Diet and Drugs in Colorectal Surgery ( Part 1 )

5gia

Taken From :

Title: Colon and Rectal Surgery, 5th Edition

Editors: Corman, Marvin L.

Copyright ©2005 Lippincott Williams & Wilkins

Guest Contributor John L. Petrini

I have asked a former colleague, John Petrini, to provide this contribution to the fifth edition of this book. Dr. Petrini is Chief of the Department of Gastroenterology at the Sansum Medical Clinic in Santa Barbara, California. During our 12 years of association, I have relied on him for his expertise and insight into the management of some of the difficult conditions that colon and rectal surgeons face. I believe that a chapter on diet and drugs for the benefit of general surgeons, as well as colon and rectal surgeons, should be a useful addition to this text.

--MLC

A drug is a substance that, when injected into a rat, produces a scientific paper.

--Anonymous

The role of diet in a healthy bowel has been a stimulating and controversial subject for two millennia. There are data to support numerous statements and recommendations, but controlled clinical trials defining the benefits of various foods and therapies are quite limited. In general, diets high in fiber and roughage help facilitate the normal passage of stool. In addition, they may be beneficial to the overall health of an individual by reducing cholesterol, maintaining blood sugar in the normal range, and decreasing the incidence of diverticulosis. Cruciferous plants also contain anticarcinogens that may reduce the incidence of colonic neoplasms. Furthermore, aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs) appear to reduce the incidence of colon cancer. Other ideas—for example, that cow's milk and dairy products may be harmful for young children and most adults—have some validity. There are a host of other claims, but the data in support of them are very weak.

Patients may solicit the opinion of a physician for concerns that do not necessarily require surgical intervention, or they may experience gastrointestinal symptoms that are consequences of an operation. For many, dietary manipulations and medical therapy may provide relief of the discomfort and disability. Initial therapy for most disorders of the colon and rectum is usually dietary adjustment. This approach is often instituted by the patient himself or herself. The symptoms of certain conditions, such as irritable bowel syndrome (IBS), inflammatory bowel disease, diverticulitis, diarrhea, and constipation, can often be ameliorated by dietary manipulation, even though the cause of the disorder may not be related to a specific food. The addition of medication, either for symptomatic relief or to treat the specific disease state, may also contribute to the relief of a patient's symptoms. It is important, however, to understand the pathophysiology underlying the bowel symptoms in order to offer the appropriate treatment. Unfortunately, there is a paucity of information available for many disorders affecting the gastrointestinal tract that may aid the physician in appropriate therapeutic decision making. This chapter focuses on some of the more common symptoms and conditions for which patients seek the attention of physicians trained in gastrointestinal disease and gastrointestinal surgery.

BOWEL MANAGEMENT PROBLEMS

Constipation

Constipation can be defined as either a decrease in the frequency of stools or an increase in the difficulty of passage of stool. Patients may also complain of hard bowel movements, small actions, inability to evacuate, or the sensation of incomplete evacuation. Some studies have demonstrated that 95% of healthy adults will have a minimum of three bowel movements per week.25,33 Those with fewer than three stools a week are considered to have “constipation,” but they may not be truly symptomatic or seek medical attention. Those who do request help usually complain of either decreased frequency or difficulty in passing stool. Therapy is therefore directed at either increasing the water content (i.e., softening the stool) or increasing the frequency of bowel movements.

History

In order to make a recommendation concerning therapy, a carefully obtained history is essential. This should include the duration of the complaints, dietary habits, the use of medications, and lifestyle. These often provide the information necessary to arrive at the source of the patient's complaints. It is not within the purview of this chapter to present a complete discussion of all the disease states, endocrine abnormalities, medications, neurologic disorders, and dietary issues that are associated with constipation. However, it is important to note the more common endocrine conditions that may affect the bowels and that should be considered: hypothyroidism, diabetes mellitus, and hyperparathyroidism. Other diseases that predispose to constipation include uremia, porphyria, amyloidosis, and short-segment Hirschsprung's disease.

As mentioned, medications are a frequent cause of constipation, so it is important to obtain a history of all medications used, including those available over the counter. Although the list is extensive, the more common ones to consider include the opiate/analgesics, antipsychotics (particularly the monoamine oxidase inhibitors and tricyclic antidepressants), anticholinergics, iron and other heavy metals, antacids, anticonvulsants, calcium channel blockers, and diuretics.

Evaluation

The perineum should be carefully inspected for obvious pathologic entities that may impede the passage of stool. Instrument examination, contrast studies, transit studies, gynecologic examination, ultrasonography, computed tomography, and physiologic studies may be required in selected patients. Certainly, gastrointestinal evaluation at some point must be accomplished to rule out the presence of a specific etiologic factor. These are discussed in the following chapters.

Treatment

The standard treatment of nonspecific constipation begins with dietary manipulation, usually through increasing dietary fiber and fluid intake. In addition, several classes of medication are available to increase stool water or stool frequency. These include bulk laxatives, stool softeners, osmotic or saline laxatives, cathartics, and motility-enhancing drugs (prokinetics).

Those who have constipation usually benefit from increasing the water content of the stool by increasing their intake of fiber and water. It is well known that individuals who live in so-called developing countries consume a large amount of unprocessed fiber. However, the diet in most developed countries contains inadequate roughage or unprocessed dietary fiber.6,18 Dietary fiber consists of plant products that are not digested or absorbed by the small intestine. These include cellulose, lignin, gums, pectins, hemicelluloses, and polysaccharides. Increasing fluid intake without adding fiber to the diet is usually ineffective for correcting constipation. Fiber, however, will improve stool consistency irrespective of the water intake.45 Interestingly, fiber with small amounts of water can be used to treat diarrhea. Some foods, particularly dairy products, actually decrease stool water content and contribute to constipation. Good sources of dietary fiber include fresh fruits and vegetables, whole grain cereals, and unprocessed carbohydrates such as bran, whole wheat, and brown rice (Table 3-1). Total daily fiber intake should be adjusted to approximately 30 g or more.

TABLE 3-1 Fiber Content of Selected Dietary Items

Food Group
Low Fiber
High Fiber
Fruits
Apples (cooked)
Oranges
Pears
Bananas
Grapes
Fruit juices
Prunes (stewed)
Raspberries
Apples (with peel)
Dates (dried)
Vegetables
Cabbage
Celery
Lettuce
Summer squash
Vegetable juices
Eggplant
Spinach
Sweet potato
Corn
Broccoli
Turnips
Greens
Starches
Bagel
White bread
Flour, white
Potato (mashed, chips)
Pasta
Popcorn
Lentils
Bran
Barley
Kidney beans
Peas
Brown rice
Granola
Flour, whole wheat
Other
Meats, seafood
Dairy products, eggs
Nuts and seeds
Oils

Fiber Products

Those individuals whose diet remains inadequate in fiber can increase stool water-carrying capacity by adding a fiber-containing bulk laxative. Psyllium husk, either as powder or granules, is obtained from various species of plantain. Bran is a product of the milling of wheat. Either, when taken with adequate dietary water, will provide additional bulk to the stool and increase the water content, trapping it in a mucin within the stool.

Other bulk laxatives utilize hydrophilic substances, such as polycarbophil and powdered karaya (sterculia) gum. The amount of bulking agents can be adjusted to what is required to alleviate the patient's constipation. This range is usually between 4 and 10 g/day, with the administration divided if a higher dose is required. The major disadvantage of bulking agents is the bloating and gas commonly associated with the cellulose and lignin-based products. Fiber products with a base of hemicellulose or pectin seem to reduce these side effects, as does the use of the polycarbophil bulk agents. However, patients seem to require higher doses of the latter than of the cellulose-based products in order for similar results to be achieved. One of the side benefits of the use of bulk agents is the lowering of serum cholesterol. This is probably effected through the binding of bile salts and reducing their reabsorption, so that the bile salt pool is lowered. Problems associated with the use of bulking agents include intestinal obstruction and fecal impaction, particularly if there is an underlying pathologic entity. Additionally, allergic reactions have been reported.

Stool Softeners

Patients who are resistant to the bulking agents alone can increase the water content further with stool softeners or emollients. The principal agent is docusate (dioctyl sulfosuccinate), which is available as the sodium, calcium, or potassium salt. These products inhibit the normal water-absorptive capacity of the colon while producing only a minimal decrease in the transit of fecal contents. Once one of these products has been administered, it may take 1 to 3 days to see an effect. In essence, they act to soften the stool but do not promote defecation. The usual adult does is from 50 to 250 mg/day. Ducosate should not be given with mineral oil because absorption of the oil as well as other medications is enhanced.

Osmotic and Saline Laxatives

Should bulking agents and surfactants fail to enhance the passage of stool, the next preferred step would be to employ an osmotic or saline laxative. Magnesium phosphate, sodium sulfate, and potassium tartrate are poorly absorbed chemicals. Ingestion increases the stool water content through an osmotic effect. Surgeons are familiar with the use of saline laxatives for bowel preparations before operative or diagnostic procedures. In smaller doses, they can be utilized for their cathartic effect. However, they should be used only intermittently. Certain antacid products contain magnesium, and it is this agent that produces the side effect of diarrhea. There is, furthermore, some evidence that magnesium may actually increase motility of the small intestine through stimulation the release of cholecystokinin from the duodenum.16 The phosphate-containing solutions may cause a high serum phosphate level and impair cardiac contractility. They should therefore be used with caution in individuals with renal, cardiac, or hepatic disease. Dehydration can also be a consequence of the use of saline laxatives. Patients should be cautioned to take adequate fluids when using these agents.

Modified doses of colonic purgatives used to clear the colon prior to surgery and gastrointestinal procedures are also available to treat constipation.10 Miralax provides increased water to the colon by adding an osmotically neutral fluid to the gastrointestinal tract. The osmotically nonabsorbed, active agents, polyethylene glycol and a mixture of sodium and potassium sulfate, are not absorbed. The usual dose is 17 g mixed with water; it can be given on a daily basis. There is minimal fluid or electrolyte shift, and side effects are rare.

Polysaccharides

Some carbohydrates are also poorly absorbed. This results in an osmotic effect that leads to enhanced water in the stool. These products include lactose, lactulose, and sorbitol. Lactulose has been particularly useful in the treatment of hepatic encephalopathy, but lower doses (30 to 60 mL/day) can be an effective laxative for patients with chronic constipation. Side effects include gas, bloating, cramps, flatulence, and, of course, fluid loss at high doses.

Lubricants

Mineral oil, a petroleum distillate, has been employed for the treatment of constipation. The mechanism of action appears to be penetration of the stool by the oil with resulting softening. However, because of the potential for complications, long-term use should be avoided. These include decreased absorption of fat-soluble vitamins and essential fatty acids. Furthermore, penetration of the mucosa can occur, and a foreign-body reaction in the mesenteric lymph nodes, mucosa, and spleen has been reported. As previously mentioned, mineral oil should not be used with surfactants, because there is the potential for increased absorption of the mineral oil.

Stimulant Laxatives

What rhubarb, senna or what purgative drug, would scour these English hence?

--William Shakespeare: Macbeth V, iii, 55

Cathartic laxatives are mucosally active agents that reduce net water and electrolyte absorption in addition to increasing bowel motility. The most frequently employed substances include phenolphthalein and the anthraquinone cathartics (senna, cascara sagrada, danthron). These drugs act primarily to increase periodic mass movements within the colon and to decrease the segmental contractions that slow bowel activity. Generally, they become effective in 4 to 6 hours. The primary side effect, in addition to diarrhea, is that of cramping. Another drug, bisacodyl (Dulcolax), is a synthetic diphenylmethane that is similar to phenolphthalein. However, it is available not only available for oral administration but also for rectal use. Because of the problem of gastric irritation, it is enteric coated. The standard adult dose is 10 to 15 mg.

Senna is an anthraquinone cathartic obtained from Cassia acutifolia or Cassia angustifolia. Preparations of the whole plant, leaflets, pods, and extracts are commercially available. Cascara sagrada is another anthraquinone; it is obtained from the bark of the buckthorn tree. Like all cathartics, these are variously effective depending on the dosage but can cause a problem with cramping. Furthermore, melanosis coli, a dark pigmentation of the colon mucosa, may be a consequence of long-term use of senna and cascara.

Another cathartic, castor oil, a triglyceride of ricinoleic acid, acts in the small intestine by pancreatic hydrolysis, thereby decreasing water and electrolyte absorption and decreasing transit time. Because it is quite potent, it should be employed with special care. Long-term use should be avoided.

Motility Agents

Three agents are currently available that decrease transit time through acceleration of the muscular activity of the bowel. Gastrointestinal motility can be enhanced through the use of metoclopramide, erythromycin, and tegaserod. Another agent, the subject of considerable investigational effort, is cisapride, but it has been taken off the market in the United States. Metoclopraminde and erythromycin have little or no effect on the colon, but tegaserod has been shown to increase bowel activity and ease constipation in those patients with IBS in whom constipation predominates.22 Tegaserod is a partial agonist of the type 4 serotonin receptor (5-HT4) with high binding affinity and little or no affinity for other serotonin receptors. It appears to enhance motor activity in the colon and elsewhere in the gastrointestinal tract by normalizing motility and stimulating intestinal secretion. Another beneficial effect in patients with IBS appears to be reduction in visceral sensitivity, thus ameliorating abdominal pain. Tegaserod is approved for oral administration, 6 mg twice daily, before meals for 4 to 6 weeks, with another 6-week course if needed.

Summary

Long-term use of intestinal stimulants and cathartics can lead to fluid and electrolyte disturbances, including dehydration, hypokalemia, hyponatremia, hypoalbuminemia, steatorrhea, protein-losing enteropathy, and secondary hyperaldosteronism. Furthermore, patients may become dependent upon laxatives, and what is known as a “cathartic colon,” or a chronically flaccid colon, may develop. A good general principle is that if laxatives are to be used, the lowest effective dose should be given. Long-term use should be discouraged. Most individuals will benefit from a program of increasing fiber and water content of the stool, with the addition of laxatives intermittently as needed to produce at least two or three bowel movements per week. The application of surgical intervention as a treatment for constipation should be offered only after an adequate trial of medical therapy and appropriate evaluation of the gastrointestinal tract (see Chapter 16).

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Continue to Part 2…

REFERENCES

1. Baron JA, Beach M, Mandel JS, et al. Calcium supplements for the prevention of colorectal adenomas. N Engl J Med 1999;340:101–107.

2. Baron JA, Cole BF, Sandler RS. A randomized trial of aspirin to prevent colorectal adenomas. N Engl J Med 2003;248: 891–899.

3. Benson MJ, Roberts JP, Wingate DL, et al. Small-bowel motility following major intra-abdominal surgery: the effects of opiates and rectal cisapride. Gastroenterology 1994; 106:924–936.

4. Bonacini M, Quiason S, Reynolds M, et al. Effects of intravenous erythromycin on postoperative ileus. Am J Gastroenterol 1993;88:208–211.

5. Bradette M, Delvaux M, Staumont G, et al. Octreotide increases thresholds of colonic visceral perception in IBS patients without modifying muscle tone. Dig Dis Sci 1994;39: 1171–1178.

6. Burkitt DP, Walker ARP, Painter NS. Effect of dietary fibre on stools and transit times, and its role in the causation of disease. Lancet 1972;2:1408–1412.

7. Byrne TA, Persinger RL, Young LS, et al. A new treatment for patients with short-bowel syndrome: growth hormone, glutamine, and a modified diet. Ann Surg 1995;222:243–254.

P.52

8. Creed F, Guthrie E. Psychological factors in the irritable bowel syndrome. Gut 1987;28:1307–1318.

9. Dapoigny M, Abitbol J-L, Fraitag B. Efficacy of peripheral kappa agonist fedotozine versus placebo in treatment of irritable bowel syndrome. Dig Dis Sci 1995;40:2244–2248.

10. Di Palma JA, De Ridder PH, Orlando RC, et al. A randomized, placebo-controlled, multicenter study of the safety and efficacy of a new polyethylene glycol laxative. Am J Gastroenterol 2000;95:446–450.

11. Drossman D. Rome II critera. Am J Gastroenterol 1999;94: 2912–2917.

12. Drossman DA, Leserman J, Nachman G, et al. Sexual and physical abuse in women with functional or organic gastrointestinal disease. Ann Intern Med 1900;113:828–833.

13. Duma RJ, Kellum JM. Colonic diverticulitis: microbiologic, diagnostic and therapeutic considerations. Curr Clin Topics Infect Dis 1991;11:218–247.

14. Edes TE, Walk BE, Austin JL. Diarrhea in tube-fed patients: feeding formula not necessarily the cause. Am J Med 1990; 88:91–93.

15. Giondretti P, Rizzello F, Venturi A, et al. Oral bacteriotherapy as maintenance treatment in patients with chronic pouchitis: a double-blind, placebo-controlled trial. Gastroenterology 2000;119:305–309.

16. Harvey RF, Read AE. Mode of action of the saline purgatives. Am Heart J 1975;89:810–212.

17. Hasler WL, Soudah HC, Owyang C. Somatostatin analog inhibits afferent response to rectal distention in diarrhea-predominant irritable bowel patients. J Pharmacol Exp Ther 1994;268:1206–1211.

18. Heller SN, Hackler LR. Changes in the crude fiber content of the American diet. Am J Clin Nutr 1978;31:1510–1514.

19. Hislop IG. Psychological significance of the irritable colon syndrome. Gut 1971;12:452–457.

20. Jepson S, Klaerke A, Nielsen PH, et al. Negative effect of metoclopramide in postoperative adynamic ileus: a prospective, randomized, double-blind study. Br J Surg 1986;73: 290–291.

21. Kellow JE, Phillips SF. Altered small-bowel motility in irritable bowel syndrome is correlated with symptoms. Gastroenterology 1987;92:1885–1893.

22. Lacy BE, Yu S. Tegaserod: a new 5-HT4 agonist. J Clin Gastroenterol 2002;34:27–33.

23. Longo WE, Vernava AM III. Prokinetic agents for lower gastrointestinal motility disorders. Dis Colon Rectum 1993; 36:696.

24. Manning AP, Thompson WG, Heaton KW, et al. Towards positive diagnosis of the irritable bowel. BMJ 1978;2: 653–654.

25. Martelli H, Duguay C, Devroede G, et al. Some parameters of large bowel function in man. Gastroenterology 1978; 75:612–618.

26. Mathias JR, Clench MH, Reeves-Darby VG, et al. Effect of leuprolide acetate in patients with moderate to severe functional bowel disease. Dig Dis Sci 1994;39:1155–1162.

27. Munakata J, Naliboff B, Harraf F, et al. Repetitive sigmoid stimulation induces rectal hyperalgesia in patients with irritable bowel syndrome. Gastroenterology 1997;112:55–63.

28. Nordgaard I, Nortensen PB. Digestive processes in the human colon. Nutrition 1995;12:35–45.

29. Ogilvy AJ, Smith G. The gastrointestinal tract after anesthesia. Eur J Anaesthesiol Suppl 1995;10:35–42.

30. Painter NS, Burkitt DP. Diverticular disease of the colon: a deficiency disease of Western civilization. BMJ 1971;2: 450–454.

31. Papi C, Ciaco A, Koch M, et al. Efficacy of rifaximin in the treatment of symptomatic diverticular disease of the colon: a multicentre double-blind placebo-controlled trial. Aliment Pharmacol Ther 1995;9:33–39.

32. Parks TC. Natural history of diverticular disease of the colon. Clin Gastroenterol 1975;4:53–69.

33. Rendtdorff RC, Kashgarian M. Stool patterns of healthy adult males. Dis Colon Rectum 1967;10:222–228.

34. Ritchie JA, Truelove SC. Treatment of irritable bowel syndrome with lorazepam, hyoscine butylbromide and ispaghula husk. BMJ 1979;1:376–378.

35. Roberts JP, Benson MJ, Rogers J, et al. Effect of cisapride on distal colonic motility in the early postoperative period following left colonic anastamosis. Dis Colon Rectum 1995; 38:139–145.

36. Sandler RS, Halabi S, Baron JA, et al. A randomized trial of aspirin to prevent colorectal adenomas in patients with previous colorectal cancer. N Engl J Med 2003;348:883–889.

37. Snape WJ Jr, Carlson GM, Cohen D. Colonic myoelectrical activity in the irritable bowel syndrome. Gastroenterology 1976;70:326–330.

38. Stefanini GF, Saggioro A, Alvisi V, et al. Oral cromolyn sodium in comparison with elimination diet in the irritable bowel syndrome, diarrheic type. Scand J Gastoenterol 1995; 30:535–541.

39. Talley NJ, Owen BK, Boyce P, et al. Psychological treatments for irritable bowel syndrome: a critique of controlled treatment trials. Am J Gastroenterol 1996;91:277–286.

40. Verlinden M, Michiels G, Boghaert A, et al. Treatment of postoperative gastrointestinal atony. Br J Surg 1987;74: 614–617.

41. Walker EA, Byrne PP, Katon WJ. Irritable bowel syndrome and psychiatric illness. Am J Psychiatry 1990;147:565–572.

42. Walker EA, Katon WJ, Roy-Byrne PP, et al. Histories of sexual victimization in patients with irritable bowel syndrome or inflammatory bowel disease. Am J Psychiatry 1993;150: 1502–1506.

43. Walker EA, Roy-Byrne PP, Katon WJ, et al. Psychiatric illness and irritable bowel syndrome: a comparison with inflammatory bowel disease. Am J Psychiatry 1990;147:1656–1661.

44. Whitehead WE, Holtkotter B, Enck P, et al. Tolerance for recto-sigmoid distention in irritable bowel syndrome. Gastroenterology 1990;98:1187–1192.

45. Zieghagen DJ, Tewinkel G, Kruis W, et al. Adding more fluid to wheat bran has no significant effects on intestinal functions of healthy subjects. J Clin Gastroenterol 1991;13:525–530.

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