Clinical Image
1 Resident Physician, Department of Medicine, University of Wisconsin Hospitals and Clinics, Madison, Wisconsin, USA
Address correspondence to:
Kirsten Marie Lipps
Department of Medicine, University of Wisconsin Hospitals and Clinics, 1685 Highland Avenue, 5158 Medical Foundation, Centennial Building, Madison, WI 53705-2281,
USA
Message to Corresponding Author
Article ID: 101191Z01KL2021
No Abstract
Keywords: Acute respiratory distress syndrome, Mechanical ventilation, Pulmonary barotrauma
A 57-year-old woman with chronic obstructive pulmonary disease (COPD), decompensated cirrhosis, and hepatopulmonary syndrome developed severe acute respiratory distress syndrome (ARDS) of presumed viral etiology. The patient was intubated and mechanically ventilated for management of hypoxemic respiratory failure. During a standard interruption of sedation on Hospital Day 5, the patient self-extubated. She was initially supported with non-invasive positive pressure ventilation, but she developed recurrent, progressive, hypoxemic respiratory failure. Thus, she was electively re-intubated and mechanically ventilated on Hospital Day 11.
Shortly after re-intubation, the patient had evidence of pulmonary barotrauma, with mild crepitus in her chest. This rapidly progressed to overt distention of her face, neck, trunk, and extremities. Radiographic (Figure 1) and computed tomographic (Figure 2, Figure 3A and Figure 3B) imaging following re-intubation demonstrated diffuse subcutaneous emphysema, a large pneumomediastinum, and a small, right-sided pneumothorax. The extensive pulmonary barotrauma was presumed due to alveolar rupture, precipitated by reduced lung compliance, which is characteristic of severe ARDS. However, direct airway trauma, particularly related to endotracheal tube removal by the patient, could not be entirely excluded.
Although manifestations of the patient’s pulmonary barotrauma were apparent clinically and radiographically, her hemodynamic status and pulmonary mechanics were unaffected. Consequently, the patient was managed conservatively with lung-protective mechanical ventilation and remained hemodynamically stable. However, she developed progressive lung injury related to severe ARDS, which was refractory to salvage therapies, including deep sedation, neuromuscular paralysis, prone positioning, high-dose glucocorticoids, and inhaled epoprostenol. Four weeks after admission, the patient was terminally extubated and expired.
Pulmonary barotrauma is caused by alveolar rupture in the setting of elevated trans-alveolar pressures. The consequences of an extrapulmonary air leak include subcutaneous emphysema, pneumothorax, pneumomediastinum, and pneumoperitoneum [1]. The incidence of pulmonary barotrauma is estimated between 2% and 10% and varies based on the presence of underlying pulmonary disease [2]. The incidence in ARDS patients is approximately 10% [2],[3],[4]. Positive-pressure mechanical ventilation is the most important risk factor leading to the development of pulmonary barotrauma [5]. However, underlying pulmonary disease is also typically present in patients who develop this complication. Disease processes associated with reduced lung compliance and/or dynamic lung hyperinflation increase the risk for development of pulmonary barotrauma. Decreased compliance is typical of ARDS, pneumonia, and interstitial lung disease, whereas hyperinflation is seen in COPD and asthma [2],[6].
Early recognition of pulmonary barotrauma is essential for prevention of hemodynamic and respiratory collapse. For patients who develop pneumothorax or pneumomediastinum, pulmonary barotrauma is typically diagnosed via imaging. Plain chest radiography is first line, though in mechanically ventilated patients, free air may accumulate in atypical locations due to supine or semi-recumbent positioning. Further, pneumothorax and pneumomediastinum may be obscured by the presence of extensive subcutaneous emphysema. In such cases, chest computed tomography may be required for diagnosis. Pulmonary barotrauma may also be diagnosed clinically, particularly in patients with extensive subcutaneous emphysema. For patients with a non-tension pneumothorax, clinical signs include absent or reduced unilateral breath sounds, acute increase in peak and plateau pressures, decrease in expired tidal volume, and patient–ventilator dyssynchrony.
Although rare cases of tension pneumomediastinum and compartment syndrome have been reported, most incidences of pulmonary barotrauma are well tolerated [7]. Conservative management focuses on treating underlying pulmonary disease and utilizing lung-protective mechanical ventilation strategies. Plateau pressure, which is the pressure applied to the small airways and alveoli, should be limited to 35 cm H2O or less, as higher values are associated with the development of pulmonary barotrauma [8],[9]. Low tidal volumes are also an important component of lung-protective mechanical ventilation. However, large randomized controlled trials have failed to demonstrate a reduction in the incidence of pulmonary barotrauma in ARDS patients ventilated with low tidal volumes [4],[10],[11]. For patients with obstructive lung disease, avoidance of dynamic hyperinflation is critical, as elevated intrinsic positive end-expiratory pressure (PEEP) increases plateau pressure. In contrast, high levels of extrinsic PEEP are not associated with a higher incidence of pulmonary barotrauma [3],[12].
Pulmonary barotrauma typically has minimal effect on cardiorespiratory status and is rarely a direct cause of mortality. However, pulmonary barotrauma is associated with poor overall prognosis for patients with ARDS, as it occurs with greater frequency in patients with severe lung injury [13],[14]. Consequently, early identification and targeted management of the etiology of ARDS are essential to prevent irreversible lung injury.
Pulmonary barotrauma is precipitated by positive-pressure mechanical ventilation in the setting of underlying lung disease. It occurs in approximately 10% of mechanically ventilated patients with ARDS. Although cases of pulmonary barotrauma may be clinically and radiographically striking, this complication typically has minimal effect on hemodynamic or pulmonary mechanic parameters. Conservative management is standard of care in stable patients and focuses on treating underlying pulmonary disease and utilizing lung-protective mechanical ventilation strategies. Pulmonary barotrauma is rarely a direct cause of mortality but is a poor prognostic marker in patients with ARDS, as it most often occurs in patients with severe underlying lung injury.
1.
2.
Anzueto A, Frutos-Vivar F, Esteban A, et al. Incidence, risk factors and outcome of barotrauma in mechanically ventilated patients. Intensive Care Med 2004;30(4):612–9. [CrossRef] [Pubmed]
3.
Brower RG, Lanken PN, MacIntyre N, et al. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med 2004;351(4):327–36. [CrossRef] [Pubmed]
4.
Acute Respiratory Distress Syndrome Network, Brower RG, Matthay MA, et al. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000;342(18):1301–8. [CrossRef] [Pubmed]
5.
Haake R, Schlichtig R, Ulstad DR, Henschen RR. Barotrauma. Pathophysiology, risk factors, and prevention. Chest 1987;91(4):608–13. [CrossRef] [Pubmed]
6.
Gammon RB, Shin MS, Groves RH Jr, Hardin JM, Hsu C, Buchalter SE. Clinical risk factors for pulmonary barotrauma: A multivariate analysis. Am J Respir Crit Care Med 1995;152(4 Pt 1):1235–40. [CrossRef] [Pubmed]
7.
Shennib HF, Barkun AN, Matouk E, Blundell PE. Surgical decompression of a tension pneumomediastinum. A ventilatory complication of status asthmaticus. Chest 1988;93(6):1301–2. [CrossRef] [Pubmed]
8.
Boussarsar M, Thierry G, Jaber S, Roudot-Thoraval F, Lemaire F, Brochard L. Relationship between ventilatory settings and barotrauma in the acute respiratory distress syndrome. Intensive Care Med 2002;28(4):406–13. [CrossRef] [Pubmed]
9.
Amato MB, Barbas CS, Medeiros DM, et al. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med 1998;338(6):347–54. [CrossRef] [Pubmed]
10.
Brochard L, Roudot-Thoraval F, Roupie E, et al. Tidal volume reduction for prevention of ventilator-induced lung injury in acute respiratory distress syndrome. The Multicenter Trail Group on Tidal Volume reduction in ARDS. Am J Respir Crit Care Med 1998;158(6):1831–8. [CrossRef] [Pubmed]
11.
Brower RG, Shanholtz CB, Fessler HE, et al. Prospective, randomized, controlled clinical trial comparing traditional versus reduced tidal volume ventilation in acute respiratory distress syndrome patients. Crit Care Med 1999;27(8):1492–8. [CrossRef] [Pubmed]
12.
Santa Cruz R, Rojas JI, Nervi R, Heredia R, Ciapponi A. High versus low positive end-expiratory pressure (PEEP) levels for mechanically ventilated adult patients with acute lung injury and acute respiratory distress syndrome. Cochrane Database Syst Rev 2013;2013(6):Cd009098. [CrossRef] [Pubmed]
13.
Schnapp LM, Chin DP, Szaflarski N, Matthay MA. Frequency and importance of barotrauma in 100 patients with acute lung injury. Crit Care Med 1995;23(2):272–8. [CrossRef] [Pubmed]
14.
Weg JG, Anzueto A, Balk RA, et al. The relation of pneumothorax and other air leaks to mortality in the acute respiratory distress syndrome. N Engl J Med 1998;338(6):341–6. [CrossRef] [Pubmed]
Kirsten Marie Lipps - Conception of the work, Design of the work, Acquisition of data, Drafting the work, Revising the work critically for important intellectual content, Final approval of the version to be published, Agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.
Anatoliy V Nechyporenko - Conception of the work, Design of the work, Acquisition of data, Drafting the work, Revising the work critically for important intellectual content, Final approval of the version to be published, Agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.
Guarantor of SubmissionThe corresponding author is the guarantor of submission.
Source of SupportNone
Consent StatementWritten informed consent was obtained from the patient for publication of this article.
Data AvailabilityAll relevant data are within the paper and its Supporting Information files.
Conflict of InterestAuthors declare no conflict of interest.
Copyright© 2021 Kirsten M Lipps et al. This article is distributed under the terms of Creative Commons Attribution License which permits unrestricted use, distribution and reproduction in any medium provided the original author(s) and original publisher are properly credited. Please see the copyright policy on the journal website for more information.