Chest Imaging

Tuberculous lymphadenopathy

After inhalation of mycobacterial tuberculous bacilli a pneumonia or inflammatory response occurs in a peripheral portion of lung. Macrophage ingestion of the bacilli and transport of the bacilli into the interstitial space then ensues, with resultant lymphatic spread of bacilli to ipsilateral bronchopulmonary and hilar lymph nodes. Subsequent spread to mediastinal lymph nodes is relatively common. Thus lymphadenopathy with tuberculosis is seen with primary infection and not typically with postprimary disease. The lymphadenopathy observed with primary tuberculosis is usually ipsilateral hilar and occasionally mediastinal. Bilateral hilar adenopathy is unusual and should suggest other possibilities including sarcoidosis or lymphoma. Tuberculous lymph nodes in the hilum and mediastinum may calcify, presenting with irregular calcific opacities within the hila and mediastinum (see calcification mediastinal lymph node). If treated with effective antituberculous agents the lymphadenopathy will slowly resolve. If the disease is unsuspected and untreated the lymph nodes will in time generally decrease in size as the patient's host defences effectively combat the tuberculous bacillus. Calcification in hilar or mediastinal lymph nodes is observed in approximately 35% of cases. Tuberculous lymphadenopathy may also produce extrinsic compression of central airways resulting in atelectasis. This is particularly true in the right middle lobe in children and this finding alone should suggest the possibility of primary tuberculosis. The combination of a peripheral calcified lung nodule and ipsilateral hilar calcified lymph nodes is called a Ranke complex and is virtually pathognomonic of primary tuberculosis.

PGO