Solitary ulcer of the cecum was first described by Cruveilhier in 1832. The subject of cecal ulcers is confusing and complicated because they are uncommon and have multiple causes. A variety of terms, including solitary cecal ulcer, acute cecal ulcer, and benign solitary cecal ulcer, have been used to describe these lesions. Case inclusion varies. For example, Ong et al, in a recent review of “solitary caecal ulcer syndrome,” excluded cecal ulcers associated with colon cancer, infectious causes, nonsteroidal antiinflammatory drug (NSAID) use, and inflammatory bowel disease, whereas the case report and literature review of “benign solitary cecal ulcer” by Chi and Hanauer described a case that was caused by an infectious agent. Perhaps it is more useful to consider cecal ulcers in the context in which they are found, after which the potential causes can be considered and treatment can be tailored. Knowledge of the possible causes is essential to this approach.
Box 45-1 provides an outline of possible causes of cecal ulceration. With so many possibilities, cecal ulceration is likely the end point of several pathologic pathways. A detailed history including current medications, family history of irritable bowel disease or colon cancer, immune status, and travel history, correlated with presenting symptoms, may point to a possible cause.
Ulcerated submucosal tumor
Nonsteroidal antiinflammatory drugs
Chronic kidney disease
Inflammatory bowel disease
Cecal cancer can be confused with less common causes of cecal ulcer, such as ulcerated submucosal tumors, mycobacterial or ischemic strictures with ulceration, and drug-induced ulceration. These conditions can cause profound inflammation with a mass effect so as to suggest an ulcerated cancer.
In an aging society, drug-related cecal ulcers are common. NSAIDs can damage the stomach, small bowel, and colon. Colonic ulceration is predominantly right sided. Possible mechanisms of injury include reactive oxygen species and Na + /H + exchange alteration with resultant increased acidification.
A variety of infections can produce cecal ulcers, especially in immunocompromised patients who are prone to cytomegalovirus (CMV)-induced cecal ulcers.
Cecal ulcers can be identified at the time of colonoscopy or during the evaluation of symptoms ( Box 45-2 ). The former scenario is probably most commonly seen in patients taking NSAIDs. Occult blood loss or blood loss anemia may also be seen in asymptomatic patients who take NSAIDs. About 3% of regular NSAID users have colonic ulcers, which are more common with enteric-coated formulations and usually are found in the cecum or right colon. Terminal ileal ulceration also may be present. The cecal ulceration can be solitary or multiple. Upon colonoscopy, these ulcers are commonly found on the anterior wall of the cecum or on the antimesenteric border within 2 cm of the ileocecal valve. Significant edema typically surrounds these ulcers, which may have the appearance of a simple peptic ulcer. Biopsy results are nonspecific, but fibrinous granulation tissue and lymphocyte and fibroblast infiltration with disruption and thickening of the muscularis mucosae have been described. Microvascular thrombosis in submucosal vessels due to fibrin deposition may be seen. In patients with CMV infection, viral inclusions within endothelial cells and fibroblasts in the lamina propria are seen.
Some patients with cecal ulcers will present with right lower quadrant (RLQ) pain simulating acute appendicitis. A history of NSAID use or immunosuppression should at least lead to consideration of the possibility of a cecal ulcer as a cause of the pain. A strong family history of colon cancer potentially related to Lynch syndrome raises suspicion of a right-sided colon cancer. The usual evaluation of a patient with RLQ pain includes a complete blood cell count and differential, routine chemistries, and imaging studies. Computed tomography scan findings are nonspecific but include cecal wall thickening, inflammation (streaky or dirty fat) in the adjacent mesocolon, and occasionally the appearance of a cecal mass, which suggests cancer. In the appropriate clinical scenario, appendicitis and Crohn disease may be considered. A barium or water-soluble enema may similarly suggest cancer. Cecal ulcers, whether idiopathic or associated with a known cause, can appear to be ulcerated colon malignancies, and an ulcerated lipoma can mimic an ulcerated colonic malignancy. Colonoscopy with a biopsy will help settle this differential, although the clinical setting will dictate whether a colonoscopy is deemed to be safe. Nonoperative management and delayed colonoscopy is often prudent.