Management of advanced ARDS complicated by bilateral pneumothoraces with high-frequency oscillatory ventilation in an adult{dagger}

I. Galvin, R. Krishnamoorthy and R. S. G. Saad*

Intensive Care Unit, Royal Albert Edward Infirmary, Wigan Lane, Wigan WNI 2NN, UK

* Corresponding author. E-mail: rsgsaad{at}hotmail.com

Accepted for publication February 2, 2004.


    Abstract
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 Footnotes
 Abstract
 Introduction
 Case report
 Discussion
 References
 
We report the case of a 33-yr-old patient with adult respiratory distress syndrome (ARDS) complicated by bilateral pneumothoraces, who was successfully treated with high-frequency oscillatory ventilation following failure to respond to conventional ventilation. The role of high-frequency ventilation in the management of ARDS and air leaks is discussed.

Keywords: complications, adult respiratory distress syndrome ; complications, air leaks ; complications, pneumothoraces ; ventilation, high frequency oscillatory


    Introduction
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
High-frequency oscillatory ventilation (HFOV) achieves oxygenation and ventilation by oscillating the lung around a constant mean airway pressure, with small tidal volumes (1–3 ml kg–1) at a high frequency (up to 2400 bpm). Its use in adults has remained contentious since its introduction in 1972,1 but recently there has been a resurgence of interest in its possible application in adults with severe adult respiratory distress syndrome (ARDS), supported by a number of promising studies.25 These studies and the discussions they have triggered,69 suggest that HFOV may both reduce ventilator associated lung injury and improve gas exchange by maintaining alveolar patency throughout the respiratory cycle. Although there are a number of reports of the successful use of high-frequency ventilation in children with severe air leaks,1113 an extensive literature search failed to find any reports regarding its application in adults with pneumothoraces associated with severe ARDS.


    Case report
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
A 33-yr-old lady was admitted via the accident and emergency department (A&E) following an overdose of amitryptiline, ibuprofen, and paracetamol. She had a long history of depression but no other medical history. On arrival in A&E, her Glasgow Coma Scale was 6. She had been unconscious for approximately 30 min. She was haemodynamically stable, her was 97% in air, and there were no signs of aspiration. The trachea was intubated and she was artificially ventilated. She developed a right-sided pneumothorax following central line placement and this was treated by insertion of a chest drain. In intensive care she was sedated with propofol 50 mg h–1 and fentanyl 100 µg h–1, and ventilated on the Hamilton Amadeus ventilator with SIMV, 0.45, rate 12 bpm and PEEP 5 cm H2O. Three hours after admission, she had a generalized seizure associated with a broad complex tachycardia that progressed to pulseless electrical activity. Cardiac output was restored after one cycle of cardiopulmonary resuscitation and epinephrine 1 mg. Post arrest she was commenced on amiodarone 900 mg daily i.v.. The following day she had two further tonic clonic seizures and phenytoin 300 mg daily was started. CT scan of brain was normal. Sedation was stopped 4 days after admission but she remained unresponsive while breathing spontaneously on oxygen 50% with a of 14 kPa. Over the next 24 h, her condition deteriorated. She became pyrexial and tachypnoeic, her decreased to 8 kPa despite increasing the to 1. Chest X-ray showed left basal consolidation and diffuse bilateral infiltrates. She was re-sedated, paralysed with atracurium 20 mg h–1 and ventilated on the Drager Evita 2 ventilator, 1, tidal volume 400 ml (estimated body weight 55 kg), rate 17 bpm, I:E ratio 1:2 and a PEEP of 10 cm H2O. Inverse I:E ratio was tried but it did not improve oxygenation and her remained between 8.5 and 9.5 kPa. She responded well to prone positioning with the increasing to 15 kPa. Haemophilus influenza was grown from sputum and streptococcus from blood cultures. She was therefore commenced on cefotaxime i.v.. She remained unstable, requiring frequent proning to maintain her above 90%.

Over the next week, her ventilatory variables remained essentially the same. She developed bilateral spontaneous pneumothoraces and her was between 8 and 9 kPa with an of 1. Her tidal volumes were reduced to 300–350 ml, ventilatory rate increased to 25 bpm and she was started on hydrocortisone 800 mg daily, and diuretics to achieve a negative fluid balance. Her oxygenation failed to improve over the next 4 weeks and she developed two further pneumothoraces, such that she now had five chest drains in situ.

She was started on HFOV 40 days after admission to ITU. The initial settings were as follows: amplitude 55 cm H2O, mean airway pressure 22.5 cm H2O, frequency 5 Hz, and 0.95. Over the next 24 h, her oxygenation improved with a of 10.5 kPa and within 1 week it was possible to reduce the to 0.8. Her oxygen requirements continued to decrease as her oxygenation improved. She remained haemodynamically stable and did not develop any further pneumothoraces. The existing pneumothoraces resolved whilst on the oscillator. After 16 days on HFOV, she was changed back to conventional ventilation. She went back onto the Drager Evita 2 ventilator on BIPAP ASB (assisted spontaneous breathing) with an of 0.6, pressures adjusted to give a tidal volume of 300–350 ml, rate 22 bpm, I:E ratio 1:2 and PEEP 15 cm H2O. She remained on BIPAP for the next 30 days. During this time her oxygenation continued to improve.

By 86 days post-admission, she was able to tolerate CPAP. She was finally discharged to the ward 123 days after admission on oxygen 28% via facemask. She was discharged home 3 weeks later with no neurological deficit and no supplementary oxygen requirement.


    Discussion
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 Footnotes
 Abstract
 Introduction
 Case report
 Discussion
 References
 
The basic defect in ARDS is one of oxygenation rather than of ventilation, as a consequence of widespread alveolar collapse with resultant ventilation perfusion mismatch and hypoxaemia. The volume of normally functioning lung is significantly reduced and there is marked variation in alveolar compliance and time constants. This heterogenous pathology makes the lung particularly susceptible to the volutrauma and barotrauma inherent in the mechanics of conventional ventilation. Any successful ventilatory strategy has to address the balance between the need to optimize alveolar patency and avoid alveolar over-distension and damage.

This has led to the introduction of a more ‘lung friendly’ form of ventilation with small tidal volumes, rapid rates, and high PEEP.10 The rationale of this is that in ARDS the normal lung is essentially small, hence the small tidal volumes and the use of a high PEEP serves to increase ventilated lung volume and prevent end-expiratory alveolar collapse. The rapid rates facilitate carbon dioxide clearance with the acceptance that carbon dioxide elimination is not the priority in ARDS.

HFOV may be regarded as the extreme end of this lung protective spectrum. The very small tidal volumes (1–3 ml kg–1), allow use of a higher end-expiratory lung volume, achieving greater alveolar recruitment while avoiding damage as a result of excessive end-inspiratory lung volumes. The combination of a high continuous distending pressure with minimal pressure changes prevents the damage caused by cyclical alveolar collapse. HFOV also provides a rapid rate (up to 2400 bpm) and an active expiratory phase, both of which decrease air trapping and maintain normal or near normal carbon dioxide levels. It is for these reasons that HFOV has a well-established position in paediatric and neonatal practice, and is now emerging as a promising prospect in the treatment of ARDS. Recent studies25 show an association between early introduction of HFOV in ARDS and improved survival. Its use in adults is still, however, in its infancy and a trial of its effectiveness in comparison with the gold standard conventional ventilation recommended by the ARDS network10 is awaited.

When HFOV was first introduced, there was considerable concern that the benefits it provides in improved oxygenation and better alveolar stability might be outweighed by the possibility of increased risk of pneumothoraces and haemodynamic compromise as a result of the high mean airway pressures used. Recent studies2 4 indicate that haemodynamic instability is not a problem and that HFOV may both decrease the risk of and have a role in the treatment of air leaks.1115 Animal studies have supported the role of HFOV in the management of air leaks. Wang and colleagues14 ventilated surfactant depleted rabbits with bilateral pneumothoraces using high-frequency ventilation. The peak airway pressure was found to decrease significantly as the frequency setting was increased. There were no significant differences in mean airway pressure when high frequency was compared with conventional ventilation and during high-frequency ventilation; peak airway pressures measured at the mouth were actually decreased. An association between increasing frequency and decreasing chest tube flow was also noted in the treatment of experimental pneumothoraces in piglets.15 In this study, Ellsbury and colleagues suggest that the very short inspiratory time and small tidal volume of each HFOV breath minimize dilation of existing air leaks. The resultant decrease in diameter of the leak may then increase the resistance to gas flow and promote its closure. This is supported by their findings that increasing inspiratory time increased chest tube flow. There have also been reports of the successful use of high-frequency ventilation in children with air leaks,1113 and in neonatal pulmonary interstitial emphysema; however, we did not find any information regarding its use in adults with air leaks. It is also interesting to note that Derek and colleagues2 excluded patients with more than one chest tube per hemithorax and a persistent air leak for more than 120 h from their randomized controlled trial.

The case we present posed a difficult challenge to the success of HFOV not only because she had 40 days conventional ventilation before starting oscillation, but also because of the fact that she had multiple bilateral air leaks and had five chest drains in situ at the time of starting oscillation. Her oxygenation improved, she did not develop any further air leaks, and the existing pneumothoraces resolved while she was on the oscillator.

It may well be that this unconventional form of ventilation not only has a role in the management of ARDS but that its success in the treatment of air leaks in children,1113 and in animal studies,14 15 may also be applicable to adults.


    Footnotes
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 Footnotes
 Abstract
 Introduction
 Case report
 Discussion
 References
 
{dagger} This article is accompanied by Editorial II. Back


    References
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 Footnotes
 Abstract
 Introduction
 Case report
 Discussion
 References
 
1 Lukenheimer PP, Rafflenbeul W, Keller H, et al. Application of transtracheal pressure oscillations as a modification of diffusing respiration. Br J Anaesth 1972; 44: 627[ISI][Medline]

2 Derek S, Mehta S, Stewart T, et al. High frequency oscillatory ventilation for acute respiratory distress syndrome in adults. Am J Resp Crit Care Med 2002; 166: 801–8[Abstract/Free Full Text]

3 Metha S, Lapinsky SE, Hallet DC, et al. Prospective trial of high frequency oscillatory ventilation in adults with acute respiratory distress syndrome. Crit Care Med 2001; 29: 1360–9[ISI][Medline]

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5 David M, Weiler N, Heinrichs W, et al. High-frequency oscillatory ventilation in adult acute respiratory distress syndrome. Intensive Care Med 2003; 29: 1656–65[CrossRef][ISI][Medline]

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8 Singh J, Mehta S Kacmarek R. Pro/con clinical debate: is high frequency ventilation useful in the management of adult patients with respiratory failure? Crit Care 2002; 6: 183–5[ISI][Medline]

9 Froese A. The incremental application of lung protective high frequency oscillatory ventilation. Am J Resp Crit Care Med 2002; 166: 786–7[Free Full Text]

10 The Acute Respiratory Distress Syndrome Network. 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: 1301–8[Abstract/Free Full Text]

11 Varnholt V, Lasch P, Kachel W, et al. High frequency oscillatory ventilation of infants with severe respiratory disorders: possibilities, risks and limits. Klin Padiatr 1994; 206: 161–6[ISI][Medline]

12 Pizov R, Shir Y, Eimerl D et al. One-lung high frequency ventilation in the management of traumatic bronchial tear in a child. Crit Care Med 87; 15: 1160–1

13 Shen HN, Leigh F, Wu HD et al. Management of tension pneumatocele with high frequency oscillatory ventilation. Chest 2002; 121: 284–6[Abstract/Free Full Text]

14 Wang C, Nichol M, Chakrabarti M, et al. Cardio respiratory effects of conventional ventilation and high frequency ventilation in rabbits with bilateral pneumothoraces and surfactant depleted lungs. Pediatr Pulmonol 1993; 354–7

15 Ellsbury D, Klein J, Segar J. Optimization of high-frequency oscillatory ventilation for the treatment of experimental pneumothorax. Crit Care Med 2002; 30: 1131–5[CrossRef][ISI][Medline]





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