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The anal canal is the terminal portion of the large intestine. It is divided into three zones: the upper (covered with rectal mucosa), the middle (partially covered with a transitional mucosa),

and the lower (covered by stratified squamous mucosa). The tumors located in this anatomic location are designated as carcinoma of the anal canal. Patterns of differentiation

include a basaloid pattern, squamous cell carcinoma, and adenocarcinoma.

Anal canal carcinoma with basaloid differentiation is a tumor populated by immature proliferative cells derived from the basal layer of a stratified squamous epithelium. These tumors may

occur sporadically and be uniform in their histologic features. Alternatively, basaloid differentiation may be a component of a tumor that exhibits more genuine squamous cell

differentiation and/or the mucin vacuole-containing features of adenocarcinoma. All such tumors remain classified as anal canal carcinoma.

Pure squamous cell carcinomas of the anal canal are closely associated with chronic HPV infection.[96] Some rare cases are also related to immunosuppression, as encountered in renal

transplantation and in AIDS patients. As with the genital tract, chronic HPV infection of the anal canal often causes precursor lesions such as condyloma acuminatum, squamous epithelium

dysplasia, and carcinoma in situ.

Pure adenocarcinoma of the anal canal is often the extension of rectal adenocarcinoma. Rarely, other tumors may arise from the anal canal, notably Paget disease, small-cell carcinoma,

and melanoma.



The appendix is an underdeveloped residuum of the otherwise voluminous cecum. The adult appendix averages 6 to 7 cm in length, is partially anchored by a mesenteric extension from the

adjacent ileum, and has no known function. The appendix has the same four layers as the remainder of the gut and possesses a colonic-type mucosa. A distinguishing feature of this organ

is the extremely rich lymphoid tissue of the mucosa and submucosa, which in young individuals forms an entire layer of germinal follicles and lymphoid pulp. This lymphoid tissue

undergoes progressive atrophy during life to the point of complete disappearance in advanced age. In the elderly the appendix, particularly the distal portion, sometimes undergoes fibrous



Diseases of the appendix loom large in surgical practice; appendicitis is the most common acute abdominal condition the surgeon is called on to treat. Appendicitis is one of the best-known

medical entities and yet may be one of the most difficult diagnostic problems to confront the emergency physician. A differential diagnosis must include virtually every acute process that

can occur within the abdominal cavity, as well as some emergent conditions affecting organs of the thorax.

Acute Appendicitis

Inflammation in the right lower quadrant was considered a nonsurgical disease of the cecum (typhlitis or perityphlitis) until Fitz recognized acute appendicitis as a distinct entity in 1886.

Appendiceal inflammation is associated with obstruction in 50% to 80% of cases, usually in the form of a fecalith and, less commonly, a gallstone, tumor, or ball of worms (oxyuriasis

vermicularis). Continued secretion of mucinous fluid in the obstructed viscus presumably leads to a progressive increase in intraluminal pressure sufficient to cause eventual collapse of the

draining veins. Ischemic injury then favors bacterial proliferation with additional inflammatory edema and exudation, further embarrassing the blood supply. Nevertheless, a significant

minority of inflamed appendices have no demonstrable luminal obstruction, and the pathogenesis of the inflammation remains unknown.


At the earliest stages, only a scant neutrophilic exudate may be found throughout the mucosa, submucosa, and muscularis propria. Subserosal vessels are congested, and often there is a

modest perivascular neutrophilic infiltrate. The inflammatory reaction transforms the normal glistening serosa into a dull, granular, red membrane; this transformation signifies early acute

appendicitisfor the operating surgeon. At a later stage, a prominent neutrophilic exudate generates a fibrinopurulent reaction over the serosa ( Fig. 17-66 ). As the inflammatory process

worsens, there is abscess formation within the wall, along with ulcerations and foci of suppurative necrosis in the mucosa. This state constitutes acute suppurative appendicitis. Further

appendiceal compromise leads to large areas of hemorrhagic green ulceration of the mucosa and green-black gangrenous necrosis through the wall, extending to the serosa, creating acute

gangrenous appendicitis,which is quickly followed by rupture and suppurative peritonitis.

The histologic criterion for the diagnosis of acute appendicitis is neutrophilic infiltration of the muscularis propria. Usually, neutrophils and ulcerations are also present within the mucosa.

Since drainage of an exudate into the appendix from alimentary tract infection may also induce a mucosal neutrophilic infiltrate, evidence of muscular wall inflammation is requisite for the


Figure 17-66Acute appendicitis. The inflamed appendix shown below is red, swollen, and covered with a fibrinous exudate. For comparison, a normal appendix is shown above.

Figure 17-67Mucinous cystadenocarcinoma of the appendix, with spread into the immediate periappendiceal tissues.


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