Intestinal failure syndrome. Intestinal motor failure. Intestinal diseases caused by vascular pathology

p>V.S. Savelyev, V.A. Petukhov, A.V. Karalkin, D.A. Son, P.V. Podachin,
K.V. Romanenko, V.V. Ivanov
Department of Faculty Surgery, Russian State Medical University, First City Hospital, Moscow

Patients with surgical diseases of the abdominal organs were always classified as difficult. This is mainly due to intestinal failure syndrome (IFS), which develops in many diseases (peritonitis, intestinal obstruction, pancreatic necrosis, etc.) and still causes high mortality due to progressive endogenous intoxication and associated multiple organ disorders. Although surgery remains the main stage of treatment, it is not always able to save the patient.
This can to a certain extent be explained by the fact that ICI is formed long before surgery and includes a violation of the motor, secretory, absorption and barrier functions of the intestine. Intestinal paresis and disturbances in the transit of intestinal contents dramatically change the quantity and quality of intraluminal and parietal microflora, disrupt the barrier function of the intestine and promote the translocation of toxins and microorganisms themselves into the bloodstream and into the lumen of the abdominal cavity. The gastrointestinal tract with SCI becomes a source of endogenous intoxication of a bacterial and dysmetabolic nature.
Treatment of SCI, regardless of the pathology that caused it, is aimed primarily at active sanitation and removal of toxic products from the intestinal lumen. Taking into account the pathogenesis of SCI, the absolute indication is drainage of the entire small intestine in order to remove intestinal contents, reduce intraluminal pressure to ensure restoration of circulatory processes in the intestinal wall, normalize its motor and metabolic functions and, most importantly, reduce portal and systemic endotoxemia.
There is reason to believe that the additional use of sorbents has a positive effect on these processes. Unfortunately, known enterosorbents have a low sorption capacity, are not able to absorb toxic bile, which plays an important role in maintaining the “vicious endotoxin circle,” and are poorly evacuated through a nasointestinal tube (NIT). In addition, it is unknown whether SCI is completely relieved after removal of NCDs and restoration of intestinal motility and evacuation function and what metabolic consequences of endotoxemia persist in patients after discharge from the hospital.
The purpose of this study was to evaluate the results of using a new method of treating intestinal failure syndrome.

Material and research methods
We examined 44 patients aged from 15 to 90 years with SCI that developed as a result of acute surgical diseases of the abdominal organs. After laparotomy, all of them underwent nasointestinal intubation: 23 patients (group 1) underwent enterosorption (ES) with a liquid form of micropectin emulsion (MPE) FISHant-S® (Penta Med, Russia, permission of the Ministry of Health of the Russian Federation No. 005469); 21 patients (group 2, control) did not use ES. The distribution of patients in both groups by age, gender and cause of SCI is presented in Table. 1.
In patients of both groups, the content of endotoxin (ET) in blood plasma, peritoneal effusion and intestinal contents was studied at outcome (during laparotomy), 3, 6, 9, 12, 24 and 48 hours after surgery using the LAL test. Motor-evacuation function gastrointestinal tract during the enterosorption process, it was monitored by electrogastroenterography using a gastroenteromonitor "GEM-01" (NPO "Istok"), the data was processed according to a program using fast Fourier and Wavelet transform algorithms.
Depending on the volume of contents aspirated from the intestine during surgery, the amount required for a single administration of enterosorbent was calculated as the quotient of dividing the product of the volume of contents separated by the tube in three hours and the maximum concentration of ET in the intestinal contents by the sorption capacity of the enterosorbent.
Based on the results of these calculations, a curve was constructed for the practical determination of a single dose (volume) of MPE FISHant-S® administered every three hours (Fig. 1) and the main parameters of ES were developed: the calculated dose of FISHant-S® was administered every three hours, the nasointestinal tube was clamped with a clamp for one hour, then the clamp was removed and free outflow of intestinal secretions along with the sorbent was carried out.
In patients of the first group, on the eve of discharge from the hospital, bile synthetic and bile excretory functions of the liver were studied using hepatobilis scintigraphy. The half-life (T1/2) of the radiopharmaceutical from the liver, the time of its entry into the duodenum, and the motor-evacuation function of the gallbladder were assessed. The functions of the reticuloendothelial system (RES) of the liver and hepatic blood flow were studied using the method dynamic scintigraphy liver. Functional status Kupffer cells were assessed by the time of maximum uptake of the radiopharmaceutical by liver RES cells. The structural and metabolic imbalance of the colon microbiocenosis was studied at the Moscow Research Institute of Microbiology and Epidemiology named after. G.N. Gabrichevsky using gas-liquid chromatography, determined the levels and spectra of volatile fatty acids in feces (biochemical study).

Results and its discussion
Changes in the concentration of ET in the studied media during the treatment of SCI are presented in Table. 2. The concentration of ET in the blood plasma decreased by half after just three hours; then, up to 12 hours of treatment, it also decreased (Fig. 2). This time period (12 hours) should be considered the most important period in the treatment of SCI for the following reasons.
In the first 12 hours, according to the literature, the main pathobiochemical processes unfold, initiating the entry into the bloodstream of numerous mediators of pathological, often irreversible, processes. In other words, the most intensive measures to prevent the development of abdominal sepsis and infectious-toxic shock should be carried out in the first hours after surgery. During this period, in the majority of patients receiving ES, the most important life-supporting systems of the body were stabilized and intestinal motility was restored. In addition, in the first 12 hours after ES, we obtained the most significant, from a clinical practical point of view, correlations of ET content indicators in various study objects with objective criteria (the results are presented below).
Similar dynamics were found when studying the ET content in peritoneal effusion (Table 2, Fig. 3). After 9 hours, its concentration decreased by 2.2 times, and a further decrease was noted up to 48 hours of observation, but, unlike the first 12 hours of enterosorption, further dynamics were not so significant.
It should be noted that the decrease in ET concentration was accompanied by a decrease in the total amount of effusion in the abdominal cavity, the volume of which after 12 hours no longer increased and amounted to 20-25 ml per day.
A significant decrease in ET in peritoneal effusion is important evidence of stabilization of the SCN, creating favorable conditions for the restoration of chyme transit and peristalsis.
In the control group of patients, the content of ET in the peritoneal effusion over the entire period of observation changed little and decreased by only 20% compared to the initial values, while even at the time of removal of the drainage from the abdominal cavity (3-5 days) its concentration was 1. 7-1.5 U/ml, and the amount of peritoneal effusion was two to three times higher than that in patients of the first group.
A study of intestinal contents in SCI revealed the following. The volume of contents removed during surgery through a nasointestinal tube in the first group was 2.3 ± 0.5 l, in the control group 2.1 ± 0.4 l (p > 0.05). The concentration of ET in the intestinal contents at outcome was the same (Table 2, Fig. 4): 9.6 ± 1.2 U/ml in the first group and 9.5 ± 1.5 U/ml in the control group.
In patients of the first group, already in the first three hours, the concentration of ET in the intestinal contents decreased by 61%, i.e. ES using MPE FISHant-S® is most effective in the first three hours. Subsequently, the concentration of ET in the contents also decreased, but less intensely: after 6 hours - by another 11.5% (72.9%), after 9 hours - by almost 80%. The second day of enterosorption practically did not change the content of ET in the chyme.
In the control group of patients, with adequate outflow of contents from the intestine through a nasointestinal tube in the first 12 hours, the concentration of ET remained practically unchanged. After 12 hours, this figure decreased by 20% and only after two days by 44%. This period (48 hours) coincided with the appearance of the first signs of intestinal peristaltic activity in some patients in the control group (36 ± 6 hours). Note that in patients of the first group, against the background of enterosorption, the motor-evacuation function of the gastrointestinal tract was restored three times faster - after 10.9 ± 2 hours (p) The timing of restoration of intestinal motility in patients with SCI had a positive effect on the duration of nasointestinal intubation. With enterosorption the probe was removed after 2.5 ± 0.4 days, and in patients in the control group after 5.2 ± 1.6 days (p Detailed analysis The correlation between the concentration of ET in the blood, effusion and intestinal contents with monitoring data of the electrical activity of the gastrointestinal tract during enterosorption proved the need for intensive elimination of ET from the intestinal lumen in the first 12 hours after surgery.
The positive effect of enterosorption in SCI is largely explained by the characteristics of the sorbent. Microemulsion FISHant-S® is absolutely neutral in terms of its effect on metabolism, is not absorbed during transit through the gastrointestinal tract, and does not enter into chemical interactions and a drug that does not form new chemical compounds toxic to the body. Its structure contains prebiotic components (pectin and agar-agar) and white oil– a completely inert product from a chemical point of view. It is located inside a pectin-agar capsule, which actively transports bile acids inside and ideally dissolves them. Toxic bile acids dissolved in oil are sorbed by FISHant-S® microemulsion and removed from the intestine through a nasointestinal tube.
MPE FISHant-S® has another property that is unusual for enterosorbents. Mixing with chyme and covering the mucous membrane with a thin film, it reduces the absorption of ET.
Thus, enterosorption in SCI using liquid microemulsion FISHant-S® allows in the first 12 hours after surgery to reduce endotoxemia, prevent the development of multiple organ failure and the progression of abdominal sepsis, quickly restore peristalsis and motor-evacuation function of the intestine, reduce the time of nasointestinal intubation, and avoid drug intestinal stimulation. An important and fundamental difference between the FISHant-S® microemulsion and other enterosorbents is its high sorption capacity, low desorption, sorption of ET not only from the intestinal contents, but also the absorption of toxic complexes of bile acids - ET, as well as a physicochemical obstacle to the absorption of ET.
The objective of the second part of the study was to assess changes in the concentration of ET in the blood plasma and intestinal contents (in feces) after completion of the rational treatment required for SCI. antibacterial therapy in patients of the first group. The data is presented in Fig. 5 and 6. The ET concentrations in the blood plasma, which had decreased by 67% by the time of extraction compared to the initial values, increased by 44% after 7-10 days and were 4.7 times higher normal values(p The logical negative outcome of such an increase in ET in the studied environments is the preservation of the pathophysiological conditions for SCI, but not in the “acute” phase, as is commonly believed in the case of an abdominal catastrophe, but in the “chronic”, i.e., less aggressive dysmetabolic form. The result of this chronic course SCI is not sepsis and multiple organ failure, characteristic of the acute phase of SCI, but the development of chronic pathology, primarily lipid distress syndrome.
Evidence of the validity of this assumption is provided by data from our study conducted 15 years ago in patients with pancreatogenic peritonitis. Let us recall that out of 34 patients discharged after surgery, 21 patients (62%) died from various cardiovascular diseases within 4-10 years. When examining young patients (up to 45 years old), it was found that 8 of them (73%) have ischemic disease heart (one suffered myocardial infarction), one patient (9.1%) suffered an acute disorder cerebral circulation, 8 (73%) have hypertonic disease, and 7 (64%) had obliterating atherosclerosis.
The most important biochemical marker in these patients upon discharge from the hospital was an extremely low (53%) concentration of high-density lipoproteins, considered in the classical sense as an important antiatherogenic factor.
According to currently available scientific information, this fact can be considered from other positions, namely from the point of view of endotoxemia. High-density lipoproteins are among the most important endotoxin-binding elements in the blood, and their low values ​​in the above study are strong evidence of persistent endotoxemia in the near future. postoperative period.
These data served as the main reason for studying in patients with SCI the causes of the development and progression of diseases included in lipid distress syndrome in 1988. For this purpose, studies of blood plasma lipids, hepatobiliscintigraphy were performed, and indicators of liver RES activity were assessed upon discharge of patients with SCI from the hospital (Table 4).
Indicators of lipid metabolism in general were characteristic of dyslipoproteinemia, while the absolute plasma concentrations of cholesterol, triglycerides and low-density lipoproteins were slightly changed, the antiatherogenic potential was 54.8% (p Significant changes were established in the study of radionuclide hepatobiliscintigraphy indicators: bile synthesis by hepatocytes and bile transport from the liver were slowed down by 57 and 43%, respectively (p Liver scintigraphy against the background of redistribution of portal blood flow fractions revealed depression of the cells of the reticuloendothelial system of the liver, their activity was reduced by 77% (p When studying the correlations of these indicators with ET concentrations in the blood plasma and In stool, a high negative relationship was found with the concentration of high-density lipoproteins (rblood = -0.78, rfeces = -0.76), positive with indicators characterizing bile secretion (Tmax) (rblood = +0.59, rstool = +0.67) and bile excretory function of hepatocytes (T12) (r-blood = +0.84, r-stool = +0.71), as well as with a value characterizing the activity of Kupffer cells of the liver (r-blood = +0.54, r-stool = +0.74).
The continuation of antibacterial therapy, which is extremely necessary for the patient with SCI, after removal of the NCD, significantly affected the microbiocenosis of the colon (Table 4). Upon discharge of patients operated on for various urgent surgical diseases, there was pronounced dysbiosis of the large intestine, expressed in a decrease general level volatile fatty acids and an increase in the anaerobic index, characteristic of inhibition of the activity of resident intestinal microflora.
The data obtained allow us to conclude that liver dysfunction after surgical treatment of SCI is a direct consequence of disrupted symbiosis in the “microbiota-host” system as a result of initial and persisting disorders after surgery, generating mutual aggression between the microbiota and the “host”. The microbiota wins this “metabolic duel” by activating the “shock” enzymatic apparatus of bacteria and releasing ET. Forming new or persistent old damage to the epithelium of the ileocecal intestine disrupts the cycle of enterohepatic circulation of bile acids, significantly changing their metabolism. These changes in bile acid metabolism become an important pathogenetic link in lipid distress syndrome.
Thus, two phases can be distinguished in SCI for various acute surgical diseases of the abdominal organs. The first starts at the onset of the disease and is characterized by endogenous intoxication and multiple organ disorders. The second phase of SCI begins after surgery against the background of restored motor-evacuation function of the intestine, subjective and objective improvement of the patient’s condition. It is characterized by persistent endogenous intoxication caused by increased concentrations of ET in the blood and feces against the background of colon dysbiosis, impaired metabolic functions of the liver, depression of the liver RES and conditions for the formation and progression of lipid distress syndrome.
For the treatment of SCI in the second phase, we have developed a special complex, which is based on the principles of treatment of LDS - restoration of cycles of enterohepatic circulation of bile acids, sorption of endotoxins, normalization of metabolic functions of the liver and correction of intestinal dysbiosis.
After removal of NCDs, patients are prescribed a paste form of the enterosorbent FISHant-S®, which has good taste, 100 g once a day, the probiotic Hilak Forte 40-60 drops per 100 ml of water three times a day, the herbal hepatoprotective agent hepabene 1- 2 capsules three times a day and a water-soluble collection of dry extracts of medicinal plants detoxical 2.5 g (1 sachet) three times a day.
The rationale for this choice of drugs for the treatment of the second phase of SCI was as follows. Microemulsion FISHant-S® has the highest sorption capacity for endotoxin from gram-negative microflora compared to many market enterosorbents (Table 5). The drug restores the enterohepatic circulation of bile acids, sorption of endotoxin from bile (remember that this does not happen when using other enterosorbents), eliminates secondary deficiency of pancreatic enzymes, restoring their activity, homeostasis the chyme, creating favorable conditions for the normalization of intestinal motility and digestion.
The use of hepabene makes it possible to increase choleresis due to a fraction independent of the amount of bile acids synthesized, to activate the synthesis of endogenous cholecystokinin and secretin, which results in an increase in the secretion of water and bicarbonates by the epithelium bile ducts helps restore the motor-evacuation function of the gallbladder, reduce the neurogenic tone of the sphincter of Oddi, ensuring a greater flow of bile into the intestines and creating all the metabolic conditions for restoring the mechanism of enterohepatic circulation of bile acids and digestion.
The water-soluble hepatoprotective agent detoxical (NPP “Saluta”) is prescribed immediately after removal of NCDs. It consists of dry extracts of medicinal plants: sandy immortelle, knotweed, St. John's wort, bearberry, licorice root, nettle leaves, lingonberry, white cabbage, milk thistle fruits.
Hilak forte is a sterile concentrate of waste products of gram-positive and gram-negative microorganisms - synbionts of the small and large intestines, forming lactic acid, amino acids, lactose, short-chain fatty acids, contains important metabolic products of lactobacilli, E. coli and lactic acid. The drug creates an optimal intestinal pH, has a positive effect in any pathological condition of the intestinal microflora, is compatible with the use of antibiotics, promotes the rapid restoration of indigenous flora, as well as maintaining the physiological function of the mucous membrane.
After patients are discharged from the hospital for ambulatory treatment The treatment regimen for SCN is modified: enterosorbent FISHant-S® is taken once a week, 200 g for two to three months, the dose of Hilak Forte is reduced to 15-20 drops - three times a day for 6 weeks, hepabene, one capsule twice - three times a day – 6-8 weeks.
The results of the second phase of SCI treatment for various diseases of the abdominal organs will be presented in a separate report.

conclusions
1. Enterosorption in SCI using MPE FISHant-S® allows in the first 12 hours after surgery to reduce endotoxemia, prevent the development of multiple organ failure and the progression of abdominal sepsis, quickly restore peristalsis and motor-evacuation function of the intestine, reduce the time of nasointestinal intubation, and avoid drug stimulation of the intestine .
2. An important and fundamental difference between MPE FISHant-S® and other enterosorbents is its high sorption capacity, low desorption, sorption of ET not only from the intestinal contents, but also the absorption of toxic complexes of bile acids - ET, as well as a physicochemical obstacle to the absorption of ET.
3. During SCI in acute surgical diseases of the abdominal organs, it is necessary to distinguish two phases. The first is characterized by severe endogenous intoxication and multiple organ disorders. The second phase of SCI begins after surgery against the background of restored motor-evacuation function of the intestine and is characterized by persistent endogenous intoxication caused by increased concentrations of ET in the blood and feces against the background of colon dysbiosis, impaired metabolic functions of the liver, and depression of the liver RES.
4. To stop the second phase of SCI and prevent the progression of lipid distress syndrome, it is necessary to continue enterosorption for two to four months after removal of NCDs, restore the microbiocenosis of the colon and normalize the impaired metabolic functions of the liver.

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Intoxication, which causes multiple organ abnormalities in chronic diseases of the digestive system (pancreatic necrosis, peritonitis), forms intestinal failure syndrome (IF). The pathology is characterized by secretory, barrier, and motor dysfunction of the small intestine.

When the ability to remove waste products is impaired (paresis), the composition and quantity of microflora changes due to increased bacterial growth. The lost barrier function allows taxa and metabolites to enter the blood and abdominal cavity. Thus, the gastrointestinal tract is the starting point of endogenous intoxication, the dynamics of which does not exclude death.

Causes of intestinal failure

The pathogenesis of the syndrome involves a number of factors that directly depend on the nature of the disorder. If there is a weakening of the excretory function, the reasons for this are:

• myocardial infarction;
• spinal column, abdominal or traumatic brain injuries;
• rapid progression of pneumonia;
• liver failure, cirrhosis;
• acute form of diseases of the abdominal organs (pancreatitis, peritonitis, obstruction);
• intestinal infections in young children.

Weak motor skills are caused by excessive stimulation of sympathetic nerve endings due to inhibition of parasympathetic ones. Paresis can be provoked by surgical intervention in acute diseases of the abdominal (located in the peritoneum) organs. Vegetative system also inhibits contractile activity. The nerves do not transmit impulses to the smooth muscle structure of the intestinal wall. An important role in the etiology of defective motor activity is played by the humoral factor. In this case, there is an increased production of adrenaline or acetylcholine.

In the development of pathology caused by mechanical damage to the intestinal wall, the main role is played by endotoxins that penetrate into the bloodstream. Lipopolysaccharide complexes formed due to the death of microorganisms are distributed throughout the body, localizing in liver cells and lymph nodes.

The cause of the development of SCI is a secondary infection during trauma due to the translocation of bacteria. The intestinal mucosa affected by endotoxins is not only the cause of pathology, but also a symptom of complicated necrotizing enterocolitis.

Classification and main features

Despite poor motility, the pattern of development of intestinal failure varies depending on the degree of manifestation and period of its course. The anomaly is classified into three types. The first stage is the debut of SCN, which occurs against the background of:

• normal blood circulation in the intestinal walls;
• unimpaired suction function;
• absence of paresis;
• natural accumulation of fluid in the lumen;
• normal gas formation.

The location of the anterior abdominal wall is visually noted above the normal level. Peristaltic sounds are easily heard. The first stage is characterized by independent restoration of motor skills.

The second degree includes disorders of motor activity and reflex blood circulation. A characteristic feature is an increased level of secretion with poor absorption. The abnormal condition provokes the accumulation of fluid in the lumen of the small intestine and increased gas formation. Against this background, the following is formed:

• circulatory disorders;
• loop stretching;
• intraintestinal hypertension.

An increase in pressure to the systemic diastolic level triggers the following pathological processes:

• complete cessation of suction function;
• stretching loops to a critical state;
• loss of blood supply to the walls;
• lack of physical activity;
• increased production of gastric secretions;
• transudation of fluid into the lumen of the distended small intestine.

The second stage of the disease is accompanied by the active growth of pathogenic microorganisms in the proximal parts of the digestive tract.

The third stage of the clinical course of SCI is characterized by critical stretching of the loops. This process affects the barrier function of the diaphragm and increases hypertension in the intestine, which leads to disruption of:

• microcirculation of arterial and venous blood;
• the act of breathing, as a consequence - to tissue hypoxia;
• functions of digestion and absorption;
• metabolic processes between electrolytes and proteins;
• peristalsis.

An increased volume of fluid enters the lumen, in which the presence of plasma is observed.

Symptoms

Signs of the disease depend on the degree of intestinal insufficiency and obstruction. Common manifestations of dysfunction include:

• bloating;
• poor passage of gases;
• rumbling;
• weakening of peristalsis;
• specific odor from the mouth;
• unpleasant taste;
• tachycardia;
• increased breathing;
• instability blood pressure.

Spasmodic pain is concentrated in the umbilical region, radiating to the epigastrium or lower abdominal cavity. Characteristic symptoms include vomiting and nausea. The higher the obstacle is located in the small or large intestine, the stronger the symptoms. As the pathology progresses, the symptoms are complemented by a prolonged absence of bowel movements; in rare cases, constipation alternates with diarrhea.

Diagnostic tests

To determine intestinal failure, activities are carried out, including questioning the patient for concomitant symptoms, studying a history of diseases, laboratory and instrumental examinations. By palpation of the abdominal cavity the following is analyzed:

• localization of pain;
• muscle tone to exclude or confirm spasms, neoplasm;
• parameters, elasticity of the abdominal organs.

Appointed laboratory test feces taking into account:

• consistency (solid, liquid);
• colors - dark color indicates bleeding in the upper gastrointestinal tract;
• composition - the presence of plasma in excrement indicates a violation of the integrity of the intestinal vessels.

Instrumental diagnostics are carried out differentially using:

1. Radiology, which allows you to determine the degree of anomaly, functional or mechanical disorder. The initial stage is accompanied by a slight increase in the intestine near the inflammatory focus. The second phase has a pronounced picture - obvious swelling of the loops, accumulation of exudate. The third stage of pathology is determined by strong gas formation, a large number liquid and critical stretching of loops.
2. Probe enterography scanning the size of the small intestine: at the onset of the disease - 4 cm, the second degree of SCI - 5 cm, at the final stage of development - 6 cm.
3. Computed tomography (CT), which allows you to determine the condition of the digestive tract and the cavity behind the peritoneum.
4. Scintigraphy using a radiopharmaceutical. The procedure shows how long it takes for the contents of the stomach to enter the large intestine. The test allows you to determine the degree of motor function.
5. Electrogastrography, which determines the electrical dynamics of the intestine.

Motor activity is analyzed by inserting catheters into different parts of the digestive tract, which indicate the level of pressure and the size of the lumen.

Treatment

The principles of influence are aimed at restoring gastrointestinal function and resuscitation. In case of acute intestinal failure, emergency surgery is performed. Pharmacological therapy to eliminate the inflammatory process involves the use of drugs:

1. Steroid hormones: Budesonide, Prednisolone, Methylprednisolone - in severe forms of the third degree, when the intestinal mucosa is affected. Prescription of drugs in this group is carried out if previous therapy was ineffective. The dosage depends on the body weight and age of the patient. Due to the existing risk of addiction, the course of treatment hormonal drugs not lasting.
2. Aminosalicylates: “Pentasalazine”, “Sulfasalazine”, “Mesalazine”, which are prescribed for exacerbation of the syndrome, as well as to speed up recovery.
3. Immunosuppressants: Cyclosporine, Azathioprine, Methotrexate. In case of hormonal dependence, medications have a cumulative effect, so therapy is carried out over a long course.
4. Antibacterial agents - Ciprofloxacin, Metronidazole.

In order to correct dysfunction of the digestive organs, treatment is aimed at eliminating the symptoms:

• to restore metabolic processes - “Hemodez”, “Reopoliglyukin”;
• immunomodulators are used: “Ribomunil”, “Levamisole”, “Timalin”;
• probiotics that improve the state of microflora - “Bifiform”, “Lactofiltrum”;
• for pain, antispasmodics are taken: “Platifillin”, “Drotaverine”, “Papaverine”;
• treatment of constipation is carried out with the stimulating drug “Mosid”;
• diarrhea is relieved with Loperamide, Trisol, and Reopoliglucin.

If a neoplasm of an oncological nature develops, chemoradiation intervention is prescribed. If the disease is complicated by perforation, obstruction, or a tumor has formed in the abdominal cavity, resection is resorted to.

The development of intestinal failure syndrome after surgery involves the use of medications, the purpose of which is:

• blockade of reflexogenic areas;
• withdrawal pain syndrome(“No-shpa”, “Papaverine”);
• relaxation of the distal zones of the stomach for its emptying (“Cerucal”, “Metoclopramide”);
• restoration of motor skills (“Kalimin”, “Aceclidine”);
• normalization of water and electrolyte metabolism (“Albumin”).

Measures are being taken to prevent hypoxia. By means of enterosorption, endogenous substances are removed.

In gross sectional material it occurs with a frequency of about 0.4%. It is more often observed in people 40-60 years old.

Acute arterial insufficiency occurs with embolic occlusion of the visceral branches of the abdominal aorta in patients with mitral disease, especially against the background of arrhythmias; or with thrombosis of visceral vessels involved in atherosclerosis - Fig. 4.58. Intestine in shock (Imuna aortic rupture with tamponade process; or non-occlusive intestinal lesions in

(Fig. 4.58). According to its clinical significance, severity and role in thanatogenesis pathological changes in the intestines during shock are inferior to those in the kidneys, heart, brain and lungs. However, nonspecific manifestations of shock are multiple superficial ulcers (Cushing's ulcers) and hemorrhagic syndrome

chronic heart failure (especially in connection with the simultaneous use of kaliuric diuretics in combination with digitalis); or in patients in shock.

In children, this type of intestinal infarction is rare, usually in combination with various disorders of the anatomical structure and development of the intestine, for example, with atresia (Fig.

Rice. 4.61. Fibrinous-purulent diffuse peritonitis

Rice. 4.60. Acute arterial insufficiency of the intestine in combination with partial atresia

Rice. 4.59. Hemorrhagic intestinal infarction (bacterial endocarditis)

Arterial blood pressure drops during occlusion, and venous blood filling the empty circulation gives infarcts a pronounced hemorrhagic appearance.

Chronic arterial insufficiency often occurs with stenotic atherosclerosis of the branches of the abdominal aorta with predominant stenosis in the area of ​​the mouths of the mesenteric arteries. This process more often leads to the development of ischemic enterocolitis than to localized hemorrhagic infarctions.

Venous thrombosis also often leads to hemorrhagic infarction of the intestine. Several mechanisms can be distinguished here: descending portal thrombosis in liver cirrhosis as a manifestation of portal hypertension, ascending thrombosis in invasive intestinal infections and spontaneous thrombosis. A special place is occupied by non-occlusive thrombosis in polycythemia vera.

Various shapes intestinal obstruction(hernias, torsions, adhesive disease) can also lead to disruption of local blood flow and the development of a heart attack, but they should be considered in terms of nosological conditions in accordance with the recommendations of the ICD.

Obstructive intestinal obstruction with hemorrhagic infarction, accompanied by the involvement of a significant area of ​​the intestine, may subsequently be complicated by secondary paralytic intestinal obstruction. Primary and secondary paralytic forms of intestinal obstruction must be differentiated based on the intensity of hemorrhagic damage, which is more pronounced in secondary forms.

Intestinal diseases caused by vascular pathology

Intestinal diseases associated with vascular pathology usually manifest as abdominal pain, bleeding, or both.

Mesenteric circulation disorders

Disturbances of mesenteric circulation can manifest themselves in very different ways, ranging from periodic attacks of abdominal pain after eating (abdominal angina) to unbearable abdominal pain with thrombosis of the mesenteric vessels. With a mild form of abdominal toad, patients may otherwise feel well, but acute occlusive intestinal ischemia is associated with severe consequences. Occlusion of one of the mesenteric vessels as a result of thrombosis or embolism occurs abruptly, and its causes are obvious. However, ischemia may not be associated with occlusion, and such ischemia may be more common. In these cases, it is caused by insufficient blood supply to the intestines, the causes of which may be insufficient mesenteric blood flow after meals (leading to attacks of abdominal angina) or its drop due to heart failure and arrhythmias, and is manifested by bleeding and abdominal pain. Intestinal vascular pathologies are more common in the elderly, and their prevalence is increasing as the population ages.

Blood supply to the gastrointestinal tract

The blood supply to the stomach and intestines is provided by three unpaired arteries. The volume of blood flow through them is almost 30% of cardiac output at rest. From the last row of arcade anastomoses formed by the branches of the superior mesenteric artery at the level of the small intestine, and from the marginal colon artery at the level of the colon, small straight vessels arise, penetrating through the muscular layer of the intestine and forming a dense submucosal plexus. In the small intestine, arterioles extend from the submucosal plexus to each intestinal villi. The central arteriole runs along the axis of the villus and branches at its end, forming a network of capillaries; The outflow of blood is carried out through the venule running parallel to the central arteriole. Oxygen within the villus diffuses directly from the arteriole into the venules, which creates a countercurrent, reducing its concentration at the tip of the villus. When blood flow in the intestines decreases, the decrease in oxygen concentration is even more pronounced. This may explain that ischemia of the small intestine leads first to the destruction of the tips of the villi, and then to disruption of the integrity of the mucosa, which facilitates the penetration of bacteria through it. In the colon, arterioles and venules also lie very close together, which similarly predisposes to mucosal ischemia.

Occlusive intestinal ischemia

Pathogenesis. Occlusion of mesenteric vessels can also be a consequence of dissecting aortic aneurysm. With insufficient collateral circulation, intestinal ischemia develops, which is manifested by severe abdominal pain. The most common reason thrombosis of mesenteric arteries - atherosclerosis. Embolism is possible with myocardial infarction, left ventricular aneurysm, atrial fibrillation, heart valve damage and infective endocarditis.

Symptoms and signs. Occlusion of one of the abdominal arteries as a result of thrombosis or embolism causes acute abdominal pain. At first it may be cramping, but as intestinal infarction and peritonitis develop, it becomes constant and intensifies. Tachycardia appears arterial hypotension fever, leukocytosis and bleeding. Careful examination may reveal an abdominal aortic aneurysm, vascular murmurs, and changes in peripheral arterial pulsations.

Differential diagnoses include dissecting abdominal aortic aneurysm, intestinal obstruction, perforation of a hollow viscus, acute cholecystitis, appendicitis, diverticulitis, peptic ulcer disease, pancreatitis, and pancreatic cancer. With aortic dissection, occlusion of the mesenteric arteries is also possible. Acute intestinal obstruction and intestinal perforation can also be confused with thrombosis or embolism of the mesenteric arteries. Inflammatory diseases - cholecystitis, appendicitis, diverticulitis - are usually accompanied by local symptoms, but sometimes they are difficult to distinguish from ischemic colitis if it is accompanied by fever and leukocytosis. At peptic ulcer, pancreatitis and pancreatic cancer, symptoms are usually not so acute.

Laboratory and instrumental studies. With intestinal ischemia, leukocytosis and increased amylase activity are observed, but amylase activity rarely exceeds the norm by more than 5 times. Higher activity indicates acute pancreatitis. As ischemia increases, metabolic acidosis develops. A plain X-ray of the abdomen shows distended loops of intestine with fluid levels. The distance between the loops is increased due to swelling of the intestinal wall and intramural hemorrhages. X-ray contrast examination with barium is not indicated for acute intestinal ischemia. The diagnosis is confirmed by angiography, but if the condition rapidly worsens and perforation is suspected, immediate surgery is indicated.

Treatment. A nasogastric tube is installed, infusion therapy is carried out to correct the water-electrolyte balance, if necessary, blood transfusion, and, if necessary, vasopressors. Radical treatment consists of surgical removal of the affected segment of the intestine.

Non-occlusive intestinal ischemia

• Pathogenesis. Abdominal toad - rare disease with a characteristic clinical picture; A correct diagnosis usually makes it possible to alleviate the patient’s condition through surgical treatment. As a rule, with abdominal angina there is atherosclerosis of at least two of the three main visceral arteries. Usually there is also atherosclerosis of the coronary and other arteries, sometimes complicated by diabetes mellitus. Pain from abdominal angina occurs a few minutes after eating and is caused by the fact that the blood flow through the affected arteries is simply not enough to satisfy the energy needs of the intestines that increase during digestion.
• Symptoms and signs. The main symptom is pain in the middle part of the abdomen, severe, almost unbearable. Patients try not to eat and as a result lose weight, often by 5-15 kg. The clinical picture is very similar to pancreatic cancer, with which toad belly can be confused. Weight loss may also be partly due to malabsorption. On physical examination, weight loss is striking. On auscultation of the abdomen, vascular murmurs may be heard, but this finding is nonspecific.
• Diagnostic tests and differential diagnosis. Abdominal pain and weight loss are nonspecific symptoms that may indicate malignant tumor, as well as on the most various diseases gastrointerology. The diagnosis of abdominal toad is made with a characteristic clinical picture in the absence of other causes of abdominal pain and weight loss and arteriography revealing stenosis or occlusion of at least two of the three main visceral arteries.
• Treatment. The methods of choice are bypass surgery of the affected artery or surgical endarterectomy. In some cases, it is possible to perform endovascular endarterectomy. In rare cases, when the surgical risk is too high, it is necessary to resort to conservative treatment: the patient is transferred to nutrition with elemental mixtures or constant parenteral nutrition.

Pathogenesis. Ischemic colitis develops as a result of a periodic decrease in blood flow in the mucosa when the mesenteric vessels are damaged. The elderly and people with cardiovascular conditions such as heart failure or arrhythmias are typically affected, as these conditions predispose to periodic reductions in blood flow through the intestines. Ischemia can occur in any part of the small or large intestine, but most often affects the descending colon in the region of the splenic angle or the sigmoid colon. This is due to the fact that the splenic angle is located at the junction of the blood supply of the superior and inferior mesenteric arteries, and the sigmoid colon is at the junction of the blood supply of the inferior mesenteric and internal iliac artery. Ischemic colitis develops in almost 10% of patients who have undergone surgery for an aortic aneurysm due to impaired blood flow in the inferior mesenteric artery with insufficient collateral circulation. There is also evidence that ischemic colitis can be triggered by taking oral contraceptives, estrogens, raloxifene and pseudoephedrine.

Symptoms and signs. Characterized by sudden pain in the lower abdomen and bloody stools. On physical examination, the picture may be different. Possible low-grade fever. The abdomen is usually soft and less painful to palpation than would be expected with this type of severe pain. In most cases, the disease goes away on its own, but occasionally, from the very beginning or after some time, symptoms of peritoneal irritation appear and bowel sounds disappear, which indicates intestinal infarction and the development of peritonitis. In this case, surgery is required.

Diagnostic tests and differential diagnosis. Ischemic colitis must be differentiated from most diseases that are accompanied by abdominal pain and rectal bleeding, in particular with nonspecific ulcerative colitis, Crohn's disease, infectious colitis, bleeding from a colonic diverticulum. Plain radiographs of the abdomen reveal a characteristic symptom - a “thumb print”, caused by nodular protrusions into the intestinal lumen due to edema and hemorrhages in the submucosal layer. With sigmoidoscopy (it should be done very carefully), it is possible to identify nonspecific colitis, ulcers and soft bluish nodules, which are identified x-ray as a “thumb print”. If the patient's condition remains stable within 24-48 hours, a colonoscopy or irrigoscopy is performed, which can also show changes characteristic of the “thumbprint” symptom in the affected part of the intestine. Angiography, as a rule, is not very informative, but in cases where surgical treatment is necessary, it can help the surgeon assess the location of the mesenteric vessels.

Treatment. Food and liquid intake is prohibited and infusion therapy is started. The patient is examined several times a day so as not to miss the development of peritonitis. For heart failure and arrhythmias, appropriate treatment is carried out. Antibiotics are prescribed only for persistent fever and symptoms of peritoneal irritation. In most cases, surgery can be avoided. Some experts recommend repeat irrigoscopy after 2 months to exclude the formation of a stricture.

Angiodysplasia

Pathogenesis. Angiodysplasia is multiple accumulations of dilated, deformed vessels in the submucosal layer, consisting of arteries. _veins and capillaries. Angiodysplasia can affect any part of the gastrointestinal tract, but most often occurs in the cecum and ascending colon. Angiodysplasia can cause acute or chronic bleeding, especially in the elderly.

In most cases, angiodysplasia appears to be a consequence of the normal aging process. 15% of patients with bleeding caused by angiodysplasia have aortic stenosis, but it is not clear whether there is a pathogenetic relationship between these diseases. In hereditary hemorrhagic telangiectasia, angiodysplasia affects all parts of the gastrointestinal tract. With this disease, telangiectasia can also develop on the skin, nail beds, mucous membranes of the mouth and nasopharynx.

Symptoms and signs. Until bleeding begins, angiodysplasia does not manifest itself in any way. Therefore, such patients have a history of nothing but bleeding from the gastrointestinal tract. Most often, angiodysplasia manifests itself as acute bleeding from the lower gastrointestinal tract. The cause is often not found or is attributed to another, concomitant disease, such as peptic ulcer disease or diverticulosis. Before a correct diagnosis is made, several bleeding events often occur, sometimes over a period of months.

Instrumental research. Colonoscopy and angiography are used to diagnose angiodysplasia.

1. Colonoscopy. Red elements resembling spider veins are found in the submucosal layer. However, in order to detect angiodysplasia, the intestine during colonoscopy must be free of blood and clots, which is not always achievable in case of acute bleeding.
2. Angiography. Angiodysplasia is characterized by the following: early contrasting of veins; accumulations of dilated vessels; delay of contrast in the veins.

Treatment. The traditional method of treatment is resection of the affected area, usually the ascending colon. In 30% of cases, recurrent bleeding is observed either from newly emerging angiodysplasia or from an incompletely removed old one. Instead of surgical treatment, a method of electrocoagulation of bleeding sources during colonoscopy has been proposed.

Vascular-intestinal fistulas

Pathogenesis. Rare reason gastrointestinal bleeding - a fistula between the vessel and the gastrointestinal tract. The most common fistula occurs between the aortic prosthesis and the horizontal part duodenum, which forms several months or even years after aortic replacement. In addition, a fistula can form between an unoperated aneurysm and the intestine. Less commonly, fistulas are localized in sigmoid colon, cecum and esophagus. Fistulas between an aortic aneurysm or smaller vessels and almost any part of the gastrointestinal tract have been described.

Symptoms and signs. Fistulas between main vessels and intestines are manifested by massive bleeding from the rectum or vomiting blood. The presence of an aortic aneurysm, including a prosthetic aneurysm, increases the likelihood that the cause of bleeding is a fistula. Mortally dangerous bleeding may be preceded several hours or days by a small so-called signal bleeding.

Diagnosis and treatment. Endoscopic examination makes it possible to exclude other causes of bleeding, but rarely reveals a fistula. Angiography often fails to detect a fistula. Barium studies are not informative and also carry a risk of severe bleeding. A CT scan of the abdomen can show a ruptured aortic aneurysm or fistula, which in doubtful cases helps to make a decision about the need for surgery. A high degree of clinical suspicion for aortocolic fistula with a history of prosthetic or non-prosthetic aortic aneurysm is more important than the results of instrumental studies, since if the results of endoscopy do not clarify the diagnosis, emergency surgery is usually indicated.

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Mesenteric intestinal thrombosis

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Every day I anointed my feet with the rub.

Thrombosis in the human body always reflects serious health problems and is potentially life-threatening. But if a blood clot appears in the vessels supplying blood to internal organs, such a disease is doubly serious. For example, intestinal thrombosis, or thrombosis of mesenteric veins and arteries, is a very serious disease that leads to the death of a significant proportion of patients if they are not promptly provided with first aid and surgical treatment.

Features of the disease

The intestine is supplied with blood by 2 large vessels, which drain from the aorta. They are called the superior and inferior mesenteric (mesenteric) arteries. In this case, the outflow of blood is carried out through the superior and inferior mesenteric veins. The superior mesenteric artery supplies all parts of the small intestine, as well as some of the large intestine. The inferior mesenteric artery supplies the sigmoid and rectum. The small branches of the arteries are connected in a special way: the upper vessel in a critical situation helps to nourish the lower part of the large intestine, but the lower mesenteric artery cannot replace “foreign” functions. Therefore, with thrombosis of the intestinal arteries, the blood supply to the small intestine is disrupted.

The venous outflow from the intestinal arteries is organized in such a way that when the superior mesenteric vein is blocked, the small intestine is also left without nutrition, and therefore the processes of tissue hypoxia and death will be observed in it. If a mesothrombus, or thrombus in the intestine, clogs one of the vessels, one or another part of the small intestine will undergo necrosis. This condition is called “acute mesenteric thrombosis,” or intestinal infarction. Intestinal thrombosis, therefore, can be arterial or venous, and in especially advanced cases it can form a mixed form.

In 90% of situations, thrombosis affects the superior mesenteric artery, which supplies the largest part of the intestine, so this type of pathology will have the most severe consequences. It is believed that after thrombosis of this artery develops, acute mesenteric arterial insufficiency, or AMA, develops. Since replacement (collateral) blood circulation does not occur in this disorder, there will be no compensation of blood flow with all the ensuing consequences. Only with segmental thrombosis or embolism of the inferior mesenteric vein can the blood circulation be compensated, and only the ileum is affected.

Thrombosis of mesenteric vessels is practically not recorded in patients under 50 years of age. Age-related changes, namely, atherosclerotic decrease in the lumen of blood vessels, which occurs in the second half of life, is the main “provocateur” of this pathology. Mortality in this disease is very high, even after surgery to remove the blood clot due to the rapid progression of necrotic processes.

Causes of intestinal thrombosis

In the development of the disease, the main role may be played by embolism of a blood clot, which formed not in the intestinal vessels, but in another part of the circulatory system, or the direct formation of a blood clot - a blood clot or atherosclerotic plaque. The most common causes of a blood clot in the mesenteric vessels are:

• atherosclerosis of blood vessels with the formation of plaques, their rupture or detachment, or with the growth of plaque and blockage of the lumen of the vessel;
• myocardial infarction or cardiac aneurysm - diseases in which blood clots form that can cause embolism in the mesenteric vessels;
• thrombophlebitis and phlebothrombosis - lead to the separation of a blood clot and blockage of a peritoneal vessel;
• condition after surgery, during which massive tissue dissection was performed due to the risk of multiple blood clots;
• childbirth with severe blood loss - for a similar reason;
• injuries to the vessels of the mesentery as a result of injury or a blow to the abdomen, as a result of which the intima of an artery or vein is peeled off, which blocks the lumen of the vessel;
• a tumor of the surrounding tissues, which compresses the vessel and leads to its blockage.

The following factors and past diseases provoke the appearance of a blood clot in the mesenteric vessels:

• hypertension;
• heart defects;
• rheumatism;
• endocarditis;
• obliterating endarteritis;
• sepsis;
• chronic or acute heart failure;
• cirrhosis of the liver;
• Ormund's disease (circulatory disorder of internal organs);
• severe dehydration of the body.

Despite the different etiology, the pathogenesis of intestinal thrombosis is approximately the same and comes down to one result - intestinal ischemia. Both in the case of thrombus formation directly in the mesenteric vessels and in thromboembolism, a significant part of the vessel is closed (more than 75%), or a vein or artery is completely blocked. Next, a reflex vascular spasm is observed, further aggravating the situation. The nutrition of the intestines is disrupted, its walls begin to die. With absence emergency assistance Peritonitis develops quickly.

Stages and symptoms of intestinal thrombosis

At the very first stages, it can be very difficult to distinguish intestinal thrombosis from other diseases of the peritoneum and internal organs. But there are some symptoms related to the acute abdomen clinic that you need to immediately pay attention to and urgently call a doctor. These include:

• sudden abdominal pain;
• increased pain after eating;
• pallor;
• pallor of the conjunctiva of the eyes;
• dry mouth;
• increased sweating;
• fever above 38 degrees;
• constipation or diarrhea;
• nausea, vomiting with bile;
• increased gas formation;
• pressure drop;
• blood in stool.

Typically, the symptoms of the disease develop in stages. The duration of the stages and their characteristics can be as follows:

1. Ischemic stage - 6-12 hours. The pain in the abdomen is very strong, the person cannot find a place for himself. Pain from intestinal thrombosis cannot be relieved even with the most powerful analgesics; it becomes diffuse, cutting, stabbing. By the end of this stage, the pulse begins to slow down, the skin is pale, with a bluish tint. Unlike appendicitis and other pathologies accompanied by the clinical picture of an acute abdomen, the latter remains mild. ¼ of patients experience constipation, the rest have bloody diarrhea.
2. Heart attack stage - up to 3 days. The pain subsides as pain receptors become necrotic. The wall of the small or large intestine dies. Despite the subsidence of symptoms, intoxication increases and the pulse quickens. A person’s behavior at this stage may become inappropriate.
3. Stage of peritonitis. It begins towards the end of the infarction stage, approximately hours after the onset of the disease. Pain in the abdomen reappears, which intensifies when palpating, moving, or coughing. Rapid dehydration of the body occurs, the balance of electrolytes is disturbed, the tongue is dry, the skin turns grey, and the pulse is thready. Death occurs from peritonitis and intoxication. The stages of venous thrombosis may last longer than with arterial thrombosis - up to 5-6 days, but the result without treatment will be similar.

The clinical picture of mesenteric thrombosis develops differently in different patients. It can vary in the severity of symptoms, and, depending on this, there are three degrees of severity of the disease:

1. Decompensated ischemia - rapid development of irreversible changes, complete intestinal ischemia. The prognosis is the most unfavorable.
2. Subcompensated ischemia - collateral blood flow is partially formed, so the disruption of the intestinal blood supply is partial.
3. Compensated ischemia is a chronic condition in which the formation of collateral circulation is observed.

With chronic intestinal ischemia, abdominal pain is observed regularly, frequent diarrhea is noted, and the abdomen is constantly bloated. At any moment, the pathology can become acute with all the characteristic symptoms described above.

Possible complications

The consequences of thrombosis of mesenteric vessels without timely medical intervention will be the most serious. With rapid progression of small intestinal ischemia, an unfavorable outcome can be observed already on the first day from the onset of the disease. After a blood clot completely blocks a vessel, an intestinal infarction inevitably occurs - circulatory impairment and tissue death. Consequences of this condition:

If the blood clot was not removed at an early stage of the disease, or part of the affected intestine was not excised at the stage of ischemia, then a person with any form of intestinal thrombosis faces death.

Carrying out diagnostics

When a patient seeks help, the doctor must correctly collect anamnesis, find out the time of onset of the pain syndrome, as well as existing chronic diseases, including cardiovascular and autoimmune diseases. Physical tests are required, which reveal some characteristic symptoms:

• Mondor's sign. If there is a dough-like swelling between the navel and pubis, this most often indicates intestinal thrombosis.
• Shchetkin-Blumberg symptom. A surgical symptom characteristic of some pathologies with the clinical picture of an acute abdomen. When you press on the anterior abdominal wall and suddenly release your hand, the pain intensifies.

Intestinal thrombosis has a similar clinical picture to other diseases of the peritoneum - appendicitis, acute pancreatitis, gynecological pathologies, acute cholecystitis. For differentiation, instrumental and laboratory examinations are urgently carried out. The most important methods The following studies are used to diagnose thrombosis of mesenteric vessels:

• selective angiography or CT;
• colonoscopy;
• FGS with examination of the small intestine;
• laparoscopy;
• blood test for ESR, leukocytes (indicators will be greatly increased).

Usually, a patient with similar symptoms is immediately placed on the operating table, because with a decompensated course of the disease, the surgeon has only 2-3 hours left to save the person. As a rule, the diagnosis is established after laparoscopic surgery, which, if necessary, is immediately supplemented by abdominal surgery or laparotomy.

Treatment methods

First aid to a patient with the symptoms described above should consist of calling an ambulance as early as possible, or independently transporting the person to the hospital. The patient must be transported in a lying position. If necessary, the person should be given a heart drug - Cardiamine, Corvalol. All further treatment should be carried out in a hospital, where the person is admitted urgently.

Depending on the stage of development of the pathology, the doctor chooses a treatment method.

Conservative therapy for thrombosis of mesenteric vessels is used in very rare cases - when intestinal necrosis has not yet occurred. To rid an artery or vein of a blood clot, anticoagulants are used, which thin the blood and dissolve the blood clot. Typically, intravenous infusions of heparin and its analogues are performed. Additionally, injections of antiplatelet drugs and antithrombolytics are given. It should be remembered that only timely treatment can lead to the dissolution of the clot and prevent serious consequences. Unfortunately, early diagnosis The disease occurs rarely, so in the vast majority of cases, surgery has to be performed to save the sick person.

Intestinal surgery for thrombosis

An operation almost always becomes the only chance to save a person’s life. Despite its emergency implementation, intensive preoperative preparation is required. In addition to thorough intestinal lavage, drug correction of central hemodynamic disorders is carried out. Next, the patient is positioned on the operating table and endotracheal anesthesia is administered.

First, a laparotomy is performed, during which an inspection of the intestine is performed, examination of the mesenteric vessels, starting from their mouth, to search for a blood clot. If there is no necrotic tissue, the vessel is dissected and the blood clot is removed. Often the clot has to be literally squeezed out of a vein or artery with your fingers. A prosthesis is placed in place of the removed part of the vessel. When areas of necrosis are identified, the affected part of the intestine is excised. In some cases, bypass surgery, angioplasty, and reconstructive procedures are performed. Without restoration of normal blood flow, even after removal of gangrenous tissue, up to 80% of patients die after surgery, so the creation of collateral circulation in the mesenteric vessels is extremely important.

After the operation, the patient is prescribed large doses of antibiotics to stop the infectious process in the peritoneum; direct anticoagulants are necessarily administered, sometimes in high doses. But this also threatens with serious consequences in the form of suture failure, a drop in fibrin levels and the development of severe bleeding. After the intervention, the patient spends at least 2-3 weeks in the hospital. Further, for a long period, physical activity is strictly contraindicated for him; a person must spend a lot of time in bed, but at the same time give himself a light abdominal massage and warm-up for the legs. For 2-4 months you should adhere to a plant-dairy diet to normalize intestinal function.

Prognosis and prevention

The prognosis for thrombosis of the mesenteric arteries is unfavorable, mortality reaches 90%. The earlier treatment is started, the greater the chance of survival. The prognosis for mesenteric vein thrombosis is more favorable, since the intestine continues to be supplied arterial blood and does not undergo necrosis. The prognosis for early treatment for this variant of the disease is optimistic.

Disease prevention measures come down to preventing the development and progression of atherosclerosis and other cardiac pathologies. To do this you need to adhere proper nutrition, eat more vegetables and whole grains. Need to give up junk food, limit consumption of sweets and fatty foods. You should definitely stop smoking, because it provokes vasospasm. A healthy lifestyle and sports should be practiced from youth, and then intestinal thrombosis will not occur and will not lead to serious consequences for a person.

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Thrombosis of intestinal mesenteric vessels

Thrombosis of arteries and veins of the intestine is called “mesenteric” after the name of the vessels. Most often it is a complication of acute myocardial infarction, an attack of atrial fibrillation, or slow sepsis. Mesenteric thrombosis usually affects the superior mesenteric artery. Much less often it is found in the inferior artery and mesenteric veins.

Thrombosis in veins is less common than in mesenteric arteries. The mixed form, in which blockage of both veins and arteries occurs, is rarely observed in very advanced cases.

The disease is difficult to diagnose. 1/10 of deaths from intestinal infarction occur in people under 40 years of age. Women are more susceptible to this type of pathology than men.

In the International Classification of Diseases (ICD-10), embolisms and thromboses of the iliac artery are coded I 74.5 and are included in the zonal group of pathology of the abdominal aorta. Venous mesenteric thrombosis is a component of acute vascular diseases of the intestine and has code K55.0.

Features of the blood supply to the intestines

The intestinal loops are in a “suspended” state and are secured in place by a dense mesenteric ligament. Arterial and venous vessels pass between the leaves. They are located almost parallel. The arteries (superior and inferior mesenteric) arise from the abdominal aorta and divide the blood supply into sections:

• The superior mesenteric artery carries blood to the small intestine, cecum, ascending colon, and most of the transverse colon. It carries out 90% of the blood supply, so the lesions are more widespread and clinically severe.
• The inferior mesenteric artery supplies a much smaller area (30% of the transverse colon, descending, sigmoid, rectum).

Between the main arteries there are “spare” collateral vessels. Their task is to help blood supply to the damaged area. A feature of intestinal collaterals is that they pump blood in only one direction: from the area of ​​the superior artery to the inferior mesenteric. Therefore, in the case of upper-level thrombosis, no help can be expected from anastomoses.

Venous drainage from the intestine goes to the portal vein. Difficulty occurs when it narrows due to liver disease. Collateral circulation is formed by a group of portocaval anastomoses between the portal and vena cava. The small intestine is in the worst position. It does not have a developed collateral network.

Where do blood clots and emboli come from?

Through the arterial system, the embolus can reach the mesentery:

• from the heart in case of detachment of a parietal thrombus from the wall of a post-infarction aneurysm, during atrial fibrillation, from the inner layer (epicardium) during sepsis, destruction of valves;
• from the thoracic and abdominal aorta during vessel dissection, softening of atherosclerotic plaques;
• is formed in the mesenteric artery after traumatic damage to the inner layer.

Venous blood, having the opposite direction and a tendency to decrease speed and increase viscosity, is more susceptible to the formation of its own thrombotic masses. The formation of blood clots in the veins is caused by:

• inflammatory bowel diseases, affecting the entire wall, also involve venous vessels, local thrombophlebitis is formed;
• drop in blood pressure caused by various situations;
• portal hypertension in liver diseases;
• congestion in the underlying vessels due to portal vein thrombosis;
• any reasons that increase blood viscosity (diseases of the hematopoietic system, condition after splenectomy, long-term use of hormonal drugs to prevent pregnancy).

Types of intestinal vascular damage

Pathology classification includes different sides mechanism of injury.

The reasons are distinguished:

• arterial thrombosis and embolism;
• venous thrombosis;
• secondary thrombosis of mesenteric vessels in diseases of the aorta;
• impaired vascular patency due to compression by germinating tumors;
• consequence of vascular ligation during surgery.

Depending on the degree of blood flow disturbance, stages are distinguished:

The pathological consequences of thrombosis can be:

• ischemia of the intestinal wall;
• site of infarction;
• diffuse peritonitis.

Light areas are viable tissues, dark areas are the infarct area.

In surgery there is a stage of functional acute obstruction mesenteric vessels, in which there is no organic lesion, and the pathology is caused by a temporary spasm.

The maximum damaging factor is abdominal trauma. Compensation does not have time to develop into to the fullest. Protective mechanisms increase blood clotting are activated, which aggravates the patient’s condition.

During operations on the aorta (narrowing of the isthmus, change in position during congenital defects, replacement of a site of an aneurysm with a graft), doctors know the possible mechanism of thrombosis of the mesenteric vessels: restored full blood circulation leads to a high flow rate through thoracic aorta into the abdominal area and the femoral artery to the legs. In this case, partial “robbing” of the mesenteric vessels occurs due to the additional suction action of the jet. Small blood clots may form in the capillaries supplying the intestinal wall.

Stages and forms of blood supply disorders

Any circulatory disorders cause intestinal ischemia.

In the compensated stage, the damaged lumen of the vessel is completely replaced by the flow of blood through collaterals. This form is characteristic of chronic ischemia with a gradual course of the disease.

Subcompensation also depends on collaterals, but has clinical manifestations.

During decompensation, the entire period is divided into 2 phases:

1. in the first 2 hours, reversible changes are possible with complete restoration of blood supply to the damaged area;
2. after 4–6 hours, the irreversible phase of gangrenous changes begins.

Clinical signs of thrombosis

Symptoms of acute thrombosis of mesenteric vessels are determined by the level of circulatory blockage and the form of ischemia.

1. Abdominal pain is intense in the subcompensation stage. Localized throughout the abdomen or in the navel and lower back. During the transition to decompensation (after 4–6 hours), the nerve endings on the intestinal wall die off, and the pain decreases. Such an “improvement” does not correspond to the actual extent of the pathology.
2. Intoxication of the body is manifested by nausea, vomiting, and decreased blood pressure. Noteworthy is the discrepancy between the general severe condition and moderate abdominal pain.
3. Peritoneal phenomena: the abdomen is tense, swollen, dense muscles are felt on palpation. The symptom is more typical of small intestinal thrombosis. During the stage of decompensation, peristalsis disappears, although in the subcompensated form it retains increased activity.
4. Stool disorders - frequent diarrhea mixed with blood is possible in initial stages ischemia. With decompensation, when there is no intestinal motility, diarrhea stops.
5. A state of shock is characterized by pale skin, thread-like pulse, tachycardia, cyanosis of the lips, and a drop in blood pressure.

Any, even short-term, pain in the abdomen requires attention.

Signs of pre-thombosis caused by arterial insufficiency can be identified by questioning and clarifying the patient’s complaints:

• pain in the abdomen along the intestines becomes more intense after eating or long walking;
• tendency to unstable stool, alternating diarrhea and constipation;
• unclear weight loss.

Thrombosis of mesenteric veins is milder and slower. More often it is a chronic process.

Diagnostics

In order to make a correct diagnosis, it is important for the doctor to get answers to questions about the initial manifestations, duration of pain, and characteristics of the stool.

The decisive method is diagnostic laparoscopy, which allows you to examine the intestines and clarify the stage of ischemic changes and the localization of the area.

Leukocytosis with a shift of the formula to the left does not provide certain information, since it is characteristic of many diseases. Increased level lactate dehydroginase enzyme indicates the presence of necrotic tissue.

Some help in differential diagnosis Ultrasound of the abdomen and fluoroscopy may provide assistance. Preparing the patient and wasting time on angiography is not rational.

Inspection of the intestine allows you to detect a blood clot or ischemic area

If laparoscopy is not possible, doctors proceed to laparotomy - an operation with a large incision in the midline of the abdomen:

• examine (perform an audit) the abdominal organs and intestines;
• palpate the mesenteric vessels to identify a thrombus;
• assess the sufficiency of arterial pulsation;
• determine the boundaries of viable tissues.

Treatment

For vein thrombosis, fibrinolytic therapy is indicated in the first 6 hours.

During the operation, the doctor must find ways to:

• in the absence of necrotic changes, restore the patency of blood flow through the vessel to relieve ischemia from the affected area of ​​the intestine;
• remove the altered intestine or part of it and sew the upper and lower ends.

Restoring blood supply is carried out in the following way:

• squeezing out a blood clot with your fingers;
• creation of a bypass shunt between the upper and lower levels of the stenosis, bypassing the thrombosed area.

In the postoperative period, the patient is prescribed large doses of Heparin to thin the blood.

An angiogram of the intestinal arteries in an emergency is difficult because it requires patient preparation

How does the chronic form of thrombosis manifest?

The chronic form of thrombosis should be considered in patients with heart failure complicated by myocardial infarction. The clinic distinguishes 4 stages:

• I - the patient has no complaints, the thrombus is an accidental finding during angiography;
• II - typical complaints of pain along the intestines after eating, the person refuses food because of this;
• III - constant pain, flatulence, impaired absorption of the small intestine, diarrhea;
• IV - the occurrence of intestinal obstruction, which manifests itself " acute stomach", with peritonitis and gangrene.

Forecast

Mesenteric thrombosis, according to clinical studies, is observed much more often than the number of cases diagnosed. This pathology is masked by various acute conditions: cholecystitis, renal colic, appendicitis. The limited time for diagnosis does not always allow the disease to be detected.

Fatal cases, according to pathologists, are 1–2.5% of hospital mortality. These are thrombosis in the stage of infarction and diffuse peritonitis. Late surgery (after 12 hours) means high mortality (up to 90%).

Good prognosis for recovery surgical treatment chronic form thrombosis in the first two stages. Timely seeking surgical help for abdominal pain allows the patient to be operated on in a favorable time frame and prevent perforation of the intestinal wall.

Vascular diseases of the intestines (K55)

Spicy:

• fulminant ischemic colitis
• intestinal infarction
• small bowel ischemia

Mesenteric, [arterial, venous]:

• embolism
• heart attack
• thrombosis

Subacute ischemic colitis

Ischemic narrowing of the intestine

Mesenteric:

• atherosclerosis
• vascular insufficiency

Intestinal angiodysplasia NOS

In Russia International classification of diseases of the 10th revision (ICD-10) was adopted as a single normative document for recording morbidity, reasons for the population’s visits to medical institutions of all departments, and causes of death.

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. No. 170

The release of a new revision (ICD-11) is planned by WHO in 2017-2018.

With changes and additions from WHO.

Processing and translation of changes © mkb-10.com

Acute intestinal obstruction is a disorder in the movement of food through the gastrointestinal tract. This pathology can be caused by mechanical, dynamic or functional reasons. Thus, intestinal obstruction is divided into mechanical and dynamic.

Causes of acute intestinal obstruction

To the main mechanical factors causing intestinal obstruction include:

• Strangulated hernia.

• Formation of adhesions after surgery on the abdominal cavity and their blocking of the lumen. Intussusception of the intestinal wall (retraction of one section of the intestine into another, which blocks its lumen).

• The presence of a tumor on a nearby organ or colon cancer.

• Nodulation and volvulus.

• Obstruction of the intestinal lumen by fecal or gallstones, foreign bodies or a ball of worms.

Dynamic intestinal obstruction may develop immediately after surgery in the abdominal cavity, in case of poisoning (for example, lead) or peritonitis (inflammation of the peritoneum).

The development of intestinal obstruction can be facilitated by inflammatory diseases of the abdominal organs, previous operations in this area, abdominal trauma (open and closed), abnormally long sigmoid colon, diverticular disease of the large intestine, hernia of the anterior wall of the abdominal cavity.

Symptoms of acute intestinal failure

Acute intestinal obstruction develops gradually. Usually the disease is preceded by symptoms of intestinal dysfunction: periodic bloating, rumbling, abdominal pain; alternating diarrhea with constipation.

Symptoms of this disease are varied and mainly depend on the degree of intestinal obstruction. The obstruction may be in the upper or lower parts of the large or small intestine.

The main symptoms of acute intestinal obstruction include: pain, increased peristalsis, constipation, vomiting, abdominal tension and bloating, shock.

From the very beginning of the disease, the pain is pronounced. It is usually localized around the navel or in the epigastrium (under the stomach), less often it occurs in the lower abdomen. The pain is in the nature of spasms.

One of the most persistent symptoms this disease is vomiting. The higher the intestinal obstruction is located, the more severe the vomiting will be. If there is an obstruction of the colon, there may be no vomiting, but there will certainly be nausea.

A rather late symptom (12-24 hours after the onset of the disease) is the absence of stool.

With the development of acute intestinal failure, increased intestinal motility can be heard from a distance: rumbling, splashing, seething in the stomach.

Treatment of acute intestinal failure

All patients, regardless of the cause of the disease, are prescribed rest and hunger.

In order to empty the stomach and stop vomiting, a nasogastric tube is inserted into the stomach through the nose. Then intravenous administration is carried out medicines and antiemetic, analgesic, antispasmodic solutions.

If a hernia is strangulated, emergency surgery is performed. In other cases, if ineffective conservative treatment surgery is also indicated.

One of the problems in the treatment of patients after surgery on the abdominal organs is the prevention and restoration of disorders of the motor-evacuation function of the stomach and intestines. Timely evacuation of metabolic products, toxic substances, undigested food residues, etc. helps maintain a constant internal environment and prevents the development of endotoxicosis and septic complications. Unfortunately, a delay in the passage of gas and stool for several days is the recognized “norm” for the course of the postoperative period.

The reasons for the development of intestinal failure in the early postoperative period may be:
- high morbidity of surgical intervention;
- prolonged ischemia and hypoxia of the walls of the stomach and intestines;
- development of an intestinal inhibitory reflex, realized through the autonomic nervous system, in conditions of a long-lasting powerful reflexogenic zone after surgery;
- negative impact on the motility of certain medications (narcotic analgesics), mediators, hormones, both local and general action, electrolytes (hypokalemia), endotoxins and other biologically active substances.

The opinion of many surgeons and resuscitators that early stimulation of the intestine is contraindicated in patients after operations on the stomach and intestines has no basis and is deeply misleading. Microcirculation disorders and intestinal atony are the cause of intestinal failure against the background of enteritis. In addition to the development of stress ulcers and translocation, this also leads to anastomotic failure - ischemic, edematous and “lolling” - the swollen intestine is not capable of healing! It is quite stupid to associate peristalsis with anastomotic failure - the amplitude of peristaltic waves rarely exceeds 0.5 cm, but in the minds of some doctors this amplitude is such that it breaks the anastomosis, i.e. is at least 10-20cm. Need to know pathophysiological mechanisms and it is realistic to imagine that in the absence of peristalsis - passage of contents, stagnation begins - filling the intestines with rotting and gas-forming liquid, which swells the intestines and “tears” the anastomoses. That is why early stimulation of intestinal motor function is necessary - from the first hours after surgery.

Modern methods of prevention and treatment of postoperative intestinal failure:
1. Blockade of reflexogenic zones, nociceptive impulses. The method of choice is epidural analgesia (block). Extended epidural blockade most completely turns off the flow of pathological impulses from the area of ​​the performed operation, turns off the negative influence of sympathetic innervation and does not affect the parasympathetic department of the autonomic nervous system.
2. The use of non-narcotic analgesics in combination with antispasmodics (No-shpy (drotaverine hydrochloride) or papaverine) is aimed at eliminating the high tonic state of the smooth muscles of the intestinal tube. It has been proven that the administration of a 2% solution of No-shpa, 2.0 ml every 6 hours, within 2 days after surgery leads to the relief of colon spasm and rapid restoration of peristalsis, which can be an alternative to an epidural block.
3. Metoclopramide (cerucal, raglan) relaxes mainly the distal parts of the stomach, promotes its emptying by central blockade of dopamine receptors. Inject 2 ml of a 0.5% solution every 8 hours in the first 2 days to restore gastric emptying.
4. Parenteral administration of anticholinesterase (proserin, neostigmine) or cholinomimetic drugs (aceclidine, ubretide, kalimine) in small doses in the first 2 days to restore small intestinal motility. The administration of large doses of cholinomimetics will lead to increased peristalsis only in the small intestine and increased tone/spasm of the large intestine, depletion of energy reserves of the gastrointestinal tract and progression of intestinal paresis.
5. Measures for the treatment and prevention of hypoxia: normalization of external respiration function, elimination of ischemia, anemia - up to extended mechanical ventilation, barotherapy.
6. Correction of water-electrolyte metabolism (maintain plasma potassium at upper limit norms). Taking into account water retention and its accumulation in the surgical area, the daily volume of infusion therapy in the first 48 hours is prescribed at a rate of no more than 40 ml/kg of patient weight. Clear control of the water balance is necessary, taking into account all losses - it must be maintained at zero level.
7. Correction of hypoproteinemia with albumin. Routine use of synthetic colloids is contraindicated because they are able to accumulate in the interstitium and maintain intestinal edema.
8. Constant drainage of the upper and lower gastrointestinal tract.
9. Early enteral or tube feeding. Once the tube is in the stomach or small intestine, insertion can begin. isotonic solutions 6-8-12 hours after planned operations (restoration of the absorption function of the small intestine usually coincides with the appearance of peristaltic noises).
10. Effective method prevention of postoperative intestinal paresis is enterosorption. Enterosorption (ES) is a method based on the binding and removal from the gastrointestinal tract for therapeutic or prophylactic purposes of endogenous and exogenous substances, supramolecular structures and cells.