Etiology and pathogenesis
The main theory links the onset of the disease to the obstruction of the lumen of the vermiform appendix. Causes of obstruction may include intraluminal or extraluminal adhesions, fecaliths (coproliths), and lymphoid hyperplasia of the wall.
However, clinical and morphological observations often criticize this concept: in most cases of acute appendicitis, fecaliths are not detected, and the volume of lymphoid tissue corresponds to age norms. Hyperplasia itself may not be the cause, but rather a secondary reaction to inflammation that has already begun.
Alternative mechanisms of development include:
- Ischemic factor: central ischemia of the wall leads to the formation of ulceration foci on the mucosa. Through these defects, microorganisms penetrate deep into the tissues, causing secondary infection.
- Hematogenous route: a rare variant in which infection is carried by the bloodstream from other organs.
Morphological forms of acute appendicitis
Microscopically, four successive stages of the development of the acute inflammatory process are distinguished:
- Simple appendicitis: initial changes. Characterized by vascular congestion, erythrocyte stasis in capillaries and venules, wall edema, and diapedetic hemorrhages.
- Superficial appendicitis: the result of the progression of the simple form. Macroscopically, the appendix swells, the serosa becomes dull, hyperemic, and granular. Microscopically, changes in the mucosa are visible, starting from the distal section.
- Phlegmonous appendicitis: the appendix is significantly enlarged. The serosa is covered with a fibrin deposit with petechial hemorrhages. The wall is thickened and diffusely infiltrated with pus (neutrophilic leukocytes), and small abscesses may form within the thickness. If the mucosa ulcerates, it is referred to as the phlegmonous-ulcerative form.
- Gangrenous appendicitis: progression of phlegmonous inflammation with the addition of putrefactive microflora. The key factor in the transition is thrombosis of the appendiceal artery and the spread of the process to the mesentery (mesenteriolitis). Macroscopically, purple-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 determined.
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 mesentery of the appendix (vascular obliteration against the background of atherosclerosis or diabetes mellitus).
If acute inflammation subsides, it can transform into chronic appendicitis, which is prone to periodic exacerbations. Its reliable morphological criteria are:
- Connective tissue obliteration (scarring) of the lumen.
- Accumulations of adipose tissue.
- Diffuse mononuclear infiltrate within the wall thickness.
Complications
The pathology is dangerous due to the development of severe consequences, which are divided into several groups:
- Local and abdominal: perforation or rupture of the wall, formation of localized abscesses (including pelvic), diffuse peritonitis (morphologically manifested by adhered loops of bowel).
- Vascular and systemic: septicemia, shock, DIC syndrome. Of note is pylephlebitic abscess — a liver abscess arising due to infectious thrombophlebitis.
- Rare: subphrenic or lumbar abscess, anaerobic gangrene of the abdominal wall, skin and urinary bladder fistulas.
Specific lesions and artifacts
Inflammation of the appendix may be associated with infectious agents: bacteria (yersinia Yersinia enterocolitica), viruses, or parasites (amebae Entamoeba histolytica, schistosomes). The association with pinworms (Enterobius vermicularis) is considered minor. In inflammatory bowel diseases, such as ulcerative colitis (pancolitis), the appendix is also involved in the process, but perforation does not occur.
Mechanical pathologies also occur: torsion (dilation of the distal end due to tumors or lipomas, which can lead to autoamputation) and intussusception, often associated with foci of endometriosis or reactive lymphoid hyperplasia.
Note for pathologists: it is important to distinguish true inflammation from intraoperative artifacts. Surgeon manipulations can cause the serosa to become soaked with exudate and cause pinpoint traumatic hemorrhages, which microscopically yields only minimal changes that are not a sign of acute appendicitis.
Briefly: answers to topical questions
Through which veins does the infection spread from the appendix during the development of a pylephlebitic liver abscess?
Infection from the appendix during the development of a pylephlebitic liver abscess spreads via the venous pathways of the mesentery and the branches of the portal vein draining the area of the inflamed appendix. The process begins as suppurative thrombophlebitis of the mesentery, which then spreads to the branches of the portal vein, leading to pylephlebitis and thrombo-bacterial embolism in the liver with the formation of liver abscesses.
What types of peritonitis, according to the nature of the exudate, develop upon perforation of the vermiform appendix?
Perforation of the vermiform appendix leads to diffuse (generalized) purulent peritonitis, which may be accompanied by fibrinous-purulent or putrefactive exudate. This complication occurs in the absence of localization of the inflammatory process.
The stages of acute appendicitis are easy to remember by the increasing depth of the lesion: Simple (vascular reactions) → Superficial (mucosa) → Phlegmonous (all layers, pus) → Gangrenous (necrosis and thrombosis). The rule "SSPG".
Class and exam questions
How does phlegmonous appendicitis differ from gangrenous appendicitis?
In phlegmonous appendicitis, the wall is diffusely infiltrated with neutrophils and pus, while in gangrenous appendicitis, total mucosal necrosis, appendiceal artery thrombosis, and the addition of putrefactive microflora are added.
What is primary gangrenous appendicitis?
This is a form of the disease occurring predominantly in elderly people due to circulatory disturbances in the vessels of the appendiceal mesentery (e.g., in atherosclerosis), bypassing the initial stages of exudative inflammation.
What does chronic appendicitis look like under a microscope?
It is characterized by connective tissue obliteration of the lumen, accumulations of adipose tissue, and a diffuse mononuclear infiltrate in the wall of the appendix.
What else to study on this topic
- The role of ischemia in primary mucosal ulceration
- Pylephlebitic liver abscess as a systemic complication
- Intussusception and torsion of the vermiform appendix
- Appendiceal involvement in ulcerative colitis
- Infectious and parasitic appendicitis (yersiniosis, amebiasis)
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