ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Alifano, M.
Right arrow Articles by Regnard, J. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Alifano, M.
Right arrow Articles by Regnard, J. F.
Related Collections
Right arrow Pleura

Ann Thorac Surg 2006;81:761-769
© 2006 The Society of Thoracic Surgeons

Review

Thoracic Endometriosis: Current Knowledge

Marco Alifano, MD a , b , * , Rocco Trisolini, MD c , Alessandra Cancellieri, MD d , Jean François Regnard, MD a

a Department of Thoracic Surgery, Hotel-Dieu, AP-HP, Paris, France
b Department of Thoracic Surgery, Ospedale Maggiore, Bologna, Italy
c Department of Thoracic Endoscopy, Ospedale Maggiore, Bologna, Italy
d Department of Pathology, Ospedale Maggiore, Bologna, Italy

Accepted for publication July 13, 2005.

* Address correspondence to Dr Alifano, Unitè de Chirurgie Thoracique, Hôtel-Dieu, 1, Place du Parvis Notre-Dame, 75181 Paris, France (Email: marcoalifano{at}yahoo.com).


   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Epidemiology
 Etiologic Mechanisms
 Pathology
 Clinical Presentations
 Diagnosis
 Treatment
 Outcome
 References
 
Thoracic endometriosis syndrome includes four well-recognized clinical entities, namely catamenial pneumothorax, catamenial hemothorax, catamenial hemoptysis and lung nodules, as well as some exceptional presentations. The etiological mechanisms of this syndrome are not well understood, and different theories have been proposed. Controversies exist about optimal management, as experience has been drawn from case reports and small clinical series. Surgery, hormonal treatments and combined approaches have all been proposed, with variable results in terms of short and long term outcome.


   Introduction
Top
 Abstract
 Introduction
Material and Methods
 Epidemiology
 Etiologic Mechanisms
 Pathology
 Clinical Presentations
 Diagnosis
 Treatment
 Outcome
 References
 
Endometriosis is characterized by the growth of endometrium outside the uterine cavity or myometrium. The pelvis and, less frequently, the rest of the peritoneal cavity are the sites most frequently involved, but endometriosis of virtually all the body compartments has been reported [1].

Almost all the structures in the pelvis can be involved, the leading localizations being the cul-de-sacs, ovaries, posterior broad ligaments, uterosacral ligaments, and uterus [1]. Although pelvic endometriosis is asymptomatic in many patients, the disorder is associated with a wide variety of symptoms, none of which is pathognomonic [1]. Infertility, pelvic pain (dysmenorrhea, dyspareunia, or even noncyclic lower abdominal pain), and dysfunctional uterine bleeding are common presentations of pelvic endometriosis [1]. Treatment of pelvic endometriosis includes symptomatic relief of pain, hormonal manipulation, surgery, and combined approaches. Hormonal treatment is effective in diminishing the anatomical extent of the disease, and reducing pain, but recurrence rates are substantial [2] and such treatment has not been shown to have an impact on endometriosis-associated infertility [2]. Conservative surgery (preserving the woman's ability to conceive) may enable excision of all apparent endometrial implants and, possibly, restore normal anatomical relations [2]. Laparoscopic excision of endometrial foci has been proven to be more effective than placebo in reducing pain and improving quality of life [3], but has not been demonstrated to have any impact on infertility, at least in initial stages of the disease [2, 4].

Thoracic endometriosis syndrome (TES) [5] is the term used to refer to the varying clinical and radiological manifestations associated with the growth of endometrial glands and stroma in the lungs or on the pleural surface. Unlike abdominopelvic endometriosis, TES is a rare condition that includes four well-recognized clinical entities (namely, catamenial pneumothorax [CP], catamenial hemothorax [CHt], catamenial hemoptysis [CH], and lung nodules) [5], but less frequent presentations are possible. The etiological mechanisms of this syndrome are not well understood, and controversies exist about optimal management. The aim of this review is to summarize the current knowledge on thoracic endometriosis syndrome.


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Epidemiology
 Etiologic Mechanisms
 Pathology
 Clinical Presentations
 Diagnosis
 Treatment
 Outcome
 References
 
Literature searches were carried out using Medline for articles published up to December 2004 containing the associations of words "catamenial pneumothorax," "catamenial hemothorax," "catamenial hemoptysis," "pneumothorax endometriosis," "hemothorax endometriosis," "hemoptysis endometriosis," "lung nodule endometriosis," "thoracic endometriosis," "diaphragmatic endometriosis," "pulmonary endometriosis," "bronchial endometriosis," and "pleural endometriosis." We also reviewed the references from these articles.


   Epidemiology
Top
 Abstract
 Introduction
 Material and Methods
 Epidemiology
Etiologic Mechanisms
 Pathology
 Clinical Presentations
 Diagnosis
 Treatment
 Outcome
 References
 
Endometriosis is thought to affect 5% to 15% of women in reproductive age [1]. Clinical and radiologic manifestations of thoracic endometriosis are generally thought to be extremely rare, but specific figures are scanty and come almost completely from case reports and small retrospective series. The most consistent, albeit retrospective, series on TES included 110 patients and showed that the mean age at presentation was 35 ± 0.6 years, with a range from 15 to 54 years [5]. Interestingly, the peak incidence for pelvic endometriosis in the patients of this series occurred between 24 and 29 years, whereas the peak incidence for TES occurred approximately 5 years later [5].

The most detailed epidemiologic data are available for CP, which is thought to be the most common clinical presentation of TES [5]. Catamenial pneumothorax was, until recently, considered a rare entity. In a large retrospective study [6] evaluating 664 women with spontaneous pneumothorax, only 6 cases of CP were identified. Another group [7] reported having identified 11 cases of CP among 196 women with spontaneous pneumothorax (5.6%) seen over a 21-year period. However, in a recent prospective study [8], 8 of 32 women hospitalized in an 18-month period for surgical treatment of spontaneous pneumothorax had a CP. Thus, it is plausible that thoracic endometriosis is an under-recognized cause of secondary spontaneous pneumothorax in an age group of women in whom most cases of pneumothorax have so far thought to be primary [9, 10].


   Etiologic Mechanisms
Top
 Abstract
 Introduction
 Material and Methods
 Epidemiology
 Etiologic Mechanisms
Pathology
 Clinical Presentations
 Diagnosis
 Treatment
 Outcome
 References
 
There is general agreement that thoracic endometriosis is the only cause of CHt [11], CH [12, 13], and of the exceedingly rare endometriotic lung nodules [5]. Catamenial pneumothorax, although very frequently associated with thoracic endometriosis, may also have other etiological mechanisms [5, 8]. The clinical manifestations of CHt, CH, and endometriosis-related pneumothorax imply the presence of intrathoracic endometrial tissue undergoing cyclical changes in response to the physiologic hormonal variations [5]. Most clinical manifestations of CHt, CH, and endometriosis-related CP are thought to be a consequence of sloughing of thoracic endometrial tissue, whereas CP not related to endometriosis should be considered as an abnormal consequence of physiologic changes typical of the menstrual period [14, 15]. Endometrial implants may be found in the lung parenchyma, visceral and parietal pleura, diaphragm, and more rarely in the tracheobronchial tree [5]. The clinical picture obviously depends on the affected structures.

Three theories have been proposed to explain the presence on intrathoracic endometrial implants: coelomic metaplasia, lymphatic or hematogenous embolization from the uterus or pelvis, and retrograde menstruation with subsequent transperitoneal-transdiaphragmatic migration of endometrial tissue. None of these theories can per se explain all the clinical manifestations of TES, and the disease probably has a multifactorial etiology [5, 8].

The theory of coelomic metaplasia [16] is based on the concept that endometrium as well as pleural and peritoneal mesothelium share the same embryologic origin. Pathogenic stimuli could then be responsible for inducing precursor cells in the pleura or the peritoneum to differentiate into endometrial cells. This theory cannot explain the occurrence of intrapulmonary endometriosis or the right-sided predominance of the disease.

The theory of transplantation of endometrium through lymphatic or vascular embolization [1, 5] could explain not only the intrapulmonary endometriosis but also the other extrapelvic localizations. Trauma or manipulation of uterine tissue would be a factor predisposing to microembolization [17]. Endometrial tissue might not only enter the lymphovascular circulation in the uterus but also in the pelvic peritoneum, especially if pelvic endometriosis coexists [5, 18, 19]. In the review by Joseph and Sahn [5], pelvic endometriosis was documented in 84% of the patients with TES in whom it was reliably searched for.

A review of autopsy data [20] showed that patients with pulmonary endometriosis usually had bilateral lesions, whereas pleural and diaphragmatic lesions were always right-sided. Thus, parenchymal lesions were hypothesized to originate from embolization, whereas pleural and diaphragmatic ones were explained by a third theory, transperitoneal-transdiaphragmatic migration of endometrial tissue.

Sampson's theory [21] of retrograde menstruation with subsequent peritoneal implantation of endometrial tissue is now the most favored explanation of the pathogenesis of pelvic endometriosis [1]; it presumes impaired clearance mechanisms at the peritoneal level that allow the endometrial tissue to survive, implant, and proliferate. The spread to thoracic structures would occur as a consequence of lymphovascular embolization [5] or of transabdominal-transdiaphragmatic migration.

This last theory is based on the concept that movement of fluids in the peritoneal cavity follows predictable patterns: this "peritoneal circulation" implies a preferential flow of fluids (air, cell aggregates, pus) from the pelvis to the right subdiaphragmatic area through the right paracolic gutter [22].

The transdiaphragmatic passage of endometrial tissue could occur through either congenital diaphragmatic defects (which are thought to exist in many individuals and to predominate on the right side [22]) or acquired defects of the diaphragm (sometimes called fenestrations or porosities) [5, 8, 23]. This passage would be favored by both the thoracoabdominal pressure gradient, and the "piston" action of the liver [22]. Once the viable endometrial tissue has entered the pleural space, it may colonize either the diaphragm or the rest of the pleural space. Although isolated diaphragmatic endometriosis is a frequent feature, the association of diaphragmatic and pleural endometriosis is possible [8, 24].

Diaphragmatic defects could also be acquired. The endometrial implants in the abdominal aspect of the diaphragm undergo cyclical necrosis and subsequent cycles may lead to the production of holes. The diaphragm may undergo progressive involution as a consequence of endometriosis [25]; it has been suggested that sloughing of full-thickness endometrial implants could cause the formation of holes, and coalescence of small holes might in turn produce larger defects [25].

How Does Intrathoracic Endometrial Tissue Cause Clinical Manifestations?
The pulmonary implants responsible for CH may be located in the parenchyma or, more rarely, in bronchi. In the case of CHt, the endometrial implants are found on the pleural surface. Bleeding from endometrial implants results from fluid shifts during menstruation causing capillary rupture within the lesions [26].

Lung nodules may, rarely, be the only presenting manifestation of thoracic endometriosis [5]. Remarkably, endometriosis-related lung nodules are not responsible for catamenial symptoms [5]. As compared with other clinical-radiological manifestations of TES, lung nodules are more frequently observed in older women who probably have less pronounced hormonal activity [5]. This factor, along with the frequent location in the periphery of the lung, is probably responsible for the indolent clinical course of these lung nodules [5].

The Anomaly of Catamenial Pneumothorax
Four mechanisms have been advocated to explain the pathogenesis of CP: (1) spontaneous rupture of blebs; (2) transdiaphragmatic passage of air from the genital tract; (3) sloughing of endometrial implants from visceral pleura with subsequent air leak; and (4) alveolar rupture caused by prostaglandin-induced bronchiolar constriction or by a check-valve mechanism exerted by bronchiolar endometrial implants.

Mayo [27] suggested that contemporaneous pneumothorax and menstruation could simply be a coincidence. However, the recurrent character of CP renders this hypothesis statistically unlikely; furthermore, it cannot explain the right-sided predominance of the condition or the response to hormonal manipulation.

The mechanism of transdiaphragmatic passage of air was initially suggested by Maurer and colleagues [28]. The cervical mucus plug is absent during the menstrual period, thus the peritoneal cavity is in communication with the outside through the uterine cavity and Fallopian tubes. Air may be forced into the peritoneum by uterine contractions, physical efforts, or sexual intercourse, and from there may reach the pleural space, through diaphragmatic defects (Fig 1), because of the negative intrathoracic pressure [8, 22, 25]. Previous clinical experience showed that pleural or diaphragmatic endometriosis could be ruled out in most cases of CP, and diaphragmatic defects were seen in only a relatively low percentage of patients [5, 14]. According to a recent review of literature [23] taking into account the 229 cases of CP published so far, thoracic endometriosis was diagnosed in 52.1% of cases, whereas 38.8% of patients had diaphragmatic lesions. In the prospective series reported by Alifano and colleagues [8], diaphragmatic abnormalities (Fig 2) were found in all the patients with CP and endometriosis was pathologically confirmed in all cases but one.


Figure 1
View larger version (102K):
[in this window]
[in a new window]
  		Fig 1. A diaphragmatic resection from a case of thoracic endometriosis: backlighting shows tiny defects in the diaphragmatic wall.

 

Figure 2
View larger version (122K):
[in this window]
[in a new window]
  		Fig 2. Thoracoscopic view of endometrial implants and holes in the pleural aspect of the diaphragm.

 
The transdiaphragmatic passage of air implies the occurrence of a pneumoperitoneum as an intermediate step. Downey and colleagues [29] reported on a patient with catamenial pneumothorax who had simultaneous pneumoperitoneum and pneumothorax. Roth and colleagues [30] had the opportunity to "photograph" the transdiaphragmatic passage of air bubbles.

The theory of transdiaphragmatic passage of air is further strengthened by the observation that tubal ligation prevented the recurrence of catamenial pneumothorax in a patient with diaphragmatic defects [31]. The mechanism of transdiaphragmatic passage of air is currently the most favored, although it cannot explain the pathogenesis of all the reported cases of CP.

Sloughing of endometrial tissue from the visceral pleura with subsequent alveolar leak may be another cause of catamenial pneumothorax, as documented in some patients previously undergoing hysterectomy [32, 33]. In many cases, CP has been related to endometriosis of the visceral pleura in women with an intact genital apparatus: in the review by Korom and colleagues [23], this casual relationship was advocated in approximately 30% of cases.

Several authors were unable to find diaphragmatic defects or pleural endometriosis in patients with CP, especially in the past decades. Rossi and Gopleurod [14] postulated that CP may be a consequence of increased circulating levels of prostaglandin F2-alpha in the menstrual period. According to this theory, prostaglandin F2-alpha would be responsible for vascular and bronchiolar constriction, with subsequent alveolar rupture. More recently, on the basis of the consideration of the paracrine action of prostaglandin F2-alpha, it has been suggested that vasospasm and bronchospasm are more likely to occur if there is local secretion of the prostaglandin (possibly from intrapulmonary menstrual debris) [33].

Lillington and colleagues [34], who coined the term "catamenial pneumothorax," proposed that pulmonary endometrial implants may swell inside terminal bronchioles during the menstrual period, thus causing localized hyperinflation by a check-valve mechanism, which, in turn, might cause pneumothorax. Although this theory may explain the cases of CP without diaphragmatic abnormalities, it does not explain the well-known right-sided predominance of the disease.


   Pathology
Top
 Abstract
 Introduction
 Material and Methods
 Epidemiology
 Etiologic Mechanisms
 Pathology
Clinical Presentations
 Diagnosis
 Treatment
 Outcome
 References
 
Thoracic endometriosis is represented by the presence of morphologically normal endometrial tissue within the thoracic cavity (Figs 3 and 4). Go Regardless of the site, endometriotic foci consist of both stroma and glands in different proportions, often with ectatic glands, mostly lined by pseudostratified cuboidal to cylindrical epithelium. Flieder and colleagues [35] provided a definite description of nine cases of pleuropulmonary endometriosis. They described the presence of proliferative-type glands, with inconspicuous nucleoli, scanty eosinophilic cytoplasm and frequent mitoses. Stromal cells, with scanty cytoplasm, constantly admixed with extravasated erythrocytes and hemosiderin-laden macrophages were observed. Remarkably, secretory changes are not a feature [36].


Figure 3
View larger version (190K):
[in this window]
[in a new window]
  		Fig 3. An endometriotic focus, composed of both glands and stroma, within the diaphragm (hematoxylin and eosin, original magnification x40). The rupture into the pleural space is evident.

 

Figure 4
View larger version (175K):
[in this window]
[in a new window]
  		Fig 4. An endometriotic focus mainly composed of stroma, lining the peritoneal aspect of the diaphragm (hematoxylin and eosin, original magnification x200).

 
Pleural (either visceral or parietal) and diaphragmatic endometriosis is characterized by the presence of both endometrial stroma and glands in the form of blue-brown implants or "chocolate cysts," almost invariably associated with hemorrhage, fibrosis and inflammatory infiltrates to various extents [37].

Most cases of pleural involvement exhibit either a nodular or nodulocystic pattern, associated with pleural thickening, adhesions, and hemorrhage [35]. The endometriotic foci may also rarely appear as dark red dimples, less than 5 mm in diameter [35]. Sometimes, the endometriotic foci may be identified only in deeper sections [35].

Pulmonary endometriosis can either take the form of solitary or multiple circumscribed nodules, or appear as thin-walled cavities or bullae, often associated with old and recent hemorrhages in the surrounding parenchyma [35]. Parenchymal lesions are often represented by microscopic foci within the bronchovascular bundles, and may be associated with prominent acute and chronic hemorrhage [35]. More rarely, endometrial stroma may be found outside the bronchovascular bundle, within the adjacent alveolar septa [35]. Endometriotic nodules may show a pseudoinfiltrative pattern, although lacking both cytologic atypia and epithelial crowding [35].

In a single case, the presence of intimal hyperplasia within pulmonary arterial branches, some obliterated by fibrosis, was observed in the setting of parenchymal endometriosis; vessel lumina were lined by endometrium [12].

Immunohistochemically, in the series reported by Flieder and associates [35], most glands showed cytoplasmic positivity with broad spectrum cytokeratin, cytokeratin 7 and BER-EP4, and strong nuclear staining for estrogen (Fig 5) and progesterone receptors. Most stromal cells showed strong cytoplasmic staining for vimentin, and approximately 30% stained for actin, smooth- muscle actin, and desmin. Half of the stromal cells in each case of this series showed intense nuclear staining for estrogen (Fig 5) and progesterone receptors. Neither epithelial nor neuroendocrine markers were expressed in the stromal cells.


Figure 5
View larger version (151K):
[in this window]
[in a new window]
  		Fig 5. A focus of diaphragmatic endometriosis. Immunohistochemistry shows strong nuclear staining for estrogen receptors (original magnification x100).

 

   Clinical Presentations
Top
 Abstract
 Introduction
 Material and Methods
 Epidemiology
 Etiologic Mechanisms
 Pathology
 Clinical Presentations
Diagnosis
 Treatment
 Outcome
 References
 
Catamenial pneumothorax is the most frequent presentation of TES, accounting for approximately 80% of cases [5]. Catamenial pneumothorax is generally defined as a recurrent pneumothorax occurring within 72 hours after the onset of menstruation [8], but somewhat different time frames are possible. There are reports of recurrence in relation to the immediate premenstrual period [24, 38] and the ovulatory phase [39]. Furthermore, recurrent endometriosis-related pneumothorax may also be observed in the intermenstrual period [25]. Catamenial pneumothorax does not necessarily occur with every menstrual cycle. In our recent prospective study, 1 to 4 episodes had occurred in the studied population before videothoracoscopy [8], but reports exist of patients who had had more than 10 episodes before receiving treatment [14]. Catamenial pneumothorax is unilateral and right-sided in almost all cases [5, 8, 24], although there are exceptional reports of left-sided pneumothorax [14, 40]. Bilateral CP is also possible, but it extremely rare [41, 42]. The presentation of CP includes cough, chest pain, and shortness of breath. The chest pain may be the same as that usually seen in patients with spontaneous pneumothorax or present as periscapular or neck-irradiated pain ("diaphragmatic pain"). In most cases, symptoms are mild or moderate but very severe presentations are possible [15].

Catamenial hemothorax is an infrequent manifestation of TES, occurring in 14% of the cases of this syndrome [5]. Catamenial hemothorax may present in association with CP, but this occurrence is uncommon [5, 8]. The right side is involved in almost all the cases, although one case of associated right pneumothorax and left hemothorax has been reported [43]. The most common presenting symptoms are nonspecific and include cough, chest pain, and shortness of breath [5]. In some instances, signs can mimic those of pulmonary embolism [11, 44]. The entity of the bloody effusion is variable [5], and severe anemia is possible [11]. In almost all the cases, chest roentgenogram shows the presence of pleural effusion without specific characteristics [5]. Computed tomography scan may show additional features such as nodular lesions of pleura, multiloculated effusions [44], or bulky pleural masses [45].

Cyclical hemoptysis occurring during menses is an extremely rare condition; approximately 30 cases have been reported in the English literature [18]. The entity of bleeding is quite variable, but neither cases of massive hemoptysis nor deaths have been described. The source of bleeding is an endometrial implant located in the pulmonary parenchyma or in the large airways [18]. A temporal association of symptoms with menses may not be appreciated, and diagnostic delays of up to 4 years from the onset of symptoms have been reported [12]. Chest roentgenogram may reveal pulmonary opacities or nodular infiltrates, but findings are normal even in a significant number of patients with current bleeding [12, 19, 45–48]. Computed tomography signs of pulmonary endometriosis include ill-defined or well-defined opacities, nodules, thin-walled cavities, bullous formations, and ground glass opacities [12, 19, 46–50]. All of these lesions, which are expressions of the endometrial implants or secondary hemorrhage, may change in size during the menstrual cycle. Unfortunately, computed tomography seems to have a low diagnostic yield in tracheobronchial endometriosis without parenchymal involvement [48–51]; virtual bronchoscopy has been suggested to have some additional value in this setting [48]. Bronchial angiography has been employed, but normal angiograms are found in as many cases [46, 47] as pathologic ones [52, 53].

Lung nodules in the setting of TES are not infrequent radiological features. In most cases, they are associated with catamenial hemoptysis [5, 12, 18, 19, 46], although in rare instances, single or multiple asymptomatic nodules can be the presentation of TES; this event was reistered in only 7 of 110 patients (6%) of the series by Joseph and Sahn [5].

In the setting of TES, catamenial chest pain is almost always related to CP or CHt. Two small gynecologic series reported cases of diaphragmatic endometriosis diagnosed at laparoscopy in which chest pain without pneumothorax or hemothorax was the only clinical complaint [37, 54]. Shoulder pain was frequently associated and this radiated to the neck or the arm [37]. In other instances, epigastric or right upper quadrant pain was reported [54]. In most patients it was a pure catamenial pain, whereas in some others it appeared several days before menstruation [37, 54]. The possibility of persistent pain with exacerbation during menses has also been reported [37].


   Diagnosis
Top
 Abstract
 Introduction
 Material and Methods
 Epidemiology
 Etiologic Mechanisms
 Pathology
 Clinical Presentations
 Diagnosis
Treatment
 Outcome
 References
 
In accordance with the preferential peripheral location of endometrial tissue in the lung of patients with CH, bronchoscopy does not show visible lesions in most cases [12, 18, 19, 46, 47], although it frequently allows localization of the bleeding lobe or segment [12, 46, 47]. Descriptions of bronchoscopic findings are, therefore, extremely rare with fewer than 10 cases having been reported [48, 51–53, 55, 56]. Multiple, bilateral purplish-red submucosal lesions, which ooze easily if touched, seem to be the commonest feature, but the spectrum of tracheobronchial abnormalities ranges from a striking diffuse hyperemia with pronounced mucosal oozing [52] to a single, tiny red mucosal spot [48]. Curiously, bronchial biopsy almost constantly fails to provide a tissue diagnosis regardless of the bronchoscopic findings, whereas brush cytology frequently shows distinctive features of endometrial cells [53]. Even when all the sampling bronchoscopic procedures have failed to yield a diagnosis of endometriosis, follow-up bronchoscopic examination in the middle of the menstrual cycle typically documents the disappearance of the previously reported findings, thus strengthening the clinical suspicion [52].

Video-assisted thoracoscopy is currently the preferred method for surgical assessment of patients with CP [8, 23]. Diaphragmatic abnormalities are nowadays the most commonly described abnormality [8, 23, 24]. The tendinous portion is the most frequently involved part of the diaphragm; the perforations are generally a few millimeters wide [8], although larger defects have been reported [57]. Endometrial deposits in both diaphragm and pleura have a similar appearance. Their size usually ranges between some millimeters and 1 cm [8, 33], and their color varies from brown to violet, according to the period of menstrual cycle. In the review by Joseph and Shan [5], pleural endometriosis was found in 5 of 7 patients submitted to thoracoscopy or thoracotomy for CHt and in all the cases diaphragmatic defects coexisted, but this last finding has not been reported by others [11]. The morphologic appearance, observed at either thoracoscopy or thoracotomy in patients with Cht, varies from nodular blue-brown lesions to orange-red plaquelike pleural nodules [11] or even to bulky masses [45]. Video-assisted thoracoscopy has also been useful in assessing patients with lung nodules that were subsequently proven to be endometriotic [58].

Video-assisted laparoscopy has been employed in patients with catamenial chest pain suggestive of diaphragmatic endometriosis. The observed abnormalities range from small, single nodular lesions to wide involvement characterized by the presence of lesions a few centimeters large in one (generally the right one) or even both (much more rarely) hemidiaphragms [37, 54].

Exploratory thoracotomy now plays only a limited role as a merely diagnostic tool, since video-assisted thoracoscopy is generally sufficient to provide a diagnosis. Open surgery was, however, widely used in the past and contributed to the knowledge of the mechanisms of disease [5, 14, 28, 59]. Exploratory thoracotomy is currently employed in cases of failure of prior thoracoscopic exploration [24, 60].


   Treatment
Top
 Abstract
 Introduction
 Material and Methods
 Epidemiology
 Etiologic Mechanisms
 Pathology
 Clinical Presentations
 Diagnosis
 Treatment
Outcome
 References
 
In the era of video-assisted surgery, treatment of TES is best achieved by video-assisted thoracoscopy. Once the pathogenic mechanism has been identified by exploration, targeted treatment may be carried out in most instances [8]. Diaphragmatic involvement by either endometrial tissue or perforations is probably best managed by diaphragmatic resection [8]. Simple suturing of the holes has been reported to be followed by recurrence [64], and it does not provide tissue for diagnosis. What is more, if endometrial implants are left in place, they can be responsible for formation of further holes and, possibly, for further intrathoracic spread. The diaphragm can be resected and sutured using endoscopic stapler devices [8, 30], provided that the resected surface is relatively small. For more extended resection, we advocated the use of a minithoracotomy to allow diaphragmatic repair with X-shaped stitches [8, 25]. Furthermore, concomitant bullous dystrophy can be resected, as usually done in the treatment of pneumothorax [8], whereas endometrial foci of visceral pleura or deeper lung parenchyma can be removed with a wedge resection. Partial pleurectomy is required if the parietal pleura is involved [8, 33]. Pleural abrasion at completion of the procedure has been proposed [8], but pleurectomy is another option [24].

Small endometrial foci can be removed from the peritoneal aspect of the diaphragm during video-assisted laparoscopy [54]. Superficial lesions can be successfully vaporized using a combination of hydrodissection and carbon dioxide laser, whereas deeper implants require sharp dissection. However, some concerns have been raised about this approach [37]: the operating field on the right side is small because of the bulk of the liver; access to the posterior aspect of the right hemidiaphragm is difficult, and full-thickness resections are difficult to repair. Redwine and colleagues [37] suggested that laparoscopy should be used for diagnosis and open surgery for treatment of endometriosis of the peritoneal aspect of the diaphragm.

Video-assisted laparoscopy has also been advocated to carry our tubal ligation in patients with CP not desiring to became pregnant [31]. This treatment is obviously ineffective in those cases in which the mechanism of pneumothorax is not the transabdominal/transdiaphragmatic passage of air.

In spite of the advances of video-assisted surgical techniques, open surgery maintains an important role in the treatment of TES. Standard thoracotomy continues to be employed in cases of previous unsuccessful surgery for CP [8, 24]. The repair of possible diaphragmatic holes and the resection of endometrial implants is easily accomplished [8]. Lesions close to the phrenic nerve or its main divisions are best treated by limited resection (if possible) and repair [8]. Because of the fear to leave occult defects, Bagan and colleagues [24] proposed the insertion of a polygalactin mesh to cover the tendinous part of the diaphragm.

Experience with the surgical treatment of CHt is much more limited. Medical treatment has been adopted in some patients, and only a few have been submitted to surgery. Two recent reports have focused on the successful treatment of CHt by surgical pleurectomy [44, 45].

In cases of CH, surgery has been advocated if medical treatment fails [65], intolerable drug-related side effects occur, or if symptoms recur after the cessation of hormonal therapy [18], but it has also been proposed as an alternative to it [12, 66]. Open surgery may be employed in the treatment of CH when video-assisted thoracoscopy or video-assisted thoracic surgery is not adequate. Parenchymal-sparing procedures should be employed whenever possible [18, 66], but lobectomy may occasionally be necessary [65].

A single case of bronchoscopic treatment of airway endometriosis by Nd-YAG laser under rigid bronchoscopy has been reported in the literature [48]: a small endometriotic implant at the origin of the left upper lobe bronchus was successfully treated, and there had been no recurrence at the 17-month clinical and bronchoscopic follow-up.

Theoretically, the possibility of treating endometrial implants endoscopically depends on both their location in the airway and the characteristics of the tissue involvement. Biopsy-proven endometrial lesions of limited size and extension would obviously be those most suitable for endobronchial treatment. Nevertheless, diffuse hyperemia which may involve an extremely large area and extend beyond endoscopic visibility has been observed in some cases of catamenial hemoptysis [52]. The possible role of endobronchial treatments in diffuse widespread hyperemia due to vascular engorgement not clearly associated with endometrial tissue is less predictable and has never been assessed to our knowledge.

Simple rest has been employed in the treatment of CP in patients experiencing mild symptoms [15, 61], and thoracenthesis has been used for symptomatic relief [7]. Tube thoracostomy has been used in the treatment of some patients with CP [5]. Instillation of sclerosing agents may be performed, but visualization of the causative lesion is obviously impossible. Tetracycline pleurodesis failed in both patients in whom this treatment option was used [5]. On the other hand, talc pleurodesis was effective in all the 3 patients who underwent this treatment, with no recurrence at the 1-year follow-up [5]. Needle thoracentesis [62] and tube thoracostomy [63] have also been employed in the treatment of CHt or catamenial hemopneumothorax.

Hysterectomy with bilateral salpingo-oophorectomy is the definitive treatment of endometriosis, but it should be considered only in case of failure of other treatment modalities; remarkably, if hormonal replacement therapy is undertaken in this setting, the manifestations of thoracic endometriosis may recur [5].

Medical Treatment
Medical treatment has long been considered the first choice in patients with TES. It is aimed at blocking the hormonal support from the ovary to the existing endometrial tissue, and at preventing further seeding. Theoretically, this aim may be achieved by inducing either a pseudopregnancy or a pseudomenopause, creating a suboptimal milieu for growth and maintenance of endometrial tissue [1]. The literature contains a variety of reports on the use of oral contraceptives, progestational drugs, danazol, and gonadotropin-releasing hormone (GnRH) agonists, although controlled trials on the efficacy of these drugs in patients with TES are lacking [5, 18, 19, 46, 47, 52, 53, 66, 67].

As no specific drug has been shown to be superior to the others, the decision on which to use is influenced by costs, side-effects, duration of treatment, and the patient's wish to become pregnant [5]. That said, experience in the last 2 decades has been greatest with danazol and GnRH agonists.

Danazol is a isoxazol derivative of 17{alpha}-ethinyltesterone that causes anovulation by attenuating the mid-cycle surge of luteinizing hormone secretion, inhibiting several enzymes in the steroidogenic pathway, and increasing serum concentrations of free testosterone [2]. The recommended dosage of danazol is 600 to 800 mg per day, a regimen that is well known to be associated with androgenic side effects and, rarely, liver damage [2]. Treatment with lower doses has been tried in small uncontrolled studies [68], but case reports documenting failure or incomplete response to low-dose treatment of TES have been published [18, 46, 52, 53].

The GnRH agonists reduce the secretion of follicle-stimulating hormone and luteinizing hormone, thus leading to hypogonadotropic hypogonadism [2]. The side effects are those of hypoestrogenism, and can be limited by adding estrogen and progesterone, in the doses usually given to postmenopausal woman, to the treatment; this approach maintains the efficacy of the GnRH agonists while reducing their side effects [2].

The results of medical treatment in comprehensive series of patients with TES are, however, disappointing. The recurrence rate exceeds 50%, regardless of the drug used [5]. These data suggest that hormonal therapy does not achieve complete regression of endometrial implants or that recurrent embolization from pelvic foci is a continuous process in a large number of cases [5].

The highest rates of recurrence after hormonal therapy are seen in patients with CP [5]. Interestingly, in the retrospective analysis by Joseph and Sahn [5], surgical treatment of CP resulted in a far lower recurrence rate than did hormonal therapy: the 6- and 12-month recurrence rates of CP were, in fact, 50% and 60%, respectively, for medical treatment, and 5% and 25%, respectively, for surgical management [5]. Among the medical options, GnRH agonists have been found to be the most effective in preventing CP recurrence when given for prolonged periods of as long as 1 year [66, 69, 70].

Combined and Sequential Approaches
As medical treatment of TES has been shown to prevent recurrences in 50% of cases at most, the utility of combined and sequential treatments has been seriously considered in the last years by many authors. A sequential medical-surgical or surgical-medical approach may become necessary for patients who do not achieve a satisfactory response to the first treatment option employed [5].

That is particularly true for patients with CP and CHt, who frequently experience recurrence after medical treatment and are subsequently managed surgically [5]. For patients with CH, surgery is usually considered after medical treatment, if the latter is not effective [65], if it is refused or causes intolerable side effects, or if symptoms recur after it is discontinued [18]. On the other hand, there are reports of CP that recurred after surgical treatment but then responded to subsequent hormonal therapy [32].

Based on the suboptimal response rates associated with either the surgical or medical option alone, many authors have tried a combined approach in patients with CP consisting in surgery followed, in the immediate postoperative period, by hormonal treatment [8, 25, 33, 38, 60]. The reported results are encouraging and in spite of the absence of randomized controlled studies on the topic, the opinion that the combined approach should be regarded as the best option for treating patients with CP is gaining increasing popularity [8, 69, 70].


   Outcome
Top
 Abstract
 Introduction
 Material and Methods
 Epidemiology
 Etiologic Mechanisms
 Pathology
 Clinical Presentations
 Diagnosis
 Treatment
 Outcome
References
 
Information about the outcome of manifestations of thoracic endometriosis are scanty and have significant limitations because they are derived from case reports or small series, and refer to short-term follow-up periods. That is especially true for CH and CHt, whereas the outcome of CP is better known. Bagan and colleagues [24] reported the outcome of a retrospective series of 10 patients who were followed up for a mean period of 55.7 months: the recurrence rate among patients treated by simple thoracoscopic pleurodesis was high (3 of 5), whereas none of the patients who had diaphragmatic abnormalities identified and treated experienced recurrence [24]. In a prospective study by Alifano and colleagues [8] the mean follow-up was shorter (6.6 months); diaphragmatic abnormalities were identified and treated in all the 8 patients, and a single recurrence was observed. The literature data seem to indicate that the recurrence rate of CP after treatment is much higher than that of primary pneumothorax, probably regardless of treatment modality. The optimal management of these patients needs further evaluation.


   References
Top
 Abstract
 Introduction
 Material and Methods
 Epidemiology
 Etiologic Mechanisms
 Pathology
 Clinical Presentations
 Diagnosis
 Treatment
 Outcome
 References
 

  1. Olive DL, Schwartz LB. Endometriosis N Engl J Med 1993;328:1759-1769.[Free Full Text]
  2. Olive DL, Pritts EA. Treatment of endometriosis N Engl J Med 2001;345:266-275.[Free Full Text]
  3. Abbott J, Hawe J, Hunter D, Holmes M, Finn P, Garry R. Laparoscopic excision of endometriosisa randomized, placebo-controlled trial. Fertil Steril 2004;82:878-884.[Medline]
  4. Parazzini F. Ablation of lesions or no treatment in minimal-mild endometriosis in infertile women: a randomized trial. Gruppo Italiano per lo Studio dell'Endometriosi Hum Reprod 1999;14:1332-1334.[Abstract/Free Full Text]
  5. Joseph J, Sahn SA. Thoracic endometriosis syndromenew observations from an analysis of 110 cases. Am J Med 1996;100:164-170.[Medline]
  6. Nakamura H, Konishiike J, Sugamura A, Takeno Y. Epidemiology of spontaneous pneumothorax in women Chest 1986;89:378-382.[Medline]
  7. Shearin RPN, Hepper NGG, Payne WS. Recurrent spontaneous pneumothorax concurrent with menses Mayo Clin Proc 1974;49:98-101.[Medline]
  8. Alifano M, Roth Th, Camilleri Broet S, Schussler O, Magdeleinat P, Regnard JF. Catamenial pneumothorax. A prospective study Chest 2003;124:1004-1008.[Medline]
  9. Gupta D, Hansell A, Nichols T, Duong T, Ayres J, Strachan D. Epidemiology of pneumothorax in England Thorax 2000;55:666-671.[Abstract/Free Full Text]
  10. Sadikot RT, Green T, Meadows K, et al. Recurrence of primary spontaneous pneumothorax Thorax 1997;52:805-809.[Abstract]
  11. Shepard MK, Mancini MC, Campbell GD, George R. Right-sided hemothorax and recurrent abdominal pain in a 34-year-old woman Chest 1993;103:1239-1240.[Medline]
  12. Cassina PC, Hauser M, Kacl G, Imthurn B, Schroder S, Weder W. Catamenial hemoptysis. Diagnosis with MRI Chest 1997;111:1447-1450.[Medline]
  13. Wood DJ, Krishnan K, Ward MJ. Catamenial hemoptysisa rare cause. Thorax 1993;48:1048-1049.[Abstract/Free Full Text]
  14. Rossi NP, Goplerud CP. Recurrent catamenial pneumothorax Arch Surg 1974;109:173-176.[Medline]
  15. Carter EJ, Ettensohn DB. Catamenial pneumothorax Chest 1990;98:713-716.[Medline]
  16. Meyer R. Zur Frage der heterotopen Epithelwucherung, insbesondere des Peritonealepithels und in die Ovarien Virch Arch Path Anat Phys 1924;250:595-610.
  17. Lattes R, Shepard F, Tovell H, et al. A clinical and pathological study of endometriosis of the lung Surg Gyecol Obstet 1956;103:552-556.
  18. Terada Y, Chen F, Shoji T, Itoh H, Wada H, Hitomi S. A case of endobronchial endometriosis treated by subsegmentectomy Chest 1999;115:1475-1478.[Medline]
  19. Yu Z, Fleischman JK, Rahman HM, Mesia AF, Rosner F. Catamenial hemoptysis and pulmonary endometriosisa case report. Mt Sinai J Med 2002;69:261-263.[Medline]
  20. Kovaric JL, Toll GD. Thoracic endometriosis with recurrent spontaneous pneumothorax JAMA 1966;196:595.[Medline]
  21. Sampson JA. Peritoneal endometriosis due to the menstrual dissemination of endometrial tissue into the peritoneal cavity Am J Obstet Gynecol 1927;14:422-469.
  22. Kirschner PA. Porous diaphragm syndromes Chest Surg Clin North Am 1998;8:449-472.[Medline]
  23. Korom S, Canyurt H, Missbach A, et al. Catamenial pneumothorax revisitedclinical approach and systematic review of the literature. J Thorac Cardiovasc Surg 2004;128:502-508.[Abstract/Free Full Text]
  24. Bagan P, Le Pimpec Barthes F, Assouad J, Souilamas R, Riquet M. Catamenial pneumothoraxretrospective study of surgical treatment. Ann Thorac Surg 2003;75:378-381.[Abstract/Free Full Text]
  25. Alifano M, Cancellieri A, Fornelli A, Trisolini R, Boaron M. Endometriosis-related pneumothoraxclinico-pathological observations from a newly diagnosed case. J Thorac Cardiovasc Surg 2004;127:1219-1221.[Free Full Text]
  26. Foster DC, Stern JL, Buscema J, et al. Pleural and parenchymal pulmonary endometriosis Obstet Gynecol 1981;58:552.[Abstract/Free Full Text]
  27. Mayo P. Recurrent spontaneous pneumothorax concomitant with menstruation J Thorac Cardiovasc Surg 1963;46:415-416.[Medline]
  28. Maurer CR, Schaal JA, Mendez FL. Chronic recurring spontaneous pneumothorax due to endometriosis of the diaphragm JAMA 1958;168:2013-2014.
  29. Downey DB, Towers MJ, Poon PY, Thomas P. Pneumoperitoneum with catamenial pneumothorax AJR Am J Roentgenol 1990;155:29-30.[Free Full Text]
  30. Roth Th, Alifano M, Schussler O, Magdeleinat P, Regnard JF. Catamenial pneumothoraxchest X-ray sign and thoracoscopic treatment. Ann Thorac Surg 2002;74:563-565.[Abstract/Free Full Text]
  31. Muller NL, Nelems B. Postcoital catamenial pneumothorax. Report of a case not associated with endometriosis and successfully treated with tubal ligation Am Rev Respir Dis 1986;134:803-804.[Medline]
  32. Sakamoto K, Ohmori T, Takei H. Catamenial pneumothorax caused by endometriosis in the visceral pleura Ann Thorac Surg 2003;76:290-291.[Abstract/Free Full Text]
  33. Alifano M, Venissac N, Mouroux J. Recurrent pneumothorax associated with thoracic endometriosis Surg Endosc 2000;14:680.[Medline]
  34. Lillington GA, Mitchell SP, Wood GA. Catamenial pneumothorax JAMA 1972;219:1328-1332.[Medline]
  35. Flieder DB, Moran CA, Travis WD, Koss MN, Mark EJ. Pleuro-pulmonary endometriosis and pulmonary ectopic deciduosisa clinico-pathologic and immunohistochemical study of 10 cases with emphasis on diagnostic pitfalls. Hum Pathol 1998;29:1495-1503.[Medline]
  36. Inoue T, Kurokawa Y, Kaiwa Y, et al. Video-assisted thoracoscopic surgery for catamenial hemoptysis Chest 2001;120:655-658.[Medline]
  37. Redwine DB. Diaphragmatic endometriosisdiagnosis, surgical management, and long-term results of treatment. Fertil Steril 2002;77:288-296.[Medline]
  38. Yamazaki S, Ogawa J, Koide S, Shohzu A, Osamura Y. Catamenial pneumothorax associated with endometriosis of the diaphragm Chest 1980;77:107-109.[Medline]
  39. Brown RC. A unique case of catamenial pneumothorax Chest 1989;95:1368.[Medline]
  40. Lee CY, DiLoreto PC, Beaudoin J. Catamenial pneumothorax Obstet Gynecol 1974;44:407-411.[Abstract/Free Full Text]
  41. Laws HL, Fox LS, Younger B. Bilateral catamenial pneumothorax Arch Surg 1977;112:627-628.[Abstract]
  42. Wilhelm JL, Scommegna A. Catamenial pneumothoraxbilateral occurrence while on suppressive therapy. Obstet Gynecol 1977;50:227-231.[Abstract/Free Full Text]
  43. Joseph J, Reed CL, Sahn SA. Thoracic endometriosis recurrence following hysterectomy with bilateral salpingo-oophorectomy and successful treatment with talc pleurodesis Chest 1994;106:1894-1896.[Medline]
  44. Ziedalski TM, Sankaranarayanan V, Chitkara RK. Thoracic endometriosisa case report and literature review. J Thorac Cardiovasc Surg 2004;127:1513-1514.[Free Full Text]
  45. Byanyima RK. Menstruation in an unusual placea case of thoracic endometriosis in Kampala, Uganda. Afr Health Sci 2001;1:97-98.[Medline]
  46. Elliot DL, Barker AF, Dixon LM. Catamenial hemoptysis. New methods of diagnosis and therapy Chest 1985;87:687-688.[Medline]
  47. Katoh O, Yamada H, Aoki Y, Matsumoto S, Kudo S. Utility of angiograms in patients with catamenial hemoptysis Chest 1990;98:1296-1297.[Medline]
  48. Puma F, Carloni A, Casucci G, Puligheddu C, Urbani M, Porcaro G. Successful endoscopic Nd-YAG laser treatment of endobronchial endometriosis Chest 2003;124:1168-1170.[Medline]
  49. Volkart JR. CT findings in pulmonary endometriosis J Comput Assist Tomogr 1995;19:156-157.[Medline]
  50. Kiyan E, Kilicaslan Z, Caglar E, Yilmazbayhan D, Tabak L, Gurgan M. An unusual radiographic finding in pulmonary parenchymal endometriosis Acta Radiol 2002;43:164-166.[Medline]
  51. Wang HC, Kuo PH, Kuo SH, Luh KT. Catamenial hemoptysis from tracheobronchial endometriosisreappraisal of diagnostic value of bronchoscopy and bronchial brush cytology. Chest 2000;118:1205-1208.[Medline]
  52. Hope-Gill B, Prathibha BV. Catamenial haemoptysis and clomiphene citrate therapy Thorax 2003;58:89-90.[Abstract/Free Full Text]
  53. Kuo PH, Wang HC, Liaw YS, Kuo SH. Bronchoscopic and angiographic findings in tracheobronchial endometriosis Thorax 1996;51:1060-1061.[Abstract/Free Full Text]
  54. Nezhat C, Seidman DS, Nezhat F, Nezhat C. Laparoscopic surgical management of diaphragmatic endometriosis Fertil Steril 1998;69:1048-1055.[Medline]
  55. Butler H, Lake KB, Dyke JJV. Bronchial endometriosis and bronchiectasis Arch Intern Med 1978;138:991-992.[Medline]
  56. Bateman ED, Morrison SC. Catamenial haemoptysis from endobronchial endometriosis. A case report and review of previously reported cases Respir Med 1990;84:157-161.[Medline]
  57. Cowl CT, Dunn WF, Dechamp C. Visualization of diaphragmatic fenestration associated with catamenial pneumothorax Ann Thorac Surg 1999;68:1413-1414.[Abstract/Free Full Text]
  58. Shimizu I, Nakanishi R, Yoshino I, Yasumoto K. An endometrial nodule in the lung without pelvic endometriosis J Cardiovasc Surg (Torino) 1998;39:867-868.[Medline]
  59. Stern H, Toole AL, Merino MD. Catamenial pneumothorax Chest 1980;78:480-482.[Medline]
  60. Blanco S, Hernando F, Gomez A, Gonzalez MJ, Torres AJ, Balibrea JL. Catamenial pneumothorax caused by diaphragmatic endometriosis J Thorac Cardiovasc Surg 1998;116:179-180.[Free Full Text]
  61. Hinson JM, Brigham KL, Daniell J. Catamenial pneumothorax in sisters Chest 1981;80:634-635.[Medline]
  62. Margolis MT, Thoen LD, Mercer LJ, Keith LG. Hemothorax after Lupron therapy of a patient with pleural endometriosis. A case report and literature review Int J Fertil Menopausal Stud 1996;41:53-55.[Medline]
  63. Wilkins SB, Bell-Thomson J, Tyras DH. Hemothorax associated with endometriosis J Thorac Cardiovasc Surg 1985;89:636-638.[Abstract]
  64. Fonseca P. Catamenial pneumothoraxa multifactorial etiology. J Thorac Cardiovasc Surg 1998;116:872-873.[Free Full Text]
  65. Kristianen K, Fjeld NB. Pulmonary endometriosis causing haemoptysis. Report of a case treated with lobectomy Scand J Thorac Cardiovasc Surg 1993;27:113-115.[Medline]
  66. Slabbynck H, Laureys M, Impens N, De Vroey P, Schandevyl W. Recurring catamenial pneumothorax treated with a Gn-RH analogue Chest 1991;100:851-861.[Medline]
  67. Metalliotakis IM, Goumenou AG, Koumantakis GE, Neonaki MA, Koumantakis EE, Arici A. Pulmonary endometriosis in a patient with unicornuate uterus and noncommunicating rudimentary horn Fertil Steril 2002;78:183-185.[Medline]
  68. Vercellini P, Trespidi L, Panazza S, Bramante T, Mauro F, Crosignani PG. Very low dose danazol for relief of endometriosis-associated pelvic paina pilot study. Fertil Steril 1994;62:1136-1142.[Medline]
  69. Tripp HF Thomas LP, Obney JA. Current therapy of catamenial pneumothorax Heart Surg Forum 1998;1:146-149.[Medline]
  70. Tripp HF, Obney JA. Consideration of anatomic defects in the etiology of catamenial pneumothorax J Thorac Cardiovasc Surg 1999;117:632-633.[Free Full Text]



This article has been cited by other articles:


Home page
 Am. J. Respir. Crit. Care Med.Home page
M. Alifano, C. Jablonski, H. Kadiri, P. Falcoz, A. Gompel, S. Camilleri-Broet, and J.-F. Regnard
Catamenial and Noncatamenial, Endometriosis-related or Nonendometriosis-related Pneumothorax Referred for Surgery
Am. J. Respir. Crit. Care Med., November 15, 2007; 176(10): 1048 - 1053.
[Abstract] [Full Text] [PDF]

Home page
 Eur Respir JHome page
J-C. Cutz, J. S. Woods, J. H. Mitchell, T. V. Colby, and K. O. Leslie
A common presentation with a rare cause
Eur. Respir. J., September 1, 2007; 30(3): 594 - 597.
[Full Text] [PDF]

Home page
 Eur Respir JHome page
S. Gyorik, S. Erni, U. Studler, R. Hodek-Wuerz, M. Tamm, and P. N. Chhajed
Long-term follow-up of thoracoscopic talc pleurodesis for primary spontaneous pneumothorax
Eur. Respir. J., April 1, 2007; 29(4): 757 - 760.
[Abstract] [Full Text] [PDF]

Home page
 RadioGraphicsHome page
C. M. Park, J. M. Goo, H. J. Lee, C. H. Lee, E. J. Chun, and J.-G. Im
Nodular Ground-Glass Opacity at Thin-Section CT: Histologic Correlation and Evaluation of Change at Follow-up
RadioGraphics, March 1, 2007; 27(2): 391 - 408.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited