Apendicitis

Appendicitis typically begins with blockage of the appendiceal lumen by fecaliths, tumors, lymphoid hyperplasia, parasites, or foreign bodies. This obstruction prevents normal mucosal drainage, causing secretions to accumulate and pressure to build within the appendix. The increased pressure compresses venous outflow before arterial supply, leading to congestion and reduced blood flow.

Obstruction causes pressure buildup that impairs arterial blood flow, resulting in ischemia and weakening of the epithelial lining. This damage creates ulceration and compromises the mucosal barrier, allowing gut bacteria such as E. coli and Bacteroides to invade deeper layers of the appendiceal wall, triggering acute suppurative inflammation similar to intestinal obstruction pathophysiology.

Bacterial invasion triggers an acute inflammatory response with neutrophil infiltration into the mucosa and submucosa. The appendix becomes swollen and fills with pus. Inflammation typically begins at the tip but spreads throughout the entire organ as pressure and infection increase, marking the hallmark of suppurative appendicitis.

Continued pressure from inflammation further impairs arterial blood flow, worsening ischemia. Prolonged oxygen deprivation leads to tissue necrosis and gangrenous appendicitis. If the appendiceal wall weakens significantly, perforation can occur, releasing infectious contents into the peritoneal cavity and causing abscess formation or diffuse peritonitis.

The appendix is a narrow, blind-ended pouch that extends from the cecum, the first part of the large intestine. Its tubular structure and limited lumen make it susceptible to blockage by various materials including fecaliths, lymphoid hyperplasia often following viral infections, parasites, tumors, and foreign bodies.

Ischemia develops when increased intraluminal pressure compresses blood vessels, reducing oxygen supply to the appendiceal tissue. This weakens the mucosal lining, causing ulceration and allowing bacterial invasion. Continued ischemia from worsening inflammation leads to tissue death, gangrene, and potential perforation if untreated.

Simple luminal obstruction can rapidly progress through ischemia and suppurative inflammation to gangrenous appendicitis and perforation. Perforation releases infectious contents into the peritoneal cavity, causing life-threatening peritonitis or abscess formation. This cascade of pathological changes transforms appendicitis into a surgical emergency requiring immediate diagnosis and treatment.