Inflammation of Vermiform Appendix

Updated: Aug 27, 2021
  • Author: Steven L Lee, MD; Chief Editor: John Geibel, MD, MSc, DSc, AGAF  more...
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Practice Essentials

In 1886, Reginald H Fitz, a Harvard pathologist, first described the clinical condition of acute appendicitis (ie, inflammation of the vermiform appendix). [1]  He correctly pointed out the importance of its early diagnosis and timely treatment, as indicated by his analysis of 257 cases of perforating inflammation of the appendix and 209 cases of typhlitis or perityphlitis. [2]

A few years later, Charles McBurney described the clinical findings prior to rupture and advocated early surgical intervention. Despite aggressive intervention, mortality and morbidity remained high through the rest of the 19th century and the first half of the 20th century. The mortality associated with appendicitis declined with the introduction of antibiotics and with the development of anesthesia and better perioperative care.

Acute appendicitis remains one of the most common surgical diseases encountered by physicians. When appendicitis manifests in its classic form, it is easily diagnosed and treated. Unfortunately, these classic symptoms occur in just over half of patients with acute appendicitis. Atypical presentations often lead to a delay in diagnosis, perforation, prolonged hospitalization, and increased morbidity. [3, 4]

Consequently, accurate and timely diagnosis of atypical appendicitis remains clinically challenging, and this condition is still one of the most commonly missed problems in the emergency department. Controversy continues over the most accurate, cost-effective, and rapid method of making the diagnosis of atypical appendicitis. Surgical consultation remains the most effective method of determining what additional diagnostic tools are needed.

There is growing interest in treatment of acute appendicitis with antibiotics without appendectomy, [5] as well as in the use of biomarkers to improve the accuracy of diagnosis.

For patient education resources, see the Digestive Disorders Center, as well as Appendicitis and Abdominal Pain in Adults.



The appendix was probably first noted in ancient Egypt as early as 3000 BCE. During the mummification process, abdominal parts were removed and placed in canopic jars with inscriptions describing the contents. When these jars were uncovered, inscriptions referring to the "worm of the intestine" were discovered. [6]

Aristotle and Galen did not identify the appendix, because they both dissected lower animals, which do not have appendices. Celsus, however, probably discovered the appendix because he was allowed to dissect criminals executed by the Roman emperor. [6]

Leonardo da Vinci first depicted the appendix in anatomic drawings in 1492. In 1521, Jacopo Beregari da Capri, a professor of anatomy in Bologna, identified the appendix as an anatomic structure. In the 1500s, Vesalius (1543) and Pare (1582) referred to the appendix as the caecum. Laurentine compared the appendix to a twisted worm in 1600, and Phillipe Verheyen coined the term appendix vermiformis in 1710. [6]

Embryologically, the appendix is a continuation of the cecum and is first delineated during the fifth month of gestation. The appendix does not elongate as rapidly as the rest of the colon, thus forming a wormlike structure. [1]

The average length of the appendix is 10 cm, but its length can range from 2 to 20 cm. The wall of the appendix consists of both an inner circular and an outer longitudinal layer of muscle. The longitudinal layer is a continuation of the taeniae coli. The appendix is lined by colonic epithelium. [1]

Few submucosal lymphoid follicles are noted at birth. These follicles enlarge, peak between age 12 and 20 years, then decrease. This correlates with the incidence of appendicitis.

Blood supply to the appendix is mainly from the appendicular artery, a branch of the ileocolic artery. This artery courses through the mesoappendix posterior to the terminal ileum. An accessory appendicular artery can branch from the posterior cecal artery. Damage to this artery can lead to significant intraoperative and postoperative hemorrhage and should be searched for carefully and ligated once the main appendicular artery is controlled. [7]

The base of the appendix is consistently located at the posteromedial wall of the cecum, about 2.5 cm below the ileocecal valve. This is also where the taeniae converge. [7]

While the appendiceal base is in a constant location, the position of the tip of the appendix varies widely. In 65% of patients, the tip is located in a retrocecal position; in 30%, it is located at the brim or in the true pelvis; and, in 5%, it is extraperitoneal, situated behind the cecum, ascending colon, or distal ileum. The location of the tip of the appendix determines early signs and symptoms of appendicitis.



Appendicitis progresses through four stages, as follows [7] :

  • Acute or focal appendicitis
  • Suppurative appendicitis
  • Gangrenous appendicitis
  • Perforated appendicitis

The basic pathophysiology of appendicitis is obstruction of the lumen of the appendix followed by infection. In 60% of patients, obstruction is caused by hyperplasia of the submucosal follicles. This form of obstruction is mostly observed in children and is known as catarrhal appendicitis. A fecalith or fecal stasis causes luminal obstruction 35% of the time and is usually observed in adults. Obstruction may also be caused by foreign bodies (4%) and tumors (1%).

Following obstruction, an increase in mucus production occurs, leading to increased intraluminal pressure. With increased pressure and stasis from obstruction, bacterial overgrowth ensues. The mucus then turns into pus that causes a further increase in luminal pressure. This leads to distention of the appendix and visceral pain, which is typically located in the epigastric or periumbilical region.

As the luminal pressure continues to increase, lymphatic obstruction occurs, leading to edema in the appendiceal wall. This stage is known as acute or focal appendicitis. The overlying parietal peritoneum becomes irritated, causing the pain to localize to the right lower quadrant (RLQ). This series of events results in the classic migrating abdominal pain described in patients with appendicitis.

Further increases in pressure lead to venous obstruction, causing edema and ischemia of the appendix. The ensuing bacterial invasion of the wall of the appendix is known as acute suppurative appendicitis. Finally, with continued pressure increases, venous thrombosis and arterial compromise occur, leading to gangrene and perforation. [7]

If the body successfully walls off the perforation, the pain may actually improve. However, symptoms do not completely resolve. Patients may still have underlying RLQ pain, decreased appetite, change in bowel habits (eg, diarrhea, constipation), or intermittent low-grade fever. If the perforation is not successfully walled off, then diffuse peritonitis develops.



Appendicitis results from obstruction of the lumen of the appendix. Obstruction may be due to lymphoid hyperplasia (60%), fecalith or fecal stasis (35%), foreign body (4%), or tumors (1%). [7]



In Western countries, approximately 7% of individuals develop appendicitis at some point during their lives. Approximately 200,000 appendectomies are performed annually in the United States. [1]

The annual incidence of acute appendicitis has gradually declined by nearly 50% from its peak incidence in the early 20th century to its current levels of 1 case per 1000 population in the United States and 86 cases for every 100,000 persons worldwide. [8, 9]

Acute appendicitis is less common in Africa and in parts of Asia because of the high-residue diets of the inhabitants.



The outcome following appendectomy for acute or suppurative appendicitis is excellent. Although most patients return to full activity within 2 weeks, prolonged hospitalization and additional diagnostic and therapeutic procedures may be required when perforated appendicitis is encountered.

The prognosis for all stages of appendicitis is excellent, with a mortality of less than 1%. This low death rate is largely the result of early diagnosis and treatment, antibiotics, and improved anesthesia care.

Numerous prospective randomized trials have compared laparoscopic appendectomy with open appendectomy. The two techniques have been found to be similar with respect to the negative appendectomy rate (laparoscopic, 14.4%; open, 14.5%), length of hospital stay (laparoscopic, 3 days; open, 3.7 days), and incidence of intra-abdominal abscess formation (laparoscopic, 1.9%; open, 0.8%).

Laparoscopic appendectomy appears to have a slightly lower wound infection rate (3%) than open appendectomy does (7.5%). [10]

The benefits of a laparoscopic approach seem to be more pronounced among obese patients. One study found a significantly shorter length of hospital stay (laparoscopic, 3.4 days; open, 5.5 days) and a higher wound closure rate (laparoscopic, 90%; open, 68%) in patients with a body mass index (BMI) higher than 30. [11]

Data from the Nationwide Inpatient Sample (NIS) from 2006 to 2008 demonstrated that laparoscopic appendectomy was associated with lower morbidity, lower mortality, and a shorter hospital stay in both perforated and nonperforated appendicitis. Laparoscopic appendectomy was also associated with lower hospital charges in patients with perforated appendicitis. [12]

Studies by Frazee et al suggested that in the setting of uncomplicated appendicitis, outpatient laparoscopic appendectomy is effective and safe, with low morbidity and low readmission rates. [13, 14]

A systematic review and meta-analysis by Neogi et al found that laparoscopic appendectomy had a better complication profile than open appendectomy even in children with complicated appendicitis. [15]