Appendicitis

Etiology and Pathogenesis

The primary theory links the onset of the disease to the occlusion of the vermiform appendix lumen. Causes of obstruction include intra- or extraluminal adhesions, fecaliths (coproliths), and lymphoid hyperplasia of the wall.

However, clinical and morphological observations frequently challenge this concept: in most cases of acute appendicitis, fecaliths are not found, and the volume of lymphoid tissue corresponds to the age norm. Hyperplasia itself may not be the cause, but rather a secondary reaction to an already initiated inflammation.

Alternative developmental mechanisms include:

• Ischemic factor: Central ischemia of the wall leads to ulceration of the mucosal membrane. Microorganisms penetrate deeper tissues through these defects, causing secondary infection.
• Hematogenous route: A rare variant where infection spreads via the bloodstream from other organs.

Morphological Forms of Acute Appendicitis

Microscopically, four sequential stages of acute inflammation are distinguished:

1. Simple appendicitis: Initial changes characterized by vascular congestion, erythrocyte stasis in capillaries and venules, wall edema, and diapedetic hemorrhages.
2. Superficial appendicitis: A result of simple form progression. Macroscopically, the appendix swells, and the serosa becomes dull, hyperemic, and granular. Microscopically, mucosal changes are visible, starting from the distal portion.
3. Phlegmonous appendicitis: The appendix is significantly enlarged. The serosa is covered with a fibrin exudate and petechial hemorrhages. The wall is thickened and diffusely infiltrated with pus (neutrophilic leukocytes), and small abscesses may form within the muscular layer. Ulceration of the mucosa indicates the ulcerative-phlegmonous form.
4. Gangrenous appendicitis: Progression of phlegmonous inflammation with the addition of putrefactive microflora. The key transition factor is thrombosis of the appendicular artery and the spread of the process to the mesoappendix (mesoappendicitis). Macroscopically, purplish-bluish patches and greenish fibrin deposits are visible, and the lumen is filled with pus and dirty-gray necrotic detritus. Microscopically, total mucosal necrosis and extensive hemorrhages are identified.

Special Forms and Chronic Process

In middle-aged and elderly individuals, primary gangrenous appendicitis occurs. It develops not as an outcome of phlegmon, but due to primary circulatory disorders in the appendicular mesoappendix (vascular obliteration secondary to atherosclerosis or diabetes mellitus).

If acute inflammation subsides, it may transition into chronic appendicitis, which is prone to periodic exacerbations. Its reliable morphological criteria include:

• Connective tissue obliteration (fibrosis) of the lumen.
• Accumulations of adipose tissue.
• Diffuse mononuclear infiltration within the wall.

Complications

The pathology is dangerous due to severe consequences divided into several groups:

• Local and abdominal: Perforation or rupture of the wall, formation of localized abscesses (including pelvic), and generalized peritonitis (morphologically manifested by matted intestinal loops).
• Vascular and systemic: Septicemia, shock, disseminated intravascular coagulation (DIC). Pylephlebitic abscess—a liver abscess arising from infectious thrombophlebitis—deserves special mention.
• Rare: Subdiaphragmatic or retroperitoneal abscess, anaerobic gangrene of the abdominal wall, and cutaneous or urinary bladder fistulas.

Specific Lesions and Artifacts

Appendix inflammation may be associated with infectious agents: bacteria (Yersinia enterocolitica), viruses, or parasites (Entamoeba histolytica, schistosomes). Association with pinworms (Enterobius vermicularis) is considered minor. In inflammatory bowel diseases, such as ulcerative colitis (pancolitis), the appendix is also involved, but perforation does not typically occur.

Mechanical pathologies also occur: torsion (distal dilation due to tumors or lipomas, which can lead to auto-amputation) and intussusception, frequently associated with foci of endometriosis or reactive lymphoid hyperplasia.

Note for pathologists: It is important to differentiate true inflammation from intraoperative artifacts. Surgeon manipulation can cause exudate imbibition of the serosa and traumatic petechial hemorrhages, yielding minimal microscopic changes that do not indicate acute appendicitis.