A rectal ulcer is an open sore or lesion that develops in the mucosal lining of the rectum, the final section of the large intestine before the anus. These lesions are a physical manifestation of an underlying issue causing damage to the delicate rectal tissue. The formation of these ulcers results from various destructive processes, ranging from chronic autoimmune responses to physical trauma and circulatory compromise.
Ulcers Caused by Inflammatory Bowel Disease
Autoimmune inflammation represents a major, systemic cause of rectal ulceration, primarily through Inflammatory Bowel Disease (IBD). IBD includes Ulcerative Colitis (UC) and Crohn’s Disease (CD), both involving the immune system mistakenly attacking the gastrointestinal tract. The resulting chronic inflammation in the rectal lining leads to its eventual breakdown and the formation of ulcers.
In Ulcerative Colitis (UC), inflammation typically starts in the rectum and extends continuously upward into the colon, a pattern often referred to as proctitis. The ulcers characteristic of UC are generally superficial, limited only to the innermost mucosal layer of the intestinal wall. This continuous, shallow erosion of the lining causes bleeding and the production of pus and mucus.
Crohn’s Disease (CD) can affect any part of the digestive tract, but when it involves the rectum, the lesions are structurally different. Crohn’s inflammation is transmural, meaning it extends deep through all layers of the rectal wall, often leading to deep, penetrating ulcers. Unlike the continuous involvement seen in UC, CD is known for its patchy distribution, where inflamed areas are separated by sections of healthy tissue, referred to as “skip lesions.” The deep nature of Crohn’s ulcers can also lead to complications like fistulas.
Mechanical Injury and Chronic Strain
Physical stress and structural issues are a significant cause of rectal ulcers, most notably contributing to Solitary Rectal Ulcer Syndrome (SRUS). Despite its name, SRUS often presents with multiple lesions, but its origin is rooted in chronic mechanical trauma. The primary mechanism involves repeated, excessive straining during difficult bowel movements, which is frequently associated with long-term constipation.
This chronic straining can cause the rectal mucosa to prolapse into the anal canal, creating localized friction and pressure. The excessive force can also cause paradoxical contraction of the puborectalis muscle, preventing the anal canal from properly opening. This uncoordinated effort traps the rectal wall, leading to a temporary blockage of blood flow and subsequent localized ischemic injury to the mucosa.
Other forms of mechanical injury can also lead to ulceration through direct physical trauma to the rectal lining. These less common causes include attempts at manual disimpaction of hardened stool or the insertion of foreign bodies into the rectum. In each case, the ulcer forms as a direct consequence of frictional damage or pressure-induced injury.
Infections and Pathogenic Causes
A wide variety of external pathogens can directly invade and erode the rectal lining, resulting in infectious proctitis, which is often characterized by ulceration. These infectious agents cause a swift inflammatory response as the body attempts to fight the invading organisms. The direct attack by the pathogen and the subsequent immune response lead to the breakdown of the mucosal barrier and the development of acute ulcers.
Pathogens associated with infectious proctitis include:
- Bacterial infections, such as Shigella species, Salmonella, and Campylobacter
- Sexually transmitted infections, including Neisseria gonorrhoeae, Chlamydia trachomatis, and the bacterium responsible for syphilis
- Viruses like Herpes Simplex Virus (HSV) and Cytomegalovirus (CMV)
Acute ulcers caused by these infectious agents are typically self-limited or resolve rapidly once the infection is identified and treated with appropriate antibiotics or antiviral medications. A bacterium called Clostridioides difficile, often associated with antibiotic use, can also cause severe inflammation and ulceration in the rectum and colon.
Damage from Radiation and Reduced Blood Flow
Two distinct processes involving tissue damage due to external factors or circulatory compromise can lead to rectal ulcer formation. Radiation proctitis is a delayed complication following radiation therapy directed at pelvic cancers, such as prostate or cervical cancer. The high-energy radiation initially damages the fast-dividing cells of the rectal lining, leading to acute symptoms.
The chronic effects of radiation damage the small blood vessels within the rectal wall, causing a progressive loss of blood supply and the buildup of scar-like tissue. This process, which can occur months or even years after the completion of treatment, leads to chronic tissue starvation, or ischemia, causing the delayed formation of ulcers and strictures.
Reduced blood flow to the rectum from non-radiation causes is known as ischemic ulceration. While the rectum has a robust dual blood supply, reduced systemic circulation due to severe hypotension, shock, or underlying vascular disease like atherosclerosis can compromise this supply. Acute Hemorrhagic Rectal Ulcer (AHRU) is sometimes observed in critically ill or elderly patients who are non-ambulatory, where impaired blood flow is the trigger for ulcer formation.