Appendicitis is an acute or chronic inflammation of the vermiform process the caecum (Appendix). In the occurrence of appendicitis important role of microorganisms present in the large intestine (Escherichia coli, enterococci , and others).
Microbes penetrate the wall of the vermiform process of its clearance through one or another part of the mucous membrane. The reasons for the transformation of saprophytic flora in pathogenic and its mechanism of action on the mucous membrane of the Appendix remain outstanding. Predisposing moments can be particularly anatomical structure of the Appendix (narrow channel, the blood supply of not only having anastomoses artery), the nature of the power of the patient (the abundance of meat food), acute inflammatory diseases of other organs.

Appendix (appendicitis; from lat. appendix - appendage) - inflammation of the vermiform process cecum. There are acute and chronic appendicitis.
Acute Appendicitis takes the first place among acute diseases of the abdomen. Acute appendicitis sick people of all ages, mostly women.
Chronic Appendicitis occurs much less acute, also mostly in women.
The etiology and pathogenesis
At the present time are not yet established a firm view on etiology and pathogenesis of acute A. Undoubtedly plays an important role microflora, vegetating in the gut (You. coli commune, Staphylococcus, Streptococcus, Pneumococcus, Diplo-coccus intestinalis, anaerobes), and in the first place is You. coli. The reasons for the sudden transformation of saprophytic flora in pathogenic, as the mechanism of its action on the mucous membrane of the Appendix, remain outstanding. For a long time cause inflammation believed mechanical stagnation content in the process because of the excess it and narrowing (A. A. Bobrov)and feces stones or foreign inclusions. But numerous observations have shown that mechanical damage of mucous membranes do not entail serious consequences, as easily heal. Feces stones are often found in healthy shoots without causing pathological changes. Championed (L. Championniere) believed that acute appendicitis occurs in connection with a hearty meat meals. Indeed, in the famine years the incidence of breast cancer was sharply reduced. Suspected valid hematogenous route influenza infection [Fasan (Faisans)].
Brunn, Ricker (Briinn, G. Ricker) and Century A. Rusakov has developed a neurovascular the theory that best covers the clinical and pathological manifestations of acute appendicitis, though not explain the cause of primary vascular pathological reflex. According to this theory, first of all develop the disorder of blood circulation, depending on the violation of the regulation of blood flow due to irritation of the nervous system. There are functional changes in the process of the preceding obvious micro - and macroscopic changes. Will in the navel or in podlojecna area, which usually starts attack, forced Ricker to think about the initial changes in plexus solaris. Neuro-vascular theory helps to understand why with clearly pronounced clinic of acute appendicitis in 20-30% in the first two days of appendectomy vermiform process is unchanged or observed only signs of catarrhal inflammation. Even taking into account possible errors diagnostics clearly expressed by a discrepancy between clinical picture and morphological changes. This discrepancy can only be explained by different strength and duration of pathological reflex.
Pathologic anatomy
There are the following morphological forms of appendicitis: surface (simple) acute (primary affect); acute purulent (phlegmonously, flegmonas-ulcer, epistemology); gangrenous (primary, secondary); chronic (without relapse or with them).
Acute inflammation of the Appendix begins with the formation of ocaka destruction at the bottom of one of the crypts of the mucous membrane with swelling and leukocyte infiltration of the adjacent area submucosal (primary affect, Fig. 1); in some cases simultaneously formed several of these affects. If the inflammation subsides quickly and purulent infiltration does not apply (surface appendicitis), defect mucous membrane soon epithelialized.
In other cases, leukocytic infiltration captures all layers of the wall of the process; the latter is thickened, full-blooded, like his peritoneum, covered with soft, loose fibrose nature (phlegmonously appendicitis). Bruecke process also worthwhile, edematous, infiltrated by leukocytes. Often, the mucous membrane is subjected to degradation at a considerable distance, or is preserved only in the form of Islands (flegmonas-ulcer A., Fig. 2 and 3),

Fig. 1. Acute appendicitis. Primary affect. Fig. 2. Flegmonas-ulcer appendicitis (prodolny the section of the Appendix). The wall is thickened considerably due to infiltration of all layers her leukocytes; mucous membrane nekrotizirovanne; in the lumen of the purulent exudate.
Fig. 3. Flegmonas-ulcer appendicitis.
Diffuse purulent infiltration submucosal shell; necrosis mucosa.
Fig. 4. Chronic appendicitis. A significant narrowing of the lumen of the Appendix.

Sometimes in the wall of the ridge formed a separate pustules (epistemology appendicitis)
Purulent inflammation may be accompanied by marked venous thrombosis intramural vessels, lymphangitis and melting of tissues that leads to eliminate them and the destruction of the Appendix, partial or widespread (gangrenous appendicitis). The process becomes dirty or black and green breaks or tears easily, has a putrid smell; flegmonas inflammation extends to bruecke. More common are described secondary gangrenous appendicitis; sometimes on the basis of the expressed vascular spasms and angioneurotic of stasis mortification process occurs in the first 12 hours of the disease - primary gangrenous A.
Acute purulent and necrotic form A. can be complicated peritonitis (see), as limited, and spilled. This is facilitated by the perforation of the wall of the process (when aposematism and gangrenous appendicitis) and of Microperforation (flegmona and flegmonas-ulcer). Purulent inflammation may spread to the wall the caecum (see Tiflis), peritoneum (perityphlic) and surrounding tissue (paratively). In the retroperitoneal fat may occur ulcers, and spread it suppuration is sometimes complicated by parametrical (see) and ulcers in the pelvis. Flegmonas inflammation and blood clots phlebitis bruecke process can be complicated by pylephlebitis and metastatic abscesses of the liver. Sometimes there is a septic generalization of infection.
Acute appendicitis can become chronic; while in the wall of the ridge there is a significant growth of fibrous connective tissue, which is accompanied by atrophy of the mucous membrane and muscle layer (sclerosing A.). If wounded, the mucous membrane only partially recovered, but mostly replaced by scar tissue, there is a chronic ulcerative A. Progressive growth of fibrous connective tissue leads to the narrowing of the lumen (Fig. 4) and even obliteration process. If the ground clearance closes his part, in the distal, ampliarse extended Department accumulate serous fluid (edema of the Appendix), pus (empyema) and mucus (mucocele). Sometimes slime sliding into lumps running process (microglobulin). Sclerosis process is accompanied by atrophy of the muscle membrane, hypertrophy of muscle layer of blood vessels that passes in scar tissue, and destructive changes intramural nervous knots.
Chronic inflammation of the Appendix is accompanied by formation periappendicular adhesions, zamurovali process and leading to its excesses; adhesions can summability periappendicular ulcers. If the found ampliarse advanced process in the abdominal cavity flows out mucus and get the cells that produce it (these cells are implanted in the abdomen), the accumulation of mucus sumawinata and a so-called false myxoma (see Pseudomyxoma peritoneum). Chronic appendicitis can often escalate, leading to the development of the already mentioned acute complications, and to the progression of chronic changes in the process and its surroundings.
Morphological changes in the process can be expressed differently in different departments, so histological specimens should be done at least three sections of the Appendix. To detect the presence and character of distribution of leukocytes it is recommended to paint the slices on the method of I. B. Goldman (Sudan III + alpha-naphthol). We must bear in mind that one white blood cells in the wall of the process does not, however, appendicitis and can take place without the clinical picture of the disease (for example, in cases of sudden death). On the other hand, the absence of morphological signs of acute inflammation does not give the right to take into doubt the existence of some clinical manifestations common to A. true, because the attacks of pain in the right iliac region may arise as a result of functional, transient vasomotor disorders, muscle spasms shoot blind intestine (called appendiabiti). From the true appendicitis is necessary to distinguish A. false (pseudoephedine), when a number of symptoms that simulates the inflammation of the Appendix, is caused by diseases of other organs (kidney, gall bladder, stomach, duodenum). Should not be attributed to A. follicular hyperplasia of the apparatus of the Appendix, which is a manifestation of the General lymph status, and atrophic-sclerotic involutive change process.

Clinical presentation and course