjunction with an approach involving low tidal volume and limited plateau pressure. ^[18]

Across the differing study protocols, the levels of PEEP used in the higher-PEEP group averaged 13-15 cm H₂O, compared with those in the lower-PEEP group, which averaged 6-8 cm H₂O. No mortality benefit was found with any of the trials, but improvement was noted in secondary study endpoints in two of the three main trials, with improvement in hypoxemia, acidosis, use of rescue therapies, ventilator-free days, and organ failure–free days in the higher-PEEP group. ^{[19, 20]}

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% to 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. No barotrauma was noted in either group, with average PEEPs of 12 and 18 cm H₂O administered in the two groups. Technical issues and limited availability of expertise may limit the use of this approach while the results of larger trials are being awaited. ^[21]

In 2017, results were published from the Alveolar Recruitment for ARDS Trial (ART), which was designed to determine whether lung recruitment associated with PEEP titration according to the best respiratory-system compliance decreased 28-day mortality in patients with moderate-to-severe ARDS as compared with a conventional low-PEEP approach. ^[22]  The former strategy was found to increase 28-day all-cause mortality; accordingly, the investigators concluded that routine use of lung recruitment and PEEP titration was not supported in these patients.

In summary, using low tidal volumes ^[23] 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 H₂O. No mortality benefit has been conclusively demonstrated with higher PEEP ^{[24, 25]} (though one meta-analysis did find a benefit in a subset of patients ^[26] ), 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 assessing neuromuscular blockade with 48 hours of cisatracurium against placebo (N = 340), there was a statistically lower proportion with barotrauma in the treatment group (5% vs 11.7%). ^[10]  No increase was noted in plateau pressure readings prior to the episode of barotrauma (primarily pneumothoraces), but patients with barotrauma did have higher minute ventilation than control subjects did.

Pneumothoraces also occurred earlier in the course of this study, ^[10] which may provide further support for the barotrauma-protective effects with early use of cisatracurium. A mortality benefit for cisatracurium was suggested, but statistical significance was not achieved. There was no increased in neuromuscular weakness associated with cisatracurium use.

The findings from this study notwithstanding, the potential for adverse effects with neuromuscular blockade has given rise to uncertainty regarding the minimally effective duration of such blockade and the concentration of benefit among those with the most severe ARDS (PaO₂/FIO₂ < 120). A meta-analysis of 431 patients, all from the same study group, also noted a reduction in barotrauma (5% vs 9.7%). ^[27]  A subsequent meta-analysis of 1598 ARDS patients reported a significant decrease in the incidence of barotrauma with the use of neuromuscular blockade. ^[28]

There remains a need for additional confirmatory investigations before neuromuscular blockade can be endorsed for routine use in this setting.

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 in the 2000s were generally disappointing. ^{[29, 30]}  No mortality difference was demonstrated, and the possibility of increased adverse events in patients treated with corticosteroids late (>14 days) into the course was suggested. However, a multicenter randomized controlled study from 2020 found that early administration of dexamethasone reduced the duration of mechanical ventilation and overall mortality in patients with moderate-to-severe ARDS. ^[31]

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 the proposition that corticosteroid therapy reduces barotrauma. However, a small study in which corticosteroids were administered 3 days after the onset of ALI or ARDS documented a definite, albeit nonsignificant, decrease in the incidence of pneumothorax in the control group (8% vs 21%). 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 supine. 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- to 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-tip 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 three dilators, which are passed over the wire one 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.

The main issue in the subsequent management of pneumothoraces related to barotrauma involves the duration of placement of the thoracostomy tube and its removal. (See Tube Thoracostomy Management.)

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 two 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 dislodgment of the tube or kinking of the tubing and thereby prevent the egress of pleural air.

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.

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.

Optimizing ventilator settings by 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.

In view of the deleterious effects of alveolar overdistention, limiting plateau pressures to less than 30 cm H₂O 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.

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, it may be necessary to consult a thoracic surgeon for assistance in the management of a persistent air leak in a patient with a long-standing chest tube.