Acute phlegmonous appendicitis. Clinic

Acute appendicitis develops in response to an attack of a nonspecific type of infection by inflammatory phenomena in the appendix - the appendix. The cause of infection is a disruption of the normal relationship between the human body and the environment of microorganisms. Connecting exogenous and endogenous factors to the “conflict” accelerates the urgent need for immediate removal of the appendage. There are several manifestations of inflammation of the appendix, systematized by the nature of the disease, course and distribution. The pathanatomical and clinical classification of acute appendicitis is most often used.

Classification of acute appendicitis

The proposed classification includes anatomical, morphological and clinical manifestations, and also takes into account the diversity of inflammatory processes of appendicitis.

In practice, the following forms of inflammation of the appendix are encountered:

• Acute simple appendicitis, its second name, is superficial in the concept of many doctors.
• Acute appendicitis of destructive form:
  • simple phlegmonous;
  • beginning ulcers with phlegmonous form;
  • abscesses replacing ulcers - apostematous appendicitis with and without perforation;
  • gangrenous type with and without perforation.
• Acute complicated:
  • peritonitis, which can be local limited (not limited) or widespread diffuse (less often diffuse);
  • appendiceal infiltrate located in different places;
  • appendicular and periappendicular abscess;
  • pylephlebitis;
  • local abscess in the liver;
  • sepsis;
  • unrestricted inflammatory phenomena of a purulent nature in the retroperitoneal tissue.

According to the clinical course, there are 4 degrees of acute appendicitis:

• regressive type;
• no progress;
• with slow progress;
• with rapid progress.

In children, there is a discrepancy between the clinical picture of the disease and pathological changes in the tissues of the affected organ.

Etiology and pathogenesis of inflammation

Nonspecific inflammation

The etiology and pathogenesis of acute appendicitis causes a lot of controversy and evidence of different points of view, resulting in theories. To date, at least 12 theories are known that consider the possible causes, mechanism of development, termination and conditions for the development of the disease.

1. Proponents of the infectious theory believe that the source of inflammation of the appendix is ​​microorganisms that penetrate the cavity of the appendix and invade the mucous membrane of the organ.
2. According to the cortico-visceral theory, there is an increased impulse from the nervous system to the organs of the digestive system, causing contraction of the smooth muscles of certain organs. As a result, there is a decrease in the nutrition of groups of cells, causing their necrosis. The cells of the appendix mucosa are the most vulnerable. Later, infection invades the necrotic areas for the second time.
3. The etiology of acute appendicitis, according to the theory of fecal stagnation, is associated with the accumulation of fecal stones in the cavity of the appendix, and the pathogenesis considers fecalitis as the cause of microerosive phenomena in the mucous membrane of the appendix with the subsequent invasion of infection and, together, the development of the inflammatory process.
4. Closed cavity theory. When the outflow of contents from the appendix is ​​disrupted, stretching of its walls contributes to the formation of problems with blood supply. In addition, stagnant contents are an excellent environment for the proliferation of pathogenic microflora, both conditional and secondary.
5. The pathogenesis of appendicitis is associated with the invasion of pathogenic microflora from foci of infection localized in other organs. Migration of microorganisms occurs with the bloodstream (hematogenous theory).
6. The theory of nutrition as a source of inflammation. The etiology of the infection is associated with the activation of pathogenic microflora of a secondary nature and a conditional level of pathogenicity when meat foods with a small amount of fiber predominate in the diet and, as a result, appendicitis develops. Meat food takes a long time to digest and causes the development of putrefactive bacteria, which create an environment for pathogenic microorganisms. The validity of the theory is obvious, because in children under 2 years of age the insidious disease is not detected due to a diet not related to meat. If inflammation occurs in young children, the cause is associated with the intensive development of the lymphatic follicles of the appendix; normally they do not grow in children under 7 years of age. The increase in inflammatory reactions in the appendix in children over 7 years of age is explained by mature follicles.
7. The pathogenesis of acute appendicitis, according to the psychosomatic theory, is associated with frequent nervous stress, overexertion, phobias, and chronic fatigue.
8. Congenital curves cause stagnation in the lumen of the appendix and disruption of blood flow in the organ, and this is the best environment for the life of pathogenic microflora.
9. The theory of spasm of the bauhinian valve. The valve between the colon and ileum of the small intestine, under the influence of provoking factors, is capable of entering a state of spasm. In this case, the outflow of contents from the appendix is ​​disrupted, which is the cause of the onset of phlegmonous appendicitis. Inflammation increases with tissue swelling during spasms.
10. A specific virus, the effect of which is poorly understood, causes inflammation of the appendix. Occurs in most cases in children.
11. The allergy theory is similar to the nutrition theory, but has a view on the emphasized influence of food protein, against which an immune response is formed in the body. With increased protein nutrition and insufficient intake of plant fiber from food, putrefactive processes are added to the allergic reaction. Together, these factors cause the activation of a secondary infection.
12. The theory of blockage of the appendicular artery. As a result of poor blood supply to the tissues of the appendix by the appendicular artery, necrotic phenomena begin in the organ, followed by perforation of the organ.

A special form of inflammation occurs in children - hemorrhagic appendicitis. For inflammation of any etiology to begin, several conditions must be maintained:

• damage to the mucosa and disruption of its protective functions;
• an increase in the number of pathogenic microorganisms and activation of microflora of the secondary and conditional level of pathogenicity;
• reducing the body's immune response to the invasion of pathogenic bacteria.

Specific inflammation

When inflammation of the appendix is ​​of a specific nature, provoking factors are included that do not have a negative effect during the normal functioning of the body. These include helminthic infestations (flat and roundworms, Giardia, etc.), protozoa (amoebas, Trichomonas, etc.), fungi (actinomycetes, dimorphic yeasts).

Specific inflammation of the appendix is ​​detected after its removal. It is extremely rare and causes destructive appendicitis. The body responds to the aggression of microorganisms with serous inflammation, which develops in stages regardless of etiology: from the phlegmonous form to the gangrenous form.

For children, helminthic etiology is more common, since helminthic infestations (pinworms, children's roundworms) are more common in children.

Etiology, pathogenesis, classification, clinical picture and diagnosis of acute appendicitis.

Acute appendicitis– inflammation of the vermiform appendix of the cecum. One of the most common surgical diseases. Often: between the ages of 20 and 40, women get sick 2 times more often. Mortality 0.1 - 0.3%, postoperative complications 5-9%.

Etiology. Nutritional factor: food rich in animal protein contributes to impaired intestinal evacuation function, which should be considered a predisposing factor in the development of the disease. In childhood, helminthic infestation plays some role.

The main route of infection of the appendicular wall is enterogenic. Hematogenous and lymphogenous variants are rare. Pathogens: various microorganisms (bacteria, viruses, protozoa) located in the process. Most often, 90% is anaerobic non-spore-forming flora (bacteroides and anaerobic cocci). Aerobic bacteria are found less frequently (6-8%) - Escherichia coli, Klebsiella, enterococci.

Vascular theory believes that systemic vasculitis is one of the causes of acute appendicitis.

Pathogenesis. Due to the fact that mucus continues to be released during occlusion, the pressure of the contents quickly increases in the cavity of the appendix. The walls of the appendix are stretched under the pressure of mucus, effusion and gases, so first the venous and then the arterial blood supply is disrupted (ischemia).

With a lack of blood, comfortable conditions are created in the walls of the appendix for the spread of pathogenic flora. Microorganisms produce a lot of toxins, which cause disruption of the epithelial tissue of the appendix and the formation of ulcers on the mucosa. Cells of the immune system - leukocytes, lymphocytes, macrophages and others - begin to fight the activity of bacteria. They produce interleukins, adhesion molecules and other inflammatory mediators. By contacting each other, as well as with epithelial tissue cells, they limit the inflammatory focus. As a result, the process is not generalized, and the body does not produce a general reaction to the existing problem. Interleukins are released in huge quantities, which leads to a gradual destructive process in the wall of the appendix.

Classification.

The classification of acute appendicitis is clinical and morphological in nature and is based on the severity and diversity of inflammatory changes and clinical manifestations.

Forms of acute appendicitis.

 Acute simple (superficial) appendicitis. Catarrhal (leukocyte infiltration of the mucous membrane only).

 Acute destructive appendicitis.

o Phlegmonous (leukocyte infiltration of all layers of the mucous membrane, including the serous membrane, blood, leukocytes in the lumen, fibrin, leukocytes on the serous membrane).

o Gangrenous (with and without perforation) necrosis of the process wall, diffuse neutrophilic infiltration, peritonitis.

 Complicated acute appendicitis

o Complicated by peritonitis - local, limited, diffuse, diffuse

o Appendicular infiltrate

o Periappendiceal abscess

o Phlegmon of retroperitoneal tissue

o Sepsis, generalized inflammatory reaction

o Pylephlebitis

Clinic and diagnostics. The clinical picture of acute appendicitis is variable due to the peculiarities of its anatomy and the different localizations of the apex of the appendix. In typical cases, the main symptom of the disease is pain, which at the onset of the disease is localized in the epigastric or mesogastric regions or does not have a clear localization. A few hours after the onset of the disease, the pain intensifies and shifts to the right iliac region. This characteristic displacement of pain is called the Kocher-Volkovich symptom.

The pain is often accompanied by nausea, sometimes vomiting, which is reflexive in nature and occurs in 30-40% of patients. In most cases, there is a lack of appetite.

Upon examination, the general condition of patients in the initial stages of the disease practically does not suffer. There is moderate tachycardia, an increase in body temperature, usually no more than 37.5°C.

When examining the abdomen, it is most often not possible to identify any features; it is not swollen, and is involved in the act of breathing. On percussion, pain is noted in the right iliac region - a positive Razdolsky sign. On palpation, pain is determined here, even at the beginning of the disease, when the patient may feel pain in the epigastric or mesogastric areas. Also, palpation can reveal a number of symptoms:

Rovsing's sign. the appearance of pain in the right iliac region with jerky palpation of the left parts of the colon

 Sitkovsky’s symptom – increased pain in the right iliac region when the patient is positioned on the left side.

 Bartomier-Michelson's symptom - increased pain on palpation of the right iliac region with the patient positioned on the left side.

One of the most important symptoms of appendicitis is muscle tension in the right iliac region. This is the main symptom indicating the spread of inflammation to the parietal peritoneum. Other peritoneal symptoms are the Shchetkin-Blumberg, Voskresensky symptom (the “shirt” symptom - a hand is quickly passed through the patient’s shirt from the costal arch to the inguinal ligament - while increased pain is noted on the right).

Laboratory and instrumental diagnosis of acute appendicitis.

A blood test reveals moderate leukocytosis in the vast majority of patients; a shift in the leukocyte count to the left is possible.

With radiography In the abdominal cavity, no specific signs of acute appendicitis can be identified. Performing radiography is rather intended to exclude some other diseases that can simulate the picture of acute appendicitis, for example, a perforated ulcer of the stomach and duodenum, right lower lobe pneumonia, etc.

CT scan is a very informative method for diagnosing appendicitis. In many cases, it is possible to visualize the appendix with signs of inflammation - an increase in its diameter and wall thickness, and free fluid in the abdominal cavity is detected. Among the disadvantages of the method, it should be noted the presence of radiation exposure, which makes the use of CT impossible in some patients (pregnant women, children), as well as the insufficient availability of the method in most medical institutions.

Ultrasound. Signs of acute appendicitis are an increase in the diameter of the appendix and thickening of its wall.

The most informative diagnostic method is diagnostic laparoscopy. Direct examination of the appendix allows a diagnosis to be made, and in most cases, laparoscopic intervention is not only a diagnostic, but also a therapeutic procedure.

Symptoms of cholangitis.

The clinical picture of acute cholangitis develops suddenly and is characterized by Charcot's triad: high body temperature, pain in the right hypochondrium and jaundice.

Acute cholangitis manifests itself with fever: a sharp rise in body temperature to 38-40°C, chills, severe sweating. At the same time, intense pain appears in the right hypochondrium, reminiscent of biliary colic, radiating to the right shoulder and scapula, and neck. In acute cholangitis, intoxication quickly increases, weakness progresses, appetite worsens, headaches, nausea with vomiting, and diarrhea bother you. Somewhat later, with acute cholangitis, jaundice appears - visible yellowing of the skin and sclera. Against the background of jaundice, itching of the skin develops, usually worsening at night and disrupting normal sleep. As a result of severe itching on the body of a patient with cholangitis, skin scratching is detected.

In severe cases, disturbances of consciousness and shock phenomena may join Charcot's triad - in this case, a symptom complex called Reynolds' pentad develops.

Diagnosis of cholangitis.

Cholangitis is usually suspected based on the characteristic Charcot triad; clarifying diagnostics is carried out on the basis of laboratory and instrumental studies.

Imaging methods for diagnosing cholangitis include ultrasound of the abdominal cavity and liver, ultrasonography of the biliary tract, and CT. With their help, it is possible to obtain an image of the bile ducts, identify their expansion, and determine the presence of structural and focal changes in the liver.

Among the instrumental methods for diagnosing cholangitis, the leading role is given to endoscopic retrograde cholangiopancreatography, magnetic resonance cholangiopancreatography (MRCP), and percutaneous transhepatic cholangiography. The obtained radiographs and tomograms clearly visualize the structure of the biliary tract, which makes it possible to identify the cause of their obstruction.

Differential diagnosis of cholangitis is necessary with cholelithiasis, noncalculous cholecystitis, viral hepatitis, primary biliary cirrhosis, pleural empyema, and right-sided pneumonia.

12\13\14\15. Acute pancreatitis.

Acute pancreatitis is a very dangerous disease, which is based on complete or partial self-digestion (necrosis) of the pancreas.

Treatment of acute pancreatitis

In case of acute pancreatitis, hospitalization is indicated. All patients were prescribed bed rest. The main goals of therapy are to relieve pain, reduce the load on the pancreas, and stimulate its self-healing mechanisms.

Therapeutic measures:

· novocaine blockade and antispasmodics to relieve severe pain;

· hunger, ice on the area of ​​gland projection (creating local hypothermia to reduce its functional activity), parenteral nutrition, gastric contents are aspirated, antacids and proton pump inhibitors are prescribed;

· deactivators of pancreatic enzymes (proteolysis inhibitors);

· necessary correction of homeostasis (water-electrolyte, acid-base, protein balance) using infusion of saline and protein solutions;

· detoxification therapy;

· antibiotic therapy (broad-spectrum drugs in large dosages) as a prevention of infectious complications.

Surgical treatment is indicated if:

· stones in the bile ducts;

· accumulations of fluid in or around the gland;

· areas of pancreatic necrosis, cysts, abscesses.

Operations performed for acute pancreatitis with the formation of cysts or abscesses include: endoscopic drainage, cyst marsupialization, cystogastrostomy, etc. When areas of necrosis form, depending on their size, necrectomy or resection of the pancreas is performed. The presence of stones is an indication for surgery on the pancreatic duct.

Surgical intervention can also be resorted to in cases of doubt about the diagnosis and the likelihood of missing another surgical disease that requires surgical treatment.

The postoperative period involves intensive measures to prevent purulent-septic complications and rehabilitation therapy.

Treatment of mild forms of pancreatitis, as a rule, does not present any difficulties, and positive dynamics are noted within a week. It takes significantly longer to cure severe pancreatitis.

Complications of acute pancreatitis divided into early and late.

Early complications of acute pancreatitis are caused by the generalized action of pancreatic enzymes, biologically active amines and other vasoactive substances. These include shock, enzymatic diffuse peritonitis, acute hepatic-renal failure, early acute ulcers and gastrointestinal bleeding, jaundice, pneumonia, vascular thrombosis, psychoses of an intoxication nature

1. Pancreatogenic peritonitis. We can talk about pancreatogenic peritonitis only in the presence of effusion with high activity of pancreatic enzymes in combination with signs of inflammation of the peritoneum (hyperemia, subserous hemorrhages, foci of fat necrosis). The genesis of pancreatogenic peritonitis is complex and is associated not only with the exudative process in the gland; the complication most likely arises as a result of the spread of an autolytic process involving peripancreatic fibrous-ligamentous formations, peritoneum and retroperitoneal tissue.
2. Pancreatogenic shock.

16. Infected pancreatitis: clinical picture, classification, diagnosis, treatment tactics.

Infected pancreatitis (pancreatic necrosis) is a complication of acute pancreatitis.

Classification:

Pancreatic necrosis is characterized by the development of local and systemic complications.

Local complications:

In the aseptic phase of pancreatic necrosis: parapancreatic infiltrate, necrotic phlegmon of retroperitoneal tissue, enzymatic (abacterial) peritonitis, pseudocyst (late complication);

In the phase of infected pancreatic necrosis: purulent-necrotic phlegmon of the retroperitoneal tissue, abscesses of the retroperitoneal tissue spaces or abdominal cavity, internal and external pancreatic, gastrointestinal fistulas, arrosive bleeding (intra-abdominal and in the gastrointestinal tract).

· Extra-abdominal complications (systemic): pancreatogenic (enzymatic) shock, septic shock, multiple organ failure.

Clinical picture.

Infected pancreatic necrosis, which is widespread, usually forms within 1-2 weeks of the disease. It is characterized by hectic body temperature, chills, arterial hypotension and multiple organ disorders. Phenomena of intestinal paresis and intestinal obstruction. Objective symptom - Kerte - painful resistance in the projection of the pancreas.

Voskresensky's symptom is the absence of pulsation of the abdominal aorta in the projection of the pancreas. Mayo-Robson sign - pain in the left costovertebral angle.

Diagnostics.

Laboratory research:

1.OAC - leukocytosis, shift of the formula to the left, acceleration of ESR

2.OAM-proteinuria, microhematuria, cylindruria.

3. Biochemical blood test - hyperamelasemia, hyperbilirubinemia, hyperglycemia.

4.methods for diagnosing infections and complications - microbiologist studies of biopsy material obtained from fine-angle biopsy; procalcitonin test

Instrumental:

1.Ultrasonography

3.diagnostic laparoscopy

Treatment tactics.

Surgical treatment. When infected pancreatic necrosis forms in combination with an abscess, at the first stage, the surgeon uses minimally invasive technologies for percutaneous drainage of the purulent-necrotic lesion under ultrasound or CT control, providing optimal conditions for simultaneous and complete necrectomy and sequestrectomy with minimal intraoperative blood loss.

In case of widespread infected pancreatic necrosis, a laparotomy is performed, necrotic tissue or sequestration is removed, the affected areas are sanitized and the retroperitoneal tissue is extensively drained.

Surgical approaches: midline laparotomy, bisubcostal approach, lumbotomy.

Classification of bleeding

To assess the source of bleeding, the most convenient classification is J. Forrest (1987):

Ongoing bleeding:

F-I-A - jet, pulsating, arterial bleeding from the ulcer;

F-I-B - drip (venous) bleeding from an ulcer

bleeding occurred:

F-II-A - visible large thrombosed vessel at the bottom of the ulcer;

F-II-B - thrombus-clot fixed to the ulcer crater;

F-II-C - small thrombosed vessels in the form of colored spots

bleeding occurred:

no signs of bleeding

F-III - absence of stigmata of bleeding in the ulcerative crater (no stigmata).

Treatment tactics

· medical

· -solve diagnostic problems: bleeding from the stomach or other sources

Hemostatic therapy, hemodynamic restoration

· replacement therapy, hospitalization

· surgical

urgent hospitalization

· complex treatment + examination (1-24 hours)

· choice of method in accordance with the diagnosis:

· urgent surgery

· conservative treatment

· local

The basis of treatment tactics for acute gastrointestinal bleeding is conservative therapy.

Endoscopic bleeding control: It is highly effective and allows temporary hemostasis in most patients. Provides the opportunity to adequately prepare them for urgent surgical intervention. Therapeutic endoscopy may be the only justified method of treatment in a group of patients with extremely high surgical risk, when surgery is impossible. Methods of endoscopic hemostasis: mono- and biactive diathermocoagulation, thermocauterization, argon plasma coagulation, endoclipation methods, injection methods of administering epinephrine, 96% ethanol solution, as well as special sclerosants.

Infusion-transfusion therapy: necessary to restore the basic parameters of hemostasis. The primary tasks are the introduction into the vascular bed of an adequate amount of colloid and crystalloid solutions to eliminate the deficiency of bcc, normalization of microcirculation and blood rheology, correction of water and electrolyte metabolism.

Drug therapy: antisecretory drugs - parenteral forms of H2 antagonists - histamine receptors, proton pump inhibitors. Optimal conditions are created in the gastric cavity to prevent recurrent bleeding and healing of the ulcer, the operation is postponed to the stage of planned surgery or the operation is abandoned. It is advisable to monitor the effectiveness of therapy with antisecretory drugs with 24-hour pH measurements.

For the speedy healing of ulcerative and erosive lesions - antacids, synthetic analogues of prostaglandins. Anti-Helicobacter agents accelerate regenerative processes.

Nutrition is an integral part of conservative therapy.

Surgical tactics: bleeding from gastroduodenal ulcers is an indication for emergency surgery:

Emergency if it cannot be stopped using non-surgical methods.

Urgent. When the threat of relapse is too great.

The following patients are operated on as an emergency: patients with profuse ongoing bleeding, hemorrhagic shock and clinical and anamnestic data indicating bleeding of an ulcerative nature. Patients with massive bleeding, if conservative measures, including endoscopic methods, were ineffective. Patients with recurrent bleeding in the hospital.

If bleeding is stopped by conservative methods and the risk of its recurrence is low, emergency surgery is not indicated; such patients are treated conservatively.

Elderly patients with a maximum degree of surgical and anesthetic risk are not operated on. Control endoscopic examinations are carried out daily until the risk of recurrent bleeding disappears.

Choosing a surgical method depends on the severity of the patient’s condition, the degree of surgical and anesthetic risk, and the location of the bleeding ulcer.

Organ-preserving procedures with vagotomy– stopping bleeding from a duodenal ulcer involves pyloroduodenotomy, excision and/or suturing of the source of bleeding with separate sutures.

Antrumectomy with vagotomy- indicated for patients with a relatively low degree of surgical risk.

Pyloroplasty with excision or suturing of the ulcer without vagotomy are performed forcedly due to ongoing bleeding, which cannot be stopped endoscopically, usually in elderly and senile patients with an extremely high operational and anesthetic risk.

Gastric resection– indicated for a bleeding ulcer, if the degree of surgical risk is relatively low.

Excision of an ulcer or suturing of a gastric ulcer through gastrotomy access (forced nature) can be undertaken in patients with an extremely high degree of surgical risk.

Diagnostics.

Clinical symptoms.

Instrumental diagnostic methods

Laboratory diagnostics

Differential diagnosis.

Instrumental diagnostic methods:

X-ray examination –

in the compensation stage there is some enlargement of the stomach, cicatricial and ulcerative deformation of the pyloroduodenal zone, a slowdown in gastric evacuation for up to 12 hours.

With subcompensated stenosis, signs of beginning decompensation of gastric motility are detected - an increase in its size, a weakening of peristaltic activity. Symptom of a “three-layer stomach” (contrast agent, mucus, air). Evacuation delay of more than 12 hours.

The stage of decompensation is characterized by a significant increase in the size of the stomach, decreased peristalsis, a sharp narrowing of the pyloroduodenal canal and severe disturbances in gastric evacuation.

FEGDS – in the first stage, pronounced cicatricial deformation of the pyloroduodenal canal is noted with a narrowing of its lumen to 0.5-1 cm, hypertrophy of the gastric mucosa and increased peristalsis. In the second stage there is a significant narrowing of the pyloroduodenal canal, delayed evacuation of gastric contents, and an increase in the size of the stomach. In the third stage - a sharp narrowing of the pyloroduodenal canal, thinning of the gastric mucosa, lack of peristalsis of the gastric wall and excessive expansion of the lumen of the stomach.

Study of motor function using ionomanometry gives an idea of ​​the tone, frequency, amplitude of contractions of the stomach on an empty stomach and after taking a food irritant, allows you to determine the delay time of the initial evacuation. Compensated stenosis is a rare rhythm of active gastric contractions. Subcompensated – motor function is weakened. Decompensated – a sharp decrease in the tone and motor activity of the stomach.

Ultrasound – useful for express diagnostics. Not accurate in terms of determining the stage of stenosis.

Laboratory diagnostics.

Determine the signs of metabolic alkalosis, exicosis, hypoglycemia, hypoproteinemia.

Differential diagnostics.

With a tumor lesion of the antrum of the stomach, a tumor of the head of the pancreas with invasion into the duodenum.

Treatment.

Conservative therapy:

Aimed at healing active ulcers using modern antisecretory agents and anti-Helicobacter drugs. With the help of parenteral administration of salt and protein preparations, it is necessary to ensure the correction of disturbances in water-electrolyte metabolism, the protein composition of the blood plasma and the restoration of body weight. In the later stages of stenosis, one of the most effective ways to prepare a patient for surgery is enteral tube feeding. To improve the motor function of the stomach, continuous or fractional aspiration of gastric contents, gastric lavage with cold water are performed, and modern prokinetic agents are prescribed.

Surgical tactics:

Pyloroduodenal stenosis is an indication for surgical treatment. When choosing a method, one should take into account the stage of development of stenosis and the degree of disturbances in the motor function of the stomach and duodenum, as well as the characteristics of gastric secretion and the degree of surgical risk.

Truncal vagotomy in combination with stomach drainage operations– The most substantiated indications for this operation are for compensated pyloroduodenal stenosis. It can also be performed with subcompensated stenosis, when adequate preoperative preparation has been carried out.

Laparoscopic truncal vagotomy with pyloroplasty from a mini-access– with compensated stenosis.

Truncal vagotomy with anthrumectomy for stenoses with signs of subcompensation and decompensation.

Gastric resection with compensated stenosis and reduced acid-forming function of the stomach.

Gastroenterostomy as a final method of treatment, it is indicated for elderly patients, in serious condition, with late stages of stenosis.

Clinic.

With this complication, vomiting of scarlet blood or the color of “coffee grounds”, a sharp deterioration in the general condition of the patient (tachycardia, decreased blood pressure, general weakness, sweating), and dark stool (melena) are observed.

Diagnostics.

The diagnosis of bleeding from dilated veins of the esophagus is made on the basis of the above-described clinical picture and additional research methods. In order of application, they should be divided into simple diagnostic (insertion of a probe), radiological and instrumental methods.

X-ray methods primarily include examination of the esophagus and stomach with a barium suspension to determine the extent of the lesion. For the same purpose, esophagogastroscopy is performed in specialized institutions.

Establishment of the localization of bleeding in the esophagus is made on the basis of anamnesis indicating the possibility of cirrhosis of the liver, bleeding in the form of vomiting of scarlet blood, objective signs of portal hypertension determined by splenoportography and splenoportomanometry, portohepatography, azygography, etc.,

Laboratory data (leukopenia, thrombocytopenia, hyperbilirubinemia, hypocholesterolemia, hypoproteinemia with a shift towards gamma globulins, positive bromsulfalein test, etc.).

Treatment.

Treatment of patients with bleeding from the veins of the esophagus begins with conservative measures. If bleeding continues, the most effective is local exposure to the source of bleeding using a probe. Blackmore type-Sengstaken. The probe is left in the esophagus for up to 48-72 hours, while for hemostasis it is necessary to introduce 100-120 cm of air into the gastric balloon and up to 100 cm of air into the esophageal balloon. The probe with inflated cuffs is left in the stomach for 4 hours, after which the air should be released from the esophageal cuff and the patient should be observed for 1.5-2 hours. At this time, the stomach is washed through an obturator probe to clean water and complex conservative hemostatic therapy is carried out.

In cases of recurrent bleeding (40%), the obturator probe should be reinserted, leaving it in the stomach for at least 24 hours.

Endoscopic hemostasis:

More often used as a measure to prevent recurrent bleeding.

Main implementation options: endoscopic ligation, endoscopic

sclerotherapy (tetradecyl sulfate, ethoxysclerol); obliteration of varicose veins with adhesive compositions (tissucol, histoacrylate, bucrylate, cyanoacrylate); esophageal stenting.

Surgery.

Recommended intervention - operation PATIENTS (transverse gastrotomy in the subcardial part of the stomach, circular stitching and ligation over a significant extent of all dilated veins of the submucosal layer in the area of ​​the cardial-esophageal junction).

Clinic.

Clinically, Mallory-Weiss syndrome will be manifested by the presence of blood in the vomit. Moreover, blood may be absent during the first attacks of vomiting, when the mucous membrane just ruptures. It may also be accompanied by abdominal pain, pale skin, severe weakness, black stools (melena), cool sticky sweat.

Diagnostics.

Of the instrumental methods for diagnosing Mallory-Weiss syndrome, endoscopic examination (fibroesophagogastroduodenoscopy) is of greatest value. This study allows you to see a longitudinal tear in the mucous membrane of the esophagus. In addition, if bleeding is detected, an attempt can be made to stop it endoscopically.

In the anamnesis of patients with Mallory-Weiss syndrome, one can often find mention of drinking alcoholic beverages in large quantities, which resulted in vomiting.

When examining a patient with Mallory-Weiss syndrome, one can detect common signs of all bleeding: pale skin, cold sticky sweat, lethargy, tachycardia, hypotension, and possibly even the development of shock.

In a clinical blood test, there will be a decrease in the number of red blood cells, hemoglobin levels, and an increase in the number of platelets, which indicates the presence of bleeding.

Treatment.

A. Conservative therapy for Malory-Weiss syndrome is used to restore circulating blood volume. For this purpose, various

Crystalloids (NaCl 0.9%, glucose 5%, Ringer's solution, etc.),

Colloidal solutions (albumin, aminoplasmal, etc.); in case of severe blood loss, blood transfusion (packed red blood cells, fresh frozen plasma) may be used.

For vomiting (or retching), metoclopramide (Cerucal) is used.

To stop bleeding, it is possible to apply

• sodium ethamsylate,
• calcium chloride,
• aminocaproic acid,
• octreatide.

b. When performing fibroesophagogastroduodenoscopy and detecting a longitudinal rupture of the mucous membrane of the esophagus with bleeding, you can try to stop this bleeding endoscopically. This uses:

1. Injection of the bleeding site with adrenaline.

A solution of epinephrine hydrochloride is injected into the area of ​​bleeding, as well as around the source of bleeding. The hemostatic effect is achieved due to the vasoconstrictor effect of adrenaline.

2. Argon plasma coagulation

This method is one of the most effective and at the same time one of the most technically difficult. The use of argon plasma coagulation method allows achieving stable hemostasis.

3. Electrocoagulation

Also quite an effective method. The use of electrocoagulation is often combined with the administration of adrenaline.

4. Administration of sclerosants

This method consists in the fact that the hemostatic effect is achieved through the introduction of slerating drugs (polidocanol).

5. Vessel ligation

For Mallory-Weiss syndrome, endoscopic ligation of bleeding vessels is often used. The use of endoscopic vascular ligation is especially justified in the combination of Mallory-Weiss syndrome and portal hypertension with esophageal varices.

6. Vessel clipping

In essence, this method is similar to the previous one. The only difference is that not a ligature is applied to the bleeding vessel, but a metal clip. Clip application is possible using an applicator. Unfortunately, endosopic clipping of vessels is not always possible due to the technical difficulties of applying clips to vessels.

V. For Mallory-Weiss syndrome, surgical treatment is resorted to in case of ineffectiveness of conservative therapy and endoscopic treatment methods. For Mallory-Weiss syndrome, a Bayeux operation will be performed:

Access: median laparotomy.

Operation: gastrotomy, suturing of bleeding vessels.

25. Predisposing and producing factors for the formation of abdominal hernias. Classification of hernias.

Abdominal hernia is the exit of viscera from the abdominal cavity along with the parietal layer of the peritoneum through natural or pathological openings under the integument of the body or into another cavity.

Classification:

Etiological characteristics:

Congenital

Purchased

Localization:

Inguinal

Femoral

Umbilical

Linea alba

Rare (lumbar, xiphoid, Spigelian line, ischial, perineal)

Clinical course:

Uncomplicated (reducible hernia)

Complicated (strangulation, irreducibility, inflammation, coprostasis)

Recurrent

Predisposing factors include the characteristics of the human constitution (asthenic physique, tall stature), hereditary weakness of connective tissue, gender, age, both obesity and rapid weight loss, frequent childbirth, postoperative scars, paralysis of the nerves innervating the abdominal wall.

Producing factors are those that contribute to a significant increase in intra-abdominal pressure or its sharp fluctuations. These are conditions that occur with frequent crying and screaming of a child in infancy, prolonged coughing; heavy physical labor exceeding the degree of muscle fitness of a particular person; difficulty urinating, prolonged constipation, complicated pregnancy and difficult childbirth with a long period of pushing.

Treatment of the disease

A strangulated hernia is subject to immediate surgical treatment, regardless of the timing, type and location of the strangulation. Any attempt to reduce a hernia at the pre-hospital stage or in the hospital is unacceptable. The exception is for patients in extremely serious condition, for whom more than 2 hours have passed since the strangulation - you can try to carefully push the hernial contents into the abdominal cavity, first you need to administer atropine to the patient, empty the bladder, rinse the stomach with a probe, and perform a cleansing enema with warm water .

A patient diagnosed with a strangulated hernia is immediately sent to the emergency surgical department. The administration of analgesics and antispasmodics is contraindicated. If a patient with a strangulated hernia undergoes spontaneous reduction, he must also be hospitalized

A patient with a strangulated hernia should not do the following:

1. wash in the bath;

2. give a laxative;

3. administer morphine;

4. reduce the hernia:

There may be false reduction;

Break gr. bag;

Recession of dead areas inward.

Classification of inguinal hernias

According to anatomical Features include oblique, direct and combined inguinal hernias.

Oblique inguinal hernias can be of congenital or acquired origin. In this case, the elements of the hernial contents enter the inguinal canal through the internal inguinal ring and are located along the inguinal canal among the anatomical structures of the spermatic cord. Among the forms of oblique inguinal hernia, there are canal hernia (the bottom of the hernial sac is located at the level of the external opening of the inguinal canal), cordic (the bottom of the hernial sac is located in the inguinal canal at different levels of the spermatic cord), inguinal-scrotal hernia (the bottom of the hernial sac descends into the scrotum, leading to its increase).

Acute appendicitis (acute inflammation of the appendix of the cecum) is one of the most common causes of “acute abdomen” and the most common pathology of the abdominal organs requiring surgical treatment. The incidence of appendicitis is 0.4-0.5%, it occurs at any age, most often from 10 to 30 years, men and women are affected with approximately the same frequency.

Anatomical and physiological information. In most cases, the cecum is located in the right iliac fossa mesoperitoneally, the vermiform appendix arises from the posteromedial wall of the intestinal dome at the junction of three longitudinal muscle bands (tenia liberae) and is directed downward and medially. Its average length is 7 - 8 cm, thickness 0.5 - 0.8 cm. The vermiform appendix is ​​covered with peritoneum on all sides and has a mesentery, thanks to which it has mobility. The blood supply to the appendix occurs through a. appendicularis, which is a branch of a. ileocolica. Venous blood flows through v. ileocolica in v. mesenterica superior and v. portae. There are many options for the location of the appendix in relation to the cecum. The main ones are: 1) caudal (descending) - the most common; 2) pelvic (low); 3) medial (internal); 4) lateral (along the right lateral canal); 5) ventral (anterior); 6) retrocecal (posterior), which can be: a) intraperitoneal, when the process, which has its own serous cover and mesentery, is located behind the dome of the cecum and b) retroperitoneal, when the process is completely or partially located in the retroperitoneal retrocecal tissue.

Etiology and pathogenesis of acute appendicitis. The disease is considered as a nonspecific inflammation caused by factors of various nature. Several theories have been proposed to explain it.

1. Obstructive (stagnation theory)

2. Infectious (Aschoff, 1908)

3. Angioneurotic (Rikker, 1927)

4. Allergic

5. Nutritional

The main reason for the development of acute appendicitis is obstruction of the lumen of the appendix, associated with hyperplasia of lymphoid tissue and the presence of fecal stones. Less commonly, the cause of outflow disturbance may be a foreign body, neoplasm or helminths. After obstruction of the lumen of the appendix, a spasm of the smooth muscle fibers of its wall occurs, accompanied by vascular spasm. The first of them leads to a violation of evacuation, stagnation in the lumen of the appendix, the second leads to a local disruption of the nutrition of the mucous membrane. Against the background of activation of the microbial flora, which penetrates the appendix by enterogenous, hematogenous and lymphogenous routes, both processes cause inflammation, first of the mucous membrane, and then of all layers of the appendix.

Classification of acute appendicitis

Uncomplicated appendicitis.

1. Simple (catarrhal)

2. Destructive

• phlegmonous
• gangrenous
• perforated

Complicated appendicitis

Complications of acute appendicitis are divided into preoperative and postoperative.

I. Preoperative complications of acute appendicitis:

1. Appendiceal infiltrate

2. Appendiceal abscess

3. Peritonitis

4. Phlegmon of retroperitoneal tissue

5. Pylephlebitis

II. Postoperative complications of acute appendicitis:

Early(occurring during the first two weeks after surgery)

1. Complications from the surgical wound:

• bleeding from a wound, hematoma
• infiltrate
• suppuration (abscess, phlegmon of the abdominal wall)

2. Complications from the abdominal cavity:

• infiltrates or abscesses of the ileocecal area
  • abscess of the pouch of Douglas, subphrenic, subhepatic, interintestinal abscesses
• retroperitoneal phlegmon
• peritonitis
• pylephlebitis, liver abscesses
• intestinal fistulas
• early adhesive intestinal obstruction
• intra-abdominal bleeding

3. General complications:

• pneumonia
• thrombophlebitis, pulmonary embolism
• cardiovascular failure, etc.

Late

1. Postoperative hernias

2. Adhesive intestinal obstruction (adhesive disease)

3. Ligature fistulas

The causes of complications of acute appendicitis are:

1. 1. Failure of patients to seek medical care in a timely manner
2. 2. Late diagnosis of acute appendicitis (due to an atypical course of the disease, diagnostic errors, etc.)
3. 3. Tactical errors of doctors (neglect of dynamic monitoring of patients with a questionable diagnosis, underestimation of the prevalence of the inflammatory process in the abdominal cavity, incorrect determination of indications for drainage of the abdominal cavity, etc.)
4. 4. Technical errors of the operation (tissue injury, unreliable ligation of vessels, incomplete removal of the appendix, poor drainage of the abdominal cavity, etc.)
5. 5. Progression of chronic or occurrence of acute diseases of other organs.

Clinic and diagnosis of acute appendicitis

In the classic clinical picture of acute appendicitis, the patient's main complaint is abdominal pain. Often pain occurs first in the epigastric (Kocher's sign) or periumbilical (Kümmel's sign) region, followed by gradual movement after 3-12 hours to the right iliac region. In cases of atypical location of the appendix, the nature of the occurrence and spread of pain may differ significantly from that described above. With pelvic localization, pain is noted above the womb and in the depths of the pelvis, with retrocecal localization - in the lumbar region, often with irradiation along the ureter, with a high (subhepatic) location of the process - in the right hypochondrium.

Another important symptom that occurs in patients with acute appendicitis is nausea and vomiting, which is often one-time, and stool retention is possible. General symptoms of intoxication in the initial stage of the disease are mild and manifest as malaise, weakness, and low-grade fever. It is important to assess the sequence of symptoms. The classic sequence is the initial occurrence of abdominal pain, followed by vomiting. Vomiting preceding the onset of pain casts doubt on the diagnosis of acute appendicitis.

The clinical picture of acute appendicitis depends on the stage of the disease and the location of the appendix. At an early stage, there is a slight increase in temperature and increased heart rate. Significant hyperthermia and tachycardia indicate the occurrence of complications (perforation of the appendix, abscess formation). With the usual location of the process, palpation of the abdomen causes local pain at McBurney's point. With pelvic localization, pain is detected in the suprapubic region, dysuric symptoms (frequent painful urination) are possible. Palpation of the anterior abdominal wall is not very informative; it is necessary to perform a digital rectal or vaginal examination to determine the sensitivity of the pelvic peritoneum (“Douglas cry”) and assess the condition of other pelvic organs, especially in women. With a retrocecal location, the pain is shifted to the right flank and right lumbar region.

The presence of protective tension in the muscles of the anterior abdominal wall and symptoms of peritoneal irritation (Shchetkin - Blumberg) indicates the progression of the disease and the involvement of the parietal peritoneum in the inflammatory process.

The diagnosis is facilitated by identifying the characteristic symptoms of acute appendicitis:

• Razdolsky - pain on percussion over the source of inflammation
• Rovzinga - the appearance of pain in the right iliac region when pushing in the left iliac region in the projection of the descending colon
• Sitkovsky - when the patient turns on his left side, pain in the ileocecal region intensifies due to movement of the appendix and tension of its mesentery
• Voskresensky - when the hand quickly slides along a stretched shirt from the xiphoid process to the right iliac region, in the latter there is a significant increase in pain at the end of the movement of the hand
• Bartomier-Mikhelson - palpation of the right iliac region with the patient positioned on the left side causes a more pronounced pain reaction than on the back
• Obraztsova - when palpating the right iliac region with the patient in the supine position, the pain intensifies when raising the straightened right leg
• Koupa - hyperextension of the patient's right leg when he is positioned on the left side is accompanied by sharp pain

Laboratory data. A blood test usually reveals moderate leukocytosis (10 -16 x 10 9 / L) with a predominance of neutrophils. However, a normal number of leukocytes in the peripheral blood does not exclude acute appendicitis. In the urine there may be single red blood cells in the field of view.

Special research methods usually performed in cases where there is doubt about the diagnosis. In case of inconclusive clinical manifestations of the disease, if there is an organized specialized surgical service, it is advisable to begin further examination with a non-invasive ultrasound examination (ultrasound), during which attention is paid not only to the right iliac region, but also to the organs of other parts of the abdomen and retroperitoneal space. An unambiguous conclusion regarding the destructive process in the organ allows you to adjust the surgical approach and the option of pain relief in case of an atypical location of the appendix.

In case of inconclusive ultrasound data, laparoscopy is used. This approach helps to reduce the number of unnecessary surgical interventions, and if special equipment is available, it makes it possible to move from the diagnostic stage to the therapeutic stage and perform endoscopic appendectomy.

Development acute appendicitis in elderly and senile people has a number of features. This is due to a decrease in physiological reserves, a decrease in the body’s reactivity and the presence of concomitant diseases. The clinical picture is characterized by a less acute onset, mild severity and diffuse nature of abdominal pain with the relatively rapid development of destructive forms of appendicitis. Abdominal bloating and non-passage of stool and gas are often noted. Muscle tension in the anterior abdominal wall and pain symptoms characteristic of acute appendicitis may be mild and sometimes not detectable. The overall response to the inflammatory process is weakened. A rise in temperature to 38 0 and above is observed in a small number of patients. In the blood there is moderate leukocytosis with a frequent shift of the formula to the left. Careful observation and examination with the widespread use of special methods (ultrasound, laparoscopy) are the key to timely surgical intervention.

Acute appendicitis in pregnant women. In the first 4-5 months of pregnancy, the clinical picture of acute appendicitis may not have any features, however, later the enlarged uterus displaces the cecum and the appendix upward. In this regard, abdominal pain can be determined not so much in the right iliac region, but along the right flank of the abdomen and in the right hypochondrium; irradiation of pain into the right lumbar region is possible, which can be erroneously interpreted as a pathology from the biliary tract and the right kidney. Muscle tension and symptoms of peritoneal irritation are often mild, especially in the last third of pregnancy. To identify them, it is necessary to examine the patient in a position on the left side. For the purpose of timely diagnosis, all patients are advised to monitor laboratory parameters, ultrasound of the abdominal cavity, joint dynamic observation of a surgeon and obstetrician-gynecologist, and laparoscopy can be performed if indicated. Once the diagnosis is made, emergency surgery is indicated in all cases.

Differential diagnosis for pain in the right lower abdomen, it is carried out with the following diseases:

1. 1. Acute gastroenteritis, mesenteric lymphadenitis, food toxic infections
2. 2. Exacerbation of peptic ulcer of the stomach and duodenum, perforation of ulcers of these localizations
3. 3. Crohn's disease (terminal ileitis)
4. 4. Inflammation of Meckel's diverticulum
5. 5. Gallstone disease, acute cholecystitis
6. 6. Acute pancreatitis
7. 7. Inflammatory diseases of the pelvic organs
8. 8. Rupture of ovarian cyst, ectopic pregnancy
9. 9. Right-sided renal and ureteral colic, inflammatory diseases of the urinary tract

10. Right lower lobe pleuropneumonia

Treatment of acute appendicitis

An active surgical position in relation to acute appendicitis is generally accepted. Absence of doubt about the diagnosis requires emergency appendectomy in all cases. The only exception is patients with a well-demarcated dense appendiceal infiltrate, requiring conservative treatment.

Currently, surgical clinics use various options for open and laparoscopic appendectomy, usually under general anesthesia. In some cases, it is possible to use local infiltration anesthesia with potentiation.

To perform a typical open appendectomy, the Volkovich-Dyakonov oblique variable (“slide”) access through the McBurney point is traditionally used, which, if necessary, can be expanded by dissecting the wound down the outer edge of the sheath of the right rectus abdominis muscle (according to Boguslavsky) or in the medial direction without crossing the rectus muscle (according to Bogoyavlensky) or with its crossing (according to Kolesov). Sometimes the Lenander longitudinal approach (along the outer edge of the right rectus abdominis muscle) and the transverse Sprengel approach (used more often in pediatric surgery) are used. In case of complications of acute appendicitis with widespread peritonitis, with severe technical difficulties during appendectomy, as well as erroneous diagnosis, a median laparotomy is indicated.

The vermiform appendix is ​​mobilized in an antegrade (from apex to base) or retrograde (first, the appendix is ​​cut off from the cecum, the stump is processed, then isolated from the base to the apex) method. The stump of the appendix is ​​treated with a ligature (in pediatric practice, in endosurgery), intussusception or ligature-intussusception method. As a rule, the stump is tied with a ligature of absorbable material and immersed in the dome of the cecum with purse-string, Z-shaped or interrupted sutures. Often, additional peritonization of the suture line is performed by suturing the stump of the mesentery of the appendix or fatty suspension, fixing the dome of the cecum to the parietal peritoneum of the right iliac fossa. Then the exudate is carefully evacuated from the abdominal cavity and, in the case of uncomplicated appendicitis, the operation is completed by suturing the abdominal wall tightly in layers. It is possible to install a microirrigator to the bed of the appendix for administering antibiotics in the postoperative period. The presence of purulent exudate and diffuse peritonitis is an indication for sanitation of the abdominal cavity with its subsequent drainage. If a dense inseparable infiltrate is detected, when it is impossible to perform an appendectomy, as well as in the case of unreliable hemostasis after removal of the appendix, tamponing and drainage of the abdominal cavity are performed.

In the postoperative period for uncomplicated appendicitis, antibacterial therapy is not carried out or is limited to the use of broad-spectrum antibiotics in the next 24 hours. In the presence of purulent complications and diffuse peritonitis, combinations of antibacterial drugs are used using various methods of their administration (intramuscular, intravenous, intra-aortic, into the abdominal cavity) with a preliminary assessment of the sensitivity of the microflora.

Appendicular infiltrate

Appendicular infiltrate - this is a conglomerate of loops of the small and large intestine, greater omentum, uterus with appendages, bladder, parietal peritoneum welded together around the destructively altered appendix, which reliably limit the penetration of infection into the free abdominal cavity. Occurs in 0.2 - 3% of cases. Appears 3-4 days after the onset of acute appendicitis. In its development, two stages are distinguished - early (formation of loose infiltrate) and late (dense infiltrate).

In the early stage, an inflammatory tumor forms. Patients have a clinical picture close to the symptoms of acute destructive appendicitis. At the stage of formation of a dense infiltrate, the phenomena of acute inflammation subside. The general condition of the patients is improving.

The decisive role in diagnosis is played by a clinical history of acute appendicitis or upon examination in combination with a palpable painful tumor-like formation in the right iliac region. At the stage of formation, the infiltrate is soft, painful, has no clear boundaries, and is easily destroyed when the adhesions are separated during surgery. In the delimitation stage, it becomes dense, less painful, and clear. Infiltrate is easily determined with typical localization and large size. To clarify the diagnosis, rectal and vaginal examination, ultrasound of the abdominal cavity, and irrigography (scopy) are used. Differential diagnosis is carried out with tumors of the cecum and ascending colon, uterine appendages, hydropyosalpix.

Tactics for appendiceal infiltrate are conservative and expectant. Complex conservative treatment is carried out, including bed rest, a gentle diet, in the early phase - cold applied to the infiltrated area, and after normalization of the temperature, physical therapy (UHF). Antibacterial, anti-inflammatory therapy is prescribed, perinephric novocaine blockade is performed according to A.V. Vishnevsky, blockade according to Shkolnikov, therapeutic enemas, immunostimulants, etc. are used.

In the case of a favorable course, the appendiceal infiltrate resolves within 2 to 4 weeks. After complete subsidence of the inflammatory process in the abdominal cavity, no earlier than 6 months later, a planned appendectomy is indicated. If conservative measures are ineffective, the infiltrate suppurates with the formation of an appendiceal abscess.

Appendiceal abscess

Appendicular abscess occurs in 0.1 - 2% of cases. It can form in the early stages (1 - 3 days) from the moment of development of acute appendicitis or complicate the course of the existing appendiceal infiltrate.

Signs of abscess formation are symptoms of intoxication, hyperthermia, an increase in leukocytosis with a shift in the white blood count to the left, an increase in ESR, increased pain in the projection of a previously identified inflammatory tumor, a change in consistency and the appearance of softening in the center of the infiltrate. An abdominal ultrasound is performed to confirm the diagnosis.

The classic treatment option for an appendiceal abscess is opening the abscess using an extraperitoneal approach according to N.I. Pirogov with a deep, including retrocecal and retroperitoneal location. In case of a tight fit of the abscess to the anterior abdominal wall, the Volkovich-Dyakonov approach can be used. Extraperitoneal opening of the abscess avoids the entry of pus into the free abdominal cavity. After sanitizing the abscess, a tampon and drainage are inserted into its cavity, and the wound is sutured to drainage.

Currently, a number of clinics use extraperitoneal puncture sanitation and drainage of the appendiceal abscess under ultrasound control, followed by washing the abscess cavity with antiseptic and enzyme preparations and prescribing antibiotics, taking into account the sensitivity of the microflora. For large abscesses, it is proposed to install two drains at the upper and lower points for the purpose of flow-through rinsing. Considering the low invasiveness of puncture intervention, it can be considered the method of choice in patients with severe concomitant pathology and weakened by intoxication against the background of a purulent process.

Pylephlebitis

Pylephlebitis is purulent thrombophlebitis of the branches of the portal vein, complicated by multiple liver abscesses and pyaemia. It develops as a result of the spread of the inflammatory process from the veins of the appendix to the ileocolic, superior mesenteric, and then portal veins. More often it occurs with a retrocecal and retroperitoneal location of the appendix, as well as in patients with intraperitoneal destructive forms of appendicitis. The disease usually begins acutely and can be observed both in the preoperative and postoperative periods. The course of pylephlebitis is unfavorable and is often complicated by sepsis. Mortality rate is more than 85%.

The clinical picture of pylephlebitis consists of hectic temperature with chills, heavy sweating, and icteric discoloration of the sclera and skin. Patients are bothered by pain in the right hypochondrium, often radiating to the back, lower chest and right collarbone. Objectively, enlarged liver and spleen and ascites are found. An X-ray examination reveals a high position of the right dome of the diaphragm, an enlarged liver shadow, and a reactive effusion in the right pleural cavity. Ultrasound reveals areas of altered echogenicity of the enlarged liver, signs of portal vein thrombosis and portal hypertension. In the blood - leukocytosis with a shift to the left, toxic granularity of neutrophils, increased ESR, anemia, hyperfibrinemia.

Treatment consists of performing an appendectomy followed by complex detoxification intensive therapy, including intra-aortic administration of broad-spectrum antibacterial drugs, the use of extracorporeal detoxification (plasmapheresis, hemo- and plasmasorption, etc.). Long-term intraportal administration of drugs is carried out through a cannulated umbilical vein. Liver abscesses are opened and drained, or punctured under ultrasound guidance.

Pelvic abscess

Pelvic localization of abscesses (abscesses Douglas space) occurs most often in patients who have undergone appendectomy (0.03 - 1.5% of cases). They are localized in the lowest part of the abdominal cavity: in men excavatio retrovesicalis, and in women in excavatio retrouterina. The occurrence of ulcers is associated with poor sanitation of the abdominal cavity, inadequate drainage of the pelvic cavity, and the presence of an abscess infiltrate in this area when the appendix is ​​located in the pelvis.

An abscess of the pouch of Douglas forms 1 to 3 weeks after surgery and is characterized by the presence of general symptoms of intoxication, accompanied by pain in the lower abdomen, behind the womb, dysfunction of the pelvic organs (dysuric disorders, tenesmus, mucus discharge from the rectum). Per rectum, tenderness of the anterior wall of the rectum and its overhang are found; a painful infiltrate along the anterior wall of the intestine with areas of softening can be palpated. Per vaginam there is pain in the posterior fornix and intense pain when the cervix is ​​displaced.

To clarify the diagnosis, ultrasound and diagnostic puncture are used in men through the anterior wall of the rectum, and in women through the posterior vaginal fornix. After obtaining pus, the abscess is opened using a needle. A drainage tube is inserted into the abscess cavity for 2 - 3 days.

A pelvic abscess that is not diagnosed in time can be complicated by a breakthrough into the free abdominal cavity with the development of peritonitis or into adjacent hollow organs (bladder, rectum and cecum, etc.)

Subphrenic abscess

Subdiaphragmatic abscesses develop in 0.4 - 0.5% of cases, and can be single or multiple. According to localization, they distinguish between right and left-sided, anterior and posterior, intra- and retroperitoneal. The reasons for their occurrence are poor sanitation of the abdominal cavity, infection through the lymphatic or hematogenous route. They can complicate the course of pylephlebitis. The clinical picture develops 1-2 weeks after surgery and is manifested by pain in the upper abdominal cavity and lower parts of the chest (sometimes radiating to the scapula and shoulder), hyperthermia, dry cough, and symptoms of intoxication. Patients can take a forced semi-sitting position or on their side with their legs adducted. The chest on the affected side lags behind when breathing. The intercostal spaces at the level of 9 - 11 ribs above the abscess area bulge (V.F. Voino-Yasenetsky's symptom), palpation of the ribs is sharply painful, percussion - dullness due to reactive pleurisy, or tympanitis over the area of ​​the gas bubble with gas-containing abscesses. On a survey X-ray, there is a high position of the dome of the diaphragm, a picture of pleurisy, a gas bubble with a liquid level above it can be determined. Ultrasound reveals a limited accumulation of fluid under the dome of the diaphragm. The diagnosis is clarified after a diagnostic puncture of the subdiaphragmatic formation under ultrasound guidance.

Treatment consists of opening, emptying and draining the abscess using extrapleural, extraperitoneal access, less often through the abdominal or pleural cavity. Due to the improvement of ultrasound diagnostic methods, abscesses can be drained by inserting single- or double-lumen tubes into their cavity through a trocar under ultrasound guidance.

Interintestinal abscess

Interintestinal abscesses occur in 0.04 - 0.5% of cases. They occur mainly in patients with destructive forms of appendicitis with insufficient sanitation of the abdominal cavity. In the initial stage, symptoms are scant. Patients are bothered by abdominal pain without clear localization. The temperature rises, intoxication symptoms increase. In the future, a painful infiltrate in the abdominal cavity and stool disorders may appear. On a survey radiograph, areas of darkening are found, in some cases with a horizontal level of liquid and gas. To clarify the diagnosis, lateroscopy and ultrasound are used.

Interintestinal abscesses adjacent to the anterior abdominal wall and adherent to the parietal peritoneum are opened extraperitoneally or drained under ultrasound guidance. The presence of multiple abscesses and their deep location is an indication for laparotomy, emptying and drainage of abscesses after preliminary delimitation with tampons from the free abdominal cavity.

Intra-abdominal bleeding

The causes of bleeding into the free abdominal cavity are poor hemostasis of the appendix bed, slipping of the ligature from its mesentery, damage to the vessels of the anterior abdominal wall and insufficient hemostasis when suturing the surgical wound. Disorders of the blood coagulation system play a certain role. Bleeding can be profuse and capillary.

With significant intra-abdominal bleeding, the condition of the patients is serious. There are signs of acute anemia, the abdomen is somewhat swollen, tense and painful on palpation, especially in the lower parts, symptoms of peritoneal irritation may be detected. Percussion reveals dullness in sloping areas of the abdominal cavity. Per rectum is determined by the overhang of the anterior wall of the rectum. To confirm the diagnosis, ultrasound is performed, in difficult cases - laparocentesis and laparoscopy.

For patients with intra-abdominal bleeding after appendectomy, urgent relaparotomy is indicated, during which an inspection of the ileocecal area, ligation of the bleeding vessel, sanitation and drainage of the abdominal cavity are performed. In case of capillary bleeding, tight packing of the bleeding area is additionally performed.

Limited intraperitoneal hematomas give a more sparse clinical picture and can manifest themselves in the presence of infection and abscess formation.

Abdominal wall infiltrates and wound suppuration

Infiltrates of the abdominal wall (6 - 15% of cases) and wound suppuration (2 - 10%) develop as a result of infection, which is facilitated by poor hemostasis and tissue injury. These complications often appear on days 4–6 after surgery, sometimes at a later date.

Infiltrates and abscesses are located above or below the aponeurosis. By palpation, a painful lump with unclear contours is found in the area of ​​the postoperative wound. The skin over it is hyperemic, its temperature is elevated. When suppuration occurs, a symptom of fluctuation can be detected.

Treatment of infiltration is conservative. Broad-spectrum antibiotics and physical therapy are prescribed. A short novocaine blockade of the wound with antibiotics is performed. Suppurating wounds are opened wide and drained, and subsequently treated taking into account the phases of the wound process. Wounds heal by secondary intention. For large granulating wounds, the application of secondary early (8-15) days or delayed sutures is indicated.

Ligature fistulas

Ligature fistulas observed in 0.3 - 0.5% of patients who have undergone appendectomy. Most often they occur in the 3rd to 6th week of the postoperative period due to infection of the suture material, suppuration of the wound and its healing by secondary intention. A clinic of recurrent ligature abscess appears in the area of ​​the postoperative scar. After repeated opening and drainage of the abscess cavity, a fistula tract is formed, at the base of which there is a ligature. In case of spontaneous rejection of the ligature, the fistula tract closes on its own. Treatment consists of removing the ligature during instrumental revision of the fistula tract. In some cases, the entire old postoperative scar is excised.

Other complications after appendectomy (peritonitis, intestinal obstruction, intestinal fistulas, postoperative ventral hernia, etc.) are discussed in the relevant sections of private surgery.

Control questions

1. 1. Early symptoms of acute appendicitis
2. 2. Clinical features of acute appendicitis with atypical location of the appendix
3. 3. Features of the clinic of acute appendicitis in the elderly and pregnant women
4. 4. Surgeon’s tactics for a questionable picture of acute appendicitis
5. 5. Differential diagnosis of acute appendicitis
6. 6. Complications of acute appendicitis
7. 7. Early and late complications after appendectomy
8. 8. Surgeon’s tactics for appendiceal infiltrate
9. 9. Modern approaches to the diagnosis and treatment of appendiceal abscess

10. Diagnosis and treatment of pelvic abscesses

11. Surgeon’s tactics when detecting Meckel’s diverticulum

12. Pylephlebitis (diagnosis and treatment)

13. Diagnosis of subphrenic and interintestinal abscesses. Treatment tactics

14. Indications for relaparotomy in patients operated on for acute appendicitis

15. Examination of work capacity after appendectomy

Situational tasks

1. A 45-year-old man has been ill for 4 days. I am worried about pain in the right iliac region, temperature 37.2. On examination: The tongue is moist. The abdomen is not swollen, participates in the act of breathing, is soft, painful in the right iliac region. Peritoneal symptoms are inconclusive. A tumor-like formation 10 x 12 cm, painful and inactive, is palpated in the right iliac region. Regular stool. Leukocytosis - 12 thousand.

What is your diagnosis? Etiology and pathogenesis of this disease? What pathology should be considered for differential pathology? Additional examination methods? Treatment tactics for this disease? Treatment of a patient at this stage of the disease? Possible complications of the disease? Indications for surgical treatment, nature and extent of the operation?

2. Patient K., 18 years old, was operated on for acute gangrenous-perforated appendicitis, complicated by diffuse serous-purulent peritonitis. An appendectomy and drainage of the abdominal cavity were performed. The early postoperative period occurred with symptoms of moderately severe intestinal paresis, which were effectively relieved by the use of drug stimulation. However, by the end of 4 days after the operation, the patient’s condition worsened, increasing bloating and cramping pain throughout the abdomen appeared, gases stopped passing, nausea and vomiting appeared, general signs of endogenous intoxication.

Objectively: the condition is of moderate severity, pulse 92 per minute, A/D 130/80 mm Hg. Art., the tongue is wet, coated, the abdomen is evenly swollen, diffuse pain in all parts, peristalsis is increased, peritoneal symptoms are not determined, upon examination per rectum - the rectal ampulla is empty

What complication of the early postoperative period occurred in this patient? What additional examination methods will help determine the diagnosis? The role and scope of x-ray examination, interpretation of data. What are the possible reasons for the development of this complication in the early postoperative period? Etiology and pathogenesis of disorders developing in this pathology. The scope of conservative measures and the purpose of their implementation in the development of this complication? Indications for surgery, scope of surgical treatment? Intra- and postoperative measures aimed at preventing the development of this complication?

3. A 30-year-old patient is in the surgical department for acute appendicitis in the stage of appendiceal infiltration. On the 3rd day after hospitalization and on the 7th day from the onset of the disease, the pain in the lower abdomen and especially in the right iliac region intensified, the temperature became hectic.

Objectively: Pulse 96 per minute. Breathing is not difficult. The abdomen is of regular shape, sharply painful on palpation in the right iliac region, where a positive Shchetkin-Blumberg sign is determined. The infiltrate of the right iliac region increased slightly in size. Leukocytosis increased compared to the previous analysis.

Formulate a clinical diagnosis in this case? Patient treatment tactics? Nature, scope and features of surgical treatment for this pathology? Features of the postoperative period?

4. A 45-year-old man underwent appendectomy with drainage of the abdominal cavity for gangrenous appendicitis. On the 9th day after the operation, the flow of small intestinal contents from the drainage canal was noted.

Objectively: The patient’s condition is moderate. Temperature 37.2 - 37.5 0 C. The tongue is wet. The abdomen is soft, slightly painful in the wound area. There are no peritoneal symptoms. Independent stool once a day. In the drainage area there is a channel approximately 12 cm deep, lined with granulating tissue, through which intestinal contents are poured. The skin around the canal is macerated.

What is your diagnosis? Etiology and pathogenesis of the disease? Classification of the disease? Additional research methods? Possible complications of this disease? Principles of conservative therapy? Indications for surgical treatment? The nature and scope of possible surgical interventions?

5. By the end of the first day after appendectomy, the patient has severe weakness, pale skin, tachycardia, a drop in blood pressure, and free fluid is detected in the sloping areas of the abdominal cavity. Diagnosis? Surgeon's tactics?

Sample answers

1. The patient has developed an appendiceal infiltrate, confirmed by ultrasound data. The tactics are conservative and expectant; in case of abscess formation, surgical treatment is indicated.

2. The patient has a clinical picture of postoperative early adhesive intestinal obstruction; in the absence of effect from conservative measures and negative radiological dynamics, emergency surgery is indicated.

3. Abscess formation of the appendiceal infiltrate has occurred. Surgical treatment is indicated. Preferably, extraperitoneal opening and drainage of the abscess.

4. The postoperative period was complicated by the development of an external small intestinal fistula. An X-ray examination of the patient is necessary. In the presence of a formed tubular low small intestinal fistula with a small amount of discharge, measures for its conservative closure are possible; in other cases, surgical treatment is indicated.

5. The patient has bleeding into the abdominal cavity, probably due to the slippage of the ligature from the stump of the mesentery of the appendix. Emergency relaparotomy is indicated.

LITERATURE

1. Batvinkov N.I., Leonovich S.I., Ioskevich N.N. Clinical surgery. - Minsk, 1998. - 558 p.
2. Bogdanov A.V. Fistulas of the digestive tract in the practice of a general surgeon. - M., 2001. - 197 p.
3. Volkov V. E., Volkov S. V. Acute appendicitis - Cheboksary, 2001. - 232 p.
4. Gostishchev V.K., Shalchkova L.P. Purulent pelvic surgery - M., 2000. - 288 p.
5. Grinberg A. A., Mikhailusov S. V., Tronin R. Yu., Drozdov G. E. Diagnosis of difficult cases of acute appendicitis. - M., 1998. - 127 p.
6. Clinical surgery. Ed. R. Conden and L. Nyhus. Per. from English - M., Praktika, 1998. - 716 p.
7. Kolesov V.I. Clinic and treatment of acute appendicitis. - L., 1972.
8. Krieger A. G. Acute appendicitis. - M., 2002. - 204 p.
9. Rotkov I. L. Diagnostic and tactical errors in acute appendicitis. - M., Medicine, 1988. - 203 p.
10. Savelyev V.S., Abakumov M.M., Bakuleva L.P. and others. Guide to emergency surgery of the abdominal organs (edited by V.S. Savelyev). - M.: Medicine. - 1986. - 608 pp.

The infectious process in the appendix should be understood as a biological interaction between the body and microbes.

However, seeing the essence of the disease only in microbes is just as wrong as reducing it only to the reactions of the body.

In acute appendicitis there is no specific microbial pathogen.

Theories of the occurrence of acute appendicitis.

1. The theory of stagnation. Violation of peristalsis of the appendix with a narrow lumen often leads to stagnation of contents rich in a variety of bacterial flora, which leads to inflammatory changes in the appendix.

2. The literature discusses the issue of the occurrence of acute appendicitis under the influence of helminthic infestation. In particular, Reindorf tried to provide evidence in favor of the occurrence of acute appendicitis due to the adverse effects of oxiurs on the mucous membrane of the appendix. In addition, the possibility of chemical effects of toxic substances secreted by worms on the mucous membrane of the appendix cannot be ruled out. As a result of such exposure, the mucous membrane appears to be damaged and a picture of catarrhal inflammation occurs.

3. A fundamentally new point of view was put forward by Ricker, who proposed the angioneurotic theory of the pathogenesis of acute appendicitis. As a result, tissue nutrition is so severely disrupted that foci of necrosis may appear in the wall of the appendix. Pathologically changed tissues become infected. The argument in favor of vascular disorders is that acute appendicitis is often characterized by a rapid course with sharp abdominal pain and an increase in clinical symptoms. It is vascular disorders that explain the rapidly developing gangrenous appendicitis, where tissue necrosis of the appendix can be noted within a few hours from the onset of the disease.

4. In 1908, the famous German pathologist Aschoff put forward an infectious theory of the occurrence of acute appendicitis, which until recently was recognized by most clinicians and pathologists.

According to Aschoff, disturbances in the structure of the appendix are caused by the influence of microbes located in the appendix itself. Under normal conditions, the presence of this flora does not lead to either functional or morphological disorders.

According to supporters of the infectious theory, the pathological process begins only if the virulence of microbes increases. For some reason, the bacteria living in the lumen of the appendix cease to be harmless: they acquire the ability to cause pathological changes in the cells of the mucous membrane, which lose their protective (barrier) function.

5. Krech identified a connection between tonsillitis and acute appendicitis. The author found that in 14 cases, people who died from appendiceal peritonitis had clear changes in the tonsils. These were infectious foci, which the author considered to be the source of bacteremia.

Acute appendicitis in this case can be considered as a result of metastatic infection. Leuven, while operating on sick children for acute appendicitis during diphtheria, found the diphtheria bacillus in the appendix.

6. I. I. Grekov attached great importance to the functional dependence of the bauginian valve and pylorus, which determines the relationship between diseases of the cecum and stomach. In his opinion, various irritants (infection, food intoxication, worms, etc.) can cause spasm of the intestines and especially spasm of the bauhinium valve. Consequently, I. I. Grekov recognized the root cause of appendicitis as a violation of the neuroreflex function, which acts as a provocateur for the further development of the disease.

Today, the most acceptable concept of the development of acute appendicitis is as follows - acute appendicitis is caused by a primary nonspecific infection. A number of reasons predispose to the occurrence of an infectious process. These predisposing factors include the following:

1. Changes in the body’s reactivity after illnesses. Sore throat, catarrh of the upper respiratory tract and various concomitant diseases weaken the body to some extent, which contributes to the occurrence of acute appendicitis.

2. Nutritional conditions can undoubtedly become a predisposing cause for the occurrence of an infectious process in the appendix. Excluding meat and fatty foods from the diet leads to changes in the intestinal microflora and helps to a certain extent reduce the incidence of acute appendicitis.

On the contrary, an abundant diet with a predominance of meat foods, a tendency to constipation and intestinal atony lead to an increase in acute appendicitis.

3. Stagnation of the contents of the appendix contributes to the occurrence of acute appendicitis

4. The structural features of the appendix predispose to the occurrence of inflammatory processes in it. What matters is the tendency of lymphoid tissue to an inflammatory reaction due to its so-called barrier function. The abundance of tonsils and lymphoid tissue of the appendix often leads to inflammation and even phlegmonous melting of both organs.

5. Vascular thrombosis often underlies gangrenous appendicitis. In such cases, tissue necrosis predominates due to circulatory disorders, while the inflammatory process is secondary.

However, the main theory of the pathogenesis of acute appendicitis should be considered the infectious theory. The infectious theory of the pathogenesis of acute appendicitis, supplemented by a modern understanding of infection, reflects the essence of changes in the appendix and throughout the body. Elimination of the infectious focus leads to the recovery of patients, which is the best proof that it is precisely such a focus that constitutes the starting point of the disease itself.

Despite the huge number of works on acute appendicitis, the pathogenesis of this disease has not yet been sufficiently studied and is perhaps the most unclear chapter in the doctrine of acute appendicitis. And although everyone recognizes that most cases of acute appendicitis occur with distinct inflammatory changes in the appendix, more and more new theories for the development of this common disease are being proposed.

In conclusion, it should be said that in the modern understanding, acute appendicitis is a nonspecific inflammatory process. The main factor in its occurrence should be considered a change in the reactivity of the body under the influence of various conditions. Anatomical features in the structure of the appendix and the richness of its nerve connections determine the uniqueness of the course of the infection and, with the appropriate reaction of the body, create a characteristic clinical picture of the disease that distinguishes acute appendicitis from other nonspecific inflammations of the gastrointestinal tract.

ETIOLOGY AND PATHOGENESIS

Despite the huge number of observations of acute appendicitis that modern surgery has, the causes of this disease have not been fully studied.

The etiology of acute appendicitis includes the following factors: nutritional (consumption of food rich in animal protein); stagnation of the contents of the appendix, helminthic infestation (especially in childhood); changes in the body's reactivity during infections; thrombosis of the vessels of the mesentery of the process.

It has been established that the nutritional factor, i.e., the nature of nutrition, plays a certain role in the etiology of acute appendicitis. In Western European countries, where the population eats mainly meat, the incidence of appendicitis is much higher than in India, Japan and other countries where the population prefers vegetarian food.

It is known that food rich in animal protein, more than plant protein, tends to cause putrefactive processes in the intestines and contributes to its atony. Abundant, predominantly protein diet and the associated tendency to constipation and intestinal atony lead to an increased incidence of acute appendicitis. One might think that an excess amount of amino acids - protein breakdown products - provides the best environment for the growth of microorganisms. Perhaps this changes the acid-base balance, increases the excitation of the sympathetic nervous system, and the vermiform appendix is ​​equipped with a powerful nervous apparatus. This should be considered a predisposing factor in the development of acute appendicitis.

The infectious theory of the pathogenesis of acute appendicitis was put forward in 1908 by Ludwig Aschoff: appendicitis is caused by a local infection spreading from the cecum. Specific pathogens do not play a role here. For the occurrence and development of infection in the appendix, certain predisposing factors are necessary: ​​a large length of the appendix with a narrow lumen; sluggish peristalsis, favoring stagnation of contents; narrowing of the appendix caused by fecal stones and adhesions.

In childhood, helminthic infestation with pinworms, whipworms and roundworms, which are found in 15-20% of vermiform appendices removed from children for acute appendicitis, plays some role in the occurrence of acute appendicitis. Nematodes themselves. They do not cause an inflammatory process in the appendix, but when they get into it, they contribute to the stagnation of the contents and activate the microflora located in it.

Numerous attempts to detect a specific microbial causative agent of acute appendicitis have been unsuccessful. From the lumen of the affected vermiform appendix, most often E. coli, enterococcus are sown, and less often - pyogenic microbes: staphylococcus, streptococcus, etc. In gangrenous forms it is often possible to find b. perfringens and other anaerobes.

The listed polymicrobial flora is usually found in the intestines of any healthy person. This indicates, first of all, that for the occurrence of a disease, the presence of virulent microflora alone is not enough, and certain pathological changes on the part of the microorganism that carries this flora are also necessary.

The angioneurotic theory of the pathogenesis of acute appendicitis was put forward in 1927 by Ricker and Bruhn: inflammation of the appendix occurs as a result of dysfunction of vasomotors in the wall of the appendix, which leads to impaired blood circulation, and the role of bacteria in this case is secondary.

Consequently, in the etiology and pathogenesis of acute appendicitis, the main theories - infectious, angioneurotic, nutritional - do not exclude, but complement each other.

Pathological changes in acute appendicitis develop as follows. The process begins with functional disorders, which consist of spastic phenomena from the ileocecal angle (baugitsospasm), the cecum and the appendix. It is possible that the spastic phenomena are initially based on digestive disorders, such as increased putrefactive processes with a large amount of protein food. Spasms can also be provoked by helminthic infestation, fecal stones, foreign bodies, etc. Due to the commonality of autonomic innervation, spasm of smooth muscles is accompanied by vascular spasm. The first of them leads to a violation of evacuation, stagnation in the appendix, the second - to a local one. disturbance of nutrition of the mucous membrane, as a result of which a primary affect is formed. In turn, stagnation in the appendix helps to increase the virulence of the microflora located in it, which, in the presence of a primary affect, easily penetrates the wall of the appendix.

From this moment, a typical suppurative process begins, expressed in massive leukocyte infiltration, first of the mucous and submucosal layer, and then of all layers of the appendix, including its peritoneal cover. Infiltration is accompanied by rapid hyperplasia of the lymphoid apparatus of the appendix. The presence of necrotic tissue in the area of ​​one or more primary affects causes the appearance of pathological enzymes of suppuration: cytokinase, etc. These enzymes, having a proteolytic effect, cause destruction of the wall of the appendix, which ultimately ends with its perforation, the release of purulent contents into the free abdominal cavity and the development of purulent peritonitis as one of the severe complications of acute appendicitis.

From a clinical point of view, damage to the mucous membrane and submucosal layer corresponds to the catarrhal form of appendicitis; the transition of inflammation to all layers of the appendix, including the peritoneum, means phlegmonous appendicitis; complete or almost complete destruction of the appendix corresponds to the concept of “gangrenous appendicitis”.

The morphological changes observed in the inflamed appendix are very diverse and depend mainly on the stage of the inflammatory process. It is advisable to consider separately the morphological picture for each of the clinical forms of acute appendicitis.

Catarrhal appendicitis. This form of acute appendicitis is otherwise called simple. It represents the initial stage of the disease. Macroscopically, the vermiform appendix looks somewhat thickened, its serous cover is dull, and many small vessels filled with blood are visible underneath, which creates the impression of bright hyperemia. On a section, its mucous membrane is swollen, purple in color, and sometimes spots of hemorrhages can be seen in the submucosal layer. The lumen of the appendix often contains a blood-like fluid.

Microscopically, on serial histological sections, it is possible to note small defects of the mucous membrane, covered with fibrin and leukocytes. Sometimes from a small defect the lesion spreads into deeper tissues, having the shape of a wedge, the base of which is directed towards the serous cover. This is a typical Aschoff primary affect. There is moderate leukocyte infiltration in the submucosal layer. The muscle layer is unchanged or slightly changed. The serous cover contains a large number of dilated vessels, which can also be observed in the mesentery of the appendix.

In the abdominal cavity, occasionally, with the catarrhal form of acute appendicitis, a transparent sterile reactive effusion is found.

Phlegmonous appendicitis. This form is the next stage of the inflammatory process. Macroscopically, the appendix looks significantly thickened, the serosa and mesentery covering it are swollen and clearly hyperemic. The vermiform appendix is ​​covered with fibrin deposits, which in the phlegmonous form are always found to a greater or lesser extent. Due to the fact that the process passes to the peritoneal cover, fibrinous deposits may be observed on the dome of the cecum, parietal peritoneum, and adjacent loops of the small intestines. There may be a significant cloudy effusion in the abdominal cavity due to a large admixture of leukocytes. Due to impaired biological permeability of the tissues of the appendix, the effusion may become infected.

The lumen of the appendix usually contains liquid, foul-smelling pus. The mucous membrane of the appendix is ​​swollen and easily vulnerable; It is often possible to see multiple erosions and fresh ulcers.

Microscopically, massive leukocyte infiltration is observed in all layers of the appendix, the integumentary epithelium of the mucous membrane is often desquamated, and multiple primary Aschoff affects can be seen. In the mesentery of the appendix, in addition to pronounced hyperemia, leukocyte infiltrates are visible.

Empyema of the appendix. This form of acute appendicitis is a type of phlegmonous inflammation of the appendix, in which, as a result of blockage with fecal stone or cicatricial process, a closed cavity filled with pus is formed in the lumen of the appendix. The morphological feature of this form of acute appendicitis is that here the process rarely spreads to the peritoneum. In empyema, the vermiform appendix is ​​flask-shaped and sharply tense, and there is a clear fluctuation. Along with this, the serous cover of the appendix looks like in the catarrhal form of acute appendicitis: it is dull, hyperemic, but without fibrin overlays. Serous sterile effusion may be observed in the abdominal cavity. When the appendix is ​​opened, a large amount of foul-smelling pus flows out.

Microscopically, in the mucous and submucosal layers there is a significant leukocyte infiltration, which decreases towards the periphery of the appendix. Typical primary affects are rarely observed.

Gangrenous form acute appendicitis is characterized by necrosis of the appendix or any part of it.

Macroscopically, the necrotic area is dirty green in color, loose and easily torn. If not the entire appendix is ​​necrotic, then the rest of it looks the same as in the phlegmonous form of acute appendicitis. There are fibrinous deposits on the organs and tissues surrounding the appendix. The abdominal cavity often contains purulent effusion with a fecal odor. Sowing this effusion on a nutrient medium produces the growth of typical colonic flora. Microscopically, in the area of ​​destruction, the layers of the appendix cannot be differentiated; they have the appearance of typical necrotic tissue.

Perforated form- this is the stage of acute appendicitis, in which, as a result of perforation, extremely virulent contents are poured into the abdominal cavity. As a result, local peritonitis initially occurs, which can subsequently either be limited and retain its local character, or develop into diffuse (diffuse) peritonitis.

Macroscopically, the vermiform appendix, when perforated, differs little from that in the gangrenous form of acute appendicitis. Areas of necrosis are the same dirty green color, in one or more of them there are perforations from which the fetid contents of the appendix pour out. The surrounding peritoneum is covered with massive fibrinous deposits. The abdominal cavity contains abundant purulent effusion and often fecal stones that have fallen out of the appendix.

Microscopically, there are no differences from the gangrenous form of acute appendicitis; foci of necrosis and thrombosis of venous vessels can be observed in the mesentery of the appendix.

As a rule, the catarrhal stage of acute appendicitis lasts 6-12 hours from the onset of the disease. The phlegmous form of acute appendicitis develops within 12-24 hours, the gangrenous form - 24-48 hours, and after 48 hours, with progressive appendicitis, perforation of the appendix may occur.

It must be emphasized that the above periods are typical for most cases of progressive acute appendicitis, but they are not absolute. In clinical practice, certain deviations in the course of the disease are often observed. In this case, we mean only the typical course of acute appendicitis, when the process progresses and does not have a tendency to reverse development.