Pleuropulmonary Tuberculosis - Chest X-Ray

A 45 years old male came to radiology department for X-ray chest with history of cough, mild fever and weight loss. The x ray is shown below:

X-ray chest shows fibro infiltrative lesions in right upper zone with areas of early calcification and moderate pleural effusion on left sidewith minimal tracheal pull to right side.

Comments And Explanation: Pleural effusion is the accumulation of fluid in the pleural space, i.e.
between the visceral and parietal layers of pleura. The fluid may be transude, exudate, blood, chyle or rarely bile.
Pleural fluid casts a shadow of the density of water on the chest radiograph. The most dependent recess of the pleura is the posterior costophrenic angle. A small effusion will, therefore, tend to collect posteriorly, however, a lateral decubitus view is the most sensitive film to detect small quantity of free pleural effusion (as small as 50 ml). 100–200 ml of pleural fluid is required to be seen above the dome of the diaphragm on frontal chest radiograph. As more fluid is accumulated, a
homogeneous opacity spreads upwards, obscuring the lung base.
Typically this opacity has a fairly well-defined, concave upper edge (as seen in picture above), which
is higher laterally and obscures the diaphragmatic shadow. Frequently the fluid will track into the pleural fissures.
A massive effusion may cause complete radiopacity of a hemithorax. The underlying lung will retract
towards its hilum, and the space occupying effect of the effusion will push the mediastinum towards the opposite side.
USG chest confirms the presence or absence of the pleural fluid; it also shows the septations within the pleural fluid with or without solid component within the lesion. USG helps in guiding aspiration of pleural fluid.
CT scan is the most sensitive modality for detection of presence of minimal fluid. It allows distinction between free and loculated fluid showing its extent and localization.


Diagnosis: Pleuropulmonary tuberculosis.

Clinical Discussion:
Pleural effusion is either transudate or exudate. In transudate, the protein level is 1.5–2.5 g/dL and is seen in congestive heart failure, constrictive pericarditis, cirrhosis, nephrotic syndrome and hypothyroidism.
Exudate results from increased permeability of abnormal pleural capillaries with release of high-protein fluid into pleural space, protein level > 3 g/dL seen in empyema, tuberculosis and actinomycosis.

Tuberculous pleural effusions occur in up to 30% of patients with tuberculosis.
The current hypothesis for the pathogenesis of tuberculous pleural effusion is that a subpleural caseous focus in the lung ruptures into the pleural space 6–12 weeks after a primary infection. Mycobacterial antigens enter the pleural space and interact with T-cells previously sensitized to
mycobacteria, resulting in a delayed hypersensitivity reaction and the accumulation of fluid. It seems that this reaction of the pleura augments the entry of fluid into the pleural space by increasing the permeability of pleural capillaries to serum proteins, and thereby increasing the oncotic
pressure in the pleural fluid.
It appears that tuberculous pleurisy is due to a delayed hypersensitivity reaction rather than to a tuberculous infection.
Involvement of the lymphatic system probably also contributes to the accumulation of pleural fluid. An impaired clearance of protein from the pleural space has been reported in human tuberculous effusions. It is known that the clearance of proteins and fluid from the pleural space is carried out by lymphatics in the parietal pleura. Fluid gains access to the lymphatics through openings in the parietal pleura.