Clinical cure of pulmonary tuberculosis. Posttuberculous changes, complications and consequences of tuberculosis
3.1. CLINICAL CLASSIFICATION OF TUBERCULOSIS
The clinical classification of tuberculosis used in the Russian Federation is based on the following principles:
1. Clinical and radiological features of the tuberculous process (including localization and prevalence).
2. Phases of its flow.
3. The presence of bacterial excretion.
The classification consists of four main sections:
1. Clinical forms of tuberculosis.
2. Characteristics of the tuberculous process.
3. Complications of tuberculosis.
4. Residual changes after cured tuberculosis. Clinical forms of tuberculosis vary in location and
clinical and radiological signs, taking into account the pathogenetic and pathomorphological characteristics of the tuberculosis process.
Tuberculosis intoxication in children and adolescents.
Tuberculosis of the respiratory organs:
Primary tuberculosis complex.
Tuberculosis of the intrathoracic lymph nodes.
disseminated pulmonary tuberculosis.
Miliary pulmonary tuberculosis.
Focal pulmonary tuberculosis.
Infiltrative pulmonary tuberculosis.
Caseous pneumonia.
Tuberculoma of the lungs.
Cavernous pulmonary tuberculosis.
Fibrous-cavernous pulmonary tuberculosis.
Cirrhotic pulmonary tuberculosis.
Tuberculous pleurisy (including empyema).
Tuberculosis of the bronchi, trachea, upper respiratory tract.
Tuberculosis of the respiratory organs, combined with occupational lung diseases (coniotuberculosis). Tuberculosis of other organs and systems:
Tuberculosis of the meninges, central nervous system. Tuberculosis of the intestines, peritoneum and mesenteric lymph nodes.
Tuberculosis of bones and joints. Tuberculosis of the urinary, genital organs. Tuberculosis of the skin and subcutaneous tissue. Tuberculosis of peripheral lymph nodes. Eye tuberculosis. Tuberculosis of other organs.
Characteristics of the tuberculosis process is given according to the localization of the process, clinical and radiological signs and the presence or absence of Mycobacterium tuberculosis (MBT) in the diagnostic material obtained from the patient.
Localization and prevalence are indicated:
In the lungs by lobes and segments;
According to the localization of the lesion in other organs. Phase:
a) infiltration, decay, seeding;
b) resorption, compaction, scarring, calcification. Bacterioexcretion:
a) with the isolation of Mycobacterium tuberculosis (MBT+);
b) without isolation of Mycobacterium tuberculosis (MBT-). Complications of tuberculosis:
Hemoptysis and pulmonary bleeding, spontaneous pneumothorax, pulmonary heart failure, atelectasis, amyloidosis, fistulas, etc.
Residual changes after cured tuberculosis:
A) respiratory organs:
Fibrous, fibrous-focal, bullous-dystrophic, calcifications in the lungs and lymph nodes, pleuropneumosclerosis, cirrhosis, condition after surgery, etc.;
b) other organs:
Cicatricial changes in various organs and their consequences, calcification, condition after surgical interventions.
3.2. CLINICAL CLASSIFICATION OF RESPIRATORY TUBERCULOSIS
3.2.1. TUBERCULOSIS INTOXICATION IN CHILDREN AND ADOLESCENTS
Primary forms of tuberculosis develop after first infection of the body with MBT.
Primary tuberculosis affects mainly children and adolescents and much less often adults.
From the moment of the introduction of tuberculosis infection to the manifestation of tuberculosis as a disease, a period of so-called latent infection passes.
The period of primary infection has characteristic features:
1) high sensitization of the organism;
2) a tendency to generalize the process in the lymphohematogenous way;
3) involvement in the process of the lymphatic system;
4) tendency to caseous degeneration of lymph nodes;
5) ability to spontaneous healing.
Tuberculous intoxication as an independent disease characterizes the period of the disease without a clear localization of tuberculosis, and its clinical manifestations reflect functional disorders in various body systems.
To identify the localization of tuberculosis lesions due to their small size by available X-ray and other methods impossible. Most often, the source of intoxication is minimal tuberculous foci in the lymph nodes, especially the mediastinum. Less commonly, foci are found in the liver, bones, tonsils, etc.
The diagnosis of tuberculous intoxication is established on the basis of tuberculin diagnostics data (positive, increasing in the process of observation and hyperergic reactions to tuberculin), clinical signs of the disease in the absence of local manifestations determined by x-ray and other research methods.
The specificity of the described functional disorders should be confirmed by a thorough examination of the child (adolescent) to exclude nonspecific diseases. On examination
it is necessary to use modern radiation diagnostic methods, including, if possible, computed tomography, bronchoscopy, complex tuberculin diagnostics, as well as bacteriological examination.
The diagnosis of tuberculosis intoxication is established only after examination in a specialized anti-tuberculosis institution.
The variety of clinical manifestations of primary tuberculosis is expanding due to paraspecific changes in the body:
1) keratoconjunctivitis;
2) erythema nodosum (erythema nodosum);
3) Poncet's rheumatoid;
4) acute diffuse nephritis.
In the clinic of tuberculosis intoxication, two periods are distinguished - early and chronic.
Early tuberculosis intoxication in children and adolescents
Symptoms of early tuberculous intoxication are manifested primarily in the imbalance of the nervous system, which is expressed in a change in the child's behavior: irritability, excitability, decreased attention, sleep disturbance and headaches.
Often during this period, poor appetite, pallor of the skin, intermittent low subfebrile temperature, some swelling of the external lymph nodes are noted. In thin children, it is easy to feel the enlarged liver, spleen. There may be a violation of digestion: relaxation of the action of the intestines or constipation.
4-6 weeks after the initial infection, a positive tuberculin test appears in children. (tuberculin test turn).
Often found erythema nodosum (erythema nodosum).
(fig. 3-1, see insert). Its appearance is preceded by a high temperature, a few days after which, mainly on the anterior surfaces of the legs, dense infiltrates appear, hot to the touch, very painful, red, with a cyanotic tint. Most often, erythema occurs in preschoolers and younger students, being an allergic, paraspecific reaction, and not a tuberculous skin lesion. It accompanies primary tuberculosis or an outbreak and is considered a manifestation
high allergy onset of the primary disease. Most often, it is found on the anterior surfaces of the legs in the form of painful swelling of a reddish color. The boundaries of erythema are either clearly delineated or appear diffuse. Erythema nodosum never ulcerates (unlike erythema induratum). More often nodes protrude on the skin in the area tibia, less often on the forearms and keep from 3 to 6 weeks. Erythema nodosum is a reaction to various factors. In the first place is tuberculosis, which can be observed with sarcoidosis. Rheumatism may also be accompanied by erythema nodosum. Nodular periarteritis gives similar nodes.
The most important differential diagnostic sign of early tuberculous intoxication is the coincidence of these functional disorders and morphological changes with the turn of tuberculin reactions.
If this period was imperceptible to the parents and the doctor, the child may develop a tuberculous process in the lungs with the involvement of regional lymph nodes or damage to other organs. If the patient receives rational anti-tuberculosis therapy in a timely manner, then all phenomena subside rather quickly, and then disappear; only a moderate positive tuberculin test persists.
During this period, the child must be provided with a sanatorium-hygienic regimen at home or in a medical institution - a hospital, a sanatorium kindergarten, a forest school. Against the background of a properly adjusted diet, rich in the whole complex of vitamins, depending on the severity of intoxication, it is necessary to carry out antibacterial therapy. Treatment should be long and continue after the effects of early intoxication subside.
Chronic tuberculosis intoxication in children and adolescents
characteristic signs are the child's lag in development, pallor, micropolyadenia(6-9 groups of enlarged lymph nodes are palpable - from an elastic consistency to pebbles).
In chronic tuberculosis intoxication, it is important that after the turn of tuberculin tests 1 year or more has passed, and tuberculin tests remain positive or increase.
With chronic tuberculosis intoxication morphological changes of a tuberculous nature are found in one or
multiple organs: in the bone marrow, lymph nodes and sometimes in parenchymal organs.
In contrast to early tuberculous intoxication, in chronic intoxication, all symptoms are more pronounced and more stable.
Patients have chronic conjunctivitis, conflicts, which appear and disappear.
Appetite is sharply reduced. Sometimes there are dyspepsia or constipation. Depending on the duration of chronic tuberculous intoxication, there is lagging behind in physical development, growth, and especially body weight child.
As a rule, there is a decrease in the turgor of all tissues, skin, subcutaneous tissue.
There is a slight periodic temperature increase with fluctuations from 37 to 37.5 ° С.
The reaction of a sick child to noisy games, favorite activities, communication with children changes dramatically. As a rule, children get tired quickly, tend to retire and, which is not typical of childhood, often go to bed early. Schoolchildren become distracted.
Neither clinically nor radiologically in the lungs can detect obvious pathological changes. In "older" children, who are carriers of long-term chronic tuberculous intoxication, one can detect a healed primary complex: Gon's focus and cicatricial changes in the root with petrificates in it.
Chronic tuberculosis intoxication can be prevented correct and long-term treatment. Treatment of already developed chronic tuberculous intoxication presents great difficulties. Due to the formation of a fibrous capsule and an avascular zone around the lesion, anti-tuberculosis drugs do not fully saturate the tuberculous focus, and the MBT in it do not lose their viability.
3.2.2. PRIMARY TB COMPLEX
The pathological anatomy of the primary tuberculosis complex is presented in Chapter 1. Etiology and pathogenesis of tuberculosis.
Clinic. In infants, in conditions of massive tuberculosis infection, the primary tuberculosis complex proceeds
by the type of pneumonia, with extensive damage to the intrathoracic lymph nodes. The disease develops with high fever and fever up to 39-40 ° C, complaints of cough, dry or mucous sputum, chest pain.
Pneumonia (lobar or segmental) takes on a diffuse character, which depends on hyperergic reactions and incomplete differentiation of the lungs in babies. Older children develop small primary foci in the lungs, and some have various complications of the primary tuberculosis complex.
When examining a child, enlarged peripheral lymph nodes (cervical, axillary) of a dense elastic consistency, mobile, without perifocal inflammation in the surrounding tissue are found. With a large pneumonic focus, there is a lag in the act of breathing of one half of the chest; above it, dullness of the percussion tone; Wet fine bubbling rales are heard. With small pulmonary foci, there are no physical changes.
In the washing water of the bronchi, stomach Mycobacterium tuberculosis is found, which come not only from infiltrative-pneumonic foci located in the lungs, but also from specific changes in the bronchi.
Blood test reveals moderate leukocytosis with a shift of the neutrophilic formula to the left, eosinopenia, monopenia and accelerated ESR.
Diagnostics. For the diagnosis of the primary complex, the anamnesis is of great importance - an indication of contact with a bacillus excretor, positive tuberculin tests. Especially valuable is the turn of tuberculin tests, which, with a fresh and active primary complex, is manifested by hyperergic skin tuberculin reactions.
Of great importance is the study of sputum, washings of the bronchi and stomach for the presence of tuberculous mycobacteria. X-ray examination reveals fresh pulmonary lesions with concomitant adenitis.
X-ray picture of the primary tuberculosis complex
The classic primary complex consists of three main elements: the pulmonary, glandular components and the lymphangitis that binds them. However, before the bipolarity becomes distinct on a dorsoventral x-ray of the lungs, the infiltrate phase passes. The infiltrate is a rather intense darkening associated with the root of the lung, sometimes it is superimposed on the root. As a rule, the infiltrate is not homogeneous. Its boundaries are somewhat blurred. Vessels and bronchi appear through the infiltrate. The sizes of infiltrates are various and depend on degree of defeat of a lung; they can be lobar, segmental, and broncholobular. More often, the primary complex is localized in the upper and middle segments of the lungs. With the resorption of the infiltrate, its subpleural location is more clearly visible.
The primary complex has four stages of development:
I stage - pneumonic(Fig. 3-2a). Three components of the complex are visible on the radiograph:
1) focus in the lung tissue 2-4 cm in diameter or more, oval or irregular in shape, of varying intensity (often medium and even high), with a fuzzy, blurry contour;
2) outflow to the root, lymphangitis, which is defined as linear strands from the focus to the root;
3) at the root - enlarged infiltrated lymph nodes. The root appears to be enlarged, its structure is lubricated, the intensity is increased. The contours delineating the lymph nodes are either blurred or more clearly outline the enlarged nodes.
II stage - resorption(Fig. 3-2b). The focus in the lung tissue decreases, its intensity increases, the contours become clear. The outflow to the root and the infiltration of the lymph nodes are reduced.
III stage - compaction(Fig. 3-2c). A focus up to 1 cm in diameter remains in place of the focus, calcareous inclusions appear in it in the form of small points of sharp intensity. The same inclusions of lime are also noticeable in the lymph nodes of the root of the lungs. Between the focus and the root, thin bands from lymphangitis are determined.
Rice. 3-2. Primary tuberculosis complex:
Stage I - pneumonic (a); Stage II - resorption (b); Stage III - compaction (c); IV stage - calcification (g)
IV stage - calcination(Fig. 3-2d). The focus in the lung tissue becomes even smaller, denser, its intensity is high, the contour is clear, often jagged, uneven. Increased calcifications in the lymph nodes of the root. Calcifications in some cases appear to be a continuous dense formation, in others they have less intense shadows of inclusions, which indicate incomplete calcification of the focus and the preservation of caseous areas in them. With a favorable outcome of the primary tuberculous complex, over time, in the center of the former caseosis, located in the peripheral parts of the lungs, calcification increases - up to the appearance of bone tissue in some cases. This is the focus of Gon (Fig. 3-3).
Rice. 3-3. Gon's hearth
Rice. 3-4. CT calcification in mediastinal lymph node
In cases where the primary complex is detected in a timely manner and the patient receives a full-fledged treatment, the pathological changes in the lung tissue and root often completely resolve, with a complete restoration of their original pattern.
The greatest difficulties arise in the diagnosis of tuberculous intoxication and a small form of tuberculosis of the intrathoracic lymph nodes. In the absence of radiographic signs of obvious lymphadenopathy, great diagnostic value is attached to computed tomography (CT), which allows visualizing slightly enlarged lymph nodes and calcium salt deposits (Fig. 3-4).
In small forms of tuberculosis of the intrathoracic lymph nodes, the radiological diagnosis is based on the detection of deformation and enrichment (intensification, redundancy) of the basal pulmonary pattern as a reflection of congestive lymphangitis, a violation of the root structure and blurring of its contours.
Complications of primary tuberculosis complex
The observed complications in the primary tuberculous complex are reduced to the progression of the process: the involvement of neighboring organs (bronchi, pleura) in the process, the formation of destruction in the lung tissue, the occurrence of lymphohematogenous dissemination (Fig. 3-5, 3-6).
Rice. 3-5. Pleural effusion (2) resulting from rupture of the pulmonary component (1) of the primary complex
Rice. 3-6. Thin-walled cavity (1), formed as a result of destruction of the bronchial wall by the primary process in the lung. Mycobacteria from this cavity can spread to other parts of the lungs.
Differential Diagnosis primary tuberculosis complex with nonspecific pneumonia is not difficult.
The onset of nonspecific pneumonia is acute, stormy, accompanied by chills, fever up to 39-40 °C. Herpetic eruptions on lips. Objectively - rich stetoacoustic data: intense dulling of lung sound, increased voice trembling, bronchial breathing with an abundance of wheezing. The blood picture is characterized by high leukocytosis (15,000-20,000), neutrophilia. Pneumonia proceeds with a stormy clinical picture and ends in a crisis in a short period.
In the primary tuberculosis complex, the general condition is relatively good, there are hyperergic tuberculin tests, the presence of MBT in the sputum, the presence of paraspecific reactions of the sclera, skin and joints, and a slow reverse dynamics of the process.
3.2.3. TUBERCULOSIS OF INTRATHORACIC LYMPH NODES (BRONCHADENITIS)
Bronchoadenitis- disease of the lymph nodes of the root of the lungs and mediastinum. With this form of primary tuberculosis, the intrathoracic lymph nodes are mainly involved in the inflammatory process.
According to its anatomical structure, the lymph glandular system of the lung is regional to the lymphatic vascular system of the lung, and the lymph nodes of the root of the lung - as if collector, where lymph collects. With the development of tuberculosis in the lung, the root lymph nodes react to it with an inflammatory process. However, in the lymph nodes of the mediastinum and the root of the lung, pathological processes can occur regardless of the disease in the lungs.
Clinic of tuberculous bronchoadenitis
Tuberculous bronchoadenitis, as a rule, begins with intoxication, with its inherent clinical symptoms: subfebrile temperature, deterioration in general condition, loss of appetite, weight loss, adynamia or excitation of the nervous system. Sweating, poor sleep are sometimes noted.
With progression, especially in young children, appears bitonic cough, those. two tone cough. It is called squeezing
bronchial tubes enlarged in volume by lymph nodes containing caseous masses. In adults, due to the loss of elasticity of the bronchus wall, compression is observed very rarely and occurs only in patients with a long-term current disease, when the lymph nodes are massive, dense, contain caseous masses with calcification elements.
In adults, there is dry, paroxysmal, hacking, tickling cough. It is caused by irritation of the bronchial mucosa or appears due to the formation of a bronchopulmonary fistula. As a result of damage to the nerve plexuses located in the zone of tuberculous changes, bronchospasm may occur.
In young children, the volume of the bifurcation group of lymph nodes rapidly increases, and as caseosis accumulates in them and an extensive perifocal reaction, suffocation may occur. These terrible symptoms of asphyxia are accompanied by cyanosis, intermittent breathing, swelling of the wings of the nose and retraction of the intercostal spaces. Turning the child into a position on the stomach alleviates the condition due to the movement of the affected lymph node forward.
Blood tests- no features compared with hemograms in a tuberculous patient with a different localization of the lesion. However, with the disintegration of caseous masses of lymph nodes and their breakthrough into the bronchus, higher ESR numbers are noted, leukocytosis increases to 13,000-15,000.
detection of Mycobacterium tuberculosis. Tuberculosis bacilli can be found in the washings of the stomach, especially often they are found in sputum and washings of the bronchus when caseous masses break through into the bronchus.
X-ray picture of bronchoadenitis
Clinical and radiological bronchoadenitis have two options: infiltrative And tumorous (tumor-like). The infiltrative form is more common (Fig. 3-7, 3-8). After the infiltration phase, with proper treatment, resorption develops quite quickly. The lymph nodes are compacted, a fibrous capsule forms around them, lime deposits are visible on the x-ray. If treatment is started in a timely manner, calcifications may not form, and cicatricial seals remain at the site of the affected lymph nodes.
The tumorous form is observed in young children infected with a massive infection (Fig. 3-9). Often, tumorigenesis
Rice. 3-7. Infiltrative bronchoadenitis. On the survey radiograph, the shadow of the root is expanded, its outer contour is blurred, the structure is blurred, the intensity is increased
Rice. 3-8. Infiltrative bronchoadenitis of paratracheal lymph nodes. On the survey radiograph, the shadow in the region of the paratracheal lymph nodes on the right is expanded, its outer contour is fuzzy, the structure is blurred, the intensity is increased
ny bronchoadenitis proceeds accompanied by tuberculosis of the eyes, bones, skin. During the period of illness, the affected lymph nodes undergo changes typical of tuberculosis.
With tumorous bronchoadenitis reverse development is slower. Resorption takes place inside the capsule, caseous masses are calcified. Calcifications are formed in greater numbers than with the infiltrative form, and on the radiograph they take the form of uneven shadows of a rounded or oval shape.
Rice. 3-9. Left-sided tumorous bronchoadenitis, massive enlargement of bronchopulmonary lymph nodes on the left (a - overview image and b - tomogram)
Rice. 3-10. The stage of petrification (calcification) of the lymph nodes
Compacted areas are interspersed with less dense shadows. The focus resembles a mulberry or raspberry (Figure 3-10).
Complications of tuberculous bronchoadenitis. In a complicated course, massive hilar fibrosis, extensive unevenly petrified lymph nodes are observed, containing the remains of caseosis with the presence of MBT, giving the possibility of exacerbation or recurrence of the tuberculous process.
With a smooth course and complete resorption of infiltrative processes bronchoadenitis documented by small calcifications and coarsening of the root of the lungs.
Complications of tuberculosis of intrathoracic lymph nodes
Possible with bronchoadenitis tuberculous lesions of the bronchi with the formation of glandular-bronchial fistulas(Figure 3-11). With a complete violation of bronchial patency due to blockage of the bronchus by caseous masses or compression of its massive lymph nodes affected by tuberculosis (tumor bronchoadenitis), atelectasis of the lung area, collapse of a lobe or segment of the lung (1), located above the site of blockage of the bronchus, may occur. With a complete violation of bronchial patency due to blockage of the bronchus by caseous masses or compression of its massive lymph nodes affected by tuberculosis (tumor bronchoadenitis), atelectasis may occur (2).
Rice. 3-11. Collapse of a lobe or segment of the lung (1), atelectasis of the lower lung (2)
A frequent complication may be pleurisy, in particular, interlobar. Even after its resorption, a compacted pleura of both lobes remains - the mooring. Subsequently, the mooring becomes somewhat thinner, but such evidence of the transferred pleurisy remains for life.
In rare cases, when there is a connection between the affected lymph node and the draining bronchus, emptying from it may occur.
caseous masses with the subsequent formation of a lymphogenous cavity at this site.
In chronically ongoing bronchoadenitis, there are lymphohematogenous seedings, found in both lungs, predominantly in the upper lobes.
Treatment of tuberculous bronchoadenitis should be complex, with the use of antibacterial drugs and vitamins against the background of a sanatorium-hygienic regimen. During the period of the process calming down, the patient can return to his professional work and continue outpatient treatment. Early initiation of treatment of tuberculous bronchoadenitis in children and adults and its continuous implementation for a long time guarantees the recovery of the patient and prevents the complicated course of the disease. Intensive specific and pathogenetic therapy quickly gives good results.
differential diagnosis. When establishing a diagnosis, tuberculous bronchoadenitis has to be differentiated from bronchoadenitis of another etiology. It is necessary to study the anamnesis well, the presence of contact with a bacillary patient, the nature of tuberculin tests, past diseases that can be associated with tuberculosis intoxication or with small manifestations of primary tuberculosis. A number of diseases of the intrathoracic lymph nodes have some similarities with tuberculous bronchoadenitis.
Lymphogranulomatosis- tumor lesion of the lymph nodes. The nature of the defeat of the nodes themselves with lymphogranulomatosis differs sharply from their changes in tuberculosis.
With lymphogranulomatosis, the lymph nodes are affected symmetrically, often with the involvement of the entire group of peripheral nodes in the pathological process. Tuberculin tests are negative or weakly positive.
Characterized by a wave-like increase in temperature with gradually increasing ups and downs, pain in the chest, limbs and joints.
Blood changes are not similar to those of tuberculosis. Anemia, leukocytosis, neutrophilia and lymphopenia are more often determined.
When treated with antibiotics, therapy does not work.
The diagnosis of lymphogranulomatosis is confirmed cytologically with a biopsy of the lymph node.
Sarcoidosis Besnier-Beck-Schaumann- a disease characterized by infiltrative changes in the intrathoracic lymph nodes. It occurs mainly at the age of 20-40 years, more often in women.
Sometimes it is difficult to diagnose, since the general condition, despite the duration of the disease, remains good, tuberculin tests are negative. Antibacterial therapy has no effect.
In adults, tuberculous bronchoadenitis should be differentiated from metastases of central cancer and lymphosarcoma.
When making a differential diagnosis between tuberculous bronchoadenitis and hilar form of central lung cancer the following should be taken into account.
Cancer develops, as a rule, in older people, mainly in men.
There is a hacking cough, shortness of breath, chest pain, signs of compression of large vessels.
When cancer metastasizes, an increase in the subclavian lymph nodes (Virchow's glands) is detected.
Tuberculin tests may be negative.
The diagnosis is confirmed by bronchological examination: finding a tumor in the lumen of the bronchus, and in the biopsy material of the bronchial mucosa - elements of the tumor.
On a chest x-ray with peripheral development of central lung cancer, intense, irregularly shaped darkening is determined. Tomography reveals the shadow of a tumor in the lumen of a large bronchus, narrowing of its lumen, and an increase in intrathoracic lymph nodes.
With endobronchial growth, the tumor early leads to bronchial obstruction, the development of cancerous pneumonitis and atelectasis.
The hemogram is characterized by anemia, a shift in the leukocyte formula to the left, an acceleration of the ESR (40-60 mm/h).
Lymphosarcoma, with which it is necessary to differentiate tuberculous bronchoadenitis, is manifested by various clinical symptoms.
Patients complain of fever, weakness, sweating, exhaustion of the body quickly sets in.
Patients with lymphosarcoma much more often than those with tuberculous bronchoadenitis suffer from excruciating cough, shortness of breath, and severe chest pain.
The hemogram is characterized by severe lymphopenia, sharply accelerated ESR. Tuberculin tests are negative.
All groups of lymph nodes are quickly involved in the malignant process. Peripheral nodes are enlarged and form large packages, they are dense, painless.
Cytohistological examination of the lymph node reveals a large number of lymphoid elements (90-98%), which contain large nuclei surrounded by a narrow rim of protoplasm.
3.2.4. DISSEMINATED PULMONARY TUBERCULOSIS
Disseminated forms of tuberculosis include all disseminated processes in the lungs of hematogenous, lymphogenous and bronchogenic origin.
In accordance with the clinical classification of tuberculosis, hematogenous disseminated forms are divided into three main groups:
1) acute disseminated (miliary) pulmonary tuberculosis;
2) subacute disseminated pulmonary tuberculosis;
3) chronic disseminated pulmonary tuberculosis.
1. Acute miliary pulmonary tuberculosis was known to clinicians earlier than all other forms of hematogenous origin.
With hematogenous disseminated pulmonary tuberculosis, pathophysiological disorders and clinical symptoms are diverse. The clinic of miliary tuberculosis is characterized by general intoxication and functional disorders. They will manifest themselves in the form of a decrease in appetite, weakness, subfebrile temperature. Patients have a dry cough. In the anamnesis there is an indication of contact with bacillary patients, previously transferred exudative pleurisy, lymphadenitis.
With an acute onset of the disease there is a rise in temperature to 39-40 ° C, shortness of breath, dry cough, sometimes with the release of a small amount of mucous sputum. Patients on examination noted cyanosis (lips, fingertips).
Percussion a pulmonary sound with a tympanic shade is detected, hard or weakened breathing is auscultated, a small amount of dry or small moist rales, especially in the paravertebral space.
Spleen and liver slightly enlarged.
Marked labile pulse and tachycardia.
Tuberculin tests usually false negative (negative anergy).
Blood changes characterized by leukocytosis, monocytosis, eosinopenia, neutrophilic shift to the left, increased ESR. Protein is determined in the urine.
X-ray picture miliary tuberculosis in the first days of the disease is expressed by a diffuse decrease in the transparency of the lungs with blurring of the vascular pattern, the appearance of a finely looped mesh due to inflammatory compaction of the interstitial tissue. Only on the 7th-10th day of the disease, on the survey radiograph, one can see multiple, rounded, well-delimited and arranged in a chain of foci the size of a millet grain, followed by a total symmetrical seeding of the lung fields in both lungs with small foci of the same type (Fig. 3-12) . All important features of miliary lung disease can be detected using CT (Fig. 3-13). If the process progresses, then the pleura and meningeal membranes are affected.
With the reverse development of miliary tuberculosis, the foci can completely dissolve or calcify. The number of calcified foci is less than during the period of rash, since focal changes are partially absorbed.
Rice. 3-12. Acute miliary pulmonary tuberculosis
Rice. 3-13.
Patients with generalized and unrecognized tuberculosis die with symptoms of severe tuberculosis intoxication, hypoxemia and hypoxia.
Miliary pulmonary tuberculosis often has to be differentiated from typhoid fever. With miliary tuberculosis, as well as with typhoid fever, there are clearly expressed symptoms of intoxication, severe headaches, high fever, delirium, and darkened consciousness. However, a careful analysis of the symptoms that contradict typhoid fever will help to make the correct diagnosis.
Unlike miliary tuberculosis, typhoid begins with a gradually developing malaise and fever. With typhoid, bradycardia is observed, with miliary tuberculosis - tachycardia. In favor of tuberculosis and against typhoid, symptoms such as shortness of breath, cyanosis, tachycardia, fever of the wrong type, absence of dyspeptic disorders testify.
The blood picture also differs in diseases: typhoid is characterized by leukopenia and lymphocytosis, for tuberculosis - leukocytes within the normal range or leukocytosis up to 15,000-18,000.
Vidal's reaction can resolve doubts: it will be positive only in typhoid fever.
X-ray of the lungs confirms the suspicion of miliary pulmonary tuberculosis.
In the early diagnosis of miliary tuberculosis, it is important to study the fundus of the eye, where a rash of tuberculous tubercles is detected relatively early.
2. Subacute disseminated pulmonary tuberculosis. Manifestations of this clinical form of tuberculosis are diverse. Functional disorders resemble a picture of an acute infectious disease, for example, typhoid fever. The disease can proceed under the guise of influenza, focal pneumonia.
The reason for the visit of patients to the doctor is often hemoptysis. Patients go to the doctor also in connection with tuberculous lesions of other organs, for example, the larynx, when hoarseness of the voice appears, sore throat when swallowing.
With a limited extent of dissemination, the course of a subacute hematogenous process may be in the absence of symptoms. The above process is detected during preventive fluorographic examinations. Patients complain of a slight cough with sputum production, fever.
Physically, a slight shortening of the percussion sound is detected in the lungs, a small amount of fine bubbling moist rales in the interscapular space, and a pleural friction noise are auscultated. During the formation of the cavity, as a rule, fine and medium bubbling rales are heard above the cavity.
Mycobacterium tuberculosis is found in sputum.
Blood changes manifest as leukocytosis (12,000-15,000), an increase in stab neutrophils, lymphopenia, elevated ESR (20-30 mm/h).
X-ray examination reveals numerous scattered foci of different sizes symmetrically on both sides, they are located mainly in the upper parts of the lungs (Fig. 3-14). The interstitial tissue of the lungs is presented in the form of a compacted fine mesh.
With an unfavorable development of the process focuses increase, merge (infiltrate). Caverns form at the site of infiltration. The process extends to the middle and lower parts of the lungs.
Sometimes, with the progression of disseminated tuberculosis, due to trophic changes in the lungs, there is a breakdown of the lung tissue in the form of characteristic multiple thin-walled
Rice. 3-14. Tuberculous miliary dissemination in the lungs on the 10th day of illness. CT
Rice. 3-15. Chronic disseminated tuberculosis (survey direct radiographs): a - compaction phase; b - residual changes after chronic disseminated pulmonary tuberculosis
cavities Usually the caverns are round, identical in shape and size. Therefore they are named "stamped". They can be located in a chain, often symmetrically in both lungs.
Damage to blood vessels, their thrombosis and obliteration play a role in the origin of cavities. The nutrition of the affected areas of the lungs is disturbed, and destruction is formed in them.
Under the influence of chemotherapy, the temperature normalizes, coughing and the amount of sputum secreted decrease. Functional disorders are eliminated; the hemogram normalizes, bacilli excretion stops. There is a partial resorption of foci. Positive results in the treatment are achieved within 9-12 months.
3. Chronic hematogenous disseminated pulmonary tuberculosis develops with a long course of the disease and ineffective treatment. Accompanied by complaints of cough with sputum, shortness of breath, aggravated by physical exertion, weakness, weakness, fever (subfebrile temperature).
A frequent harbinger of exacerbation of chronic hematogenous disseminated pulmonary tuberculosis is exudative pleurisy. Tuberculosis of the kidneys, bones or other organs precede or accompany chronic hematogenous disseminated pulmonary tuberculosis.
Physically, in the lungs, in the paravertebral space, scattered dry and finely bubbling, moist rales, pleural friction noise are heard.
Characteristic is the dysfunction of the nervous system and the cerebral cortex: mental lability, irritability, decreased ability to work, loss of sleep, neurotic reactions. There are endocrine disorders - hyper or hypothyroidism.
Patients have hemoptysis and pulmonary bleeding, symptoms of obstructive bronchitis with symptoms of bronchospasm. There are signs of pulmonary heart failure: cyanosis, tachycardia, shortness of breath, congestion in the lungs, liver, kidneys, edema of the lower extremities.
In the hemogram, there is a nuclear shift of neutrophils to the left, lymphopenia, monocytosis, and accelerated ESR.
Patients become bacillary.
The X-ray picture is characterized by compaction of the connective tissue of the lungs, uneven reticulation and coarse heaviness of the lung pattern. Against this background, mainly in the upper parts of the lungs, there are scattered foci of various polymorphism. In the marginal and lower sections, there are signs of emphysema
With the progression of chronic hematogenous disseminated tuberculosis, there is an increase in shortness of breath, an increase in the amount of sputum, and the appearance of hemoptysis. In the lungs, above the caverns, against the background of bronchial breathing, widespread moist, medium bubbling rales are heard. A specific lesion of the upper respiratory tract, intestines, serous membranes and other organs joins.
Under the influence of various methods of treatment (chemotherapy, pathogenetic treatment), cough decreases, bacilli excretion stops, fresh foci and disseminations resolve.
The clinical and radiological picture of various forms of disseminated tuberculosis resembles a number of diseases that are characterized by focal dissemination in the lungs. These are infectious-inflammatory diseases, bacterial, viral, fungal lesions of the lungs, reticuloses, collagenoses, lung tumors.
Differentiated diagnosis. The largest group of lung diseases, with which disseminated forms of tuberculosis should be compared, are lobular bronchopneumonia of various etiologies (post-measles, influenza, septic, etc.).
Treatment. Acute miliary tuberculosis is curable even if the meningeal membranes are affected. Treatment should be comprehensive, taking into account all pathophysiological disorders.
See Chap. 5.
As a result of treatment, complete resorption of the foci occurs with the restoration of a normal pulmonary pattern and the normalization of all body functions. In some cases, the foci are partially absorbed, and the remaining foci are subjected to compaction, calcification.
Treatment of patients with disseminated forms of tuberculosis, as already mentioned, should be comprehensive. Chemotherapy is of primary importance; in the acute phase of the process, intravenous administration of antibacterial drugs is necessary. Long-term chemotherapy is indicated until the complete resorption of fresh foci in the lungs or their compaction. Of the pathogenetic agents in the acute period, hormonal therapy is performed with the appointment of corticosteroids (prednisone, prednisolone).
In patients with subacute and chronic hematogenous disseminated tuberculosis in the presence of decay, collapse therapy is indicated - the imposition of pneumoperitoneum. If cavities in the lungs persist during treatment, surgical methods of treatment are used.
3.2.5. FOCAL PULMONARY TUBERCULOSIS
A summary of the pathological anatomy of focal tuberculosis is presented in section 1.4.
Focal pulmonary tuberculosis is referred to as post-primary (secondary), which arose in the body with primary tuberculosis foci, previously cured.
Focal pulmonary tuberculosis accounts for about 50% of all newly diagnosed tuberculosis diseases. It can proceed without subjective sensations and is detected only during a mass fluorographic examination. But with an additional examination, it is often found that patients did not attach importance to a number of symptoms of tuberculous intoxication for a long time.
Clinical and radiographically, two forms of focal tuberculosis are distinguished: fresh soft focal and chronic fibro-focal. In the process of healing of various forms of tuberculosis, focal changes are formed. These lesions are replaced by fibrous tissue, encapsulated, and are considered fibrous residual lesions.
The pathogenesis of focal tuberculosis is different, diverse and complex. This form may be a manifestation of the primary or, more often, the secondary period of tuberculosis.
Secondary focal forms occur in adults under the influence of exogenous superinfection or endogenous spread of MBT from latent, earlier foci. Such foci contain caseosis and MBT and are located in the lymph nodes or in any organ.
During the exacerbation of the MBT process from the foci spread through the lymphatic tracts and small bronchi. Most often, fresh foci appear in the tops of the lungs. Initially, endobronchitis develops, then the lesion covers all the small branches of the bronchi of this zone. There comes a curdled necrosis of the walls of the altered bronchi, followed by a transition to the lung tissue, mainly in the apical region. A small focus such as caseous, acinous or lobular pneumonia is formed. The lymphatic network is involved in the pathological process only around the focus. Regional lymph nodes usually do not respond to lesions in the lungs. Exudative phenomena are small and are quickly replaced by a productive reaction.
Hematogenous spread characterized by a symmetrical arrangement of foci, the remains of which are located in the apical regions of the lungs.
clinical picture. Some of the patients identified by fluorography do not really have any clinical symptoms. However, most of them react to the occurrence of rare focal pulmonary tuberculosis with weakness, sweating, decreased ability to work and appetite. Patients complain of the appearance of heat in the cheeks and palms, short-term chills and low subfebrile temperature in the middle of the day. Sometimes observed intermittent cough, dry or with scanty amount of sputum, pain in the side.
On examination, the patient is noted slight soreness of the muscles of the shoulder girdle on the affected side. Lymph nodes are not changed. In the lungs, there may be a shortening of the percussion sound only when the lesions merge. In the fresh phases of the development of focal tuberculosis, in the presence of infiltrative changes, when coughing, hard breathing and small, wet single rales are heard.
Tuberculin tests usually expressed moderately.
From the side of the blood nothing characteristic of this form of the disease is noted, and blood changes depend on the phase of the disease. With mild fresh forms, blood counts are normal, in the infiltration phase, ESR is somewhat accelerated, the left shift of the formula reaches 12-15% of stab forms, and slight lymphopenia.
In the chronic course of the process focal tuberculosis, the so-called productive form is observed. Foci of small and medium sizes (3-6 mm), rounded or irregular in shape, clearly defined, of medium and sharp intensity are determined.
On the radiograph foci up to 1 cm in diameter, rounded or irregular in shape are determined. Their contours can be clear or blurry, the intensity is weak or medium. The foci are single and multiple, more often located in one lung, mainly in the upper sections: in I, II and VI segments; often merge with each other. Wide linear intertwining shadows are visible around the foci - lymphangitis (Fig. 3-16-3-18).
With progression, an increase in the number of fresh lesions, increased lymphangitis, and decay cavities appear.
Rice. 3-16. Soft-focal pulmonary tuberculosis (scheme)
Rice. 3-17. Soft-focal pulmonary tuberculosis in the left lung (plain picture and tomogram)
Treatment. With modern antibacterial treatment, fresh tuberculous foci and lymphangitis usually resolve within 12 months. On the radiograph, you can see a complete restoration of the lung pattern or residual slight heaviness and small outlined foci. Less often, after full-fledged treatment, fresh foci do not resolve, but are encapsulated, and coarse fibrosis develops at the site of lymphangitis.
Rice. 3-18. Focal tuberculosis in segments 1 and 2 of the right and S of the left lung in the infiltration phase (general view and tomogram). In these segments, numerous foci of small and medium sizes, low and medium intensity are determined.
3.2.6. INFILTRATIVE PULMONARY TUBERCULOSIS
Infiltrative tuberculosis is considered as a phase of progression of focal pulmonary tuberculosis, in which infiltration, perifocal inflammation are leading. With this form of tuberculosis is extremely diverse proliferative, lung tissue response.
The mechanism and causes of the occurrence of various infiltrates in their course are complex. As a rule, the infiltrative-pneumonic process develops against the background of a hyperergic reaction of the body, hypersensitization of the lung tissue, and great lability of the neurovegetative and endocrine systems.
There are the following clinical and radiological types of infiltrates (Fig. 3-19):
1) broncholobular infiltrate;
2) rounded infiltrate;
3) cloudy infiltrate;
4) caseous pneumonia.
6) periscissuritis.
Rice. 3-19. Schematic representation of radiographic types of tuberculous infiltrates in the lungs
Broncholobular infiltrate- this is a focus located in the cortical sections of I or II segments of the upper lobe of the lung, irregularly rounded, with fuzzy contours, 1-3 cm in diameter. On tomography, it consists of 2-3 or several merged fresh foci. It is asymptomatic, without functional changes and bacilli excretion (Fig. 3-20).
Rounded infiltrate- these are darkening foci of a round or oval shape, unsharply contoured, 1.5-2 cm in diameter, located more often in segments I-II or VI of the lungs. From them to the root of the lung there is an inflammatory "path", against which the projection of the bronchus is determined (Fig. 3-21a, 3-21b).
An X-ray tomographic study can reveal inclusions of denser or calcified foci, the presence of small decay cavities, pleural changes, and scar formations. With the progression of round infiltrates, there is an increase in the zone of perifocal inflammation, the appearance of signs of decay of the caseous center with the formation of a cavity. The cavity contains sequesters and a small amount of fluid - a pneumonogenic cavity.
Rice. 3-20.(a-b). Broncholobular tuberculous infiltrate [overview image (a) + (b) tomogram]. In the upper lobe of the left lung, an irregularly shaped infiltration area 6X7 cm in size is determined. The intensity of the area is average, without clear contours
Rice. 3-21. Infiltrative pulmonary tuberculosis [overview image (a) + tomogram (b)]. In the upper lobe of the right lung, there are 2 foci 3X3 cm in size, with uneven contours, heterogeneous structure. Numerous small focal shadows of medium intensity are defined around.
As a result of bronchogenic seeding, foci of various sizes appear in healthy areas of the lungs.
Cloudy infiltrate X-ray is an uneven darkening, the contours of the shadow of which are blurry
chats, it extends to one or more segments of the upper lobe of the lung (Fig. 3-22). Tuberculous infiltrate resembles a picture of nonspecific pneumonia, but differs from it in the resistance of radiological changes, the tendency to disintegration and the formation of cavities.
Rice. 3-22. Cloud-like infiltrate in the upper lobe of the right lung [overview image (a) + tomogram (b)]. In the upper lobe of the right lung, there are 2 foci sized 3x4 and 2.5x3 cm, of medium intensity, with uneven and fuzzy contours, heterogeneous structure due to decay cavities. Multiple hearths around
Lobit- an inflammatory tuberculous process that spreads to the entire lobe of the lung. Lobit is distinguished by its structural forms (many caseous foci) and severe clinical picture. As the process progresses, the entire lobe of the lung is affected, which is delimited by a clear interlobar groove. Observations over time have shown that lobitis is often preceded by the development of a small infiltrative focus (Fig. 3-23).
Periscissuritis, or marginal infiltrate,- this is a cloud-like infiltrate located at the interlobar sulcus. The top of the triangle is facing the root of the lung, the base is outward. The upper borders are vague and pass without sharp outlines into little-modified lung tissue. The lower border corresponds to the interlobar pleura, and therefore clear (Fig. 3-24).
Rice. 3-23. tuberculous infiltrate. Infiltrative shadow occupying the lobe of the right lung (lobitis), with an underlined lower border. Interlobar fissure shifted upward
Rice. 3-24. Periscisuritis
Caseous pneumonia. In some patients with insufficient immunobiological resistance, the infiltrate takes on the character of caseous pneumonia. Caseous pneumonia is characterized by the development of an inflammatory reaction in the lung tissue with a predominance of necrosis, and caseous-pneumonic foci occupy a lobe and even the entire lung.
The development of caseous pneumonia is promoted by a number of unfavorable factors: malnutrition, pregnancy, diabetes, massive infection with highly virulent Mycobacterium tuberculosis.
Caseous pneumonia can develop after pulmonary bleeding as a result of aspiration of blood with tuberculous mycobacteria.
The clinical picture of caseous pneumonia is determined by the prevalence and intensity of morphological changes.
Clinic of infiltrative tuberculosis. The severity of clinical symptoms generally corresponds to the scale of specific lesions in the lungs. In most cases, infiltrative tuberculosis begins acutely with a high temperature and can proceed as lobar pneumonia or influenza. The clinic of an acute illness appears against the background of complete health. Only with a thorough survey of patients is it possible to identify the symptoms of tuberculous intoxication that appeared before the onset of an acute illness.
Often the first symptom of infiltrative-pneumonic tuberculosis is hemoptysis or bleeding. The duration of the acute period of the disease is different: from several days to several weeks.
Of complaints most often there are chest pains on the affected side (in the side or in the area of the shoulder blades), a dry cough or with scanty sputum. The phenomena of tuberculosis intoxication are expressed: poor appetite, sweating, sleep disturbance, irritability, tachycardia, general weakness.
With caseous pneumonia the onset of the disease is acute: with high temperature up to 40-41°C, hectic type, with large differences between morning and evening temperature. The symptoms of tuberculous intoxication quickly increase, there is a sharp adynamia, profuse sweats, chest pains, cough with purulent sputum, shortness of breath, patients quickly lose weight.
During physical examination, the initial signs of infiltrative tuberculosis are: lagging of the chest on the side of the lesion during breathing, tension and soreness of the muscles of the chest, increased voice trembling.
Percussion and auscultation data become more pronounced with massive pneumonia such as lobitis and with the incipient decay of the infiltrate with the formation of a cavity. At this time, it is possible to determine the dullness of percussion over the lesion site.
nogo sound, bronchophony, bronchial breathing, moist, sonorous persistent rales of various calibers.
Differential diagnosis of infiltrates. The acute onset of the disease and the rapid development of the pneumonic process in persons who do not have a history of tuberculosis serve as a reason for making a diagnosis of nonspecific pneumonia.
Especially difficult is the diagnosis of infiltrative-pneumonic tuberculosis, which occurs with influenza syndrome. Its important differential diagnostic differences from pneumonia are:
1) signs of tuberculosis intoxication;
2) gradual onset of the disease;
3) absence of catarrhal inflammation of the upper respiratory tract;
4) relatively satisfactory condition of patients, despite the high temperature.
With nonspecific pneumonia with high fever, the condition of the patients is severe, while the specific (tuberculous) process proceeds with the absence of physical data at the onset of the disease and their appearance only with the progression of the process. In the blood tests of patients with tuberculosis, there are slight shifts in the leukocyte formula and a slight acceleration of ESR, in contrast to croupous pneumonia, when high leukocytosis with a shift to the left and a sharply accelerated ESR are noted.
X-ray shows that tuberculous infiltrates are localized mostly in the upper sections (I, II and VI segments), and nonspecific inflammatory processes - in the middle and lower fields.
A "path" to the root of the lung departs from the tuberculous infiltrate; usually, individual focal shadows are noticeable along the periphery of the main focus of the lesion, the latter can also be in other parts of the same or opposite lung as a result of bronchogenic seeding.
In some cases, only dynamic monitoring of the patient's condition, the lack of effect of treatment with non-specific antibacterial agents, the appearance of Mycobacterium tuberculosis in sputum make it possible to establish the diagnosis of tuberculosis.
Long-term reverse development of the process makes it possible to distinguish infiltrative-pneumonic pulmonary tuberculosis from eosin-
nophilic pneumonia, the main symptom of which is rapid, within a few days, resorption of the focus. In addition, with eosinophilic pneumonia, eosinophilia in the blood reaches 30-45%. Eosinophilic pneumonia disappear without a trace: after 7-10 days, complete restoration of the lung tissue occurs.
In addition to malignant neoplasms, tuberculous infiltrate sometimes has to be differentiated from echinococcosis of the lung, actinomycosis, lymphogranulomatosis, dermoid cysts, syphilis of the lung, etc. Only a comprehensive examination of the patient and a thorough analysis of clinical and X-ray laboratory data can correctly recognize the nature of the process in the lung tissue.
Treatment. If infiltrative tuberculosis is detected, treatment is started in a hospital with first-line antibacterial drugs using pathogenetic therapy. Treatment of the patient is carried out until complete resorption of infiltrative changes, an average of 9-12 months, followed by anti-relapse courses of chemotherapy under dispensary observation.
Approximate standardized doses of anti-TB drugs for tuberculosis chemotherapy, see Chap. 5.
The clinical diversity of forms of infiltrative tuberculosis necessitates the complex use of various methods of treatment. In the absence of a long-term effect and preservation of destruction, it is sometimes advisable to add collapse therapy (artificial pneumothorax) or surgical intervention.
3.2.7. TUBERCULEMA OF THE LUNG
A summary of the pathological anatomy of tuberculosis is presented in section 1.4.
Tuberculoma of the lungs unites encapsulated caseous foci of various genesis, larger than 1 cm in diameter. The source of tuberculoma formation Basically, there are two forms of pulmonary tuberculosis: infiltrative-pneumonic and focal. In addition, tuberculomas are formed from cavernous tuberculosis by filling the cavity with caseosis.
Filled cavities refer to tuberculomas only conditionally, since the filling of the cavity occurs mechanically, while tuberculomas are a peculiar phenomenon in the lung tissue.
On the radiograph tuberculomas are detected in the form of a rounded shadow with clear contours. In the focus, crescent-shaped enlightenment due to decay, sometimes perifocal inflammation and a small number of bronchogenic foci, as well as areas of calcification can be determined (Fig. 3-25, 3-26).
Rice. 3-25. Tuberculoma in the decay phase. On the survey radiograph (a) in the upper lobe of the left lung, a polygonal shadow with clear contours, 6x9 cm in size, of medium intensity, is determined. The tomogram (b) reveals crescent-shaped enlightenment due to the decay
Rice. 3-26. Multiple tuberculomas with decay [overview image (a) + tomogram (b)]. In the upper lobe of the right lung there are multiple rounded shadows with a diameter of 1.5-2 cm of medium intensity, with enlightenment in the center, clear contours. The presence of decay in tuberculomas is confirmed by tomographic examination
There are 3 clinical variants of tuberculoma course:
1) progressive, which is characterized by the appearance at some stage of the disease of decay, perifocal inflammation around the tuberculoma, bronchogenic seeding in the surrounding lung tissue;
2) stable, in which there are no radiological changes in the process of monitoring the patient or there are rare exacerbations without signs of progression of tuberculoma;
3) retrogressive, which is characterized by a slow decrease in tuberculoma, followed by the formation of a focus or a group of foci, an induction field, or a combination of these changes in its place.
In relation to all forms of pulmonary tuberculosis, patients with tuberculomas account for 6-10%. This is explained by the fact that extensive infiltrative-pneumonic processes under the influence of treatment and an increase in the body's resistance are limited, compacted. However, the process does not stop completely, remaining a clearly defined dense formation.
clinical picture. Since tuberculoma itself is an indicator of high body resistance, patients with this form of pulmonary tuberculosis are often detected by chance during fluorographic examinations, preventive examinations, etc. Patients practically do not show complaints.
On physical examination the patient pathology in the lungs is also not detected. Wheezing is heard only with a massive outbreak with widespread infiltrative changes in the lung tissue around the tuberculoma.
blood picture also without features, with exacerbations, a moderate acceleration of ESR and moderate leukocytosis are observed.
With stable tuberculomas, MBT is not found in sputum. In the presence of decay in tuberculomas, bacilli excretion occurs in cases where there is a connection with the drainage bronchus.
Tuberculin tests. Patients with pulmonary tuberculomas in most cases respond positively to tuberculin, the Mantoux test often has a hyperergic character.
Treatment. Before the discovery of antibacterial drugs, the prognosis for tuberculomas was poor - tuberculomas gave massive outbreaks, followed by a transition to severe forms of pulmonary tuberculosis. Now, in 80% of patients with tuberculomas, the process of regression
ruet or proceeds chronically without exacerbations. Approximate standardized doses of anti-TB drugs for tuberculosis chemotherapy, see Chap. 5.
When identifying patients with pulmonary tuberculomas, hospitalization and long-term treatment are necessary. If decay persists in tuberculoma for a long time and the patient continues to secrete MBT, and long-term antibiotic therapy does not lead to the desired results, it is recommended to resort to surgical intervention.
Surgery. Usually, the operation is performed with minimal removal of lung tissue - segmental resection. Surgical treatment is also indicated in cases where there is no certainty that the patient has tuberculosis, since it can be difficult to distinguish tuberculoma from other lung diseases, especially tumors.
For the diagnosis of tuberculoma, it is necessary to conduct a bronchological examination with a catheter biopsy, as well as with a puncture of the bifurcation lymph nodes. These techniques make it possible to make a correct diagnosis in almost 90% of cases.
3.2.8. CAVERNOUS PULMONARY TUBERCULOSIS
A summary of the pathological anatomy of tuberculosis is presented in section 1.4.
Distinctive features of the cavernous form of pulmonary tuberculosis is the presence of a thin-walled cavity located on
against the background of slightly changed lung tissue in the absence of pronounced infiltrative and fibrous changes (Fig. 3-27, 3-28).
Rice. 3-27. Cavernous pulmonary tuberculosis. Overview photo. In the upper sections of the left lung, a group of formed decay cavities is presented, without a pronounced perifocal zone of inflammation and limited focal seeding.
Rice. 3-28. Elastic cavity in the upper lobe of the right lung. An annular, thin-walled shadow with clear contours, 6x5 cm in size, is determined. Dense foci and fibrosis are detected in the adjacent part of the lung. Size share not reduced
Cavernous tuberculosis develops in patients with infiltrative, disseminated focal tuberculosis during the decay of tuberculomas.
An X-ray examination determines a round-shaped cavity with a thin two-layer wall and the usual localization in the subclavian region.
Physical manifestations are usually absent. Only when coughing at the height of inspiration, separate finely bubbling wet rales are heard. Catarrhal phenomena occur later, with the appearance of perifocal inflammatory changes around the cavity, thickening of its wall.
Blood changes in patients with cavernous tuberculosis are also poorly expressed: the number of leukocytes is normal, ESR is often accelerated (20-40 mm/h).
Mycobacterium tuberculosis and elastic fibers are detected in sputum or bronchial washings. But to detect MBT, it is necessary to use not only bacterioscopy, but also seeding methods.
Treatment patients with cavernous pulmonary tuberculosis should be comprehensive, with the inclusion of methods of collapse therapy and surgical intervention.
Approximate standardized doses of anti-TB drugs for tuberculosis chemotherapy, see Chap. 5.
Surgical removal of the cavity is an important stage in the treatment of patients with cavernous forms.
The combination of chemotherapy with surgical methods of treatment gives a clinical cure for patients with cavernous forms.
3.2.9. FIBROUS-CAVERNOUS PULMONARY TUBERCULOSIS
A summary of the pathological anatomy of tuberculosis is presented in section 1.4.
Fibrous-cavernous pulmonary tuberculosis- a chronic disease that proceeds for a long time and in waves, with intervals of remission of inflammatory phenomena. It is characterized by the presence of one or more caverns of great age with pronounced sclerosis of the surrounding tissues, fibrous degeneration of the lungs and pleura.
Pathogenesis. Pathogenetically, this form does not arise independently, but is a consequence of infiltrative tuberculosis. The hematogenous disseminated form also serves as a source of fibrous-cavernous processes in the lungs.
Of course, with a far advanced fibrous-cavernous form, it is not always easy to determine what caused its development.
The extent of changes in the lungs can be different. The process is unilateral and bilateral, with the presence of one or many cavities.
For fibrous-cavernous tuberculosis, foci of bronchogenic screening of various prescriptions are characteristic. As a rule, the bronchus draining the cavity is affected. Other morphological changes in the lungs also develop: pneumosclerosis, emphysema, bronchiectasis.
History of patients with fibrous-cavernous lesions of the lungs is characterized by complaints about the duration of the disease of tuberculosis, its undulating course. The intervals between flare and clinical well-being may be very long or, conversely, there may be frequent recurrence of flares. In some cases, patients subjectively do not feel the severity of the disease.
Clinical manifestations of fibrous-cavernous tuberculosis are diverse, they are due to the tuberculous process itself, as well as the developed complications.
There are two clinical variants of the course of fibrous-cavernous pulmonary tuberculosis:
1) limited and relatively stable, when a certain stabilization of the process occurs due to chemotherapy and an exacerbation may be absent for several years;
2) progressive, characterized by a change of exacerbations and remissions, with different periods between them.
During periods of exacerbations, there is a rise in temperature, which is explained by specific outbreaks of the process, the development of infiltration around the cavity. The temperature can be high in those cases when a secondary infection joins the disease.
The defeat of the bronchi is accompanied by a prolonged "hacking" cough, during which viscous mucopurulent sputum is separated with difficulty.
Frequent complications are:
1) hemoptysis;
2) pulmonary bleeding caused by perforation of large vessels due to caseous-necrotic process.
The appearance of a patient with long-term fibrous-cavernous tuberculosis is very characteristic and is called habitus phthisicus. The patient is distinguished by a sharp weight loss, flaccid dry skin, easily gathering into wrinkles, muscle atrophy, mainly of the upper shoulder girdle, back and intercostal groups.
Patients suffer from constant intoxication. With frequent outbreaks of the tuberculous process, respiratory failure of II and III degrees develops. Stagnation, acrocyanosis are noted. Later, the liver enlarges. Edema may appear. With the progression of the process, a specific lesion of the larynx and intestines is observed, which leads to a sharp decrease in
body resistance. With the development of cachexia, amyloid nephrosis and pulmonary heart failure, the prognosis becomes difficult.
Percussion gives distinct symptoms: shortening of the sound in places of thickening of the pleura and massive fibrosis. During outbreaks with a significant extent and depth of pneumonic and infiltrative processes, a shortening of the percussion sound can also be noted. There are no regularities in the distribution of these processes; therefore, it is impossible to speak of their predominant topography.
auscultatory in places of fibrosis and thickening of the pleura, weakened breathing is detected. In the presence of infiltrative-pneumonic exacerbations, bronchial breathing, fine moist rales can be detected. Above the caverns of large and giant sizes, bronchial and amphoric breathing and large-bubble, sonorous, moist rales are heard. Over small caverns, rales are less sonorous, not plentiful, and are better heard when coughing. Above the old cavity, a "creak of a cart", a "squeak" is heard, caused by cirrhosis of the cavity wall and surrounding tissue.
Thus, in the fibrous-cavernous process, an abundance of stetoacoustic symptoms can be detected. However, there are "mute" and "pseudo-mute" cavities that do not give any percussion or auscultatory symptoms.
On the radiograph, a picture of fibrosis and wrinkling of the lung, an old fibrous cavity (one or more), pleural stratifications are usually determined.
X-ray picture fibrosis and wrinkling of the lung is most often found in the upper lobes with a predominant lesion of one of them. The mediastinum and trachea are displaced towards a larger lesion. The upper lobes are reduced in volume, their transparency is sharply reduced due to hypoventilation. The pattern of the lung tissue is sharply deformed as a result of the development of coarse fibrosis. In the lower parts of the lungs, transparency is often increased, indicating emphysema. Roots, as a rule, are displaced upwards. Large vessels are determined in the form of straight, even shadows - the so-called symptom of a "stretched string". Usually in both lungs groups of foci of various sizes and intensity are visible.
Rice. 3-29. On the survey radiograph, the following are determined: a picture of fibrosis and wrinkling of the lung, multiple old fibrous caverns, pleural layers in the upper sections of the left lung
Rice. 3-30. Cavern with liquid level (general view). In the middle sections of the right lung, a cavity with a diameter of 6x7 cm is determined, which is located among coarse fibrosis of the lungs, its walls are deformed and dense. At the bottom of the cavity, a small liquid level is determined
In the fibrous-cavernous process, the cavity is located among the coarse fibrosis of the lungs, its walls are deformed, dense, most often thickened. Quite often, a small liquid level is determined at the bottom of the cavity (Fig. 3-30). With exacerbation and progression of the process around the cavity, areas of infiltration are visible. In the process of treatment, slow resorption of these changes, partial reduction and wrinkling of the cavity are noted. Sometimes a fibrous cavity is detected only with tomography, since on a conventional radiograph the shadow of the cavity can be covered by superimposed shadows of foci, fibrosis and pleural layers.
In a laboratory study of sputum a constant bacilli excretion is found, sometimes massive, as well as coral-like elastic fibers.
Blood. The state of the blood in patients with fibrous-cavernous tuberculosis depends on the phase of the disease. With an outbreak, it is the same as with active tuberculosis, but with a change in the formula towards lymphopenia, a left shift and an accelerated ESR up to 30-40 mm / h. With severe bleeding, anemia is detected, sometimes very pronounced. With a secondary infection, a higher leukocytosis is observed - up to 19,000-20,000 and an increase in neutrophils.
in the urine with amyloidosis of the kidneys, which often develops in patients with fibrous-cavernous pulmonary tuberculosis, the protein content is usually high.
Treatment. Prior to the use of chemotherapy, the average life expectancy of such patients was limited to 2-3 years. At present, there are all possibilities to prevent the development of the fibrous-cavernous process. To do this, at the very beginning of a particular form of the disease, good contact between the doctor and the patient must be established. It is equally important that the doctor achieves the full implementation of his appointments and prescriptions regarding the regimen, the time of taking medications. An authoritative doctor can and should convince the patient to give up bad habits (alcohol abuse, smoking, etc.).
Patients in whom fibro-cavernous tuberculosis has not been prevented in a timely manner can also be effectively treated. Their treatment should be complex, continuous and long. If patients have resistance or intolerance to the main drugs, 2nd-line antibacterial drugs should be carefully selected.
The healing of cavities with a fibrous wall always proceeds very slowly. If necessary, general therapy is supplemented with surgical intervention. With a one-sided process and good functional indicators, a lung resection of various sizes is performed. Currently, operations with a bilateral process also give quite satisfactory results in most cases: the patient retains his ability to work, his life expectancy is significantly lengthened, and the release of mycobacteria stops.
3.2.10. CIRRHOTIC PULMONARY TUBERCULOSIS
A summary of the pathological anatomy of tuberculosis is presented in section 1.4.
Clinical manifestations of cirrhotic tuberculosis are diverse. The most characteristic complaints of patients are progressive dyspnea and cough with sputum. If at the beginning of the disease shortness of breath appears during physical exertion, then in the future it occurs even at rest. Hemoptysis and pulmonary hemorrhages occur when angioectasias rupture.
Temperature increase associated with exacerbation of chronic pneumonia or bronchiectasis.
Hemogram changes are caused by exacerbations of pneumonia: moderate leukocytosis, ESR acceleration up to 20-30 mm/h.
When examining the patient, there is a deformation of the chest, it is flattened, the ribs are beveled, the intercostal spaces are narrowed. There is a sinking of the supraclavicular and subclavian fossae, the lower parts of the chest are emphysematously expanded. In patients with unilateral cirrhosis, the displacement of the trachea towards the affected lung is determined.
Percussion over the area of cirrhosis, the pulmonary sound is shortened. Above the areas of emphysematous lung tissue, a box tone of sound is determined.
auscultatory weakened hard or bronchial breathing and dry, scattered, wheezing rales are heard. Above the bronchiectatic cavities, sonorous moist rales with a “creaky” shade characteristic of cirrhosis are heard. With unilateral cirrhosis, the boundaries of relative cardiac dullness are shifted towards the affected lung.
For x-ray picture Unilateral cirrhosis is characterized by the presence of a massive darkening, occupying a whole lobe of the lung. The cirrhotically wrinkled lobe of the lung is reduced in volume, its lower border is determined 1-2 intercostal spaces higher. The root on the side of the lesion is pulled up and displaced outwards. On the side of the lesion, there is a narrowing of the lung field, an oblique course of the ribs. The mediastinal organs are displaced to the affected side (Fig. 3-31, 3-32).
With bilateral cirrhosis, a diffuse decrease in the transparency of the lung fields is radiologically determined; darkening is presented in the form of intertwining, clearly defined linear
shadows. The pulmonary roots are pulled up, and the heart suspended from them has a “drip/hanging” shape.
Rice. 3-31. Cirrhotic pulmonary tuberculosis (plain radiograph). Massive cirrhosis of the entire right lung, mediastinal shift to the right
Rice. 3-32. Cirrhotic pulmonary tuberculosis (plain radiograph). Massive cirrhosis of the upper parts of the left lung, mediastinal shift to the left
Purely cirrhotic forms of the tuberculous process are rare. Most often, there are peculiar forms of cavernous
but-cirrhotic tuberculosis, when, along with massive cirrhosis in the lungs, decay cavities of various sizes and shapes can be detected. These can be cleaned old cavities, and cavities that retain specific inflammatory changes in their walls, and bronchiectasis cavities. Such processes lead to the exclusion of the lung from the act of breathing and the complete loss of its function, such a lung is called a “destroyed lung”.
Morphological picture of the "destroyed lung" tuberculosis etiology is characterized by a 2-3 times decrease in lung size compared to the norm, lung compaction, fusion and thickening of the pleural sheets. "Destroyed lung" develops on one side, most often the left.
Alveolar lung tissue almost completely replaced by fibrous. Against the background of fibrotic changes, there are small and medium-sized cavities, multiple bronchiectasis. Sometimes one or two large cavities are observed against a cirrhotic background.
Depending on the sclerotic changes in the lung parenchyma and cavitary formations, three types of "destroyed lung" of tuberculous etiology can be distinguished:
1. Cavernous-cirrhotic type - one large, “leading” cavity is visible against a cirrhotic background.
2. Polycavernous-cirrhotic type - the presence of many small cavities against the background of cirrhosis of the rest of the lung.
3. Pneumato-cirrhotic type - complete replacement of the lung parenchyma with fibrous tissue with a large number of bronchiectasis and small residual cavities.
Treatment should be carried out in the following areas:
1) treatment of the underlying pulmonary process;
2) improvement of bronchial patency (bronchodilators, expectorants);
3) treatment of pulmonary heart failure. The principles of tuberculosis treatment are presented in Chap. 5. Prevention tuberculous cirrhosis consists in the correct and
timely treatment of pulmonary tuberculosis.
3.2.11. TUBERCULOSIS PLEURITIS (INCLUDING EMPIEMAS)
The diagnosis of pleurisy is established by a combination of clinical and radiological signs, and the nature of pleurisy is determined by the results of a study of diagnostic material obtained by puncture of the pleural cavity or biopsy of the pleura.
A summary of the pathological anatomy of tuberculosis is presented in section 1.4.
Pleurisy may be the first clinical manifestation of tuberculosis, especially in adolescents and young adults. Often it develops in primary tuberculosis. Pleurisy may be the only clinical manifestation of the disease when it occurs in the presence of latent fresh foci located in the lungs subpleurally, or foci in the lymph nodes.
Clinically, pleurisy is divided into dry and exudative.
According to clinical manifestations, pleurisy is divided into acute, subacute and chronic.
According to localization, the following pleurisy is distinguished:
a) bone-diaphragmatic;
b) diaphragmatic;
c) costal;
d) interlobar;
e) paramediastinal;
e) apical.
More often, the effusion is located in the pleural cavity freely, but it can also be encysted.
Dry (fibrinous) pleurisy is an inflammation of limited areas of the pleura with the deposition of fibrin on its surface. The main clinical manifestations are chest pain, dry cough, impaired general condition and subfebrile temperature. Localization of pain depends on the location of the lesion. Pain is aggravated by deep breathing, coughing and pressure on the intercostal space.
On physical examination patients revealed lagging of the affected side of the chest during breathing, a slight dullness of the percussion tone.
auscultatory: the main diagnostic sign is a pleural friction noise, which increases with pressure with a stethoscope and does not disappear after coughing.
Blood analysis in patients with pleurisy, it reveals moderate leukocytosis, a shift of neutrophils to the left and an acceleration of ESR.
On x-ray examination restriction of mobility of the dome of the diaphragm is revealed, the contours of the diaphragm become uneven, the transparency of the affected parts of the lungs decreases.
Dry pleurisy proceeds favorably and ends with healing. Sometimes it becomes recurrent. Antibacterial treatment is carried out according to standard schemes, depending on the resistance of the MBT and the body's tolerance to anti-tuberculosis drugs.
Exudative (serous) pleurisy is a common form of pleurisy of tuberculous etiology. It begins gradually with general malaise, weakness, periodic chest pains, occasionally with a cough, subfebrile temperature. Then the temperature rises, chest pain intensifies, shortness of breath appears. As exudate accumulates, shortness of breath increases due to the collapse of the lung and pressure on the mediastinal organs.
Relatively rarely, pleurisy begins in a period of complete health with chills, high fever, chest pain, dry, painful cough.
The course of acute serous pleurisy of tuberculous etiology can be divided into three periods: exudation; process stabilization; effusion resorption.
On physical examination patients with pleurisy, in the phase of exudation, there is a limitation of the respiratory excursion of the affected side, smoothness of the intercostal spaces and even their bulging with large amounts of fluid. Dullness of percussion sound is characteristic with an upper border in the form of an Ellis-Damoiseau oblique line, which goes up from the spine, reaches the top point along the axillary lines and then descends in front along the anterior wall of the chest. The displacement of the mediastinal organs to the healthy side is usually observed when a large amount of fluid accumulates in the pleural cavity.
Phases of stabilization and resorption of exudate characterized by the subsidence of signs of the disease, a decrease in temperature, a decrease in pain and shortness of breath. Objective pathological symptoms gradually disappear, but a pleural friction rub may appear.
Hemogram changes in the acute phase, they are characterized by the presence of leukocytosis (up to 12,000-15,000), lympho- and eosinopenia, a neutrophilic shift to the left, and an ESR acceleration of up to 50-60 mm/h. When the process subsides, blood counts return to normal.
With exudative pleurisy, there are significant changes in the proteinogram. In the acute phase, the amount of albumin decreases and globulins increase. With the involution of the process, the normal content of globulins is restored.
If fluid accumulates above the diaphragm, then during x-ray examination the patient in an upright position, it is often not visible. In such cases, examination in the lateral position is necessary. With an increase in effusion, a homogeneous darkening appears in the region of the external sinus. The lung pattern is poorly differentiated. Free fluid can move depending on the position of the patient's body. Pleural fluid can accumulate in the interlobar fissures, paramediastinally and in the dome of the diaphragm, where blackout is determined during a polypositional x-ray examination (Fig. 3-33, 3-34).
Rice. 3-33. Left-sided exudative pleurisy (general view)
Rice. 3-34. Pleural layers (general view). Residual changes after pleurisy, left
To determine the nature of the exudate and etiology pleurisy is extremely important is the study of pleural effusion. Serous effusion in tuberculosis is usually transparent, yellowish in color, with a specific gravity of 1015 to 1025 and a protein content of 3-6%. In the acute phase of exudation, lymphocytes predominate in the effusion (50-60%),
there is a small amount of eosinophils, erythrocytes and mesothelial cells.
In tuberculosis, cholesterol pleurisy can be observed with a yellow-green or brown effusion containing a significant amount of cholesterol. Such effusions are formed during a very long course of serous pleurisy (up to 20 years), when there is a breakdown of cellular elements containing a lot of cholesterol.
Purulent tuberculous pleurisy (pyothorax, pleural empyema)
Purulent pleurisy characterized by the accumulation of purulent exudate in the interpleural fissure. In addition to tuberculosis, the cause of purulent pleurisy in a patient with tuberculosis can be a lymphohematogenous spread of pyogenic infection in various purulent and infectious diseases. Non-tuberculous empyema in these cases may retain its character until cured or quickly turn into a mixed one as a result of an exacerbation of the tuberculous process.
Tuberculous lesion of the pleura with the formation of purulent exudate often develops with severe progression of serous and hemorrhagic pleurisy or occurs when a cavity breaks into the pleural cavity. Tuberculous empyema can be chronic. At the same time, the patient's condition worsens, the temperature rises, chills, night sweats, shortness of breath, and weight loss appear.
Empyema is especially severe with primary caseous pleurisy and violation of the integrity of the cavity, when bronchopleural fistulas are formed. With prolonged accumulation of a large amount of pus in the pleural cavity, a pleurothoracic fistula may also form.
Chronic empyema leads to the development of amyloidosis of internal organs. With purulent pleurisy, there are pronounced shifts in the leukogram and proteinogram, hypochromic anemia develops. Mycobacterium tuberculosis is found in purulent exudate in 90% of cases.
Differential diagnosis should be carried out in relation to:
1) pleurisy with nonspecific pneumonia;
2) pleurisy with collagenoses;
3) pleurisy of a tumor nature;
4) primary cancer of the pleura.
A very effective research method is currently a biopsy of the parietal pleura with a needle, and a valuable diagnostic method is pleuroscopy.
Antibacterial therapy tuberculous pleurisy - the main method of treatment. In the acute period of the disease, bed rest, good nutrition with restriction of carbohydrates, salt and liquid are indicated, food should be rich in proteins, fats and vitamins (especially vitamin C).
The principles of tuberculosis treatment are presented in Chap. 5.
Treatment effectiveness increases with the use of corticosteroid hormones in the initial phase of the disease for 3-4 weeks. During the period of resorption of pleurisy, electrophoresis treatment with calcium preparations and breathing exercises are prescribed.
With purulent pleurisy systematic and frequent evacuations of pus with washing of the pleural cavity and the introduction of antibiotics into the pleural cavity are necessary. Treatment of patients with chronic tuberculous or mixed empyema is complex. In the absence of the effect of therapeutic methods, especially in the presence of a bronchial fistula, surgical treatment is advisable.
3.2.12. TUBERCULOSIS OF THE BRONCH, TRACHEA, UPPER RESPIRATORY WAYS
There are three main forms of tuberculosis of the bronchi and trachea: infiltrative; ulcerative; fistulous (lymphobronchial, bronchopleural fistulas).
Of the complications it should be noted stenoses of varying degrees, granulations, broncholiths.
Under the influence of treatment, a clinical cure can occur without residual changes and with residual changes in the form of scars, fibrous thickenings, stenosis, etc.
Tuberculosis of the mouth, tonsils and tongue
Oral tuberculosis is rare. If tuberculosis occurs, it is usually localized on the gums. Tuberculosis of the oral cavity is manifested by relatively painless, often ulcerative swellings, sometimes accompanied by an increase in regional lymph nodes.
Tuberculous infections of the oral cavity and tonsils are similar, occur in connection with the consumption of infected milk or other food infected with tuberculosis, or by airborne droplets. Tuberculous lesions of the tonsils may not be clinically manifested.
Tuberculosis of the tongue can be both primary and secondary in advanced pulmonary tuberculosis. Tuberculous lesions on the tongue often ulcerate and can be very painful. They respond well to chemotherapy.
Clinic.
1. The patient may have cough and sputum for some time, since tuberculosis of the larynx, pharynx occurs with severe pulmonary tuberculosis. Weight loss and other symptoms of intoxication may also be observed.
3. Pain in the ear.
4. Pain when swallowing, which is a sign of damage to the epiglottis. The pain may be intense.
5. In severe tuberculosis, specific lesions of the tongue may ulcerate.
6. Examination may reveal ulceration of the vocal cords or other areas of the upper respiratory tract.
7. Sputum examination reveals the presence of MBT.
8. A chest x-ray for tuberculosis reveals lung involvement.
Differential diagnosis. The main disease with which it is first of all necessary to carry out a differential diagnosis is cancer. Malignant cancer of the larynx is rarely painful. MBT is usually found in sputum, but a biopsy may be necessary to diagnose the tuberculous nature of the disease. If a biopsy is not possible, diagnostic specific therapy is prescribed.
Treatment. Tuberculosis of the larynx responds well to chemotherapy. If there is significant pain that is not relieved by specific treatment, prednisolone is prescribed, if possible, for faster resolution of inflammatory changes.
3.2.13. RESPIRATORY TUBERCULOSIS COMBINED WITH OCCUPATIONAL LUNG DISEASES (CONIOTUBERCULOSIS)
Term "coniotuberculosis" consists of 2 words (coniosis- Greek. conia or conis- dust, ashes) - dusting and tuberculosis.
This group includes all forms of pulmonary tuberculosis with the simultaneous presence of dust occupational diseases: silicosis, asbestosis, etc. When formulating a diagnosis, one should first write coniotuberculosis, then give a detailed description of coniosis - anthracosis, silicosis, etc. and a detailed description of the tuberculosis process.
Coniotuberculosis belongs to a large group of pulmonary diseases - pneumoconiosis. Pneumoconiosis is caused by continuous long-term inhalation of certain types of dust particles and can result in peribronchial fibrosis, disability, and even death.
Classification of dust occupational lung diseases
Depending on the nature of the inhaled dust, up to six types of pneumoconiosis are distinguished.
1. Silicosis- a disease caused by the inhalation of dust containing free silicon dioxide (SiO 2).
2. silicatoses- arise from the inhalation of dust of silicates containing silicon dioxide in a bound state.
3. Metalconiosis- conioses arising from the inhalation of dust of rare earth hard and heavy alloys.
4. Carboconioses- diseases are the result of inhalation of carbonaceous dust.
5. Pneumoconiosis- due to inhalation of mixed dust, including those containing free silicon dioxide.
6. Pneumoconiosis- occur when organic dust is inhaled (cotton, grain, cork, cane koniosis).
Pneumoconiosis have a similar pattern of changes in the lungs. The most characteristic picture gives silicosis. However, there are no distinguishing features between the two types of pneumoconiosis. Pneumoconiosis masses can be detected in the lung by microscopic examination. Thus, the specific cause of pneumoconiosis can be determined using specific diagnostic methods. For example, silicone
for the brief information on the pathogenesis, clinic and diagnosis of pneumoconiosis.
The most common cause of silicosis is quartz, so any dust is harmful depending on the amount of quartz it contains. Only the smallest quartz particles, 10 microns in size or less, can cause disease.
The most common complication of silicosis is tuberculosis - silicotuberculosis.
Epidemiology. Tuberculosis is 3-7 times more likely to develop in persons with manifestations of silicosis than in persons without its manifestations (when working under the same conditions). According to average estimates, 20-25% of patients with silicosis develop tuberculosis during their lifetime.
Tuberculosis is one of the important factors in the mortality of patients with silicosis. With the same radiological manifestations of silicosis, the risk of death is higher in patients with tuberculosis.
Epidemiological and experimental data suggest that exposure to dust containing quartz, even in the absence of radiographic evidence of silicosis, is a factor in the increased prevalence of pulmonary tuberculosis.
Pathogenesis. Several pathogenic processes are common to both tuberculosis and silicosis, co-involving in the accelerated development of fibrosis and in the increased susceptibility to mycobacterial infection or reactivation of the site of latent infection. The quartz particles are phagocytosed by alveolar macrophages. Within these cells, quartz particles are exposed to phagolysosomes. Quartz has the ability to damage the cell membrane, leading to the death of the macrophage and the entry of the released particles into other macrophages.
Presumably, humoral and cell-mediated immune responses are suppressed by silicosis. Cell-mediated immunity is an important factor in suppressing the reproduction of mycobacteria. Fibrosis of the lung tissue, which develops with tuberculosis and silicosis, leads to impaired removal of macrophages containing dust particles or mycobacteria from the lungs. Violation of the activity of the lymphatic system contributes to the accumulation of macrophages in the intermediate lung tissue.
If the process continues, small round nodules or tangles of collagen develop in the lungs, forming along the
lymphatic tracts. As the disease progresses, these clear-cut structures give way to large patchy areas of fibrosis or collagen accumulations in all areas of the lung. Large accumulations of collagen are found in the upper sections of the lower lobes of the lungs.
Clinic. Manifestations of tuberculosis in patients with silicosis have no features. Since fatigue, shortness of breath, and night sweats are observed with silicosis, it is difficult to detect clinical manifestations of associated tuberculosis.
Diagnostics. Most often, focal, disseminated tuberculosis and tuberculoma are combined with silicosis. The diagnosis of active tuberculosis in patients with silicosis requires high vigilance.
The presence of tuberculosis in a patient with silicosis should be suspected in cases where x-ray changes are noted in the apical regions of both lungs. These manifestations are characterized by poorly demarcated infiltrates of various sizes that do not cross the boundaries of the lobes of the lung. Seals of lung tissue may surround pre-existing silicotic formations. The presence of caverns in the area of silicotic changes is a sign of tuberculosis. The formation of cavities in the absence of tuberculosis is so rare that from a practical point of view, any evidence of lung destruction can be taken as a sign of tuberculosis.
Signs indicating the possible presence of tuberculosis in patients with silicosis:
1) the location of the pulmonary pathology in the upper sections of the lungs;
2) the presence of decay;
3) relatively fast dynamics of the process;
4) the presence of pleural effusion.
Establishing the diagnosis of pulmonary tuberculosis in a patient with silicosis by bacteriological methods is difficult. Therefore, regular microscopy for the presence of acid-fast mycobacteria in sputum is recommended.
Treatment. There are no fundamental differences in the treatment of coniotuberculosis and tuberculosis. Tuberculosis associated with silicosis is recommended to be treated with standard regimens (see Chapter 5).
Prevention. Since tuberculosis is very common among patients with silicosis, anti-tuberculosis chemoprophylaxis is indicated for them.
Any complications such as tuberculosis, emphysema, spontaneous pneumothorax or dilatation of the heart give a very poor prognosis in patients with silicosis.
3.2.14. RUSSIAN CLINICAL CLASSIFICATION OF TUBERCULOSIS AND CODES (ICD-10)
In most countries of the world, the International Statistical System for Recording Diseases and Problems of the Tenth Revision (ICD-10), approved by the World Health Organization (WHO), is used.
The basis of the ICD-10 is an alphanumeric code for coding diseases, in which the first character is denoted by a letter, the next three by numbers. The letter denotes the classes (there are 21 in ICD-10), the first two digits are the block. For greater detail, a fourth character has been introduced - the number after the dot.
The use of the ICD-10 ensures the unity of the collection of information and the comparability of materials on public health, the prevalence of diseases and their epidemiology both within the same country and in different countries of the world. ICD-10 makes it possible to convert verbal formulations of diagnoses into alphanumeric codes that provide computer storage of information and its accumulation. The use of ICD-10 creates the conditions for automating information about human health. This allows for a comprehensive in-depth comparative analysis of data, including an assessment of the quality of health care in different regions of the country and the completeness of information collection.
A15-A16 Tuberculosis of the respiratory organs.
A15 Tuberculosis of the respiratory organs, confirmed bacteriologically and histologically.
A16 Tuberculosis of the respiratory system, not confirmed bacteriologically or histologically.
A17 Tuberculosis of the nervous system.
A18 Tuberculosis of other organs and systems (extrapulmonary localization of tuberculosis).
A19 Miliary tuberculosis.
The Tuberculosis block includes infections caused by M. tuberculosis And M. bovis. Congenital tuberculosis (P37.0), pneumoconiosis associated with tuberculosis (J65), consequences of tuberculosis (B90) were excluded from the Tuberculosis block.
The clinical classification of tuberculosis in Russia largely does not comply with ICD-10. At the same time, the classification used in our country is quite complete, at least currently meets the requirements of Russian phthisiatricians. In this regard, it is very important to adapt the domestic classification of tuberculosis to the ICD-10 and develop an adapted coding option that meets both the requirements of the international classification and domestic phthisiology.
Russian clinical classification of tuberculosis approved by order of the Ministry of Health of Russia? 109 of March 22, 2003
Tables 3-1 and 3-2 of this section present the clinical classification of tuberculosis currently used and the codes recommended for coding diseases according to ICD-10. Some provisions of this classification may be revised in subsequent years. In accordance with this, code signs will also be changed. To accurately record patients with different localizations of tuberculosis, when establishing a diagnosis marked with a special sign (f), additional coding for a different class of disease is required.
The ICD-10 does not provide for coding a number of essential features that Russian phthisiologists use when diagnosing tuberculosis and determining the tactics of managing a patient. In this regard, it is proposed to use additional characters to encode some of the most important features (Table 3-3). Code dictionaries have been developed to indicate the corresponding signs in the domestic clinical classification of tuberculosis in accordance with the ICD-10 code.
Table 3-1. The main clinical forms of tuberculosis
Note. If a term is dual-classified (according to etiology and disease manifestation), both codes are given: the first is followed by a special sign (t) and the second by an asterisk (*).
Table 3-2. Residual changes after cured tuberculosis
Table 3-3. Characteristics of additional signs
Question 7. Secondary tuberculosis
Focal tuberculosis occurs in people aged 20–25 years and older.
To date, there is no unequivocal hypothesis regarding the pathogenesis of focal tuberculosis. Some believe that this is a consequence of exogenous infection (or exogenous superinfection) in a previously infected person. When a fresh portion of Mycobacterium tuberculosis, as a rule, enters the upper lobe, limited foci of inflammation develop, because a person in this case, previously infected or having had some form of primary tuberculosis in childhood, becomes infected with a weakly virulent strain against the background of good reactivity of the organism. A number of experts believe that this is a consequence of retrograde lymph flow in persons who had tuberculosis of the lymph nodes in childhood, in which residual changes remained after tuberculosis in the form of petrificates, and at some stage, when the reactivity of the body falls (due to stressful situations, respiratory diseases), Mycobacterium tuberculosis is released from petrificates, which are brought into the upper segments of the lungs with a current of lymph. According to the first hypothesis, focal tuberculosis is the result of exogenous infection, according to the second - endogenous.
The focus is a pathomorphological concept. The focus is such a focus of inflammation, which does not exceed 10 mm in size. Pathologists divide them into small (within 3-5 mm), medium (5-8 mm), large (10 mm). With focal tuberculosis, these foci cannot be more than 10 mm, because in this process the nature of the inflammation is productive. There are tuberculous tubercles here, in which there is a large number of epithelioid cells, delimiting caseous small foci containing Mycobacterium tuberculosis. Given that these changes are localized, these foci are limited in scope, and, accordingly, the clinical symptoms in focal tuberculosis are very, very poor. Morphological changes are localized in the I and II segments of the right, less often the left, lung and are characterized by the presence of one or two Abrikosov reinfection foci. The process is usually one-sided. With timely treatment, the process subsides, the exudative tissue reaction is replaced by a productive one, the foci of caseous necrosis are encapsulated and petrified, Ashoffpool foci appear, and the process may end there.
2. Infiltrative tuberculosis develops with the progression of acute focal, while exudative changes go beyond the segment. Infiltrative pulmonary tuberculosis is areas of tuberculous bronchopneumonia larger than 1.0-1.5 cm, formed within the lobular structure of the lung. It belongs to the secondary period of tuberculosis, develops, as a rule, against the background of already existing fresh or already healed foci of inflammation.
In the morphological characteristics of round infiltrates, the specific granulation part significantly predominates over the caseous part, and there is almost no perifocal exudative reaction. Such a focus is called the Assmann-Redeker infiltrate focus, after the scientists who first described its x-ray picture. Nonspecific perifocal inflammation can resolve, and then during the healing period, only one or two non-resolved small caseous foci remain, which are subsequently encapsulated. When inflammation covers the entire lobe, they speak of lobitis as a special form of infiltrative tuberculosis.
3. Caseous pneumonia observed with the progression of infiltrative tuberculosis, as a result of which caseous changes begin to predominate over perifocal ones. Acinous, lobular, segmental caseous-pneumonic foci are formed, which, when merged, occupy larger areas of the lungs and even the entire lobe. Caseous pneumonia, which developed against the background of lobit, has a lobar character. It is observed in debilitated patients and always against the background of older changes (fibrous-focal, infiltrative-pneumonic tuberculosis or tuberculoma). Caseous pneumonia usually occurs in the terminal period of any form of tuberculosis, which is facilitated by the weakening of the body's defenses. The lung with caseous pneumonia is enlarged, dense, on the cut it is yellow in color, fibrinous overlays are found on the pleura.
4. Tuberculoma- a form of secondary tuberculosis, which develops as a kind of phase in the evolution of infiltrative tuberculosis, when the perifocal inflammation resolves and a focus of cheesy necrosis remains, surrounded by a mild capsule. Tuberculoma is an encapsulated area of specific inflammation with a diameter of more than 1 cm (can reach 2-5 cm), which is located in segments I and II, more often on the right. In the structure of the incidence of pulmonary tuberculosis, it is 10-15%. It is more common in men aged 20-40. Tuberculomas occur in people with local hyperergy and high body resistance, which is expressed by the restriction of the pathological process in the lung from healthy tissue to a fibrous capsule. The patho- and morphogenesis of tuberculomas is different. They may occur in the primary period of infection, but are more characteristic of secondary tuberculosis. According to the nature of pathomorphological changes, 3 main types of tuberculomas are distinguished (M. M. Averbakh, 1976):
1) infiltrative-pneumonic type;
2) caseoma;
3) type of filled cavity (pseudotuberculoma).
Infiltrative-pneumonic tuberculoma is more often formed from infiltrative tuberculosis, less often from focal and disseminated. Pseudotuberculoma is formed from a cavity when the draining bronchus is closed or obliterated by an inflammatory or cicatricial process. In contrast, caseoma can be considered a "true" tuberculoma, since it occurs in the lungs as an independent form of tuberculosis without any previous forms. According to the anatomical structure, caseomas can be:
1) homogeneous, consisting of caseous masses and enclosed in a fibrous capsule;
2) layered, in which concentric tuberculomas are caused by a sequence of processes of perifocal caseous pneumonia and its connective tissue fibrous encapsulation;
3) conglomerate, formed by the merger and encapsulation of several small foci.
Question 8. Secondary tuberculosis
Cavernous tuberculosis is a form of the disease, which is characterized by the rapid formation of a decay cavity and a cavity at the site of an infiltrate focus or tuberculoma. The cavern in this form of tuberculosis is localized in the I or II segment, has an oval or round shape, 2–5 cm in diameter, and communicates with the lumen of the segmental bronchus. The wall of the cavity is heterogeneous, its inner layer consists of caseous masses, the outer layer consists of lung tissue compacted as a result of inflammation.
Destruction (cavity) is formed in the center of tuberculous inflammation, where, under the influence of proteolysis and fibrinolysis, there is a melting and subsequent rejection of caseous-necrotic masses through the draining bronchus, which creates an open path for the release of mycobacteria into the external environment and their introduction into other segments of the same or another lung. . The place of the rejected caseosis is filled with air and the lung tissue defect is seen on the X-ray film in the form of a clearing inside the blackout area.
From a morphological point of view, pneumopyogenic, bronchogenic and hematogenous cavities are distinguished. The walls of pneumopyogenic cavities that form in areas of tuberculous bronchopneumonia are non-rejected caseous-necrotic masses hanging into the lumen of the cavity. A bronchogenic cavity often occurs against the background of fibrous-focal pulmonary tuberculosis and is formed from a bronchus affected by a tuberculous process. In such a cavity, a layer of caseous necrosis and granulation is poorly represented with a good level of connective tissue development. Hematogenous caverns occur only in the subacute course of hematogenous disseminated tuberculosis due to impaired vascularization, when melting and rejection of necrotic masses occur in areas of aseptic necrosis with the formation of a thin-walled cavity, the wall of which is mainly represented by granulations.
These 3 variants of decay cavities have different epidemiological and prognostic severity. The pneumopyogenic cavity, surrounded by a wide layer of caseosis that has not yet been rejected, is a source of constant massive bacterial excretion, but the absence of sclerotic changes and the preservation of the vascular bed provide it with a high efficiency of treatment with anti-tuberculosis drugs. A bronchogenic cavity with a thin layer of caseosis secretes tuberculosis bacteria only periodically and in scant amounts, but, developing in a sclerotically altered, sharply deformed lung tissue, it is weakly amenable to drugs, quickly forms a fibrous capsule and often needs surgical treatment, despite its small size ( more than 1.0–1.5 cm in diameter). A hematogenous or stamped cavity practically does not contain caseous masses and is not accompanied by bacterial excretion. Tuberculous inflammation in the granulations surrounding the cavity is represented by separate productive tubercles. With the progression of the process, a caseous layer appears on the inner surface of the granulations, and fibrous tissue along their periphery. Thus, a tuberculous cavity with a typical three-layer wall structure is formed. Any manifestation of destructive tuberculosis is characterized by the presence of a direct radiological sign of a cavity in the lung tissue in the form of an area of enlightenment, limited by a closed blackout around the entire perimeter, while maintaining this isolation in two mutually perpendicular projections: direct and lateral. At the same time, for the decay phase or for the emerging cavity, the width of the boundary darkening is characteristic, having an average intensity of more than 0.5 cm; and the shape of the enlightenment itself is irregular with fuzzy bay-shaped inner outlines. In addition to the indicated radiographic characteristics of a cavity that has recently arisen in the lung tissue, other radiological and clinical symptoms are also detected that are characteristic of earlier forms of pulmonary tuberculosis. At the same time, in the cavernous form of pulmonary tuberculosis, which represents a later stage in the development of a specific process, the clinical and radiological features inherent in the previous forms of pulmonary tuberculosis completely disappear, and a relatively isolated cavity remains in place of the former process, which radiologically is characterized by a rounded shape, even and clear internal contours with a width of the surrounding darkening exceeding 0.5 cm. There are no pronounced focal, infiltrative changes in the surrounding sections of the lung tissue, with poor or negative physical symptoms from the respiratory organs, clinical manifestations are mild.
2. Fibrous-cavernous tuberculosis(chronic pulmonary consumption) develops from acute cavernous tuberculosis, when the process becomes chronic. Fibrous-cavernous pulmonary tuberculosis is the final phase of the development of any initial process during its progression. The formation of fibrous-cavernous tuberculosis from previous forms of the disease can occur gradually, sometimes for years. Over time, the original forms of pulmonary tuberculosis, passing through various stages of their development in the form of a phase of infiltration, decay, bronchopulmonary seeding, transforming into a cavernous form, may lose their morphological and clinical and radiological signs and acquire the features of fibrous-cavernous tuberculosis. So, for example, as a result of repeated exacerbations of the cavernous form of pulmonary tuberculosis, a gradual thickening of the cavity wall occurs due to a more pronounced development of connective tissue in it, the appearance of numerous stringy shadows in areas of the lung tissue adjacent to the cavity, a decrease in transparency in the upper sections of the affected lung due to thickening of the apical pleura with the development of signs of pleurogenic fibrosis, which usually indicates the transition of cavernous pulmonary tuberculosis to fibrous-cavernous. The wall of the cavity becomes dense, it is built from 3 layers: the inner one is pyogenic, rich in decaying leukocytes, the middle one is a layer of tuberculous granulation tissue, the outer layer is connective tissue. Morphological changes are expressed in the right lung, the cavity occupies one or both segments, filled with purulent contents and a large number of mycobacteria.
In patients with fibrous-cavernous tuberculosis, the lung tissue is characterized by the appearance of an old or fibrous cavity, in the wall of which the granulation tissue is replaced by connective tissue. The inner surface of such a cavity is only in places covered with curdled masses, and sometimes with tuberculous granulations.
The result of the progression of the fibrous-cavernous process is the appearance in other segments of the affected and opposite lung of foci of bronchogenic seeding of active tuberculous changes in the bronchi. Gradually, the process from a relatively limited becomes more and more widespread, polysegmental. In addition, morphological changes in the lung tissue are formed due to the development of gross structural changes with the growth of connective tissue in the parenchyma, interstitium, along the interalveolar and interlobular septa, bronchi and vascular trunks. Due to the involvement of the visceral and parietal pleura in them, perifocal inflammation first occurs, followed by the formation of tubercles, foci, and then limited or widespread planar adhesions (mooring).
Question 9. Clinical classification of tuberculosis. Clinical forms of primary tuberculosis
1. Main clinical forms
Group 1st. Primary tuberculosis:
1) pre-local: tuberculosis intoxication in children and adolescents;
2) local:
a) tuberculosis of intrathoracic lymph nodes;
b) primary tuberculosis complex.
Group 2. Secondary: tuberculosis of the respiratory organs (tuberculosis against the background of previous primary tuberculosis):
1) miliary;
2) disseminated;
3) focal;
4) infiltrative;
5) caseous pneumonia;
6) tuberculoma;
7) cavernous;
8) fibrous-cavernous;
9) cirrhotic.
Group 3. Tertiary: tuberculosis of other organs and systems:
1) tuberculosis of the meninges and central nervous system;
2) tuberculosis of the intestine, peritoneum and mesenteric lymph nodes;
3) tuberculosis of bones and joints;
4) tuberculosis of the urinary, genital organs;
5) tuberculosis of the skin and subcutaneous tissue;
6) tuberculosis of peripheral lymph nodes;
7) tuberculosis of the eye;
8) tuberculosis of other organs.
Group 4th. Separate forms:
1) tuberculous pleurisy;
2) pleural empyema;
3) sarcoidosis.
Characteristics of the tuberculosis process
Localization and extent: in the lungs by lobes and segments, and in other organs - by the location of the lesion.
a) infiltration, decay, seeding;
b) resorption, compaction, scarring, calcification.
Bacterioexcretion:
a) with the isolation of Mycobacterium tuberculosis (MBT+);
b) without isolation of Mycobacterium tuberculosis (MBT-).
Complications:
hemoptysis and pulmonary bleeding, spontaneous pneumothorax, pulmonary heart failure, atelectasis, amyloidosis, renal failure, bronchial, thoracic fistulas, etc.
Residual changes after pulmonary tuberculosis:
a) respiratory organs: fibrous, fibrous-focal, bullous-dystrophic, calcifications in the lungs and lymph nodes, pleuropneumosclerosis, cirrhosis, condition after surgery, etc.;
b) changes in other organs: cicatricial changes in various organs and their consequences, calcification, condition after surgical interventions.
In accordance with the clinical classification of tuberculosis, the diagnosis is formulated as follows. Indicate the clinical form of tuberculosis, the localization of the lesion by lobes or segments, then characterize the phase of the process, the presence (MBT+) or absence (MBT-) of bacterial excretion, complications. For example: infiltrative tuberculosis of the VI segment of the right lung in the phase of decay and seeding; MBT+; hemoptysis.
2. Primary tuberculosis complex is a local form of primary tuberculosis, consisting of 3 components: primary pulmonary affect, glandular component - lymphadenitis and inflammatory path - lymphangitis, connecting both components.
Clinical symptoms depend on the size of the caseous focus, the severity of the zone of perifocal inflammation, and also on the degree of involvement of intrathoracic lymph nodes in a specific process. In cases where the size of the primary focus is small, the area of perifocal infiltration is absent or unsharply represented, changes in the intrathoracic nodes are limited, the clinical manifestations of the primary tuberculosis complex are erased and oligosymptomatic. In some cases, the primary complex has an asymptomatic course and is detected already in the calcification phase. It is customary to distinguish between smooth and complicated course. A clinically pronounced primary tuberculous complex corresponds to the infiltration phase of a specific process. According to the nature of the onset of the disease, it is divided into influenza-like, pneumonic and typhoid forms. With the severity of the infiltration phase of the primary complex, an acute onset of the disease is more often noted, which is accompanied by general signs of intoxication: a rise in temperature to febrile numbers, a decrease in appetite, lethargy, and fatigue. In some cases, the primary complex may have a gradual development (over several weeks, and sometimes months), while the infected person becomes lethargic, emotionally labile, there is a decrease in appetite, a decrease in body weight, subfebrile condition of the wrong type is noted when measuring temperature. In some infected individuals, the primary complex may have a latent course and is detected as a result of a preventive study. The patient during the period of temperature rise can maintain a relatively satisfactory state of health, which is typical for a specific process. In some cases, one can note a runny nose, redness in the throat, a slight cough, which is explained by the development of paraallergy in tuberculosis.
On examination, pallor of the skin, a decrease in turgor, and body weight are revealed. Peripheral lymph nodes are palpable in more than 5 groups, soft elastic consistency, mobile, painless, enlarged to the size of a pea or more. Percussion changes in the primary tuberculous complex prevail over auscultatory ones: a shortening of the percussion sound or its dullness is determined over the site of infiltration in the lung tissue. The same percussion data correspond to regional intrathoracic lymph nodes. When listening over the zone of shortening of the percussion sound, the weakening of breathing with an extended exhalation is determined. With fresh processes in a limited area, moist small bubbling rales are occasionally heard. As the resorption of perifocal phenomena and the compaction of the primary focus, dullness decreases, breathing becomes more rigid. On the part of the cardiovascular system, diffuse changes in the myocardium are noted, which leads to an expansion of the boundaries of the heart, arrhythmias, tachycardia, systolic murmur, and a decrease in blood pressure. Abdominal examination reveals enlargement of the liver and spleen.
Laboratory data
Tuberculin diagnostics. A study of the patient's sensitivity to tuberculosis using the Mantoux test with 2TE usually establishes a turn of tuberculin reactions, hyperergy, or a period immediately following the turn.
Patients with primary forms of tuberculosis rarely produce sputum. In this regard, to determine bacterial excretion, bronchial lavage is examined, and in young children, gastric lavage.
In the peripheral blood, moderate leukocytosis, a shift of the leukocyte formula to the left, lymphopenia, eosinopenia, and an acceleration of the erythrocyte sedimentation rate are noted.
X-ray data
X-ray during the primary tuberculosis complex, 4 phases are distinguished:
1) pneumonic, or infiltrative;
2) resorption;
3) seal;
4) calcification.
In the phase of infiltration, the shadow of the primary affect is homogeneous, its contours are blurred. This phase is associated with a pathologically altered root - a path in the form of indistinct linear formations. Changes in the intrathoracic lymph nodes are most often regional in nature and relate to one group. At the same time, a volume increase, or expansion, of the lung root, a violation of the differentiation of its structural elements and blurring of the contours are determined. In the resorption phase, a decrease in the inflammatory response is observed. The shadow of the primary affect decreases in size and becomes heterogeneous due to a decrease in its intensity in the peripheral sections and a more intense area in the center, the contours are fuzzy. The ribbon-like shadow becomes narrower. In the compaction phase, a rounded focus with clear contours, a heterogeneous structure due to the inclusion of lime, is determined. 3-5 linear shadows are kept in the track area. In the calcification phase, intense focal shadows with clear contours appear, not associated with the root. At the site of the pulmonary affect, a center of Gon is formed. Structural elements of the root become differentiated, and sclerotic restructuring in certain parts of the root and partial calcification in regional lymph nodes can be detected.
Clinical examination
If a child has had this disease, then after the end of the main course of chemotherapy in the clinic, he is observed in group I (1–2 years) of dispensary registration, then in group II (1–2 years). At this time, in the autumn-spring months, 2 times a year, the child receives anti-relapse treatment with two drugs in a sanatorium. Then he is transferred to the III group of dispensary registration. With pronounced residual changes in the lungs in the form of large calcifications and pneumosclerosis, children who have undergone a primary tuberculosis complex are observed in the III group of dispensary registration until adulthood.
Among the infectious diseases that lead to death, the most common is pulmonary tuberculosis and its extrapulmonary forms. The causative agent is Mycobacterium tuberculosis, which penetrate into the body of a healthy person mainly by airborne droplets.
Further, mycobacteria, if the human immune forces are weakened, begin to actively multiply and spread throughout the body, affecting the internal organs. If the diagnosis of tuberculosis and the main course of treatment are not carried out in a timely manner, the complications and consequences of tuberculosis may be irreversible. Possible disability of the patient, and in severe cases, death occurs from pulmonary tuberculosis.
Post-tuberculosis changes significantly reduce the patient's quality of life. Therefore, everyone who has been touched by this terrible disease must understand what is dangerous and what causes pulmonary tuberculosis, how to survive it, know the features of tuberculosis treatment methods and signs of pathological abnormalities in case of complications.
The most common complications include chronic non-specific respiratory diseases. Often they talk about the so-called residual changes after tuberculosis. Various formations in the lung tissues, tubercles, seals that remained at the time of the patient's clinical recovery are implied. These are fibroses, scars, (calcifications) of various sizes and shapes, which can either dissolve completely over time, or lead to the development of new complications, for example, pneumothorax (more details below).
Secondary tuberculosis
Often doctors have to deal with the so-called secondary tuberculosis. That is, the focus of infection, which after the treatment was considered extinct, under the influence of certain factors becomes active again and the disease develops again. The cause of secondary tuberculosis in most cases is repeated contact with active mycobacteria, a sharp decrease in immunity due to another disease, stress, injury, and poor lifestyle.
Complications of primary tuberculosis
Atelectasis
Atelectasis occurs as a complication of tuberculous pathology if the treatment was carried out incorrectly or was not completed. Due to blockage of the bronchi, part of the lung collapses. The alveoli of the lung stick together, air does not enter the affected lung. Thus, the process of gas exchange is disturbed, symptoms of respiratory failure develop.
The severity of atelectasis directly depends on which parts of the bronchi are affected. If there is a blockage of the main bronchus, then gas exchange is disturbed throughout the whole part of the lung. If the patency of the small branches of the bronchi is disturbed, then only one segment of the lung collapses. Metatuberculous changes are detected in atelectasis with the following symptoms:
- chest pain;
- bouts of shortness of breath;
- increased heart rate with a decrease in blood pressure;
- cyanosis of the skin.
To stop further pathological changes in the tissues of the lungs, it is first necessary to restore the patency of the bronchi.
pneumosclerosis
Pneumosclerosis is one of the most severe residual changes in pulmonary tuberculosis. As a rule, it develops with advanced atelectasis: the ventilation of the segment of the affected lung is disturbed, as a result, the lung tissues are replaced by connective tissue. Pneumosclerosis is often found after surgery on the lungs, scarring of the affected tissues.
Pneumosclerosis manifests itself with the same symptoms as atelectasis. The most important thing with such a complication is to prevent secondary infection, the formation of a "cellular lung" or heart failure.
Fistulas
Fistulas as a complication of severe tuberculosis are bronchial and thoracic. The fistula is a pathological channel connecting several points of the respiratory system. How clearly the fistula will manifest itself clinically depends on its diameter and anatomical location.
Also plays a role the presence and severity of inflammatory processes in the pleura, as well as the "age" of the fistula. Often, such complications are formed after surgery on the bronchi or lungs. Bronchopleural fistulas may not manifest themselves at all, or make themselves felt only from time to time with bouts of dry cough with the release of a small amount of sputum.
Pneumothorax
This complication is considered more dangerous than the others, but it does not develop so often. It is usually caused by other diseases of the respiratory system, in which the pleura, the inner lining of the lungs, becomes inflamed. is formed when the integrity of the pleura is violated, resulting in a message with the airways. Pneumothorax can be recognized by the following signs:
- Sharp pain in the chest, preceded by sneezing, laughing, coughing, especially violent.
- Dyspnea.
- Attacks of weakness, cold sweat, rapid pulse, pallor of the face.
- Drop in blood pressure, difficult, heavy breathing.
Treatment of pneumothorax is carried out in a hospital, a delay in diagnosis and proper therapy can lead to the death of the patient.
A. MAIN CLINICAL FORMS
Tuberculosis intoxication in children and adolescents.
Tuberculosis of the respiratory organs:
Primary tuberculosis complex;
Tuberculosis of intrathoracic lymph nodes;
Disseminated pulmonary tuberculosis;
miliary tuberculosis;
Focal pulmonary tuberculosis;
Infiltrative pulmonary tuberculosis;
Caseous pneumonia;
Pulmonary tuberculosis;
Cavernous pulmonary tuberculosis;
Fibrous-cavernous pulmonary tuberculosis;
Cirrhotic pulmonary tuberculosis;
Tuberculous pleurisy (including empyema);
Tuberculosis of the bronchi, trachea, upper respiratory tract, etc. (nose, mouth, pharynx);
Tuberculosis of the respiratory organs, combined with dust occupational lung diseases (coniotuberculosis).
Tuberculosis of other organs and systems:
Tuberculosis of the meninges and central nervous system;
Tuberculosis of the intestine, peritoneum and mesenteric lymph nodes;
Tuberculosis of bones and joints;
Tuberculosis of the genitourinary, genital organs;
Tuberculosis of the skin and subcutaneous tissue;
Tuberculosis of peripheral lymph nodes;
Tuberculosis of the eye;
Tuberculosis of other organs.
B. CHARACTERISTICS OF THE TUBERCULOSIS PROCESS
Localization and extent in the lungs: by lobes, segments, and in other organs - by the location of the lesion.
Phase:
Infiltration, decay, seeding;
Resorption, compaction, scarring, calcification
Bacterioexcretion:
With the release of Mycobacterium tuberculosis (BK+);
Without isolation of Mycobacterium tuberculosis (BK-). B. COMPLICATIONS
Hemoptysis and pulmonary hemorrhage. Spontaneous pneumothorax. Pulmonary heart failure. Atelectasis. Amyloidosis.
Fistulas bronchial, thoracic, etc.
D. RESIDUAL CHANGES AFTER CURED TB
Respiratory organs:
fibrous;
Fibrofocal;
Bullous-dystrophic calcifications in the lungs and lymph nodes;
Pleuropneumosclerosis;
Condition after surgery.
Other Bodies:
Cicatricial changes in various organs and their consequences;
Calcification;
Condition after surgery.
Residual changes. The final stage of the formulation of the diagnosis is the characterization of residual changes in cured tuberculosis, which can be in the form of:
Fibrous;
Fibrofocal;
bullous changes;
Calcifications in the lungs and lymph nodes;
Pleuropneumosclerosis;
cirrhosis;
bronchiectasis;
Conditions after surgery.
10.3. TUBERCULOSIS INTOXICATION IN CHILDREN AND ADOLESCENTS
Tuberculous intoxication in children and adolescents occurs when infected with tuberculosis and the development of primary tuberculosis infection without local manifestations, determined by x-ray and other methods of investigation. Tuberculosis intoxication is detected in children (adolescents) with first positive, increasing in the process of observation and hyperergic reactions to tuberculin. It is characterized by the activity of the tuberculous process and is accompanied by a deterioration in the general condition of the child (adolescent), which is expressed in the following:
Periodic increase in body temperature to subfebrile numbers;
Loss of appetite;
The appearance of neurovegetative disorders (increased nervous excitability or its depression, headache, tachycardia);
A slight increase in peripheral lymph nodes (micropolyadenia) with symptoms of periadenitis;
A slight increase in the liver, less often in the spleen;
Stopping physiological gain or lack of body weight;
Tendency to intercurrent diseases;
Change in the picture of peripheral blood (unsharply expressed acceleration of ESR, shift of the neutrophilic formula to the left, esinophilia, lymphopenia);
Change in immunological status (decrease in the number of lymphocytes and their functional activity).
The specificity of the described functional disorders should be confirmed by a thorough examination of the child (adolescent) to exclude nonspecific diseases. During the examination, it is necessary to use modern diagnostic methods, including direct and lateral radiographs, tomograms of the mediastinum in various projections, bronchoscopy, tuberculin provocation tests (hemotuberculin, immunotuberculin, etc.) before and after subcutaneous injection of tuberculin - 10-20 TU PPD-L, as well as bacteriological study.
Diagnosis includes a mandatory examination to exclude rare localizations of tuberculosis with lesions of the abdominal organs or small forms of tuberculosis of the intrathoracic lymph nodes.
Differential diagnosis is carried out with chronic non-specific lesions of the ENT organs, helminthic invasions and other diseases accompanied by signs of a general intoxication syndrome.
General information about the clinical cure of pulmonary tuberculosis.
The criteria for the clinical cure of pulmonary tuberculosis is understood as a set of signs indicating the elimination of active pulmonary tuberculosis, determined by clinical, radiological, laboratory, biological and functional research methods. Spontaneous cure of pulmonary tuberculosis in the anatomical aspect has been established for a long time. Based on the results of the study of sectional material and experimental data, scientists in the 80s of the 19th century established that a completely cured pulmonary tubercles can be considered cured only in cases where only one cicatricial seal or completely calcified curdled nodes remains at the site of the former pathological process. . At the beginning of the 20th century, 3 variants of healing were already distinguished with an outcome in a scar, in a petrificate, or in small epithelialized cavities.
Cure rates for pulmonary tuberculosis in adults.
It is known that the change in the number of contingents of patients with tuberculosis is determined by 2 factors. On the one hand, the contingents are increasing due to newly diagnosed patients and patients with relapses of the disease, on the other hand, the contingents are decreasing depending on the outcomes of treatment, or on the number of cured and deceased patients. Consequently, the rate of decrease in the incidence of tuberculosis in the population depends on the combination of these factors and on which one prevails among them.
The cure factor has a great influence on the reduction of contingents of patients with pulmonary tuberculosis. At the same time, the frequency of cure largely depends on the effectiveness of the treatment methods used.
Clinical criteria for the cure of pulmonary tuberculosis and methods for their determination.
The objective clinical signs characterizing the involution of pulmonary tuberculosis include clinical signs of tuberculosis intoxication and local symptoms of the disease, determined on the basis of complaints and physical methods of investigation.
Clinical signs of tuberculosis intoxication.
Intoxication is expressed in a violation of thermoregulation, a deterioration in the patient's well-being, a decrease in his ability to work, increased fatigue, insomnia or drowsiness, a rapid change in mood: increased irritability or, conversely, apathy, lethargy and indifference to the environment, tearfulness and euphoria. At the same time, signs of autonomic NS dysfunction are often observed: sweating, tachycardia, anorexia, vasomotor and dyspeptic disorders.
Under the influence of treatment, primarily a/b drugs, the clinical signs of tuberculous intoxication gradually disappeared within 1 to 3 months. Mild signs of intoxication in most patients disappeared within 1 and 2 months of treatment, and pronounced signs - somewhat later, by the end of 2 and 3 months. Of the clinical signs, the leading one is an increase in body temperature. As the temperature normalizes, the patient's well-being, mood, sleep, appetite gradually improve, weakness, malaise disappear, sweating stops. The disturbed function of external respiration, blood circulation and central nervous system is gradually normalized. The disappearance of clinical signs of tuberculosis intoxication is one of the first indicators of effective treatment and the beginning of a cure for tuberculosis.
Local signs of pulmonary tuberculosis, determined on the basis of complaints and physical research methods.
With physical research methods of a patient with pulmonary tuberculosis reveal a variety of local signs of the disease: cough, sputum production, asymmetry and deformation of the chest, changes in the type and nature of breathing, as well as percussion tone, dry and moist rales. With the onset of reparative processes in the lungs, signs appear that indicate the development of fibrosis and compaction of areas of the lung tissue at the site of a tuberculous lesion and around it. Of the numerous local signs, 4 main ones were identified: cough, sputum production, moist rales and altered breathing. These signs are easy to take into account, they disappear with effective treatment and are not found in the cured.
The disappearance of local signs of active pulmonary tuberculosis, the restoration of vesicular respiration indicates that the exudative phase of tuberculous inflammation in the lungs has largely decreased. X-ray during this period, resorption of infiltrative and focal changes is detected.
The dynamics of the main local signs of active pulmonary tuberculosis characterizes the course of the tuberculosis process. That is why, when determining the clinical cure for pulmonary tuberculosis, it is necessary to take into account the dynamics of these signs in combination with other clinical, radiological and laboratory data. The cessation of coughing, sputum production, the disappearance of moist rales and the restoration of vesicular respiration are objective signs of the involution of the tuberculous process.
The value of ESR and hemograms for determining the clinical cure of pulmonary tuberculosis.
The main significance of the hemogram is revealed when determining the quality of the tuberculous process, its activity and the reaction of the body to it. Changes in hemogram and ESR in various forms of pulmonary tuberculosis run parallel to the clinical status of the patient. A number of repeated hemograms, their dynamics allows us to judge the course of the disease, the prognosis and the effectiveness of treatment. Simultaneously with the development of reparative processes in the area of changes in the lungs, the hemogram and ESR gradually normalize and remain stable during clinical cure.
The value of biochemical parameters for determining the clinical cure of pulmonary tuberculosis.
In pulmonary tuberculosis, first of all, protein, carbohydrate and lipid metabolism is disturbed. The total content of protein, protein fractions of blood serum, C-reactive protein was studied depending on the clinical form of pulmonary tuberculosis, the activity of the tuberculosis process, the effectiveness of the treatment before and after subcutaneous injection of tuberculin.
As the tuberculous process subsides, there are shifts towards the normalization of b / x indicators.
Changes in b / x indicators are nonspecific and are equally determined in various inflammatory and infectious-allergic diseases.
Abacillation as a criterion for the cure of pulmonary tuberculosis.
One of the main criteria for the clinical cure of pulmonary tuberculosis is abacillation. Currently, to prove abacillation, a complex of studies is used, including bacterioscopic, bacteriological and biological methods. Until the 80s of the 20th century, it was generally accepted that a bacilli excretor can be deregistered 2 years after the disappearance of the MBT in sputum, bronchial washings or stomach. At the same time, the need for multiple studies of sputum or bronchial washings was emphasized. But they consider it advisable to focus on the nature and timing of reparative processes in the patient's body when determining the effectiveness of treatment. By the end of effective treatment, when the disappearance of signs of tuberculosis disease can be established by clinical, radiological and laboratory data, the patient should be deregistered as a bacillus excretor. In such cases, abacillation is indisputable and is consistent with clinical and radiological data characterizing the end of the process of involution of tuberculous changes.
X-ray criteria for the clinical cure of pulmonary tuberculosis.
X-ray examination is of great importance for determining the clinical cure of pulmonary tuberculosis. Based on the data of the R-study, one can judge the main stages of the involution of the pulmonary process, the nature of the residual post-tuberculosis changes and further reparative transformations in them.
In determining the clinical cure of pulmonary tuberculosis, the main role is given to the dynamic R-study. Many radiologists recommend using plain radiographs in standard projections and tomograms.
Inactive residual post-tuberculous changes are characterized by the presence of a small size of well-defined foci with areas of calcification (or without them) and fibrosis.
The nature of fibrosis is focal-like, linear or mesh.
With each clinical form of pulmonary tuberculosis, some features of reparative processes are noted. So, in focal pulmonary tuberculosis, compaction and fibrosis of foci were observed equally often. In addition, the processes of resorption, fibrosis and compaction were combined. Complete resorption was rarely observed.
In patients with infiltrative pulmonary tuberculosis, resorption prevailed over other regeneration processes. Compaction and calcification were observed less frequently.
The completion of the regression of infiltrative pulmonary tuberculosis is indicated by the following R-signs, which are detected during dynamic monitoring during treatment:
1.complete resorption of the infiltrative focus;
2. the development of fibrosis at the site of the former infiltrate, and the formation of fibrosis is characterized by the appearance in the center of the former infiltrate of a cellular structure with linear shadows along the periphery;
3. the emergence of small dense foci at the site of the former infiltrative focus against the background of limited fibrosis;
4. closure of the decay cavity (scar, fibrous focus).
The reverse development of the process in disseminated pulmonary tuberculosis is distinguished by the following features. Radiologically, complete resorption or with slight fibrosis is observed only in its fresh forms. In the process of resorption of fresh foci, a fine mesh was revealed radiologically, which is formed as a result of the appearance of narrow strips of enlightenment along the edge of the lesion. With numerous foci, the lines of enlightenment and darkening stripes are connected, creating a fine mesh. In the process of resorption, the foci "melt", the fine mesh gradually disappears. But sometimes the mesh remains, indicating the formation of mesh fibrosis.
In place of conglomerates of foci or foci, dense or calcified foci may remain. Fibrosed foci radiologically have a fine-mesh structure.
In some cases, during the completion of the reverse development of chronic disseminated pulmonary tuberculosis, thin-walled sanitized cavities are formed, which can persist for a long time. These cavities almost always close with scarring or cellular fibrosis.
In the process of involution in patients with chronic disseminated pulmonary tuberculosis, pleural stratifications were often observed, which persisted upon completion of reparative processes.
To distinguish a fibrous focus from a caseous one, it is necessary to take posterior images and tomograms. Healing of cavities most often occurs with the formation of residual changes in the form of a scar or focus at the site of the former cavity. There is an open healing of caverns, when a thin-walled cavity is preserved in its place. Such cavities are characterized by very thin walls with even, as if emphasized contours, subpleural localization, thickening of the pleura and sclerosis of the draining bronchi.
In most cases, complete, true healing of the decay cavity occurs (without a trace, the formation of a scar or limited fibrosis at the site of the former cavity), in other patients, incomplete healing (encapsulation of the filled cavity like tuberculoma, preservation of the residual cavity).
It is possible to judge the absence of process activity in residual changes in the treatment of disseminated pulmonary tuberculosis radiographically based on the detection of dense and calcified foci, fibrosis in the form of linear shadows, small- and medium-sized lucidities without foci and cellularity of focal-like shadows.
That. X-ray criteria for the clinical cure of pulmonary tuberculosis is the completion of the involution of the pulmonary process, which is expressed in the resorption of areas of tuberculous inflammation in the lungs and pleura, the completion of the processes of fibrosis, compaction and calcification of foci and foci, in the closure of decay cavities. In some patients, clinical cure of pulmonary tuberculosis can occur while maintaining the residual cavity.
The stability of the clinical cure of pulmonary tuberculosis is confirmed by the stability of the R-pattern of residual changes in the lungs and pleura in the long-term follow-up period.
After effectively completed treatment, R-graphy of the lungs in a direct projection should be repeated every 6 months. Within 2-3 years. If necessary, follow-up at a later date, control R-grams of the lungs should be done once a year.
The value of tuberculin tests for determining the clinical cure of pulmonary tuberculosis
Therefore, it is not possible to focus on the Pirquet reaction when determining the clinical cure for pulmonary tuberculosis in adults.
Intradermal Mantoux test. When studying the dynamics of the intensity of the Mantoux reaction in the same individuals during the period of the regression of the disease, it was found that in 70% of patients cured of tuberculosis, the intensity of the Mantoux reaction decreased, in 20% it increased and in 5% it did not change.
The Mantoux reaction cannot be a convincing criterion for the clinical cure of pulmonary tuberculosis in adults, since in 30% of clinically cured patients with residual changes, its intensity increases compared to the initial one or remains unchanged.
Subcutaneous Koch test. Use of s / c tubes. tests in determining the clinical cure of pulmonary tuberculosis turned out to be reasonable and in most cases could help in solving this difficult issue. However, the results of this test, as well as the results of other tubes. samples should be taken into account only in combination with the data of clinical, radiological and laboratory research methods.
Conclusion
Modern methods of clinical, radiological, laboratory, biological and functional examination of the patient allow timely and correct determination of the state of clinical cure of pulmonary tuberculosis.
Based on the research, a set of main criteria for the clinical cure of pulmonary tuberculosis, identified in the course of observation, was determined:
1. absence of clinical signs of tuba. intoxication;
2. normalization of hemogram and ESR;
3. disappearance of local signs of active tuberculosis, determined on the basis of complaints (cough, sputum) and physical examination methods (wheezing, abnormal breathing)
4. persistent abacillarity of sputum, bronchial and stomach washings, determined by a complex of bacterioscopic and bacteriological examinations;
5. the absence of R-signs of pulmonary tuberculosis as a result of the completion of its involution, which is expressed in the cessation of the process of resorption of the tubes. changes in the lungs and pleura, the end of the processes of fibrosis, compaction and calcification of foci and foci, in the healing of decay cavities;
6. the presence of a negative general and focal reaction to the subcutaneous injection of tuberculin;
7. restoration of working capacity, taking into account residual pathomorphological changes and functional disorders.