Tuberculosis natural history, complications and prognosis: Difference between revisions
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Pulmonary arteries and veins in an area of active tuberculous infection may demonstrate vasculitis and thrombosis; thus, acid-fast staining should be performed in any case of necrotizing granuloma- tous pulmonary vasculitis to exclude a tubercu- lous cause (8). Bronchial arteries may be enlarged in bronchiectasis associated with tuberculosis or in parenchymal tuberculosis itself (36,37). High- resolution CT has been regarded as the imaging modality of choice in patients suspected of having bronchiectasis. In patients with bronchiectasis, nodular and tubular structures with an appear- ance unlike that of lymph nodes or normal vessels in the mediastinum and around the central airway on high-resolution CT scans are suggestive of hypertrophied bronchial arteries (Fig 13). Recog- nition of this finding is important so that the bronchoscopist will not biopsy the hypertrophied bronchial arteries protruding into the airway lu- men (36). | |||
Rasmussen aneurysm is a rare phenomenon caused by weakening of the pulmonary artery wall from adjacent cavitary tuberculosis (Figs 14, 15). A review of autopsy findings in patients with a history of chronic cavitary tuberculosis showed a 5% prevalence of Rasmussen aneurysm (38). He- moptysis is the usual presenting symptom and may be life-threatening when it is massive. Pro-gressive weakening of the arterial wall occurs as granulation tissue replaces both the adventitia and the media. The granulation tissue in the ves- sel wall is then gradually replaced by fibrin, re- sulting in thinning of the arterial wall, pseudoan- eurysm formation, and subsequent rupture (38,39). | |||
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===Mediastinal Lesions=== | ===Mediastinal Lesions=== | ||
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Lymph Node Calcifica-tion and Extranodal Extension | |||
Tuberculous mediastinal lymphadenitis is a fre- quent manifestation of primary pulmonary tuber- culosis. Although enlarged nodes occur in 83%– 96% of pediatric cases, the prevalence of lymph- adenopathy decreases with increasing age (40 – 42). Pubertal and young adult women, the elderly, and patients with acquired immunodefi- ciency syndrome are the most commonly affected among adult patients (43). Tuberculous mediasti- nal lymphadenitis is caused by the formation of tuberculous caseating granulomas in lymph nodes, which more commonly involves the right side. In the active stage, the nodes have central low attenuation and peripheral rim enhancement at CT, which correspond to caseation or liquefac- tion necrosis and granulation tissue with inflam- matory hypervascularity, respectively, at patho- logic analysis. With treatment, the nodes change in appearance, first becoming homogeneous and finally disappearing or resulting in a residual mass composed of fibrotic tissue and calcifications without low-attenuation areas (44,45) (Fig 16). Extranodal extension may occur into adjacent structures such as the bronchus, pericardium, and esophagus (Figs 17–21). | |||
Esophagomediastinal Fistula | |||
Esophageal involvement by tuberculosis is rare. The most common cause of esophageal tubercu- losis is secondary involvement from adjacent tu- berculous lymphadenitis. Esophageal involvement results in strictures due to granulomatous inflammatory tissue in active disease and scar tis- sue after healing, tracheobronchial or mediastinal fistulas, and traction diverticula (8,46). Present- ing symptoms may include fever, cough, weight loss, dysphagia, chest discomfort, or back pain. The preferential involvement of the subcarinal region occurs mainly because of the anatomic proximity of the esophagus to diseased lymph nodes (47). When tuberculous lymph nodes erode the adjacent esophageal or bronchial wall, an esophagonodal or esophagobronchial fistula may be formed, which manifests as a localized gaseous collection within the mediastinum (46,47) (Figs 19, 20). | |||
Pericardial Tuberculosis | |||
Tuberculous pericarditis is reported to compli- cate up to 1% of cases of tuberculosis (48). Peri- cardial involvement is commonly caused by ex- tranodal extension of tuberculous lymphadenitis into the pericardium because of the close ana- tomic relationship between the lymph nodes and the posterior pericardial sac. The pericardium can also be involved in miliary spread of the disease (12). At CT, lymphadenopathy and pericardial thickening with or without effusion may be seen (Fig 21). | |||
Constrictive pericarditis occurs in about 10% of patients with tuberculous pericarditis. It is characterized by fibrous or calcific constrictive thickening of the pericardium, which prevents normal diastolic filling of the heart (49). CT shows pericardial thickening of more than 3 mm with or without pericardial effusion. Secondary CT findings are dilatation of the inferior vena cava secondary to right-sided heart failure and acute angulation or sinus configuration of the in- terventricular septum, which may be related to redundancy of the septum secondary to the re- striction of expansion of the pericardium (49). Visceral pericardial calcification may occur at the atrioventricular grooves, the interventricular grooves, or especially the crux of the heart (49) (Fig 22). | |||
Fibrosing Mediastinitis | |||
Fibrosing mediastinitis is uncommon and in- volves the presence of excessive fibrosis in the mediastinum (50). Although tuberculosis is an important cause of chronic mediastinitis, tubercu- lous mediastinitis is rare; the most common cause of mediastinitis is histoplasmosis (51). Tubercu- lous mediastinitis progresses insidiously without significant clinical symptoms and may result in mild symptoms, including cough and low-grade fever, and symptoms due to compression of the superior vena cava, esophagus, and tracheobron- chial tree (52). The mediastinal granulomatous lymph nodes coalesce, and the development of multiple tuberculous granulomas creates both reactive fibrous changes and acute inflammatory changes in the mediastinum. The granulomas evolve into fibrosing mediastinitis when reactive changes predominate (50). | |||
The radiographic findings include mediastinal widening or a localized mass. CT findings include a mediastinal or hilar mass, calcification in the mass, tracheobronchial narrowing, pulmonary vessel encasement, superior vena cava obstruc- tion, and pulmonary infiltrates (Fig 23). Pulmo- nary lesions in fibrosing mediastinitis may be caused by bronchial obstruction with subsequent obstructive pneumonia or atelectasis or by ob- struction of major pulmonary veins with resultant pulmonary infarction (50,52). | |||
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===Pleural Lesions=== | ===Pleural Lesions=== | ||
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Chronic Tuberculous | |||
Empyema and Fibrothorax | |||
Pleural infection is usually caused by rupture of a subpleural caseous focus into the pleural space; less commonly, it is caused by hematogenous dissemination and contamination by adjacent infected lymph nodes. Tuberculous pleurisy progresses to become chronic tuberculous empy- ema, which may be defined as persistent, grossly purulent pleural fluid containing tubercle bacilli (53–57). However, it may be difficult to culture the bacilli in chronic empyema. | |||
In chronic tuberculous empyema, CT scans show a focal fluid collection with pleural thicken- ing and calcification and with or without ex- trapleural fat proliferation (Fig 24). Fibrothorax with diffuse pleural thickening but without effu- sion on CT scans suggests inactivity (Fig 24) (55– 57). Chyliform or pseudochylous pleural effusion is a high-lipid nonchylous effusion and is most commonly caused by tuberculous empyema. The diseased pleura may result in an abnormally slow transfer of cholesterol and other lipids, originating from degenerated red and white blood cells, out of the pleural space and lead to accumulation of cholesterol in the pleural fluid (58,59). CT shows a fat-fluid or fat-calcium level (Fig 25). | |||
Bronchopleural Fistula | |||
Bronchopleural fistula associated with tuberculo- sis usually follows trauma or a surgical procedure but can also occur spontaneously, presumably due to an open pathway between bronchus and pleura established by tuberculosis. High mortality can result from both the acute and chronic phases. The former occurs because of toxicity, spread of disease, and tension pneumothorax; the latter progresses to repeat small seedings and massive aspiration of empyema fluid (60). The diagnosis is based on an increasing amount of sputum production, air in the pleural space, a changing air-fluid level, and contralateral spread of pneumonic infiltration. CT can demonstrate the sites of communication between the pleural space and either one or more airways or the lung parenchyma in patients with bronchopleural fistula (61) (Fig 26). | |||
Pneumothorax | |||
Pneumothorax secondary to tuberculosis often heralds severe and extensive pulmonary involve- ment by the infectious process and the onset of bronchopleural fistula and empyema. It occurs in approximately 5% of patients with postprimary tuberculosis, usually in severe cavitary disease (Fig 27) but rarely in miliary tuberculosis (Fig 28). The pathogenesis involves pleural caseous infiltrates that undergo liquefaction, resulting in pleural necrosis and rupture. If any apical abnor- mality is seen after reexpansion of a spontaneous pneumothorax, active tuberculosis should be con- sidered. In some cases, the lung will seal and re- expand over a long period in response to chemo- therapy. However, tube drainage is the treatment of choice (62,63). | |||
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===Chest Wall Lesions=== | ===Chest Wall Lesions=== | ||
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Chest Wall Tuberculosis | |||
Tuberculosis occasionally involves the sternum, the sternoclavicular joint, or a rib, leading to osse- ous destruction and localized abscess formation. Such involvement may occur by direct extension from a pleuropulmonary tuberculous lesion or | |||
by hematogenous spread from a distant focus (64,65). When spontaneous discharge of empy- ema through the parietal pleura into the chest wall forms a subcutaneous abscess, it is termed empyema necessitatis (66). | |||
Tuberculosis of the chest wall is characterized by bone or costal cartilage destruction and soft- tissue masses that may demonstrate calcification or rim enhancement with or without evidence of underlying lung or pleural disease at CT (64,65) (Fig 29). Bone or cartilage may be intact in chest wall tuberculosis (64). Rarely, it is associated with development of retromammary or intramammary tuberculous abscesses (Fig 30). | |||
Tuberculous Spondylitis | |||
Tuberculous spondylitis (Pott disease) is caused primarily by hematogenous spread of pulmonary infection and most commonly affects the lower thoracic and upper lumbar spine. The early radio- graphic manifestations of spinal involvement con- sist of irregularity of the vertebral end plates, de- creased height of the intervertebral disk space, and sclerosis of the adjacent bone. With progres- sion of disease, there is a tendency toward ante- rior wedging of the vertebral body, leading to ky- phosis and development of a paravertebral ab- scess. CT demonstrates paravertebral abscesses with peripheral rim enhancement and low-attenu- ation centers after enhancement (Fig 31) (67– 69). | |||
Malignancy Associated with Chronic Empyema | |||
Malignancy associated with chronic empyema, especially tuberculous empyema, is rare (70 –72). The mean duration of chronic empyema before diagnosis of malignancy is reported to be about 25 years. The histopathologic diagnoses in re- ported cases have been malignant lymphoma, squamous cell carcinoma, mesothelioma, malig- nant fibrous histiocytoma, liposarcoma, rhabdo- myosarcoma, angiosarcoma, and hemangioendo- thelioma, in order of frequency (72). The patho- genesis of malignancy developing in chronic empyema may be a long-standing severe inflam- matory process of a nonautoimmune nature in malignant lymphoma or chronic stimulation of mesothelial cells or the action of oncogenic sub- stances contained in the pleura in other malig- nancy, including mesothelioma (70,71,73). | |||
Radiographic findings that suggest the occur- rence of malignancy include increased opacity in the thoracic cavity, soft-tissue bulging and blur- ring of fat planes in the chest walls, destruction of bone near the empyema, and extensive medial deviation of the calcified pleurae (72). CT can demonstrate an abnormal mass with soft-tissue attenuation around the empyema and usually shows enhancement of the mass (Fig 32). Biopsy is necessary because differentiation between ma- lignancy and infection is rather difficult. | |||
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==Prognosis== | ==Prognosis== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]
Overview
Natural History
Without treatment, 1/3 of patients with active tuberculosis dies within 1 year of the diagnosis, and more than 50% during the first 5 years. Patients who have a positive sputum smear test for M. tuberculosis have a 5-year mortality rate of 65%. Those who survive past these 5 years, have 60% of probability of undergoing spontaneous remission. [1]
According to its clinical manifestations, pulmonary tuberculosis may be classified as primary or secondary (or post-primary) tuberculosis:[1]
Primary Pulmonary Tuberculosis
Primary tuberculosis develops soon after infection with M. tuberculosis and differs from clinical illness. In endemic regions, this form of TB is frequently seen at younger ages. Primary TB may be asymptomatic, or include mild symptoms, such as cough, fever and chest pain, related to pleurisy. Some patients may develop concomitant symptoms, such as erythema nodosum in the lower limbs and phlyctenulosis. The initial lesion (Ghon focus) often resolves spontaneously, becoming a calcified nodule that may be identified on the chest X-Ray. Pleuritic chest pain often results from the pleural reaction to the underlying Ghon focus.[1]
Primary tuberculosis progresses more rapidly in patients with impaired immune system and in children, who commonly have immature cellular immunity. Progression of the disease leads to the enlargement of the Ghon focus. The disease may be manifested with:[1]
- Pleural effusion - results from invasion of the pleural space by M. tuberculosis. This occurs more frequently when the focus of infection is subpleural.
- Cavitation - results from rapid enlargement of the Ghon focus, with ensuing necrosis of its nucleus.
- Lymphadenopathy - the spread of M. tuberculosis from the lungs to lymph leads to the enlargement of lymph nodes, especially of the paratracheal and perihilar regions.
- Airway obstruction - with symptoms of shortness of breath and wheezing. Commonly occurs in cases of severe enlargement of the lymph nodes, that compress the airways and possibly lead to distal collapse, partial obstruction with wheezing, or hyperinflation.
- Pneumonia - may occur when there is rupture and leakage of lymph node content into the airways.
- Bronchiectasis - progressive pneumonia may damage a specific segment of the lung, or an entire lobe, leading to bronchiectasis.
Primary infection leads to dissemination of M. tuberculosis through the blood. Hematogenous dissemination is often contained by an healthy immune system, however, in cases of compromised immune response, miliary tuberculosis may occur. Dissemination of the mycobacteria may lead to the formation of granulomatous lesions in other organs, which may develop different forms of the disease.[1]
Secondary Pulmonary Tuberculosis
Also known as "adult-type" or "post primary tuberculosis". May result from recent infection with M. tuberculosis, or from the reactivation of an endogenous focus that contained the latent form of the disease. Without treatment, about 1/3 of patients dies within months of disease onset. Of the remaining 2/3, some may experience remission, while others develop a chronic condition with debilitating symptoms. The surviving patients may show fibrotic and calcified lesions, as well as cavitations in some areas of the lungs, which may be later appreciated on a chest X-Ray.[1]
Disease onset is insidious and unspecific, presenting with symptoms that may include:
- Fever
- Night sweats
- Weakness
- Malaise
- Anorexia
- Weight loss
- Cough (90% cases) - nonproductive at the outset, more frequent during the morning, that gradually progresses to productive cough, with purulent sputum, with occasional streaks of blood
- Hemoptysis (20-30% cases) may occur in the following cases:
- Rupture of a blood vessel on a cavity wall (severe hemoptysis)
- Rupture of a pulmonary artery aneurysm adjacent or within a tuberculous cavity (Rasmussen's aneurysm)
- Formation of an aspergilloma in a lung cavity
- Pleuritic chest pain
- Dyspnea (in severe disease)
- ARDS
Complications
Tuberculosis may be localized to the lungs, or involve other organs and regions of the body. Depending on the pulmonary, or extrapulmonary nature of the lesion, potential complications that may arise include:[3]
Parenchymal Lesions
| Complication | Description |
|---|---|
| Tuberculoma |
|
| Cicatrization |
|
| Thin-walled cavity |
|
| Aspergilloma |
|
| Lung destruction[3] |
|
| Bronchogenic carcinoma[3] |
Airway Lesions
| Complication | Description |
|---|---|
| Bronchiectasis |
|
| Tracheobronchial stenosis |
|
| Broncholithiasis |
|
Vascular Lesions
| Complication | Description |
|---|---|
| Pulmonary or bronchial arteritis and thrombosis | |
| Bronchial artery dilatation | |
| Rasmussen's aneurysm |
Mediastinal Lesions
| Complication | Description |
|---|---|
| Esophagobronchial fistula | |
| Esophagomediastinal fistula | |
| Constrictive pericarditis | |
| Lymph node calcification | |
| Fibrosing mediastinitis | |
| Extranodal extension |
Pleural Lesions
| Complication | Description |
|---|---|
| Bronchopleural fistula | |
| Chronic empyema | |
| Pneumothorax | |
| Fibrothorax |
Chest Wall Lesions
| Complication | Description |
|---|---|
| Tuberculous spondylitis | |
| Rib tuberculosis | |
| Malignancy |
Prognosis
If untreated, active tuberculosis is often fatal. According to studies performed in several countries, 1/3 of the untreated patients died within 1 year after the diagnosis, while > 50% died within the first 5 years. However, with adequate treatment, these patients have a good prognosis.[1]
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Longo, Dan (2012). Harrison's principles of internal medicine. New York: McGraw-Hill. ISBN 007174889X.
- ↑ "Wikimedia Commons".
- ↑ 3.0 3.1 3.2 3.3 Kim HY, Song KS, Goo JM, Lee JS, Lee KS, Lim TH (2001). "Thoracic sequelae and complications of tuberculosis". Radiographics. 21 (4): 839–58, discussion 859-60. doi:10.1148/radiographics.21.4.g01jl06839. PMID 11452057.
- ↑ 4.0 4.1 Woodring JH, Vandiviere HM, Fried AM, Dillon ML, Williams TD, Melvin IG (1986). "Update: the radiographic features of pulmonary tuberculosis". AJR Am J Roentgenol. 146 (3): 497–506. doi:10.2214/ajr.146.3.497. PMID 3484866.
- ↑ 5.0 5.1 5.2 Lee KS, Song KS, Lim TH, Kim PN, Kim IY, Lee BH (1993). "Adult-onset pulmonary tuberculosis: findings on chest radiographs and CT scans". AJR Am J Roentgenol. 160 (4): 753–8. doi:10.2214/ajr.160.4.8456658. PMID 8456658.
- ↑ Palmer PE (1979). "Pulmonary tuberculosis--usual and unusual radiographic presentations". Semin Roentgenol. 14 (3): 204–43. PMID 472765.
- ↑ Fraser, Richard (1994). Synopsis of diseases of the chest. Philadelphia: W.B. Saunders. ISBN 0721636691.
- ↑ Logan PM, Müller NL (1996). "CT manifestations of pulmonary aspergillosis". Crit Rev Diagn Imaging. 37 (1): 1–37. PMID 8744521.
- ↑ Miller WT (1996). "Aspergillosis: a disease with many faces". Semin Roentgenol. 31 (1): 52–66. PMID 8838945.
- ↑ Thompson BH, Stanford W, Galvin JR, Kurihara Y (1995). "Varied radiologic appearances of pulmonary aspergillosis". Radiographics. 15 (6): 1273–84. doi:10.1148/radiographics.15.6.8577955. PMID 8577955.
- ↑ Snider GL, Placik B (1969). "The relationship between pulmonary tuberculosis and bronchogenic carcinoma. A topographic study". Am Rev Respir Dis. 99 (2): 229–36. PMID 4975011.
- ↑ Ting YM, Church WR, Ravikrishnan KP (1976). "Lung carcinoma superimposed on pulmonary tuberculosis". Radiology. 119 (2): 307–12. doi:10.1148/119.2.307. PMID 1265261.
- ↑ Lee KS, Hwang JW, Chung MP, Kim H, Kwon OJ (1996). "Utility of CT in the evaluation of pulmonary tuberculosis in patients without AIDS". Chest. 110 (4): 977–84. PMID 8874255.
- ↑ Hatipoğlu ON, Osma E, Manisali M, Uçan ES, Balci P, Akkoçlu A; et al. (1996). "High resolution computed tomographic findings in pulmonary tuberculosis". Thorax. 51 (4): 397–402. PMC 1090675. PMID 8733492.
- ↑ 15.0 15.1 Galdermans D, Verhaert J, Van Meerbeeck J, de Backer W, Vermeire P (1990). "Broncholithiasis: present clinical spectrum". Respir Med. 84 (2): 155–6. PMID 2371439.
- ↑ 16.0 16.1 Kowal LE, Goodman LR, Zarro VJ, Haskin ME (1983). "CT diagnosis of broncholithiasis". J Comput Assist Tomogr. 7 (2): 321–3. PMID 6833568.
- ↑ 17.0 17.1 Conces DJ, Tarver RD, Vix VA (1991). "Broncholithiasis: CT features in 15 patients". AJR Am J Roentgenol. 157 (2): 249–53. doi:10.2214/ajr.157.2.1853800. PMID 1853800.