Gastrointestinal complications such as constipation, fecal impaction, bowel obstruction, diarrhea, and radiation enteritis are common problems for patients with cancer. The growth and spread of cancer, as well as its treatment, contribute to these conditions.
This summary reviews the definitions, causes, assessment, and treatment of each of these common gastrointestinal side effects. For information about treatment-related nausea and vomiting, see Nausea and Vomiting Related to Cancer Treatment.
Constipation is the slow movement of feces through the large intestine that results in the passage of dry, hard stool. This condition can result in discomfort or pain.[1] The longer the transit time of stool in the large intestine, the greater the fluid absorption and the drier and harder the stool becomes.
Constipation may be annoying and uncomfortable, but fecal impaction can be life-threatening. Impaction is the accumulation of dry, hardened feces in the rectum or colon. The patient with a fecal impaction may present with circulatory, cardiac, or respiratory symptoms rather than with gastrointestinal symptoms.[2] If the fecal impaction is not recognized, the signs and symptoms may progress and result in death.
In contrast to constipation and impaction, a bowel obstruction is a partial or complete occlusion of the bowel lumen by a process other than fecal impaction. Intestinal obstructions can be classified by the type of obstruction, the obstructing mechanism, and the part of the bowel involved.
Diarrhea can occur throughout cancer care, and the effects can be physically and emotionally devastating. Although less prevalent than constipation, diarrhea remains a significant symptom burden for people with cancer. Specific definitions of diarrhea vary widely. Acute diarrhea is generally considered to be an abnormal increase in stool liquid and the passage of more than three unformed stools during a 24-hour period.[3] Diarrhea is considered chronic when it persists longer than 4 weeks. This condition can have a significant impact on quality of life and, if severe, may even be life-threatening. Furthermore, diarrhea can lead to increased caregiver burden.
Radiation enteritis is a functional disorder of the large and small bowel that occurs during or after a course of radiation therapy to the abdomen, pelvis, or rectum. One report also documented radiation-induced diarrhea in individuals with lung or head and neck cancers who were receiving radiation with or without chemotherapy.[4]
In this summary, unless otherwise stated, evidence and practice issues as they relate to adults are discussed. The evidence and application to practice related to children may differ significantly from information related to adults. When specific information about the care of children is available, it is summarized under its own heading.
Constipation can be a presenting symptom of cancer, or it can occur later as a side effect of a growing tumor or treatment of the tumor. For patients with cancer, other causative factors include the following:[1,2]
Any of these factors can occur because of the disease process, aging, debilitation, or treatment.
Constipation is frequently the result of autonomic neuropathy caused by vinca alkaloids, oxaliplatin, taxanes, and thalidomide. Other drugs, such as opioid analgesics and anticholinergics (including antidepressants and antihistamines), may lead to constipation by causing decreased sensitivity to the defecation reflex and decreased gut motility. Because constipation is common with the use of opioids, a bowel regimen should be initiated when opioids are prescribed and continued for as long as the patient takes them. Opioids produce varying degrees of constipation, suggesting a dose-related phenomenon. One study suggested that clinicians should not prescribe laxatives based on the opioid dose, but rather should titrate the laxative according to bowel function. Lower doses of opioids or weaker opioids, such as codeine, are just as likely to cause constipation as higher doses and stronger opioids.[3] For more information about opioid-induced constipation, see the Constipation section in Cancer Pain.
A normal bowel pattern is having at least three stools per week and no more than three stools per day; however, these criteria may be inappropriate for patients with cancer.[4,5]
The following questions may provide a useful assessment guide:
A thorough history of the patient’s bowel pattern, dietary changes, and medications, along with a physical examination, can identify possible causes of constipation. The evaluation also includes assessment of associated symptoms such as distention, flatus, cramping, or rectal fullness. The following tests may be part of the clinical evaluation:[6]
Physical assessment will determine the presence or absence of bowel sounds, flatus, or abdominal distention. Patients with colostomies are assessed for constipation. Dietary habits, fluid intake, activity levels, and use of opioids in these patients are examined.
Comprehensive management of constipation includes prevention (if possible), elimination of causative factors, and judicious use of laxatives. Some patients can be encouraged to increase dietary fiber (fruits; green, leafy vegetables; 100% whole-grain cereals and breads; and bran) and to drink eight 8-oz. (240-mL) glasses of fluid daily unless contraindicated. For more information, see Nutrition in Cancer Care.
The following interventions may be done before or with the use of pharmacological agents:
Rectal agents should be avoided in patients with cancer at risk of thrombocytopenia, leukopenia, and/or mucositis from cancer and its treatment. In immunocompromised patients, manipulation of the rectum and anus should be avoided (i.e., no rectal examinations, no suppositories, and no enemas). These actions can lead to the development of anal fissures or abscesses, which are portals of entry for infection. Also, the stoma of a patient with neutropenia should not be manipulated unnecessarily.
Transanal irrigation is a procedure in which water is introduced into the bowel through the anus. A systematic review suggested that this procedure may be beneficial for patients with neurogenic bowel disease, low anterior resection syndrome, fecal incontinence, and chronic constipation. However, its efficacy is unknown in patients with cancer who have constipation.[7]
There are different medical agents used to treat constipation. Table 1 lists these agents in more detail.
| Name | Action | Caution/Side Effects | Onset | Selected Drugs/Dosages | |
|---|---|---|---|---|---|
| GI = gastrointestinal; IBS = irritable bowel syndrome; N/A = not applicable; PO = orally. | |||||
| Bulk producers | Natural or semisynthetic polysaccharide and cellulose that work with the body’s natural processes to hold water in intestinal tract, soften stool, and increase frequency of stool passage. | To reduce risk of bowel obstruction, take with two 8-oz. (240-mL) glasses of water and maintain adequate hydration. | 12–24 h (may be delayed up to 72 h) | Methylcellulose: 2 g dissolved in 8-oz. (240-mL) glass of water PO up to three times daily. Increase as needed by 2 g. | |
| Avoid if fecal impaction or intestinal obstruction is suspected. | |||||
| Not advised for opioid-induced constipation. | Psyllium: 2.5-30 g PO daily in divided doses. | ||||
| Saline laxatives | High osmolarity attracts water into lumen of the intestines. Fluid accumulation alters stool consistency, distends bowel, and induces peristaltic movement. | Repeated use can alter fluid and electrolyte balance. | 0.5–6 h | Magnesium sulfate: 10–20 g dissolved in 8-oz. (240-mL) glass of water orally. May repeat in 4 h. Do not exceed two doses daily. | |
| Magnesium hydroxide: | |||||
| – 400 mg/5 mL liquid: 30–60 mL/day once daily at bedtime or divided. | |||||
| – 800 mg/5 mL liquid: 15–30 mL/day once daily at bedtime or divided. | |||||
| – 1,200 mg/5 mL liquid: 10–20 mL/day once daily at bedtime or divided. | |||||
| Avoid magnesium-containing laxatives in patients with renal dysfunction. Avoid sodium-containing laxatives in patients with edema, congestive heart failure, megacolon, or hypertension. | Magnesium citrate: 195–300 mL as single dose or divided doses over 24 h. | ||||
| Used to clear bowels for rectal or bowel examination. | Sodium phosphate enemas can cause acute phosphate nephropathy. Cramps may occur. | Sodium phosphate: 4.5-oz. enema as single dose. | |||
| Stimulant laxatives | Increase motor activity of bowels by direct action on smooth muscle of the intestine. | Prolonged use causes laxative dependency and loss of normal bowel function. | 6–24 h (oral), 0.25-1 h (bisacodyl suppository) | Sennosides: 17.2–34.4 mg PO once or twice daily. | |
| Bisacodyl must be excreted in bile to be active and is not effective with biliary obstruction or diversion. Avoid bisacodyl with known or suspected ulcerative lesions of the colon. May cause cramping. | |||||
| Used to clear bowels for rectal or bowel examination. | Avoid taking bisacodyl within 1 h of taking antacids, milk, or cimetidine; causes premature dissolving of enteric coating, which results in gastric or duodenal stimulation. | Bisacodyl: 5–15 mg PO once daily or 10-mg suppository once daily. | |||
| Lubricant laxatives | Lubricate intestinal mucosa and soften stool to help prevent straining in patients for whom straining would be dangerous. | Give on empty stomach at bedtime. Mineral oil prevents absorption of oil-soluble vitamins and drugs. | 6–8 h (oral), 2-15 min (rectal) | Mineral oil (oral): | |
| With older patients, avoid mineral oil due to aspiration potential that can cause lipid pneumonitis. | |||||
| Can interfere with postoperative healing of anorectal surgery. | – Nonemulsified: 15–45 mL in 24 h. | ||||
| – Emulsified: 30–90 mL daily as single dose or divided. | |||||
| Avoid giving with docusate sodium, which causes increased systemic absorption of mineral oil. | Mineral oil (rectal): 118 mL as single dose. | ||||
| Fecal softeners | Promote water retention, softening stool to prevent straining; most beneficial when stool is hard. Stool softeners and emollient laxatives are of limited use because of colonic resorption of water from the forming stool. | May increase systemic absorption of mineral oil when administered together. | Up to 3 d | Docusate sodium: 50–240 mg taken with full glass of water. | |
| Docusate calcium: 240 mg daily until bowel movement is normal. | |||||
| Not used as sole regimen but may be useful in combination with stimulant laxatives. | Docusate potassium: 100–300 mg daily until bowel movement is normal; increase daily fluid intake. | ||||
| Lactulose | Synthetic disaccharide that passes to colon undigested. When broken down in colon, it produces lactic acid, formic acid, acetic acid, and carbon dioxide. These products increase osmotic pressure, increasing amount of water held in stool, which softens stool and increases frequency of passage. | Excessive amounts may cause diarrhea with electrolyte losses. | 24–48 h | 10–20 g PO daily; may increase to 40 g daily. | |
| Avoid in patients with acute abdomen, fecal impaction, or bowel obstruction. | |||||
| Polyethylene glycol and electrolytes | Used to clear bowel with minimal water and sodium loss or gain. | Contraindicated in patients with bowel obstruction. | 24–96 h | 17 g dissolved in 4-8 oz. (120–240 mL) of beverage once daily. | |
| Opioid antagonists | Restricted ability to cross blood-brain barrier. | Give only if other drugs have failed. Contraindicated in patients with bowel obstruction. | In a study of patients with advanced, cancer and other diseases, about 50% of patients defecated within 4 h of receiving the injection.[8,9] | Naloxone: Oral oxycodone: naloxone combination in ratio of 2:1[10] | |
| Methylnaltrexone: Subcutaneous 0.15 mg/kg daily or every other day to treat opioid-induced constipation. | |||||
| Naldemedine: 0.2 mg PO daily for 2 wk[11] | |||||
| Block opioid receptors peripherally in the GI tract to reverse opioid-induced decreases in intestinal motility. | Side effects: Dizziness, nausea, abdominal pain, flatulence, diarrhea. | No evidence of withdrawal or other central effects of the opioid; pain scores remained unchanged. | Naloxegol: 12.5–25 mg PO daily | ||
| Lubiprostone | Chloride channel activator that acts to increase intestinal fluid secretion and improve fecal transit, bypassing antisecretory effects of opiates. | Contraindicated in patients with bowel obstruction. | 24–48 h in chronic constipation.[12] | 24 µg PO twice daily (8 µg PO twice daily in IBS). | |
| Dyspnea and chest tightness may occur within 30-60 min of first dose and resolve within a few hours. Syncope and hypotension, some requiring hospitalization, may also occur. | |||||
| Used for chronic idiopathic constipation, IBS with constipation, and opioid-induced constipation. | Side effects: Diarrhea, nausea, headache, abdominal pain. | ||||
| Linaclotide | Guanylate cyclase-C agonist that causes increased chloride and bicarbonate secretion into the intestinal lumen, leading to increased intestinal fluid and GI transit. | Contraindicated in patients <2 y and in patients with mechanical GI obstruction. | N/A | 145 µg PO daily (72 µg PO daily for tolerability or 290 µg PO daily in IBS). | |
| May cause severe diarrhea associated with syncope, hypertension, and electrolyte abnormalities. | |||||
| Used for chronic idiopathic constipation, IBS with constipation. | Side effects: Diarrhea, headache, abdominal pain. | ||||
| Prucalopride | Selective 5-HT4 receptor agonist that stimulates peristaltic reflux and increases intestinal secretions and GI motility. | Contraindicated in patients with intestinal perforation or obstruction due to structural or functional disorder of the gut wall, obstructive ileus, or severe inflammatory conditions of the GI tract. | N/A | 2 mg PO daily | |
| Used for chronic idiopathic constipation. | Side effects: Diarrhea, nausea, headache, abdominal pain. | ||||
Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available.
Constipation, if left untreated, may lead to fecal impaction. The causes of impaction are the same as the causes of constipation.[1] For more information, see the Causes of Constipation section.
The patient may exhibit symptoms similar to those of constipation or present with symptoms unrelated to the gastrointestinal system. If the fecal impaction presses on the sacral nerves, the patient may experience back pain. If the impaction presses on the ureters, bladder, or urethra, urinary symptoms, such as urinary retention or increased or decreased frequency or urgency of urination, may develop.
When abdominal distention occurs, movement of the diaphragm may be compromised, which can lead to insufficient aeration with subsequent hypoxia and/or left ventricular dysfunction. Hypoxia can, in turn, precipitate angina or tachycardia. If the vasovagal response is stimulated by the pressure of impaction, the patient may become dizzy and hypotensive.
Movement of stool around the impaction may result in diarrhea, which can be explosive. Coughing or activities that increase intra-abdominal pressure may cause leakage of stool. The leakage may be accompanied by nausea, vomiting, abdominal pain, and dehydration and is virtually diagnostic of the condition. The patient with an impaction may present in an acutely confused and disoriented state, with signs of tachycardia, diaphoresis, fever, elevated or low blood pressure, and/or abdominal fullness or rigidity.
Assessment of fecal impaction includes the same questions as for the patient with constipation. Additional assessment includes auscultation of bowel sounds to determine if they are present, absent, hyperactive, or hypoactive. The abdomen is inspected for distention and gently palpated for any masses, rigidity, or tenderness. A rectal examination will determine the presence of stool in the rectum or sigmoid colon. An abdominal x-ray (flat and upright) will show loss of haustral markings, gas patterns reflecting gross amounts of stool, and dilatation proximal to the impaction.[2] For more information, see the Assessment of Constipation section.
The primary treatment of impaction is to hydrate and soften the stool so that it can be removed or passed. Enemas (oil retention, tap water, or hypertonic phosphate) lubricate the bowel and soften the stool. Caution must be exercised in that fecal impaction can irritate the bowel wall, and excess enemas may perforate the bowel. The patient may need to be digitally disimpacted if the stool is within reach. This is best done after administering an enema to lubricate the bowel.
Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available.
There are four types of bowel obstruction that include the following:
The obstructing mechanism can be extrinsic or intrinsic.[1]
Extrinsic causes include the following:
Intrinsic causes include the following:
Bowel obstructions are more common in the small intestine than in the colon.[3] Bowel obstructions are frequently seen in the ileum. Small bowel obstructions are often caused by adhesions or hernias, while large bowel obstructions are usually caused by carcinomas, volvulus, or diverticulitis. The presentation of obstruction will relate to whether the small or large intestine is involved.
The most common malignancies that cause bowel obstruction are cancers of the colon, stomach, and ovary.[3] Patients who have had abdominal surgery or abdominal radiation are also at higher risk of developing bowel obstruction. Bowel obstructions are most common during advanced stages of disease.
Possible symptoms of malignant bowel obstruction include abdominal pain, cramps, distention, nausea, vomiting, absence of gas and stool passage, and, rarely, overflow diarrhea.[3] A complete blood cell count, electrolyte panel, and urinalysis are obtained to evaluate fluid and electrolyte imbalance and/or sepsis. An elevated white blood cell count (15,000–20,000/mm3) suggests bowel necrosis.
Traditionally, flat and upright abdominal films have been used for diagnosis. However, x-rays have only modest sensitivity to detect a bowel obstruction and limited ability to detect the exact site, cause, or complications. Contrast computed tomography (CT) delivers enhanced diagnostic precision. A CT of the abdomen and pelvis with intravenous contrast and/or a CT enterography may be used to diagnose patients suspected of having a small bowel obstruction.[4,5]
Careful serial examinations are necessary to manage patients with progressive abdominal symptoms that may be due to acute bowel obstruction. The principles of supportive care in this setting include bowel rest, volume resuscitation, correction of electrolyte imbalances, and transfusion support if necessary. These measures may precede or accompany decompression efforts.
When bowel obstruction is partial, decompression of the distended bowel may be attempted with nasogastric tubes (NGTs) or intestinal tubes. The use of these tubes may reduce edema, relieve fluid and gas accumulation, or decrease the need for multiple stage procedures.[6] However, surgery may be necessary within 24 hours if there is complete, acute obstruction. The use of self-expandable stents to decompress complete, acute malignant bowel obstruction has been noted to decrease the frequency of unnecessary surgery. The stents permit staging of the disease, increase the rate of primary anastomosis relative to colostomy, and decrease morbidity in patients with left-sided colon and rectal malignancies. Further study is warranted, including cost analysis.[7]
Patients with advanced cancer may have chronic, progressive bowel obstruction that is inoperable.[8,9] The most frequent causes of inoperability are extensive tumor and multiple partial obstructions.[10,11][Level of evidence: II][12] A retrospective review evaluated surgical palliation of malignant bowel obstruction secondary to peritoneal carcinomatosis in 63 patients with nongynecological cancers. The ability to tolerate solid food at hospital discharge was the criterion for successful palliation. Multiple logistic regression analysis identified the absence of ascites and obstruction not involving the small bowel as predictors of successful surgical palliation in this population. Successful palliation was achieved in 45% of patients and was maintained in 76% of this group at a median follow-up of 78 days, for an overall success rate of 35%. The postoperative mortality rate was 15%, and postoperative complications occurred in 44% of patients.[13]
For some patients with malignant obstructions of the gastrointestinal tract, the use of expandable metal stents may provide palliation of obstructive symptoms. Esophageal, biliary, gastroduodenal, and colorectal stents are available.[7,14-19] They may be placed under endoscopic guidance, with or without fluoroscopy, or by an interventional radiologist using fluoroscopy. Morbidity with stent placement may be lower than with surgery. Adequate imaging of the stricture itself and the gastrointestinal tract distal to the stricture is recommended to assess stricture length, detect multifocal disease, and determine the appropriateness of stenting.[20,21][Level of evidence: II][22]
When neither surgery nor stenting is possible, the accumulation of the unabsorbed secretions produce nausea, vomiting, pain, and colicky activity as a result of the partial or complete occlusion of the lumen. In this case, temporary decompression may be accomplished using an NGT; however, NGTs are not favored as a long-term solution.[3] Instead, a gastrostomy tube is commonly used to provide decompression of air and fluid that may accumulate and cause visceral distention and pain. The gastrostomy tube is placed into the stomach and is attached to a drainage bag that can be easily concealed under clothing. When the valve between the gastrostomy tube and the bag is open, the patient may be able to eat or drink by mouth without creating discomfort since the food is drained directly into the bag. Dietary discretion is advised to minimize the risk of tube obstruction by solid food. If the obstruction improves, the valve can be closed, and the patient may once again benefit from enteral nutrition.
Sometimes, decompression is difficult even with a gastrostomy tube in place. Accumulation of fluid may interfere with decompression because several liters of gastrointestinal secretions may be produced per day. Pharmacological symptom management may be necessary. In the case of complete obstruction, avoid oral administration of medications if possible. To relieve continuous abdominal pain, opioid analgesics may be necessary. Associated nausea and vomiting may be treated with several different medications, including scopolamine, octreotide, dexamethasone, haloperidol, metoclopramide, dimenhydrinate, prochlorperazine, serotonin antagonists, and olanzapine.[3] Effective antispasmodics in this situation include anticholinergics (such as scopolamine) [23] and possibly corticosteroids, as well as centrally acting agents.
Careful use of laxatives may be considered for constipation associated with partial bowel obstruction. However, a 2022 systematic review did not identify any studies that examined laxatives in this setting.[3] Osmotic laxatives, such as polyethylene glycol 3350, pull water into the lumen of the bowel, softening stool and increasing peristalsis. Bulk-forming laxatives such as psyllium should be avoided because they increase stool volume and can worsen the obstruction. Finally, manual disimpaction may be necessary if fecal impaction is noted during physical examination.
Another option for management of refractory pain and/or nausea is the synthetic somatostatin analogue octreotide. This agent inhibits the release of several gastrointestinal hormones and reduces gastrointestinal secretions.[24,25][Level of evidence: I][26]
Octreotide is usually given subcutaneously at 50 to 200 µg three times per day and may reduce the nausea, vomiting, and abdominal pain of malignant bowel obstruction. For select patients in whom octreotide alone is ineffective, the addition of an anticholinergic such as scopolamine may help reduce the associated painful colic of malignant bowel obstruction. When either scopolamine or octreotide is used alone, each is ineffective.[14,27-29] Corticosteroids are widely used to treat bowel obstruction, but empirical support is limited.[30]
Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available.
The prevalence and severity of diarrhea in patients with cancer vary greatly. Some chemotherapeutic regimens, particularly those containing fluoropyrimidines or irinotecan, are associated with diarrhea rates as high as 50% to 80%.[1] Gastrointestinal toxicity, ranging from diarrhea to severe colitis, is an immune-related adverse effect associated with immune checkpoint inhibitor (ICI) treatment. The rate of diarrhea appears to be dose dependent with anti-CTLA-4 inhibitors and greater with dual checkpoint inhibitor regimens compared with a single agent.[2,3] Rates of any grade diarrhea are 16% to 37% for single-agent PD-L and PD-L1, 32% to 49% for single-agent anti-CTLA-4, and 17% to 44% for dual ICI regimens.[4-6] Diarrhea is also commonly observed in patients with carcinoid tumors who are receiving radiation therapy to abdominal/pelvic fields or undergoing bone marrow transplantation or surgical intervention of the gastrointestinal tract.[7] In a large heterogeneous sample of patients with cancer in various stages of treatment, the prevalence of moderate-to-severe diarrhea was 14%.[8] Among children with cancer during the last month of life, 19% experienced diarrhea.[9]
The consequences of diarrhea can be significant and life-threatening. According to the National Cancer Institute’s (NCI’s) Common Terminology Criteria for Adverse Events, more than half of patients who received chemotherapy for colorectal cancer experienced diarrhea of grade 3 or 4, requiring treatment changes or the reduction, delay, or discontinuation of therapy (see Table 2).[10,11] A review of several clinical trials of irinotecan plus high-dose fluorouracil and leucovorin for colorectal cancer treatment revealed early death rates of 2.2% to 4.8%, primarily due to gastrointestinal toxicity.[12] With the advent of more aggressive anticancer therapies, the potential physical and psychosocial consequences of diarrhea and its indirect effect on cancer treatment outcomes are likely to expand.[13]
| Grade | Description |
|---|---|
| ADL = activities of daily living. | |
| aAdapted from National Cancer Institute.[11] | |
| bDefinition: A disorder characterized by an increase in frequency and/or loose or watery bowel movements. | |
| cInstrumental ADL refers to preparing meals, shopping for groceries or clothes, using the telephone, managing money, etc. | |
| dSelf-care ADL refers to bathing, dressing and undressing, feeding oneself, using the toilet, taking medications, and not being bedridden. | |
| 1 | Increase of <4 stools/day over baseline; mild increase in ostomy output compared with baseline |
| 2 | Increase of 4–6 stools/day over baseline; moderate increase in ostomy output compared with baseline; limiting instrumental ADLc |
| 3 | Increase of ≥7 stools/day over baseline; hospitalization indicated; severe increase in ostomy output compared with baseline; limiting self-care ADLd |
| 4 | Life-threatening consequences; urgent intervention indicated |
| 5 | Death |
In patients being treated for cancer, diarrhea is most commonly induced by therapy.[14] Conventional methods of diarrhea-causing treatment include the following:
Other causes of acute diarrhea include the following:[15]
Typical infections are of viral, bacterial, protozoan, parasitic, or fungal etiology. They may also be caused by pseudomembranous colitis, which often does not respond to treatment.[7] Clostridium difficile is a common cause of pseudomembranous colitis.
Other causes of diarrhea in patients with cancer include the underlying cancer, responses to diet, or concomitant diseases (see Table 3). Common causes of diarrhea in patients receiving palliative care are difficulty adjusting the laxative regimen and impaction leading to leakage of stool around the fecal obstruction.
Surgery, a primary treatment modality for many cancers, can affect the body by mechanical, functional, and physiological alterations. Postsurgical complications of gastrointestinal surgery that affect normal bowel function may contribute to diarrhea.[16]
Certain chemotherapeutic agents can alter normal absorption and secretion functions of the small bowel, resulting in treatment-related diarrhea (see Table 3 and Table 5). Patients who are receiving concomitant abdominal or pelvic radiation therapy or recovering from recent gastrointestinal surgery will often experience more severe diarrhea.
Radiation therapy to abdominal, pelvic, lumbar, or para-aortic fields can result in changes to normal bowel function. Factors contributing to the occurrence and severity of intestinal complications include the following:
Acute intestinal side effects occur at approximately 10 Gy and may last up to 8 to 12 weeks posttherapy. Chronic radiation enteritis may occur months to years after therapy ends. This condition necessitates dietary modification, pharmacological management, and, in some instances, surgical intervention. For more information, see the Radiation Enteritis section.
Graft-versus-host disease (GVHD) is a major complication of allogeneic transplantation. It commonly affects the intestinal tract, skin, and liver. Symptoms of gastrointestinal GVHD include nausea and vomiting, severe abdominal pain and cramping, and watery diarrhea.[17] The volume of accompanying GVHD-associated diarrhea may reach up to several liters per day and is an indicator of the degree and extent of mucosal damage.[17] Acute GVHD is usually manifested within 100 days posttransplant, although it can occur as early as 7 to 10 days posttransplant. It may resolve or develop into a chronic form requiring long-term treatment and dietary management.
| Cancer [18,19] | Carcinoid syndrome |
| Colon cancer | |
| Lymphoma | |
| Medullary carcinoma of the thyroid | |
| Pancreatic cancer, particularly islet cell tumors (Zollinger-Ellison syndrome) | |
| Pheochromocytoma | |
| Surgery or procedure [20] | Celiac plexus block |
| Cholecystectomy, esophagogastrectomy | |
| Gastrectomy, pancreaticoduodenectomy (Whipple procedure) | |
| Intestinal resection (malabsorption due to short bowel syndrome) | |
| Vagotomy | |
| Chemotherapy | See Table 4 for more information. |
| Radiation therapy (For more information, see the Radiation Enteritis section.) [21] | Irradiation to the abdomen, para-aortics, lumbar, and pelvis or radiation for lung and head and neck cancers |
| Bone marrow transplantation [22] | Conditioning chemotherapy, total-body irradiation, graft-versus-host disease after allogeneic bone marrow or peripheral blood stem cell transplants |
| Drug adverse effects [18,19] | Antibiotics, magnesium-containing antacids, antihypertensives, colchicine, digoxin, lactulose, laxatives, methyldopa, metoclopramide, misoprostol, potassium supplements, propranolol, theophylline |
| Concurrent disease [18,19] | Diabetes, hyperthyroidism, inflammatory bowel disease (Crohn disease, diverticulitis, gastroenteritis, HIV/AIDS, ulcerative colitis), obstruction (tumor related) |
| Infection [23] | Clostridium difficile, Clostridium perfringens, Bacillus cereus, Giardia lamblia, Cryptosporidium, Salmonella, Shigella, Campylobacter, Rotavirus |
| Fecal impaction [18,19] | Constipation leading to obstruction |
| Diet [18,19] | Alcohol, milk, dairy products (particularly in patients with lactose intolerance) |
| Caffeine-containing products (coffee, tea, chocolate); specific fruit juices (prune juice, unfiltered apple juice, sauerkraut juice) | |
| High-fiber foods (raw fruits and vegetables, nuts, seeds, whole-grain products, dried legumes); high-fat foods (deep-fried foods, high fat–containing foods) | |
| Lactulose intolerance or food allergies | |
| Sorbitol-containing foods (candy and chewing gum); hot and spicy foods; gas-forming foods and beverages (cruciferous vegetables, dried legumes, melons, carbonated beverages) | |
| Psychological factors [19] | Stress |
Some chemotherapeutic agents result in grade 3 or 4 treatment-related diarrhea. Table 4 and Table 5 list the toxicity of intravenous and oral agents used to treat cancer, respectively.
| Chemotherapy Agent | Grade 3 or 4 Diarrhea Rate (%)b | Reference |
|---|---|---|
| aIncludes drugs with 5% or greater grade 3 or 4 toxicity. | ||
| bHighest percentage listed in current manufacturer prescribing information (single-agent rate of diarrhea listed if provided; excludes irinotecan-based combinations). | ||
| Irinotecan | 31 | [24] |
| Ziv-aflibercept | 19 | [24] |
| Irinotecan, liposomal | 13 | [24] |
| Fluorouracil | 12.7 | [25] |
| Clofarabine | 12 | [24] |
| Pertuzumab | 12 | [24] |
| Ipilimumab + nivolumab | 11 | [24] |
| Bortezomib | 7 | [24] |
| Atezolizumab | 6 | [24] |
| Azacitidine | 6 | [24] |
| Brentuximab vedotin | 6 | [24] |
| Cabazitaxel | 6 | [24] |
| Docetaxel | 6 | [24] |
| Nab-paclitaxel | 6 | [24] |
| Cetuximab | 5 | [24] |
| Copanlisib | 5 | [24] |
| Elotuzumab | 5 | [24] |
| Ipilimumab | 5 | [24] |
| Nivolumab | 5 | [24] |
| Busulfan | 5 | [26] |
| Chemotherapy Agent | Grade 3 or 4 Diarrhea Rate (%)b | Reference |
|---|---|---|
| aIncludes drugs with 5% or greater grade 3 or 4 toxicity. | ||
| bHighest percentage listed in current manufacturer prescribing information (single-agent rate of diarrhea listed if provided; excludes irinotecan-based combinations). | ||
| Selumetinib | 24 | [24] |
| Tucatinib (with capecitabine/trastuzumab) | 13 | [27,28] |
| Vandetanib | 10–11 | [29,30] |
| Umbralisib | 10 | [31] |
| Vorinostat | 5–8 | [32,33] |
| Sunitinib | 4–10 | [24] |
| Sotorasib | 4 | [34,35] |
| Selinexor | 3–7 | [36-38] |
| Sorafenib | 2–8 | [39-41] |
Rapid yet thorough assessment of diarrhea is imperative because of its potentially life-threatening nature. Few standardized assessment tools are available. As a result, standardized assessment is rare in the clinical setting.[7] For a complete assessment, one author suggests obtaining background information from the patient that includes the type and extent of the patient’s cancer, anticancer treatment, comorbid factors, coexisting symptoms, patient and provider perceptions, and a thorough description of the diarrhea. Stringent monitoring conducted at least weekly is indicated during therapy using chemotherapeutic agents known to cause diarrhea.[12] The NCI’s Common Terminology Criteria for Adverse Events (see Table 2) evaluate diarrhea by the following:[11]
The patient history also includes questions regarding the frequency of bowel movements during the past 24 hours, the character of the fecal material, and the time course of the development of diarrhea.[42] A visual tool to assist patients and families in characterizing the consistency of the stool has been developed.[43] Six diagrams illustrate fecal material consistency ranging from well-formed, formed, and semiformed to loose, very loose, and liquid.
Patients are questioned regarding related symptoms that might indicate hemodynamic compromise or the underlying etiology. Specific questions include information about the following:
These symptoms are classified as complicated or uncomplicated, with therapy based on these classifications.[44]
Uncomplicated diarrhea includes grade 1 or 2 diarrhea with no other signs or symptoms. Management is conservative.
Complicated diarrhea includes grade 1 or 2 diarrhea with any one of the following risk factors:
Grade 3 or 4 diarrhea is also classified as complicated. Thorough evaluation and close monitoring is warranted.[44]
The time course of diarrhea and concomitant symptom development are key to determining the underlying etiology.[42] Medication and dietary intake, as well as a history of recent travel, may provide additional clues. Weight loss and reduced urine output provide additional data regarding the severity of the effects of diarrhea.
The goal of physical examination is to identify potential causes of diarrhea and its complications as quickly as possible to reduce morbidity. The physical examination includes vital signs and evaluation of skin turgor and oral mucosa to assess hemodynamic status and dehydration. Abdominal examination includes evaluation for rebound tenderness, guarding, hypoactive or hyperactive bowel sounds, and stool collection. A rectal exam can rule out fecal impaction but is performed judiciously in neutropenic or thrombocytopenic patients.[18]
Laboratory tests may include the following:[18]
In some cases, radiographic procedures are conducted to identify ileus, obstruction, or other abnormalities. In rare cases, endoscopy may be indicated.
A review analyzed early toxic deaths in two NCI-sponsored cooperative trials of irinotecan plus high-dose fluorouracil and leucovorin for advanced colorectal cancer. It led to the revision of clinical practice guidelines for the treatment of cancer treatment–induced diarrhea, with a heightened emphasis on assessment and early aggressive interventions. The guidelines distinguish between uncomplicated and complicated diarrhea.[44]
The treatment of cancer-related diarrhea is often empiric and nonspecific. Whenever possible, treat underlying causes such as fecal impaction or modify the stimulant laxative regimen as necessary. Medications such as bulk laxatives and promotility agents (e.g., metoclopramide) are discontinued. Dietary changes are commonly made to stop or lessen the severity of cancer treatment–related diarrhea.[10,22,45] In some cases, these changes include advising patients to eat small, frequent meals and avoid the following:[46]
When experiencing diarrhea, patients are encouraged to increase their intake of clear liquids to at least 3 L per day (e.g., water, sports drinks, broth, weak decaffeinated teas, caffeine-free soft drinks, clear juices, and gelatin).[15,47] For more information, see the Behavioral strategies for symptom management section in Nutrition in Cancer Care.
Some case reports suggest the efficacy of glutamine in relieving diarrhea and other gastrointestinal symptoms associated with cancer therapy. However, a randomized controlled trial that used oral glutamine to prevent pelvic radiation-induced diarrhea did not show any benefit.[48][Level of evidence: I][49,50]
The goals of pharmacological therapy include inhibition of intestinal motility, reduction in intestinal secretions, and promotion of absorption. Absorbents include agents that form a gelatinous mass that gives density to fecal material. Methylcellulose and pectin are most commonly used, but little data support their efficacy. Some patients may not tolerate these bulk-forming agents because of the large volume required for therapeutic effect and the associated abdominal discomfort and bloating. Adsorbents such as kaolin, clays, and activated charcoals have been used extensively, but no data support their use. Furthermore, they may inhibit absorption of other oral antidiarrheals.
Opioids bind to receptors within the gastrointestinal tract and reduce diarrhea by reducing transit time. Loperamide is the most common opioid used, due to its availability and reduced effect on cognition, although codeine and other opioids can also be effective.[42] Common loperamide doses begin with 4 mg, followed by 2 mg after each unformed stool, with a maximum of approximately 12 mg/day.[18,42] Regardless of the dose, however, loperamide may be less effective in patients with grade 3 or 4 diarrhea.[51][Level of evidence: I]
Mucosal prostaglandin inhibitors, also referred to as antisecretory agents, include the following:
Other pharmacological therapies for the relief of diarrhea may be specific to the underlying mechanism. Delayed diarrhea (>24 hours) occurs with irinotecan. In a small study, six of seven patients obtained relief with oral neomycin (1,000 mg three times daily). This relief occurred without reduction in the active metabolite of irinotecan, SN-38. Thus, the poorly metabolized antibiotic did not alter the efficacy of the chemotherapeutic agent.[52][Level of evidence: II] In another small study, 37 patients with non-small cell lung cancer received irinotecan. Investigators alkalized the patients' feces through oral administration of sodium bicarbonate, basic water, and ursodeoxycholic acid, while speeding transit time of the drug metabolites (thought to reduce damage to the intestinal lumen by reducing stasis of the drug) using magnesium oxide. The incidence of delayed diarrhea was significantly reduced in this group when compared with 32 patients who received the same chemotherapeutic regimen without oral alkalization and controlled defecation.[53][Level of evidence: III]
In addition to antidiarrheal agents and immunosuppressive medications, a specialized, five-phase dietary regimen may be started to effectively manage diarrhea associated with GVHD:[22]
Probiotics are nutritional supplements that contain a defined amount of viable microorganisms and, upon administration, confer a benefit to the patient.[54] The use of probiotic functional foods (beneficial live microorganisms) to modify gut microflora has been suggested in clinical conditions associated with diarrhea, gut-barrier dysfunction, and inflammatory response.[55] There are a vast number of different strains of probiotics; however, much of the clinical research has investigated species belonging to the families of Lactobacillus and Bifidobacterium. Probiotics have been promoted for the following:[56-62][Level of evidence: I]
In a double-blind, randomized, controlled trial, 450 adults with cancer who were receiving radiation to the pelvic region were randomly assigned to receive the blend probiotic product VSL #3 or placebo during radiation therapy. The authors reported a decrease in the incidence and severity of diarrhea. No adverse events were reported.[63]
Patients with complicated diarrhea may require further evaluation and more aggressive management. When patients are receiving chemotherapy, additional evaluation includes stool testing (including blood, fecal leukocytes, C. difficile, Salmonella, E. coli, Campylobacter, and infectious colitis), complete blood count, and electrolyte profile.[44] This workup and treatment is also considered for patients who progress to grade 3 or 4 diarrhea while taking loperamide.
The patient's symptoms will determine the level of care and type of treatments. A panel of experts suggested that severe radiation therapy–induced diarrhea may not require hospitalization. An alternative outpatient unit or intensive home care nursing may be able to provide the same level of care and monitoring.[44] The same panel recommended intravenous fluids, subcutaneous octreotide, and antibiotics for complicated diarrhea. While the optimal dose of octreotide has not been determined, octreotide may be started at a dose of 100 to 150 μg subcutaneously (SC) three times a day or 25 to 50 μg/hour intravenously (IV) with a dose escalation to 500 μg three times a day. This regimen continues until the patient has been diarrhea free for 24 hours.[44]
Octreotide, a somatostatin analogue, is currently the most promising agent in the management of severe diarrhea caused by a variety of diseases and treatments. The doses used in clinical trials have varied widely, and there is no consensus regarding optimal dose. Nevertheless, octreotide has been shown to be effective in relieving diarrhea associated with AIDS, carcinoid syndrome, and vasoactive intestinal polypeptide tumors.[64][Level of evidence: II][19]
Several open-label and randomized controlled studies of octreotide for chemotherapy-induced diarrhea have demonstrated the efficacy of this therapy.[65-67][Level of evidence: I];[68-70][Level of evidence: II] In a prospective trial of 32 patients who had chemotherapy-induced diarrhea that was refractory to loperamide, octreotide 100 µg SC three times a day produced complete resolution in 30 patients. Resolution occurred rapidly, with 5 patients responding within 24 hours after beginning treatment, 14 patients responding within 48 hours, and 11 patients responding within 72 hours. No adverse effects were noted.[71] Octreotide has also been shown to be effective for treating diarrhea associated with GVHD.[72,73]
An expert panel recommended using high-dose loperamide (2 mg q2h) for the first day of chemotherapy-induced, low-grade diarrhea (grade 1 or 2), followed by octreotide (100 µg–150 µg q8h).[42] If the patient presents with severe diarrhea (grade 3 or 4), octreotide (500 μg–1,500 µg SC or IV q8h) may be given as first-line therapy. A phase III, double-blind study of depot octreotide for the prevention of diarrhea during pelvic radiation treatment did not show any benefit.[74] In fact, some gastrointestinal symptoms, such as cramping, may have been worse. Parenteral hydration and electrolyte supplementation may be indicated, and in severe cases, total parenteral nutrition may be initiated. For more information, see Nutrition in Cancer Care.
Irinotecan is notorious for causing diarrhea. Irinotecan is associated with both acute diarrhea (occurring immediately after drug administration) and delayed diarrhea (occurring more than 24 hours after drug administration). Acute diarrhea is related to acute cholinergic excess and responds well to atropine. Delayed diarrhea, however, is typically managed with antidiarrheals and other supportive measures, as outlined above.[1]
Immune-mediated colitis is a potential side effect of ICIs. CTLA-4 inhibitors typically cause diarrhea and colitis more frequently than PD-1 and PD-L1 inhibitors, with the highest rates of colitis seen in patients receiving a combination of ICIs.[75] The onset of these events can be unpredictable, but they typically occur within the first ten doses of an ICI and may occur after cessation of an ICI.[76] Symptoms are treated according to the grade of diarrhea/colitis. Patients with mild diarrhea/colitis may be managed symptomatically with fluids and antidiarrheals. More severe diarrhea/colitis may necessitate treatment with systemic steroids and even permanent discontinuation of ICI therapy. Detailed management of ICI-induced diarrhea is further outlined in National Comprehensive Cancer Network guidelines for the management of immunotherapy-related toxicities.[77]
The U.S. Food and Drug Administration has approved four PI3K inhibitors, two of which (idelalisib and duvelisib) carry a boxed warning for gastrointestinal complications, including diarrhea.[78,79] Given the severity of diarrhea that may be seen with idelalisib, an expert panel convened to develop management strategies for idelalisib-associated diarrhea.[80] Panelists commented that it is not clear whether diarrhea is a class effect of PI3K inhibitors. The authors noted that for idelalisib, two types of diarrhea may be seen. The first type appears to be self-limiting, occurring within the first 8 weeks of treatment. The second type tends to respond poorly to antidiarrheal therapy and occurs later, approximately 7 months after the start of treatment. In the second type of diarrhea, the histological appearance of the colon is consistent with lymphocytic colitis. In this case, the panel recommended considering treatment with steroids or budesonide.[80]
Use our advanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General information about clinical trials is also available.
Almost all patients undergoing radiation to the abdomen, pelvis, or rectum will show signs of acute enteritis. Injuries are clinically evident during or within 3 months after irradiation, with the greatest prevalence during the fourth and fifth weeks.[1] Chronic radiation enteritis may present months to years after the completion of therapy, or it may begin as acute enteritis and persist after treatment ends. Only 10% to 20% of people treated with radiation to the abdomen develop chronic problems.[2]
The large and small bowel are sensitive to ionizing radiation. Although the probability of tumor control increases with the radiation dose, so does the damage to normal tissues. Acute side effects to the intestines occur with an exposure of approximately 10 Gy. Because curative radiation doses for many abdominal or pelvic tumors range between 25 and 76 Gy, enteritis is likely to occur.[2]
Factors that influence the occurrence and severity of radiation enteritis include the following:[2]
In general, the higher the daily and total dose delivered to the normal bowel and the greater the volume of normal bowel treated, the greater the risk of radiation enteritis. In addition, the individual patient variables listed above can decrease vascular flow to the bowel wall and impair bowel motility, increasing the chance of radiation injury.
Radiation therapy exerts a cytotoxic effect mainly on rapidly proliferating epithelial cells, like those lining the large and small bowel. Crypt cell wall necrosis can be observed 12 to 24 hours after a daily dose of 1.5 to 3 Gy.[3] Progressive loss of cells, villous atrophy, and cystic crypt dilation occur in the ensuing days and weeks. Patients suffering from acute enteritis may complain of nausea, vomiting, abdominal cramping, tenesmus, and watery diarrhea.[1,2] With diarrhea, the digestive and absorptive functions of the gastrointestinal tract are altered or lost, resulting in malabsorption of fat, lactose, bile salts, and vitamin B12. Symptoms of proctitis—including mucoid rectal discharge, rectal pain, and rectal bleeding (if mucosal ulceration is present)—may result from radiation damage to the anus or rectum.
One study of radiation for lung and head and neck cancers, with or without chemotherapy, noted significant diarrhea despite no direct radiation to the large or small intestine. Higher rates were noted for chemoradiation (42%) than for radiation alone (29%). Additionally, this radiation-induced diarrhea was associated with worse health outcomes and increased resource utilization. Individuals with moderate or severe diarrhea were more likely to have a gastrostomy tube placement, weight loss, unplanned office visits, more inpatient days, and longer radiation breaks. This early report requires additional validation studies to fully evaluate the prevalence and impact of this phenomenon.[4]
Acute enteritis occurs during or within 3 months after irradiation, with the greatest prevalence during the fourth and fifth weeks. Acute enteritis symptoms usually resolve 2 to 3 weeks after the completion of treatment, and the mucosa may appear nearly normal.[1]
Medical management includes treating diarrhea, dehydration, malabsorption, and abdominal or rectal discomfort. Symptoms usually resolve with medications, dietary changes, and rest. If symptoms become severe despite these measures, a treatment break may be warranted.
Medications may include the following:[1,5]
Damage to the intestinal villi from radiation therapy results in a reduction or loss of enzymes, such as lactase. Lactase is essential in the digestion of milk and milk products. Although there is no evidence that a lactose-restricted diet will prevent radiation enteritis, a diet that is lactose free, low fat, and low residue can help manage symptoms.[6][Level of evidence: I]
Foods to avoid
Foods to encourage
Helpful hints
Only 10% to 20% of patients who receive abdominal or pelvic irradiation develop chronic radiation enteritis. Signs and symptoms include the following:[2]
Less common symptoms are bowel obstruction, fistulas, bowel perforation, and massive rectal bleeding.
The initial signs and symptoms occur 6 to 18 months after radiation therapy. Radiological findings include submucosal thickening, single or multiple stenoses, adhesions, and sinus or fistula formation.[8] Microscopic findings include villi that are fibrotic or may be lost altogether. Ulceration is common, varying from simple loss of epithelial layers to ulcers that may penetrate to different depths of the intestinal wall, even to the serosa. Lymphatic tissue is often atrophic or absent. The submucosa is severely diseased. Arterioles and small arteries show profound changes, with hyalinization of the entire wall thickness. The muscularis is often distorted or focally replaced by fibrosis.
The diagnosis of chronic radiation enteritis may be difficult to make. Clinically and radiologically recurrent tumor needs to be ruled out. Because of the possible latency of the illness, it is essential to obtain a detailed history of the patient's radiation therapy course. It is often advisable to include the radiation therapy physician in managing the patient's care.
Medical management of the patient's symptoms (which are similar to symptoms of acute radiation enteritis) is indicated, with surgical management reserved for severe damage.[6][Level of evidence: I]
The timing and choice of surgical techniques remain somewhat controversial. A lower operative mortality rate (21% vs. 10%) and incidence of anatomic dehiscence (36% vs. 6%) have been reported with intestinal bypass compared with resection.[9][Level of evidence: II][10] Clinicians who favor resection point out that the removal of diseased bowel decreases the mortality rate for resection and is comparable to the bypass procedure.[9] All agree that simple lysis of adhesions is inadequate and that fistulas require bypass.
Surgery is undertaken only after careful assessment of the patient's clinical condition and extent of radiation damage. Wound healing is often delayed, necessitating prolonged parenteral feeding after surgery. Even after apparently successful operations, symptoms may persist in a significant share of patients.[11]
Treatment techniques that can minimize the risk of severe radiation enteritis include the following:
The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.
Added Eghbali et al. as reference 62.
This summary is written and maintained by the PDQ Supportive and Palliative Care Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ® Cancer Information for Health Professionals pages.
This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the pathophysiology and treatment of gastrointestinal complications, including constipation, impaction, bowel obstruction, diarrhea, and radiation enteritis. It is intended as a resource to inform and assist clinicians in the care of their patients. It does not provide formal guidelines or recommendations for making health care decisions.
This summary is reviewed regularly and updated as necessary by the PDQ Supportive and Palliative Care Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).
Board members review recently published articles each month to determine whether an article should:
Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.
The lead reviewers for Gastrointestinal Complications are:
Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website's Email Us. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.
Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Supportive and Palliative Care Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.
PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as “NCI’s PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary].”
The preferred citation for this PDQ summary is:
PDQ® Supportive and Palliative Care Editorial Board. PDQ Gastrointestinal Complications. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: https://www.cancer.gov/about-cancer/treatment/side-effects/constipation/GI-complications-hp-pdq. Accessed <MM/DD/YYYY>. [PMID: 26389211]
Images in this summary are used with permission of the author(s), artist, and/or publisher for use within the PDQ summaries only. Permission to use images outside the context of PDQ information must be obtained from the owner(s) and cannot be granted by the National Cancer Institute. Information about using the illustrations in this summary, along with many other cancer-related images, is available in Visuals Online, a collection of over 2,000 scientific images.
The information in these summaries should not be used as a basis for insurance reimbursement determinations. More information on insurance coverage is available on Cancer.gov on the Managing Cancer Care page.
More information about contacting us or receiving help with the Cancer.gov website can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the website’s Email Us.