Primary small intestinal ulcer

　　1. Etiology

　　Bailli first reported the disease in 1795, and the etiology is unknown. Central nervous system diseases, infections, trauma, malnutrition, and endocrine secretion disorders have all been considered as causes of the disease, but there is no definitive conclusion.

　　A retrospective survey in the 1960s showed that more than half of the patients had a history of taking thiazide diuretics and potassium chloride. In animal experiments, local stimulation of the small intestine can cause the disease. Administering 500 to 1000 mg of potassium chloride enteric-coated tablets to monkeys daily can cause typical small intestinal ulcers, but this was not confirmed in dogs. Due to the confirmed potassium chloride-induced small intestinal ulcers in monkeys, it is widely believed that after oral administration, the enteric-coated potassium chloride tablets dissolve rapidly in a certain segment of the small intestine, are absorbed at high concentration, causing spasms of the intestinal and mesenteric blood vessels, and insufficient blood supply to the intestinal wall. This leads to ischemia, necrosis, and ulcers. This indicates that small intestinal ulcers are of vascular origin, and it is speculated that any cause of local ischemia in the intestinal wall may lead to ulcers.

　　It has also been noted that the age of onset of this disease is mostly over 50, and those with atherosclerosis, hypertension, and cardiovascular disease are more susceptible. The occurrence of small intestinal ulcers in the elderly may be related to vascular sclerosis, insufficient blood supply to the intestines, and thrombosis of the small intestinal blood vessels. Clinical observations have found that most ulcers are located on the side opposite the mesentery, which also suggests a relationship with insufficient blood supply.

　　Since the 1980s, with the widespread use of enteric-coated aspirin, the incidence of the disease has shown an increasing trend. Therefore, some scholars believe that enteric-coated non-steroidal anti-inflammatory drugs are related to the occurrence of the disease. The mechanism is that these drugs can inhibit prostaglandin synthesis, leading to a decrease in the integrity of the intestinal mucosa and increased permeability. Administering substances that are normally not easily absorbed to patients with the disease can detect these substances in the urine, supporting this theory. Due to the increased permeability of the mucosa, certain pathogenic factors such as pathogenic microorganisms (which can be bacteria, viruses, or others), toxins, and bile acids can enter the intestinal mucosa, leading to the formation of ulcers.

　　2. Pathogenesis

　　Ulcers are mostly solitary, but can also be multiple. Reports indicate that lesions located in the ileum are twice as common as those in the jejunum, with the distal ileum more common than the proximal ileum. However, some authors report that lesions in the jejunum are more common. Ulcers are usually small elliptical, circular, or annular, with relatively regular edges, showing a chisel-like margin, and clear boundaries. The base is covered with inflammatory granulation tissue, surrounded by mild edema. The lesions mainly affect the mucosa and submucosa. Manifestations include mucosal necrosis, ulcers, inflammatory cell infiltration, and fibrosis; the mucosa around the ulcers is metaplastic to pyloric glands, with organized thrombi in small blood vessels, except for perforation, generally not invading the muscular layer. In patients with multiple ulcers, the mucosa between the ulcers is normal. The diameter of the ulcers ranges from 0.5 to 4.0 cm, with most being 1.0 to 2.0 cm. Ulcers are mostly located on the mucosa opposite the mesenteric margin, with occasional occurrence of ulcers encircling the intestinal tract. In a few patients, a fibromuscular diaphragm surrounding the intestinal lumen can be seen, which is also the pathological basis for intestinal obstruction. Acute ulcers lack an inflammatory response and are prone to perforation.

　　1. Toxic megacolon is a severe complication. It is seen in acute fulminant ulcerative colitis and acute severe cases. The incidence is about 2%, often induced by taking anticholinergic drugs such as codeine, benzylpiperazine, and atropine, or by taking laxatives such as castor oil. It can also be induced during barium enema examination of patients with acute stage or severe diarrhea. The dilated colon is often located in the transverse colon and splenic flexure. Patients present with intermittent high fever, depression, and a severe toxic state, with the abdomen quickly distending, tenderness, and reduced or absent bowel sounds. Due to the rapid expansion of the colon, the wall becomes thin, blood supply is impaired, and intestinal necrosis and perforation are prone to occur, with a very high mortality rate, reaching 30% to 50%.

　　2. Colon perforation often occurs on the basis of toxic megacolon. After perforation, it can lead to diffuse peritonitis or localized abscess, with the perforation site often located at the sigmoid colon or splenic flexure. Patients often present with high fever and symptoms of infection and intoxication, abdominal distension, and widespread muscle tension on the left side of the abdomen. Subtraction radiography often shows free air under the diaphragm.

　　3. Lower gastrointestinal bleeding can cause widespread bleeding in the rectum and colon, with the vast majority presenting as hematochezia or mucous stool. In a statistical analysis of 2077 cases of lower gastrointestinal bleeding, ulcerative colitis accounted for 8.3%. Sometimes, a small number of cases (about 4%) may experience recurrent massive lower gastrointestinal bleeding, with a single bleeding volume that can reach thousands of milliliters, even leading to shock, requiring emergency surgical treatment.

　　4. Intestinal obstruction of the rectum and colon is a late complication, but it rarely causes intestinal obstruction.

　　5. Internal fistulas between intestinal lumens or between intestinal lumens and other hollow visceras (such as bladders, vaginas, etc.) form internal fistulas; intestinal lumens communicating with the skin form external fistulas, although rare, they occasionally occur.

　　6. Anal and perianal diseases such as anal fissures, perirectal abscesses, anal fistulas, and hemorrhoids.

　　7. Other systemic complications include non-specific arthritis, nodular erythema, gangrenous pyoderma, iritis, iridocyclitis, keratitis, stomatitis, and parotitis, as well as fatty liver, pericholangitis, and others.

　　People have noticed that this disease is related to oral enteric-coated potassium chloride tablets, enteric-coated aspirin, and other drugs. Therefore, those with a history of allergy to the aforementioned drugs or those who experience明显, severe gastrointestinal reactions after taking the aforementioned drugs should avoid using them or discontinue them promptly to prevent increasing the stimulation of the gastrointestinal tract and triggering the disease. Therefore, discontinuing or reducing the dosage of medication can play a preventive role in this disease.

　　1. X-ray examination Barium enema X-ray can detect intestinal stenosis and other lesions, but it is not easy to show ulcers. When there is intestinal obstruction, the X-ray film can show the expansion of small intestinal loops and liquid levels. Barium enema double-contrast X-ray of the small intestine can show ulcers, improve the diagnostic positive rate, and the lesions of the distal ileum can also be examined by enema.

　　2. Small bowel endoscopy can directly observe the lesion and take a biopsy.

　　Patients with primary small intestinal ulcers should avoid spicy and irritating foods such as chili, tobacco, and alcohol in their diet. They should also avoid eating hard, rough, and sticky foods. During the recovery period, patients should eat soft and easily digestible foods such as congee, soup, and egg custard. Gradually return to normal diet later. Pay attention to eating light, reducing the intake of greasy foods, and eggs, milk, dairy products, vegetables, and fruits can be consumed appropriately.

　　1. Treatment

　　For those who have been taking enteric-coated non-steroidal anti-inflammatory drugs or enteric-coated potassium chloride tablets for a long time, they should temporarily discontinue use. If the original disease requires medication, other medications or dosage forms can be changed after the disease is cured. Animal experiments have shown that prostaglandin analogs, such as misoprostol, can effectively prevent and treat gastrointestinal mucosal damage caused by non-steroidal anti-inflammatory drugs. Theoretically, they can also be used for the treatment of this disease, but its clinical efficacy still needs to be accumulated through a large number of case reports. Metronidazole is also recommended for the disease, based on the drug's ability to kill anaerobic bacteria and other pathogenic bacteria in the small intestine. There is currently no evidence to show that adrenal corticosteroid hormones are effective in treating this disease. Emergency surgical treatment should be performed if intestinal obstruction or perforation occurs. If medical treatment for gastrointestinal bleeding is ineffective, emergency angiography can be performed to determine the bleeding site, and local drug perfusion or embolization can be performed. If bleeding persists, surgical treatment can be performed. The main surgical procedure is the resection of the diseased intestinal segment and end-to-end anastomosis of the small intestine.

　　2. Prognosis

　　This disease is self-limiting. If it is caused by medication, discontinuing the medication that may cause the disease can lead to spontaneous healing of the lesion, and there is usually no recurrence after stopping the medication. Only a few cases may die due to diffuse peritonitis or massive hemorrhage caused by perforation, or accompanied by serious heart, lung, or brain diseases.