Rectal ulcers are a break in the protective lining of the rectum, which is the final section of the large intestine. These sores can range from small, superficial lesions to deeper wounds that penetrate the tissue wall. The presence of a rectal ulcer can lead to several non-specific symptoms, including bleeding, which is often bright red, the passage of mucus, and a sensation of incomplete evacuation or pain during bowel movements. Various factors can cause these ulcers, ranging from chronic physical strain and functional disorders to systemic inflammatory conditions, specific infections, and external tissue damage. Understanding the root cause is necessary for effective management.
Mechanical Stress and Functional Disorders
Chronic physical trauma is a common cause of rectal ulcers, often leading to Solitary Rectal Ulcer Syndrome (SRUS). This syndrome is frequently associated with long-term straining during defecation, typically due to chronic constipation or a functional disorder called dyssynergic defecation. This excessive effort puts immense mechanical stress on the rectal wall, causing the mucosa to become damaged.
The primary mechanism involves internal prolapse, where the rectal lining folds in on itself and slides down into the anal canal during straining. This repeated folding restricts blood flow to the affected area, leading to localized tissue death, or ischemia, which manifests as an ulceration. The paradoxical contraction of the puborectalis muscle in dyssynergic defecation further compresses the tissue, exacerbating the trauma and restricting blood supply. Though the name suggests a single sore, SRUS can present with multiple ulcers, inflammation, or polyp-like lesions.
Rectal ulcers can also result from direct trauma, including injury from attempts to manually remove impacted stool or the insertion of foreign objects. Prolonged friction or localized pressure against the delicate mucosal lining disrupts the epithelial barrier. Once broken, the underlying tissue is exposed to bacteria and digestive enzymes, leading to inflammation and ulcer formation.
Chronic Inflammatory Conditions
Systemic inflammation is a major cause of rectal ulcers, most notably Inflammatory Bowel Disease (IBD). IBD encompasses Ulcerative Colitis (UC) and Crohn’s Disease (CD), both resulting from a chronic immune response directed against the intestinal tract. This persistent immune activation generates an inflammatory state that breaks down the intestinal lining.
In Ulcerative Colitis, the inflammation typically begins in the rectum and spreads in a continuous pattern upward through the colon. This immune attack is generally confined to the innermost lining (the mucosa), causing it to become swollen, fragile, and covered in ulcers. These ulcers are often superficial but can bleed and produce pus and mucus, which are characteristic symptoms of the condition.
Crohn’s Disease inflammation can be patchy, affecting any part of the gastrointestinal tract, and often involves the rectum. Unlike UC, Crohn’s inflammation is transmural, meaning it penetrates through all layers of the bowel wall. This deeper inflammation leads to characteristic deep, fissure-like ulcers that can resemble a rake-mark pattern on the intestinal surface. This full-thickness damage can ultimately lead to complications like strictures and fistulas.
Specific Infectious Agents
Infectious pathogens cause rectal ulceration, typically resulting in infectious proctitis. These infections directly invade and damage the rectal mucosa, causing an inflammatory and ulcerative response. Several sexually transmitted infections (STIs) are common culprits, particularly in individuals who engage in anal receptive intercourse.
Herpes Simplex Virus (HSV), usually type 2, can cause severe rectal pain and the formation of small, painful vesicles that rupture into ulcers. The virus invades nerve endings, which can lead to neurological symptoms like sacral paresthesia. Syphilis, caused by the bacterium Treponema pallidum, results in the formation of a chancre, a typically painless, firm ulcer that develops on the rectal lining.
Bacterial infections like Chlamydia trachomatis, particularly the serovars that cause Lymphogranuloma Venereum (LGV), also cause rectal ulcers. LGV-related ulcers are often accompanied by severe inflammation and swelling of the local lymph nodes. Non-sexually transmitted infections such as amoebiasis, caused by the parasite Entamoeba histolytica, can also lead to deep, flask-shaped ulcers in the rectum and colon through direct tissue invasion.
External Factors and Vascular Issues
Rectal ulcers can result from external medical treatments or compromised blood flow. Radiation Proctitis is tissue damage occurring after pelvic radiation therapy (e.g., for prostate or cervical cancer). The ionizing radiation damages the DNA and cellular structures of mucosal cells, leading to acute inflammation and ulceration.
In the long term, radiation causes progressive damage to the small blood vessels that supply the rectal wall. This injury, known as obliterative endarteritis, results in the narrowing and blockage of tiny arteries, restricting oxygen and nutrient delivery. This chronic lack of blood flow (ischemia) leads to tissue death and fibrosis, manifesting as persistent, non-healing ulcers that can develop months or even years after the initial treatment.
Vascular issues can cause ischemic ulcers even without radiation history. This occurs when systemic diseases, such as severe atherosclerosis or a significant drop in blood pressure, compromise the blood supply to the rectum. The tissue becomes starved of oxygen, and the cells die off, resulting in ulcer formation. Certain medications, particularly nonsteroidal anti-inflammatory drugs (NSAIDs), can also be associated with intestinal ulceration, and the rectum remains a potential site for this damage.