PULMONARY TUBERCULOSIS Dr Prakash Sapkale
• Caused by infection with “Mycobacterium Tuberculosis.” •
Accounts for 95 % of pulmonary mycobacterial infections. Other mycobacteria- M.Avium-intracellulare complex, M.kansasii.
Predisposing factors • • • • • •
Pregnancy Diabetes Mellitus Alcoholism Silicosis Malignancy Immune compromise – including HIV infection • Socio-economic factors- inner city poverty, homelessness, immigration trends • Occupation- Nurses, vagrants, people in closed institutions.
Two forms1)Primary Tuberculosisin previously unexposed individuals especially in infants and children hypersensitivity to tuberculoprotein is absent 2)Post-primary tuberculosis (secondary,reactivation,reinfection,adult tuberculosis.) In a patient who already possesses hypersensitivity to tuberculoprotein. # Progressive primary tuberculosisWhen the primary disease passes directly into the postprimary form without a break.
PRIMARY TUBERCULOSIS • Clinical Features• Primary tuberculosis develops about 1-2 months after the exposure. • Mainly infants and children. • Usually occult. • Occasionally it may result in a transient self limited illness (pyrexia and erythema nodosum) • Very occasionally a clinically significant illness in infants and children.
PRIMARY TUBERCULOSIS • Pathology• Small area of peripheral consolidationGhon focus. • Lymph node involvement and complications due to lymphadenopathy due to compression of adjacent airways, vessels, and serosal membranes. • Pleural effusion may be the only feature • Healing is by fibrosis; with or without calcification • Tuberculoma -repeated episodes of arrest
PRIMARY TUBERCULOSIS Radiological findings• Radiographic patterns are related to the competence or maturity of the immune response and not to the timing. • 5 to 15% patients may have normal chest films.
PRIMARY TUBERCULOSIS • Radiological findings3)Consolidation: • Can occur in any lobe • Ghon focus- small area of peripheral consolidation. • Homogenous consolidation which mimics community acquired pneumonias • Suspect tuberculosis if a consolidation is indolent or associated with nodal enlargement • Multifocal involvement and cavitation rare • Cavitation suggests progressive primary
PRIMARY TUBERCULOSIS •
Radiological findings-
2) Lymphadenopathy: • Most common manifestation of primary tuberculosis • Sometimes may be obscured by a large consolidation • Can occur With consolidation-nodes draining the consolidated area are enlarged. Without consolidation-unilateral hilar, unilateral hilar plus paratracheal adenopathy, isolated paratracheal adenopathy -mediastinal adenopathy -bilateral hilar adenopathy is uncommon, when present , is almost always asymmetrical Features of complications due to lymphadenopathy may be seen.
PRIMARY TUBERCULOSIS •
Radiological findings-
•
Features of complications due to lymphadenopathy(pressure/erosion)d) Airways• Obstructive overinflation • Segmental or lobar collapse-commonly anterior segment of upper lobe and the middle lobe • Segmental consolidation -bronchial perforation and aspiration of caseous material in distal segment/hypersensitivity phenomenon.
•
•
Bronchial perforation-scattered heterogeneous consolidation similar to bronchopneumonia; -It consists of acinar nodules, ipsilateral or contralateral lung involved, segmental distribution Healing of bronchial or segmental lesions- bronchostenosis, bronchiectasis, parenchymal fibrosis, volume loss, bulla formation
PRIMARY TUBERCULOSIS •
Radiological findings-
• Features of complications due to lymphadenopathy b)Blood vessels• Isolated lesion- e.g. soft tissue abscess • Generalized- miliary tuberculosis • May remain dormant for years to present later as bone,joint or renal tuberculosis c) Pericardium – • Pericarditis(erosion by node; can also occur in miliary tuberculosis. • Constrictive pericarditis and pericardial calcification- late sequelae d) Pleura –pleural effusion e) Others- esophageal involvement, phrenic and recurrent laryngeal nerve paresis, SVC obstruction, fistula formation.
PRIMARY TUBERCULOSIS •
Radiological findings-
3) Pleural effusionUsually unilateral except in miliary TB • Seen in children, teenagers and young adults • In teenagers and young adults large effusion-slow and painless accumulation • Pleural thickening or calcification uncommon –associated with empyema 4)Miliary tuberculosis: • Seen in both primary and secondary tuberculosis • Multiple small (1-2 mm ) discrete nodules of soft tissue density, scattered throughout both lungs. Characteristically very well defined. • Clear with therapy,slowly often over months,no residual changes,no calcification. 5) Tuberculoma (described later)
PRIMARY TUBERCULOSIS • Radiological findings6)Inactive primary tuberculosis: -Normal chest radiograph with positive montoux reaction -A well defined rounded or irregular(linear) opacity with or without calcification – Ghon focus -Ghon focus with ipsilateral lymph node calcification- Ranke complex.
POST-PRIMARY TUBERCULOSIS • In contrast to primary tuberculosis, lymphadenopathy is notably absent in patients with postprimary tuberculosis, with the exception of patients with HIV/AIDS infection. • Characterized by strong site preference, chronicity, cavity formation and fibrosis • Usually initial lesion in apicoposterior segment of an upper lobe or the superior segment of a lower lobe. • The lesion consists of coarse nodular and linear opacities • Changes may be unilateral or bilatral • Volume loss seen later when fibrosis occurs
POST-PRIMARY TUBERCULOSIS Clinical Features• The findings of reactivation tuberculosis typically become radiographically apparent within 2 years of the initial infection or many years later, often as a result of comorbid states: old age, malnutrition, and/or neoplasm. • lethargy, • anorexia, • weight loss, • low-grade fever, • cough, • hoarseness, • hemoptysis
POST-PRIMARY TUBERCULOSIS • Radiological findings3)Cavitation-40-80% cases -Common in apicoposterior segment of an upper lobe or the superior segment of a lower lobe -single or multiple, large or small, varying thickness of wall from hairline to few millimeters -smooth walled -sometimes air fluid levels may be seen -Rasmussen aneurysm- granulomatous weakening of the pulmonary vessel wall.A life threatening complication-hemoptysis
POST-PRIMARY TUBERCULOSIS • Radiological findings2) Healing-healing occurs by fibrosis-scar formation -cavities usually obliterated but may remain as thin walled rings -well defined upper lobe nodular and linear opacities -severe volume loss -pleural thickening -calcification less common han with primary tuberculosis -bronchiectasis -cysts and bullae
POST-PRIMARY TUBERCULOSIS • Radiological findings3) Endobronchial spread: -with or without cavitation, - ipsi- or contralateral -segmental distribution -results in bronchopneumonic consolidationnodular,with acinar lesions that may become confluent 4) Endobronchial infection: -tuberculous bronchitis -may result in bronchostenosis, bronchiectasis
POST-PRIMARY TUBERCULOSIS • Radiological findings5)Pleural effusion: -usually an empyema -results in pleural thickening and calcification. -occasionally directly involves the chest wall 6)Miliary tuberculosis: -Cryptic,typically presenting in old men as pyrexia of unknown origin with nonspecific symptoms -usually no evidence of known primary
POST-PRIMARY TUBERCULOSIS • Radiological findings7)Tuberculoma: -Localized parenchymal disease that alternately activates and heals -frequently remains stable for years but can anytime reactivate and disseminate -a nodule 10-15 mm size -most common in right upper lobe but can be situated in any lobe -usually single, can be multiple, when multiple all may be confined to single segment -satellite lesions can be seen nearby -calcification may occur
POST-PRIMARY TUBERCULOSIS • Radiological findings8)Mycetma formation: -colonization by fungus , usually Aspergillus Fumigatus -usually in cavities more than 25 mm in diameter -CT is more sensitive 9)Chest wall involvement: -haematogenous seeding or direct spread -usually associated with drug abuse -can affect soft tissue, rib or costal cartilage
PROGRESSIVE PRIMARY TUBERCULOSIS • Progressive primary tuberculosis occurs in the setting of acute infection in patients with minimal or marked immune compromise. Patients with progressive primary tuberculosis become acutely ill, and they may have extensive lung parenchymal opacities and cavitation. Hypoxia and death may occur.
Diagnostic approach • Diagnosis is based on a combination of tuberculin skin testing ,sputum examination, and radiography. Bronchoscopy may be required to obtain specimens.
• Chest Radiograph-cost efective -less sensitive-may not show any findings in 515% cases.
Diagnostic approach •
CT scan-more sensitive but costly.Used especially in progressive primary or postprimary tuberculosis -helps confirm the presence of an ill-defined parenchymal infiltrate -CT is the examination of choice for evaluating lymphadenopathy and involvement of the tracheobronchial tree. -Broncholiths may be identified in rare cases. -Associated mediastinitis and even mediastinal abscesses -Small pleural effusions are detected more readily on CT scans . Contrast enhancement may be useful in identifying evolution into an empyema. -Cavitation and mycetoma formation -Tuberculomas -The bronchogenic spread of tuberculosis -Miliary tuberculosis -Bronchial stenosis -Bronchiectasis -Empyema is visualized on contrast-enhanced CT scans with enhancement of the parietal and visceral pleurae. -Involvement of the pericardium and spine
Diagnostic approach • MRI-may be used to evaluate complications of thoracic disease. • USG-pleural effusion,soft tissue involvement • PET in tuberculosis – -on pet tuberculosis may be indistinguishable from malignancy -can be used to assess response to therapy, to distinguish active from inactive lesion -costly, not widely available.
ACTIVITY AND RESPONSE TO THERAPY •
Active lesion-ill defined coalesced nodules. -poorly marginated linear opacities -thick walled cavity surrounded by consolidation.
•
•
Inactive lesion-well defined small nodular and linear shadows -calcification Compare with previous radiograph
•
However exceptions exist, and many patients show intermediate pattern and even inactive lesions can undergo reactivation
•
Response to therapy is suggested by -resolution of abnormal opacities, a decrease in cavity size, volume loss by fibrosis
END