Adult Chest Surgery

Chapter 79. Overview 

Benign tumor, bronchogenic cyst, pulmonary hamartoma, pulmonary sequestration, bronchiectasis, and arteriovenous malformation (AVM) are the principal benign and acquired conditions of the lung encountered in thoracic surgery. This chapter reviews the etiology, clinical presentation, diagnosis, and therapeutic modalities for these benign and acquired conditions. Established surgical techniques are described in the ensuing chapters of this section.

BRONCHOGENIC CYSTS

Definition

Bronchogenic cysts are thought to be congenital lesions that arise from the primitive foregut. They are usually found within the mediastinum or lungs. The mediastinal lesions can be found close to the carina, main stem bronchi, trachea, esophagus, or pericardium. Bronchogenic cysts of the skin and subcutaneous tissue are also reported.

Etiology

The precise embryonic pathway leading to the development of bronchogenic cysts is still unknown. The respiratory tree develops by an outpouching of the primitive foregut. Some have theorized that this process fails when a cyst develops in place of the mature structure. As with other structures of the bronchus, bronchogenic cysts are lined by ciliated columnar or squamous epithelial cells (respiratory and gastrointestinal). Mucus-secreting bronchial glands found in the epithelium cause the cysts to fill. As the cysts grow, pressure is exerted on surrounding structures, particularly the membranous trachea or bronchi, which may lead to severe respiratory obstruction. Cartilage and smooth muscle cells are also found in the cyst wall.

Clinical Features

Symptoms may be evident in both children and adults depending on many factors such as the presence of a communication between the lumen of the cyst and the airways, infection of the fluid within the cyst, and bleeding. If the cyst grows large enough to cause obstruction in adjacent structures, the main symptoms will be cough, dyspnea, dysphagia, and chest pain of varying degrees as a result of irritation of the airways and esophagus or inflammation of the mediastinal or parietal pleura. Infectious complications may cause symptoms of high body temperature, elevated leukocyte count, and cough with purulent sputum. Pneumonia localized to the pericystic parenchyma may accompany chronically recurring cysts. Hemoptysis is a sign of an ulcerative process in the cyst wall. Rare complications include cardiac arrhythmias, superior vena cava syndrome, and cancer.

Diagnosis

Plain chest radiographs are diagnostic only when the cavity of the cyst contains an air-fluid level. This finding, especially when the cyst is located in the mediastinum, excludes enterogenous cysts from the differential diagnosis. Plain chest radiography alone can diagnose accurately approximately 80–90% of cases and is useful for initial screening.1

CT scanning and MRI give greater detail regarding anatomic and topographic localization, especially with respect to surrounding structures. These imaging modalities also provide detail about wall composition and content of the cysts (Fig. 79-1).

Figure 79-1.

 

CT scan showing a large bronchogenic cyst of the right lower lobe.

Ultrasound is useful when the cyst is close to the chest wall because it may give information about wall thickness and internal content. Transesophageal endoscopic ultrasound is indicated with paraesophageal cysts.

Bronchoscopy performed as part of the diagnostic workup for a bronchogenic cyst usually reveals extrinsic bronchial compression. Occasionally, there is evidence of a fistulous communication between the cyst and the bronchial tree.

Any patient who presents with clinical findings suggestive of bronchogenic cyst requires a plain chest radiograph followed by a CT scan of the chest.

Therapy

Elective treatment by surgical excision is justified to relieve symptoms in symptomatic patients and to prevent complications in asymptomatic patients. Generally, the excision is technically feasible and easy to perform. However, if there are tight adhesions to the membranous portion of the trachea or mainstem bronchus, or if there is severe inflammation, the excision could be challenging. Video-assisted thoracoscopic surgical (VATS) resection of bronchogenic cysts is now easily performed and can be considered standard therapy for peripheral lesions.2 Other techniques, such as aspiration, cyst wall biopsy, and instillation of sclerosant, can be done with mediastinoscopy.3 Complete resection is preferred over aspiration because removing the entire cyst prevents the possibility of malignant degeneration (Fig. 79-2).

Figure 79-2.

 

Intraoperative specimen: right lower lobe after excision. A large bronchogenic cyst is visible on the pleural surface.

PULMONARY HAMARTOMAS

Definition

Pulmonary hamartomas are benign biphasic lesions consisting of epithelial and mesenchymal tissues.

Etiology

Hamartomas arise more often in men than in women. The lesions are extremely slow-growing. Although often arising in young adulthood, they usually are not detected until the sixth or seventh decade. Most individuals have a history of smoking.

Clinical Features

Most pulmonary nodules are located peripherally in the lung without preference for any particular lobe. In this location they are generally asymptomatic. Central endobronchial hamartomas are less common and are associated with signs and symptoms of obstruction mimicking malignant neoplasms or other benign conditions, including pneumonia or atelectasis. The typical hamartoma is less than 2.5 cm in diameter (range 1–8 cm) and contains fat or calcification with fat. Rare giant hamartomas have been reported,4 and instances of multiple endobronchial hamartomas also have been reported.5

Diagnosis

Pulmonary hamartoma has a distinctive appearance on high-resolution CT scanning that distinguishes it from lung cancer nodules. Fine-needle aspirates also have been used as a diagnostic tool. The differential diagnosis for peripheral hamartomas includes other benign or malignant lung tumors, secondary metastasis, infectious granulomas, amyloidoma, or Carney's triad (i.e., gastric epithelioid leiomyosarcoma, extraadrenal paraganglioma, or pulmonary chondroma). The differential diagnosis for endobronchial hamartomas includes bronchogenic carcinoma, papilloma, granular cell tumor, adenoid cystic carcinoma, mucoepidermoid carcinoma, carcinoid tumor, leiomyoma, lipoma, tracheobronchopathia osteochondroplastica, and secondary metastasis.

Therapy

Elective treatment by surgical excision is justified to prevent complications in asymptomatic patients and to relieve symptoms in symptomatic patients. Peripheral nodules can be resected surgically via thoracotomy or wedge resection or using VATS. Endobronchial lesions are removed bronchoscopically. Rarely, hamartomas are observed to undergo malignant transformation, reinforcing the need for surgical resection.

PULMONARY SEQUESTRATIONS

Definition

Pulmonary sequestrations are rare congenital malformations of the lung (see Chap. 82). They consist of masses of nonfunctioning pulmonary tissues that lack normal communication with the bronchial tree.6 The condition may occur within the lobar lung tissue (intralobar sequestration) or external to the lobe (extralobar sequestrations), but each type has a direct arterial blood supply from the thoracic or abdominal aorta or from one or more of the intercostal branches of the aorta. Extralobar sequestrations are peculiar because they can be surrounded by pleura, similar to an accessory pulmonary lobe; differentiation is based on the lack of normal communications with the bronchial tree. Although there is no single unifying embryonic hypothesis, it is nonetheless thought that these lesions arise as an accessory bud that then migrates with the developing esophagus.7Others have suggested an acquired etiology (inflammatory) for pulmonary sequestrations.

Congenital cystic adenomatoid malformations have been observed within extralobar pulmonary sequestrations, suggesting similar etiologic factors. Eighty-five percent of pulmonary sequestrations are localized in the lower lung zones, more often on the left side. Twenty-eight percent of intralobar sequestrations have a homogeneous appearance, 33% are inhomogeneous, and 39% are cystic. Seventy-seven percent of extralobar sequestrations are homogeneous, and 23% are cystic.8 Extralobar sequestrations sometimes are associated with diaphragmatic hernias (16%), lung hypoplasia (25%), bronchogenic cysts, and cardiovascular malformations.

Pathology

The macroscopic characteristics of intralobar sequestrations do not differ from the normal tissues around them. Sequestration is suspected when severe adhesions between mediastinal or diaphragmatic structures or parietal pleura and lung are found. Extrapulmonary sequestrations have a more typical pathologic appearance consisting of a pyramidal or ovoid lesion of approximately 0.5–15 cm in length surrounded by its own pleura. Cystic lesions secondary to chronic inflammation and fibrosis replacing normal lung tissue may be observed in the extralobar sequestration.

The inner layer of the cyst consists of respiratory epithelium or, rarely, squamous epithelium with an eosinophilic amorphous fluid-filled center. In extralobar sequestrations, bronchus/alveolar-like structures lined with respiratory epithelium may be observed. Both types have their own systemic arterial supply, but venous flow occurs through the pulmonary veins for the intralobar type and through the systemic veins for the extralobar type. The arteries that supply the sequestrations have a large caliber (up to 0.5 cm in diameter). In 80% of cases they arise both from the thoracic and abdominal aorta. In this event, the arteries run through the triangular ligament toward the lower lobes. Abnormal origin in a sequestration arising from the coronary artery has been reported.9

Clinical Features

The two main forms of pulmonary sequestration are associated with different symptoms. In elderly patients, sequestration may be asymptomatic and observed as an incidental finding on chest radiographs, especially the extralobar sequestration. The intralobar types, because of their bronchial communications, may lead to recurrent pneumonia and respiratory distress symptoms (i.e., dyspnea, cyanosis). Hemoptysis is rare but has been reported as an acute symptom.10

Diagnosis

Plain chest radiography is nonspecific in the diagnosis of sequestration. Sometimes it shows the presence of a mass in the lower lobes or, if there is communication with the tracheobronchial tree, a cystic lesion. CT scan of the chest is the standard diagnostic tool, and it can demonstrate the presence of a systemic artery supplying the sequestration. Duplex Doppler ultrasound may be used to demonstrate the abnormal systemic vessel feeding the sequestration. MRI can be useful in the differential diagnosis (bronchogenic cyst versus bronchiectasis versus solitary lung abscess) and for demonstrating mediastinal structures.

Therapy

Medical therapy is based on anti-inflammatory and antimicrobial drugs. Elective treatment is surgical. Anatomic lobectomy is the treatment for intralobar sequestrations. Posterolateral thoracotomy through the lower intercostal spaces is performed for sequestrations of the lower lobes. Retroperitoneal or abdominal sequestrations may require a laparotomy or a thoracoabdominal approach. Use of the VATS approach has been reported for management of sequestration.11

BRONCHIECTASIS

Definition

Bronchiectasis was first described by Laennec (Paris, France) in the 1800s as a bronchial dilatation. This definition is still valid, but it must be added that it is always associated with an alteration of the structural layers of the bronchial wall. The surgical management of bronchiectasis is presented in Chapter 83.

Pathophysiology

Various congenital and acquired disease processes can lead to bronchiectasis. During pulmonary infections, obstructive endobronchial processes localized to the peripheral lung may cause bronchial dilatation. Repeated infections damage the epithelial cilia, mucoelastic tissue, and even cartilage. Healing and replacement of these tissues with fibrous tissue results in loss of elasticity with contraction of the peribronchial tissues and traction on the bronchial tree leading to bronchial dilatation. True bronchiectasis is distinct from pseudobronchiectasis (bronchocele). This latter form of bronchial dilatation is reversible and lasts only a few weeks or months after an episode of bronchopneumonia. The epithelial damage is not severe and is without necrosis.

Sometimes bronchiectasis is caused by bronchial obstruction. The obstruction is created by tiny aspirated endoluminal foreign bodies,12 benign lymphoadenomatoid-bronchial syndromes, or slow-growth tumorlets such as carcinoids.13,14

Bronchial obstruction also can be caused by extrinsic compression from the peribronchial lymph nodes (middle lobe or lingula) in the case of neoplasms or by chronic infections (e.g., histoplasmosis, coccidioidomycosis, aspergillosis, tuberculosis, and AIDS-related infections).15–18 Three steps are implicated in the pathophysiology of extrinsic obstruction, namely, secretion retention, chronic infection, and bronchiectasis, as seen before.

Congenital and familial diseases are an uncommon cause of bronchiectasis (Table 79-1). The most important is Kartagener's syndrome, or primary ciliary dyskinesia, a rare autosomal recessive disorder involving the combination of situs inversus, bronchiectasis, and sinusitis. A dynein deficiency leads to ciliary dyskinesia.19 The yellow nail syndrome is a rare clinical entity that combines three main features: yellow discoloration of the nails, chronic lymphedema, and pleural effusion. This syndrome is often complicated by bronchiectasis.20 The classification of bronchiectasis is morphologic, consisting of three types: (1) cylindrical or tubular, (2) saccular or cystic, and (3) varicose. Saccular bronchiectasis is characterized by an evident dilatation at the distal end, often associated with postinfectious and postobstructive bronchiectasis. Cylindrical bronchiectasis has a uniform caliber of dilatation and is often associated with tuberculosis. Varicose bronchiectasis is a mixed form and presents with alternating areas of saccular and cylindrical dilatation. The subclassification of bronchiectasis is based on blood perfusion.21 Two types of bronchiectasis are recognized: perfused and nonperfused. Whereas perfused bronchiectasis has intact pulmonary artery flow and cylindrical bronchiectatic changes, the nonperfused type is characterized by a lack of pulmonary artery flow, retrograde filling of the pulmonary artery through the systemic circulation, and cystic bronchiectatic changes.

Table 79-1. Congenital and Familial Diseases that Cause Bronchiectasis

Etiology

Syndromes and Diseases

Bronchial malformations

Primitive tracheomalacia

 

Williams-Campbell syndrome

Vascular and lymphatic malformations

Sequestration

 

Yellow nails syndrome

Chest malformations

Kyphoscoliosis

 

Phrenic eventration/relaxation

Systemic diseases

Cystic fibrosis

 

1-Antitrypsin deficiency

Bronchiectasis in other complex syndromes

Kartagener's syndrome (primary ciliary dyskinesia)

 

Mounier-Kuhn syndrome

 

The location of the bronchiectasis may reveal its pathogenesis. Bronchiectasis related to congenital and familial diseases is always bilateral and involves different segments of the lung. Bronchiectasis related to tuberculosis is located primarily in the upper lobes. Obstructive and inflammatory bronchiectasis is found in the lower lobes. The middle lobe syndrome is a selective localized form of bronchiectasis. The middle lobe bronchus arises with a 30-degree downward open angle from the intermediate bronchus and runs for approximately 2 cm. Lymph node hypertrophy of the angle may easily compress the middle bronchus, leading to atelectasis and bronchiectasis.22

Clinical Features

Bronchiectasis may be symptomatic or asymptomatic. The symptoms are typical: chronic cough, productive sputum (as much as 600 mL/d), and recurrent respiratory infections. Hemoptysis, even if rare, may occur and has been reported as a symptom of the type of bronchiectasis associated with coronary fistula.23

Chest physical examination may reveal coarse expiratory rhonchi and dullness over localized areas, especially during periods of acute infectious exacerbation.

Diagnosis

Standard chest radiography is often not useful because it shows only nonspecific inflammatory radiologic signs (Fig. 79-3). In the past, the ideal radiographic method was, and in some cases still is, a bronchogram. This procedure provides information about the morphology, localization, and extent of the bronchiectasis (Fig. 79-4). High-resolution, fine-cut CT scan represents the procedure of choice for the diagnosis of bronchiectasis.24

Figure 79-3.

 

Chest radiograph showing bronchiectasis.

 

Figure 79-4.

 

Bronchograms of bronchiectasis of the lower lobe.

 

CT is able to show the extent of the disease bilaterally and gives information about the walls of the bronchioles, including the presence of peribronchial inflammation and parenchymal disease (Fig. 79-5).

Figure 79-5.

 

High-resolution spiral CT scan of diffuse cylindrical bronchiectasis. (Courtesy of Dr. Nunzio Calia.)

Flexible fiberoptic bronchoscopy is useful for evaluating bronchial neoplasms and endoluminal foreign bodies or obtaining samples for bacterial culture to start specific antibiotic therapy. Bronchoscopy permits biopsy of the respiratory mucosa to diagnose hereditary mucociliary disorders.

Therapy

MEDICAL

The goal of medical therapy is to treat the secretions and infections. Postural drainage is the most effective treatment to mobilize the thick bronchial secretions but requires the skills of a trained respiratory physiotherapist. To prevent infections, a sputum culture should be performed. Targeted antibiotic therapy is started if an acute infection of the lung is present or for a preoperative workup.

The conservative therapeutic approach should be continued for several months. Annual shots of antiinfluenza and pneumococcal vaccines are recommended.

SURGICAL

Complete excision of the bronchiectatic parenchyma is the goal of surgery. Patients considered candidates for surgical resection must meet the following criteria: (1) localized bronchiectasis that is completely resectable, (2) adequate respiratory reserve, (3) irreversible process versus an early treatable condition, (4) significant symptoms with a continued chronic productive cough, significant hemoptysis, or major recurring episodes of pneumonia sufficiently severe to warrant surgery, and (5) failed prolonged attempts at medical therapy.25

For massive pulmonary hemorrhage, endobronchial suction with balloon tamponade, embolization of the bleeding vessel (usually a bronchial artery), or emergency resection can be lifesaving. The surgical approach involves anatomic resection of all targeted areas. The anatomic resection depends on the origin of the bronchiectasis: (1) Tuberculous bronchiectasis requires resection of the upper lobes, and (2) postinfective bronchiectasis requires resection of the lower lobes and lingula (Fig. 79-6). Abundant mucopurulent secretions must be treated with particular attention to prevent contamination of the normal airways. Surgical treatment of bronchiectasis is more effective in patients with localized disease. Excision in such patients is satisfactory with an acceptable rate of morbidity and mortality.26 Mortality and morbidity rates range from 1.7% to 3.5% in different case series26–28 (Table 79-2).

Figure 79-6.

 

Resected lingular lobe with bronchiectasis.

Table 79-2. Results of Surgical Resection for Bronchiectasis

Reference

Patients

Mortality Rate

Morbidity Rate

Kutlay et al., 200226

166

1.7%

10.5%

Agasthian et al., 199627

134

2.2%

24.0%

Dogan et al., 198928

487

3.5%

11.0%

 

Surgical treatment of bronchiectasis is used widely, but there appear to be no randomized, controlled trials. It is not possible to provide an unbiased estimate of its benefit compared with conservative therapy.29 Addition of a vascularized muscle flap should be considered to prevent postoperative infection.

PULMONARY ARTERIOVENOUS MALFORMATION (AVM)

Definition

Pulmonary AVMs are caused by abnormal communications between pulmonary arteries and pulmonary veins and are most commonly congenital in nature (see Chap. 84). Although these lesions are quite uncommon, they are an important part of the differential diagnosis of common pulmonary problems such as hypoxemia and pulmonary nodules. Since their first description at autopsy in 1897, these abnormal communications have been given various names, including pulmonary arteriovenous fistulas, pulmonary arteriovenous aneurysms, hemangiomas of the lung, cavernous angiomas of the lung, pulmonary telangiectasias, and pulmonary arteriovenous malformations.30 Abnormal communications among blood vessels of the lung also may be found in a variety of acquired conditions. Right-to-left shunting as a result of communications between pulmonary arteries and pulmonary veins has been reported in many diseases. Communications between bronchial arteries and pulmonary arteries causing left-to-right shunting can develop in chronic inflammatory conditions such as bronchiectasis. Many patients with pulmonary AVMs have hereditary hemorrhagic telangiectasia.

Embryology

By the fourth week of gestation, the respiratory tract can be seen as a groove in the ventral wall of the foregut. The blood vessels of the lung are derived from two sources, namely, the plexiform network of vessels developing in the pulmonary mesenchyme and the heart. Like bronchi, the vessels may vary in their course based on the eventual development of channels from the preexisting mesenchymal network.31 During blood vessel development, primitive arteriovenous connections form to initiate the flow of blood. Subsequent vascular remodeling results in normal vessel development. AVMs result from unknown stimuli during the stage of arteriovenous communications in the retiform plexus.

Diagnosis and Clinical Features

Clinical symptoms of AVM are based on the grade of the right-to-left shunt. Hemoptysis,32 dyspnea on exertion, congestive heart failure, or a major neurologic event such as stroke or cerebral abscess may be present.33 In patients with Rendu-Osler-Weber syndrome, cutaneous and mucosal spider angiomas are present.34

On physical examination of the thorax, a continuous murmur may be heard over the involved area of the thorax, especially if the AVM is quite large. Standard chest radiographs may reveal a solid round or oval mass of uniform density, frequently lobulated but sharply defined, more commonly located in the lower lobes, and ranging from 1 to 5 cm in diameter. As such, it may be difficult to differentiate from a lung tumor (Fig. 79-7).

Figure 79-7.

 

Chest radiograph showing a round mediastinal mass of uniform density in the right lower lobe.

 

CT scan of the chest may provide information about the vascular origin of the mass (Fig. 79-8), but a selective angiogram of the pulmonary artery is essential to localize, determine the extent, and map the AVM for preoperative workup (Fig. 79-9). Right-to-left shunt entities may be measured by radionuclide perfusion scans of the lung.35

Figure 79-8.

 

High-resolution CT scan confirming the arteriovenous malformation of the right lower branch of the pulmonary artery.

 

Figure 79-9.

 

Selective pulmonary angiogram of the same patient confirming the arteriovenous malformation.

Therapy

Localized and large AVMs require a surgical approach. Lobectomy (Fig. 79-10), wedge resection,36 and VATS lobectomy are the standard procedures.37,38 Multiple bilateral AVMs may require a bilateral approach and multiple resections.39 Small-sized AVMs may be treated conservatively with angiographic embolization using different techniques such as balloons, springs, coils, and thrombogenic materials.40–42

Figure 79-10.

 

Large arteriovenous malformation of the right lower lobe after complete surgical excision.

EDITOR'S COMMENT

Although these conditions are very rare, the authors have presented a comprehensive review of the workup and management of benign lung conditions. Surgery is not always needed; however, in carefully selected cases a minimally invasive approach may be helpful. The importance of careful diagnostics including radiographic imaging is emphasized.

–MJK

REFERENCES

1. Suen HC, Mathisen DJ, Grillo HC, et al: Surgical management and radiological characteristics of bronchogenic cysts. Ann Thorac Surg 55:476–81, 1993.[PubMed: 8431062]

2. Lewis R, Caccavale R, Sisler G: Imaged thoracoscopic surgery: A new thoracic technique for resection of mediastinal cysts. Ann Thorac Surg 53:318–20, 1992.[PubMed: 1731675]

3. Ginsberg RJ, Atkins RW, Paulson DL: A bronchogenic cyst successfully treated by mediastinoscopy. Ann Thorac Surg 13:266–8, 1972.[PubMed: 4623113]

4. Hutter J, Reich-Weinberger S, Hutarew G, Stein HJ: Giant pulmonary hamartoma: A rare presentation of a common tumor. Ann Thorac Surg 82:e5–7, 2006. 

5. Kang MW, Han JH, Yu JH, et al: Multiple central endobronchial chondroid hamartoma. Ann Thorac Surg 83:691–3, 2007.[PubMed: 17258021]

6. Halkic N, Cuenoud PF, Corthesy ME, et al: Pulmonary sequestration: A review of 26 cases. Eur J Cardiothorac Surg 14:127–33, 1998.[PubMed: 9754996]

7. Jeanfaivre T, Afi M, L'Hoste P, Tuchais E: Simultaneous discovery of bilateral intralobar and extralobar pulmonary sequestrations. Ann Thorac Surg 63:1171–3, 1997.[PubMed: 9124934]

8. Grabenwoger F, Kober I, Dock W: [The radiologic appearances of pulmonary sequestration: Evaluation of 11 of our own cases and 123 cases published in the literature.] Rofo 148:353–38, 1988.[PubMed: 2834777]

9. Van Langenhove G, Convens C, Seynaeve P, et al: Intralobar pulmonary sequestration supplied by the right coronary artery. Catheter Cardiovasc Intervent 47:218–20, 1999. 

10. Freeman R, Maxwell J: Intralobar bronchopulmonary sequestration presenting as hemoptysis: Evidence for an acquired cause. Mil Med 163:502–3, 1998.[PubMed: 9695620]

11. Della Porta M, Galli A, Rebuffat C: [Videothoracoscopic approach in the treatment of intralobar pulmonary sequestration: Report of a case.] Chir Ital 52:299–302, 2000. 

12. Adegboye VO, Osinowo O, Adebo OA: Bronchiectasis consequent upon prolonged foreign body retention. Cent Afr J Med 49:53–8, 2003.[PubMed: 15214283]

13. Dewan M, Malatani TS, Osinowo O, et al: Carcinoid tumourlets associated with diffuse bronchiectasis and intralobar sequestration. J R Soc Health 120:192–5, 2000.[PubMed: 11077809]

14. Canessa PA, Santini D, Zanelli M, Capecchi V: Pulmonary tumourlets and microcarcinoids in bronchiectasis. Monaldi Arch Chest Dis 52:138–9, 1997.[PubMed: 9203810]

15. Kaestel M, Meyer W, Mittelmeier HO, Gebhardt C: Pulmonary aspergilloma: Clinical findings and surgical treatment. Thorac Cardiovasc Surg 47:340–5, 1999.[PubMed: 10599966]

16. Freixinet JG, Rivas JJ, Rodriguez De Castro F, et al: Role of surgery in pulmonary tuberculosis. Med Sci Monit 8:CR782–6, 2002. 

17. Allen D, Ng S, Beaton K, Taussig D: Sternal osteomyelitis caused by Aspergillus fumigatus in a patient with previously treated Hodgkin's disease. J Clin Pathol 55:616–8, 2002.[PubMed: 12147658]

18. Chechani V, Allam AA, Smith PR, et al: Bronchitis mimicking opportunistic lung infection in patients with human immunodeficiency virus infection/AIDS. NY State J Med 92:297–300, 1992.[PubMed: 1518586]

19. Etzel S, Plotz J, Heidegger H, von Hugo R: [The Kartagener syndrome.] Anaesthesist 43:463–5, 1994.[PubMed: 8092456]

20. Rigau NC, Daele JJ: The yellow nail syndrome. Acta Otorhinolaryngol Belg 57:221–4, 2003.[PubMed: 14571658]

21. Ashour M: Hemodynamic alterations in bronchiectasis: A base for a new subclassification of the disease. J Thorac Cardiovasc Surg 112:328–34, 1996.[PubMed: 8751499]

22. Akilov K, Ismailov D, Madatov K: [Treatment of middle-lobe syndrome.] Khirurgiia (Mosk) 17–8, 2003. 

23. Jim MH, Lee SW, Lam L: Localized bronchiectasis is a definite association of coronarobronchial artery fistula. J Invas Cardiol 15:554–6, 2003.[PubMed: 12947219]

24. Kang EY, Miller RR, Muller NL: Bronchiectasis: Comparison of preoperative thin-section CT and pathologic findings in resected specimens. Radiology 195:649–54, 1995.[PubMed: 7753989]

25. Hodder V, Cameron R, Todd T: Bacterial Infections. New York, Churchill-Livingstone, 1995:463

26. Kutlay H, Cangir AK, Enon S, et al: Surgical treatment in bronchiectasis: Analysis of 166 patients. Eur J Cardiothorac Surg 21:634–7, 2002.[PubMed: 11932159]

27. Agasthian T, Deschamps C, Trastek VF, et al: Surgical management of bronchiectasis. Ann Thorac Surg 62:976–8; discussion 979–80, 1996. 

28. Dogan R, Alp M, Kaya S, et al: Surgical treatment of bronchiectasis: A collective review of 487 cases. Thorac Cardiovasc Surg 37:183–6, 1989.[PubMed: 2669228]

29. Corless J, Warburton C: Surgery vs non-surgical treatment for bronchiectasis. Cochrane Database Syst Rev CD002180, 2000. 

30. Churton T: Multiple aneurysms of the pulmonary artery. Br Med J 1:1223–5, 1897. 

31. La Quaglia M: Congenital Anomalies. New York, Churchill-Livingstone, 1995:463.

32. Thung KH, Sihoe AD, Wan IY, et al: Hemoptysis from an unusual pulmonary arteriovenous malformation. Ann Thorac Surg 76:1730–3, 2003.[PubMed: 14602328]

33. Shioya H, Kikuchi K, Suda Y, et al: [Recurrent brain abscess associated with congenital pulmonary arteriovenous fistula: A case report.] No Shinkei Geka 32:57–63, 2004.[PubMed: 14978925]

34. Marchesani F, Cecarini L, Pela R, et al: Pulmonary arteriovenous fistula in a patient with Rendu-Osler-Weber syndrome. Respiration 64:367–70, 1997.[PubMed: 9311054]

35. Lu G, Shih WJ, Chou C, Xu JY: Tc-99m MAA total-body imaging to detect intrapulmonary right-to-left shunts and to evaluate the therapeutic effect in pulmonary arteriovenous shunts. Clin Nucl Med 21:197–202, 1996.[PubMed: 8846563]

36. Morikawa T, Kaji M, Ohtake S, et al: Video-assisted anatomic mediobasal segmentectomy of lung. Surg Endosc 17:1678, 2003.[PubMed: 14703631]

37. Storck M, Mickley V, Abendroth D, Sunder-Plassmann L: Pulmonary arteriovenous malformations: Aspects of surgical therapy. Vasa 25:54–9, 1996.[PubMed: 8851266]

38. Braun J, Kaiser D, Liebig S: Lung resection in arteriovenous fistula. Pneumologie 44:511–2, 1990.[PubMed: 2114637]

39. Matsuda S, Hamada M, Sumimoto T, et al: [A case of surgical treatment of multiple bilateral pulmonary arteriovenous fistulas in a senile patient.] Nihon Kyobu Shikkan Gakkai Zasshi 28:1348–52, 1990.[PubMed: 2273664]

40. Takahashi K, Fukuoka K, Konishi M, et al: [A case of pulmonary arteriovenous malformation treated by transcatheter embolization using coils.] Nihon Kokyuki Gakkai Zasshi 40:900–4, 2002.[PubMed: 12645112]

41. Vernhet H, Bousquet C, Durand G, et al: [Interventional radiology of the thorax.] Rev Pneumol Clin 56:115–24, 2000.[PubMed: 10810197]

42. Ghani M, Yusuf W, Sdringola S, Smalling R: Percutaneous coil embolization of multiple arteriovenous malformations in left lung causing persistent hypoxia. Circulation 102:E118, 2000. 



If you find an error or have any questions, please email us at admin@doctorlib.info. Thank you!