References

1. Culhane B: Constipation. In: Yasko J, ed.: Guidelines for Cancer Care: Symptom Management. Reston, Va: Reston Publishing Company, Inc., 1983, pp 184-7.
2. Wright BA, Staats DO: The geriatric implications of fecal impaction. Nurse Pract 11 (10): 53-8, 60, 64-6, 1986. [PubMed: 3785769]
3. Hampton BG, Bryant RA, eds.: Ostomies and Continent Diversions: Nursing Management. St. Louis, Mo: Mosby Year Book, Inc., 1992.
4. Tuchmann L, Engelking C: Cancer-related diarrhea. In: Gates RA, Fink RM, eds.: Oncology Nursing Secrets. 2nd ed. Philadelphia, Pa: Hanley and Belfus, 2001, pp 310-22.
5. Perez CA, Brady LW, eds.: Principles and Practice of Radiation Oncology. 3rd ed. Philadelphia, Pa: Lippincott-Raven Publishers, 1998.

Etiology of Constipation

Common factors that contribute to the development of constipation in the general population include the following:

• Diet.
• Altered bowel habits.
• Inadequate fluid intake.
• Lack of exercise.

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, additional causative factors are the following:[1]

• The tumor itself.
• Cancer-related problems.
• Effects of drug therapy for cancer or for cancer pain.
• Other concurrent processes such as organ failure, decreased mobility, and depression.

Physiologic factors include the following:

• Inadequate oral intake.
• Dehydration.
• Inadequate intake of dietary fiber.
• Organ failure.

Any or all of these factors can occur because of the disease process, aging, debilitation, or treatment.

Causes of Constipation

Medications

• Chemotherapy (e.g., any agent that can cause autonomic nervous system changes such as vinca alkaloids, oxaliplatins, taxanes, and thalidomide).*
• Opioids or sedatives.
• Anticholinergic preparations (e.g., gastrointestinal antispasmodics, antiparkinsonism agents, and antidepressants).
• Phenothiazines.
• Calcium- and aluminum-based antacids.
• Diuretics.
• Vitamin supplements (e.g., iron and calcium).
• Tranquilizers and sleeping medications.
• General anesthesia and pudendal blocks.

Diet

• Inadequate fluid intake.*

Altered bowel habits

• Repeatedly ignoring defecation reflex.
• Excessive use of laxatives and/or enemas.

Prolonged immobility* and/or inadequate exercise

• Spinal cord injury or compression, fractures, fatigue, weakness, or inactivity (including bedrest).
• Intolerance with respiratory or cardiac problems.

Bowel disorders

• Irritable colon, diverticulitis, or tumor.*

Neuromuscular disorders (disruption of innervation leads to atony of the bowel)

• Neurological lesions (cerebral tumors).
• Spinal cord injury or compression.*
• Paraplegia.
• Cerebrovascular accident with paresis.
• Weak abdominal muscles.

Metabolic disorders

• Hypothyroidism and lead poisoning.
• Uremia.*
• Dehydration.*
• Hypercalcemia.*
• Hypokalemia.
• Hyponatremia.

Depression

• Chronic illness.
• Anorexia.
• Immobility.
• Antidepressants.

Inability to increase intra-abdominal pressure

• Emphysema.
• Any neuromuscular impairment of the diaphragm or abdominal muscles.
• Massive abdominal hernias.

Atony of muscles

• Malnutrition.
• Cachexia, anemia, or carcinoma.*
• Senility.

Environmental factors

• Inability to get to the bathroom without assistance.
• Unfamiliar or hurried environment.
• Excess heat leading to dehydration.
• Change in bathroom habits (e.g., use of a bedpan).
• Lack of privacy.

Narrowing of colon lumen

• Related to scarring from radiation therapy, surgical anastomosis, or compression from growth of extrinsic tumor.

[Note: *Frequently seen in oncology patients.]

Constipation is frequently the result of autonomic neuropathy caused by the vinca alkaloids, taxanes, and thalidomide. Other drugs such as opioid analgesics or anticholinergics (antidepressants and antihistamines) may lead to constipation by causing decreased sensitivity to the defecation reflexes and decreased gut motility. Since constipation is common with the use of opioids, a bowel regimen will be initiated at the time opioids are prescribed and continued for as long as the patient takes opioids. Opioids produce varying degrees of constipation, suggesting a dose-related phenomenon. One study suggests that clinicians should not base laxative prescribing on the opioid dose, but rather titrate the laxative according to bowel function. Lower doses of opioids or weaker opioids, such as codeine, are just as likely to cause constipation.[2] (Refer to the Side Effects of Opioids section in the PDQ summary on Pain for more information.)

Other diseases, such as diabetes (with autonomic neuropathy) and hypothyroidism, may cause constipation. Metabolic disorders, such as hypokalemia and hypercalcemia, also predispose cancer patients to developing constipation. Once these disorders are corrected, constipation will subside.[1]

Assessment of Constipation

A normal bowel pattern is having at least three stools per week and no more than three per day; however, these criteria may be inappropriate for cancer patients.[1,3] Constipation is viewed as a subjective symptom involving the complaints of decreased frequency with incomplete passage of dry, hard stool. 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. A digital rectal examination is done to rule out fecal impaction at the level of the rectum. A test for occult blood will be helpful in determining a possible intraluminal lesion. A thorough examination of the gastrointestinal tract is necessary if cancer is suspected.[4]

The following questions may provide a useful assessment guide:

1. What is normal for the patient (frequency, amount, and timing)?
2. When was the last bowel movement? What was the amount, consistency, and color? Was blood passed with it?
3. Has the patient been having any abdominal discomfort, cramping, nausea or vomiting, pain, excessive gas, or rectal fullness?
4. Does the patient regularly use laxatives or enemas? What does the patient usually do to relieve constipation? Does it usually work?
5. What type of diet does the patient follow? How much and what type of fluids are taken on a regular basis?
6. What medication (dose and frequency) is the patient taking?
7. Is this symptom a recent change?
8. How many times a day is flatus passed?

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.

Management of Constipation

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 increase fluid intake to one-half ounce per pound of body weight daily (if not contraindicated by renal or heart disease). (Refer to the PDQ summary on Nutrition in Cancer Care for more information.) A study that involved geriatric patients compared the efficacy, cost, and ease of administration of a natural laxative mixture (raisins, currants, prunes, figs, dates, and prune concentrate) with protocols using stool softeners, lactulose, and other laxatives. Results indicated lower costs, more natural and regular bowel movements, and increased ease of administration with natural laxatives. Even though generalization from these findings was limited by small sample size, additional exploration of natural laxatives in cancer patient populations might be useful.[5] A program for prevention of constipation in cancer patients is described below.

Assessment:

• Establish the patient’s normal bowel pattern and habits (time of day for normal bowel movement, consistency, color, and amount).
• Explore the patient’s level of understanding and compliance relating to exercise level, mobility, and diet (fluid, fruit, and fiber intake).
• Determine normal or usual use of laxatives, stimulants, or enemas.
• Determine laboratory values, specifically looking at platelet count.
• Conduct a physical assessment of the rectum (or stoma) to rule out impaction.

Commonly used interventions:

• Record bowel movements daily.
• Encourage patient to increase fluid intake, with a goal of drinking eight 8-oz (240-mL) glasses of fluid daily unless contraindicated.
• Encourage regular exercise, including abdominal exercises in bed or moving from bed to chair if the patient is not ambulatory.
• Encourage adequate fiber intake. Experts recommend that:

  -

  Healthy adults consume 20 g to 35 g of fiber per day (average consumption is 11 g).

  -

  Children and adolescents consume the number of grams of fiber equal to their age plus 5—for example, a 10-year-old consumes 15 g of fiber per day (10 + 5). This guideline applies until age 18 years; at that time, the adult recommendations are followed.

  While there are no specific fiber recommendations for cancer patients, they are encouraged to eat more high-fiber foods such as fruits (e.g., raisins, prunes, peaches, and apples), vegetables (e.g., squash, broccoli, carrots, and celery), and 100% whole-grain cereals, breads, and bran. Increased fiber intake must be accompanied by increased fluid intake, or constipation may result. High fiber intake is contraindicated in patients at increased risk for bowel obstruction, such as those with a history of bowel obstruction or status postcolostomy.

• Provide a warm or hot drink approximately one-half hour before time of patient’s usual defecation.
• Provide privacy and quiet time at the patient’s usual or planned time for defecation.
• Provide toilet or bedside commode and appropriate assistive devices; avoid bedpan use whenever possible.

Another approach, shown below in two parts, is adapted from the MD Anderson Cancer Center practice consensus algorithm for the prevention and management of opioid-induced constipation. [Note: Copyright 2008 The University of Texas MD Anderson Cancer Center]

MD Anderson Cancer Center Algorithm for the Prevention of Opioid-induced Constipation

• Unless there are existing alterations in bowel patterns (e.g., bowel obstruction or diarrhea), patients receiving opioids are started on a laxative bowel regimen and receive education for bowel management.

  1. Stimulant laxative plus stool softener (e.g., Senokot-S [senna 8.6 mg plus docusate 50 mg]), two tablets per day and titrate up (maximum nine tablets per day).
  2. Ensure adequate fluids, dietary fiber, and exercise, if feasible.
  3. Prune juice followed by warm beverage may be considered.

MD Anderson Cancer Center Algorithm for the Management of Opioid-induced Constipation

1. Assess potential cause of constipation (e.g., recent opioid dose increase, use of other constipating medications, or new bowel obstruction).
2. Increase Senokot-S (or senna and docusate tablets, if using separately), and add one or both of the following:

   1. Milk of magnesia oral concentrate (1170/5 mL), 10 mL by mouth 2 to 4 times per day.
   2. Polyethylene glycol (MiraLAX), 17 g in 8-oz beverage daily.
3. If no response to above, perform digital rectal examination to rule out low impaction. Continue above steps AND:

   1. If impacted, disimpact manually if stool is soft. If not, soften with mineral oil fleets enema before disimpaction. Follow up with milk of molasses enemas until clear with no formed stools.
   2. Consider use of rescue analgesics before disimpaction.
   3. If not impacted on rectal examination, patient may still have higher level impaction; if history is appropriate, consider abdominal imaging and/or administer milk of molasses enema with magnesium citrate 8 oz by mouth. Consider bowel management consult.
4. If patient is neutropenic or thrombocytopenic, arrange for bowel management consult.

• Start one of the following regimens if the patient has not had a stool in 3 days or on the first day that any patient starts taking drugs associated with constipation:

  -

  Stool softeners (e.g., docusate sodium, one to two capsules per day). For opioid-related constipation, stool softeners may be used in combination with a stimulant laxative. Bulk-producing agents are not recommended in a regimen used to counteract the bowel effects of opioids.

  -

  Two tablets of a senna preparation twice daily.

  -

  One bisacodyl tablet at bedtime.

  -

  Milk of magnesia, 30 to 45 mL, if a bowel movement is not achieved in 24 hours after other methods are instituted.

• If the amount of stool is still inadequate, increase stool softeners up to six capsules per day or a senna preparation (e.g., Senokot) gradually to a maximum of eight tablets (four tablets twice a day); bisacodyl may be increased gradually to three tablets.
• If the amount of stool is still inadequate, a glycerin or bisacodyl suppository or enema (phosphate/biphosphate, oil retention, or tap water) is used with caution, especially in patients with neutropenia or thrombocytopenia.

Medical management includes the administration of saline or chemical laxatives, suppositories, enemas, or agents that increase bulk.

Medical Agents for Constipation

Bulk producers

• Bulk producers are natural or semisynthetic polysaccharide and cellulose. They work with the body’s natural processes to hold water in the intestinal tract, soften the stool, and increase the frequency of the passage of stool. Bulk producers are not recommended for use in a regimen to counteract the bowel effects of opioids.
• Onset: 12 to 24 hours (may be delayed up to 72 hours).
• Caution: Patients take the bulk producer with two full 8-oz (240-mL) glasses of water and maintain adequate hydration to avoid the risk of developing a bowel obstruction. Avoid administering psyllium with salicylates, nitrofurantoin, and digitalis because psyllium decreases the actions of these drugs. Avoid use if intestinal obstruction is suspected.
• Use: Effective in managing irritable bowel syndrome.
• Drugs and dosages:

  -

  Methylcellulose (Cologel): 5 to 20 cc 3 times per day with water.

  -

  Barley malt extract (Maltsupex): Four tablets with meals and at bedtime or 2 tbsp powder or liquid 2 times per day for 3 to 4 days, then 1 to 2 tbsp at bedtime.

  -

  Psyllium: Varies from 1 tbsp to one packet, depending on brand, 1 to 3 times per day.

Saline laxatives

• The high osmolarity of the compounds in saline laxatives attracts water into the lumen of the intestines. The fluid accumulation alters the stool consistency, distends the bowel, and induces peristaltic movement. Cramps may occur.
• Onset: 0.5 to 3 hours.
• Caution: Repeated use can alter fluid and electrolyte balance. Avoid magnesium-containing laxatives in patients with renal dysfunction. Avoid sodium-containing laxatives in patients with edema, congestive heart failure, megacolon, or hypertension.
• Use: Mostly as a bowel preparation to clear the bowels for rectal or bowel examinations.
• Drugs and dosages:

  -

  Magnesium sulfate: 15 g in a glass of water.

  -

  Milk of magnesia: 10 to 20 cc if concentrated, 15 to 30 cc if regular.

  -

  Magnesium citrate: 240 cc.

  -

  Sodium phosphate: 4 to 8 g dissolved in water.

  -

  Monobasic and dibasic sodium phosphate (Fleet Phospho-soda): 20 to 40 mL mixed with 4 oz of cold water.

Stimulant laxatives

• Stimulant laxatives increase motor activity of the bowels by direct action on the intestines.
• Onset: 6 to 10 hours.
• Caution: Prolonged use of these drugs causes laxative dependency and loss of normal bowel function. Prolonged use of danthron discolors rectal mucosa and discolors alkaline urine red. 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. These medications may cause cramping.
• Drug interactions: Avoid taking bisacodyl within 1 hour of taking antacids, milk, or cimetidine because they cause premature dissolving of the enteric coating, which results in gastric or duodenal stimulation. There is an increased absorption of danthron when it is given with docusate.
• Use: To evacuate bowel for rectal or bowel examinations. Most of the stimulant laxatives act on the colon.
• Drugs and dosages:

  -

  Danthron: 37.5 to 150 mg with evening meal or 1 hour after evening meal.

  -

  Calcium salts of sennosides: 12 to 24 mg at bedtime; senna: Senolax, Seneson, or Black-Draught (two tablets); Senokot (two tablets or 10–15 cc at bedtime).

  -

  Bisacodyl: 10 to 15 mg swallowed whole, not chewed, or a 10-mg suppository.

Lubricant laxatives

• Lubricant laxatives lubricate intestinal mucosa and soften stool.
• Caution: Administer on empty stomach at bedtime. Mineral oil prevents absorption of oil-soluble vitamins and drugs. With older patients, aspiration potential suggests that mineral oil be avoided because it can cause lipid pneumonitis. It can interfere with postoperative healing of anorectal surgery. Avoid giving with docusate sodium. Docusate sodium causes increased systemic absorption of mineral oil.
• Use: Prophylactically to prevent straining in patients for whom straining would be dangerous.
• Drugs and dosages:

  -

  Mineral oil: 5 to 30 cc at bedtime.

Fecal softeners

• Fecal softeners promote water retention in the fecal mass, thus softening the stool. Up to 3 days may pass before an effect is noted. Stool softeners and emollient laxatives are of limited use because of colonic resorption of water from the forming stool.
• Fecal softeners are not used as the sole regimen but may be useful given in combination with stimulant laxatives.
• Caution: May increase the systemic absorption of mineral oil when administered together.
• Use: Prophylactically to prevent straining. Most beneficial when stool is hard.
• Drugs and dosages:

  -

  Docusate sodium: 50 to 240 mg taken with a full glass of water.

  -

  Docusate calcium: 240 mg each day until bowel movement is normal.

  -

  Docusate potassium: 100 to 300 mg each day until bowel movement is normal; increase daily fluid intake.

  -

  Poloxamer 188: 188 mg (480 mg at bedtime).

Lactulose (Cholac, Cephulac)

• Lactulose is a synthetic disaccharide that passes to the colon undigested. When it is broken down in the colon, it produces lactic acid, formic acid, acetic acid, and carbon dioxide. These products increase the osmotic pressure, thus increasing the amount of water held in the stool, which softens the stool and increases the frequency of passage.
• Onset: 24 to 48 hours.
• Caution: Excessive amounts may cause diarrhea with electrolyte losses. Avoid giving to patients with acute abdomen, fecal impaction, or obstruction.
• Dosage: 15 to 30 cc each day (contains 10–20 g of lactulose).

Polyethylene glycol and electrolytes (Golytely, Colyte)

• Five packets are mixed with 1 gallon (3.785 L) of tap water and contain the following: polyethylene glycol (227.1 g), sodium chloride (5.53 g), potassium chloride (2.82 g), sodium bicarbonate (6.36 g), and sodium sulfate (anhydrous, 21.5 g). Do not add flavorings. Serve chilled to improve palatability. Can be stored up to 48 hours in the refrigerator.
• Use: To clear bowel with minimal water and sodium loss or gain.

Opioid antagonists (naloxone, methylnaltrexone)

• Caution: Administer only if other drugs have failed.
• Subcutaneous methylnaltrexone, 0.15 mg per kilogram of body weight, can be administered daily or every other day to treat opioid-induced constipation. In a study of palliative care patients, including those with cancer and noncancer etiologies, approximately one-half of patients defecated within 4 hours of receiving the injection, with 30% of patients having a bowel movement within the first 30 minutes.
• In two studies of palliative care patients—one a single-dose trial and the other a 2-week every-other-day-dose trial—there was no evidence of withdrawal or other central effects of the opioid, and pain scores remained unchanged.[12,13]
• Caution: This drug is contraindicated in patients with bowel obstruction.
• The most common side effects are dizziness, nausea, abdominal pain, flatulence, and diarrhea.
• A study of prolonged-released naloxone in an oxycodone:naloxone ratio of 2:1 (average results of 40:20 mg, 60:30 mg, and 80:40 mg oxycodone:naloxone combination relative to placebo) demonstrated improved bowel function without reversal of analgesia.[14]

Current Clinical Trials

Check the list of NCI-supported cancer clinical trials for supportive and palliative care trials about constipation, impaction, and bowel obstruction that are now accepting participants. The list of trials can be further narrowed by location, drug, intervention, and other criteria.

General information about clinical trials is also available from the NCI website.

References

1. Portenoy RK: Constipation in the cancer patient: causes and management. Med Clin North Am 71 (2): 303-11, 1987. [PubMed: 3029525]
2. Bennett M, Cresswell H: Factors influencing constipation in advanced cancer patients: a prospective study of opioid dose, dantron dose and physical functioning. Palliat Med 17 (5): 418-22, 2003. [PubMed: 12882260]
3. McShane RE, McLane AM: Constipation. Consensual and empirical validation. Nurs Clin North Am 20 (4): 801-8, 1985. [PubMed: 3852308]
4. Bruera E, Suarez-Almazor M, Velasco A, et al.: The assessment of constipation in terminal cancer patients admitted to a palliative care unit: a retrospective review. J Pain Symptom Manage 9 (8): 515-9, 1994. [PubMed: 7531736]
5. Beverley L, Travis I: Constipation: proposed natural laxative mixtures. J Gerontol Nurs 18 (10): 5-12, 1992. [PubMed: 1479159]
6. Emmanuel AV, Krogh K, Bazzocchi G, et al.: Consensus review of best practice of transanal irrigation in adults. Spinal Cord 51 (10): 732-8, 2013. [PubMed: 23958927]
7. Christensen P, Bazzocchi G, Coggrave M, et al.: A randomized, controlled trial of transanal irrigation versus conservative bowel management in spinal cord-injured patients. Gastroenterology 131 (3): 738-47, 2006. [PubMed: 16952543]
8. Krogh K, Ostergaard K, Sabroe S, et al.: Clinical aspects of bowel symptoms in Parkinson's disease. Acta Neurol Scand 117 (1): 60-4, 2008. [PubMed: 18095955]
9. Coggrave M, Norton C, Cody JD: Management of faecal incontinence and constipation in adults with central neurological diseases. Cochrane Database Syst Rev 1: CD002115, 2014. [PMC free article: PMC10656572] [PubMed: 24420006]
10. Christensen P, Krogh K, Buntzen S, et al.: Long-term outcome and safety of transanal irrigation for constipation and fecal incontinence. Dis Colon Rectum 52 (2): 286-92, 2009. [PubMed: 19279425]
11. Memon S, Bissett IP: Rectal perforation following transanal irrigation. ANZ J Surg : , 2014. [PubMed: 24846120]
12. Thomas J, Karver S, Cooney GA, et al.: Methylnaltrexone for opioid-induced constipation in advanced illness. N Engl J Med 358 (22): 2332-43, 2008. [PubMed: 18509120]
13. Portenoy RK, Thomas J, Moehl Boatwright ML, et al.: Subcutaneous methylnaltrexone for the treatment of opioid-induced constipation in patients with advanced illness: a double-blind, randomized, parallel group, dose-ranging study. J Pain Symptom Manage 35 (5): 458-68, 2008. [PubMed: 18440447]
14. Meissner W, Leyendecker P, Mueller-Lissner S, et al.: A randomised controlled trial with prolonged-release oral oxycodone and naloxone to prevent and reverse opioid-induced constipation. Eur J Pain 13 (1): 56-64, 2009. [PubMed: 18762438]

Etiology of Impaction

Five major factors precipitating impaction include the following:

• Opioid analgesics.
• Prolonged inactivity.
• Dietary alterations.
• Psychiatric illness.
• Chronic use of drugs for constipation.[1]

Laxatives used to decrease constipation are the drugs that contribute most to the development of constipation and impaction. Repeated and escalating dosing of laxatives renders the colon less sensitive to its intrinsic reflexes stimulated by distention. (Refer to the Etiology of Constipation section of this summary for causes of constipation that may lead to impaction.)

Signs and Symptoms of Impaction

The patient may exhibit symptoms similar to constipation or present with symptoms unrelated to the gastrointestinal system. If the impaction presses on the sacral nerves, the patient may experience back pain. If the impaction presses on the ureters, bladder, or urethra, urinary symptoms can develop. These symptoms include increased or decreased frequency or urgency of urination, or urinary retention.

When abdominal distention occurs, movement of the diaphragm is compromised, leading to insufficient aeration with subsequent hypoxia and 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. Thus, 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 Impaction

Assessment includes the questions discussed previously for the patient with constipation. (Refer to the Assessment of Constipation section of this summary for the list of questions.) 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) would show loss of haustral markings, gas patterns reflecting gross amounts of stool, and dilatation proximal to the impaction.[2]

If a diagnosis of fecal impaction is uncertain, a laboratory workup can rule out other problems. A complete blood cell count, appropriate blood chemistries, chest x-ray, and an electrocardiogram can be performed. If the patient has become dehydrated, the blood urea nitrogen, creatinine, and serum osmolality will be elevated. There may be an elevation of the hemoglobin and hematocrit indicating hemoconcentration. The white blood cell (WBC) count may be slightly elevated in the presence of a fever. If the WBC count is extremely elevated and the patient is exhibiting a high fever and abdominal pain, an obstruction, perforation, infection, or inflammatory process must be ruled out. With marked distention of the cecum (diameter ≥12 cm), there is a risk of bowel perforation.

Treatment of Impaction

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; fecal impaction can irritate the bowel wall, and enemas in excess 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.

Nonstimulating bowel softeners such as docusate can be used to help soften stool higher in the colon. Mineral or olive oil can be given to loosen the stool. Caution is used when giving docusate sodium with mineral oil because there could be an increased systemic absorption of the mineral oil leading to systemic lipid granulomas.[3] Glycerin suppositories can also be used. Any laxatives that might stimulate the bowel or cause cramping are avoided so that the bowel is not damaged further.

Current Clinical Trials

Check the list of NCI-supported cancer clinical trials for supportive and palliative care trials about constipation, impaction, and bowel obstruction that are now accepting participants. The list of trials can be further narrowed by location, drug, intervention, and other criteria.

General information about clinical trials is also available from the NCI website.

References

1. Cefalu CA, McKnight GT, Pike JI: Treating impaction: a practical approach to an unpleasant problem. Geriatrics 36 (5): 143-6, 1981. [PubMed: 7215809]
2. Bruera E, Suarez-Almazor M, Velasco A, et al.: The assessment of constipation in terminal cancer patients admitted to a palliative care unit: a retrospective review. J Pain Symptom Manage 9 (8): 515-9, 1994. [PubMed: 7531736]
3. Brandt LJ: Gastrointestinal Disorders of the Elderly. New York, NY: Raven Press, 1984.

Etiology of Bowel Obstruction

The most common malignancies that cause bowel obstruction are cancers of the colon, stomach, and ovary. Extra-abdominal cancers (such as lung and breast cancers and melanoma) can spread to the abdomen, causing bowel obstruction.[3] Patients who have had abdominal surgery or abdominal radiation are also at higher risk of developing bowel obstruction.[2] Bowel obstructions are most common during advanced stages of disease.

Assessment and Diagnosis of Bowel Obstruction

Examination of the patient will determine the presence or absence of abdominal pain, vomiting, and evidence of the passage of flatus or stool. 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. Flat and upright abdominal films as well as a barium enema may be necessary to determine where the obstruction is located. While it remains controversial, an upper gastrointestinal series is contraindicated with an acutely presenting obstruction because it can cause a partial obstruction to become complete or may further complicate a total obstruction. If the patient is exhibiting dehydration, oliguria, or shock, perforation of the bowel may have occurred, and immediate medical or surgical intervention is indicated.

Treatment of Acute Bowel Obstruction

Careful serial examinations are necessary in the management of patients with progressive abdominal symptoms that may be due to acute bowel obstruction. The principles of supportive care in this setting include 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 or intestinal tubes. Although use of these tubes may be successful in reducing edema, relieving fluid and gas accumulation, or decreasing the need for multiple stage procedures,[4] 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 by permitting staging of the disease, increasing the rate of primary anastomosis relative to colostomy, and decreasing morbidity in patients with left-sided colon and rectal malignancies. Further study is warranted, including cost analysis.[5]

Management of Chronic, Malignant Bowel Obstruction

Patients with advanced cancer may have chronic, progressive bowel obstruction that is inoperable.[6,7] The most frequent causes of inoperability are extensive tumor and multiple partial obstructions.[8,9][Level of evidence: II][10] A retrospective review evaluating surgical palliation of malignant bowel obstruction secondary to peritoneal carcinomatosis in 63 patients with nongynecological cancer used the ability to tolerate solid food at hospital discharge as 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%. Postoperative mortality was 15%, and postoperative complications occurred in 44% of patients.[11]

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.[5,12-17] Stents 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.[18,19][Level of evidence: II][20].

When neither surgery nor stenting is possible, the accumulation of the unabsorbed secretions produce nausea, vomiting, pain, and colicky activity as a consequence of the partial or complete occlusion of the lumen. In this case, a gastrostomy tube is commonly used to provide decompression of air and fluid that may be accumulating and causing 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. This problem may be caused by the accumulation of fluid, since several liters of gastrointestinal secretions may be produced per day. To relieve continuous abdominal pain, opioid analgesics via continuous subcutaneous or intravenous infusion may be necessary. Effective antispasmodics in this situation include anticholinergics (such as hyoscine butylbromide) [21] and possibly corticosteroids as well as centrally acting agents. If the bowel obstruction is thought to be functional (rather than mechanical) in origin, metoclopramide is the drug of choice because of its prokinetic effects on the bowel. For complete bowel obstruction thought to be irreversible, a trial of an antispasmodic such as hyoscyamine may decrease bowel contractions and therefore yield pain relief. Another option for management of refractory pain and/or nausea is the synthetic somatostatin analog octreotide. This agent inhibits the release of several gastrointestinal hormones and reduces gastrointestinal secretions.[22,23][Level of evidence: I][24]

Octreotide is usually given subcutaneously at 50 to 200 µg 3 times per day and may reduce the nausea, vomiting, and abdominal pain of malignant bowel obstruction. For selected patients, the addition of an anticholinergic such as scopolamine may be helpful in reducing the associated painful colic of malignant bowel obstruction when octreotide alone is ineffective. When either scopolamine or octreotide is used alone, each is ineffective.[12,25-27] Corticosteroids are widely used in treating bowel obstruction, but empirical support is limited.[28] They may be useful as adjuvant antiemetics and analgesics in this setting, given as dexamethasone at a starting dose of 6 to 10 mg subcutaneously or intravenously 3 to 4 times per day.[12,25]

Current Clinical Trials

Check the list of NCI-supported cancer clinical trials for supportive and palliative care trials about constipation, impaction, and bowel obstruction that are now accepting participants. The list of trials can be further narrowed by location, drug, intervention, and other criteria.

General information about clinical trials is also available from the NCI website.

References

1. Givens BA, Simmons SJ: Gastroenterology in Clinical Nursing. 4th ed. St. Louis, Mo: C.V. Mosby Co, 1984.
2. Bouchier IA: Gastroenterology. 3rd ed. London: Balliere Tindall, 1982.
3. Ripamonti C, De Conno F, Ventafridda V, et al.: Management of bowel obstruction in advanced and terminal cancer patients. Ann Oncol 4 (1): 15-21, 1993. [PubMed: 8435356]
4. Horiuchi A, Maeyama H, Ochi Y, et al.: Usefulness of Dennis Colorectal Tube in endoscopic decompression of acute, malignant colonic obstruction. Gastrointest Endosc 54 (2): 229-32, 2001. [PubMed: 11474399]
5. Martinez-Santos C, Lobato RF, Fradejas JM, et al.: Self-expandable stent before elective surgery vs. emergency surgery for the treatment of malignant colorectal obstructions: comparison of primary anastomosis and morbidity rates. Dis Colon Rectum 45 (3): 401-6, 2002. [PubMed: 12068202]
6. Ripamonti C, Bruera E: Palliative management of malignant bowel obstruction. Int J Gynecol Cancer 12 (2): 135-43, 2002 Mar-Apr. [PubMed: 11975672]
7. Potluri V, Zhukovsky DS: Recent advances in malignant bowel obstruction: an interface of old and new. Curr Pain Headache Rep 7 (4): 270-8, 2003. [PubMed: 12828876]
8. Jung GS, Song HY, Kang SG, et al.: Malignant gastroduodenal obstructions: treatment by means of a covered expandable metallic stent-initial experience. Radiology 216 (3): 758-63, 2000. [PubMed: 10966707]
9. Camúñez F, Echenagusia A, Simó G, et al.: Malignant colorectal obstruction treated by means of self-expanding metallic stents: effectiveness before surgery and in palliation. Radiology 216 (2): 492-7, 2000. [PubMed: 10924576]
10. Coco C, Cogliandolo S, Riccioni ME, et al.: Use of a self-expanding stent in the palliation of rectal cancer recurrences. A report of three cases. Surg Endosc 14 (8): 708-11, 2000. [PubMed: 10954814]
11. Blair SL, Chu DZ, Schwarz RE: Outcome of palliative operations for malignant bowel obstruction in patients with peritoneal carcinomatosis from nongynecological cancer. Ann Surg Oncol 8 (8): 632-7, 2001. [PubMed: 11569777]
12. Baron TH: Expandable metal stents for the treatment of cancerous obstruction of the gastrointestinal tract. N Engl J Med 344 (22): 1681-7, 2001. [PubMed: 11386268]
13. Law WL, Chu KW, Ho JW, et al.: Self-expanding metallic stent in the treatment of colonic obstruction caused by advanced malignancies. Dis Colon Rectum 43 (11): 1522-7, 2000. [PubMed: 11089586]
14. Repici A, Reggio D, De Angelis C, et al.: Covered metal stents for management of inoperable malignant colorectal strictures. Gastrointest Endosc 52 (6): 735-40, 2000. [PubMed: 11115905]
15. Harris GJ, Senagore AJ, Lavery IC, et al.: The management of neoplastic colorectal obstruction with colonic endolumenal stenting devices. Am J Surg 181 (6): 499-506, 2001. [PubMed: 11513773]
16. Aviv RI, Shyamalan G, Watkinson A, et al.: Radiological palliation of malignant colonic obstruction. Clin Radiol 57 (5): 347-51, 2002. [PubMed: 12014929]
17. Dauphine CE, Tan P, Beart RW Jr, et al.: Placement of self-expanding metal stents for acute malignant large-bowel obstruction: a collective review. Ann Surg Oncol 9 (6): 574-9, 2002. [PubMed: 12095974]
18. Lopera JE, Alvarez O, Castaño R, et al.: Initial experience with Song's covered duodenal stent in the treatment of malignant gastroduodenal obstruction. J Vasc Interv Radiol 12 (11): 1297-303, 2001. [PubMed: 11698629]
19. Razzaq R, Laasch HU, England R, et al.: Expandable metal stents for the palliation of malignant gastroduodenal obstruction. Cardiovasc Intervent Radiol 24 (5): 313-8, 2001 Sep-Oct. [PubMed: 11815836]
20. Baron TH, Rey JF, Spinelli P: Expandable metal stent placement for malignant colorectal obstruction. Endoscopy 34 (10): 823-30, 2002. [PubMed: 12244506]
21. De Conno F, Caraceni A, Zecca E, et al.: Continuous subcutaneous infusion of hyoscine butylbromide reduces secretions in patients with gastrointestinal obstruction. J Pain Symptom Manage 6 (8): 484-6, 1991. [PubMed: 1720156]
22. Ripamonti C, Mercadante S, Groff L, et al.: Role of octreotide, scopolamine butylbromide, and hydration in symptom control of patients with inoperable bowel obstruction and nasogastric tubes: a prospective randomized trial. J Pain Symptom Manage 19 (1): 23-34, 2000. [PubMed: 10687323]
23. Mystakidou K, Tsilika E, Kalaidopoulou O, et al.: Comparison of octreotide administration vs conservative treatment in the management of inoperable bowel obstruction in patients with far advanced cancer: a randomized, double- blind, controlled clinical trial. Anticancer Res 22 (2B): 1187-92, 2002 Mar-Apr. [PubMed: 12168923]
24. Fallon MT: The physiology of somatostatin and its synthetic analogue, octreotide. European Journal of Palliative Care 1 (1): 20-2, 1994.
25. Mercadante S: Assessment and management of mechanical bowel obstruction. In: Portenoy RK, Bruera E, eds.: Topics in Palliative Care. Volume 1. New York, NY: Oxford University Press, 1997, pp. 113-30.
26. Fainsinger RL: Integrating medical and surgical treatments in gastrointestinal, genitourinary, and biliary obstruction in patients with cancer. Hematol Oncol Clin North Am 10 (1): 173-88, 1996. [PubMed: 8821566]
27. Ripamonti C, Panzeri C, Groff L, et al.: The role of somatostatin and octreotide in bowel obstruction: pre-clinical and clinical results. Tumori 87 (1): 1-9, 2001 Jan-Feb. [PubMed: 11669548]
28. Feuer DJ, Broadley KE: Systematic review and meta-analysis of corticosteroids for the resolution of malignant bowel obstruction in advanced gynaecological and gastrointestinal cancers. Systematic Review Steering Committee. Ann Oncol 10 (9): 1035-41, 1999. [PubMed: 10572600]

Etiology of Diarrhea

In patients being treated for cancer, diarrhea is most commonly induced by therapy.[11] Conventional methods of diarrhea-causing treatment include the following:

• Surgery.
• Chemotherapy.
• Radiation therapy.
• Bone marrow transplantation.

Other causes of acute diarrhea include the following:[12]

• Antibiotic therapy.
• Stress and anxiety associated with cancer diagnosis and treatment.
• Infection.

Typical infections are of viral, bacterial, protozoan, parasitic, or fungal etiology; they may also be caused by pseudomembranous colitis, a cause of diarrhea that often does not respond to treatment.[3] 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 2). 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.

Another strategy for categorizing the causes of diarrhea is by putative underlying mechanisms. These include exudative (i.e., excess blood or mucous enters the gastrointestinal tract), malabsorptive, dysmotile, osmotic, and secretory (due to increased secretion of electrolytes and fluid—probably the mechanism underlying chemotherapy-induced diarrhea) factors or combinations of these factors.[13]

Surgery, a primary treatment modality for many cancers, can affect the body by mechanical, functional, and physiological alterations. Postsurgical complications of gastrointestinal surgery affecting normal bowel function that may contribute to diarrhea include the following:[14,15]

• Increased transit time.
• Gastroparesis.
• Fat malabsorption.
• Lactose intolerance.
• Fluid and electrolyte imbalance.
• Dumping syndrome.

Certain chemotherapeutic agents can alter normal absorption and secretion functions of the small bowel, resulting in treatment-related diarrhea.[7] Examples of chemotherapy agents with diarrhea-related potential are listed in Table 2. Patients 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 depend on the following:

• Total dose.
• Fractionation.
• Volume of bowel irradiated.
• Concomitant chemotherapy.

Common side effects of intestinal enteritis include the following:

• Diarrhea.
• Malabsorption.
• Gas.
• Bloating.
• Cramping.

Acute intestinal side effects occur at approximately 10 Gy and may last up to 8 to 12 weeks posttherapy. Chronic radiation enteritis may present months to years after completion of therapy and necessitates dietary modification and pharmacological management and, in some instances, surgical intervention. (Refer to the Radiation Enteritis section of this summary for more information.)

Graft-versus-host disease (GVHD) is a major complication of allogeneic transplantation, and the intestinal tract, skin, and liver are commonly affected. Symptoms of gastrointestinal GVHD include nausea and vomiting, severe abdominal pain and cramping, and watery, green diarrhea.[16] The volume of accompanying GVHD-associated diarrhea may reach up to 10 L 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.

Assessment

Rapid, yet thorough, assessment of diarrhea is imperative because of the potentially life-threatening nature of diarrhea. Few standardized assessment tools are available, and studies suggest that, as a result, standardized assessment is rare in the clinical setting.[3] 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, as well as a thorough description of the diarrhea. Stringent monitoring conducted at least weekly is indicated during therapy using chemotherapeutic agents known to cause diarrhea.[9] The NCI’s Common Terminology Criteria for Adverse Events (Table 1) evaluate diarrhea by the following:[8]

• Number of stools per day.
• Incontinence.
• Increase in ostomy output compared with baseline.

The 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.[26] One author has developed a visual tool to assist patients and families in characterizing the consistency of the stool.[27] 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:

• Dizziness.
• Orthostatic symptoms.
• Lethargy.
• Cramping.
• Abdominal pain.
• Nausea.
• Vomiting.
• Fever.
• Rectal bleeding.

These symptoms are classified as complicated or uncomplicated, with therapy based on these classifications.[28]

Uncomplicated symptoms include grade 1 or 2 diarrhea with no other signs or symptoms. Management is conservative.

Complicated symptoms include grade 1 or 2 diarrhea with any one of the following risk factors:

• Moderate to severe cramping.
• Grade 2 or higher nausea/vomiting (see Table 3).
• Decreased performance status.
• Fever.
• Sepsis.
• Neutropenia.
• Frank bleeding.
• Dehydration.

Grade 3 or 4 diarrhea is also classified as complicated. Thorough evaluation and close monitoring is warranted.[28]

The time course of diarrhea and concomitant symptom development are key to determining underlying etiology.[26] Medication and dietary intake, as well as a history of recent travel, may provide additional clues regarding etiology. 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.[5]

Laboratory tests may include stool cultures for bacterial, fungal, and viral pathogens. A complete chemistry panel and hematologic profile can provide information regarding the effect of diarrhea on kidney function and electrolytes as well as identify changes in white blood cell count in response to infection. Urinalysis with specific gravity can provide information regarding hydration status. Stool osmolality may also be measured.[5]

In some cases, radiographic procedures are conducted to identify ileus, obstruction, or other abnormalities. In rare cases, endoscopy may be indicated.

Management

A review of early toxic deaths in two NCI-sponsored cooperative trials of irinotecan plus high-dose fluorouracil and leucovorin for advanced colorectal cancer has led to the revision of previously published 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.[28]

Current Clinical Trials

Check the list of NCI-supported cancer clinical trials for supportive and palliative care trials about diarrhea that are now accepting participants. The list of trials can be further narrowed by location, drug, intervention, and other criteria.

General information about clinical trials is also available from the NCI website.

References

1. Leichman CG, Fleming TR, Muggia FM, et al.: Phase II study of fluorouracil and its modulation in advanced colorectal cancer: a Southwest Oncology Group study. J Clin Oncol 13 (6): 1303-11, 1995. [PubMed: 7751875]
2. Rothenberg ML, Eckardt JR, Kuhn JG, et al.: Phase II trial of irinotecan in patients with progressive or rapidly recurrent colorectal cancer. J Clin Oncol 14 (4): 1128-35, 1996. [PubMed: 8648367]
3. Rutledge DN, Engelking C: Cancer-related diarrhea: selected findings of a national survey of oncology nurse experiences. Oncol Nurs Forum 25 (5): 861-73, 1998. [PubMed: 9644702]
4. Cleeland CS, Mendoza TR, Wang XS, et al.: Assessing symptom distress in cancer patients: the M.D. Anderson Symptom Inventory. Cancer 89 (7): 1634-46, 2000. [PubMed: 11013380]
5. Sykes NP: Constipation and diarrhoea. In: Doyle D, Hanks GW, MacDonald N, eds.: Oxford Textbook of Palliative Medicine. 2nd ed. New York, NY: Oxford University Press, 1998, pp 513-26.
6. Wolfe J, Grier HE, Klar N, et al.: Symptoms and suffering at the end of life in children with cancer. N Engl J Med 342 (5): 326-33, 2000. [PubMed: 10655532]
7. Arbuckle RB, Huber SL, Zacker C: The consequences of diarrhea occurring during chemotherapy for colorectal cancer: a retrospective study. Oncologist 5 (3): 250-9, 2000. [PubMed: 10884503]
8. National Cancer Institute: Common Terminology Criteria for Adverse Events (CTCAE), Version 4.0. Bethesda, Md: U.S. Department of Health and Human Services, National Institutes of Health, 2010. Available online. Last accessed June 25, 2015.
9. Rothenberg ML, Meropol NJ, Poplin EA, et al.: Mortality associated with irinotecan plus bolus fluorouracil/leucovorin: summary findings of an independent panel. J Clin Oncol 19 (18): 3801-7, 2001. [PubMed: 11559717]
10. Arnold RJ, Gabrail N, Raut M, et al.: Clinical implications of chemotherapy-induced diarrhea in patients with cancer. J Support Oncol 3 (3): 227-32, 2005 May-Jun. [PubMed: 15915825]
11. Cartoni C, Dragoni F, Micozzi A, et al.: Neutropenic enterocolitis in patients with acute leukemia: prognostic significance of bowel wall thickening detected by ultrasonography. J Clin Oncol 19 (3): 756-61, 2001. [PubMed: 11157028]
12. Tuchmann L, Engelking C: Cancer-related diarrhea. In: Gates RA, Fink RM, eds.: Oncology Nursing Secrets. 2nd ed. Philadelphia, Pa: Hanley and Belfus, 2001, pp 310-22.
13. Bruckstein AH: Acute diarrhea. Am Fam Physician 38 (4): 217-28, 1988. [PubMed: 3051978]
14. Yahanda AM: Hepatobiliary cancers. In: Berger DH, Feig BW, Fuhrman GM, eds.: The M.D. Anderson Surgical Oncology Handbook. Boston, Mass: Little, Brown, 1995, pp 194-224.
15. Grant JP, Chapman G, Russell MK: Malabsorption associated with surgical procedures and its treatment. Nutr Clin Pract 11 (2): 43-52, 1996. [PubMed: 8788337]
16. McDonald GB, Shulman HM, Sullivan KM, et al.: Intestinal and hepatic complications of human bone marrow transplantation. Part I. Gastroenterology 90 (2): 460-77, 1986. [PubMed: 3510147]
17. Herrmann VM, Petruska PJ: Nutrition support in bone marrow transplant recipients. Nutr Clin Pract 8 (1): 19-27, 1993. [PubMed: 8455527]
18. Mercadante S: Diarrhea in terminally ill patients: pathophysiology and treatment. J Pain Symptom Manage 10 (4): 298-309, 1995. [PubMed: 7602180]
19. Gupta E, Lestingi TM, Mick R, et al.: Metabolic fate of irinotecan in humans: correlation of glucuronidation with diarrhea. Cancer Res 54 (14): 3723-5, 1994. [PubMed: 8033091]
20. Wadler S, Benson AB 3rd, Engelking C, et al.: Recommended guidelines for the treatment of chemotherapy-induced diarrhea. J Clin Oncol 16 (9): 3169-78, 1998. [PubMed: 9738589]
21. Crown JP, Burris HA 3rd, Boyle F, et al.: Pooled analysis of diarrhea events in patients with cancer treated with lapatinib. Breast Cancer Res Treat 112 (2): 317-25, 2008. [PubMed: 18204897]
22. Makrauer FL, Oates E, Becker J, et al.: Does local irradiation affect gastric emptying in humans? Am J Med Sci 317 (1): 33-7, 1999. [PubMed: 9892269]
23. Donaldson SS: Nutritional consequences of radiotherapy. Cancer Res 37 (7 Pt 2): 2407-13, 1977. [PubMed: 861954]
24. Charuhas PM: Medical nutrition therapy in bone marrow transplantation. In: McCallum PD, Polisena CG, eds.: The Clinical Guide to Oncology Nutrition. Chicago, Ill: The American Dietetic Association, 2000, pp 90-8.
25. DuPont HL: Guidelines on acute infectious diarrhea in adults. The Practice Parameters Committee of the American College of Gastroenterology. Am J Gastroenterol 92 (11): 1962-75, 1997. [PubMed: 9362174]
26. Kornblau S, Benson AB, Catalano R, et al.: Management of cancer treatment-related diarrhea. Issues and therapeutic strategies. J Pain Symptom Manage 19 (2): 118-29, 2000. [PubMed: 10699539]
27. Mertz HR, Beck CK, Dixon W, et al.: Validation of a new measure of diarrhea. Dig Dis Sci 40 (9): 1873-82, 1995. [PubMed: 7555436]
28. Benson AB 3rd, Ajani JA, Catalano RB, et al.: Recommended guidelines for the treatment of cancer treatment-induced diarrhea. J Clin Oncol 22 (14): 2918-26, 2004. [PubMed: 15254061]
29. Polisena CG: Nutrition concerns with the radiation therapy patient. In: McCallum PD, Polisena CG, eds.: The Clinical Guide to Oncology Nutrition. Chicago, Ill: The American Dietetic Association, 2000, pp 70-8.
30. McCallum PD, Polisena CG, eds.: The Clinical Guide to Oncology Nutrition. Chicago, Ill: The American Dietetic Association, 2000.
31. Hogan CM: The nurse's role in diarrhea management. Oncol Nurs Forum 25 (5): 879-86, 1998. [PubMed: 9644704]
32. Kozelsky TF, Meyers GE, Sloan JA, et al.: Phase III double-blind study of glutamine versus placebo for the prevention of acute diarrhea in patients receiving pelvic radiation therapy. J Clin Oncol 21 (9): 1669-74, 2003. [PubMed: 12721240]
33. Savy GK: Glutamine supplementation. Heal the gut, help the patient. J Infus Nurs 25 (1): 65-9, 2002 Jan-Feb. [PubMed: 11840007]
34. Ziegler TR, Bye RL, Persinger RL, et al.: Effects of glutamine supplementation on circulating lymphocytes after bone marrow transplantation: a pilot study. Am J Med Sci 315 (1): 4-10, 1998. [PubMed: 9427568]
35. Cascinu S, Bichisao E, Amadori D, et al.: High-dose loperamide in the treatment of 5-fluorouracil-induced diarrhea in colorectal cancer patients. Support Care Cancer 8 (1): 65-7, 2000. [PubMed: 10650901]
36. Creemers GJ, Lund B, Verweij J: Topoisomerase I inhibitors: topotecan and irenotecan. Cancer Treat Rev 20 (1): 73-96, 1994. [PubMed: 8293429]
37. Kehrer DF, Sparreboom A, Verweij J, et al.: Modulation of irinotecan-induced diarrhea by cotreatment with neomycin in cancer patients. Clin Cancer Res 7 (5): 1136-41, 2001. [PubMed: 11350876]
38. Takeda Y, Kobayashi K, Akiyama Y, et al.: Prevention of irinotecan (CPT-11)-induced diarrhea by oral alkalization combined with control of defecation in cancer patients. Int J Cancer 92 (2): 269-75, 2001. [PubMed: 11291056]
39. de Vrese M, Schrezenmeir J: Probiotics, prebiotics, and synbiotics. Adv Biochem Eng Biotechnol 111: 1-66, 2008. [PubMed: 18461293]
40. Isolauri E: Probiotics in human disease. Am J Clin Nutr 73 (6): 1142S-1146S, 2001. [PubMed: 11393192]
41. Johnston BC, Supina AL, Ospina M, et al.: Probiotics for the prevention of pediatric antibiotic-associated diarrhea. Cochrane Database Syst Rev (2): CD004827, 2007. [PubMed: 17443557]
42. Pillai A, Nelson R: Probiotics for treatment of Clostridium difficile-associated colitis in adults. Cochrane Database Syst Rev (1): CD004611, 2008. [PubMed: 18254055]
43. Huertas-Ceballos A, Logan S, Bennett C, et al.: Dietary interventions for recurrent abdominal pain (RAP) and irritable bowel syndrome (IBS) in childhood. Cochrane Database Syst Rev (1): CD003019, 2008. [PubMed: 18254014]
44. Alfaleh K, Bassler D: Probiotics for prevention of necrotizing enterocolitis in preterm infants. Cochrane Database Syst Rev (1): CD005496, 2008. [PubMed: 18254081]
45. Karimi O, Peña AS: Indications and challenges of probiotics, prebiotics, and synbiotics in the management of arthralgias and spondyloarthropathies in inflammatory bowel disease. J Clin Gastroenterol 42 (Suppl 3 Pt 1): S136-41, 2008. [PubMed: 18806706]
46. Butterworth AD, Thomas AG, Akobeng AK: Probiotics for induction of remission in Crohn's disease. Cochrane Database Syst Rev (3): CD006634, 2008. [PMC free article: PMC6544811] [PubMed: 18646162]
47. Delia P, Sansotta G, Donato V, et al.: Use of probiotics for prevention of radiation-induced diarrhea. World J Gastroenterol 13 (6): 912-5, 2007. [PMC free article: PMC4065928] [PubMed: 17352022]
48. Cello JP, Grendell JH, Basuk P, et al.: Effect of octreotide on refractory AIDS-associated diarrhea. A prospective, multicenter clinical trial. Ann Intern Med 115 (9): 705-10, 1991. [PubMed: 1929038]
49. Cascinu S, Fedeli A, Fedeli SL, et al.: Octreotide versus loperamide in the treatment of fluorouracil-induced diarrhea: a randomized trial. J Clin Oncol 11 (1): 148-51, 1993. [PubMed: 8418225]
50. Cascinu S, Fedeli A, Fedeli SL, et al.: Control of chemotherapy-induced diarrhea with octreotide. A randomized trial with placebo in patients receiving cisplatin. Oncology 51 (1): 70-3, 1994 Jan-Feb. [PubMed: 8265106]
51. Gebbia V, Carreca I, Testa A, et al.: Subcutaneous octreotide versus oral loperamide in the treatment of diarrhea following chemotherapy. Anticancer Drugs 4 (4): 443-5, 1993. [PubMed: 8400346]
52. Petrelli NJ, Rodriguez-Bigas M, Rustum Y, et al.: Bowel rest, intravenous hydration, and continuous high-dose infusion of octreotide acetate for the treatment of chemotherapy-induced diarrhea in patients with colorectal carcinoma. Cancer 72 (5): 1543-6, 1993. [PubMed: 8348489]
53. Wadler S, Haynes H, Wiernik PH: Phase I trial of the somatostatin analog octreotide acetate in the treatment of fluoropyrimidine-induced diarrhea. J Clin Oncol 13 (1): 222-6, 1995. [PubMed: 7799023]
54. Cascinu S, Fedeli A, Fedeli SL, et al.: Control of chemotherapy-induced diarrhoea with octreotide in patients receiving 5-fluorouracil. Eur J Cancer 28 (2-3): 482-3, 1992. [PubMed: 1591068]
55. Zidan J, Haim N, Beny A, et al.: Octreotide in the treatment of severe chemotherapy-induced diarrhea. Ann Oncol 12 (2): 227-9, 2001. [PubMed: 11300329]
56. Ippoliti C, Champlin R, Bugazia N, et al.: Use of octreotide in the symptomatic management of diarrhea induced by graft-versus-host disease in patients with hematologic malignancies. J Clin Oncol 15 (11): 3350-4, 1997. [PubMed: 9363865]
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58. Martenson JA, Halyard MY, Sloan JA, et al.: Phase III, double-blind study of depot octreotide versus placebo in the prevention of acute diarrhea in patients receiving pelvic radiation therapy: results of North Central Cancer Treatment Group N00CA. J Clin Oncol 26 (32): 5248-53, 2008. [PMC free article: PMC2652088] [PubMed: 18768432]

Etiology

Almost all patients undergoing radiation to the abdomen, pelvis, or rectum will show signs of acute enteritis. Injuries clinically evident during the first course of radiation and up to 8 weeks later are considered acute.[1] Chronic radiation enteritis may present months to years after the completion of therapy, or it may begin as acute enteritis and persist after the cessation of treatment. Only 5% to 15% of persons treated with radiation to the abdomen will develop chronic problems.[2]

Factors that influence the occurrence and severity of radiation enteritis include the following:

1. Dose and fractionation.
2. Tumor size and extent.
3. Volume of normal bowel treated.
4. Concomitant chemotherapy.
5. Radiation intracavitary implants.
6. Individual patient variables (e.g., previous abdominal or pelvic surgery, hypertension, diabetes mellitus, pelvic inflammatory disease, inadequate nutrition).[3,4]

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.

Acute Radiation Enteritis

Chronic Radiation Enteritis

References

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Purpose of This Summary

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 who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.

Reviewers and Updates

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:

• be discussed at a meeting,
• be cited with text, or
• replace or update an existing article that is already cited.

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:

• Joseph Bubalo, PharmD, BCPS, BCOP (Oregon Health and Science University Hospital)
• Lillian M. Nail, PhD, RN, FAAN, CNS (Oregon Health & Science University Cancer Institute)
• Maria Petzel, RD, CSO, LD, CNSC, FND (University of TX MD Anderson Cancer Center)

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.

Levels of Evidence

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.

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The preferred citation for this PDQ summary is:

National Cancer Institute: PDQ® Gastrointestinal Complications. Bethesda, MD: National Cancer Institute. Date last modified <MM/DD/YYYY>. Available at: http://www.cancer.gov/about-cancer/treatment/side-effects/constipation/GI-complications-hp-pdq. Accessed <MM/DD/YYYY>.

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