Interact CardioVasc Thorac Surg 2007;6:262-263. doi:10.1510/icvts.2006.144261
© 2007 European Association of Cardio-Thoracic Surgery
Use of silfenadil for treatment of respiratory distress after pneumonectomy for bronchogenic carcinoma
Bradley G. Thomasa and
James D. Maloneyb,*
a University of Louisville, Louisville, KY, USA
b Division of Cardiothoracic Surgery, University of Wisconsin, 600 Highland Avenue, Madison, WI, USA
Received 5 October 2006;
received in revised form 21 November 2006;
accepted 24 November 2006
*Corresponding author. Tel.: +1-608-2635215; fax: +1-608-2630547.
E-mail address: maloney{at}surgery.wisc.edu (J.D. Maloney).
 |
Abstract
|
|---|
Post-pneumonectomy respiratory failure is a devastating complication of resection for lung cancer. As proven therapy is limited, we successfully employed a novel medication silfenadil that has been effective in the treatment of pulmonary hypertension.
Key Words: Pneumonectomy; Respiratory failure; Lung cancer; Silfenadil
|
1. Introduction
|
|---|
Pneumonectomy for lung cancer remains an important procedure for patients not amenable to parenchymal sparing techniques. It is associated with a significantly higher risk of morbidity and mortality than lobar resection. Respiratory failure following pneumonectomy is of particular concern and carries a mortality rate of 50%. Acute lung injury (ALI) after surgery clinically and pathologically parallels ARDS. Nitric oxide has been used to treat both entities by decreasing pulmonary arterial pressures. Sildenafil is known to be effective in the treatment of primary pulmonary hypertension as a nitric oxide donor. We report the use of sildenafil (Viagra) in a patient with respiratory failure after pneumonectomy.
|
2. Case report
|
|---|
A 63-year-old woman with an 80-year pack history presented with left lower lobe pneumonia. Bronchoscopy demonstrated a near obstructing left lower lobe squamous cell carcinoma. Preoperative CT scan and PET showed no evidence of unresectable disease. Pulmonary function test showed that the patient had sufficient pulmonary reserve to tolerate lobectomy or pneumonectomy. Preoperative evaluation included cardiac risk stratification. Mediastinoscopy demonstrated that no evidence of N2 disease was present. During left thoracotomy we found that the cancer extended across the fissure to involve both lobes. We proceeded with pneumonectomy and mediastinal lymph node dissection. Pathology returned as a T1 tumor with single N1 nodal involvement by direct extension.
The patient tolerated the procedure and was transferred to intermediate care requiring minimal oxygen by nasal cannula to maintain satisfactory saturation levels. On post-operative day two the patient began showing increased respiratory effort. Despite increasing FIO2 support we had difficulty maintaining adequate saturation. She was transferred to the intensive care unit, diuresed aggressively and treated with bronchodilators. The patient was intubated after a short trial of BiPap and 100% FIO2. Pressure regulated volume control was used in an effort to maintain low mean and peak airway pressures. No steroids were given. Chest radiograph suggested pulmonary edema. Cardiac evaluation, including echocardiogram, did not suggest ischemia or left ventricular dysfunction as the cause of pulmonary compromise.
Inhaled nitric oxide was not immediately available. We elected to initiate sildenafil as an NO donor. It was started at a low dose (20 mg every 8 h). This was increased as the patient's hemodynamic parameters allowed. The patient was initially on 100% FIO2 after intubation. She was weaned to 40% FIO2 within 48 h and was intubated for a total of four days. She remained on sildenafil through her hospitalization. She was weaned cautiously from nasal cannula oxygen and discharged without home oxygen on 20 mg of silfenadil every 8 h. We maintained silfenadil for six weeks postoperatively at which time it was discontinued. She maintains saturations above 92% on room air but does become short of breath with strenuous exertion.
|
3. Discussion
|
|---|
Pulmonary resection is established as the most effective means of treating early stage bronchogenic carcinoma. Morbidity and mortality have improved substantially, however, acute lung injury (ALI) after surgery and subsequent respiratory failure remain a serious concern and represents the leading cause of post lung resection mortality. The incidence of ALI is difficult to determine. Estimates of 4–9% in pneumonectomy and approximately 1–3% of lobectomies have been published [1]. Other authors feel that this entity is under-recognized and may be as high as 12% in pneumonectomy populations [2]. All authors agree that clinically manifest ALI after pneumonectomy has a nearly insurmountable risk of mortality with figures ranging from 50% to 100% [1].
Clinically, patients develop hypoxemia that is not responsive to increasing FIO2 and non-cardiogenic pulmonary edema. Though some risk factors have been described, the exact etiology is unclear [2–4]. Consistent and successful treatment in the post-resection patient has not been identified. The histopathologic pattern in post surgical ALI is similar to that seen in ARDS from other causes and therapy is extrapolated from this patient group [2]. Pulmonary arterial relaxation with nitric oxide has been shown to improve oxygenation and mortality in some studies in conjunction with aggressive supportive care [3]. Sildenafil similarly has been shown to decrease pulmonary arterial pressure and is now accepted as treatment for primary pulmonary hypertension [5]. Sildenafil has not to our knowledge been used in the treatment of ALI in a post-pneumonectomy patient.
Sildenafil was started in this patient because of the delay in initiating nitric oxide therapy. Like Mathisen and colleagues we were aggressive about early intubation, diuresis, minimizing barotrauma and supportive care. Oxygen saturation and pO2 improved rapidly so we did not transition to nitric oxide. Our concern for systemic hemodynamic compromise was not realized in this case but may limit use in some patients. Though survival data are inconsistent regarding pulmonary arterial relaxation in the ARDS population, PaO2 is improved [6]. This result may allow for more latitude in ventilator management in an effort to minimize further injury. Additional study of sildenafil alone or in combination with other pulmonary arterial dilators is necessary to determine its role in the treatment of ALI after lung resection.
|
References
|
|---|
- Ruffini E, Parola A, Papalia E, Filosso PL, Mancuso M, Oliaro A, Actis-Dato G, Maggi G. Frequency and mortality of acute lung injury and acute respiratory distress syndrome after pulmonary resection for broncogenic carcinoma. Eur J Cardiothorac Surg 2000; 20:30–37.
- Jordan S, Mitchell JA, Quinlan GJ, Goldstraw P, Evans TW. The pathogenesis of lung injury following pulmonary resection. Eur Respir J 2000; 15:790–799.[Abstract]
- Mathisen DJ, Kuo EY, Hahn C, Moncure AC, Wain JC, Grillo HC, Hurford WE, Wright CD. Inhaled nitric oxide for adult respiratory distress syndrome after pulmonary resection. Ann Thorac Surg 1998; 65:1894–1902.
- Behrends M, Beierlinden M, Peters J. Postpneumonectmy pulmonary edema. A retrospective analysis of incidence and possible risk factors. Eur J Anaesth 2005; 22:155–157.[CrossRef][Medline]
- Galie N, Ghofrani HA, Torbicki A, Barst RJ, Rubin LJ, Badesch D, Fleming T, Parpia T, Burgess G, Branzi A, Grimminger F, Kurzyna M, Simonneau G. Sildenafil citrate therapy for pulmonary arterial hypertension. New Eng J Med 2005; 353:2148–2157.[Abstract/Free Full Text]
- Jain R, Dalnogare A. Pharmacological therapy for acute respiratory distress syndrome. Mayo Clinic Proceedings 2006; 81:205–212.[Abstract/Free Full Text]
|
|
Top
Abstract
1. Introduction