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Cirrhotic pulmonary tuberculosis

Alexey Kryvenko, medical expert
Last reviewed: 12.07.2025

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Cirrhotic tuberculosis develops in the final stage of a long-term tuberculosis process. In this form, fibrous changes in the lung and pleura prevail over specific manifestations of tuberculous inflammation, which are usually represented by separate encapsulated tuberculous foci, sometimes residual slit-like caverns; intrathoracic lymph nodes often contain calcifications.

Cirrhotic tuberculosis is characterized by a gradual increase in fibrotic changes and progression of pulmonary-cardiac insufficiency. Episodic exacerbations of the specific process are possible. Non-specific inflammation often joins the tuberculous lesion.

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Epidemiology of cirrhotic pulmonary tuberculosis

Cirrhotic tuberculosis is rarely diagnosed in patients with newly diagnosed tuberculosis of the respiratory organs. With age, the tendency for fibrous transformation of specific granulations and elastic fibers in the lungs increases, so cirrhotic tuberculosis is more often observed in older people many years after the onset of the disease. In childhood, cirrhotic tuberculosis usually develops when primary tuberculosis complicated by atelectasis is not detected in a timely manner.

Cirrhotic tuberculosis accounts for about 3% of all fatal tuberculosis cases. The immediate causes of death are pulmonary heart failure, pulmonary hemorrhage, and amyloidosis of internal organs.

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Pathogenesis and pathological anatomy of cirrhotic pulmonary tuberculosis

Cirrhotic tuberculosis is formed as a result of excessive development of connective tissue in the lungs and pleura due to the incompleteness of the involution of tuberculous inflammation. The development of cirrhotic tuberculosis is facilitated by the complicated course of the disease with impaired bronchial patency and hypoventilation or atelectasis of the affected area, sluggish resorption of infiltration, as well as internal and external effects that increase lipid peroxidation (LPO).

As a result, the maturation processes of connective tissue accelerate and coarse ("insoluble") collagen fibers are formed in the affected area. Over time, they form massive fibrous strands that spread peribronchially and perivascularly, along interlobular and intersegmental septa, to the root of the lung and pleura. Caseous foci are found among the fibrous tissue. Residual slit-like caverns with fibrous walls can also be found. Rough deformation of the bronchi causes the appearance of cylindrical and saccular bronchiectasis. Small vessels of the lung, especially capillaries, are obliterated, multiple arteriovenous anastomoses, arterio- and venectasias occur. When they rupture, pulmonary hemorrhage is possible. Intensive formation of connective tissue is combined with atrophy of muscle and elastic fibers, and secondary mixed-type pulmonary emphysema develops.

Depending on the extent of the lesion, a distinction is made between unilateral and bilateral, as well as segmental, lobar and total cirrhotic tuberculosis.

Cirrhotic tuberculosis may develop in complicated cases of primary tuberculosis with the spread of specific inflammation from the lymph node to the bronchial wall. Obstruction of bronchial patency leads to the development of atelectasis, in the area of which chronic inflammation and gross metabolic disorders develop. An extensive zone of bronchogenic cirrhosis is formed. In primary tuberculosis, such changes are more often localized in the upper and middle lobes of the right lung or in the 4th and 5th segments of the left lung. In these cases, unilateral lobar or segmental cirrhotic tuberculosis is diagnosed.

In the process of reverse development of chronic disseminated tuberculosis, interstitial reticular sclerosis can gradually transform into coarse trabecular diffuse cirrhosis. In these cases, bilateral upper lobe cirrhotic tuberculosis often develops.

In secondary forms of tuberculosis, especially in lobitis, slow resorption of infiltration leads to carnification of serous-fibrinous exudate and collagenization of alveolar septa. Development of fibrous changes is facilitated by lymphangitis, hypoventilation, impaired blood and lymph circulation (pneumogenic cirrhosis). Unilateral upper lobe cirrhotic tuberculosis usually develops as a result of lobitis or lobar caseous pneumonia.

Cirrhotic tuberculosis of the lungs is often preceded by fibrous-cavernous tuberculosis, in which there are pronounced fibrous changes in the wall of the cavern and pericavitary lung tissue. In these cases, pneumogenic cirrhotic changes are combined with bronchogenic cirrhosis, and in the thickness of the fibrous masses, along with encapsulated tuberculous foci, there are residual slit-like, usually sanitized, caverns.

Cirrhotic pulmonary tuberculosis may also develop after tuberculous exudative pleurisy or pneumopleurisy, usually after therapeutic artificial pneumothorax or thoracoplasty. In such cases, the tuberculous process from caseous foci on the visceral pleura spreads to the lung tissue. Tuberculous foci are formed in it, which subsequently undergo fibrous transformation and lead to pleurogenic cirrhosis of the lung.

In widespread cirrhosis, the loss of a significant portion of the lung parenchyma, anatomical and functional changes in the vessels and bronchi, and a decrease in respiratory excursions of the lungs due to pleural adhesions and emphysema lead to significant impairment of respiratory and circulatory function. Chronic pulmonary heart disease gradually develops.

Symptoms of cirrhotic tuberculosis of the lungs

Symptoms of cirrhotic tuberculosis are primarily due to disruption of the lung architecture, deformation of the bronchial tree, and significant deterioration of gas exchange. Most often, patients complain of shortness of breath, cough, and sputum production. The degree of clinical manifestations depends on the localization, prevalence, phase of the tuberculosis process, and the severity of the nonspecific component of inflammation in the lung.

Cirrhotic tuberculosis of limited extent with damage to the upper and lower lobes of the lung rarely occurs with pronounced symptoms. Patients have slight shortness of breath and periodically develop a dry cough. The addition of non-specific inflammation may not be accompanied by pronounced clinical signs due to good natural drainage of the bronchi.

Common forms of cirrhotic tuberculosis and its lower lobe localization often have a vivid clinical picture caused by gross fibrous and nonspecific inflammatory changes in the lung tissue. Patients are bothered by shortness of breath, cough with mucopurulent sputum, periodic hemoptysis. The development of chronic pulmonary heart leads to increased shortness of breath, the appearance of tachycardia and acrocyanosis. Gradually, heaviness in the right hypochondrium increases, peripheral edema occurs. With a long process, symptoms of amyloidosis of internal organs may appear.

Exacerbation of cirrhotic tuberculosis is associated with increased inflammatory response in tuberculosis foci. Symptoms of tuberculosis intoxication appear. Cough intensifies, the amount of sputum increases.

Exacerbation of tuberculosis is not easy to distinguish from a non-specific inflammatory reaction. It is often caused by the addition or exacerbation of obstructive purulent bronchitis or protracted pneumonia. An important symptom of exacerbation of tuberculosis is the resumption of bacterial excretion.

A serious complication of cirrhotic tuberculosis is recurrent pulmonary hemorrhage, which can lead to severe aspiration pneumonia or asphyxia with a fatal outcome.

An objective examination of a patient with cirrhotic tuberculosis usually reveals pale skin, acrocyanosis, and sometimes dryness and other trophic changes in the skin. The terminal phalanges of the fingers often have the appearance of "drumsticks," and the nails are shaped like "watch glasses." Tachycardia and arterial hypotension are characteristic. With unilateral damage, asymmetry of the chest is detected; on the affected side, it lags behind during breathing. Dullness of percussion sound, weakening of breathing, dry or fine-bubble monotonous wheezing over the affected area are noted. With an exacerbation of the specific process and an increase in the nonspecific component of inflammation, the number of wheezing increases, they become different in caliber. Expansion of the boundaries of cardiac dullness, muffled heart sounds, and an accentuation of tone II over the pulmonary artery are also detected. With circulatory decompensation, an increase in liver size, peripheral edema, and sometimes ascites are observed.

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X-ray picture of cirrhotic tuberculosis of the lungs

The radiographic picture largely depends on the initial form of tuberculosis. In unilateral cirrhotic tuberculosis, which developed during the involution of infiltrative or limited fibro-cavernous tuberculosis, radiographs reveal well-defined darkening of medium and, in places, high intensity. Areas of more intense darkening are due to the presence of dense, partially calcified tuberculous foci or small foci. Such darkening in extent corresponds to the affected area of the lung (segment, lobe) reduced in volume. When the entire lung is affected, the darkening extends to the entire lung field, the size of which is significantly reduced. In the darkening zone, lighter areas of a round or oval shape - bronchiectasis - can also be detected. Sometimes the enlightenment is of an irregular slit-like shape and corresponds to residual caverns. They are especially clearly visible on tomograms. The shadows of the root of the lung, trachea, large vessels and heart are shifted towards the affected side, the pleura is thickened. The parts of the lung free from darkening may have increased airiness due to emphysematous swelling. Radiographic signs of emphysema can also be found in the second lung.

Previously, bronchography was often used in patients with cirrhotic tuberculosis, which revealed gross changes in the bronchial tree associated with deformation and obstruction of small bronchi in the area of cirrhotic changes (symptom of "cut tree branches"). At present, this study is almost never performed. The existing changes are well visualized by computed tomography.

Cirrhotic tuberculosis of the middle lobe, formed as a result of complicated course of primary tuberculosis, is revealed on images by "middle lobe syndrome". In the right lung, a darkening corresponding to the volume of the wrinkled middle lobe is detected, including focal shadows of compacted and calcified foci. In the left lung, a similar picture is observed with cirrhotic damage of segments 4-5. Large calcifications are usually clearly visible in the intrathoracic lymph nodes.

Cirrhotic pulmonary tuberculosis, which developed as a result of disseminated tuberculosis, is characterized by pathological changes in the upper and middle sections of both lungs. On the plain radiograph, these sections are significantly reduced in size, their transparency is reduced. Against the background of coarse linear and cellular shadows of interstitial fibrosis, multiple focal shadows of high and medium intensity with clear contours are found in them. The visceral pleura is thickened, especially in the upper sections. The underlying sections of the pulmonary fields are emphysematous. The shadows of the fibrously compacted roots of the lungs are symmetrically pulled up, the heart is in the shape of a drop.

In pleuropneumocirrhosis, a decrease in the volume of the affected lung on radiographs is combined with coarse, sharply expressed pleural overlays, a shift in the shadow of the mediastinal organs towards the affected side, and an increase in the airiness of the remaining lung tissue.

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