Understanding the embryologic development of the appendix can aid clinicians in making the diagnosis of appendicitis. The appendix arises from the cecum during the eighth week of fetal development. It rotates from its initial position along the lateral aspect of the cecum to a more medial position near the ileocecal valve. Rotational arrest can occur at any point, resulting in variations in the final position of the appendix within the abdominal cavity. Variability in appendiceal position, especially the tip, can lead to alterations in the point of maximal tenderness on physical examination when inflammation is present.

The risk of developing appendicitis during an average lifetime has been estimated to range from 6% to 20%. The risk is lowest during infancy and greatest during adolescence. Approximately 1% of all children age 15 years or younger will develop appendicitis, with a peak incidence between 10 and 12 years. The incidence of perforation present at the time of surgery ranges between 10% and 50%.

Luminal obstruction is the most common etiology of acute appendicitis. Most often, obstruction is the result of inspissated fecal material (appendicolith). However, appendicoliths are present in only 30% to 50% of patients at the time of appendectomy.

Bacterial or viral infections can lead to periappendiceal lymphoid hyperplasia. Lymphoid hyperplasia located near the base of the appendix can result in extrinsic compression. Obstruction, either intrinsic or extrinsic, is followed by an increase in intraluminal pressure distal to the point of obstruction, secondary to increased mucus production and venous engorgement. Unabated, the inflammatory process leads to thrombosis of the vascular strictures within the wall of the appendix. Thrombosis, with progressive ischemia, results in full thickness necrosis, which ultimately leads to perforation.

Early diagnosis and treatment are essential to the successful management of patients with appendicitis. Usually, patients present with the triad of nausea (with or without vomiting), fever, and abdominal pain. The pain associated with appendicitis exhibits a classic migratory pattern, which is a result of the particular neural pathways associated with the perception of abdominal pain. Obstruction of the appendiceal lumen leads to distention of the organ; impulses via wall-stretch receptors then are relayed through visceral nerve fibers to the tenth
thoracic ganglion. Pain initially is perceived in the periumbilical region. As the inflammatory process progresses and becomes full-thickness, parietal peritonitis results. Pain localizes in the right lower quadrant (RLQ) at McBurney’s point (two-thirds of the way between the umbilicus and the anterior superior iliac spine).

Anorexia, nausea, and vomiting are important symptoms in patients with acute appendicitis. One or more of these symptoms occur subsequent to the onset of abdominal pain. The differential diagnosis of RLQ pain is extensive (Box 364.1). A detailed history and physical examination are of utmost importance and may effectively rule out a number of other conditions. Laboratory data and radiographic findings may offer additional important information.