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Volume 2, Issue 4, Pages 173-175 (2009)


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Successful use of high-frequency oscillator ventilation for acute respiratory distress syndrome with pneumomediastinum

Adriano R. TonelliabCorresponding Author Informationemail address, Orlando I. Ruiz-Rodriguezaemail address, Edgar J. Jimenezabemail address

Received 2 December 2008; accepted 12 January 2009.

Abstract 

We report the successful use of high-frequency oscillatory ventilation without recruitment maneuvers in a patient with ARDS and severe hypoxemia who developed a pneumomediastinum during conventional mechanical ventilation. High-frequency ventilation is an attractive modality for the treatment of pneumomediastinum, especially when the airway pressures cannot be reduced by variation in the settings of the conventional mechanical ventilator.

Article Outline

Abstract

1. Introduction

2. Case presentation

3. Discussion

4. Conclusion

Conflict of interest statement

References

Copyright

1. Introduction 

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Conventional mechanical ventilation, especially if large tidal volumes are used, can lead to ventilator-induced lung injury (VILI) in patients with adult respiratory distress syndrome. Pneumomediastinum is one of the manifestations of VILI. The treatment of pneumomediastinum in patients with ARDS can be challenging as a result of the high airway pressures frequently observed during conventional mechanical ventilation. High airway pressures may lead to an increase in the amount of air collected in the mediastinum and produce hemodynamic instability. A reduction in the airway pressures by using high-frequency oscillatory ventilation (HFOV) is an attractive approach for the management of pneumomediastinum in patients with ARDS.

2. Case presentation 

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A 21-year-old Haitian woman, with an ideal body weight of 75kg and known positive serology for human immunodeficiency virus, presented with febrile syndrome and new infiltrates on the chest radiography. In a matter of hours the patient developed adult respiratory distress syndrome (ARDS) with severe hypoxemic respiratory failure that required intubation and mechanical ventilation (Fig. 1, Fig. 2, panel A). Her initial settings were volume control with a tidal volume of 600ml (8ml/kg), positive end expiratory pressure (PEEP) of 18cmH2O, fraction of inspired oxygen 100% and respiratory rate of 24 per minute. With this initial setting the patient had high airway pressures (Peak pressure of 55cmH2O, Mean pressure of 26cmH2O and Plateau pressure of 49cmH20). These high airway pressures, in part due to the relatively large tidal volume used, led to the occurrence of pneumomediastinum and subcutaneous emphysema. In spite several modifications of the conventional ventilator parameters, including a rapid reduction of the tidal volume to 5ml/kg, the high airway pressures persisted despite neuromuscular blockade and diverse manipulations of the mechanical ventilator (different modes of ventilation, reduction of the inspiratory flow and inverse I/E ratio). In addition the patient's hypoxemia (PaO2/FIO2 91) aggravated. The patient remained hemodynamically stable throughout the hospitalization and did not develop a pneumothorax.


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Fig. 1 Portable chest radiography, obtained during the second day of hospitalization, showing extensive alveolar infiltrates and pneumomediastinum (arrows) (Panel A). Four weeks after the admission the chest radiography showed resolution of the infiltrates and pneumomediastinum (Panel B).



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Fig. 2 Computed tomography of the chest without intravenous contrast showing extensive alveolar infiltrates, pneumomediastinum (arrows) and subcutaneous emphysema (Panel A). A second computed tomography obtained 4 weeks after the admission showed significant improvement of the infiltrates and resolution of the pneumomediastinum and subcutaneous emphysema.


On the second day of hospitalization, prompted by worsening oxygenation, the patient was placed on high-frequency oscillator ventilation (HFOV) with mean pulmonary pressure of 24cmH2O, frequency 4.5Hz, inspiratory time 33%, power 6, amplitude of oscillation 74cmH2O and FIO2 100%. Under the possibility of increasing the pneumomediastinum, no recruitment maneuvers were used. In a few days the subcutaneous emphysema and pneumomediastinum (assessed by chest radiography) resolved. Thereafter, the FIO2 and the mean pressure were decreased and 11 days later, the HFOV was discontinued and the patient was placed on pressure control with inspiratory pressure of 18cmH2O, PEEP of 10cmH2O and FIO2 of 50%. Four weeks after the admission the lung infiltrates almost completely resolved (Fig. 1, Fig. 2, panel B) and she had adequate arterial blood gases on tracheostomy mask with FIO2 28%. The etiology of the ARDS is uncertain as the patient did not undergo necessary diagnostic studies due to her respiratory instability. Initial sputum culture only showed normal respiratory flora with negative fungal and acid fast bacilli (AFB) stains and culture. Streptococcus pneumoniae, Legionella and histoplasma urinary antigens were negative. She improved with empiric treatment for Pneumocystis jirovecii and bacterial pneumonia.

3. Discussion 

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Pneumomediastinum is manifestation of VILI and can occur in patients with ARDS due to barotrauma. The progressive accumulation of air in the mediastinum can lead to 1) hemodynamic instability by reducing venous return and compromising cardiac output, 2) atelectasis with potential increases in the airway pressures, and 3) venous air embolism.1 Its prevention and management include a reduction in the airway pressures by using a lung protective strategy, however this strategy may lead to deterioration of the already compromised oxygenation. Studies of HFOV in patients with ARDS have being associated with improvements in oxygenation when compared with conventional mechanical ventilation, nevertheless a survival advantage of the former ventilator modality needs yet to be proven.2

A potential application of HFVO is in the treatment of VILI. There are case reports supporting the use of HFVO for tension pneumatocele,3 bronchopleural fistula4 and bilateral pneumothoraces with persistent air leaks.5 A related condition, pneumomediastinum, can be difficult to treat in the context of patients with severe hypoxemia due to ARDS, as the high airway pressure frequently observed with conventional mechanical ventilation may aggravate the amount of air collected in the mediastinum. An alternative approach is to use HFOV, which is considered a lung protective ventilator strategy mainly by two mechanisms. Firstly, it generates smaller tidal volumes (1–2ml/kg) at higher frequencies (>100breath/min), resulting in less alveolar overdistension and lower peak inspiratory airway pressures. Secondly, oscillation provides adequate ventilation at relatively high mean airway pressure with smaller pressure variations, avoiding potentially injurious peak pressure and cyclical alveolar collapse.6 Although animal studies have shown less histological small airway and alveolar injury with the use of HFOV,7 in humans, the only two randomized controlled trials of HFOV versus conventional mechanical ventilation showed no differences in the rate of barotraumas between the treatment groups.8, 9

Little is known about the use of HFVO for the treatment of ARDS complicated with pneumomediastinum in adult patients. A review of the literature revealed a successful treatment with HFOV with recruitment maneuvers of ARDS complicated with pneumomediastinum in an 18-month-old patient.1

Using HFOV without recruitment maneuvers, we successfully treated an adult patient that developed severe hypoxemia due to ARDS, complicated by the occurrence of pneumomediastinum. The patient required this mode of ventilation for several days due to ARDS, whereas the pneumomediastinum rapidly resolved in a few days of treatment.

4. Conclusion 

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High-frequency oscillatory ventilation without recruitment maneuvers is a useful ventilatory modality in patients with severe hypoxemia associated with ARDS and pneumomediatinum. Further research is needed to support these findings.

Conflict of interest statement 

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The authors have no conflict of interest.

References 

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1. 1McGinley J, Corcoran T, Canny G, O'Hare B. A case of pneumomediastinum in paediatric ARDS: to oscillate or not?. Paediatr Anaesth. 2001;11:366–369. MEDLINE | CrossRef

2. 2Chan KP, Stewart TE, Mehta S. High-frequency oscillatory ventilation for adult patients with ARDS. Chest. 2007;131:1907–1916. MEDLINE | CrossRef

3. 3Shen HN, Lu FL, Wu HD, Yu CJ, Yang PC. Management of tension pneumatocele with high-frequency oscillatory ventilation. Chest. 2002;121:284–286. MEDLINE | CrossRef

4. 4Baumann MH, Sahn SA. Medical management and therapy of bronchopleural fistulas in the mechanically ventilated patient. Chest. 1990;97:721–728. MEDLINE | CrossRef

5. 5Galvin I, Krishnamoorthy R, Saad RS. Management of advanced ARDS complicated by bilateral pneumothoraces with high-frequency oscillatory ventilation in an adult. Br J Anaesth. 2004;93:454–456. MEDLINE | CrossRef

6. 6Fessler HE, Hess DR. Respiratory controversies in the critical care setting. Does high-frequency ventilation offer benefits over conventional ventilation in adult patients with acute respiratory distress syndrome?. Respir Care. 2007;52:595–605. MEDLINE

7. 7mai Y, Nakagawa S, Ito Y, Kawano T, Slutsky AS, Miyasaka K. Comparison of lung protection strategies using conventional and high-frequency oscillatory ventilation. J Appl Physiol. 2001;91:1836–1844.

8. 8Derdak S, Mehta S, Stewart TE, Smith T, Rogers M, Buchman TG, et al High-frequency oscillatory ventilation for acute respiratory distress syndrome in adults: a randomized, controlled trial. Am J Respir Crit Care Med. 2002;166:801–808. CrossRef

9. 9Bollen CW, van Well GT, Sherry T, Beale RJ, Shah S, Findlay G, et al. High frequency oscillatory ventilation compared with conventional mechanical ventilation in adult respiratory distress syndrome: a randomized controlled trial [ISRCTN24242669]. Crit Care. 2005;9:R430–R439. CrossRef

a Medical Critical Care Unit, Orlando Regional Medical Center, Orlando, FL, USA

b Division of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, University of Florida, Gainesville, FL, USA

Corresponding Author InformationCorrespondence to: Health Science Center, 1600 SW Archer Road, Room M452, P.O. Box 100225, Gainesville, FL 32610 0225, USA. Fax: +1 352 392 0821.

 Work done: Medical ICU Orlando Regional Medical Care.

PII: S1755-0017(09)00010-4

doi:10.1016/j.rmedc.2009.01.011


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