Tuberculosis of the intestines of the peritoneum and mesenteric lymph nodes. Tuberculosis of the mesenteric lymph nodes is the main form of abdominal tuberculosis

Tuberculosis of mesenteric lymph nodes. The main complaints are periodic pain in the abdomen, often in the navel area, independent of food intake. There is often constipation, less often diarrhea, and sometimes nausea and vomiting. There are always pronounced manifestations of tuberculosis intoxication. On palpation, pain is noted in different parts of the abdominal cavity; Shtenberg's pain points can be detected at the sites of attachment of the peritoneum (on the right 2-5 cm above McBurney's point and on the left at the level of the II lumbar vertebra). With tumor-like enlargement of the mesenteric lymph nodes in the area of ​​the root of the mesentery, small, clearly defined, round-shaped tumors are palpated (after cleansing the intestines); with a perifocal reaction around the nodes, their contours are unclear.

During rectal examination, deep-lying enlarged lymph nodes are sometimes identified. Diagnosis is aided by contrast X-ray examination of the intestine. Tuberculin tests are positive. Differential diagnosis should be made with nonspecific mesadenitis, chronic appendicitis, cholecystitis, pseudotuberculosis, neoplasms in the abdominal cavity, gallstones and urolithiasis, and helminthic infestations.

Tuberculosis of peripheral lymph nodes. Tuberculous lymphadenitis develops in children during the period of current primary tuberculosis with lymphogenously disseminated spread of infection. It is possible to develop a primary isolated lesion of the cervical or vertebral lymph nodes when Mycobacterium tuberculosis penetrates through the tonsils or oral cavity. The axillary and inguinal lymph nodes are less commonly affected. Clinical manifestations of the disease depend on local changes in the lymph nodes and the activity of the general tuberculosis process. During the infiltrative process or during the period of node disintegration, the child’s general condition worsens, there is a rise in temperature, loss of body weight, a cough often appears, and the ESR increases. The intensity of the Mantoux test increases.

Upon palpation, a package of dense, mobile, painless, partially fused lymph nodes is determined. With caseous decay, the nodes are emptied of caseous masses, followed by the formation of scars. In untreated young children, the lymph nodes can melt, forming fistulas with a subsequent long-term course.

Tuberculous lymphadenitis in some cases must be differentiated from lymphogranulomatosis, benign and malignant tumors (cysts, lymphosarcoma, etc.).

Treatment is complex, long-term, continuous, staged. It is necessary to create the right regime: sufficient sleep, daytime rest, long stay in the fresh air. To harden the body, air baths, water procedures, and physical therapy are used. Physical and mental stress should be reduced. Only in decompensated forms of tuberculosis or in the acute period of the disease is bed rest with extensive use of fresh air necessary.

The diet should be complete and contain an increased amount of animal proteins, fresh fruits, vegetables and additional vitamins, especially C, B1, B2, A and nicotinic acid. Vitamin B complex can be added as a yeast drink. It is recommended to increase daily caloric intake by 15-20%.

Children with early and chronic tuberculosis intoxication should be sent to a hospital to exclude other diseases with a similar clinical picture and to prevent the development of local forms of tuberculosis.

The main method of treating children with tuberculosis is the use of tuberculostatic drugs. Children with early and chronic tuberculosis intoxication are prescribed two main chemotherapy drugs - tubazid or ftivazid and PASK for at least 6 months. They are then sent to a sanatorium. For dosages of the drug, see table. 14.

Children with local forms of tuberculosis are treated in a hospital until the activity of the process subsides, then they are sent to a sanatorium until complete clinical recovery.

In case of primary tuberculosis complex, bronchoadenitis in the infiltration phase, three main drugs are used: streptomycin, drugs of the GINK group (tubazid, ftivazide, metazide, saluzide, etc.) and PASK for 1.5-2, less than 3 months, then streptomycin is canceled and continued treatment with two of these drugs for at least 8 months; for tumorous bronchoadenitis - at least 1-1.5 years. For bronchoadenitis and the primary complex in the phase of compaction and calcification, tubazide and PAS are prescribed; in the absence of clinical signs of activity - for 3 months, in the presence of activity - for 6-8 months.

For miliary and hematogenously disseminated tuberculosis, the administration of streptomycin, a drug of the GINK and PAS group, lasts from 3 to 6 months. followed by the prescription of two drugs (tubazid and PAS K) for a period of at least 1.5 years.

If bronchoadenitis is complicated by bronchial tuberculosis, then solutizone is administered in the form of an aerosol in a 1-2% solution in an amount of 1.5-3 ml; course of treatment is 1-2 months.

Only with the development of direct or cross-resistance of Mycobacterium tuberculosis to first-line tuberculostatic drugs, in the absence of clinical effect, when within 1.5-2.5 months. there are no signs of improvement or an exacerbation or complication of the process occurs during treatment, second-line drugs are used. They are weaker and more toxic. Currently, new drugs are increasingly used: ethambutol, rifampicin, rifamycin. In their activity, they are close to the drugs of the GINK group, are well absorbed, have low toxicity, and do not have cross-resistance. Treatment is carried out in combination with drugs from the GINK group.

With long-term use of anti-tuberculosis drugs, side effects develop: dizziness, headache, fever, allergic rash, eosinophilia in the blood. When taking PAS, Tibon, abdominal pain, nausea, vomiting, and flatulence are possible.

In order to weaken the hyperergic state and exudative phase, corticosteroid drugs (prednisodone, etc.) are sometimes prescribed. Duration of treatment is 1.5-2 months. with simultaneous massive chemotherapy. Indications for the use of hormonal drugs: tuberculosis of the serous membranes (pleurisy, meningitis, peritonitis), infiltrative lesions of the lungs, acute disseminated forms of tuberculosis, atelectasis, decay cavities.

To prevent side effects of drugs from the GINK group, vitamin B6 is administered intramuscularly in the form of a 2.5-5% solution, 0.5-1 ml every other day for 1.5-2 months, vitamins B12 and B, and glutamic acid.

Table 14. Antibacterial therapy for children with tuberculosis

To relieve an allergic reaction that occurs when streptomycin is administered, calcium pantotenate is prescribed at 0.4-0.8 r/day. in 2 doses throughout the course of treatment with streptomycin.

When treating with cycloserine, glutamic acid is given at 1.5-2 r/day, ATP is administered at 1 ml of a 1% solution for 1-1.5 months. and vitamin B6. For the purpose of hyposensitization, calcium supplement, diphenhydramine, suprastin or diprazine are prescribed. To improve metabolism and liver function, administration of vitamin B15 (calcium pangamate), cocarboxylase, ATP, vitamin B12 in age-related dosages is indicated; for poor appetite - gastric juice, apilak.

Stimulating therapy is used in children with chronic tuberculosis intoxication, which is difficult to treat, and then in the chronic course of primary tuberculosis in children in whom compensation for the process does not occur for a long time. For this purpose, gamma globulin and aloe are administered, and plasma transfusions are performed according to indications. Sunbathing is indicated for extrapulmonary forms of tuberculosis (lymphadenitis of the cervical lymph nodes, bone tuberculosis, mesadenitis), chronic tuberculosis intoxication.

PHENYLKETONURIA is a severe hereditary disease that is characterized mainly by damage to the nervous system.

Etiology and pathogenesis. As a result of a mutation in the gene that controls the synthesis of phenylapanine hydroxylase, a metabolic block develops at the stage of conversion of phenylalanine to tyrosine, as a result of which the main pathway for the conversion of phenylalanine becomes deamination and the synthesis of toxic derivatives - phenylpyrosinograde, phenyllactic and phenylacetic acids. The content of phenylalanine in the blood and tissues increases significantly (up to 0.2 g/l or more, with the norm being 0.01-0.02 g/l). Insufficient synthesis of tyrosine, which is a precursor of catecholamines and melanin, plays a significant role in the pathogenesis of the disease. The disease is inherited in an autosomal recessive manner.

Clinical picture. Signs of phenylketonuria are detected already in the first weeks and months of life. Children are lagging behind in physical and neuropsychic development; lethargy, excessive drowsiness or increased irritability, tearfulness are noted. As the disease progresses, epileptiform seizures may be observed - full-blown convulsive and non-convulsive seizures such as nodding, bowing, shuddering, and short-term blackouts. Hypertension of individual muscle groups is manifested by a peculiar “tailor’s pose” (tucked legs and bent arms). Hyperkinesis, hand tremors, ataxia, and sometimes central paresis may be observed. Children are often blond with light skin and blue eyes; they often have dermatitis, eczema, excessive sweating with a specific (mouse) odor of sweat and urine. A tendency to arterial hypotension is detected. If left untreated, idiocy or imbecility and profound mental disability develop.

Diagnosis. It is extremely important to establish a diagnosis in the preclinical stage, or at least no later than the 2nd month of life, when the first signs of the disease may appear. To do this, all newborns are examined according to special screening programs that detect an increase in the concentration of phenylalanine in the blood already in the first weeks of life. Any child who exhibits signs of developmental delay or minimal neurological symptoms should be examined for pathology of phenylalanine metabolism. Microbiological and fluorometric methods are used to determine the concentration of phenylalanine in the blood, as well as the Fehling test for phenylpyruvic acid in the urine (adding a few drops of a 5% solution of ferric chloride and acetic acid to the patient’s urine leads to the appearance of a green stain on the diaper). These and other similar methods are classified as indicative, therefore, if the results are positive, a special examination is required using precise quantitative methods for determining the content of phenylalanine in the blood and urine (amino acid chromatography, the use of amino acid analyzers, etc.), which is carried out by centralized biochemical laboratories.

Children require special observation of captivity in medical genetic centers (clinic offices).

Differential diagnosis is carried out with intracranial birth trauma, intrauterine infections.)

Treatment. When the diagnosis is confirmed by biochemical methods, it is necessary to transfer children to a special diet, with a restriction of phenylalanine, which, with early diagnosis, guarantees the normal neuropsychic development of the child. Milk and other products of animal origin are excluded from the diet and protein hydrolysates (cymogran, lefanolac, berlofen, hypophenate) are prescribed, which become the main food products that meet the need for protein. Protein hydrolysates are administered with fruit and vegetable juices, purees, and soups. Treatment is carried out under the control of phenylalanine content in the blood, ensuring that its level is maintained within the range of 0.03-0.04 g/l. Strict limitation of animal proteins is required during the first 2-3 years of life.

Prevention. Of great importance is special monitoring of families at risk, i.e., families where there were already children with phenylketonuria. Newborns from these families should be subjected to mandatory biochemical examination and, if indicated, early treatment. Identification and treatment of children through mass screening programs also helps prevent the development of severe mental disability.

A DNA probe has been proposed for the prenatal diagnosis of phenylketonuria in high-risk families.

PHOSPHATE DIABETES is a dominantly X-linked disease with profound disturbances in phosphorus-calcium metabolism, which cannot be restored with regular doses of vitamin D. In connection with this, another name for the disease has appeared - rickets, resistant to vitamin D; however, in reality we are not talking about rickets, but about a rickets-like disease.

Etiology, pathogenesis. It is assumed that in phosphate diabetes, the enzyme processes of converting vitamin D into active hormone-like substances are disrupted or the sensitivity of intestinal epithelial receptors to the action of these metabolites is reduced. Characteristic biochemical signs are phosphaturia, hypophosphatemia, increased activity of the parathyroid glands, high activity of blood alkaline phosphatase. Reabsorption of calcium in the intestine is reduced.

Clinical picture. Phosphate diabetes has similar features to ordinary D-deficient rickets, but also differs from it in that with this disease there are no signs of general intoxication, the general condition remains satisfactory. In contrast to rickets, the processes of osteomalacia and osteoid hyperplasia are expressed predominantly in the bones of the lower extremities (curvature of long tubular bones or deformation of the knee and ankle joints). Clinically, phosphate diabetes manifests itself not in the first months of life, but in the second half of life, after children begin to stand on their feet.

If left untreated, the disease progresses as the child grows (dystrophy, complete inability to move independently). X-rays reveal the same changes that are characteristic of rickets, but the pathology is especially pronounced in the bones of the lower extremities. One of the typical radiological signs is the coarse fibrous structure of the cancellous bone.

Similar changes in the skeletal system can be detected in one of the parents, or the influence of a mutant gene in them can only be detected during a biochemical blood test, therefore, if phosphate diabetes is suspected, it is advisable to examine the content of inorganic phosphorus in the blood of parents and siblings.

Treatment. Long-term administration of vitamin D in large doses (40,000 - 120,000 IU daily) with mandatory monitoring of calcium and phosphorus levels in the blood. Under the influence of treatment, alkaline phosphatase activity decreases rapidly. Treatment begins with lower doses, gradually increasing them. In case of increased calciuria (according to the Sudkovich test and biochemical examination data), the dose is reduced. When the condition improves, maintenance doses are prescribed - 1000-5000 IU with breaks in treatment for 3-7 days. Vitamin therapy is supplemented with the introduction of phosphorus (phosphate-rich foods, calcium glycerophosphate). Oxidevit and other vitamin D metabolites are used.

Prevention. The risk of having a sick child again in a family is high and reaches 50%, which should be explained to parents during a medical genetic consultation.

Debreu-de-Toni-Fanconi syndrome is also characterized by rickets-like osteopathy, but unlike phosphate diabetes, it manifests itself with more severe general symptoms - malnutrition, decreased resistance to infection. In addition to phosphaturia, it is characterized by aminoaciduria, glucosuria, and impaired renal function to maintain the balance of acids and bases in the blood. To restore the functions of the renal tubules, vitamin D is used in high doses, as in phosphate diabetes, the protein content in the diet is increased to 5 g/kg, and acidosis is corrected.

CELIACIA (Hy-Herter-Heubner disease, glutenenteropathy, intestinal infantilism), is characterized by impaired intestinal absorption, sub- or atrophy of the jejunal mucosa and an unconditionally positive reaction to a gluten-free diet (exclusion from food of cereals containing gluten). Celiac disease occurs with a frequency of approximately 1:3000 and is inherited in an autosomal dominant manner.

Etiology, pathogenesis. A connection has been established between the disease and the intake of gliadin, a protein from the cereals wheat, rye and oats. However, the mechanism of the pathological interaction of gliadin with the mucous membrane is not completely clear. There is an assumption of the presence of an enzyme defect - the absence or deficiency of gliadinaminopeptidase or another enzyme involved in the breakdown of gluten. There are reports of an immunological reaction (humoral and cellular) to gluten occurring in the lining of the small intestine.

Clinical picture. Among the clinical options, true celiac disease and celiac disease syndrome should be distinguished, which can develop with a wide variety of intestinal diseases (developmental anomalies, infections, prolonged use of antibiotics, etc.). The onset of celiac disease often coincides with the introduction of complementary foods containing flour products into the child’s diet. Therefore, children aged 6-12 months get sick more often. Frequent, foamy stools appear, abundant, with a pungent odor, light or with a grayish tint, and greasy. As a rule, pathogenic intestinal microflora is not detected in feces. Treatment of dyspepsia with conventional means (antibiotics, enzyme preparations, dietary reduction, etc.) does not produce any effect. The child becomes lethargic, pale, loses body weight, and decreases appetite. Dystrophy gradually develops and children acquire a typical appearance for celiac disease: severe exhaustion, dull eyes, bright mucous membranes, and a huge belly. In some cases, swelling develops in the lower extremities, and spontaneous bone fractures are common. Pseudoascites (fluid accumulation in the atonic intestine) is determined. Then there are symptoms of multivitamin deficiency (dry skin, stomatitis, dystrophy of teeth, nails, hair, etc.).

As a rule, with celiac disease, especially if it lasts for a long time, there is impaired absorption of disaccharides, fats, vitamins, iron, calcium, the transport of cystine, the metabolism of tryptophan are disrupted, i.e. we are talking about universal malabsorption. In this regard, the polymorphism of the clinical picture is understandable. Children suffer not only physically, but also mentally (lability of mood, isolation, increased excitability, negativism). An important sign of the disease during its long course is short stature.

The course of celiac disease is wavy, often accompanied by a secondary infection, which in some cases decides the fate of the patient.

Diagnosing celiac disease, if you remember about this disease, is not difficult. The totality of the medical history, the characteristic appearance of the patient and stool are sufficient to make a presumptive diagnosis of celiac disease. If, against the background of a gluten-free diet, the patient’s condition improves, and an error in the diet leads to the appearance of stools characteristic of celiac disease, the diagnosis is almost beyond doubt. Clarification of the diagnosis is possible with a thorough scatological examination (the presence of a large amount of fatty acids and soaps in the stool), a bismic blood test (hypoproteinemia, hypo-albuminemia, decreased concentrations of cholesterol and lipids, hypocalcemia, hypophosphatemia, hyposiderinemia, etc.), X-ray examination ( osteoporosis, horizontal levels in intestinal loops, intestinal dyskinesia). The final diagnosis is established by histological analysis of biopsy samples of the jejunal mucosa.

Differential diagnosis is carried out with the intestinal form of cystic fibrosis, disaccharidase deficiency, and abnormalities of the gastrointestinal tract.

Treatment for celiac disease is complex. The basis of treatment is the appointment of a gluten-free diet for a long period (years) (bread, crackers, cookies, confectionery flour and pasta, pates, sausages are excluded). Children tolerate potatoes, fruits, vegetables, corn and soy flour, vegetable fats, meat and fish, etc. well.

When following a gluten-free diet, patients' body weight begins to recover after 3 weeks. Histological changes in the intestine begin to disappear after 2-2.5 years.

Simultaneously with the prescription of a gluten-free diet, symptomatic therapy is carried out: vitamins, calcium, iron, enzyme preparations, massage, gymnastics, etc. Children suffering from celiac disease should be under clinical observation.

The prognosis with diet and proper treatment is favorable.

EXUDATIVE ENTEROPATHY is a heterogeneous group of diseases and pathological conditions characterized by increased loss of plasma proteins through the gastrointestinal tract with phenomena of impaired absorption, hypoproteinemia, edema, and delayed physical development.

Etiology, pathogenesis. There are primary (hereditary) and secondary (acquired) exudative enteropathy (for various chronic gastrointestinal diseases). In most patients, lymphangiectasia is found in a limited area or throughout the entire intestine.

Clinical picture. The disease often develops acutely after a year, but a transient and chronic course cannot be excluded. The clinical picture consists of the following symptoms: edema, delayed physical development, diarrhea, weight loss. Swelling may be small or widespread in the form of anasarca. In a small number of cases, hypocalcemic convulsions and extreme dystrophy are observed. The loss of plasma protein, which also contains all classes of immunoglobulins, sharply reduces the overall resistance of children to infections and causes a protracted course of infectious diseases.

The diagnosis is based on history and clinical symptoms.

Differential diagnosis is made with nephrotic syndrome. A distinctive feature in this case is the discrepancy between hypoproteinemia and the quantitative protein content in the urine. The presence of protein in feces, especially in large quantities, speaks in favor of exudative enteropathy.

It is advisable to start treatment as early as possible. Protein preparations (albumin, plasma, etc.) are administered parenterally, fats are limited, and unsaturated fatty acids (vegetable oils) are used; vitamins, enzymes, anabolic hormones, etc. are recommended. Specific therapy has not been developed.

The prognosis for primary exudative enteropathy is serious.

Peritoneal tuberculosis always occurs only in cases where it was preceded by a similar disease of the lungs, intestines, and bones.

The disease most often occurs in young people, but there are cases where it can occur in children and older people.

That is why the main aspects of the disease should be considered.

Tuberculosis of the abdominal organs can develop as a result of the spread of mycobacteria from the main focus by lymphogenous, hematogenous or contact routes. It is also possible that infection occurs through nutritional means, but this variant of infection is very, very rare.

The terminal ileum is most prone to damage. When conducting a macroscopic examination, swelling of the intestinal walls is observed, its darkening with manifestations of a rash of grayish-yellow color and dense consistency. With the development of the infiltrative ulcerative form of tuberculosis, the mucous membrane may have ulcerative defects that will differ in size.

Microscopic examination allows you to see destructive foci on the mucosa, which lead to the formation of ulcers; their depth can reach the muscular and serous layer of the intestine. Giant cell granulomas are also observed, which can be found in all layers of the intestinal wall.

In case of perforation of a tuberculous intestinal ulcer, peritonitis occurs.

If the peritoneum and omentum are damaged, a rash will be observed on their surface, which in appearance resembles millet, grayish-white in color.

Clinical manifestations of the disease

Tuberculosis has two forms:

• exudative;
• adhesive (adhesive).

At the same time, the lymph nodes enlarge and acquire a densely elastic consistency.

The progression of intestinal tuberculosis occurs secretly with a combination of general (fatigue, emaciation, diarrhea) and local signs (pain). As the disease progresses, there is an alternation of moments of exacerbation and remission. The pain is felt in the right iliac region, is constant and varies in intensity. Patients may have a fever, but there is a course without the presence of a rise in body temperature. Vomiting may also occur, but this is only in cases where tuberculous peritonitis has developed.

Due to intestinal tuberculosis, intestinal obstruction, ulcer perforation, bleeding and peritonitis may occur.

With the development of tuberculous mesadenitis, the patient develops wave-like abdominal pain without clear localization. The pain syndrome can be so severe that it resembles the symptoms of an acute abdomen, or it can be aching, dull, or in the form of attacks.

Intestinal tuberculosis is often associated with common diseases and therefore examination and treatment are prescribed for completely different diseases. The main and dangerous diagnosis is missed.

Effective methods of treatment and prevention

To correctly indicate the diagnosis, it is necessary to conduct x-ray and endoscopic examination. The results of the study may show the presence of calcified peritoneal lymph nodes, and this is direct evidence of tuberculous mesadenitis.

Disturbances in gastric and intestinal motility and placement of small intestinal loops may occur. In the event of tuberculous peritonitis, intestinal adhesions or intestinal obstruction may occur.

To diagnose changes in intestinal tissue, a colonoscopy is performed, taking material from the affected area for biopsy. During this period of time, ultrasound is used for diagnostic purposes.

But, despite the significant number of possible research methods, the main method for diagnosing tuberculosis (all possible forms) is still considered to be a histological examination of biopsy material.

Treatment of this disease is aimed at alleviating and removing the manifestations of intoxication, resolving local inflammatory changes, and preventing possible complications. Treatment of uncomplicated and initial forms of tuberculosis is carried out in a hospital setting.

Chemotherapeutic agents are prescribed:

1. Rifampicin.
2. Pyrazinamide.
3. Ethambutol (if MBT is sensitive to them).

In a situation where the prescribed drugs do not help, an individual treatment regimen is developed for the patient.

Symptomatic treatment is carried out with detoxification agents, vitamins, hepatoprotectors, as well as physiotherapeutic procedures, namely electrophoresis with lidase.

In severe and complicated cases of abdominal tuberculosis, treatment is carried out through surgery.

Mesadenitis, or tuberculosis of the mesenteric lymph nodes, can develop in both primary and secondary tuberculosis. Secondary tuberculous mesadenitis is observed only with a sharp decrease in the body's defenses caused by a severe progressive course of pulmonary or extrapulmonary tuberculosis; More often, the occurrence of mesadenitis can be associated with the primary form of tuberculosis.

Damage to the abdominal nodes in some patients is caused by the causative agent of bovine tuberculosis during alimentary penetration of infection. In modern conditions, tuberculous lesions of the lymph nodes of the abdominal cavity are rare, which is largely due to the timely detection and successful treatment of patients with primary tuberculosis.

All groups of lymph nodes of the abdominal cavity can be involved in the tuberculosis process, but the disease most often and more severely develops in the mesenteric lymph nodes. Mesenteric lymph nodes affected by tuberculosis may be slightly enlarged, but often reach significant sizes and are closely fused into large conglomerates. If the course of mesadenitis is unfavorable, the tuberculous process spreads to the serous membranes and intestinal walls. The formation of cold abscesses in the abdominal cavity is possible, sometimes opening into the abdominal cavity or outward, as well as the spread of tuberculosis infection in the body through the lymphogenous route. A favorable course of the disease leads to calcification of the lymph nodes, which develops with mesadenitis much earlier than with bronchoadenitis.

Histological examination can reveal various stages of the evolution of mesadenitis - from the development of a tuberculous tubercle to the formation of a glandular cavity. There are three forms of mesadenitis: infiltrative, caseous and fibrous. The course of the disease is usually long-term, but in most cases it is benign: progressive mesadenitis is extremely rare.

The most common symptom of mesadenitis is pain, usually localized in the umbilical or right iliac region, where the largest number of lymph nodes are concentrated. The nature of the pain can be varied: dull or acute, in the form of attacks. There is an increase in pain with physical exertion. In the acute period of the disease, pain can simulate the picture of appendicitis, pancreatitis and even a perforated gastric ulcer.

Almost always, various dyspeptic disorders are observed with mesadenitis: loss of appetite, occasional nausea, vomiting and irregular bowel movements. The occurrence of these symptoms is associated with the neuro-reflex effect of inflammation on the gastrointestinal tract or with the involvement of the peritoneum in the tuberculosis process.

With a long course of the disease, the development of hyperacid gastritis and impaired liver function are possible.

Examination and palpation reveal abdominal bloating, tension and pain at various points, depending on the damage to the corresponding nodes. The cause of bloating and abdominal tension is flatulence, and sometimes effusion in the abdominal cavity. In places where pain is localized, deep palpation can identify fixed or sedentary enlarged single lymph nodes or clusters of them. The most accessible for palpation are the mesenteric lymph nodes to the right of the navel above the location of the cecum and to the left along the mesentery. Here, dullness of percussion sound is also possible.

The patient's hemogram shows a decreased hemoglobin content, a shift of band neutrophils to the left, lymphocytosis, and an increased ESR.

An X-ray examination of the abdominal cavity may reveal enlarged and changed lymph nodes in the form of oval or round formations, often with a granular structure due to the deposition of lime in them (Fig. 53).

Tuberculin tests in patients with active mesadenitis are in most cases sharply positive. The body's reaction to subcutaneous injection of tuberculin is of great diagnostic importance. The appearance or intensification of pain in the abdominal cavity after the administration of tuberculin simultaneously with a general reaction may indicate the presence of an active tuberculous process in the mesenteric lymph nodes.

The commonality of some symptoms of mesadenitis with symptoms of appendicitis, pancreatitis, gastric ulcer, carcinomatosis and lymphogranulomatosis requires knowledge of the differential diagnostic differences between these diseases.

Nonspecific mesadenitis occurs during various inflammatory processes in the abdominal organs, as well as during chronic inflammatory processes in the upper respiratory tract. The clinical manifestations of nonspecific mesadenitis are extremely similar to those of tuberculous mesadenitis. Differential diagnosis is based on anamnestic data: with nonspecific mesadenitis there are often indications of chronic tonsillitis, inflammatory diseases of the abdominal organs, with tuberculous mesadenitis - indications of previous tuberculosis of other organs. The main differential diagnostic tests are hemogram and tuberculin diagnostics. With nonspecific mesadenitis, the hemogram shows leukocytosis up to 11 10 3 -15 10 3 in 1 μl (11,000-15,000), a significant shift of neutrophils to the left, lymphocytosis, and an increase in ESR. Tuberculin tests are negative or mild. The body's response to subcutaneous injection of tuberculin is not observed.

In acute appendicitis, there is a sudden onset of pain in the right iliac region. Their intensity usually increases, while with mesadenitis the pain is constant. With appendicitis, symptoms of peritoneal irritation are pronounced. With recurrent appendicitis, during an exacerbation, the pain is paroxysmal in nature, accompanied by nausea, vomiting, and fever. A blood test reveals leukocytosis and an increase in the number of band neutrophils.

The acute period of pancreatitis is also characterized by the sudden appearance of very severe pain in the epigastric region and to the left of the rectus abdominis muscle. Pain may radiate to the left iliac region and left thigh. There is an increase in the content of diastase in the urine and blood.

Gastric ulcer is accompanied by the appearance of strictly localized pain in the epigastric region; pain radiates to the back. X-ray examination reveals corresponding changes in the stomach.

Peritoneal carinomatosis is a very rare disease. The main symptoms of carcinomatosis are severe intoxication of the body, progressive course of the disease, severe anemia and negative reactions to tuberculin. Changed lymph nodes in carcinomatosis are palpated as denser formations than in tuberculous mesadenitis.

The mesenteric form of lymphogranulomatosis occurs with wave-like fever. Lymphogranulomatosis is characterized by enlargement of the lymph nodes during the period of rising temperature. The hemogram reveals leukopenia and lymphopenia, monocytosis and eosinophilia. Lymphogranulomatosis progresses rapidly.

Clinical manifestations of chronic colitis are often mistaken for tuberculous mesadenitis, but in chronic colitis, abdominal pain is often caused by eating rough and fatty foods. When palpating the abdomen, diffuse pain is determined, but mainly along the colon.

The main method of treating patients with tuberculous mesadenitis is the use of antibacterial drugs according to the generally accepted treatment regimen for patients with tuberculosis.

During the acute course of the process, the use of three main anti-tuberculosis drugs (streptomycin, isoniazid, PAS) in optimally tolerated doses with the simultaneous administration of vitamins B and C complexes is indicated. In the chronic course of mesadenitis, one can limit oneself to the prescription of drugs from the group GINK and PAS. The total duration of treatment is 12-18 months.

Tuberculosis of the intestines, peritoneum and mesenteric lymph nodes (abdominal tuberculosis)

Primary intestinal tuberculosis, which occurs as a result of ingestion of milk from animals with tuberculosis, is currently practically never encountered in developed countries. Secondary intestinal tuberculosis develops as a result of the entry of Mycobacterium tuberculosis into it with sputum (for pulmonary tuberculosis), hematogenously and (or) lymphogenously (for pulmonary tuberculosis or other organs). Before the introduction of antibiotics into medical practice, 55-90% of people who died from pulmonary tuberculosis had tuberculous intestinal damage at autopsy. In modern conditions, intestinal tuberculosis is very rare.

In approximately 90% of cases, the ileocecal region of the intestine (terminal ileum and cecum) is affected. Its other parts, as well as the stomach, are involved in the tuberculosis process extremely rarely. In the initial stage of the disease, tuberculous granulomas form in the intestinal mucosa. As the process progresses, ulcerative (in 60% of cases), hypertrophic (10% of cases) or ulcerative-hypertrophic (in 30% of cases) forms of intestinal tuberculosis develop. The ulcerative form is characterized by the formation of multiple ulcers on the intestinal mucosa: hypertrophic - thickening of the intestinal wall, spread of the inflammatory process to all its layers, including the serous membrane, as well as to the mesenteric lymph nodes (mesadenitis); ulcerative-hypertrophic - a combination of signs of both forms. With intestinal tuberculosis, pseudopolyps and fistulas often form in it; possible development of stenosis.

In the initial stage, the disease may be asymptomatic. As it progresses, cramping abdominal pain, flatulence, diarrhea, often alternating with constipation, weakness, loss of appetite, weight loss, and fever occur. Sometimes there are signs of partial intestinal obstruction . Blood may be detected in the stool, but hidden intestinal bleeding is more common. On palpation, the distal segment of the ileum is determined in the form of a compacted painful cord, the consistency of which often changes. The cecum is painful, swollen, compacted, sometimes the compaction is pear-shaped and decreases towards the ascending colon. With mesadenitis, enlarged lymph nodes or a tumor-like formation (conglomerate of lymph nodes) are palpated in the ileocecal area. The disease can be complicated by massive intestinal bleeding (rarely), intestinal perforation, and the formation of intestinal fistulas. In some cases, mesadenitis may develop malabsorption syndrome . The course of the disease is usually long, with remissions alternating with relapses.

Diagnosis of intestinal tuberculosis due to the absence of pathognomonic symptoms is difficult. The deterioration of the patient’s general condition with a stable course of tuberculosis of the lungs or another organ and the absence of signs of exacerbation or further spread of the process in them gives reason to suspect intestinal tuberculosis, especially when stool disorders and abdominal pain appear. Positive reactions to occult blood and soluble protein in feces are of important diagnostic value. Mycobacterium tuberculosis is usually not found in it. Characterized by anemia and elevated ESR. X-ray examination of the intestine reveals shortening and deformation of the cecum and terminal part of the ileum, ulcerative defects of the mucous membrane of these parts of the intestine, pseudopolyps, and sometimes cicatricial stenoses. Colonoscopy allows you to detect ulcers and stenoses. When diagnosing, it is necessary to take into account the results of tuberculin tests. Differential diagnosis is carried out with Crohn's disease , occlusive form of ischemic colitis , actinomycosis intestines, with isolated damage to the cecum - with a malignant tumor of this part of the colon , in tropical areas - with amoebiasis .

Peritoneal tuberculosis (tuberculous peritonitis) in countries with hot climates is diagnosed in approximately 25% of patients with ascites; It is rare in countries with temperate climates. More often, peritonitis is a reaction to a latent tuberculosis focus in it, resulting from hematogenous dissemination from the primary focus in the lungs. Approximately 80% of patients with peritoneal tuberculosis experience fever, anorexia, weakness, and weight loss. 75% of patients have ascites; an increased protein content and lymphocytes are detected in the ascitic fluid. Half of the patients experience diffuse abdominal pain. Possible constipation or diarrhea, vomiting.

In every fourth patient an enlarged liver is palpable. Sometimes the spleen also enlarges. The diagnosis is confirmed by the results of a histological examination of the affected area of ​​the peritoneum (biopsy is performed during laparoscopy) and biological tests (injection of ascitic fluid from the patient to a guinea pig).

Tuberculosis of the mesenteric lymph nodes does not occur as an independent disease; it usually accompanies intestinal tuberculosis.

Patients with intestinal tuberculosis require long-term (12-18 months) anti-tuberculosis chemotherapy; the combined use of isoniazid, ethambutol and rifampicin is recommended. A gentle diet and symptomatic therapy are important. In case of intestinal obstruction, intestinal perforation, or the formation of intestinal fistulas, resection of the affected area of ​​the intestine is indicated. For tuberculous peritonitis, anti-tuberculosis chemotherapy should continue for at least 18-24 months. The advisability of combining chemotherapy with the prescription of glucocorticosteroids to reduce the intensity of the adhesive process and prevent intestinal stenosis is not recognized by all specialists. Sanatorium-resort treatment of persons who have suffered abdominal tuberculosis is carried out both in local sanatoriums and in climatic resorts. The prognosis for abdominal tuberculosis is serious; high mortality is observed in the ulcerative form of intestinal tuberculosis.

In the anti-tuberculosis dispensary, persons who have had abdominal tuberculosis are observed in group V of the dispensary registration. The observation period is determined individually depending on the dynamics of the tuberculosis process and the indicated treatment and preventive measures.

Abdominal tuberculosis is never primary. The source of damage is the lungs, peribronchial lymph nodes, intestines, bones, and joints.

The routes of penetration of the tuberculosis bacillus into the peritoneum can be different. In the first place is spread through the bloodstream, then through the lymphatic vessels and, finally, through direct spread of tuberculosis from the abdominal organs (intestines, mesenteric lymph nodes, female genital organs, kidneys).

There are 3 forms of abdominal tuberculosis:

• serous (exudative) with millet-like rashes along the peritoneum and with the formation of serous fluid;
• adhesive (adhesive), also called dry, characterized by an abundant amount of adhesions between the intestines, omentum, and peritoneum. Between such adhesions there may be an encysted cavity with effusion;
• nodular-tumor-like (purulent) form, characterized by the formation of large nodular tumor-like formations due to adhesions between the intestines, omentum, and parietal peritoneum. Between these adhesions, when they are separated, large quantities of cheesy masses are found, in some places liquefied, purulently softened.

Symptoms of abdominal tuberculosis

The disease affects mainly young people, but often occurs in both childhood and old age. The course is chronic, which is sometimes worsened by acute attacks of intestinal obstruction.

Clinical signs of tuberculous inflammation of the peritoneum can be very unclear. Against the background of emaciation, mild fatigue, vague pain, dyspeptic symptoms, and diarrhea appear. The pain is cramping, sometimes dull. Patients very often have a fever, but there is a fever-free course when abdominal pain is diagnosed as acute, and when tuberculous peritonitis is unexpectedly found. There is a combination of tuberculous peritonitis and an attack. The intensity of the pain depends on the degree of narrowing of the intestines. Vomiting is very rare and appears only in acute cases or during exacerbation of latent peritonitis. Palpation usually provides little information. Pressure sensitivity is negligible. When palpated, the entire abdomen is often painful.

At the onset of the dry form of abdominal tuberculosis, the diagnosis is only presumptive based on general symptoms and the presence of tuberculosis in the patient. From the moment palpable tumor-like formations appear, the diagnosis becomes easier. It is possible to differentiate the tumor-like form of tuberculosis from true tumors on the basis of the multiplicity of lesions, age and slow general course. The exudative form is most easily recognized, especially in children.

The amount of liquid effusion in the exudative form is sometimes significant and the process resembles ascites. If there are encysted accumulations of fluid in the abdominal cavity, they are sometimes mistakenly interpreted as ovarian tumors or hydatid cysts.

Recognition is facilitated if the initial disease of any organ with tuberculosis is established, as well as the presence of a positive serological reaction.

It is sometimes very difficult to distinguish abdominal tuberculosis from peritoneal cancer. Here the issue is resolved by examining tissues taken during surgery.

Treatment of abdominal tuberculosis

Treatment of tuberculous peritonitis is carried out surgically. It is produced, which in itself often gives healing; to this is added the intraperitoneal administration of streptomycin 1 g diluted in 20 ml of 0.5% novocaine. Administration of streptomycin can be repeated in the future either through a small incision or by punctures. A puncture of the abdominal cavity and infusion of streptomycin are carried out according to the same rules as the injection of oxygen or air for diagnostic purposes. At the same time, treatment is also carried out with PAS and ftivazid. All these activities lead to good results.

There are a number of theories to explain the beneficial effect of laparotomy on the course of tuberculous peritonitis. It is believed that air entering the abdomen during laparotomy has a beneficial effect. It was further thought that laparotomy facilitates the release of a large amount of fluid from the peritoneal cavity, thereby reducing the amount of toxins, etc. Laparotomy has a beneficial effect only on exudative forms, especially during the period when the effusion reaches large sizes.