Atherosclerosis of intestinal vessels symptoms. Morphological study of the intestinal mucosa in the diagnosis of diseases occurring with diarrhea syndrome. Morphological changes in the intestinal mucosa in various diseases

Intestinal atherosclerosis is a pathology that is characterized by the deposition of cholesterol on the surface of the vascular walls, which in turn seriously impairs the supply of nutrients to the organ.

Atherosclerotic plaques can form in absolutely any vessel of the human body. Most often, this disease affects large vascular trunks, which are the intestinal vessels. Atherosclerosis of the intestinal arteries is characterized by the manifestation of atypical symptoms. A vascular surgeon treats this type of disease.

Symptoms of the disease

First of all, you need to pay attention to acute symptoms, since they are a significant factor negatively affecting general state requiring urgent medical attention. Acute ischemic colitis, which developed due to blockage of blood vessels, is characterized by the following symptoms:

If you start treatment at this stage of the disease, it is possible to completely restore the normal state of the vessel and avoid serious consequences.

It is much more difficult to determine the disease in chronic or subacute form. In this case, the symptoms are similar to those of other pathologies gastrointestinal tract, in view of which the real reason feeling unwell detected only after a thorough examination of the whole body. Chronic vascular disease in the intestine is characterized by the presence of the following symptoms:

Causes and classification

Atherosclerosis of intestinal vessels can provoke disturbances in the functioning of all digestive organs. Ischemic colitis can be caused by the following factors:

Atherosclerosis of intestinal vessels can also be triggered by the deposition of lipid molecules on the surface of the artery walls.

The following stages of development are distinguished of this disease:

Ischemia - the first stage is characterized by the development of a slight lack of blood, which initial stage does not cause pronounced discomfort. This stage can be cured with drug therapy.
Heart attack - this stage of pathology causes an increase in painful sensations in the abdomen, which is explained by the death of certain areas of the intestine.
Peritonitis - the third stage is the most severe. At this stage, the patient suffers from severe acute pain, the appearance of which is explained by the breakdown of intestinal tissues and the entry of contents into the abdominal cavity. This phenomenon often leads to death.

If the inflammatory process affects the abdominal vessels, coronary disease may develop, which entails the gradual death of intestinal tissue. However, the prognosis is most often unfavorable.

Diagnosis and treatment methods

Laboratory methods play a huge role in identifying intestinal atherosclerosis. Thanks to some tests, it is possible to identify the body's predisposition to atherogenesis. In this case, it is necessary to study the condition fat metabolism, as well as determine the tendency to increased blood clotting, which is usually observed with thrombosis.

The most common method that can effectively treat this disease is surgery.

If the disease is chronic, the doctor may prescribe the following therapeutic procedures:

a diet aimed at reducing the amount of cholesterol in the blood;
the use of drugs that have a hypocholesterol effect;
restoration of blood flow in large and medium-sized vessels (vasodilating drugs are used for this);
reduced risk of thrombosis (decreased blood density);
elimination of symptoms (reduction blood pressure, improving the functioning of the gastrointestinal tract, relieving pain).

When acute course illness, the only effective way Treatment is surgery, which is performed by a vascular surgeon. In this case, the doctor can use various methods surgical operation aimed at restoring blood access to the digestive organs.

Treatment of atherosclerosis folk remedies extremely undesirable, since in most cases such methods are ineffective. When the intestines are damaged, symptoms often do not become apparent immediately, so it is very important to have regular examinations with a doctor. This will help to identify any disease in time and increase the chances of a favorable outcome.

In recent years, due to the active implementation in clinical practice endoscopy, in the diagnosis of diseases occurring with diarrhea syndrome, methods of morphological examination of biopsy samples of the intestinal mucosa have become widespread, allowing not only to confirm a preliminary clinical diagnosis, but also to evaluate the dynamics of the process, the nature of the course of the disease, and the effectiveness of the treatment. Using electron microscopy, histochemical, immunoluminescent, enzymological and other modern methods research, a morphologist can help in diagnosing the most subtle, initial changes, when specific clinical manifestations may still be absent.

Accuracy morphological diagnostics largely depends on the technique of taking the biopsy. The biopsy specimen should be as little traumatized as possible, without coagulation damage. It is necessary that the material sent for research be absolutely informative, sufficient in the number of pieces and their sizes. Small-sized biopsies do not always provide an idea of changes in the entire surface of the mucous membrane of the small or large intestine and can cause false negative results. For diffuse lesions (for example, common forms of ulcerative colitis), biopsies should be multiple, taken from different parts of the intestine.

Research methods.

Biopsies obtained during endoscopic examination are examined primarily using light microscopy. In this case, histological methods of staining the material are usually used to obtain an overview picture. To assess the secretory function of the intestinal epithelium, histochemical methods are used to identify neutral (CHIK reaction) and acidic (Alcian blue staining) glycosaminoglycans. Material from tumors and polyps is stained with picrofuchsin according to van Gieson to detect connective tissue stroma. IN in some cases Sudan III or IV staining is used to identify lipids. To study regenerative processes in the intestinal epithelium, the Feulgen reaction (for DNA) or staining with gallocyanine and alum chromate (for DNA and RNA) is used.

Can help diagnose some diseases histoenzyme-chemical methods, allowing to identify certain enzymes and determine their activity. For example, in celiac disease, a deficiency of specific peptidases is found that ensures the deamination of gliadin in the intestine.

Indicative in in this case is a study of biopsies taken before and after a gluten-free diet.

Electron microscopic examination allows us to monitor at the ultrastructural level the most subtle changes that develop during various diseases.

By using morphometric methods you can obtain objective information about the condition of the intestinal mucosa, calculate the height and number of villi, the depth and number of crypts, the content of bordered epithelial cells and goblet cells, interepithelial lymphocytes, assess the thickness of the mucous membrane, infiltrate cells in the stroma, etc.

Histoautoradiography makes it possible to visually assess the varying degrees of intensity of biochemical processes in the cells of the intestinal mucosa and allows, based on the determination of DNA synthesis, to draw a conclusion about the dynamics of the mitotic cycle.

Immunomorphological methods(in particular, the immunoluminescent method) help to identify the components of immune reactions in tissues (antigen, antibody, complement) and establish the connection of these reactions with the nature of developing morphological changes.

The biopsy obtained by endoscopy, in addition to conventional light microscopy, can be examined using stereoscopic microscopy. This method does not require pre-treatment material and takes little time. At the same time, the intestinal mucosa retains its light, which makes it possible to evaluate intestinal villi under conditions close to natural. Finally, from a biopsy obtained during endoscopy, an impression smear can be prepared and a cytological examination can be performed. Advantage this method consists in quickly (on the same day) receiving an answer about the nature of the pathological process.

Morphological changes in the intestinal mucosa in various diseases.

At chronic enteritis, arising, for example, as a result of radiation injury, with long-term use of non-steroidal anti-inflammatory drugs, immunodeficiency states, etc., morphological changes develop, characterized by chronic inflammation, disorders of epithelial regeneration, which culminate in atrophy and structural restructuring of the mucous membrane. Therefore, the morphological classification of chronic enteritis is based on the presence or absence of atrophy. There are chronic enteritis without atrophy of the mucous membrane and chronic atrophic enteritis. In turn, chronic enteritis without atrophy of the mucous membrane is divided depending on the depth of pathomorphological changes into superficial and diffuse.

At chronic superficial enteritis mucosal thickness small intestine, as well as the ratio of the lengths of villi and crypts do not change. With this form of enteritis, uneven thickness of the villi and club-shaped thickening of their apical sections are noted. Bordered epithelial cells are dystrophic, acquire a cubic shape or become flattened; the nuclei of some cells are pyknotic, their cytoplasm is vacuolated. Some of the cells are desquamated, destruction of the basal membrane of the epithelial lining and exposure of the villous stroma occur. The number of goblet cells is unchanged or may even be increased. The lamina propria of the mucous membrane at the level of the villi is diffusely infiltrated with lymphocytes, plasma cells, and eosinophils.

Histochemical study of border epithelial cells indicates a decrease in oxidoreductases and alkaline phosphatase, a significant decrease or disappearance of neutral and acidic glycosaminoglycans in the area of the “brush” border. Electron microscopy reveals deformation, shortening and irregular arrangement of microvilli, and the absence of a glycocalyx on their surface. These changes serve as a morphological substrate for subsequent disturbances in the processes of digestion and absorption.

At chronic diffuse enteritis further progression of structural changes is noted, which is manifested by an increase in dystrophic and necrobiotic changes in the epithelium and the spread of the process to the entire depth of the mucous membrane of the small intestine. The inflammatory infiltrate from the villous area penetrates between the crypts up to the muscular plate of the mucous membrane and further into the submucosal layer. Along with infiltration in the stroma, vascular congestion, edema, the appearance of thin collagen fibers, and hyperplasia of lymphoid follicles are noted. Often, villi exposed in the apical part are found, as well as adhesions, “arcades” between the enterocytes of nearby villi, which arise as a result of healing of superficial erosions. The number of goblet cells is slightly reduced, their secretion is liquid and contains little mucin.

At chronic atrophic enteritis There are 2 types of damage. In option 1 (hyperregenerative atrophy), atrophic changes affect the villi, which thicken, shorten, and fuse together. The crypts retain their normal length, but over a long period of time they become longer due to hyperplasia. Option 2 (hyporegenerative atrophy) is characterized by significant shortening of both villi and crypts.

In both cases, along with pronounced atrophic changes in the epithelium, diffuse inflammatory infiltration of the stroma and proliferation connective tissue, displacing crypts. Deep changes in the crypts should be considered typical: their number decreases significantly, resulting in the ratio of villi to crypts being 1:3-1:2 (with the norm being 1:4-5).

The inflammatory infiltrate is usually represented by lymphocytes and plasma cells; during an exacerbation, a predominance of polymorphonuclear leukocytes and eosinophils is observed. Leukopedesis of the epithelium is noted.

A histoautoradiographic study of DNA synthesis showed that in chronic enteritis, epithelial proliferation accelerates and its differentiation is delayed (the second phase of the regenerative process). This is evidenced by the appearance of incompletely differentiated cells on the surface of the villi, the expansion of the generative zone, as well as an increase in the number of DNA-synthesizing cells in this zone.

Morphological changes in all types of enteropathies are the same and are reduced to dystrophic and atrophic processes in the mucous membrane of the small intestine without pronounced exudative reactions. The mucous membrane becomes thinner. In this case, as a rule, a hyperregenerative form of atrophy is possible: the villi are shortened, often deformed, and the crypts are elongated. The number of enterocytes is reduced, the cytoplasm of the remaining cells is vacuolated. In the lamina propria of the mucous membrane there is a moderate infiltration of lymphoplasmacytic elements and eosinophils. There are macrophages with high activity of lysosomal enzymes. Electron microscopic examination of bordered epithelial cells reveals swelling of mitochondria, fragmentation of the endoplasmic reticulum, shortening and reduction in the number of microvilli. In the later stages, total villous atrophy and severe sclerosis of the mucous membrane and submucosal layer develop.

At disaccharidase enteropathy the morphological changes described above are extremely poorly expressed. The diagnosis is made exclusively histo- and biochemically. In this case, a deficiency of enzymes that break down lactose and/or sucrose is detected.

At celiac enteropathy(non-tropical sprue, sprue-celiac disease) morphological changes are presented various types damage to the mucous membrane of the small intestine by gliadin (a fraction of gluten - a protein found in cereals). Microscopically, in addition to hyperregenerative atrophy of the mucous membrane, a significant decrease in the number of goblet cells and a sharp decrease in the RNA content in the bordered epithelial cells are detected. A characteristic feature is also a significant number of interepithelial lymphocytes in the villi of the mucous membrane of the small intestine, as well as an increase in the number of cells synthesizing IgA, IgM, IgG. In some cases of nontropical sprue, a picture of collagenous colitis is detected.

A histoautoradiographic study reveals an increase in the number of cells in the phase of DNA synthesis, indicating increased proliferation of the epithelium, as well as the appearance of incompletely differentiated epithelial cells from the generative zone in the villi. Changes develop predominantly in the proximal part of the small intestine, where, as a result of the digestion and absorption of gluten, gliadin has an adverse effect on the mucous membrane. In biopsy samples, in addition to the changes described above, using histoenzyme-chemical reactions, it is possible to detect an insufficient content of enzymes that break down gliadin.

At intestinal lipodystrophy (Whipple's disease) Rigidity of the walls and segmental expansion of the lumen of the small intestine, thickening of the folds of the mucous membrane, fibrinous deposits on the serous membrane are noted. The mesentery is dense, the mesenteric and sometimes para-aortic lymph nodes are enlarged, they contain an excess amount of chylous fluid, the nodes resemble caseous-like masses.

At histological examination biopsies of the mucous membrane of the small intestine in patients with intestinal lipodystrophy, enterocytes have a normal structure, with a preserved “brush” border. The villi are somewhat thickened and shortened. Lymphatic vessels are sharply dilated and contain protein-lipid masses in the form of lumps, which are stained red with Sudan III. In the lamina propria of the mucous membrane, diffuse infiltration of round or polygonal macrophages with a pale-colored nucleus and foamy cytoplasm containing PAS-positive inclusions is detected. PAS-positive macrophages are also found in the submucosal layer of the small intestine, para-aortic and mesenteric lymph nodes.

Electron microscopic examination reveals bacilli-like bodies about 1-3 µm long, 0.2-0.4 µm thick, with a three-circuit membrane in which the oval vacuole. Some macrophages are destroyed and bacilli-like bodies are found in the intercellular space.

Morphologically, two stages of intestinal lipodystrophy can be distinguished: at an early stage, accumulation of protein-lipid substances occurs in the lymph nodes and lymphatic vessels; at a later stage, lipogranulomas develop.

Morphological changes during nonspecific ulcerative colitis depend on the nature of the disease (acute or chronic form).

In the acute form of nonspecific ulcerative colitis, the folds of the mucous membrane are significantly thickened or, conversely, smoothed, sharply swollen, congested, covered with translucent mucus, pus-like deposits or a thin layer of fibrin. Numerous erosions and ulcers are visible in the mucous membrane. The ulcers are located randomly (unlike Crohn's disease), their definite orientation to the lumen of the colon is not observed. Ulcers vary in size, but are often large, irregular shape, with undermined overhanging edges. Even large ulcers usually remain shallow and are localized in the mucous membrane; their bottom, as a rule, is the submucosa. Often, along with typical ulcers, numerous erosions in the form of “wormholes” are visible, while the mucous membrane resembles moth-eaten felt. In the initial stages of the disease, erosions and ulcers may be absent and changes in the mucous membrane of the colon are minimal.

A characteristic sign of the acute form of ulcerative colitis are pseudopolyps. In this case, in the mucous membrane of the colon, along with ulcers, single or multiple protrusions of a stalactite nature ranging in size from several millimeters to several centimeters are found, which often resemble true glandular polyps. These formations are islands of mucous membrane preserved between ulcers (fringed pseudopolyps), or areas of granulation tissue growing at the site of healing ulcers (granulomatous pseudopolyps).

Sometimes the ulcers penetrate deep into the intestinal wall, forming pockets between the submucosal layer and the mucous membrane. In this case, the mucous membrane can be torn away and then the inner surface of the colon looks like a solid ulcer. With deep ulcers and destruction of the muscular lining, the wall of the colon becomes thinner (up to 1 mm or even less), resembling tissue paper, and the lumen of the damaged area of the intestine expands sharply.

Single or multiple microperforations may occur in a thinned intestinal wall.

Histologically in initial stage diseases in the mucous membrane of the colon, inflammatory changes predominate. The infiltrate consists mainly of lymphocytes with an admixture of polynuclear leukocytes, plasma cells, eosinophils and is located in the lamina propria of the mucous membrane, without penetrating into the submucosal layer. Hyperemia of microvessels (mainly venules and capillaries), stromal edema, and moderate hyperplasia of lymphoid follicles are pronounced.

Then polymorphonuclear leukocytes begin to accumulate in the infiltrate, which penetrate through the perivascular space into the thickness of the intestinal wall, through the integumentary epithelium through leukopedesis into the intestinal lumen, and through the epithelium of the crypts into the lumen of the latter. Cryptitis develops, in which obliteration occurs distal sections intestinal crypts (Lieberkühn glands), the number of desquamated epithelium and leukocytes sharply increases, and a crypt abscess is formed. Crypt abscesses open in the fundus, their contents break into the submucosa and an ulcer forms.

At acute form nonspecific ulcerative colitis is characterized by the dominance of destructive processes: when opening single crypt abscesses, numerous small ulcers are formed; the formation of large ulcers occurs when the merged crypt abscesses are opened and inflammation passes from the mucous membrane to the submucosa. At the bottom of the ulcer there are extensive foci of necrosis, intramural hemorrhages, and vessels with signs of fibrinoid necrosis. Fresh and organized blood clots are found in the lumen of many vessels. In some ulcers, the bottom is lined with granulation tissue, diffusely infiltrated with lymphocytes, plasma cells, a small number of neutrophilic leukocytes, and eosinophils. The destructive process may involve the intermuscular nerve plexuses, where in such cases a picture of toxic aganglionosis is revealed.

At chronic form Nonspecific ulcerative colitis in the mucous membrane is dominated by reparative sclerotic processes. Ulcers undergo granulation and scarring, while the colon is grossly deformed, often significantly shortened, its wall thickens due to hypertrophy of the muscular layer, and the lumen narrows unevenly. The mucous membrane of the colon sharply smoothes out, acquiring a whitish appearance. As a result of reparative regeneration of the epithelium around ulcers and scars, numerous granulomatous and adenomatous pseudopolyps are formed, sometimes imitating the picture of diffuse polyposis. Some ulcers scar with the formation of rough, extensive scar areas of irregular shape. Complete epithelization of ulcers, as a rule, does not occur.

Histological examination reveals a picture of chronic productive inflammation in the intestinal wall. The infiltrate contains many plasma cells, no polymorphonuclear leukocytes, and the number of eosinophils varies widely. It is characteristic that lymphoplasmacytic infiltration persists even during a period of long-term remission. In the vessels there is a picture of productive endovasculitis with sclerosis of the walls, narrowing, and sometimes obliteration of the lumen.

Regeneration of epithelium with nonspecific ulcerative colitis turns out to be imperfect, as evidenced not only by pseudopolyps, but also by the nature of the newly formed mucous membrane in the areas of epithelization of ulcers: full-fledged crypts are not formed, goblet cells remain single. In the epithelium of the atrophied mucous membrane, dysplasia of varying degrees of severity is often observed, which can be considered as a risk factor for the subsequent development of colorectal cancer.

Macroscopic changes in the intestine with Crohn's disease usually turn out to be the same type regardless of location. Inflammatory process begins in the submucosal layer and spreads to all layers of the wall. At the site of the lesion, the intestinal wall thickens and becomes dense to the touch; in appearance - depending on the length of the process (from 8-15 cm to 1.5-2 m) - it is figuratively compared to a “hose” or “suitcase handle”. Such areas are especially often found in the jejunum and ileum.

Damage in Crohn's disease is extremely rarely isolated. The process is usually multifocal in nature and spreads like “kangaroo jumping”, when foci of ulceration, which always have clear macro- and microscopic boundaries, alternate with areas of unchanged mucous membrane. This sign can be considered quite typical for Crohn's disease, allowing one to exclude nonspecific ulcerative colitis based on the macroscopic picture.

The appearance of ulcers of the intestinal mucosa turns out to be very characteristic: they are long, narrow, with smooth edges, deep, and often penetrate to the serous membrane and even into the surrounding tissue. The ulcers are arranged in parallel rows along the axis of the intestine, resembling “rake marks.” At the same time, slit-like ulcers are formed, deep, like knife wounds, oriented in the transverse direction. Islands of edematous mucous membrane, enclosed between intersecting fissure ulcers, resemble a “cobblestone street.”

Slit-like ulcers that penetrate through all layers of the intestinal wall sometimes form intramural abscesses, but more often they contribute to the formation of adhesions and fistulas between the intestinal loops and neighboring organs (urinary and gallbladder, vagina), in some cases external fistulas occur.

Microscopic changes in Crohn's disease are diverse. Most characteristic feature The disease should be considered the formation of nonspecific granulomas, formed against the background of productive inflammation, developing in all layers of the intestinal wall, and consisting mainly of epithelioid cells, sometimes with giant cells of the Pirogov-Langhans type. Granulomas do not contain foci of caseous necrosis, and tuberculous mycobacteria are never detected in them. These granulomas resemble those in sarcoidosis, but unlike the latter, they are smaller in size, do not have clear boundaries, and the giant cells detected in these granulomas contain fewer nuclei. It should be emphasized that granulomas are detected in Crohn's disease only in half of the cases, and taking into account the often single nature of granulomas, their detection requires the examination of a large number of biopsies and the preparation of serial sections.

The development of atherosclerosis leads to multiple appearance of atherosclerotic plaques in various vessels of internal organs and lower extremities. Against this background, the patient develops clinical symptoms associated with damage to a specific arterial bed, most often symptoms of myocardial ischemia or impaired blood supply to the brain.

However, there are other localizations of atherosclerotic plaques that lead to unpleasant manifestations. One of these forms of the disease is intestinal atherosclerosis. This process is associated with a number of symptoms that significantly reduce the patient’s quality of life and lead to long and difficult treatment.

Atherosclerosis develops mainly in older people, which is associated with the gradual accumulation of risk factors and negative impacts on the body.

Cholesterol plaques can form in the vessels that feed the intestines

Main causes of the disease

The main factor in the development of intestinal ischemia is the gradual blocking of the lumen of the mesenteric arteries by a growing atherosclerotic plaque. The causes of atherosclerosis are different, however, most often they appear against the background of the following factors.

Long-term irrational consumption of food, mainly consisting of fats and “fast” carbohydrates.
Lack of regular physical activity.
Tobacco smoking and alcohol abuse.
Hypercholesterolemia and increased levels of low-density lipoproteins (LDL) in the bloodstream.
A history of diabetes mellitus or other endocrinological diseases.
Genetically determined changes in fat metabolism, i.e. hereditary factor etc.

Against the background of the influence of these factors on the body, the patient’s arterial wall changes, which leads to an increase in its sensitivity to lipid molecules. LDL and cholesterol begin to be deposited in the thickness of the wall, causing inflammation and the growth of connective tissue. This is what causes the formation and progression of atherosclerotic plaque.

Smoking and alcohol are the most powerful factors in the development of atherosclerosis

Manifestations of the disease

The disease can be suspected at the earliest stages of its development, when symptoms and treatment are closely related, since with a significant increase in atherosclerotic plaques, therapy is significantly more difficult.

The disease can manifest itself in a patient in two forms: acute disruption of the blood supply to the stomach and intestines, or gradually progressive ischemia. The greatest danger to humans is the acute form of the disease, and therefore it is necessary to start with its manifestations.

The patient develops a strong, sharp pain syndrome in the abdomen, rapidly increasing in intensity.
Abdominal bloating appears due to the expansion of the intestinal lumen due to its ischemia and lack of motor activity.
Vomiting blood or bleeding from the rectum due to gastrointestinal bleeding may occur.
A drop in blood pressure due to blood loss (gastric or intestinal bleeding) and the development of tachycardia.

Most common symptom- sudden strong pain in the umbilical region

This condition requires immediate treatment and hospitalization of the patient due to the severity of the disease and possible necrosis of part of the intestine.

Diagnostics chronic forms atherosclerosis of intestinal vessels is much more complicated, since the symptoms that arise are nonspecific and are characteristic of most diseases of the stomach and intestines. The main manifestations are as follows.

Pain of low intensity, dull or pressing in nature. Most often it occurs after eating, which is associated with an increased need for blood flow from the intestinal wall, which is impossible due to the presence of atherosclerotic plaques in the vessels.
Various dyspeptic disorders in the form of nausea, vomiting, loss of appetite, diarrhea, constipation and flatulence. Symptoms may persist constantly, or they may occur from time to time, complicating the process of adequate diagnosis and delaying the time the patient seeks medical help.
As a result of loss of appetite and refusal to eat, the patient’s weight gradually decreases, which is easy to detect over time. Very often this can cause an erroneous diagnosis of tumor growth.

Such symptoms that occur against the background of atherosclerotic damage to the intestinal vessels are not an unambiguous sign of this disease. Therefore, it is very important to conduct additional laboratory and instrumental methods diagnostics to confirm the diagnosis and determine the localization of the site of arterial damage.

One of the symptoms is nausea and repeated vomiting

Diagnostic methods

The diagnostic process is based on laboratory and instrumental examination methods. From laboratory methods The greatest value is a biochemical blood test, which allows us to identify the following abnormalities.

Hypercholesterolemia, i.e. excess normal level cholesterol in the patient's blood.
Increased levels of low and very low density lipoproteins, which play an important role in the onset and progression of plaque growth.
Decreased lipoprotein concentration high density, protecting the body from the development of atherosclerosis.

It is optimal to use an integrated approach to diagnosis, and not be content with the results of only one method.

Of the instrumental methods of examination, the following methods allow identifying atherosclerosis of intestinal vessels and its complications.

Fibrogastroduodenoscopy (FGDS).Aimed at identifying erosions and ulcerative defects in the stomach and duodenum.
Ultrasound examination of intestinal loops with Dopplerography of the aorta and mesenteric arteries. Allows you to assess blood flow in the vessels and identify the degree of its disturbance.
Angiography of mesenteric vessels with the introduction of a contrast agent. The most indicative and useful method for diagnosing intestinal atherosclerosis for prescribing subsequent treatment. The method allows you to easily and quickly detect plaques in the arteries, assess their size and the degree of blood flow disturbance.

The data obtained allow us to prescribe adequate treatment, which may differ significantly from patient to patient.

Fibrogastroduodenoscopy - endoscopic examination of the internal surfaces of the esophagus, stomach and the initial part of the duodenum

Treatment of the disease

It is possible to treat atherosclerosis of intestinal vessels correctly only with a combination of medicinal methods with non-medicinal ones. And a number of patients will need and surgical intervention to restore adequate blood flow in the organ.

Non-drug therapy

It is impossible to cure atherosclerosis completely. Its progression can only be slowed down and thereby reduce the intensity of symptoms. In addition to the use of various medications, therapy is impossible without certain changes in the patient’s lifestyle. According to international recommendations, a person with atherosclerotic changes in the vessels of the intestine should follow a number of recommendations.

Consciously approach your diet, excluding from it all foods high in fat and easily digestible carbohydrates. This helps lower cholesterol and LDL levels in the blood.
Exercise regularly physical exercise medium degree intensity.
Get the right treatment concomitant diseases– diabetes mellitus, etc.
Organize regular preventive medical examinations.
Stop smoking and drinking alcohol.

If there is a slight deviation in the level of lipids in the blood, only by following these recommendations can you return them back to normal.

Use of Medicines

It is also possible to effectively reduce cholesterol and LDL levels with the help of various medications, which is actively used in medicine. The following pharmacological groups of drugs are most often used.

Ezetimibe is a lipid-lowering drug

Statins (Lovastatin, Rosuvastatin) are the most common lipid-lowering drugs approved for use in a large group of patients.
Fibrates (Gemfibrozil, Tycolor) interfere with the synthesis of cholesterol in the liver and contribute to its persistent decrease in the blood while taking the medication.
Inhibitors of cholesterol absorption in the intestine (Ezetimibe, etc.) are actively used in patients as one of the most modern drugs.

The use of medications should always be under strict medical supervision and only as prescribed by a doctor.

If the degree of stenosis of the intestinal arteries is significant (close to critical ischemia), then surgical operations to restore blood flow. As a rule, this is either bypass surgery or stenting of the affected artery.

Atherosclerosis of intestinal vessels is a serious, difficult to detect disease that occurs against the background of local or diffuse growth of atherosclerotic plaques in arterial vessels. Early detection allows you to assign effective treatment using a minimum amount medicines, and ensure a positive prognosis for recovery with an increase in the patient’s quality of life.

Atherosclerosis. Common chronic illness arteries, heart, brain, etc. with the formation of single and multiple foci of lipid, mainly cholesterol, deposits (atheromatous plaques) in the inner lining of the arteries. These plaques are made up of cholesterol, calcium and scar (connective) tissue. The affected artery wall becomes less elastic and thickens.

Overgrowth of connective tissue and calcification gradually lead to slowly progressive deformation and narrowing of the lumen of the artery until it is completely blocked (obliteration) and thereby cause chronic, slowly increasing insufficiency of blood supply (ischemia) of the organ fed through the affected artery. In addition, acute blockage (occlusion) of the artery lumen is possible either with a blood clot, or (much less often) with the contents of a disintegrated atheromatous plaque, or both at the same time, which leads to the formation of foci of necrosis (infarction) or gangrene in the organ (part of the body) supplied by the artery. . Atherosclerosis occurs more often in men aged 50-60 and in women over 60 years of age.

General damage to all arteries is very rare. Typically, there is predominant damage to the blood vessels of the brain, heart, kidneys, and legs. Progression atherosclerotic changes in the artery is manifested by the fact that with increased functional activity of the organ, the blood flow to it may be insufficient, appear discomfort from any of the above bodies.

The clinical picture varies depending on the predominant location and extent of the affected arteries. Atherosclerosis is associated with hypertension, obesity, smoking, diabetes, increased blood cholesterol levels, sedentary lifestyle, etc.

Atherosclerotic lesion of cerebral vessels leads to insufficient blood supply and deterioration of its function. One of the first symptoms is deterioration of memory for recent events. Subsequently, there is a gradual decline in intelligence, emotional instability is noted, and sometimes patients complain of “noise” and a feeling of pulsation in the head. Other symptoms depend on which part of the brain is most affected by the circulatory disorder. Atherosclerotic damage to cerebral vessels can cause ischemic stroke.

Treatment. Nootropil, sermion, cinnarizine, stugeron, cavinton, etc. are used. Regular, repeating courses of treatment lasting 1-2 months are recommended. To prevent the development of a stroke, it is very important to monitor blood pressure levels and cholesterol levels in the blood. To prevent strokes, reconstructive surgeries are performed on the vessels supplying the brain.

Atherosclerosis of the aorta is affected by gradually increasing arterial hypertension, noise heard over the ascending and abdominal aorta. Complications are possible - insufficient blood supply to the brain (strokes, dizziness, fainting) or upper extremities.

Atherosclerosis of the mesenteric arteries, feeding the intestines, is manifested by thrombosis of the arterial branches with infarction (necrosis) of the intestinal wall and mesentery, as well as abdominal angina - an attack of colic-like abdominal pain that occurs soon after eating, often with vomiting and bloating.

Treatment. The pain is relieved by nitroglycerin, fasting stops attacks of abdominal pain.

Atherosclerosis of the arteries of the lower extremities caused by ischemia of skeletal muscles. Symptoms: intermittent claudication (pain in calf muscles when walking, forcing a person to stop), chilliness of the feet, change in color of the skin and nails. Among the many risk factors for atherosclerosis, smoking is of particular importance in this form of the disease.

Treatment. Vascular drugs and medications that prevent blood clots. Reconstructive surgeries are also used; in some cases, due to the development of gangrene, limbs have to be amputated. If the patient stops smoking, the progression of the disease stops and the risk of amputation is significantly reduced.

Atherosclerosis of the renal arteries leads to insufficient blood supply to the kidneys and the development of arterial hypertension and chronic renal failure; renal function is rarely impaired.

Atherosclerosis of the coronary arteries (vessels feeding the heart muscle - myocardium). Cm. Ischemic disease hearts.

The diagnosis is made based on the clinical picture and biochemical blood test. X-rays sometimes show calcium deposits on the walls of the aorta and other arteries.

Treatment. Physical activity, smoking cessation, balanced diet, regular bowel movements. Taking medications that lower the level of cholesterol (lipids) in the blood, as well as those intended to treat diseases that contribute to the development of atherosclerosis (hypertension, etc.). Surgical treatment for narrowing (stenosis) of the main arteries (removal inner shell arteries, the application of bypass blood supply routes - shunts, the use of artificial vessels, etc.).

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Chronic abdominal ischemia (AIB, abdominal angina)

Angina abdominalis. Synonyms: intestinal ischemia, abdominal sore throat, etc.) - attacks of abdominal pain resulting from insufficient blood supply to various parts of the gastrointestinal tract due to narrowing (or blockage) of the arteries supplying the digestive organs.

Occurs approximately 0.05-0.07% of total number all diseases.

The main cause of abdominal pain is atherosclerosis of the arteries supplying blood to the organs. digestive tract, changes are observed less frequently vascular wall with nonspecific aortoarteritis, periarteritis nodosa, compression of arteries by the falciform ligament of the diaphragm, scar tissue, neoplasms, hypoplasia and developmental anomalies of visceral arteries (aneurysm, arteriovenous fistulas).

A decrease in blood flow in the mesenteric arteries leads to changes in the secretory and motor activity of the gastrointestinal tract. Ischemia is especially pronounced after eating, when adequate arterial blood flow is necessary to activate the digestion process. Collateral blood flow can prevent the development of infarction of the intestinal wall.

Clinical picture.

In the compensation stage, pain occurs only after a heavy meal, during long walking or neuropsychic stress, and is most often localized in the epigastric region, less often in the right hypochondrium or in the left iliac region. The duration of the attack ranges from several minutes to 2-3 hours.

In the subcompensation stage, in addition to the symptoms described above, belching, bloating, constipation, alternating with diarrhea (diarrhea), and weight loss appear.

With decompensation, persistent diarrhea, dehydration, and progressive exhaustion develop.

The listed symptoms allow us to suspect the possibility of developing the disease even in outpatient settings. For further examination, the patient should be referred to the vascular surgery department or to an angiologist at a consultative and diagnostic center. At acute disorders mesenteric circulation, causing a heart attack, and then, as a rule, gangrene of the intestinal wall, the clinical picture is characterized by symptoms acute abdomen, which is an indication for emergency hospitalization of the patient in the surgical department.

Palpation of the abdomen can be painful in various parts of the abdomen, however, protective, tension in the muscles of the anterior abdominal wall absent.

When the lumen of the celiac trunk or superior mesenteric artery is narrowed in the epigastric region, a systolic murmur can sometimes be heard.

Attacks of abdominal toad are stopped after taking nitroglycerin, which may have a differential diagnostic value.

Diagnosis established on the basis of clinical data, results of instrumental and laboratory diagnostic methods. Ultrasound duplex scanning allows you to determine the location and degree of narrowing of the mesenteric arteries. Angiography, spiral CT scan and magnetic resonance imaging. During gastroduodenoscopy and colonoscopy, swelling and atrophy of the mucous membrane of the stomach, duodenum and colon, and less often erosion or ulcers, are noted.

Course and prognosis. Abdominal tonsillitis can be observed for months or even years and is often preceded by thrombosis of one of the mentioned arteries or their branches.

Treatment.

Conservative treatment boils down to the prescription of antispastic agents (nitroglycerin, papaverine, aminophylline, etc.), but it is often ineffective. The diet should be prescribed one that requires as little work as possible of the digestive apparatus. For the same purpose, small separate meals should be prescribed at appropriate equal intervals. After eating, a long, complete rest is necessary (for 2-3 hours).

Obstacles to blood flow due to organic narrowing of blood vessels can only be eliminated surgically in specialized departments of vascular surgery by applying bypass anastomoses from vascular prostheses and grafts. To prevent thrombosis, it is advisable to prescribe anticoagulants.

The prognosis of the disease is always serious, since the progression of obstruction of the mesenteric arteries can lead to intestinal infarction and peritonitis, and lead to the death of the patient. Timely surgical intervention in most cases allows patients to recover and regain their ability to work.

Intestinal ischemia

There are acute and chronic ischemia of the small intestine. The four main causes of acute intestinal ischemia are considered to be: embolism of the mesenteric arteries (25-30% of cases), thrombosis of the mesenteric arteries (10-15%), thrombosis of the mesenteric veins (10%), non-occlusive mesenteric ischemia (50%).

In 90-95% of cases, the source of embolism is thrombi in the left atrium, formed during atrial fibrillation, less often - thrombosis of the left ventricle, vegetations and blood clots formed on affected or prosthetic heart valves, migration of fragments of atheromatous plaques in the aorta. The cause of thrombosis of the mesenteric arteries is, as a rule, atherosclerosis of the visceral branches of the aorta, narrowing of their lumen. Decreased perfusion in the mesenteric vessels combined with decreased cardiac output leads to non-occlusive mesenteric ischemia. Heart failure due to arrhythmias and the consequences of the vasoconstrictor effect on mesenteric blood flow of cardiac glycosides (vasopressin, pressor amines) can contribute to mesenteric thrombosis).

As a result of acute intestinal ischemia and subsequent hypoxia, irreversible intestinal necrosis develops within 2-6 hours.

This predetermines clinical picture. Most often, at the onset of the disease, acute pain appears in the abdomen (umbilical region, right upper quadrant of the abdomen). Against the background of ischemia of the intestinal wall, violent peristalsis and the urge to defecate appear. Therefore, in the initial period, patients experience nausea, vomiting, and diarrhea. Blood in the stool usually appears a few hours after the onset of the disease, when a mucosal infarction occurs. Despite the intense pain, tension in the abdominal wall muscles is low or completely absent (until intestinal perforation and the development of peritonitis). Pain that does not correspond to objective symptoms is fundamental diagnostic sign acute ischemia. The appearance of symptoms of peritoneal irritation indicates necrosis of all layers of the intestinal wall and is a poor prognostic sign. At the onset of the disease, body temperature is normal. Over time, symptoms of hypovolemia (fluid accumulation in the “third” space) progress, metabolic acidosis occurs, pronounced leukocytosis (more than 20 thousand) and hemoconcentration, as well as hyperamylasemia, are noted.

In occlusive forms of acute ischemia, selective angiography data in the lateral projection are of diagnostic value (disturbances in blood flow are detected, as a rule, 4-6 cm from the beginning of the superior mesenteric artery). Sometimes, to clarify the diagnosis, they resort to laparoscopy or exploratory laparotomy.

Treatment. During the first hours from the onset of acute ischemia, a thrombus or embolus can be removed, followed by reconstructive surgery. With the development of gangrene of the small intestine, resection of the affected area of the intestine is performed. IN postoperative period it is necessary to prescribe anticoagulants, drugs that improve the rheological properties of blood, and vasodilators.

Mortality at various forms acute mesenteric ischemia varies from 50-60% to 90-100%.

Chronic ischemia intestines, as a rule, causes atherosclerosis of the visceral arteries, affecting their first 4 cm. Less commonly, the cause of the characteristic clinical symptom complex of angina abdominalis is vasculitis. In this case, patients complain of cramping pain in the abdomen, usually occurring 20-50 minutes after eating, localized in the epigastrium, radiating throughout the abdomen. The pain decreases or goes away after taking analgesics, antispasmodics, and vasodilators. As the disease progresses, fear of eating arises, which leads to weight loss. IN initial period The disease is marked by constipation (due to a decrease in the amount of food taken) followed by diarrhea (due to impaired absorption of fats).

During physical examination, attention should be paid to a low systolic murmur in the upper abdomen (the stethoscope should be positioned midway between the navel and xiphoid process- to the projection point of the superior mesenteric artery).

Clinically significant intestinal artery occlusion (i.e. requiring surgical treatment) are identified only by the “method of exclusion”, when a comprehensive clinical examination excludes any other genesis of chronic abdominal pain. Using magnetic resonance imaging or selective angiography, critical stenosis or complete occlusion of the superior mesenteric artery is found.

Surgery comes down to a reconstructive operation aimed at restoring normal blood flow in the affected artery (endarterectomy, bypass surgery, side-to-side anastomosis with the aorta, reimplantation of the vessel after ligation of its base, retrograde vascularization). In 60-75% of patients, within the immediate period after surgery, the condition improves and the pain disappears.

When an atherosclerotic plaque forms in the branches of the aorta that feed the intestine, ischemia of its wall develops. Gradual blockage of the arteries causes attacks of pain (abdominal angina) and disruption of the organ (ischemic colitis); with sudden blockage, a local infarction occurs.

Symptoms of intestinal atherosclerosis are pain, diarrhea alternating with constipation, bleeding, nausea, and weight loss over a long period of time. Treatment is medicinal, in later stages - surgical.

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Causes of atherosclerosis of intestinal vessels

If the ratio between cholesterol, protein and phospholipid compounds in the body is disturbed, then fats are deposited in the wall of the arteries. This is facilitated by a slowdown in blood flow (places of branching of blood vessels, physical inactivity) and destruction of the inner membrane (glucose molecules in diabetes, nicotine and tar in smoking, hypertension).

Gradually, connective tissue fibers grow into places where lipids are soaked - it is formed. At this stage, it is fragile and can collapse, and its fragments move along the vascular bed, clogging smaller branches. In later stages of the disease, the plaque becomes calcified.

When an obstacle to blood flow in the form of a cholesterol plaque appears inside the intestinal artery, the supply of blood to the walls gradually decreases. This causes ischemia, manifested by abdominal pain, impaired intestinal digestion, absorption into the blood nutrients, vitamins, insufficient excretion of metabolic products from the body.

Depending on the degree of vessel overlap and the prevalence of atherosclerotic lesions of the mesenteric arteries, the pathology has three stages of progression:

initial (compensation) - no signs of illness or minor malaise (recurrent abdominal pain, flatulence, tendency to constipation or diarrhea), detected during a random examination for other vascular diseases;
clinical manifestations (subcompensation) - indigestion and intestinal excretion, abdominal pain;
complications (decompensation) - chronic pain syndrome, intestinal dysfunction, weight loss, asthenia, depression, hypochondria, with complete blockage - acute abdomen clinic, severe intoxication, addition of a septic process.

Symptoms of pathology

Intestinal atherosclerosis is manifested by a pain syndrome, which is characterized by the following properties:

occurs 20-30 minutes after eating;
may be in different parts of the abdomen;
relief occurs after taking antispasmodics, vomiting, applying heat, and adopting a knee-elbow position.

Due to decreased blood flow, the intestines lose their motor function, which leads to alternating diarrhea and constipation, bloating. The inflammatory process and weakened excretion of intestinal contents lead to intoxication - nausea, vomiting, increased body temperature to low-grade levels (37.1 - 37.4 degrees).

Insufficient digestion of food and weakened absorption from the intestines, frequent diarrhea, refusal to eat due to pain cause weight loss, total hypovitaminosis, constant weakness, and depression.

Watch the video about atherosclerosis of intestinal vessels:

What is the danger of the disease

Insufficient treatment of the disease and late diagnosis contribute to the development of complications of atherosclerosis of the mesenteric vessels. These include:

ischemic colitis or enteritis;
intestinal infarction;
peritonitis.

When a heart attack occurs, zones of necrosis form in the intestinal walls, even if it is possible to resume blood flow later with medications or surgery, tissue restoration does not occur. Microorganisms penetrate from the intestinal lumen into the abdominal cavity, causing severe inflammation of the peritoneum.

Decaying tissue increases intoxication, coma and convulsions occur, mortality at this stage of the disease reaches 100%.

Diagnosis of the condition

Very often, signs of intestinal atherosclerosis are regarded as a pathology of the digestive organs; patients are treated for a long time and unsuccessfully by a gastroenterologist. This is due to the fact that the symptoms of the disease are similar to gastritis, pancreatitis, cholecystitis or peptic ulcer.

Atherosclerosis can be suspected by the presence of risk factors in the patient, listening to noise in abdominal cavity, which coincides with the systolic contraction of the heart, but, unlike the cardiac contraction, intensifies as it moves away from the chest.

To confirm the diagnosis, instrumental examination is indicated:

phonoenterography – detects noise over the intestinal projection and its intensity;
angiography of mesenteric vessels - helps to detect blockage, narrowing of the lumen, expansion above the obstruction to blood flow, the location of the atherosclerotic plaque and the degree of disruption of blood flow;
fibrogastroduodenoscopy – swelling of the mucous membranes, atrophic changes, erosive or ulcerative defects;
stool analysis - undigested fiber and high mucus content.

In addition to these methods, patients undergo thermography.

Treatment of intestinal atherosclerosis

In the initial stages of the disease, drug therapy is carried out. Drugs from the following groups are indicated:

antispasmodics – No-shpa, Riabal, Buscopan;
disaggregants – Curantil, Pentilin;
normalizing microflora - Laktovit forte, Yogurt, Enterol;
enzymes – Mezim-forte, Panzinorm.

Nutrition plays an important role. It is necessary to take warm food in fractional quantities, exclude spicy foods, coarse vegetable fiber (brown bread, millet, pearl barley, legumes, raw vegetables), canned foods and semi-finished products. During an exacerbation, only pureed dishes without sauces are allowed; as intestinal function is restored, chopping is not required, but cooking should be longer than usual.

With persistent pain syndrome and the development of complications, surgical intervention is indicated:

release of the vessel from the falciform diaphragmatic ligament or fibrous fibers;
removal of sympathetic nodes nervous system in the solar plexus area;
decompression of the celiac trunk;
extraction of an atherosclerotic plaque with part of the inner membrane;
and stent placement.

Usually surgery, carried out in the subcompensation stage, helps prevent severe circulatory disorders in the intestinal arteries and save the lives of patients. On later the results are much worse.

Intestinal atherosclerosis occurs due to the formation of cholesterol plaque in the branches of the abdominal aorta. It can affect the celiac trunk, inferior and superior mesenteric arteries. In the initial stage it proceeds hidden, then patients complain of constant pain after eating, indigestion, and unstable stool. As complications develop, intoxication occurs, the intestinal walls are destroyed, and the peritoneum becomes inflamed.

Diagnosis requires angiography and ultrasound of the abdominal aorta. Conservative therapy indicated for minor circulatory disorders; when the stage of subcompensation occurs, surgery is performed.