Radiation enteritis is intestinal damage caused by radiation treatment of pelvic, abdominal, and retroperitoneal malignancies, which can involve the small intestine, colon, and rectum, so it is also called radioactive rectal, colon, and small intestinal inflammation. The occurrence of this disease is related to the radiation dose per treatment, the total amount of radiation per course, the nutritional status of the patient, the presence or absence of surgical treatment and chemotherapy. Radiation disease is generally classified as acute or chronic according to the size of the radiation dose to the intestine, the duration, and the urgency of the onset. According to the location of the radiation source inside and outside the body, it is divided into external radiation disease and internal radiation disease. Clinically, the disease is most common in the rectum and sigmoid colon, and is characterized by abdominal pain, diarrhea, purulent stools, intestinal stricture, intestinal obstruction, fistula formation, and hypothermia.
I. Etiology and pathogenesis
It is generally believed that short-wavelength and high-frequency X-ray or γ-ray irradiation has sufficient energy to cause ionization of the absorbed tissue, which produces charged molecules or atoms, which in turn causes damage to living cells. While the kilovoltage X-rays used in the past often damaged the skin, the high-energy rays used in recent times are less likely to damage the skin, but have an increased risk of damaging the intestine. With experience, it has been recognized that radiation intestinal injury, especially to the colon and rectum, is a serious complication.
Factors affecting radiation injury are.
1, irradiation dose and treatment interval Although there is a direct relationship between the total radiation dose and the incidence of acute radiation injury, what is more important is the dose received at each time at the same site and the interval between each radiotherapy treatment. The higher the dose each time and the shorter the interval, the heavier the damage suffered by healthy cells and the less likely it is to repair the damage already formed before new damage is produced.
In addition, radiation-induced damage to the intestinal wall is also related to the extent of the irradiated intestinal canal. At the same dose, the smaller the extent, the less likely it is that radiation enteritis will occur.
3.Increased chance and effect of irradiation In clinical practice, some factors can increase the risk of radiation injury. These factors either increase the chance of radiation damage by increasing the exposure of normal tissues, or by increasing the effect of radiation. For example, thin older women have less soft tissue to protect themselves from radiation damage, and thus the dose to normal tissue at the irradiation site increases accordingly, and the likelihood of radiation damage increases. In patients with a history of abdominal or pelvic surgery, because of the adhesion of the intestine to the pelvic cavity, the adhered intestine is relatively fixed and cannot change with the change of body position. In addition, factors that can aggravate radiation damage include cardiovascular disease and chemotherapeutic drugs. In patients with vaso-occlusive disease, after radiation therapy, the blood vessels of the intestinal wall can be further occluded, aggravating ischemia and significantly increasing the chance of intestinal wall injury. Patients with hypertension, diabetes mellitus and cardiovascular disease at the time of radiotherapy are also significantly more likely to develop radiation enteritis. Although the use of chemotherapy drugs along with radiotherapy can improve the therapeutic effect, it can also increase the chance of tissue damage from both chemotherapy and radiotherapy.
The site of radiation enteritis depends mainly on the primary tumor site or the radiotherapy site. Since the pelvis is the most frequently used site for abdominal radiation therapy, and because of the poor mobility of the rectum, 70% to 90% of radiation enteritis occurs in the rectum. The more mobile colon, such as the cecum, sigmoid colon and transverse colon, can fall into the pelvic cavity and enter the radiation field during radiotherapy, which can also be accompanied by radiation colitis. The more fixed parts of the colon, such as the ascending and descending colon, rarely occur. In addition, 25%-30% of patients have small intestine radiation enteritis, especially those who have a history of abdominal or pelvic surgery and have adhesions between small intestine and pelvic intestine.
II. Epidemiology
Since 1980, the overall incidence of radiation enteritis has been on the rise due to the increase in patients receiving radiation therapy, the increase in radiation dose, and the increase in internal radiation exposure to avoid skin damage.
III. Clinical manifestations
The small intestine is the most sensitive to radiation in the gastrointestinal tract, and radiation enteritis is most common after radiotherapy for retroperitoneal, mesenteric, and pelvic cancers. The response to radiotherapy was dose-dependent. Those who received more than 3000 cGy had obvious lesions up to 90%, those who received 1000-3000 cGy had 40%, and those who received less than 1000 cGy had only 20%.
1.Local symptoms: The incidence of radiation enteritis varies according to the way, site, dose and time of receiving radiation, and the clinical manifestations vary in severity. Acute cases mostly appear during radiotherapy, late cases can occur up to 6 months after treatment, most of them 1 to 2 years after radiotherapy, and the longest has been reported in the literature up to 10 years after radiotherapy. Clinical symptoms of abdominal pain, diarrhea, urgency and blood in the stool may occur. Blood in the stool is associated with tissue necrosis and reduction of platelets, and the amount of bleeding is generally related to the radiation dose and individual response. Most patients have only non-severe diarrheal symptoms. Late onset patients may develop clinical symptoms of rectal stricture, ulceration, and necrosis, and severe cases may develop intractable nausea, vomiting, and diarrhea, leading to dehydration, decreased blood volume, vascular failure, and death. The gastrointestinal symptoms are initially due to toxemia caused by tissue necrosis, followed by progressive atrophy of the gastrointestinal mucosa, and finally, the intestinal mucosal villi are shed so that a large amount of plasma is lost in the intestinal lumen. If the patient can pass the acute phase of 4-6 days by supplementing a large amount of plasma and active symptomatic support treatment, the intestinal mucosa of the patient may regenerate, but the patient may be left with intestinal stricture.
2. Systemic symptoms: symptoms of systemic infection mostly occur in severe cases; malnutrition.
IV. Complications
Complications caused by radiation enteritis include intestinal stricture and intestinal obstruction, rectovaginal fistula, rectovaginal vesicovaginal fistula or ileo-bigot fistula, gastrointestinal ulcer and perforation, and induced colon and rectal cancer.
V. Examination.
1, rectal finger diagnosis: in the acute stage due to inflammation and inflammation of the anorectal area, the anal sphincter muscle spasm can be palpated, the rectal wall thickens and hardens, and the finger sleeve is blood-stained. In the later stage, patients can find rectal ulcers, rectal strictures or fistulas.
2.X-ray examination: In the early stage of radiation enteritis, abdominal plain film can show functional intestinal obstruction. Barium examination often shows mucosal edema, dilated intestinal collaterals and hypotonia. In the subacute stage, edema of the abdominal wall and intestinal mesentery can occur. In severe edema, the mucosal folds are thickened and straightened, giving a spiked appearance and separating the intestinal collaterals. On barium enema examination, severe spasm of the colon and rectum is common in the acute phase, and there may be isolated ulcers in the anterior rectal wall. If diffuse ulcers are present, the mucosa of the colonic and rectal walls may appear as spicula- tions. The barium examination of the later stage of chronic radioactive small bowel colitis reveals edema of the intestinal mucosa and separation of the intestinal collaterals. If further fibrosis occurs, the intestinal lumen is seen to be narrowed, fixed, and tubular, and there may be one or several segments of the intestinal canal that are less dilated, with loss of mucosal texture. This x-ray presentation resembles intestinal strictures caused by Crohn’s disease or colonic ischemic lesions. Functional small bowel obstruction can occur due to power dysfunction. In addition, X-ray manifestations of colon and rectal lesions include narrowing of the intestinal lumen, straightening and disappearance of the colonic pouch.
3, colonoscopy: changes in the acute phase of radiation enteritis, manifested in sigmoidoscopy as congestion and edema of the mucosa of the colon and rectum, indistinct vascular texture, and even ulcer formation, fragile mucosa, and easy bleeding when touched. In the chronic phase of radioenteritis, the mucosa is seen to be edematous, pale, granular, more fragile, and with obvious submucosal capillary dilation.
4. Mesenteric arteriogram: Small artery injury with ischemic changes is the pathological basis of radioactive intestinal stenosis, and abnormalities of small mesenteric artery branches are often seen on mesenteric arteriograms.
5.CT scan: It can show non-specific changes such as thickening of perirectal fibrous tissue or widening of presacral space or tumor recurrence.
6.Radionuclide examination: determination of the absorption rate of radioactive γ-labeled bile acids to determine the function of the terminal ileum, and determination of the increase in permeability to large molecules such as chromium-EDTA have some value in the diagnosis of acute radioactive small bowel inflammation, but because the specificity of these tests is not high, they are not widely used in clinical practice.
VI. Diagnosis
Patients with previous history of malignancy and receiving radiation therapy or accidental radiation, presenting with the above gastrointestinal symptoms, combined with relevant examinations and excluding other diseases can confirm the diagnosis of this disease. However, diagnosis is difficult or almost impossible in chronic radiators who are unaware of and neglect the presence of external exposure, and possible occupational exposure must be sought. Diagnosis is also quite difficult in self-reported radiation recipients due to possible mental or emotional factors, and cannot be confirmed unless the patient has written proof of receiving internal and external radiation doses.
VII. Treatment
The main treatment of acute radiation enteritis is symptomatic, while the treatment of chronic radiation enteritis is usually poor, and general medical treatment has been successful in only a few cases. Acute radiation enteritis or small bowel-colonitis is reversible and requires only supportive therapy, with a 10% reduction in radiation dose sufficient to reduce symptoms while still controlling the cancer. Prostaglandin E2 inhibitors have been reported in the literature to reduce diarrhea symptoms in patients. Chronic radiculitis is often associated with multiple intestinal strictures and requires some dietary changes, such as limiting fat and cow’s milk intake. Intravenous high-energy nutrition can change nutrition and immune function. Acute small bowel obstruction should be treated conservatively, even if chronic intestinal stenosis is obstructed, surgery should only be used as a last resort because the lesioned intestine is hypotonic and postoperative anastomotic fistula is likely to occur. Surgical resection of the diseased intestinal segment is preferable to short-circuit surgery, as the anastomotic fistula and morbidity and mortality rates are lower in the former than in the latter, while the incidence of perforation and fistula in the latter is high due to bacterial overgrowth. At present, most domestic and foreign advocate for home gastrointestinal nutrition (home, parenteral nutrition, HPN) treatment, and has achieved good results.
Oral 5-ASA and corticosteroid enemas can be used for radiation proctitis, and it has also been reported that enemas with aluminum thioglycollate (2g/20ml) have better efficacy. It has been reported that several courses of hyperbaric oxygen therapy can stop bleeding in rectal bleeding. In individual cases of severe rectal bleeding, coagulative necrosis caused by 3.6% formaldehyde irrigation can be reduced, and its effect is similar to that of formaldehyde for hemorrhagic cystitis, but this is only the experience of individual cases. Laser and electrocoagulation hemostasis can also be tried. Low rectal stenosis can be treated with paraffin oil lavage, short segment stenosis with balloon dilatation, and long segment stenosis still needs to be considered for surgical treatment. It has been reported that resection of the left hemicolectomy in the splenic flexure can avoid complications.
VIII. Prognosis
The prognosis depends on the radiation dose, dose rate and distribution in the body. In order to determine the prognosis, it is necessary to know the patient’s medical history in detail and to perform relevant tests on the patient’s blood and bone marrow.
Prevention
It has been reported that certain drugs such as sulfhydryl compounds given prior to radiation therapy can increase the survival rate of irradiated animals, but there are no prophylactic agents of practical value for humans. Elemental diets that remove glutelin lactose have been reported in the literature to relieve patient symptoms, increase body weight, and improve patient tolerance to radiation. The only effective way to avoid lethal or severe excess radiation is to strictly enforce protective measures and to strictly prohibit exceeding the maximum allowable dose. In addition, the use of small doses of multiple exposures may reduce the incidence of radiation enteritis.