Management of Secondary Spontaneous Pneumothorax

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metaiodobenzylguanidine imaging in patients with COPD. Chest 1999; 116:1575–1581 Heindl S, Lehnert M, Criee CP, et al. Marked sympathetic activation in patients with chronic respiratory failure. Am J Respir Crit Care Med 2001; 164:597– 601 Bartels MN, Jelic S, Ngai P, et al. High-frequency modulation of heart rate variability during exercise in patients with COPD. Chest 2003; 124:863– 869 Racine N, Blanchet M, Ducharme A, et al. Decreased heart rate recovery after exercise in patients with congestive heart failure: effect of beta-blocker therapy. J Card Fail 2003; 9:296 –302 Lacasse Y, Brosseau L, Milne S, et al. Pulmonary rehabilitation for chronic obstructive pulmonary disease. Cochrane Database Syst Rev 2002; (3)CD003793 Hao SC, Chai A, Kligfield P. Heart rate recovery response to symptom-limited treadmill exercise after cardiac rehabilitation in patients with coronary artery disease with and without recent events. Am J Cardiol 2002; 90:763–765 Kligfield P, McCormick A, Chai A, et al. Effect of age and gender on heart rate recovery after submaximal exercise during cardiac rehabilitation in patients with angina pectoris, recent acute myocardial infarction, or coronary artery bypass surgery. Am J Cardiol 2003; 92:600 – 603 Tiukinhoy S, Beohar N, Hsie M. Improvement in heart rate recovery after cardiac rehabilitation. J Cardiopulm Rehabil 2003; 23:84 – 87 Lauer MS. Is heart rate recovery a modifiable risk factor? J Cardiopulm Rehabil 2003; 23:88 – 89 Sin DD, McAlister FA, Man SFP, et al. Contemporary management of chronic obstructive pulmonary disease: scientific review. JAMA 2003; 290:2301–2312 Guite HF, Dundas R, Burney PGJ. Risk factors for death from asthma, chronic obstructive pulmonary disease, and cardiovascular disease after a hospital admission for asthma. Thorax 1999; 54:301–307 Mascolo MC, Truwit JD. Role of exercise evaluation in restrictive lung disease: new insights between March 2001 and February 2003. Curr Opin Pulm Med 2003; 9:408 – 410 La Rovere MT, Bersano C, Gnemmi M, et al. Exerciseinduced increase in baroreceptor sensitivity predicts improved prognosis after myocardial infarction. Circulation 2002; 106:945–949

Management of Secondary Spontaneous Pneumothorax There’s Confusion in the Air occurrence of a spontaneous pneumothorax T herepresents a troubling milestone in the course of

patients with moderate-to-severe COPD. A pneumothorax causes rapidly progressive and alarming degrees of dyspnea usually associated with pleuritic chest pain. Hospitalization is necessary and often prolonged, and most patients require an intercostal chest tube and consideration of a surgical procedure to induce pleurodesis. But beyond these distressing experiences, a spontaneous pneumothorax represents a significant marker of mortality for patients

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with COPD. Each pneumothorax occurrence increases the chances of dying by nearly fourfold.1 In light of this lethal potential, the recurrence rate of secondary spontaneous pneumothoraces is especially alarming. Up to 40 to 50% of patients will have a second pneumothorax if pleurodesis is not performed.1–3 These observations prompt experts in pleural disease to recommend a more aggressive approach to managing secondary spontaneous pneumothorax as compared with primary spontaneous pneumothorax, which are usually well tolerated because of the absence of underlying lung disease. Despite recommendations for aggressive care, little consensus exists regarding the specifics of the management approaches that should be applied. For example, the American College of Chest Physicians (ACCP) consensus statement on pneumothorax recommends chest tubes for all patients and pleurodesis with the first episode of a secondary spontaneous pneumothorax to prevent a recurrence.4 The consensus was incomplete, however, in that 19% of the expert panel would defer pleurodesis until the second pneumothorax. The British Thoracic Society (BTS) pneumothorax guidelines recommend manual aspiration with a catheter and syringe for small pneumothoraces in patients with mild underlying lung disease, but submit that most patients will require chest tube drainage.5 The BTS recommends removal of the chest tube after lung re-expansion and resolution of air leaks, and reserves pleurodesis for patients with an unresolved air leak or a recurrent pneumothorax. Even less consensus exists regarding the ideal method for pleurodesis once it becomes indicated. The ACCP recommends medical thoracoscopy or video-assisted thoracoscopic surgery (VATS) as the primary procedure, and a limited axillary thoracotomy with pleural abrasion as a secondary approach.4 These guidelines value the lower morbidity attached to minimally invasive procedures. The BTS recommends open thoracotomy with repair with VATS reserved for patients who cannot tolerate an open procedure.5 This approach values the high effectiveness and low mortality of the open procedure and cites the limited availability of randomized controlled trials that compare VATS with thoracotomy. Considering the clinical confusion that emerges from these varying recommendations, any new data entering the arena of pneumothorax management are greatly appreciated. The study by Lee and colleagues (see page 1316) provides novel information by reporting their experience with medical thoracoscopy and talc poudrage for pleurodesis in 41 patients with moderate COPD (73% of patients, FEV1 ⱕ 30% but ⬎ 50% predicted) or severe COPD (27% of patients, FEV1 ⬍ 30% predicted) who preEditorials

sented with either an initial (66% of patients) or recurrent (34% of patients) pneumothorax. Of note, the investigators did not perform any procedures to eliminate blebs or bullae. They conclude that medical thoracoscopy was well tolerated with no major perioperative complications and a 30-day mortality of 10%, with the four deaths in the study confined to patients with severe COPD and ischemic heart disease. All patients who survived the hospitalization were discharged with resolution of their pneumothoraces after a median 5-day length of stay. Only 5% of patients had a pneumothorax recurrence during 19 to 47 months of follow-up. Further characterizing secondary pneumothorax as an ominous portent, 17% of patients died within 1 year of discharge from complications related to their underlying cardiopulmonary disease. Lee and colleagues advanced our understanding of secondary pneumothorax by limiting their investigation to patients with COPD. Other investigators6 –9 have demonstrated the efficacy of thoracoscopic poudrage in general categories of patients with primary and secondary pneumothorax. But these studies did not present data stratified by underlying lung disease. Despite its strengths, however, the present investigation remains a single-arm, observational study and, consequently, requires considerable speculation and a healthy dose of skepticism to appraise its findings. For instance, the authors note that only 44% of patients had blebs and bullae by thoracoscopic inspection of the visceral pleural, which is lower than expected for a cohort of patients with spontaneous pneumothorax due to COPD.10 As mentioned in the discussion, the investigators may have underestimated the presence of these lesions because of limitations of thoracoscopy for inspecting apical regions of the lung where most blebs and bullae occur.11 As suggested by the authors, this underestimate may create the impression that blebs and bullae do not require excision during medical thoracoscopic poudrage. Such an approach, however, differs from existing recommendations to convert patients to VATS or thoracotomy to manage bullae ⬎ 2 cm noted during medical thoracoscopy.12–14 Although removal of blebs offers little benefit for patients with primary spontaneous pneumothorax managed by thoracoscopy,13 the presence of large bullae decreases the success of thoracoscopy in managing secondary pneumothoraces.7,8 In support of their approach, the authors cite the experience of Liu and coworkers,15 who reported good results with thoracoscopic poudrage without bleb- or bullectomy in 13 patients with COPD. Of note, however, most of the patients reported by Liu and coworkers underwent Endoloop (Ethicon; Somerville, NJ) resections of blebs and www.chestjournal.org

bullae except for these 13 patients who had “diffuse emphysema” and, presumably, no resectable localized lesions.15 We remain reluctant, therefore, to conclude that blebs and bullae do not require resection, coagulation, stapling, or oversuturing, considering the relatively small size of the present study. Moreover, 59% of the patients reported by Lee and coworkers had preexisting tuberculosis, which is an independent cause of secondary pneumothorax and a confounder of their results. Nevertheless, this discussion further highlights the lack of high-quality evidence to direct therapy for blebs and bullae at thoracoscopy. One must also scrutinize the results of the study relative to its rationale. In their introduction, the authors state that they commonly encounter patients with COPD for whom general anesthesia and surgery present considerable risks. Medical thoracoscopy, in their view, offers such patients a welltolerated option for pleurodesis. Yet, the four deaths in the study occurred in patients with more advanced COPD and ischemic cardiac disease. These results prompted Lee and colleagues to recommend such patients for talc slurry pleurodesis via chest tube rather than thoracoscopy, thereby weakening the study rationale. One might alternatively conclude, however, that patients with advanced COPD require the attention of an anesthesiologist skilled in preoperative assessment and intraoperative management of high-risk patients. It has previously been observed that medical thoracoscopists need to enhance their skills in treating pain,13 which can precipitate catecholamine release and perioperative myocardial ischemia.16 Moreover, Mukaida and coworkers17 demonstrated in a small series that high-risk patients can tolerate VATS when carefully managed with local and epidural anesthesia. Once again, additional therapeutic confusion exists regarding patient selection for medical thoracoscopy relative to other available pleurodesis techniques. Finally, we note that no procedure was performed or planned during medical thoracoscopy other than talc poudrage. Other reports of medical thoracoscopy for pleurodesis emphasize the twin value of thoracoscopy in both administering talc and staging the pleural space.8 If thoracoscopy is only needed to administer talc, one could question if results would have been similar for the studied patient population had they been treated with talc slurry via a chest tube without thoracoscopy. Perhaps the most important outcome of the study by Lee and colleagues is the focus it brings to the paucity of randomized controlled trials that address management of secondary spontaneous pneumothorax for the population at greatest risk—patients with COPD. One cannot avoid catching the scent of CHEST / 125 / 4 / APRIL, 2004

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confusion in the air when attempting to interpret the numerous noncomparative studies that examine the value of markedly different pleurodesis modalities studied in aggregate populations with diverse underlying respiratory conditions. Considering the importance of spontaneous pneumothorax for patients with COPD, multicenter trials akin to those recently completed for lung volume reduction surgery are needed. Anticipating that such trials will be many years from conception to completion—if they occur at all—we need formal decision analyses to weigh the relative value of different management approaches18 as have been performed for primary spontaneous pneumothorax.19 Such analyses are especially important considering the opinion of some pleural experts that the risk of talc-induced acute lung injury does not justify its use.20 Meanwhile, we are left with our previously stated and less-than-satisfying recommendation to individualize care based on the available techniques at local institutions that match best-reported clinical outcomes.21 Albeit necessary with our present state of knowledge, such recommendations further entrench practice variation, delay implementation of best clinical practices, and perpetuate our clinical confusion. John E. Heffner, MD, FCCP John T. Huggins, MD Charleston, SC Dr. Heffner is Professor of Medicine and Executive Medical Director, Medical University of South Carolina. Dr. Huggins is a Senior Clincal Fellow in the Pulmonary/Critical Care Division at the Medical University of South Carolina. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail: [email protected]). Correspondence to: John E. Heffner, MD, FCCP, Professor of Medicine, Executive Medical Director, Medical University of South Carolina, 169 Ashley Ave, PO Box 250332, Charleston, SC

References 1 Videm V, Pillgram-Larsen J, Ellingsen O, et al. Spontaneous pneumothorax in chronic obstructive pulmonary disease: complications, treatment and recurrences. Eur J Respir Dis 1987; 71:365–371 2 Light RW, O’Hara VS, Moritz TE, et al. Intrapleural tetracycline for the prevention of recurrent spontaneous pneumothorax: results of a Department of Veterans Affairs cooperative study. JAMA 1990; 264:2224 –2230 3 Lippert HL, Lund O, Blegvad S, et al. Independent risk factors for cumulative recurrence rate after first spontaneous pneumothorax. Eur Respir J 1991; 4:324 –331 4 Baumann MH, Strange C, Heffner JE, et al. Management of spontaneous pneumothorax: an American College of Chest Physicians Delphi consensus statement. Chest 2001; 119: 590 – 602 5 Henry M, Arnold T, Harvey J. BTS guidelines for the management of spontaneous pneumothorax. Thorax 2003; 58(Suppl 2):ii39 –ii52 6 de Campos JR, Vargas FS, de Campos Werebe E, et al. 1192

Thoracoscopy talc poudrage: a 15-year experience. Chest 2001; 119:801– 806 7 Delaunois L, el Khawand C. Medical thoracoscopy in the management of pneumothorax. Monaldi Arch Chest Dis 1998; 53:148 –150 8 Tschopp JM, Brutsche M, Frey JG. Treatment of complicated spontaneous pneumothorax by simple talc pleurodesis under thoracoscopy and local anaesthesia. Thorax 1997; 52:329 –332 9 Noppen M, Meysman M, d’Haese J, et al. Comparison of video-assisted thoracoscopic talcage for recurrent primary versus persistent secondary spontaneous pneumothorax. Eur Respir J 1997; 10:412– 416 10 de Vos B, Hendriks J, Van Schil P, et al. Long-term results after video-assisted thoracic surgery for spontaneous pneumothorax. Acta Chir Belg 2002; 102:439 – 444 11 Horio H, Nomori H, Fuyuno G, et al. Limited axillary thoracotomy vs video-assisted thoracoscopic surgery for spontaneous pneumothorax. Surg Endosc 1998; 12:1155–1158 12 Loddenkemper R, Schonfeld N. Medical thoracoscopy. Curr Opin Pulm Med 1998; 4:235–238 13 Tschopp JM, Frey JG. Treatment of primary spontaneous pneumothorax by simple talcage under medical thoracoscopy. Monaldi Arch Chest Dis 2002; 57:88 –92 14 Cardillo G, Facciolo F, Giunti R, et al. Videothoracoscopic treatment of primary spontaneous pneumothorax: a 6-year experience. Ann Thorac Surg 2000; 69:357–361; discussion 361–352 15. Liu HP, Lin PJ, Hsieh MJ, et al. Thoracoscopic surgery as a routine procedure for spontaneous pneumothorax: results from 82 patients. Chest 1995; 107:559 –562 16 Sametz W, Metzler H, Gries M, et al. Perioperative catecholamine changes in cardiac risk patients. Eur J Clin Invest 1999; 29:582–587 17 Mukaida T, Andou A, Date H, et al. Thoracoscopic operation for secondary pneumothorax under local and epidural anesthesia in high-risk patients. Ann Thorac Surg 1998; 65:924 – 926 18 Massard G, Thomas P, Wihlm JM. Minimally invasive management for first and recurrent pneumothorax. Ann Thorac Surg 1998; 66:592–599 19 Morimoto T, Fukui T, Koyama H, et al. Optimal strategy for the first episode of primary spontaneous pneumothorax in young men: a decision analysis. J Gen Intern Med 2002; 17:193–202 20 Light RW. Diseases of the pleura: the use of talc for pleurodesis. Curr Opin Pulm Med 2000; 6:255–258 21 Sahn SA, Heffner JE. Spontaneous pneumothorax. N Engl J Med 2000; 342:868 – 874

C-Reactive Protein in Pneumonia Let Me Try Again description of C-reactive protein (CRP) T hewasinitial based on patients with pneumonia. CRP was identified in 1930 and subsequently considered to be an early nonspecific but sensitive marker of inflammation, so called “acute-phase protein.”1 An acutephase protein has been defined as one whose plasma concentration increases (positive acute-phase proEditorials