<B>Acute Appendicitis </B>

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Acute Appendicitis

Etiology:

• The presumed etiology is obstruction, most commonly a fecolith with parasites seen in other parts of the world
• Currently less than half of the cases with acute appendicitis have a fecolith, and in these lymphoid hyperplasia, secondary to viral or bacterial infection is implicated

Pathogenesis:

• Obstruction is thought to lead to increased intraluminal pressure due to continued secretion of fluids
• Increased intraluminal pressure eventually exceeds intravenous pressure leading to stoppage in venous flow and ischemia
• Ischemic damage leads to bacterial invasion of the mucosa with ischemic and septic necrosis

Epidemiology:

• Predominantly a disease of the Western world, presumed related to lower dietary fiber
• Incidence is decreasing due to changes in dietary fiber
• All ages affected with peak incidence in 2cd and 3rd decade
• Males 1.6>females

General Gross Description:

• Early-edema and telangiectasia of serosal vessels
• Later-Dilated lumen, thickened wall, dusky discoloration of serosa, fibrinous or fibrinopurulent serosal exudate
• Late-Mucosal necrosis often with hemorrhage,gangrenous softening of wall, heavy coating of purulent exudate on the serosa
• With complications such as perforation or abcess formation, the appendix may appear gangrenous and found in a walled off collection of pus
• An intraluminal 0bstruction, most commonly a fecalith, is found in 30 to 50% of cases

General Microscopic Description:

• Early-neutophil infiltrate of lumen, mucosa and muscularis
• Later-Mucosal necrosis, fibrinopurulent exudate on serosa
• Late-Extensive necrosis of mucosa and muscularis, with microabcesses within the appendiceal wall

Clinical Correlations:

• Sequence of symptoms: abdominal pain; nausea, vomiting, and anorexia; pain localizes over appendix, fever(see Sleisenger)
• Patient is seen and diagnosis usually made 1 to 2 days after onset of pain
• Laboratory findings are those of acute inflammation and infection
• Treatment is appendectomy
• Surgery is curative and mortality approaches 0.0 in the non-perforated patient.With perforation mortality is <1.0% except in the elderly where it is higher

References:
Cotran RS, Kumar V, Robbins SL. Robbins Pathologic Basis of Disease, 5th edition. W.B. Saunders. Philadelphia, 1994, pp.823-824 Rosai J Ackerman1s Surgical Pathology, 8th edition, Mosby St. Louis 1996 pp.711-716 Sleisenger M and Fordtran J