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Primary tuberculosis - Complications
Medical expert of the article
Last reviewed: 04.07.2025
Complications of primary tuberculosis occur with the deepening of disorders in the immune system and are associated with lymphohematogenous and bronchogenic spread of infection, as well as with the formation of destruction in the affected area and the generalization of the pathological process. The development of complications is facilitated by late diagnosis of primary tuberculosis, untimely initiation of treatment and failure to comply with the basic principles of therapy, most often complications occur in infants and preschool children.
Typical complications of primary tuberculosis: pleurisy, lymphohematogenous and bronchogenic dissemination, atelectasis with subsequent development of inflammatory and cirrhotic changes, bronchial tuberculosis, nodulobronchial fistula, as well as a primary cavity in the lung or lymph node.
Caseous pneumonia and tuberculous meningitis are considered to be very severe but currently uncommon complications of primary tuberculosis. Rarely observed complications include compression of the trachea, esophagus, vagus nerve by enlarged lymph nodes, perforation of the caseous-necrotic node into the lumen of the thoracic aorta.
[ Lymphatic hematogenous dissemination
Lymph-hematogenous dissemination leads to the appearance of fresh tuberculosis foci in the lungs, which is rarely accompanied by bright clinical symptoms. As the inflammatory reaction progresses in the focal area, the symptoms of intoxication and signs of local damage to the respiratory organs increase. In X-ray examination, focal shadows are localized in the upper parts of the lungs. In the process of reverse development, an increase in the intensity of shadows, a decrease in their size are observed, while the contours of the shadows become clearer. Sometimes calcium salt inclusions are detected. Such foci-screenings in the apices of the lungs are usually called Simon foci.
Atelectasis of the lung
Bronchial obstruction with the development of atelectasis can be suspected in the presence of persistent symptoms of intoxication, chest pain, dry cough, and the appearance of signs of respiratory failure. The nature and severity of clinical symptoms depend on the caliber of the affected bronchus and the rate of development of atelectasis. During examination, a recession or flattening of the chest, and a lag of the affected side during breathing are sometimes noted over the airless zone. The percussion sound over the atelectasis zone is muffled, breathing and vocal fremitus are weakened, and sometimes intermittent dry wheezing is heard. X-ray examination reveals a homogeneous darkening with clear, sometimes concave contours. The atelectatic lobe of the lung is reduced in volume, so the root of the lung and the mediastinum are displaced toward the side of the lesion. Other parts of the lung may be excessively transparent due to increased airiness.