Infection

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Tuberculosis

Tracheobronchial tuberculous infections seem to involve principally the lower trachea and/or main bronchi (see Figure 37 [Color Plate 16]). Acute ulcerative tuberculous tracheitis is treated medically. Polypoid tissue and then cicatricial stenosis may result as the tracheitis or bronchitis heals.1 This can occur despite adequate treatment of the tuberculosis.

Typically, the fibrosis that results is circumferential and submucosal (Figure 14-1). The airway may become extremely narrowed. Externally, the tracheal cartilages may appear to be intact, despite some peritracheal fibrosis. These days, cavitary disease is not often present with a tuberculous stenosis, as it once was. Primary parenchymal disease associated with endobronchial tuberculosis has been noted more in the lower lobes in the form of bronchiectasis. The length and severity of stenosis varies. The degree of resolution of the frequently accompanying pulmonary lesions also varies, ranging from residual parenchymal scar to lobar fibrosis or destruction (Figure 14-2). Tuberculous broncholithiasis is not often seen anymore. Rarer still are tuberculous tracheoesophageal fistulae.2

If possible, active tuberculosis should be arrested before surgical resection and reconstruction is contemplated. The linear extent of mature fibrous stenosis of the trachea and bronchi may be such that excision and reconstruction is not presently possible. This leaves the possibility of dilation and stenting. When the stenosis is more limited in extent, surgical excision and reconstruction can be performed, with the likelihood of a good result. Such resections have included excision of the lower trachea and carina, isolated resection of the left main bronchus, as well as sleeve lobectomies.3-5 Kato and colleagues, however, noted an increased frequency of postanastomotic stenosis.5

In 2 patients operated upon for acute and severe airway obstructions, the resection necessarily included a stenotic lower trachea, a stenotic right main bronchus, and a contracted and fibrotic right upper lobe. The right bronchus intermedius was anastomosed to the side of the trachea after the left main

figure 14-1 Tuberculous stenosis of lower trachea and right main bronchus. The bronchial cross section (arrow) shows the lumen nearly obliterated by circumferential fibrosis.

figure 14-2 Complete specimen from Figure 14-1, consisting ofstenosed lower trachea and right main bronchus to the bronchus intermedius. The right upper lobe was also densely fibrosed and removed in continuity.

figure 14-1 Tuberculous stenosis of lower trachea and right main bronchus. The bronchial cross section (arrow) shows the lumen nearly obliterated by circumferential fibrosis.

figure 14-2 Complete specimen from Figure 14-1, consisting ofstenosed lower trachea and right main bronchus to the bronchus intermedius. The right upper lobe was also densely fibrosed and removed in continuity.

bronchus had been joined end-to-end to the trachea (Figure 14-3). One patient with a fibrotic stenosis recovered well. In the second patient, with markedly active disease, the healing failed and the patient died. In the presence of active tuberculosis, obstruction must be managed other than by resection. This same distribution of disease and treatment has been described by others.5,6

Histoplasmosis

Histoplasmosis causes airway obstruction in several ways.7 Large fibrotic or calcified lymph nodes may compress the main bronchi by forming what is well described as subcarinal histoplasmoma or mediastinal granuloma (Figure 14-4). The center of this mass usually contains necrotic material. The periphery is characterized by a considerable thickness of dense collagenous tissue. Enlarged lymph nodes and fibrosis may compress the right or left main bronchi, and, in particular, the bronchus intermedius, at the level of the large lymph node accumulation present around the middle lobe bronchus (Figure 14-5).7,8 Calcified lymph nodes may also erode gradually into the carina, the right or left main bronchi, or the bronchus intermedius, causing obstruction and hemoptysis from granulation tissue, as well as eventual protrusion of the calcific node (Figure 14-6).

Histoplasmosis is now a principal cause of broncholithiasis, as tuberculous disease has receded (see Figure 36 [Color Plate 16]).9 Intrinsic fibrosis of the wall of the lower trachea and one or both main bronchi or of the right bronchial tree and bronchus intermedius may also occur, with accompanying lymph node involvement (see Figure 35, Color Plate 16). Varying degrees of mediastinal fibrosis can present (Figure 14-7). Pulmonary infection and fibrosis may follow bronchial obstruction, and hemorrhage

figure 14-3 Tomograms (retouched) of a 38-year-old woman with tuberculous stenosis seen in the surgical specimen in Figure 14-2. A, Lower tracheal and right main bronchial stenoses are indicated by arrows. B, Postoperative study shows anastomosis of bronchus intermedius (arrow) to side of trachea just above the end-to-end anastomosis of trachea to left main bronchus.

figure 14-3 Tomograms (retouched) of a 38-year-old woman with tuberculous stenosis seen in the surgical specimen in Figure 14-2. A, Lower tracheal and right main bronchial stenoses are indicated by arrows. B, Postoperative study shows anastomosis of bronchus intermedius (arrow) to side of trachea just above the end-to-end anastomosis of trachea to left main bronchus.

figure 14-4 Magnetic resonance image showing bilateral compression of main figure 14-5 Bronchus intermedius constricted by dense bronchi by a subcarinal mass due to histoplasmosis in a 35-year-old woman. scar which envelopes cartilages, causing them to override.

Extensive disease also encircles the bronchus intermedius. The lesion developed Nodes at the origin of this bronchus are frequently involved. radiologically in less than 5 years. This required removal of middle and lower lobes in continuity with the subcarinal mass. The main bronchi were intact.

may accompany broncholithiasis. The granulomatous process may compress the adjacent esophagus to some degree and even produce fistulae from the esophagus to the subcarinal or lobar lymph nodes or to the airway itself (see Figure 12-12 in Chapter 12, "Acquired Tracheoesophageal and Bronchoesophageal Fistula").7,10 Inability to identify Histoplasma capsulatum from biopsy specimens in many patients has led to conclusions that fibrosis is often not the result of active fungal proliferation but instead of hypersen-sitivity reaction to the healing infection.11 Although not easily established, the interval between initial infection and these later presentations appears to be of several years.

Patients present with cough (41%), dyspnea (32%), hemoptysis (31%), or recurrent postobstructive pneumonia (23%). Pleuritic pain also occurs (23%).11 Forty percent of patients may be asymptomatic. Superior vena cava syndrome is another presentation that may coexist with airway obstruction.

Computed tomography (CT) scanning with contrast has been of particular help in identifying the extent of involvement (see Figure 14-7B). Skin tests are of no use, in view of the widespread sensitization of the population in areas where the disease is endemic (up to 80%). Indeed, skin tests may be misleading, by causing conversion of serologic tests. Serial complement fixation titers may be of value and may help to determine the need for antifungal therapy in chronic states.12 Antigenuria may be present in active disseminated infection. Organisms are most often demonstrated by silver methenamine stains in pathological material rather than found in aspirates, even in the presence of bronchial erosion. Although acute documented histoplasmosis is treated with amphotericin, the use of the drug has not proved to be of benefit in late cases of fibrosis without demonstration of active organisms. The finding of organisms may indicate the use of itraconazole or ketoconazole, which have less side effects than those seen with amphotericin.

Fibrosis may be so severe and so dense that dilation finally becomes impossible (see Figures 14-7, 14-8). There may be no useful medical treatment at this stage. Large, obstructing subcarinal masses may sometimes be removed by painstaking surgical excision, without the necessity of bronchial resection.

Subcarina Excision

figure 14-6 Mass of calcified subcarinal lymph nodes due to histoplasmosis, with broncholithiasis of the left main bronchus. A, Computed tomography scan showing a calcified mass. B, Tomogram of the carina in the same patient. The arrow points to the broncholith protruding into the bronchial lumen. C, The mass excised with an attached intrabronchial extension. The bronchus was closed longitudinally in this particular patient, which is not always possible. Also, see Figure 36 (Color Plate 16).

figure 14-6 Mass of calcified subcarinal lymph nodes due to histoplasmosis, with broncholithiasis of the left main bronchus. A, Computed tomography scan showing a calcified mass. B, Tomogram of the carina in the same patient. The arrow points to the broncholith protruding into the bronchial lumen. C, The mass excised with an attached intrabronchial extension. The bronchus was closed longitudinally in this particular patient, which is not always possible. Also, see Figure 36 (Color Plate 16).

A resulting bronchial opening, if very limited, may indeed be closed with only slight ultimate narrowing of the bronchus. Small portions of the fibrotic wall of "histoplasmoma" may be left in place in the mediastinum rather than incurring serious technical problems or creating an unreconstructible situa-tion.7,8 James and colleagues essentially performed decortication of a severely stenotic trachea, which produced lasting relief despite necessarily incomplete removal of fibrosis.13 Garrett and Roper noted relief of vascular and bronchial obstructions by unroofing soft nodes, leaving the adherent fibrous capsule behind.14 In their series of 94 patients, 13 had respiratory symptoms, with major bronchial narrowing in 9 and compression in the other 4. Eleven patients had hemoptysis related to broncholithia-sis. Postobstructive destruction of the middle and right lower lobe requires resection. The technical procedure may be very difficult and often requires judicious placement of a proximal tourniquet on the pul monary artery prior to proceeding with further dissection. The calcified lymph nodes often intrinsically involve the wall of the pulmonary artery.

We reported bronchoplastic procedures for airway involvement as follows: sleeve lobectomy in 3 patients, carinal resection in 1, carinal pneumonectomy in 4, and sleeve resection of the right main bronchus in 1.7 The organism was identified in 9 of 20 patients by staining. Despite the adjacent fibrosis, the tracheobronchial anastomoses heal if there is not excessive tension. Dense cicatrization may involve a proximal pulmonary artery, necessitating intrapericardial control. Full thickness esophageal involvement or fistula is managed by careful layered esophageal closure, with firm buttressing of the suture line. Significant collateral circulation from the pleura to lung, sufficient to cause severe hemoptysis, may occur, especially where a pulmonary artery is occluded.11 Superior vena cava obstruction is also well recognized in this process. Surgical intervention does seem to be advisable, even for asymptomatic mediastinal granulomas of large size. Dines and colleagues found that 34% of their cases of mediastinal granuloma progressed to

Lungs Collateral CirculationTracheostomy Infection

figure 14-7 Massive mediastinal fibrosis in a 57-year-old man who had reached an extreme of incapacitating dyspnea. Prior thoracotomy had failed and bronchial dilation proved impossible. A, Detail of chest roentgenogram showing critical stenosis of the right main bronchus (right arrow) and bronchus intermedius plus severe stenosis of the left main bronchus (left arrow). B, Computed tomography scan demonstrating a fibrocalcific mass at the carina in the same patient. C, Bronchoscopy reveals near total obstruction of the right main bronchus and a tiny opening on the left.

figure 14-7 Massive mediastinal fibrosis in a 57-year-old man who had reached an extreme of incapacitating dyspnea. Prior thoracotomy had failed and bronchial dilation proved impossible. A, Detail of chest roentgenogram showing critical stenosis of the right main bronchus (right arrow) and bronchus intermedius plus severe stenosis of the left main bronchus (left arrow). B, Computed tomography scan demonstrating a fibrocalcific mass at the carina in the same patient. C, Bronchoscopy reveals near total obstruction of the right main bronchus and a tiny opening on the left.

figure 14-7 (continued) D, Operative treatment. Right carinal pneumonectomy was necessary, with intrapericardial division of the pulmonary artery, since calcification extended almost to the origin of the right pulmonary artery. Exposure was via a right thoracotomy. Recovery was uneventful. E, Specimen shows calcific and anthracotic lymph nodes encased by dense fibrosis. The left main bronchus is at the left (arrow). F, Photomicrograph of dense keloidal fibrosis (hematoxylin and eosin stain). Many fibroblasts are seen on the left and thick bundles of collagen on the right. Histo-plasma capsulatum was identified on silver methenamine stain.

fibrosing mediastinitis within 2 years, a result at variance with others.10,11,14 In a study of 71 patients, Lloyd and colleagues found no support for evolution of a mediastinal granuloma into mediastinal fibrosis.11

Trastek and colleagues advised surgical removal of broncholiths rather than bronchoscopic attempts at removal, since pathologic involvement so often necessitated pulmonary resection.9 We concur in this approach. The endoscopically visible broncholith is truly only the "tip of the iceberg."

Other Infections

Nocardiosis was reported as a mass in the right main bronchus in an isolated case.15

A necrotizing mucormycosis that involves the trachea, carina, or bronchi, as well as the lungs, is seen principally in diabetic patients and in patients who are immunosuppressed or undergoing chemotherapy, particularly for lymphoma. Chronic renal failure and a history of organ transplantation are factors.16 Diagnosis is made on bronchial biopsy material by direct examination. Branching, nonseptate hyphae are noted with necrosis, fibrosis, and vessel thrombosis. Cultures are difficult to obtain. Progression of the infection from the bronchus may cause severe or fatal hemorrhage from pulmonary vessels.17 Secondary bacterial infection also occurs in the lungs.

Prompt and very radical excision of the involved airway and lung, under the protection of vigorous and prolonged treatment with amphotericin or other drugs, may save some of these patients.16,18 In a young

figure 14-8 Intrinsic fibrosis of the airways often accompanies mediastinal processes due to histoplasmosis, as seen in Figure 14-7. Further examples are shown here. A, Tracheal tomogram showing narrowed trachea as well as mediastinal mass. Exploration had been previously done. B, Section of a densely fibrotic stenosed trachea in another patient. C, A carina similarly encased and invaded by fibrosis in another patient.

figure 14-8 Intrinsic fibrosis of the airways often accompanies mediastinal processes due to histoplasmosis, as seen in Figure 14-7. Further examples are shown here. A, Tracheal tomogram showing narrowed trachea as well as mediastinal mass. Exploration had been previously done. B, Section of a densely fibrotic stenosed trachea in another patient. C, A carina similarly encased and invaded by fibrosis in another patient.

diabetic woman with destructive mucormycosis in the right lung, extensive disease involving the carina and lower third of the trachea, and with infiltrates in the opposite lung, who was deteriorating on drug treatment, an aggressive right carinal pneumonectomy and lower tracheal resection, combined with continued medical treatment, led to resolution and complete recovery. Only a few instances of tracheal bronchial mucormycosis are reported.19 In a review of reported patients, Brown and colleagues confirmed the favorable results of early surgical treatment, against a high fatality with medical treatment alone.17 Tedder and colleagues compared a mortality of 68% for medical treatment versus 11% for surgical and medical treatments.16 Similar results were obtained by Donahue and Wain.18

Diphtheria in childhood may be followed many years later by tracheal stenosis or laryngotracheal stenosis; that is, involvement of the subglottic larynx as well as the upper trachea. Since most of the patients who had this disease in infancy or in early childhood were treated with one or more intubations and tra-cheostomies, it is difficult to determine whether the later stenosis is due to disease or to treatment. In several cases, the patient carried a tracheostomy for many years, later had it removed, and then appeared even later with severe stenosis. These late stenoses, which in my experience most frequently involve the subglottic larynx as well as the uppermost trachea and which lie in the region of prior tracheostomy, may be reconstructible. The anatomic and surgical considerations in such cases are the same as those for postintubation stenoses. Diminishing occurrence of these cases undoubtedly reflects the success of immunization programs.

Scleroma (rhinoscleroma) is a rare disease, which may cause fibrosing changes in the nasopharynx, larynx, and upper airways. In only 2% of cases does it occur in the trachea and bronchi.20,21 Scleroma is related to infection by Klebsiella rhinoscleromatis. The organism is identified in biopsied material. The disease occurs in Mexico, Central and South America, Eastern Europe, the Middle East, India, and only occasionally in the United States.

Scleroma is most common in the first three decades of life and in patients with poor nutrition. As the disease appears and progresses, it is characterized by nasal obstruction, nasal deformity, hoarseness, epistaxis, sore throat, and lip swelling.21 The tracheobronchial tree is kept open in these patients by repeated bronchoscopies, while prolonged and repeated antibiotic treatments (streptomycin and tetracycline) are given. A tracheostomy may become necessary. Glottic webs and subglottic scars may result as healing proceeds.

Although viral in origin, laryngotracheal papillomatosis is described in Chapter 7, "Primary Tracheal Neoplasms," because of its tumor-like appearance. Endobronchial Kaposi's sarcoma is also described in Chapter 7. Human immunodeficiency virus (HIV)-infected persons are also subject to endobronchial tuberculosis, aspergillosis, non-Hodgkin's lymphoma, and bacterial tracheitis.22

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  • celendine
    What is trachea bronchial lymph node calcification infection?
    4 years ago

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