Anesth Analg 2002;95:1189-1191
© 2002 International Anesthesia Research Society
CARDIOVASCULAR ANESTHESIA
Bronchial Stenting and High-Frequency Percussive Ventilation Treatment of Descending Aortic Aneurysm-Induced Atelectasis of the Left Lung
Matthias Heringlake, MD*,
Jan Schumacher, MD*,
Beate Sedemund-Adib, MD*,
Ludger Bahlmann, MD*,
Sawas Eleftheriadis, MD*,
Hans-Hinrich Sievers, MD PhD ,
Klaus Dalhoff, MD PhD , and
Peter Schmucker, MD PhD*
*Klinik für Anaesthesiologie, Klinik für Herzchirurgie, and Medizinische Klinik II, Medizinische Universität zu Lübeck, Germany
Address correspondence and reprint requests to Matthias Heringlake, MD, Klinik für Anaesthesiologie, Medizinische Universität zu Lübeck, Ratzeburger Allee 160, D-23538 Lübeck, Germany. Address e-mail to heringlake{at}t-online.de
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Abstract
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IMPLICATIONS: This case report shows that atelectasis of the left lunginduced by extrinsic compression of the left main bronchus by an aortic aneurysm and persisting despite aggressive conservative treatmentmay be effectively treated by bronchial stenting and high-frequency percussive ventilation.
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Case Report
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AA 34-yr-old man was admitted to the intensive care unit after a reoperative aortic valve replacement and mitral valve reconstruction. The patient also had an aneurysmatic aortic dissection of the descending aorta extending from the left subclavian artery into the iliac vessels. No physical signs of Marfans syndrome were present. The postoperative chest radiograph showed a broadening of the cardiac silhouette to the left (Fig. 1A); however, oxygenation was normal, and the patient was quickly weaned from mechanical ventilation.

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Figure 1. A, Chest radiograph immediately after reoperative aortic valve replacement and mitral valve reconstruction, showing a broadening of the cardiac silhouette and displacement and atelectasis of the left lung caused by a large aneurysmatic dissection of the descending aorta. B, Chest radiograph showing a pneumothorax, a pleural effusion, and a complete atelectasis of the left lung, leading to severe respiratory failure. C, After insertion of a chest tube and drainage of the pleural effusion and the pneumothorax, and after repeated bronchoscopic examinations, the left lung remains atelectatic. D, Chest radiograph immediately after stent implantation in the left main bronchus, showing that the left lung is still only partially ventilated. E, Chest radiograph after 36 h of high-frequency percussive ventilation showing that the left lung is reopened and no longer atelectatic.
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A few hours after tracheal extubation, the patient developed acute respiratory failure (SpO2 84% with O2 12 L/min by face mask) and was reintubated and mechanically ventilated. A subsequent chest radiograph revealed a pneumothorax, a pleural effusion, and atelectasis of the left lung (Fig. 1B). However, despite immediate drainage by a chest tube, atelectasis persisted, and arterial oxygenation was seriously compromised (Fig. 2; t1). Bronchoscopic examination showed a stenosis of the left main bronchus and purulent mucus in the distal airways of the left lung; the chest radiograph showed persistent atelectasis (Fig. 1C). Piperacillin-sulbactam was started to prevent imminent pneumonia. Cultures of bronchial aspirates were later found to be sterile.

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Figure 2. Oxygenation index (PaO2/fraction of inspired oxygen [FIO2] ratio), PaCO2, and ventilator settings (open bars: PAW = peak airway pressure; closed bars: PEEP = positive end-expiratory pressure; I:E = inspiratory/expiratory time ratio; RR = respiratory rate) immediately after reintubation (t1), 24 h after reintubation (t2), after implantation of a stent in the left main bronchus (t3), after 2 h of high-frequency percussive ventilation (HFPV) (t4), and 2 h after reinstitution of airway pressure release ventilation (APRV).
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In the following 3 days, the patient was mechanically ventilated with an assisted mode. He received intensive percussive physical therapy and large doses of mucolytics (ambroxol 1 g/d and acetylcysteine 1800 mg/d) and was repeatedly suctioned bronchoscopically. However, the atelectasis persisted, and oxygenation remained compromised (Fig. 2; t2). Additionally, he developed fever and leucocytosis. A thoracic computed tomography scan showed pulmonary infiltrates in the atelectatic left lung compatible with bronchopneumonia and the descend-ing aorta compressing the left main bronchus. Additionally, increasing infiltrates were also observed in the right lung.
Because the risk of an emergency replacement of the descending thoracic and abdominal aorta was deemed to be unacceptably high, a self-expandable uncovered endobronchial nitinol stent (Ultraflex; length, 4 cm; diameter, 12 mm; Boston Scientific Corp., Natick, MA) was implanted according to the recommendations of the manufacturer into the left main bronchus by specialists of the respiratory care unit. The procedure was performed with rigid bronchoscopy under fluoroscopic control during general anesthesia.
After the procedure, gas exchange was still moderately compromised during airway pressure release ventilation (Fig. 2; t3), a chest radiograph showed persisting atelectasis (Fig. 1D), and high-frequency percussive ventilation (HFPV) was started 4 h after stent implantation. The device used (VDR-4-G Servolator; Percussionaire Corp., Vienna, Austria) combines pressure-controlled ventilation with superimposed high-frequency oscillations induced by a flow interrupter, leading to a percussion effect and an increase in mean airway pressure without increasing peak airway pressure. The respiratory rate (15 to 20 breaths/min) and the percussive frequency (550 to 650/min) were adjusted to achieve normocapnia (Fig. 2; t4). Sedation was performed with a continuous infusion of propofol, and analgesia was achieved with piritramide administered intermittently.
After 36 h, the chest radiograph revealed that the left lung was fully ventilated (Fig. 1E), and airway pressure release ventilation was reinstituted (Fig. 2; t5). The patient was weaned from mechanical ventilation 48 h later and was successfully discharged on Day 12 after surgery.
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Discussion
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Atelectasis of the left lung caused by extrinsic compression of lung tissue is a rare complication of descending aortic aneurysms and has been treated successfully by the implantation of an expandable stent into the left main bronchus (13). However, the extrinsic pressure of the aneurysm may lead to a delayed aorto-bronchial fistula and fatal pulmonary hemorrhage after stent implantation (4).
The rationale to accept this risk was that stent implantation was considered the only alternative to reexpand this lung. Additionally, because the small airways were occluded by viscous mucus as a result of the concomitant bronchopneumonia, we used HFPV, a form of high-frequency ventilation that, in our experience, facilitates clearing the airways by mobilizing mucus very effectively. Furthermore, HFPV improves oxygenation in patients with acute respiratory distress syndrome (5,6). The mechanisms of this effect have not yet been fully elucidated.
The clinical course of the patient does not allow discrimination of whether bronchial stenting alonewithout HFPVwould have been sufficient to reexpand the left lung, because HFPV was begun immediately after the stenting procedure. Hence, it cannot be excluded that conventional ventilation with intermittent lung inflation maneuvers may have had a comparable beneficial effect. Nonetheless, the successful management of this case shows that reopening atelectatic lung tissue by bronchial stentingand possibly HFPVmay be a promising strategy for conditions in which external decompression of the lung is not feasible.
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References
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Accepted for publication July 3, 2002.
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