Pulmonary Vasculopathy and Recurrent Pneumothoraces

Pulmonary Vasculopathy and Recurrent Pneumothoraces

communications to the editor Communications for this section will be published as space and priorities permit. The comments should not exceed 350 word...

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communications to the editor Communications for this section will be published as space and priorities permit. The comments should not exceed 350 words in length, with a nutximwn offive ref erences; onefigure or table can be printed. Exceptions may occur under particular circumstances. Contributions may include comm.ents on articles published in this periodical, or they may be reports of unique educat-ional character. Please include a cot:er letter with a complete list of authors (including full first and last names and highest degree), corresponding author's address, phone number, fax number, and e-mail address (i f applicable). Specific permission to publish should be cited in the cover letter or appended a s a postscript. CHEST reserves the right to edit letters for length and clarity.

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Pulmonary Vasculopathy and Recurrent Pneumothoraces

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subjects: a clinical and pathological study. Thorax 1971; 26:409-17 Dunnill MS. Pulmonary pathology. Edinburgh: Churchill Livingstone, 1982; 464-63 Churg A. Diseases of the pleura. In: Thurlbeck WM , Churg AM , eds. Pathology of the lung. 2nd ed. New York: Thieme, 1995; 1079-80 Harris P, Heath D. The human pulmonary circulation: its form and function in health and disease. 3rd ed. Edinburgh: Churchill Livingstone, 1986; 595 Glancy DL, Frazier PO, Roberts WC. Pulmonary parenchymal cholesterol-ester granulomas in patients with pulmonary hypertension. Am J M ed 1968; 45:198-210 Kay JM , Heath D , Hasleton PS, et al. Aetiology of pulmonary cholesterol-ester granulomas. Br J Dis Chest 1970; 64:55-57 Colby TV, Yousem SA. Pulmonary histology for the surgical pathologist. Am J Surg Pathol 1988; 121:223-39 Kay JM . Vascular disease. In: Thurlbeck WM , Churg AM, eds. Pathology of the lung. 2nd ed. New York: Thieme, 1995; 1001

To the Editor:

To the Editor:

I offer the following comments on th e vascular pathology in the case reported by Schnader et al in CHEST (November 1996). 1 It is well established that in lung tissue resected from patients with idiopathic spontaneous pneumothorax, the muscular pulmonary artelies frequently show severe intimal fibrosis ,2 • 4 as illustrated in Figure 1A, 1C, and 10 1 H emosiderin-laden macrophages are also commonly present. 2 ··1 The thick-walled pleural vessels illustrated in Figure IF and 1G are modified bronchial arteries ("sperrarterien") which are commonly encountered in normal lungs.-5 Figure 1E shows a cholesterol-ester granuloma. It was previously thought that pulmonary hypertension was important in the pathogenesis of pulmonmy cholesterol-ester granulomas,6 but for some years it has been known that they are nonspecific lesions encountered in a wide variety of conditions 7 ·s In summary, all the vascular lesions described and illustrated in this case are incidental and are known to occur in idiopathic spontaneous pneumothorax. There is no reason to investigate this patient for pulmonmy hypertension. It is important for pathologists to understand that the presence of medial hypertrophy and intimal fibrosis in muscular pulmonary arteries does not necessatily indicate pulmonmy hypertension. These intimal and medial lesions may develop as a reaction to chronic inflammation and fibrosis in the adjacent lung tissue. They have no he modynamic significance 9

\Ve appreciate Dr. Kay's comments . We agree that many of the pathologic changes reported in the case presentation are nonspecific, as we point out clearly in our article.' We do not disagree with the oliginal report, which documents a "nonspecific" endartelitis. 2 But along the lines of what is most interesting about this case, 1 and as we discuss, it is unclear whether the vascular changes precede the pneumothoraces or the pneumothoraces precede the vascular changes, and whether or not there is a cause-and-effect relationship. Finally, the scenario in which these pulmonary vasculopathologic changes are uncovered fortuitously is not a common one for clinicians. Although Dr. Kay is of the opinion that such changes are "incidental" and that "the re is no reason to investigate," it is clear that clinicians are not always comfortable or confident with this approach. In our case, the impetus for an investigation was strengthened by the abnormal diffusing capacity.'

I Michael Kay, MD Department of Laboratory Medicine St. Joseph 's Hospital Department of Pathology McMaster University Hamilton, Ontario, Canada REFERENCES 1 Schnader J, Ten y PB, Field SK, et al. Clinical conference on manage ment dilemmas: pulmonary vasculopathy and recurrent pneumothoraces. Chest 1996; 110:1340-47 2 Lichter I, Gwynne JF. Spontaneous pneumothorax in young 1784

Jeff Schnader, MD, CM, FCCP Dayton VA Medical Center Wright State University School of Medicine Dayton, Ohio Peter B. Terry, MD The Johns Hopkins Hospital Baltimore Adam S. Katz, 1VID North Shore University Hospital Cornell University Medical College Manhasset, New York Stephen K. Field, MD, CM University of Calgary Calgary, Alberta, Canada Kenneth M. Moser, MD, FCCP University of California at San Diego

REFERENCES 1 Schnader J, Terry PB, Field SK, et al. Clinical conference on management dilemmas: pulmonary vasculopathy and Communications to the Editor

recurrent pneumothoraces. Chest 1996; 110:1340-47 2 Lichter I , Gwynne JF. Spontaneous pneumothorax in young subjects: a clinical and pathological study. Thorax 1971; 26:409-17

Therapeutic Thoracoscopy Under Local Anesthesia To the Editor: \-Ve read with great interest the report by Nezu et a!on thoracoscopic bullectomy performed under local anesthesia for the treatment of spontaneous pneumothorax (January 1997). 1 The authors selected patients with no pleural adhesions (by air insufflation and then x-ray), and they tried to identify their bullae preoperatively by using CT scans. They compared their results with those of a historical group in which the same procedure was performed under general anesthesia; they then concluded that the approach usin g local anesthesia is safe and is associated with a shorte r hospital stay. \-Ve would like to raise four points. First, in our experience, it is relatively unusual for recurrent ptimary spontaneous pneumothorax not to have any adhesions, as the natural history of a ruptured bulla is eventual adhesion to the chest wall. Therefore, if this selection critetia is stJictly followed, it seems that the desctibed procedure will be applicable only to a relatively small group of patients. Second, although a CT scan can confirm the presence of apical bullae, it fails to identify ruptured bullae or blebs, which can coexist with unruptured bullae. The former requires careful thoracoscopic examination? which is more difficult to cany out in a spontaneously ventilating lung. Third, the authors did not compare subj ective o r objective pain measurements ( by visual analogue scale o r naalgesic requirements ) betvveen the tvvo groups. The reported average postope rative hospital stay of 4.5 days in their local anesthesia group, although less than the 5.8 days reported in their general anesthesia group, is still longer than our result of 3.0 days in over 200 consecutive patients, whose procedures w ere all performed under general anesthesia. 3 Fourth, mechanical pleurodesis and pleurectomy, which are believed to be important components of surgical treatment,4 are difficult to perform under local anesthesia. Besides, this leaves vi rtually no safety margin if major intraoperative complications do occur. Although bullectomy under local anesthesia is technically feasible, the claim that this approach is supe tior to its counte rpatt performed under general anesthesia with s elected one-lung ventilation may be a little premature. Anthony P. C. Yim, MD, FCCP M. Bashar Izzat, MD, MCh Prince of Wales Hospital Hong Kong REFERENCES 1 Nezu K , Kushibe K, Tojo T, e t !a. Thoracoscopic wedge resection of blebs under local anesthesia ' vith sedation for treatment of a spontaneous pneumothorax. Chest 1997; 111: 230-35 2 Yim APC, Liu HP. Complications and failures of video assisted thoracic surgery: experience from two centers in Asia. Ann Thorac Surg 1996; 61 :538-41 3 Yim APC. Video-assisted thoracoscopic management of primary spontaneous pne umothorax. Ann Acad M ed Singapore 1996; 25:668-72 4 Parry GW, Juniper ME , Dussek JE. Surgical intetvention in spontaneous pneumothorax [editotial] Respir Med 1992; 86:1-2

To t h e Editor: We thank Drs. Yim and Izzat for their very pertinent comments on our article (January 1997).' First, they claimed that recurrent primary spontaneous pneumothorax \vithout any pleural adhesions is relatively unusual. However, we disagree; 56% of our patients with recurrent pneumothorax were preoperatively diagnosed b y the air-infusion test to be practically free from adhesions. We have to admit that there might have been minimal adhesions present in such patients, and that our description may have been a little extreme. However, there were many pa tients with r ecurrent pne umothorax who were practically adhesionfree. Furthermore, we ope rated on the patients within a relatively shOtt period after the onset of recurrent spontaneous pneumothorax, which may have influenced the higher r atio of the adhesion-free patients in our se ties. As for their second claim, we agree that CT scans fill! to identify ruptured bullae or blebs coexisting with unruptured bullae. Although they mentioned the difficulty in locating ruptured bullae in the lung of a patient receiving mechanical ventilation, we can c ontrol the expansion and collapse o fthe lung using a valved port with an insufflation stopcock, \vith the patient under local anesthesia and sedated, as desctibed in our paper. In response to their third question, we did not pe rform subjective or objective pain measurement between the two groups during or after the operation. However, there are no apparent clinical differences between the two groups in terms o f complaints of pain. As for the ave rage duration of postoperative hospital stay, our results (4.5 and 5.8 days for the local and general anesthetia groups, respectively) were longer than those obtained b yYim .2 However, there may be manydifferences in his circumstances and ours, such as social medical insurance systems. Under such conditions, we do not think it is approptiate to simply compare the durations of hospital stay. We agree with their fourth comment about the importance of mechanical pleurodesis or pleurectomy in the manage ment of spontaneous pneumothorax. We do only fibrin glue pleurodesis in our procedure, and other pleurodesis procedures a re hardly required because of the low recurrence rate of 3.1 %. Fibrin glue pleurodesis can b e easily performed \vith the patient under local anesthesia and sedated; this was the method we used for simple cases. Certainly, our procedure is not applicable to all of the patients with spontaneous pneumothorax a t this time. However, considering several advantages, such as its minimal invasiveness, this procedure can b e sed u asan alternative for selected patients with uncomplicated spontaneous pneumothorax. Kunimoto Nezu, MD Soichiro Kitamura, MD, FCCP Department of Surgery III Nara Medical University Nara, Japan REFERENCES 1 N ezu K, Kushibe K, Tojo T, e t al. Thoracoscopic wedge resection of blebs under local anesthesia with sedation for treatment of a spontaneous pneumothorax. Chest 1997; 111: 230-35 2 Yim APC. Video-assisted thoracoscopic management of ptimary spontaneous pneumothorax. Ann Acad Med Singapore 1996; 25:668-72 CHEST I 111 I 6 I JUNE, 1997

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