Cirrhotic pulmonary tuberculosis

Cirrhotic tuberculosis is formed in the final stage of a long-term tubercular process. With this form, fibrotic changes in the lung and pleura predominate over specific manifestations of tubercular inflammation, which are usually represented by separate encapsulated tuberculosis foci, sometimes with residual slit-like caverns; The intrathoracic lymph nodes often contain calcinates.

Cirrhotic tuberculosis is characterized by a gradual increase in fibrotic changes and progression of pulmonary-cardiac failure. Occasional exacerbations of a specific process are possible. Often, tuberculosis infection is associated with nonspecific inflammation.

[1], [2], [3], [4]

Epidemiology of cirrhotic pulmonary tuberculosis

Cirrhotic tuberculosis is rarely diagnosed in patients with newly diagnosed tuberculosis of respiratory organs. With age, the tendency to fibrous transformation of specific granulations and elastic fibers in the lungs is increasing, so Cirrhotic tuberculosis is more often observed in the elderly many years after the onset of the disease. In childhood Cirrhotic tuberculosis is usually formed when untimely detection of primary tuberculosis complicated by atelectasis.

Cirrhotic tuberculosis accounts for about 3% of all lethal outcomes of tuberculosis. The immediate causes of death are pulmonary-cardiac failure, pulmonary hemorrhage, amyloidosis of internal organs.

[5], [6], [7], [8], [9]

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 inferiority of the involution of tuberculous inflammation. Contribute to the development of cirrhotic tuberculosis complicated course of the disease with violation of bronchial patency and hypoventilation or atelectasis of the affected area, slack resorption of infiltration, as well as internal and external influences that enhance lipid peroxidation (LPO).

As a result, the maturation of the connective tissue is accelerating and coarse ("insoluble") collagen fibers are formed in the lesion zone. Over time, they form massive fibrous cords, which are peribronchial and perivascular, along interlobular and intersegmental septa extend to the lung and pleura roots. Among the fibrous tissue, caseous foci are found. There can be found and residual slit-like caverns with fibrous walls. A rough deformation of the bronchi causes the appearance of cylindrical and saccular bronchiectasises. Small vessels of the lung, especially capillaries, obliterated, there are multiple arteriovenous anastomoses, arterio- and venectasias. With the rupture of which possible pulmonary hemorrhage. Intensive formation of connective tissue is combined with atrophy of muscle and elastic fibers, secondary emphysema of mild mixed type develops.

Depending on the extent of the defeat, one-sided and two-sided, as well as segmental, lobar and total Cirrhotic tuberculosis are distinguished.

Cirrhotic tuberculosis can develop with a complicated course of primary tuberculosis with the spread of a specific inflammation from the lymph node to the bronchus wall. Violation of bronchial patency leads to the appearance of atelectasis, in the area of which chronic inflammation and gross metabolic disturbances develop. An extensive zone of bronchogenic cirrhosis is formed. With 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 mesh sclerosis can gradually be transformed into coarse trabecular diffuse cirrhosis. In these cases, two-sided upper-lobe Cirrhotic tuberculosis is often formed.

With secondary forms of tuberculosis, especially with lobitis, a slow resolution of infiltration leads to the carnification of serous-fibrinous exudate and collagenization of the alveolar septa. The development of fibrotic changes is facilitated by lymphangitis, hypoventilation, violation of blood and lymph circulation (pneumogenic cirrhosis). One-sided upper-lobe Cirrhotic tuberculosis usually develops in the outcome of a lobit 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 pericavital pulmonary tissue. In these cases, pneumogenic cirrhotic changes are combined with bronchogenic cirrhosis, and in the thickness of the fibrous masses, along with the encapsulated tuberculosis foci, residual slit-like foci are present. Usually sanitized, caverns.

Cirrhotic tuberculosis of the lung can also develop after tuberculosis exudative pleurisy or pneumo pleura, usually after therapeutic artificial pneumothorax or thoracoplasty. In such cases, the tubercular process from the caseous foci on the visceral pleura extends into the lung tissue. It forms tubercular foci, which later undergo fibrotic transformation and lead to pleurogenic cirrhosis of the lung.

With widespread cirrhosis, the loss of a significant part of the lung parenchyma, anatomical and functional changes in blood vessels and bronchial tubes, a reduction in lung respiratory excursions due to pleural fusion and emphysema lead to marked disturbances in the function of respiration and circulation. Gradually develops a chronic pulmonary heart.

Symptoms of cirrhotic pulmonary tuberculosis

Symptoms of cirrhotic tuberculosis are due primarily to a violation of the architectonics of the lung, deformation of the bronchial tree and a significant deterioration in gas exchange. Most often, patients complain of shortness of breath, coughing and spitting. 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 lesions in the upper lobe of the lung lobe rarely occurs with severe symptoms. Patients may have a short breath and periodically develop a dry cough. Attachment of nonspecific inflammation may not be accompanied by marked clinical signs due to a good natural drainage of the bronchi.

The common forms of cirrhotic tuberculosis and its lower-lying localization often have a vivid clinical picture due to coarse fibrous and nonspecific inflammatory changes in the lung tissue. Patients are concerned about shortness of breath, cough with discharge of mucopurulent sputum, periodic hemoptysis. The development of chronic pulmonary heart leads to increased dyspnea, the appearance of tachycardia and acrocyanosis. Gradually, the heaviness in the right upper quadrant increases, peripheral edema occurs. With prolonged process, symptoms of amyloidosis of internal organs may appear.

Exacerbation of cirrhotic tuberculosis is associated with increased inflammatory response in tuberculosis foci. There are symptoms of tuberculosis intoxication. Increases cough, sputum increases.

Exacerbation of tuberculosis is not easy to distinguish from a nonspecific inflammatory response. Often, it is due to the attachment or exacerbation of obstructive purulent bronchitis or prolonged pneumonia. An important symptom of exacerbation of tuberculosis is the resumption of bacterial excretion.

A severe complication of cirrhotic tuberculosis is recurrent pulmonary bleeding, which can lead to severe aspiration pneumonia or fatal asphyxia.

When an objective examination of a patient with cirrhotic tuberculosis is usually revealed pallor of the skin, acrocyanosis, sometimes dryness and other trophic changes in the skin. The terminal phalanges of the fingers often have the form of "drumsticks", and the nails - the form of "watch glass". Characteristic of tachycardia and arterial hypotension. With unilateral lesion, asymmetry of the chest is detected, on the side of the lesion it lags behind when breathing. They note dullness of percussion sound, weakening of breathing, dry or small bubble monotonous rales over the zone of injury. When the specific process becomes aggravated and the nonspecific component of inflammation becomes stronger, the number of wheezing increases, they become different. There is also an expansion of the boundaries of cardiac dullness, deafness of cardiac tones, an emphasis of tone II over the pulmonary artery. With decompensation of blood circulation, there is an increase in liver size, peripheral edema, and sometimes ascites.

Radiological picture of cirrhotic pulmonary tuberculosis

The radiological picture largely depends on the initial form of tuberculosis. With unilateral cirrhotic tuberculosis, which developed during the involution of infiltrative or restricted fibrous-cavernous tuberculosis, radiographs show a well-delineated darkening of the middle and sometimes high intensity. Areas of more intensive darkening are due to the presence of dense, partially calcified tuberculosis foci or small foci. This darkening in length corresponds to a reduced lung volume in the volume (segment, fraction). With the defeat of the entire lung, the blackout extends to the entire pulmonary field, the dimensions of which are significantly reduced. In the darkening zone, lighter areas of round or oval shape, bronchiectasis, can also be detected. Sometimes enlightenments are of an irregular slit shape and correspond to residual caverns. Especially clearly they are visible on the tomograms. Shadows of the root of the lung, trachea, large vessels and heart are biased towards the lesion, the pleura is thickened. Unobstructed sections of the lung are increased airiness due to emphysema swelling. X-ray signs of emphysema can also be found in the second lung.

Earlier, patients with cirrhotic tuberculosis often resorted to bronchography. At which severe changes were found on the part of the bronchial tree associated with deformation and obturation of small bronchi in the zone of cirrhotic changes (a symptom of "chopped branches of a tree"). Currently, this study is almost not carried out. The existing changes clearly visualize the computed tomography.

Cirrhotic tuberculosis of the middle lobe, formed as a result of a complicated course of primary tuberculosis, is revealed in the pictures according to the "average share syndrome". In the right lung, a darkening corresponding to the volume of the wrinkled middle lobe is found, including focal shadows of densified calcified foci. In the left lung, a similar picture is observed with cirrhotic lesions of 4-5 segments. In the intrathoracic lymph nodes, usually large calcinates are clearly visible.

For cirrhotic tuberculosis of the lungs, formed in the outcome of disseminated tuberculosis, pathological changes are characteristic in the upper and middle sections of both lungs. On the survey X-ray diffraction, these sections are significantly reduced in size, their transparency is reduced. Against the background of coarse linear and cellular shadows of interstitial fibrosis, they reveal multiple focal shadows of high and medium intensity with clear contours. The visceral pleura is thickened, especially in the upper parts. The underlying areas of pulmonary fields are emphysema. The shadows of the fibrous-compacted roots of the lungs are symmetrically tucked up, the heart in the form of a drop.

With pleuropneumocirrhosis, a decrease in the volume of the affected lung on radiographs is combined with coarse, pronounced pleural overlap, a blend of the shadow of the mediastinal organs towards the lesion, an increase in the airiness of the preserved pulmonary tissue.

Tuberculosis - Treatment

• Chemotherapy for tuberculosis
• Anti-TB drugs
• Artificial pneumothorax
• Pneumoperitoneum
• Surgical methods of treatment of tuberculosis
• Treatment of extrapulmonary tuberculosis
• Pathogenetic therapy of tuberculosis
• Immunotherapy in the treatment of tuberculosis
• Physical methods of treatment of tuberculosis
• Methods of extracorporal hemocorrection in tuberculosis
• Prevention of tuberculosis (BCG vaccination)
• Chemoprophylaxis of tuberculosis
• Sanitary and social prevention of tuberculosis