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Ann Thorac Surg 2004;78:335-337
© 2004 The Society of Thoracic Surgeons
a Division of General and Surgical Intensive Care Medicine, Departments of Anesthesia and Critical Care Medicine, Leopold-Franzens-University of Innsbruck, Innsbruck, Austria
b Radiology, Leopold-Franzens-University of Innsbruck, Innsbruck, Austria
Accepted for publication June 13, 2003.
* Address reprint requests to Dr Mayr, Division of General and Surgical Intensive Care Medicine, Department of Anesthesia and Critical Care Medicine, Leopold-Franzens-University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria
e-mail: andreas.j.mayr{at}uibk.ac.at
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Abstract |
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Introduction |
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Bridging the acute phase of hypoxia with ECMO, fibroproliferative changes of the lung, triggered by continuous production of proinflammatory mediators, can complicate therapy of severe ARDS. Uncontrolled studies indicated improved outcome of unresolving ARDS after steroid treatment [3]. Recently, reductions in lung injury severity (LIS) and multiple organ dysfunction syndrome (MODS) scores after steroid treatment have been reported [4]. Because statistical analysis in that small crossover study has been criticized, uncertainty persists about improvement of organ function during steroid therapy for unresolving ARDS.
We report a case of pneumonia-associated ARDS in a pneumonectomized patient who could not be treated with mechanical ventilation, but survived after implantation of ECMO. Methylprednisolone therapy caused a dramatic improvement in lung and systemic organ function.
A 51-year old, white Eurasian man underwent right-sided pneumonectomy for T1N1M0 bronchogenic carcinoma. After an uncomplicated postoperative course early bronchial stump fistula was diagnosed, and the patient had to undergo rethoracotomy on postoperative day 7. On postoperative day 11, he was transferred to the surgical intensive care unit (SICU) with pneumonia-associated ARDS (Fig 1). At admission, the patient was breathing spontaneously (respiratory rate 28/min, positive end-expiratory pressure [PEEP] 12 mbar, FiO2 0.8) exhibiting hypoxia (PaO2 60 mm Hg, PAO2/FiO2-quotient 75). Empiric antibiotic therapy was started with imipenem-cilastin and ciprofloxacin. Despite subsequently instituted invasive ventilation (airway pressure release ventilation, Ppeak 25 mbar, PEEP 12 mbar, Tinsp 1.7 seconds, Texsp 0.5 seconds, FiO2 1.0), hypoxia aggravated. Because of the impossibility of increasing PaO2 more than 50 mm Hg over 2 hours [5], veno-venous ECMO was implanted on SICU day 2 (centrifugal biopump Medtronic CBBP-80, capillary membrane oxygenator Maxima plus PRF, cannulation sites: V. jug. int. dex. [19F, 18 cm] and V. fem. dex. [23F, 50 cm]; anticoagulation with Carmeda-coated systems [Carmeda, San Antonio, TX]; and heparin infusion to achieve an activated clotting time between 120 and 180 seconds). With extracorporeal oxygenation (blood flow 4.0 L/min, O2 flow 4.0 L/min, FiO2 0.8, three oxygenator changes required during ECMO therapy) and immobilization of the failing lung (Ppeak 20 mbar, PEEP 15 mbar, Tinsp 3 seconds, Texsp 6 seconds, FiO2 0.4) hypoxia could be reversed effectively. Because of recurrence of bronchial stump fistula on SICU day 4, bronchoscopic fibrin sealing was performed. The bronchial stump dehiscence, however, reappeared on SICU day 8 and was surgically revised in a combined thoracoabdominal intervention. One day after surgery the patient was successfully weaned from ECMO.
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On SICU day 36, the patient was discharged for pulmonary rehabilitation. Spirometry performed 6 months after severe ARDS showed adequate function of the residual lung.
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Comment |
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Common justification for ECMO therapy of ARDS is that chances for survival with mechanical ventilation are so low that additional risks of ECMO therapy become acceptable [6]. Survival chances are extremely low particularly in patients with ARDS after pneumonectomy [1]. Applying the "infant lung concept" to this patient population, healthy lung compartments are reduced by almost 50% compared with common ARDS, thus making hypoxia and ventilator-associated lung injury even more imminent (Fig 1).
Therefore, a maximally effective method to treat hypoxia is of vital therapeutic interest. In contrast to nitric oxide inhalation or proning where nonresponders are reported in up to 40% [7], ECMO is highly effective in reversing hypoxia. Further advantages of ECMO therapy are pulmonary immobilization and reduction of toxic inspiratory oxygen concentrations. Pulmonary healing may be enhanced by reversal of hypoxic pulmonary hypertension and perfusion of the pulmonary capillary bed at normal blood flow with normal PO2 and PCO2 [6]. Risk of bleeding, considered the major complication in ECMO therapy, is relatively low in postpneumonectomy patients and can be treated adequately, as shown in this patient who even underwent thoracoabdominal surgery during ECMO therapy.
After explantation of ECMO, ARDS persisted in this patient, because of what we believed was pulmonary fibroproliferation. Although fibroproliferation can be diagnosed reliably only by open lung biopsy or 67gallium scan, computed tomography and bronchoalveolar lavage have been suggested as appropriate tools to discriminate between fibroproliferation and secondary pneumonia in unresolving ARDS [3].
We propose two reasons for the dramatic improvement of LIS and MODS scores and systemic inflammatory measurements after the start of methylprednisolone therapy in this patient. First, inhibiting inflammatory cell activation and stabilizing alveolocapillary membrane [8], methylprednisolone therapy reduced prolonged pulmonary inflammation and improved systemic organ function by decreasing proinflammatory mediator release into the systemic circulation. Second, initiation of ECMO therapy has been shown to be associated with the appearance of circulating endotoxin, enhanced free radical activity, and high levels of inflammatory mediators [9]. Thus, discontinuation of ECMO therapy could have contributed to the reversal of organ dysfunction and leukocytosis as well as reduction of C-reactive protein. However, because worsening in pulmonary gas exchange could be seen after a too-rapid withdrawal of methylprednisolone on day 7 of treatment, we consider methylprednisolone therapy to be the main reason for the observed improvement in pulmonary and systemic organ function.
Based on this clinical case, early use of ECMO in patients with ARDS after pneumonectomy unresponsive to conventional ventilation seems to be a lifesaving therapeutic intervention. Steroid therapy may be helpful in patients with unresolving, fibroproliferative ARDS leading to an improvement of pulmonary and systemic organ function.
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This article has been cited by other articles:
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  M. Hommel, M. Deja, V. von Dossow, K. Diemel, C. Heidenhain, C. Spies, and S. Weber-Carstens Bronchial fistulae in ARDS patients: management with an extracorporeal lung assist device Eur. Respir. J., December 1, 2008; 32(6): 1652 - 1655. [Abstract] [Full Text] [PDF]
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 B. S. Burleson and E. D. Maki Acute Respiratory Distress Syndrome Journal of Pharmacy Practice, April 1, 2005; 18(2): 118 - 131. [Abstract] [PDF]
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