Addiss and associates estimated the incidence of acute appendicitis in the United States population to be 11 cases per 10,000 population annually. The disease is slightly more common in males, with a male:female ratio of 1.4:1. In a lifetime, 8.6% of males and 6.7% of females can be expected to develop acute appendicitis. Young age is a risk factor, as nearly 70% of patients with acute appendicitis are less than 30 years of age. The highest incidence of appendicitis in males is in the 10- to 14-year-old age group (27.6 cases per 10,000 population), while the highest female incidence is in the 15- to 19-year-old age group (20.5 cases per 10,000 population). Patients at extremes of age are more likely to develop perforated appendicitis. Overall, perforation was present in 19.2% of cases of acute appendicitis. This number was significantly higher, however, in patients under 5 and over 65 years of age. Although less common in people over 65 years old, acute appendicitis in the elderly progresses to perforation more than 50% of the time.
Etiology and Pathophysiology
Appendicitis, diverticular disease, and colorectal carcinoma have been shown to be diseases of developed civilizations. Burkitt found an increased incidence of appendicitis in Western countries compared to Africa, as well as in wealthy, urban communities compared to rural areas. He attributed this to the Western diet, which is low in dietary fiber and high in refined sugars and fat, and postulated that low-fiber diets lead to less bulky bowel contents, prolonged intestinal transit time, and increased intraluminal pressure. Burkitt theorized that the combination of firm stool leading to appendiceal obstruction and increased intraluminal pressure causing bacterial translocation across the bowel wall resulted in appendicitis. In examining appendixes removed for reasons other than appendicitis, he found fecaliths to be more prevalent in Canadian (32%) than in South African (4%) adults. In a group of patients with appendicitis, fecaliths were more common in Canadians (52%) than in South Africans (23%).He felt this was confirmation that appendiceal obstruction resulted in appendicitis. Of note, however, the majority of patients with appendicitis in his study did not have evidence of a fecalith.
Wangensteen extensively studied the structure and function of the appendix and the role of obstruction in appendicitis.Based on anatomic studies, he postulated that mucosal folds and a sphincterlike orientation of muscle fibers at the appendiceal orifice make the appendix susceptible to obstruction. He proposed the following sequence of events to explain appendicitis:
(1) closed loop obstruction is caused by a fecalith and swelling of the mucosal and submucosal lymphoid tissue at the base of the appendix;
(2) intraluminal pressure rises as the appendiceal mucosa secretes fluid against the fixed obstruction;
(3) increased pressure in the appendiceal wall exceeds capillary pressure and causes mucosal ischemia; and
(4) luminal bacterial overgrowth and translocation of bacteria across the appendiceal wall result in inflammation, edema, and ultimately necrosis. If the appendix is not removed, perforation can ensue.
Although appendiceal obstruction is widely accepted as the primary cause of appendicitis, evidence suggests that this may be only one of many possible etiologies. First, some patients with a fecalith have a histologically normal appendix.Moreover, the majority of patients with appendicitis show no evidence for a fecalith.Arnbjornsson and Bengmark studied at laparotomy the appendixes of patients with suspected appendicitis. They found the intraluminal pressure of the appendix prior to removal to be elevated in only 8 of 27 patients with nonperforated appendicitis. They found no signs of obstruction in the remaining patients with nonperforated appendicitis, as well as all patients with a normal appendix. Taken together, these studies imply that obstruction is but one of the possible etiologies of acute appendicitis.