local complications general complications physiological complication
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COMPLICATIONS OF TUBERCULOSIS DR. ANKUR GUPTA S.M.O. (NODAL DRTB CENTRE, DEPTT. OF PULMONARY MEDICINE )
Complications of Tuberculosis can mimic other disease entities. Therefore, recognition and understanding of such thoracic and extratoracic sequelae and are important to facilitate diagnosis and institute proper treatment
COMPLICATIONS LOCAL Parenchymal Airway Vascular Mediastinal Pleural Chest Wall GENERAL Physiologic Tuberculous enteritis and Enteritis Secondary Amyloidosis Respiratory Failure Cor pulmonale
Parenchymal Complications Tuberculoma and Thin-walled Cavity Cicatrization and Destruction of the Lung Aspergilloma Bronchogenic Carcinoma
Tuberculoma and Thin-walled Cavity Tuberuloma - It is a round or oval granuloma caused by AFB, lined by granulomatous inflammatory tissue or connective tissue Central portion - caseation necrosis. Solitary or multiple Diameter from 0.5 to 4.0 cm or greater. Margins are smooth or sharply defined Satellite lesions are seen in up to 80%. Calcification is found in 20%–30%.
Tuberculoma
Tuberculoma and Thin-walled Cavity Thin-walled Cavity aka OPEN NEGATIVE SYNDROME OR INH CAVITIES Seen in both active and inactive disease May disappear after ATT Occasionally wall becomes paper-thin and an air-filled cystic space remains Wall thickness 1 cm to 1 mm and may be smooth, sometimes simulating an emphysematous bulla, cyst or pneumotocele
Thin-walled Cavity
Cicatrization and Lung Destruction Cicatrization atelectasis is a common finding after postprimary tuberculosis (40%) Marked fibrotic response manifests as Atelectasis of the upper lobe Retraction of the hilum Compensatory lower lobe hyperinflation and Mediastinal shift toward the fibrotic lung. Nonspecific fibrotic response Parenchymal bands, Fibrotic nodules and cavities Traction bronchiectasis
Aspergilloma ( Mycetoma ; “ Fungas Ball”) Mobile, rounded mass surrounded by a crescentic air shadow is noted inside a lung cavity ( air-crescent sign ) Aspergilloma associated with chronic TB has been reported to be 11% 25%–55% of patients with aspergilloma have a history of chronic cavitary tuberculosis. Hemoptysis is the most common clinical symptom (50%–90%),cough, weight loss, rarely fever and dyspnea
Aspergilloma ( Mycetoma ; “ Fungas Ball”) DD Organized hematoma Pus inside cavity Neoplasm, Hydatid cyst DX – Serum precipitins for aspergillus (100%), Sputum culture Skin test Bronchoscopy . Treatment – Systemic antifungal Local instillation of antifungal Surgery Wait and watch
Bronchogenic Carcinoma Bronchogenic carcinoma and PTB often coexist Manifestations of carcinoma may be obscured or misinterpreted as progression of tuberculosis. TB may favor the development of bronchogenic carcinoma by local mechanisms (scar cancer) Any predominant or growing nodule should be suspicious for coexisting lung cancer in patients with TB
Airway Complications Bronchiectasis TB Endobronchitis and Tracheitis Tracheobronchial Stenosis Broncholithiasis
Bronchiectasis Result of tuberculous involvement of the bronchial wall and subsequent fibrosis. Bronchiectasis is seen in 30%– 60% of patients with active postprimary tuberculosis and in 71%–86% of patients with inactive disease Bronchiectasis located in the apical and posterior segments of the upper lobe is highly suggestive of a tuberculous origin “ DRY BRONCHIECTASIS ”
TB Endobronchitis and Tracheitis Occur in 1/3`rd of cases. AFB Implantation may be direct, via circulation, or via lymphatics . CF- cough, hemoptysis , dyspnea , soreness or constriction in substernal region. O/E – Localized wheeze.
Rasmussen aneurysm is a rare phenomenon caused by weakening of the pulmonary artery wall from adjacent cavitary tuberculosis Progressive weakening of the arterial wall occurs as granulation tissue replaces both the adventitia and the media granulation tissue – replaced by fibrin - thinning of the arterial wall – pseudoaneurysm - rupture
Tracheobronchial Stenosis caused by 1. granulomatous changes in the tracheobronchial wall erythema - lymphocytic infiltration( submucosa ) - tubercle formation – fibrosis) 2. extrinsic pressure from enlarged peribronchial lymph nodes. Endobronchial involvement occurs in approximately 2%–4% The left main bronchus is most frequently involved.
Tracheobronchial Stenosis Active stage of stenosis Irregular luminal narrowing with wall thickening Enhancement Enlarged adjacent mediastinal nodes Fibrotic stage Concentric narrowing of the lumen Uniform thickening of the wall Involvement of a long bronchial segment
Broncholithiasis Defined as the presence of calcified or ossified material within the lumen of the tracheobronchial tree. Uncommon complication. The calcific nidus in a tuberculous lymph node erodes into the bronchial wall and may occlude the bronchus Symptoms - cough, hemoptysis , wheezing,recurrent pneumonia Change in the position or disappearance of a calcific focus on serial radiographs, development of airway obstruction, resulting in lobar or segmental atelectasis , mucoid impaction, or expiratory air trapping.
Vascular Complications Hemoptysis more common and potentially serious (30-35%) Initial manifestation, during treatment, after treatment. Cause – from cavity wall rupture of Rasmussen`s aneurysm direct erosion of capillaries d/t granulomatous inflamm d/t sec infetion d/t tubercular endobronchitis (bronchial circulation) d/t bronchiectasis (bronchial circulation) d/t aspergilomata d/t bronchioliths (bronchial circulation) d/t scar carcinoma
Lymph Node Calcification and Extranodal Extension. Tuberculous mediastinal lymphadenitis is a frequent manifestation of primary pulmonary tuberculosis. Enlarged nodes occur in 83%–96% of pediatric cases, decrease with age. Caused by the formation of tuberculous caseating granulomas in lymph nodes, commonly on right side . In the active stage, the nodes have central low attenuation and peripheral rim enhancement at CT. Extranodal extension may occur into bronchus, pericardium, and esophagus.
Esophagomediastinal Fistula Most common cause of esophageal tuberculosis is secondary involvement from adjacent Tuberculous Lymphadenitis. Rare complication. Symptoms - fever, cough, weight loss, dysphagia , chest discomfort, or back pain. Esophageal involvement results in strictures, tracheobronchial or mediastinal fistulas, and traction diverticula
Pericardial Tuberculosis Caused by extranodal extension of TB lymphadenitis into the pericardium (1% of cases of tuberculosis) Constrictive pericarditis characterized by fibrous or calcific constrictive thickening of the pericardium, which prevents diastolic filling of the heart (10%) CT findings pericardial thickening 3 mm with or without pericardial effusion. RHF Secondary dilatation of IVC acute angulation or interventricular septum,
Fibrosing Mediastinitis Fibrosing mediastinitis is presence of excessive fibrosis in the mediastinum and is uncommon TB mediastinitis is rare (most common histoplasmosis ) Symptoms – cough, fever, and symptoms d/t compression of the SVC, esophagus, and tracheobronchial tree CT findings mediastinal or hilar mass calcification in the mass tracheobronchial narrowing Pulmonary vessel encasement superior vena cava obstruction pulmonary infiltrates
Tubercular Empyema and Fibrothorax Pleural infection is usually caused by rupture of a subpleural caseous focus into the pleural space hematogenous dissemination contamination by adjacent infected lymph nodes Chronic tuberculous empyema - persistent, grossly purulent pleural fluid containing AFB CT scans - focal fluid collection with pleural thickening and calcification and with or without extrapleural fat proliferation
Tubercular Empyema and Fibrothorax Fibrothorax with diffuse pleural thickening but without effusion on CT scans suggests inactivity Chyliform or pseudochylous pleural effusion is a high-lipid nonchylous effusion and is most commonly caused by tuberculous empyema
Bronchopleural Fistula Bronchopleural fistula occurs due to an open pathway between bronchus and pleura established by tuberculosis BPF usually follows trauma, surgical procedure or spontaneously Diagnosis – increasing amount of sputum production air in the pleural space a changing air-fluid level contralateral spread of pneumonic infiltration
Bronchopleural Fistula
Pneumothorax In severe and extensive pulmonary involvement by the infectious process and the onset of bronchopleural fistula and empyema . Occcurs in 5% of patients with postprimary TB. Pathogenesis pleural caseous infiltrates -> liquefaction -> pleural necrosis and rupture. Tube drainage is the treatment of choice
Chest Wall Tuberculosis CWTuberculosis characterized by bone or costal cartilage destruction and soft tissue masses that may demonstrate calcification or rim enhancement Involves the sternum, the sternoclavicular joint, or a rib osseous destruction and localized abscess formation Occur by direct extension or by hematogenous spread. When spontaneous discharge of empyema through the parietal pleura into the chest wall forms subcutaneous abscess, it is termed empyema necessitatis
Tuberculous Spondylitis Aka Pott disease, is caused primarily by hematogenous spread of pulmonary infection and commonly affects the lower thoracic and upper lumbar spine early features irregularity of the vertebral end plates Decreased height of the intervertebral disk space, sclerosis of the adjacent bone Late features Anterior wedging of the vertebral body -> kyphosis paravertebral abscess.
Malignancy Associated with Chronic Empyema Rare complication. mean duration 25 years. The histopathologic diagnoses in reported cases have been malignant lymphoma, SqCCa , mesothelioma , malignant fibrous histiocytoma , liposarcoma , rhabdomyosarcoma , angiosarcoma , and hemangioendothelioma , Imaging clues – increased opacity in the thoracic cavity soft-tissue bulging and blurring of fat planes destruction of bone near the empyema extensive medial deviation of the calcified pleurae
Physiologic changes Airway obstruction – in 30-60% cases of PTB. Airway restriction – D/t effusion, thickening, fibrothorax Mixed defect. Type of abnormality depends upon the type and extend of involvement or residual damage left out.
Respiratory Failure & Cor Pulmonale Extensive destruction of pul . Parenchyma greater V/Q mismatch. Pleural pathology (thickening, fibrothorax ). Atropy or disuse of respiratory muscles 1+2+3 mechanical disadvantage -> Tachypnea , Hypoxia, Hypercapnia Respiratory Failure. Cor Pulmonale – Enlargement of RV due to increased RV afterload sec to pulmonary disease
Tuberculous Laryngitis In 4 – 25 % of cases, via direct implantation, lympahatics or blood vessels. CF- Soreness or pain in throat Dry, hacking cough and hoarseness of voice Laryngoscopy may reveal an ulcer, granuloma , paresis or paralysis of VC, destruction of VC or stenosis . Sputum is usually positive or AFB.
Secondary Amyloidosis Ctz by deposition of extracellular eosinophilic substance in various organs – kidneys (100%), spleen(75%), liver(63%), adrenals(21%) etc. Lag period is about 5 years in majority of cases. Now a rare complication d/t modern ATT
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