Appendicitis develops at any age, with a peak incidence in the second and third decades. Over their lifetime, 7% to 12% of the US population develops appendicitis. Appendicitis occurs more commonly in Western cultures than in Eastern cultures likely due to dietary differences between these populations (15
). Heredity may also play a role in the pathogenesis of appendicitis. Patients with a family history of appendicitis have approximately three times the risk for developing appendicitis than those with no family history (16
). Appendicitis affects males slightly more commonly than females, particularly during early childhood (17
Acute appendicitis may also develop in neonates. Although this is rare, it is associated with high morbidity and mortality rates (18
). Neonatal appendicitis usually results from the presence of neonatal necrotizing enterocolitis, cystic fibrosis, Hirschsprung disease, or from bacteremia associated with maternal chorioamnionitis (18
Despite the proclivity of appendicitis to involve younger individuals, it also affects the elderly and other age groups. The incidence of appendicitis in the elderly may be increasing due to longer life expectancy. Appendicitis in the elderly also has a high mortality and complication rate (20
), perhaps due to concomitant NSAID use. NSAIDs may impair the inflammatory processes and suppress white cell responses
increasing the risk of developing appendicitis (20
). Additionally, NSAIDs mask the symptoms so that patients present with late-stage disease.
TABLE 8.2 CAUSES OF APPENDICEAL OBSTRUCTION LEADING TO APPENDICITIS
Mucus—most often in cystic fibrosis
Kinks (angulated appendix)
Tumors in the appendix or cecum
Lymphoid hyperplasia—usually secondary to viral infection
The diagnosis of appendicitis is straightforward when it presents classically with right lower quadrant abdominal pain of short duration, abdominal rigidity, and anorexia. Appendicitis also causes acute periumbilical, colicky pain, or vomiting. Fever and leukocytosis develop early. However, there are many examples of appendices that are removed for suspected acute appendicitis in which histologic evidence of an acute appendicitis is lacking.
Normally, the appendiceal mucosa appears smooth, light yellow-tan; the serosa appears pink-tan, smooth, and glistening. When the inflammation is restricted to the mucosa, the exterior of the appendix may grossly appear normal. Dilatation and congestion of serosal vessels produces localized or generalized hyperemia and constitutes the earliest visible external change (Figs. 8.12
). Well-developed acute appendicitis shows marked congestion with a dull (rather than glistening) serosal surface or there may be a serosal granular, fibrinous, or purulent coating and vascular engorgement reflecting severe necrosis and inflammation.
The mesoappendix appears edematous, and contiguous structures may become inflamed. The appendix often exudes purulent material from the cut surface; one may sometimes identify an impacted intraluminal fecalith. Mucosal necrosis and ulceration are usually present. The acute inflammation can localize to one segment of the organ, or the entire appendix may be affected. There may be the appearance of a mucocele. If so, the appendix should be well sampled to exclude the presence of a coexisting mucinous neoplasm.
FIG. 8.13 Acute appendicitis showing vascular engorgement and serosal erythema. A white purulent membrane covers the serosal surface.
By the time full-blown gangrenous appendicitis develops, the organ appears soft, purplish, and hemorrhagic or even greenish black, sometimes with visible thrombi in the mesoappendix. These may spread along the ileocecal and upper mesenteric veins. Perforation may be present. In complicated cases, abscesses may form around a site of perforation, and inflammation may extend into the mesoappendix (Fig. 8.15
Histologic changes associated with appendicitis reflect disease duration and severity, and some changes may not reflect clinical disease at all. The term “acute intraluminal appendicitis” has been used when there are neutrophils in the appendiceal lumen, but they have not yet infiltrated the mucosa (26
). This may not be of any significance since this finding can be seen in incidental appendectomy specimens. Other minimal changes may consist of focal neutrophilic collections in the lumen and lamina propria. This is sometimes referred to as “mucosal” or “early” appendicitis. The term mucosal appendicitis has been used both in the presence and the absence of ulcers if the inflammation is restricted to the mucosa (27
). The clinical significance of pure mucosal inflammation in the absence of ulcers is uncertain. Since these changes may reflect sampling error, more sections should be taken of the appendix to be certain that there is not more extensive inflammation elsewhere in the appendix.
FIG. 8.14 Gangrenous appendicitis. The external surface of the appendix is hemorrhagic and reddened with a well-developed fibropurulent membrane.
FIG. 8.15 Diagram illustrating the complications of acute appendicitis.
In better developed disease, focal erosions, cryptitis, and crypt abscesses develop. The inflammation then extends to the submucosa. After the inflammatory process reaches the submucosa, it spreads quickly to involve the remaining appendix. Eventually, the mucosa erodes, the wall becomes necrotic, and the vessels may thrombose. Submucosal abscesses, edema, and congestion follow. Some appendices contain prominent eosinophilic infiltrates. Extravasated mucin in the bowel wall may induce a foreign body reaction or even small mucin granulomas.
Gangrenous appendicitis shows extensive suppuration, often extending deep into or through the appendiceal wall with complete mural destruction (Figs. 8.16
) with or without rupture. If perforation occurs, an intense nonspecific inflammatory process ensues. Perforation may be suspected clinically, but it is often difficult to see in the resected specimen due to the extensive inflammation. Resolving appendicitis is characterized by the presence of a predominantly lymphocytic infiltrate involving the subserosa and muscularis propria or the subserosa. When appendicitis heals, it assumes one of two basic patterns: the “usual” pattern, sometimes with an intraluminal cord of granulation tissue, and a xanthogranulomatous pattern (30
). Fibrosis may develop.
FIG. 8.16 Acute appendicitis. A: Cross section through the appendix showing the transmural inflammation. B: High magnification of the surface exudate that contains necrotic debris and bacteria. C: Below the surface of the debris shown in (B), there is acute and chronic inflammation. D: Acute and chronic inflammation with small thrombi within the dilated and congested veins. E: Cross section through a larger vessel containing an organizing thrombus at the base of the vessel (arrow). Overlying the vessel is necrotic and inflammatory debris. Under the vessel is a zone of acute and chronic inflammation. F: Cross section through a small vessel demonstrating with fibrinoid necrosis and acute and chronic inflammation. G: The serosa shows marked vascular engorgement and small thrombi in the dilated vessels (arrow). H: Lower magnification showing the extension of fibrosing stands of tissue extending into the mesoappendiceal fat. The vessels on the serosal surface are markedly engorged. The lumen of the appendix at this level is completely necrotic (star).
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