Appendicitis is caused by a blockage of the hollow portion of the appendix. This is most commonly due to a calcified "stone" made of feces. Inflamed lymphoid tissue from a viral infection, parasites, gallstone, or tumors may also cause the blockage. This blockage leads to increased pressures in the appendix, decreased blood flow to the tissues of the appendix, and bacterial growth inside the appendix causing inflammation. The combination of inflammation, reduced blood flow to the appendix and distention of the appendix causes tissue injury and tissue death. If this process is left untreated, the appendix may burst, releasing bacteria into the abdominal cavity, leading to increased complications.
The diagnosis of appendicitis is largely based on the person's signs and symptoms. In cases where the diagnosis is unclear, close observation, medical imaging, and laboratory tests can be helpful. The two most common imaging tests used are an ultrasound and computed tomography (CT scan). CT scan has been shown to be more accurate than ultrasound in detecting acute appendicitis. However, ultrasound may be preferred as the first imaging test in children and pregnant women because of the risks associated with radiation exposure from CT scans.
The standard treatment for acute appendicitis is surgical removal of the appendix. This may be done by an open incision in the abdomen (laparotomy) or through a few smaller incisions with the help of cameras (laparoscopy). Surgery decreases the risk of side effects or death associated with rupture of the appendix. Antibiotics may be equally effective in certain cases of non-ruptured appendicitis. It is one of the most common and significant causes of severe abdominal pain that comes on quickly. In 2015 about 11.6 million cases of appendicitis occurred which resulted in about 50,100 deaths. In the United States, appendicitis is the most common cause of sudden abdominal pain requiring surgery. Each year in the United States, more than 300,000 people with appendicitis have their appendix surgically removed. Reginald Fitz is credited with being the first person to describe the condition in 1886.
The presentation of acute appendicitis includes abdominal pain, nausea, vomiting, and fever. As the appendix becomes more swollen and inflamed, it begins to irritate the adjoining abdominal wall. This leads to the localization of the pain to the right lower quadrant. This classic migration of pain may not be seen in children under three years. This pain can be elicited through signs and can be severe. Signs include localized findings in the right iliac fossa. The abdominal wall becomes very sensitive to gentle pressure (palpation). There is severe pain on sudden release of deep pressure in the lower abdomen (rebound tenderness). If the appendix is retrocecal (localized behind the cecum), even deep pressure in the right lower quadrant may fail to elicit tenderness (silent appendix). This is because the cecum, distended with gas, protects the inflamed appendix from pressure. Similarly, if the appendix lies entirely within the pelvis, there is usually complete absence of abdominal rigidity. In such cases, a digital rectal examination elicits tenderness in the rectovesical pouch. Coughing causes point tenderness in this area (McBurney's point), historically called Dunphy's sign.
Acute appendicitis seems to be the end result of a primary obstruction of the appendix. Once this obstruction occurs, the appendix becomes filled with mucus and swells. This continued production of mucus leads to increased pressures within the lumen and the walls of the appendix. The increased pressure results in thrombosis and occlusion of the small vessels, and stasis of lymphatic flow. At this point spontaneous recovery rarely occurs. As the occlusion of blood vessels progresses, the appendix becomes ischemic and then necrotic. As bacteria begin to leak out through the dying walls, pus forms within and around the appendix (suppuration). The end result is appendiceal rupture (a 'burst appendix') causing peritonitis, which may lead to sepsis and eventually death. These events are responsible for the slowly evolving abdominal pain and other commonly associated symptoms.
The causative agents include bezoars, foreign bodies, trauma, intestinal worms, lymphadenitis and, most commonly, calcified fecal deposits that are known as appendicoliths or fecoliths. The occurrence of obstructing fecaliths has attracted attention since their presence in people with appendicitis is higher in developed than in developing countries. In addition an appendiceal fecalith is commonly associated with complicated appendicitis. Fecal stasis and arrest may play a role, as demonstrated by people with acute appendicitis having fewer bowel movements per week compared with healthy controls.
The occurrence of a fecalith in the appendix was thought to be attributed to a right-sided fecal retention reservoir in the colon and a prolonged transit time. However, a prolonged transit time was not observed in subsequent studies. From epidemiological data, it has been stated that diverticular disease and adenomatous polyps were unknown and colon cancer exceedingly rare in communities exempt from appendicitis. And acute appendicitis has been shown to occur antecedent to cancer in the colon and rectum. Several studies offer evidence that a low fiber intake is involved in the pathogenesis of appendicitis. This low intake of dietary fiber is in accordance with the occurrence of a right-sided fecal reservoir and the fact that dietary fiber reduces transit time.