Plastic bronchitis

Plastic bronchitis

Plastic bronchitis (pseudomembranous bronchitis, fibrinous bronchitis, bronchial croup) is rare. Characteristic is the coughing of a sick child with fibrinous casts, reminiscent of the structure of the bronchial tree. Microscopy of casts reveals fibrin, mucus, lymphocytes, eosinophils, plasma cells and banal coccal flora. The presence of eosinophils in the casts of the bronchi, Shar-Ko-Leiden crystals, and Kurshman spirals was the basis to consider this disease as a manifestation of an allergy.

Etiology of plastic bronchitis

The etiology of the disease is not clear. They allow the possibility of developing primary chronic idiopathic plastic bronchitis and its occurrence as a secondary disease in various bronchopulmonary pathologies (tuberculosis, bronchiectasis, bronchial asthma, etc.).

Clinic of Plastic Bronchitis

In addition to coughing bronchial casts, patients have a cough, mainly paroxysmal, shortness of breath, pain and discomfort in the chest. The severity of these symptoms is determined by the extent of the lesion of the obstructed bronchial tree. This also determines the prevalence of atelectasis, which is one of the constant and characteristic symptoms of plastic bronchitis.
The course of the disease can be acute or relapsing. The intervals between relapses are different (from several days to several years). There are cases of a single manifestation of the disease, without relapse in the future.
In the acute period of the disease, dense white or gray masses are completely obstructed in their lumen in the main and lobar bronchi of the affected side. The prognosis for plastic bronchitis is mostly favorable. After isolation of the cast of bronchi, atelectasis is straightened.

Plastic bronchitis treatment

In the period of exacerbation, agents are used that help dilute the bronchial contents. The main method of treatment is bronchoscopy, which allows using bronchoscopic forceps to remove fibrinous deposits that are tightly soldered to the bronchial wall. Antibiotics are indicated.

Tuberculosis of the intrathoracic lymph nodes (Bronchoadenitis)

Tuberculous bronchoadenitis can occur as without pronounced symptoms, i hk and with obvious symptoms of tuberculous intoxication. In modern conditions, “small forms” of tuberculosis of the intrathoracic lymph nodes are increasingly observed. They are determined by the main OSROM during tomographic examination. Their clinical symptoms are scarce. Bronchoadenitis can be infiltrative and tumor-like. Infiltrative forms of bronchoadenitis usually occur with severe signs of intoxication, with a prolonged increase in temperature from 37.5 to 38 ° and higher, complaints of dry cough, which is sometimes bitonal (pertussis-like) due to compression of large bronchi. Tuberculous bronchoadenitis can be accompanied by pleurisy, often interlobar. In the presence of enlarged tumor-like lymph nodes, a violation of bronchial obstruction may occur as a result of compression of the bronchus from the outside or as a result of a breakthrough of the caseous contents of the lymph node into the lumen of the bronchus (bronchofistulosis syndrome) with the formation of atelectasis and bronchogenic seeding.

Diagnosis of bronchoadenitis

Recognition of bronchoadenitis requires a comprehensive clinical and radiological examination, taking into account anamnestic data, the nature of tuberculous intoxication, the presence of severe tuberculin reactions. Often, an incorrect assessment of radiological data entails overdiagnosis of these forms of tuberculosis.
The most convincing for the radiological diagnosis of bronchoadenitis are data from a tomographic study of the roots of the lungs. Changes in the roots of the lungs have to be differentiated mainly from lymphogranulomatosis, malignant neoplasms in the mediastinum, Beck sarcoidosis. In typical cases with bronchoadenitis, dullness of percussion sound in the interscapular space at the level of IV-V thoracic vertebrae (Korani symptom) and in the parasternal region can be determined.
During auscultation, altered breathing, scanty rales in the interscapular space and at the angle of the scapula are established.
Blood changes are expressed in accelerated ESR, a neutrophilic shift to the left. The white blood cell count is usually either normal or slightly increased. Accelerated ESR in combination with a pronounced tuberculin breakdown indicates the continued activity of the process. When bronchoadenitis has lost activity, changes in the blood, like tuberculin tests, are normalized. An X-ray examination in these cases reveals compaction of the lymph nodes and their petrification.
Tuberculous mycobacteria are usually detected with infiltrative bronchoadenitis, a breakthrough of the caseous lymph node in the bronchus – bronchofistulous forms (often in old age), and specific damage to the bronchial pathways. Mycobacterium tuberculosis is more often found in the study of bronchial lavage by sowing or flotation.
Patients with active tuberculosis of the intrathoracic lymph nodes need long-term treatment in a sanatorium using antibacterial drugs, and in some cases, surgical removal of caseous degenerated large lymph nodes. They need constant monitoring of the dispensary and treatment until a lasting clinical cure is established.

Complicated bronchial asthma

Complicated bronchial asthma – bronchial asthma, aggravated by the consequences of this disease or associated infectious and inflammatory process in the lungs. The most common complications are: asthmatic status, emphysema, pneumothorax, mediastinal and subcutaneous emphysema, pulmonary heart, lung atelectasis. Emphysema, observed in 2/3 of patients with bronchial asthma, has different developmental periods. It can be acute reversible (formed during an attack due to obstruction of the bronchi) and chronic irreversible (formed during repeated exacerbations of asthma). The progression of concomitant chronic bronchitis causes secondary obstructive emphysema. Due to emphysema, the value of irreversible airway obstruction increases significantly, which worsens the course and prospects of therapy for bronchial asthma. In patients, the rhythm of breathing during an attack is disturbed, the excursion of the chest decreases, its configuration changes. The main link in the formation of the pulmonary heart in bronchial asthma is a diffuse violation of bronchial obstruction leading to a series of consecutive changes: a decrease in the clearance of the pulmonary capillaries and arterioles, an increase in pressure in the pulmonary artery, uneven ventilation of the lungs, alveolar hypoventilation, a reduction in the blood vessels of the lungs, arterial hypoxemia, and an increase in work right ventricle of the heart. Immediate allergy mediators (serotonin) are involved in the pathogenesis of pulmonary hypertension, and disorders of the androgenic and glucocorticosteroid functions of the adrenal cortex are observed. The presence of severe pulmonary hypertension, overload of the right ventricle of the heart in combination with the hypokinetic type of central hemodynamics, a change in pulmonary volumes (a steady increase in OOL and its relationship to OEL) are signs of a formed pulmonary heart. Segmental atelectasis can form during an acute attack of asthmatic status or in case of bronchial obstruction with Aspergillus fumigatus plug in case of allergic bronchopulmonary aspergillosis. The signs of this complication are different depending on the cause, location and severity of pulmonary collapse. The range of symptoms ranges from a mild cough with lack of physical data to tachypnea, cyanosis, displacement of the heart and mediastinum, elevation of the diaphragm on the side involved in the process. Persistent atelectases in the right middle lobe of the lung are manifested by constant or intermittent shortness of breath (right middle lobe syndrome). The diagnosis is established by x-ray examination. In unclear cases , additional research is indicated: bronchoscopy, bronchography. Bronchial asthma is also accompanied by hemodynamic disorders. During the attack in most patients, the pressure in the pulmonary artery system is increased, and the contractility of the right ventricle of the heart is reduced; sinus tachycardia (120 strokes or more in 1 min), various ECG disturbances, paradoxical pulse are noted. These disorders correspond to the severity of bronchial obstruction. During the period of remission, the pressure in the ductal artery remains elevated and disturbances in the phase structure of the heart remain (hypodynamia of the I – II degree of the right and left ventricles) depending on the severity of the course. Pneumothorax, mediastinal and subcutaneous emphysema can occur during asthmatic status. Treatment of complications is given according to the general rules of therapy for these conditions. Particular attention should be paid to the rehabilitation of the infectious and inflammatory focus in the lungs, which is most often represented by chronic obstructive bronchitis.

Bronchial asthma during pregnancy

Features of the course of bronchial asthma during pregnancy . Pregnancy can cause an improvement and worsening of the course of bronchial asthma. Approximately 40% of women experience remission, 35 – the course does not change, in 25% there is an exacerbation; sometimes the first attack occurs during pregnancy. A certain prognostic value is the severity of the disease before pregnancy. The course of a mild form of bronchial asthma does not change or improve; severe bronchial asthma is prone to exacerbation. Deterioration is most often observed and most pronounced in the last months of pregnancy. The effect of pregnancy on the subsequent course of the disease is variable. In 25-30% of patients, it noticeably worsens. Responsible for the immediate period after childbirth. Mothers with asthma have an increased risk of antenatal and neonatal fetal death. The mechanism of the effect of pregnancy on the course of bronchial asthma is not precisely established. Several factors are attached importance: a gradual increase in the level of plasma glucocorticosteroids by 2-2.5 times (positive factor), with which, possibly, an increase in the level of cAMP in the plasma of pregnant women, which is a good prognostic sign; increased progesterone content. having a different effect – a weak bronchodilating effect and increased shortness of breath due to excitation of the respiratory center; a decrease in the function of cellular immunity with possible consequences in the form of a change in the severity of allergies and an increase in the likelihood of an exacerbation of a bacterial infection of the respiratory tract; an increase in the size of the fetus and the associated increase in the diaphragm and a change in the respiratory volume of the lungs (the hormonal or metabolic nature of these changes is also assumed); allergic mothers with fetal antigens, which causes the development of an immunological conflict involving the lungs. The basic principles of treating bronchial asthma during pregnancy are the minimum risk for the mother and the fetus, the prevention of complications in the neonatal and perinatal periods. In the early stages of pregnancy, drugs that can stimulate uterine contractions should be avoided. Adrenergic drugs (3-stimulating drugs are well tolerated, however, since the initial clinical trials of these substances did not study their effect on pregnant women, it is not recommended to use them in the first trimester . The same applies to intal. Antibiotics of the tetracycline group for the treatment of bronchial asthma during pregnancy. contraindicated due to teratogenic effects Methylxanthines are safe and can be used, although they can increase nausea and vomiting in the first trimester of pregnancy. idnye drugs are prescribed, if necessary; the risk of complications for the mother as a result of glucocorticosteroid therapy does not increase, but may develop transient suppression of fetal adrenal glands, resulting in the glucocorticosteroid insufficiency in neonates with stress (eg, infection). In the first six weeks after birth.

Exogenous Allergic Bronchioloalveolitis

Exogenous allergic bronchioloalveolitis (synonyms of the disease: hypersensitive pneumonitis) – diseases caused by inhalation of organic dust with a particle diameter of up to 5 μm, characterized by an inflammatory process (mainly in the alveoli and bronchioles) with interstitial infiltration and the formation of granulomas, which tend to fibrosis with repeated prolonged contact antigen. For the first time, a lung disease similar to exogenous allergic bronchioalveolitis was described in 1713 by Ramazzini, in more detail in 1932, Campbell (“farmer’s lung”). The name “exogenous allergic alveolitis”, proposed by Pepis in 1967 due to the frequent involvement of bronchioles in the process, is not entirely accurate, the term “exogenous allergic bronchioloalveolitis” is considered more correct . This is a relatively rare disease, but incidence can be high in certain areas. Outbreaks of it are most often observed in years with wet summers, usually a lot of snow falls.

Etiology of exogenous allergic bronchioloalveolitis

Organic substances that cause exogenous allergic bronchioloalveolitis are very diverse. The most common cause of the disease is thermophilic actinomycetes, bacteria with a morphological characteristic of fungi that are ubiquitous and are found in earth, compost, hay, straw dust, grain, sawdust and other wet organic materials that can mold and heat up to a temperature of 40-60 ° C optimal for mushroom growth. Actinomycetes also reproduce in the heating, cooling and air conditioning systems of the recirculating type. Many microorganisms have been identified in compressors and water from vacuum pumps that can cause the disease. The most important representative of thermophilic actinomycetes is Micropolyspora faeni, whose spores with a diameter of less than 5 microns can penetrate the periphery of the lung. Actinomycetes contain three antigens: A, B, C. Antigens A and B are proteins that cross-react with antigens of fungi of other species (Aspergillus, Mucor), C is a polysaccharide that is most specific. An important group of etiological factors of the disease is whey proteins and dust from the droppings of various birds (pigeons, parrots, chickens, ducks, turkeys). Bird droppings extract (a mixture of soluble proteins, glycoproteins and polysaccharides) is a species-specific antigen – serum g-globulin. Antigens of the gastrointestinal tract of birds, cross-react with serum proteins. The frequency of exogenous allergic bronchioloalveolitis due to bird proteins is low; more often, the disease is caused by the proteins of pigeons and parrots. Exogenous allergic bronchioloalveolitis can also provoke other animal proteins, in particular, inhalation of rat serum droplets is described as the cause of the disease in laboratory workers. The disease can cause plant dust (from cotton, hemp, hemp, cork) and some medications: pituitary powder in patients with diabetes insipidus, sometimes Intal.

Pathogenesis of exogenous allergic bronchioalveolitis

Allergic predisposition factors in patients with exogenous allergic bronchioalveolitis have not been established, although HLA-BW40 and HLA-B8 are more common. Immunological and non-immunological mechanisms are involved in the development of the disease. Allergic reactions of various types are expected to be involved: delayed-type hypersensitivity, immune complexes, immediate-type allergic reactions caused by antibodies related to immunoglobulin E, mediated by cytotoxicity antibodies. There is currently no evidence of a predominance of a particular type of immunological reaction.
Existing ideas about exogenous allergic bronchioloalveolitis as a disease caused by the immune complex are questioned for the following reasons: there is no parallelism between the level of precipitating antibodies related to immunoglobulin G and the severity of the disease; precipitins are found in a large number of healthy individuals in contact with the antigen; in the acute period of the disease, granulomas are formed that are uncharacteristic of the Arthus phenomenon; skin reactions according to the type of Arthus phenomenon to specific antigens are not constantly detected in patients;
deposits of immune complexes in biopsies of human lungs are noted only at an early stage of the process; histological signs with exogenous allergic bronchioalveolitis are more characteristic of cellular reactions, fibrinoid necrosis of the vascular walls and perivascular infiltration by segmented cells. Many authors assign the leading role of HRT. The role of GNT due to immunoglobulin E is not clear, antibodies related to immunoglobulin E have not been identified, although certain antigens (pigeon proteins, pituitary powder) can cause GNT. It is assumed that immunoglobulin E does not participate in the development of a typical granulomatous lesion, but can mediate GNT. The question of the role of immunoglobulin E needs to be studied in connection with recent data on late-type allergic reactions caused by immunoglobulin E and characterized by mononuclear cell infiltration without the presence of vasculitis. Perhaps the participation of a secondary autoimmune cytotoxic mechanism associated with chronic inflammation and tissue destruction. Non-immunological mechanisms are associated with the characteristics of disease-causing antigens that are resistant to lysosomal enzymes, are not destroyed by alveolar macrophages, are able to activate the complement system in an alternative way and have a nonspecific adjuvant effect on the induction of cell-mediated reactions and activation of alveolar macrophages. Immuno-non-immunological mechanisms activate alveolar macrophages, which, through soluble mediators, induce inflammation and stimulate the activity of fibroblasts, which leads to fibrosis. There is an opinion that it is activated alveolar macrophages that occupy a central place in the pathogenesis of exogenous allergic bronchioloalveolitis.

Pathomorphology of exogenous allergic bronchioalveolitis

With the fulminant form of exogenous allergic bronchioalveolitis, ending with the rapid death of the patient, intense inflammatory exudate in the alveolar septa, hemorrhagic edema inside the alveoli, necrosis of the bronchioles with obliteration are detected. In the acute period, infiltration of the alveoli and bronchioles with lymphocytes, plasma cells and a large number of alveolar macrophages is detected. Noncaseating sarcoid-like granulomas, consisting of lymphocytes, activated macrophages, epithelioid and giant cells, are characteristic. In a very early period of the disease, deposits of immune complexes on the alveolar membrane and necrotizing vasculitis are found. In the chronic form, infiltration by lymphocytes and plasma cells is less pronounced, granulomas are scattered in areas of interstitial fibrosis, destruction of the bronchioles mural structure with macrophage obliteration of the lumen, hypertrophy of the cuboid epithelium of the alveoli, and sometimes of the “emphysema” zone due to uneven destruction of the alveoli are observed. At the final stage, destruction of the alveoli, fibrosis, and the picture of the “cell lung” develop.

Clinic of exogenous allergic bronchioloalveolitis

Clinical signs of the disease depend on the nature of the organic particles, the intensity and frequency of inhalation, and the characteristics of the immunological response of the patient. The allergy period is different – from several months to several years. Usually, 4-6 hours after inhalation of organic dust, a cough appears, dry or with viscous yellow sputum, which may contain blood; there is an increase in temperature to 38-40 ° C, heavy sweat, chills, myalgia, weakness, retrosternal pain. Inspiratory dyspnea progresses rapidly. Over the lungs, dullness of the sound and crepitus are determined. In the acute period, tachycardia and bronchial obstruction resistant to the action of bronchodilators may occur, which indicates the prevalence of inflammation over increased bronchial tone. Fever lasts up to 24 hours, shortness of breath and weakness sometimes lasts up to several weeks. In other cases, the symptoms spontaneously disappear within a day. Upon contact with certain antigens (pigeon proteins, pituitary powder), HNT can occur, which occurs rarely if actinomycetes are the cause of exogenous allergic bronchioloalveolitis. With repeated exposures of the antigen, shortness of breath intensifies, anorexia, weight loss are noted – the disease acquires a chronic course, which can develop without an acute attack – in cases of prolonged contact with small stumps of antigen. This form is formed by bird lovers, especially budgerigar owners, workers in contact with heating and conditioning systems, and is characterized by progressive shortness of breath, coughing, weakness, malaise, and emaciation. Wet cracking rales (“cracking cellophane”) are heard over the lungs, but this is less typical of a disease than an idiopathic fibrosing alveolitis; in 10% of patients, after a gradual onset, subsequent antigen inhalations cause acute symptoms and GNT. Rare clinical signs of exogenous allergic allergic bronchioalveolitis are also described: chest tightness, impaired consciousness, changes in sensitivity and paralysis of the facial nerve.

The course of the disease is usually acute or subacute when inhaled enough antigen; with massive inhalation, the disease can last no more than a day. In cases of prolonged exposure to small doses of antigen, the disease progresses with the development of fibrosis.

The prognosis for acute and subacute currents is favorable, elimination of antigen and glucocorticosteroid therapy lead to the reverse development of the process. The prognosis is less favorable if the disease lasts several years, especially in the elderly.

Diagnosis of exogenous allergic bronchioalveolitis

There are no specific diagnostic methods for exogenous allergic bronchioloalveolitis. The diagnosis is based on the following criteria: typical allergic history (contact with organic dust); dynamics of clinical signs; positive allergic diagnostic tests intradermally for the corresponding antigens such as GNT and HRT; detection of precipitating antibodies related to immunoglobulins G; lack of eosinophilia of peripheral blood and sputum; radiological changes; restrictive ventilation disorders; positive RBTL and RTML; inhibition of macrophage migration under the influence of a specific antigen; HRT, GNT or a double bronchospastic reaction or crepitation over the lungs after allergological diagnostic tests of provocative inhalation with extracts of specific antigens.

X-ray data in the acute phase of the disease may be normal. As the disease develops, bilateral middle and lower lobe focal shadows appear with a tendency to merge and diffuse. Comparison of radiographs with lung biopsy data reveals that focal shadows correspond to granulomas and interstitial infiltrates. In acute cases, the radiograph of the lungs normalizes within 10-20 days after eliminating contact with the antigen. For the chronic form of exogenous allergic bronchioloalveolitis, fibrosis is characteristic; a cell lung pattern may develop.

Functional disorders of the respiratory system consist in restrictive ventilation failure, a decrease in the diffusion capacity of the lungs and static pulmonary volumes in the absence of airway obstruction. In severe cases, hypoxemia and hypercapnia may occur. In the later stages, a third of patients develop irreversible airway obstruction with a change in the relationship between ventilation and blood flow. In the acute phase of exogenous allergic bronchioalveolitis with fever, leukocytosis of up to (15-20) 109 leukocytes per 1 liter with a neutrophilic shift is observed, eosinophilia, hypergammaglobulinemia are sometimes noted; the level of immunoglobulins is increased, with the exception of immunoglobulin E.
Positive delayed and immediate skin tests for the introduction of antigen, antibodies related to immunoglobulin E, positive cell-type reactions (RBTL and RTML) with specific antigens are observed not only in patients with exogenous allergic bronchioalveolitis, but also in a certain contingent of people in contact with the same antigens, but not having symptoms of the disease. Cell-type reactions are of great diagnostic value compared to the detection of precipitating antibodies. RBTL remains positive for many months, while the precipitation reaction quickly becomes negative after cessation of contact with the antigen. Conducting provocative inhalation tests with specific antigens is unsafe, but in some cases it is possible. The diagnosis is helped by a study of bronchial lavage water, in which an increased number of lymphocytes is detected (the larger the more acute the form of the disease) – from 35 to 90% (average 50-60%). These results differ from those obtained for persons also exposed to organic dust, but without signs of disease. Despite the presence of specific precnpitins in the latter, the cellular composition of lavage fluid remains normal, which coincides with the absence of clinical signs of the disease. Lavage fluid lymphocytosis has not only diagnostic, but also prognostic value, as it quickly disappears with effective treatment or a spontaneous favorable course and is again detected during exacerbation.

Differential diagnosis of exogenous allergic bronchioloalveolitis

Differential diagnosis of the acute form is carried out with acute viral infectious diseases (influenza, etc.), acute pneumonia, allergic bronchopulmonary aspergillosis, chronic – with other diffuse lung lesions with progressive pulmonary and general symptoms.

Treatment of exogenous allergic bronchioloalveolitis

The main event is the elimination of the etiological factor. In particular, if the cause of the disease is pituitary powder (in patients with diabetes insipidus), then when switching to synthetic vasopressin, the symptoms of the disease disappear. If the disease progresses after removal of the antigen, then pharmacological therapy is necessary. The main treatment is glucocorticosteroid drugs, which are most effective in the acute form of exogenous allergic bronchioalveolitis, with a chronic effect is insufficient. The duration of glucocorticosteroid therapy is determined by clinical and laboratory data. GNT during provocative inhalation tests with specific antigens is prevented by the intal, but its effectiveness in conditions of professional contact with organic dust has not been proved. Antihistamines and bronchodilators are not effective. In cases of infection, antibiotics are prescribed, with appropriate indications, antimycotic drugs.
Prevention consists in storing organic materials under conditions that exclude their moisture, heating and decay.

Obliterate bronchiolitis

Obliterating bronchiolitis is rarely observed, mainly in children in the first months of life, and can occur as a complication of ARVI.

Clinic of obliterating bronchiolitis

At the onset of the disease, symptoms of acute bronchiolitis or bronchopneumonia appear. At a blood test neutrophilia, sometimes moderate leukocytosis is noted. After the acute period of the disease, relative remission sets in, lasting 3 to 4 weeks. However, in this period auscultatory changes are detected (rales of different sizes, wheezing exhalation), localized on the side of the lesion.
Then comes the third period in which, at an unstable febrile body temperature, bronchopulmonary changes intensify and respiratory failure increases. With bilateral damage during the next exacerbation, a fatal outcome is possible. With a unilateral lesion, a rapid decrease in the lung occurs due to atrophy of the alveolar tissue and a significant secondary violation of the functional pulmonary blood flow. Patients develop symptoms characteristic of McLeod’s syndrome (signs of chronic bronchitis in the affected lung and severe respiratory failure).
Radiologically, in the initial period of the disease, massive shadow formations due to the presence of atelectasis are detected mainly on one side . In the period of remission, these changes disappear, however, after such relative well-being, a rapidly progressive decrease in the lung occurs with the development of pneumosclerosis.
The deformity of the proximal parts of the bronchi, ending blindly (non-filling of peripheral branches with contrast medium), is bronchographically detected.
Diffuse endobronchitis of the affected lung is bronchoscopically detected.

Treatment of obliterating bronchiolitis

In the initial period of the disease, the use of antibiotics and glycocorticoids is indicated, symptomatic therapy (oxygen, with indications – antispasmodic and antihistamine drugs). Inhalations of semisynthetic penicillins in combination with other drugs, physical therapy, chest massage, etc. are effective. The
prognosis for diffuse obliterating bronchiolitis is serious and more favorable in children in whom obliteration is limited to a small number of bronchioles.

Atherosclerosis obliterans 

Obliterating atherosclerosis of the aorta and major vessels of the lower extremities in frequency is in first place among other diseases of the peripheral arteries. It occurs mainly in men over 40 years old. The disease often causes severe limb ischemia, condemning patients to excruciating suffering and depriving them of working capacity. The process is localized mainly in large vessels (aorta, iliac arteries) or medium-sized arteries (femoral, popliteal). 

Etiology, pathogenesis of obliterating atherosclerosis

Atherosclerotic lesions of the arteries are a manifestation of general atherosclerosis. In its occurrence, the same etiological factors and pathogenetic mechanisms play a role that are responsible for the formation of atherosclerosis of any other localization. The main changes in atherosclerosis develop in the intima of the arteries. A young connective tissue appears around the foci of lipoidosis , the maturation of which leads to the formation of fibrous plaque. Platelets and fibrin clots settle on plaques. With abundant accumulation of lipids, there is a violation of blood circulation in plaques, the necrosis of which causes the appearance of atheromas, i.e. cavities filled with atheromatous masses and tissue detritus. Atheromatousmasses are rejected into the lumen of the vessel. Getting with a blood stream into the distal bloodstream, they become the cause of embolism. At the same time, calcium salts are deposited in the altered tissue of plaques, in areas of degenerating elastic fibers, which is the final stage in the development of atherosclerosis and leads to impaired patency of the vessel.

Clinic for obliterating atherosclerosis

During obliterating atherosclerosis, the same 4 stages are distinguished as with obliterating endarteritis. For several years obliteri – ruyuschy atherosclerosis may be asymptomatic, but after the first clinical manifestations progress rapidly. In some cases, due to the joined thrombosis, the clinical manifestations of the disease appear suddenly. A characteristic symptom of obliterating atherosclerosis is intermittent claudication, manifested by pain in the calf muscles, which appears when walking and disappears after a short rest. With atherosclerotic lesions of the terminal abdominal aorta and iliac arteries ( Leriche syndrome ), the pain is localized not only in the legs, but also in the gluteus, lumbar and thigh muscles. Intermittent claudication intensifies when climbing stairs or uphill. Chilliness , increased sensitivity of the lower extremities to cold, and a feeling of numbness in the feet are noted. Due to ischemia, the color of the skin of the lower extremities changes, which in the initial stages of the disease become pale, and in patients with Lerish’s syndrome have the color of ivory. In the later stages of the disease the skin of feet and toes becomes purplish-bluish okrasku.Razvitie trophic disorders leading to hair loss, breach of nail growth. One of the manifestations of occlusion of the aorto-iliac segment is impotence due to circulatory disorders in the system of internal iliac arteries. This symptom occurs in 50% of patients.

Diagnosis of obliterating atherosclerosis

When examined in patients with obliterating atherosclerosis, hypotrophy or atrophy of the muscles of the lower extremities is often noted. In obliterating atherosclerosis, the femoral- iliac segment is most often affected , therefore, starting from the place of discharge of the deep femoral artery, the pulsation in the vast majority of patients is not determined either on the popliteal artery or on the arteries of the feet. With the occlusion of the abdominal aorta and iliac arteries, it is not determined on the femoral arteries. Systolic murmur is usually heard over stenotic arteries. With stenosis of the abdominal aorta and iliac arteries, it can be determined not only above the anterior abdominal wall, but also on the femoral arteries under the inguinal ligament. Rheovasography with obliterating atherosclerosis records a decrease in the main blood flow in the lower extremities. In severe cases of lower limb ischemia, rheovasographic curves take the form of straight lines, additional teeth disappear on the catacrotis , the rheographic index decreases, the infrared radiation intensity recorded by the thermal imager decreases until the thermal pattern is completely darkened, thermal asymmetry increases. Ultrasound examination makes it possible to determine the level of atherosclerotic and the degree of blood supply to the distal parts of the affected limb. The main method of topical diagnosis in obliterating atherosclerosis is angiography. It allows you to determine the localization and extent of the pathological process, the degree of damage to the arteries (occlusion, stenosis), the nature of collateral circulation, the state of the distal bloodstream. By angio graphic signs of atherosclerosis include edge defects filling ize – degeneracy circuit portions of the arteries to the stenosis, the presence or segmental common occlusions with filling through distal collaterals network.

Differential diagnosis of obliterating atherosclerosis

Differential diagnosis should be made with obliterative endarte – Riitta and trombangiitom.Endarteriitom ill young people. Overcooling, frostbite, emotional stress contribute to its development. The arteries of the distal segments of the limbs are mainly affected, a long, undulating course of the disease is characteristic. In patients with atherosclerosis may occur symptoms of other vascular beds (heart, brain, kidneys, etc..), Giperholesterine – mia , diabetes that occurs very endarteriite redko.Differentsialnaya diagnosis of arteriosclerosis obliterans and thromboangiitis usually straightforward. The main difference lies in the fact that Trom – Bang occurs predominantly in young men and is characterized by a combination of symptoms of arterial insufficiency and migratory thrombophlebitis of superficial veins.

Etiology, pathogenesis of obliterating endarteritis

The development of endarteritis is promoted by prolonged hypothermia, frostbite, injuries of the lower extremities, smoking, vitamin deficiencies, severe shock, mental disorders, infections, disorders of autoimmune processes and other factors that cause persistent spasm of the vessels. Long-term spasm of the arteries and their accompanying vasa vasorum leads to chronic and walls, resulting in intimal hyperplasia, adventitious fibrosis and degenerative changes in the nervous system of the vascular wall. Against the background of altered intimacy, a blood clot forms, narrowing and obliteration of the lumen of the vessel occur. If at the beginning of the disease mainly the distal vessels of the lower extremities (lower leg and foot) are affected, then subsequently larger arteries (popliteal, femoral, iliac) are involved in the pathological process. A sharp weakening of blood flow through the arteries leads to a deterioration in blood flow in the vessels of the microvasculature providing tissue metabolism, reduced oxygen delivery to tissues and tissue hypoxia develops, which is enhanced by the opening of arteriovenular anastomoses. Under these conditions, blood viscosity increases, erythrocyte aggregation increases, the adhesion-aggregation increases, and the disaggregation properties of platelets decrease . Formed platelet agreganty that block the microvasculature. Chronic hypoxia leads to the disintegration of the lysosomes with the release of hydrolases, Lizzie – ruyuschih cells and tissues. Tissue necrosis, the accumulation of proteolytic enzymes. The body is sensitized to protein breakdown products. Pathological autoimmune processes occur, exacerbating microcirculation disorders and enhancing local hypoxia and tissue necrosis.

Clinic of obliterating endarteritis

Depending on the degree of insufficiency of arterial blood supply to the affected limb, 4 stages of obliterating endarteritis are distinguished:
Stage I – functional compensation. Patients note chilliness, sometimes tingling and burning at the fingertips, increased fatigue. When cooled, the limbs become pale, cold to the touch. When passing at a speed of 4-5 km / h a distance of more than 1000 m in patients with intermittent claudication. It lies in the fact that the patient begins to experience pain in the calf muscles or foot, causing him to stop. In the pathogenesis of this symptom, a number of factors are important, in particular, insufficient blood supply to the muscles, impaired oxygen utilization, and the accumulation of under-oxidized metabolic products in the tissues. The pulse on the arteries of the feet in this stage is weakened or not determined; Stage II – subcompensation . Intermittent claudication increases and at the indicated pace of walking it occurs already after passing 200 m or a little earlier, the skin of the feet and lower legs loses its inherent elasticity, it becomes dry, flaky, hyperkeratosis develops on the plantar surface. Nail growth slows down, they thicken, become brittle, dull, acquire a matte or brown color. Disturbed and hair growth on the affected limb, which leads to the appearance of areas of baldness. Atrophy of the subcutaneous base and small muscles of the foot begins to develop. Ripple in the arteries of the feet is not determined; Stage III – decompensation. There is pain in the affected limb at rest. Walking becomes possible at a distance of 25-50 m. The color of the skin changes dramatically depending on the position of the affected limb. Her rise is accompanied by blanching, lowering – by redness of the skin. The skin becomes thinner and easily vulnerable. Minor injuries – scuffs, bruises, after cutting off nails – lead to the formation of cracks and superficial painful ulcers. To alleviate the suffering, patients give the limb a forced position, lowering it down, sitting asleep. Atrophy of the muscles of the leg and foot progresses. Disability of patients is significantly reduced; IV stage – destructive changes. Pain in the foot and fingers becomes constant and unbearable. The resulting ulcers are usually located in the distal extremities, often on the fingers. Their edges and bottom are covered with a dirty gray coating, there are no granulations, and there is inflammatory infiltration in the circle. Swelling of the foot and lower leg joins. Developing gangrene of the fingers and feet often proceeds as wet. Ripple may be absent due to ascending arterial thrombosis. Disability in patients at this stage is completely lost.

The course of obliterating endarteritis is usually long, over several years. It is characterized by periods of exacerbation and remission. Exacerbation is more often observed in autumn and spring. There are two main clinical forms of the course of the disease: 1) limited, in which, as a rule, arteries of one or both lower extremities are affected. This form is benign, changes progress slowly; 2) generalized , characterized by damage not only to the vessels of the limbs, but also to the visceral vessels of the abdominal part of the aorta, branches of the aortic arch, coronary and cerebral arteries.

Diagnosis of obliterating endarteritis

Diagnosis of obliterating endarteritis is based on the clinic of the disease, the results of functional tests and special research methods. Among the functional tests, indicating a lack of arterial blood supply is certainly the most revealing symptom of plantar ischemia Oppel , sample Goldflama , Samuels and Shamova , knee phenomenon Panchenko. Rheovasography , ultrasound flowmetry , thermography and angiography of the lower extremities help to establish the diagnosis . Obliterating endarteritis is characterized by a decrease in the amplitude of the main wave of the rheographic curve in the leads from the lower leg and especially the foot, smoothness of its contours, the disappearance of additional waves, a significant decrease in the value of the rheographic index. Rheograms recorded from the distal sections of the affected limb are straight lines. Ultrasound findings usually indicate a marked decrease in pressure in the arteries of the feet, a decrease in the linear velocity of blood flow, and help to clarify the level of vascular damage.
A thermographic study reveals a decrease in the intensity of infrared radiation in the distal extremities. On angiograms , normal patency of the aorta, iliac and femoral arteries is usually visible, the popliteal artery is narrowed, often occluded , the leg arteries are usually obliterated , and a network of small corkscrew collaterals is traced. If the contrast medium fills the affected vessels, then their contours are even, there is no scalloped edges, so characteristic for obliterating atherosclerosis.

Etiology, pathogenesis of Raynaud’s disease

The disease is characterized by spasm of the vessels of the fingers of the upper and lower extremities and very rarely – the tips of the ears and nose. The process is localized mainly on the upper limbs, the lesion is usually bilateral and symmetrical. The main reasons for the development of Raynaud’s disease are prolonged hypothermia, chronic trauma to the fingers, impaired functions of some endocrine organs (thyroid, genital glands), severe emotional stress. Triggers in the development of the disease are disorders of the vascular innervation.

Raynaud’s Clinic

There are three stages of the disease:
stage I – angiospastic . It is characterized by a pronounced increase in vascular tone. There is a short-term spasm of the vessels of the terminal phalanges. Fingers (often II and III hands and I-III feet) become pale, cold to the touch and insensitive. After a few minutes, the spasm is replaced by vasodilation. Due to active hyperemia, redness occurs and the fingers darken. Patients notice a strong burning sensation and sharp pain in them, swelling appears in the area of ​​interphalangeal joints. When the vascular tone normalizes, the color of the fingers becomes normal and the pain disappears. Stage II – angioparalytic . Attacks of pallor of the “dead finger” in this stage are rarely repeated, the brush and fingers become bluish. When lowering the arms down, it intensifies and acquires a purple hue. Swelling and pastiness of the fingers become permanent. The indicated stages last on average 3 years — 5 years. Stage III – trophoparalytic . At this stage, panaritiums and ulcers appear on the fingers. Foci of necrosis are formed, capturing the soft tissues of 1-2 terminal phalanges, less often of the entire finger. With the development of demarcation, necrotic areas are rejected, after which slowly healing ulcers remain, the scars from which are pale in color, painful, fused to the bone.

Differential diagnosis of Raynaud’s disease

Differential diagnosis includes obliterans endarte – Riitta and diseases in which circulatory disorder in the upper limb caused extravasal compression subclavian artery.
In contrast to obliterating endarteritis in Raynaud’s disease, pulsation in the arteries of the feet and radial arteries persists. The disease is more benign. Compression of the subclavian artery can be caused by an additional cervical rib or a highly located I rib (costoclavicular syndrome), a hypertrophied anterior scalene muscle, or its tendon (anterior scalene syndrome), or a pathologically altered pectoral muscle (pectoralis minor syndrome). With the above syndromes, both arteries and brachial plexus are compressed, so their clinic consists of vascular and neurological disorders. Constant trauma to the artery leads to cicatricial changes in its wall, periarteritis and may result in vascular thrombosis. The result of severe disturbances in the blood supply to the upper limb are trophic disorders. The correct assessment of the clinical picture, the results of samples with a change in the position of the limb allows you to differentiate these syndromes from Raynaud’s disease . In patients with an additional VI rib, as well as costal-clavicular syndrome, an x-ray study is important in the diagnosis.