531
Nutritional Concerns in Gastrointestinal Neuropathy BETH CRONIN, MS, RD, CDE Holy Family Hospital and Medical Center Methuen, Massachusetts
development of neuropathy has been linked to hyperglycemial .2 ; however, other factors, (environmental,’1 vascular,1.2 immune,2 and genetic2) also may contribute to pathogenesis. Although the etiology of diabetic neuropathy is not fully understood, duration of diabetes, degree of hyperglycemia, presence of other diabetic complications, cigarette smoking, and reduced level of high-density lipoprotein cholesterol appear to correlate positively with the prevalence of this The
complication.’
.
Manifestations of gastrointestinal autonomic neuropathy include gastroparesis, diabetic diarrhea, and constipation 3 Gastroparesis and diabetic diarrhea typically present in individuals with a history of long-term, poorlycontrolled diabetes, peripheral neuropathy, and evidence of other autonomic impainnent.3-6 In addition to the motility disorders of the stomach and small bowel, esophageal dysfunction and changes in pancreatic exocrine function have been observed more frequently in patients with diabetes than in the general population. 3.4
of fullness, and, in about half of all cases, nausea and vomiting. Attacks of gastric stasis may be brief or the condition may become intractable. When gastroparesis persists, poor appetite, weight loss, decline in nutritional status, and reactive depression are likely to ensue. Glycemic control is more difficult to achieve because altered nutrient absorption is no longer synchronized with insulin activity. The clinical management of diabetic gastroparesis should include pharmacologic treatment, an individualized insulin administration regimen accompanied by self blood glucose monitoring, and nutritional therapy related to the degree of dysfunction (see Figure). of Treatment Pharmacologic Prokinetic usuGastroparesis agents ally are prescribed to enhance gastric emptying of solids. Metoclopramide (Reglan), taken as 10 mg three to four times per day (t/2 hour before meals and at bedtime) initially is beneficial in the treatment of gastric stasis.&dquo; Side effects of metoclopramide (agitation, depression, and involuntary movements6)
reported in up to 10% of patients.10 Domperidone (Motilium) have been
Gastroparesis Gastroparesis is thought to be due to a disturbance in the myoelectric activity of the smooth muscle of the stomach, which results in compromised clearance of solids from the adtrum. 5-7 In advanced cases, involvement of the proximal stomach leads to impaired emptying of both solids and liquids.5.8 Symptoms of gastroparesis include
abdominal bloating, a persistent feeling
Beth Cronin is
an
Outpatient Dietitian at Holy
Family Hospital and Medical Center. Correspondence to Beth Cronin, MS, RD, CDE, Holy Family Hospital and Medical Center, 70 East Street, Methuen, MAO 1844.
does not cross the blood brain barrier and therefore rarely induces side effects.1,10 With chronic administration, both pharmacologic agents have been shown to produce a refractory response.8 Cisapride (Prepulsid), an investigational drug, has been shown to promote improvement in solid as well as liquid gastric emptying, and therefore shows promise as an effective, long-term treatment of gastroparesis.$8 Erythromycin, which appears to act as a motilin agonist, also is under investigation to determine the potential long-term efficacy in the treatment of gastric stasis. In a clinical trial reported by Janssens et al,&dquo; intravenous admin-
istration of erythromycin promoted normal emptying of liquids and solids in diabetic patients with advanced gastroparesis. Oral treatment with erythromycin during a four-week period also was shown to accelerate the emptying rate for both solids and liquids in these subjects. However, a difference between solid and liquid emptying still was
observed.
Nutritional Management of Mild to Moderate Gastroparesis Individuals who present with mild to moderate symptoms of gastroparesis usually experience impaired emptying of solids from the stomach while liquid clearance remains normal.5.8 Because the defect of solid emptying is neural, there does not appear to be one single mealrelated determinant of gastric emptying rate for individuals with diabetic gastroparesis. Osmolarity, acidity, fat and amino acid composition, nutrient density, and feeding volume all influence gastric emptying in normal physiology.5 There is evidence that osmolarity has a greater effect on gastric retention than does fat.’2 Receptors located in the proximal duodenum and jejunum respond to hormonal controls to regulate
emptying. Hypertonic, high-fat, acidic, and nutrient-dense feedings tend to retard gastric emptying via the action of these receptors.3 Water soluble fiber also has been demonstrated to delay the emptying of gastric contents by mechanical means.’3 Nutritional intervention of symptomatic bouts of gastric stasis should consist of small, frequent feedings of low-fat, low-fiber foods. Solids may be blenderized to a liquid consistency to promote passage through the stomach. Oral supplementation with nutrientdense liquids should be initiated as necessary. When liquid emptying is not
impaired, milk, regular
Downloaded from tde.sagepub.com at UNIVERSITY OF SASKATCHEWAN LIBRARY on June 21, 2015
or
sugar-free
532
Meeting Nutritional Needs in
*Reproduced/adapted with penllissionfrom Cronin
BS.
Diabetic
Gastroparesis (algorithm)*
Insights into Diabetic Gastroparesis-Part 2. RD 1989; 9(2):7.
Downloaded from tde.sagepub.com at UNIVERSITY OF SASKATCHEWAN LIBRARY on June 21, 2015
533
instant breakfast drinks, meal replaceformulas or commercially available milk shakes can be calculated into the diabetic meal plan to achieve the desired balance of calories, macronutrients, vitamins, and minerals. The choice of meal replacement formula should be based on patient acceptance and tolerance. A fiber-free formula with a lower osmolarity (eg, Ensure/Ross Laboratories: 470 mosm/kg water) may be offered if instant breakfast drinks (671-758 mosmlkg water) are not well tolerated. It should be noted that fat content frequently is greater in products that have a lower ment
poorly or has been without food orally (NPO) for some time. Formula strength (isotonicity) and volume should be gradually progressed until the goal rate is achieved (usually 60 to 80 mllhr).I~,15.17 Intravenous fluids must be continued until hydration needs are met (about 30-40 mLlkg).17 The choice of formula and volume of feeding should be individualized for patients
with renal disease or in cases where fluid restriction is warranted. Patient tolerance to the feeding should be monitored frequently at this stage. Daily weights, report of fluid intake and output, nursing notes indicating changes in osmolarity. consistency of stools, and glucose and Food diaries may be compared with electrolyte values should be reviewed the results of blood glucose measure- to detect potential complications of ments and records of hypoglycemic ep- tube feeding. When the patient has adjusted to isodes to facilitate adjustments to the insulin regimen. For example, regular jejunostomy feeding, an isotonic, lacinsulin may need to be administered tose-free, meal-replacement formula shortly after a meal rather than pre- may be introduced (eg, IsocaI/Mead meal to allow for delayed glucose ab- Johnson Enteral Nutritionals or Osmosorption. Insulin requirements are lite/Ross Laboratories). This type of likely to increase with improved formulation generally is tolerated by caloric intake associated with oral the jejunum and is more economical for supplementation. long-term use. Although there have Glycemic control, although more been reports to support the role of fiber difficult to achieve with gastroparesis, in the maintenance of gut integrity and should be a focus of patient teaching. function,18 the safety and efficacy of Hyperglycemia is one of the factors feeding a fiber-containing formula into known to aggravate gastric reten- the jejunum has not been studied’-’ and tion.3.5.12.1~.15 Improved glycemia hope- therefore currently is not advised. Transition to a nocturnal-cycle feedfully will extend clinical remissions. When symptoms improve, the regis- ing schedule may be considered when tered dietitian (RD) and/or the certified long-term home tube feeding is wardiabetes educator (CDE) should en- ranted. This schedule may enable the courage the patient to resume follow- patient to resume a more routine lifeing a usual meal plan. Emotional sup- style. If the patient is able to take small port is critical as the individual may be amounts of food orally, the RD should reluctant to reintroduce solid foods. analyze food records to determine the nutritional contribution of any meals. Nutritional Therapy for Advanced The remainder of assessed nutritional Gastroparesis When nausea, vomit- needs may then be delivered via contining, and marked gastric stasis (both liq- uous overnight feeding. A 2 Kcal/mL uids and solids) do not respond to ma- formula may be initiated to allow a nipulations of oral feeding and slower rate of delivery over a 10- to pharmacologic treatment, post-pyloric 16-hour period of time. Free water feeding has proven to be an effective needs can be met by taking water means of alleviating gastric distress through the jejunostomy tube during and meeting nutritional goalS.16 Short- the day. Bolus feeding into the small term enteral alimentation can be ad- bowel is contraindicated as this is ministered via a nasoduodenal or likely to promote symptoms of dumpnasojejunal tube. However, a surgi- ing syndrome. During acute exacerbations of gascally-placed feeding jejunostomy should be considered for long-term use. troparesis, nasogastric suctioning may Continuous, pump-assisted, 24-hour be employed to empty the stomach. In feeding of an elemental formula is the event that a patient must be NPO advised if the patient has been eating for two to three weeks for suctioning,
total parenteral nutrition is advisable to achieve normal hydration and to avert protein calorie malnutrition.I~~~9 Total parenteral nutrition should be employed only when the gut is
non-functional.
Diabetic Diarrhea Diabetic diarrhea is characterized by of multiple loose stools and often is nocturnal. Remissions are unexplained and may alternate with periods of normal bowel movements or constipation.3.4.20 The diagnosis of diabetic diarrhea is made only after a complete clinical evaluation has been performed to exclude the presence of other diseases or another cause of the malabsorptive process. Celiac disease has been associated with certain genetic subgroups of type I diabetes and therefore is more frequently observed in the diabetic population.3,4.20 Jejunal biopsy is warranted when steatorrhea is present to rule-out gluten enteropathy. Neural defects of intestinal motility have been implicated in the etiology of diabetic diarrhea. Rapid transit time is believed to promote diarrhea. However, delayed transit time associated with bacterial overgrowth also may cause diarrhea. Alterations in pancreatic exocrine function and in the action of gut factors also appear to be contrib-
episodes
uting factors.3.4.20 Effective dietary
treatment of diabetic diarrhea has not been reported. Fiber, administered as Metamucil or cholestyramine resin, has not4 proven to ameliorate this condition.4 Patients who experience diabetic diarrhea should be encouraged to follow a meal plan designed to meet assessed energy and nutrient needs. Adequate hydration and supplementation with a multiple vitamin/mineral tablet are advisable. Effective treatment of diabetic diarrhea has been reported using anti-
diarrheals, metoclopramide, cyclic antibiotics, and gut factor analogues.2°.2’ The effect of
glycemic
control in the
management of diabetic diarrhea is questionable. There have been reports that achievement of euglycemia has failed to ameliorate diarrhea.2° However, the link between poor glycemic control (two or more years prior to onset) and the development of diabetic diarrhea suggest that diabetes control may be a determinant of successful treatment.
Downloaded from tde.sagepub.com at UNIVERSITY OF SASKATCHEWAN LIBRARY on June 21, 2015
535
Constipation is the most
Constipation frequently ported gastrointestinal complaint of inre-
dividuals with diabetes; up to 60% may be affected.~9.22 Neuropathy is not always associated with constipation; however, a neural defect of intestinal motility has been observed in patients with diabetes. A high-fiber diet is recommended to promote normal transit of fecal contents. The RD and/or CDE should elicit a diet history to include frequency and quantity of fiber-rich foods consumed. Sample high-fiber recipes and specific suggestions for addition of fibrous foods should be offered during the nutrition counseling session. Lentils, dried beans and peas, whole grain cereals, green leafy vegetables, and whole fruits with edible seeds and skins may be recommended to promote increased fiber consumption. These foods are identified with a green symbol in the Exchange Lists for Meal Planlling.23 Ample sugar-free fluids, at least 8 cups per day, also should be recommended. When a high-fiber diet is not well tolerated due to gastroparesis (estimated to affect about 30-35% of people with diabetes22), or when constipation is marked, laxative therapy may be indicated.
Report from Pittsburgh epidemiology of diabetes complications study. Diabetes 1989;38:1456-61. 2. Understanding diabetic neuropathy. The Lancet
1. Maser RE, Steenkiste AR, Dorman JS, et al. Epidemiological correlates of diabetic neuropathy.
636-9.
1991;338:1496-97.
Yang R, Ridha A, Chan L Gastrointestinal complications of diabetes mellitus. Arch Intern 3.
Med 1984;144:1251-56. 4. Fochios S. Duodenal, biliary tract, and pancreatic abnormalities in diabetes. Practical Diabeto-
logy 1987;6:18-20. 5. Minami H, McCallum RW. The physiology and pathophysiology of gastric emptying in humans.
Gastroenterology 1984;86:1592-1610.
6. Camilleri M, Phillips SF. Gastroparesis: an emerging disorder of gut function. Contemp Intern Med 1989;1:22-32.
Wright R, Clemente A, Wathen R. Diabetic gastroparesis: an abnormality of gastric emptying 7.
of solids. J Med Sci 1985;289:240-42. 8. Horowitz M, Roberts AP. Long-term efficacy of cisapride in diabetic gastroparesis. Am J Med
1990;88:195-96. 9. McCallum RW, Ricci DA, Rakatansky H, et al. A multicenter placebo-controlled clinical trial of oral metoclopramide in diabetic gastroparesis. Diabetes Care 1993;6:463-67.
10. Horowitz MB, Harding PE, Chatterton BE, et al. Acute and chronic effects of domperidone on gastric emptying in diabetic autonomic neuropathy. Dig Dis Sci 1985;30:1-9. 11. Janssens J, Peeters TL, Vantrappen G, et al. Improvement of gastric emptying in diabetic gastroparesis by erythromycin. N Engl J Med
1990;332:1028-31. References
13. Holt S, Heading RC, Carter DC, et al. Effect of gel fibre on gastric emptying and absorption of glucose and paracetamol. Lancet 1979;1(8117):
12. Bury KD, Jambunathan G. Effects of elemental diets on gastric emptying and gastric secretion in
man. Am J Surg 1974;127:59-64.
14. Nompleggi D, Bell S, Blackburn G, et al. Overview of gastrointestinal disorders due to diabetes mellitus: emphasis on nutritional support J Parentr Enteral Nutr 1989;13:84-91. 15. Peters AL. Enteral and parenteral nutrition in patients with diabetes. Diabetes Professional 1990;Spring:1-16. 16. Jacober SJ, Narayan A, Strodel WE, et al. Jejunostomy feeding in the management of gasDiabetes
Care
17. Wade JE. Practical aspects of tube Clin Consult Nutr Supp 1982;2:12-14.
feeding.
troparesis
diabeticorum.
1986;9:217-19.
18. Dietary fiber and bowel function in tube-fed patients. J Am Diet Assoc 1991;91:590-96,599. 19. Bell SJ. Nutrition support in diabetes mellitus. In: Shronte EP, ed. Nutrition support dietetics core curriculum. Silver Spring, Md: American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.), 1990:175-80.
20. Ogbonnaya KI, Arem R. Diabetic diarrhea. Pathophysiology and management. Arch Intern Med 1990;150:262-67. 21. Michaels PE, Cameron RB. Ocreotide is costeffective therapy in diabetic diarrhea. Arch Intern Med 1991:151:2469,2473. 22. Kim CH.
Managing GI complications of diabetes. Contemp Intern Med 1992;00:77-86. 23.
Exchange lists for meal planning. Alexandria, Va, and Chicago: American Diabetes Association and American Dietetic Association,1989.
Downloaded from tde.sagepub.com at UNIVERSITY OF SASKATCHEWAN LIBRARY on June 21, 2015
Nutritional Concerns in Gastrointestinal Neuropathy BETH CRONIN, MS, RD, CDE Holy Family Hospital and Medical Center Methuen, Massachusetts
development of neuropathy has been linked to hyperglycemial .2 ; however, other factors, (environmental,’1 vascular,1.2 immune,2 and genetic2) also may contribute to pathogenesis. Although the etiology of diabetic neuropathy is not fully understood, duration of diabetes, degree of hyperglycemia, presence of other diabetic complications, cigarette smoking, and reduced level of high-density lipoprotein cholesterol appear to correlate positively with the prevalence of this The
complication.’
.
Manifestations of gastrointestinal autonomic neuropathy include gastroparesis, diabetic diarrhea, and constipation 3 Gastroparesis and diabetic diarrhea typically present in individuals with a history of long-term, poorlycontrolled diabetes, peripheral neuropathy, and evidence of other autonomic impainnent.3-6 In addition to the motility disorders of the stomach and small bowel, esophageal dysfunction and changes in pancreatic exocrine function have been observed more frequently in patients with diabetes than in the general population. 3.4
of fullness, and, in about half of all cases, nausea and vomiting. Attacks of gastric stasis may be brief or the condition may become intractable. When gastroparesis persists, poor appetite, weight loss, decline in nutritional status, and reactive depression are likely to ensue. Glycemic control is more difficult to achieve because altered nutrient absorption is no longer synchronized with insulin activity. The clinical management of diabetic gastroparesis should include pharmacologic treatment, an individualized insulin administration regimen accompanied by self blood glucose monitoring, and nutritional therapy related to the degree of dysfunction (see Figure). of Treatment Pharmacologic Prokinetic usuGastroparesis agents ally are prescribed to enhance gastric emptying of solids. Metoclopramide (Reglan), taken as 10 mg three to four times per day (t/2 hour before meals and at bedtime) initially is beneficial in the treatment of gastric stasis.&dquo; Side effects of metoclopramide (agitation, depression, and involuntary movements6)
reported in up to 10% of patients.10 Domperidone (Motilium) have been
Gastroparesis Gastroparesis is thought to be due to a disturbance in the myoelectric activity of the smooth muscle of the stomach, which results in compromised clearance of solids from the adtrum. 5-7 In advanced cases, involvement of the proximal stomach leads to impaired emptying of both solids and liquids.5.8 Symptoms of gastroparesis include
abdominal bloating, a persistent feeling
Beth Cronin is
an
Outpatient Dietitian at Holy
Family Hospital and Medical Center. Correspondence to Beth Cronin, MS, RD, CDE, Holy Family Hospital and Medical Center, 70 East Street, Methuen, MAO 1844.
does not cross the blood brain barrier and therefore rarely induces side effects.1,10 With chronic administration, both pharmacologic agents have been shown to produce a refractory response.8 Cisapride (Prepulsid), an investigational drug, has been shown to promote improvement in solid as well as liquid gastric emptying, and therefore shows promise as an effective, long-term treatment of gastroparesis.$8 Erythromycin, which appears to act as a motilin agonist, also is under investigation to determine the potential long-term efficacy in the treatment of gastric stasis. In a clinical trial reported by Janssens et al,&dquo; intravenous admin-
istration of erythromycin promoted normal emptying of liquids and solids in diabetic patients with advanced gastroparesis. Oral treatment with erythromycin during a four-week period also was shown to accelerate the emptying rate for both solids and liquids in these subjects. However, a difference between solid and liquid emptying still was
observed.
Nutritional Management of Mild to Moderate Gastroparesis Individuals who present with mild to moderate symptoms of gastroparesis usually experience impaired emptying of solids from the stomach while liquid clearance remains normal.5.8 Because the defect of solid emptying is neural, there does not appear to be one single mealrelated determinant of gastric emptying rate for individuals with diabetic gastroparesis. Osmolarity, acidity, fat and amino acid composition, nutrient density, and feeding volume all influence gastric emptying in normal physiology.5 There is evidence that osmolarity has a greater effect on gastric retention than does fat.’2 Receptors located in the proximal duodenum and jejunum respond to hormonal controls to regulate
emptying. Hypertonic, high-fat, acidic, and nutrient-dense feedings tend to retard gastric emptying via the action of these receptors.3 Water soluble fiber also has been demonstrated to delay the emptying of gastric contents by mechanical means.’3 Nutritional intervention of symptomatic bouts of gastric stasis should consist of small, frequent feedings of low-fat, low-fiber foods. Solids may be blenderized to a liquid consistency to promote passage through the stomach. Oral supplementation with nutrientdense liquids should be initiated as necessary. When liquid emptying is not
impaired, milk, regular
Downloaded from tde.sagepub.com at UNIVERSITY OF SASKATCHEWAN LIBRARY on June 21, 2015
or
sugar-free
532
Meeting Nutritional Needs in
*Reproduced/adapted with penllissionfrom Cronin
BS.
Diabetic
Gastroparesis (algorithm)*
Insights into Diabetic Gastroparesis-Part 2. RD 1989; 9(2):7.
Downloaded from tde.sagepub.com at UNIVERSITY OF SASKATCHEWAN LIBRARY on June 21, 2015
533
instant breakfast drinks, meal replaceformulas or commercially available milk shakes can be calculated into the diabetic meal plan to achieve the desired balance of calories, macronutrients, vitamins, and minerals. The choice of meal replacement formula should be based on patient acceptance and tolerance. A fiber-free formula with a lower osmolarity (eg, Ensure/Ross Laboratories: 470 mosm/kg water) may be offered if instant breakfast drinks (671-758 mosmlkg water) are not well tolerated. It should be noted that fat content frequently is greater in products that have a lower ment
poorly or has been without food orally (NPO) for some time. Formula strength (isotonicity) and volume should be gradually progressed until the goal rate is achieved (usually 60 to 80 mllhr).I~,15.17 Intravenous fluids must be continued until hydration needs are met (about 30-40 mLlkg).17 The choice of formula and volume of feeding should be individualized for patients
with renal disease or in cases where fluid restriction is warranted. Patient tolerance to the feeding should be monitored frequently at this stage. Daily weights, report of fluid intake and output, nursing notes indicating changes in osmolarity. consistency of stools, and glucose and Food diaries may be compared with electrolyte values should be reviewed the results of blood glucose measure- to detect potential complications of ments and records of hypoglycemic ep- tube feeding. When the patient has adjusted to isodes to facilitate adjustments to the insulin regimen. For example, regular jejunostomy feeding, an isotonic, lacinsulin may need to be administered tose-free, meal-replacement formula shortly after a meal rather than pre- may be introduced (eg, IsocaI/Mead meal to allow for delayed glucose ab- Johnson Enteral Nutritionals or Osmosorption. Insulin requirements are lite/Ross Laboratories). This type of likely to increase with improved formulation generally is tolerated by caloric intake associated with oral the jejunum and is more economical for supplementation. long-term use. Although there have Glycemic control, although more been reports to support the role of fiber difficult to achieve with gastroparesis, in the maintenance of gut integrity and should be a focus of patient teaching. function,18 the safety and efficacy of Hyperglycemia is one of the factors feeding a fiber-containing formula into known to aggravate gastric reten- the jejunum has not been studied’-’ and tion.3.5.12.1~.15 Improved glycemia hope- therefore currently is not advised. Transition to a nocturnal-cycle feedfully will extend clinical remissions. When symptoms improve, the regis- ing schedule may be considered when tered dietitian (RD) and/or the certified long-term home tube feeding is wardiabetes educator (CDE) should en- ranted. This schedule may enable the courage the patient to resume follow- patient to resume a more routine lifeing a usual meal plan. Emotional sup- style. If the patient is able to take small port is critical as the individual may be amounts of food orally, the RD should reluctant to reintroduce solid foods. analyze food records to determine the nutritional contribution of any meals. Nutritional Therapy for Advanced The remainder of assessed nutritional Gastroparesis When nausea, vomit- needs may then be delivered via contining, and marked gastric stasis (both liq- uous overnight feeding. A 2 Kcal/mL uids and solids) do not respond to ma- formula may be initiated to allow a nipulations of oral feeding and slower rate of delivery over a 10- to pharmacologic treatment, post-pyloric 16-hour period of time. Free water feeding has proven to be an effective needs can be met by taking water means of alleviating gastric distress through the jejunostomy tube during and meeting nutritional goalS.16 Short- the day. Bolus feeding into the small term enteral alimentation can be ad- bowel is contraindicated as this is ministered via a nasoduodenal or likely to promote symptoms of dumpnasojejunal tube. However, a surgi- ing syndrome. During acute exacerbations of gascally-placed feeding jejunostomy should be considered for long-term use. troparesis, nasogastric suctioning may Continuous, pump-assisted, 24-hour be employed to empty the stomach. In feeding of an elemental formula is the event that a patient must be NPO advised if the patient has been eating for two to three weeks for suctioning,
total parenteral nutrition is advisable to achieve normal hydration and to avert protein calorie malnutrition.I~~~9 Total parenteral nutrition should be employed only when the gut is
non-functional.
Diabetic Diarrhea Diabetic diarrhea is characterized by of multiple loose stools and often is nocturnal. Remissions are unexplained and may alternate with periods of normal bowel movements or constipation.3.4.20 The diagnosis of diabetic diarrhea is made only after a complete clinical evaluation has been performed to exclude the presence of other diseases or another cause of the malabsorptive process. Celiac disease has been associated with certain genetic subgroups of type I diabetes and therefore is more frequently observed in the diabetic population.3,4.20 Jejunal biopsy is warranted when steatorrhea is present to rule-out gluten enteropathy. Neural defects of intestinal motility have been implicated in the etiology of diabetic diarrhea. Rapid transit time is believed to promote diarrhea. However, delayed transit time associated with bacterial overgrowth also may cause diarrhea. Alterations in pancreatic exocrine function and in the action of gut factors also appear to be contrib-
episodes
uting factors.3.4.20 Effective dietary
treatment of diabetic diarrhea has not been reported. Fiber, administered as Metamucil or cholestyramine resin, has not4 proven to ameliorate this condition.4 Patients who experience diabetic diarrhea should be encouraged to follow a meal plan designed to meet assessed energy and nutrient needs. Adequate hydration and supplementation with a multiple vitamin/mineral tablet are advisable. Effective treatment of diabetic diarrhea has been reported using anti-
diarrheals, metoclopramide, cyclic antibiotics, and gut factor analogues.2°.2’ The effect of
glycemic
control in the
management of diabetic diarrhea is questionable. There have been reports that achievement of euglycemia has failed to ameliorate diarrhea.2° However, the link between poor glycemic control (two or more years prior to onset) and the development of diabetic diarrhea suggest that diabetes control may be a determinant of successful treatment.
Downloaded from tde.sagepub.com at UNIVERSITY OF SASKATCHEWAN LIBRARY on June 21, 2015
535
Constipation is the most
Constipation frequently ported gastrointestinal complaint of inre-
dividuals with diabetes; up to 60% may be affected.~9.22 Neuropathy is not always associated with constipation; however, a neural defect of intestinal motility has been observed in patients with diabetes. A high-fiber diet is recommended to promote normal transit of fecal contents. The RD and/or CDE should elicit a diet history to include frequency and quantity of fiber-rich foods consumed. Sample high-fiber recipes and specific suggestions for addition of fibrous foods should be offered during the nutrition counseling session. Lentils, dried beans and peas, whole grain cereals, green leafy vegetables, and whole fruits with edible seeds and skins may be recommended to promote increased fiber consumption. These foods are identified with a green symbol in the Exchange Lists for Meal Planlling.23 Ample sugar-free fluids, at least 8 cups per day, also should be recommended. When a high-fiber diet is not well tolerated due to gastroparesis (estimated to affect about 30-35% of people with diabetes22), or when constipation is marked, laxative therapy may be indicated.
Report from Pittsburgh epidemiology of diabetes complications study. Diabetes 1989;38:1456-61. 2. Understanding diabetic neuropathy. The Lancet
1. Maser RE, Steenkiste AR, Dorman JS, et al. Epidemiological correlates of diabetic neuropathy.
636-9.
1991;338:1496-97.
Yang R, Ridha A, Chan L Gastrointestinal complications of diabetes mellitus. Arch Intern 3.
Med 1984;144:1251-56. 4. Fochios S. Duodenal, biliary tract, and pancreatic abnormalities in diabetes. Practical Diabeto-
logy 1987;6:18-20. 5. Minami H, McCallum RW. The physiology and pathophysiology of gastric emptying in humans.
Gastroenterology 1984;86:1592-1610.
6. Camilleri M, Phillips SF. Gastroparesis: an emerging disorder of gut function. Contemp Intern Med 1989;1:22-32.
Wright R, Clemente A, Wathen R. Diabetic gastroparesis: an abnormality of gastric emptying 7.
of solids. J Med Sci 1985;289:240-42. 8. Horowitz M, Roberts AP. Long-term efficacy of cisapride in diabetic gastroparesis. Am J Med
1990;88:195-96. 9. McCallum RW, Ricci DA, Rakatansky H, et al. A multicenter placebo-controlled clinical trial of oral metoclopramide in diabetic gastroparesis. Diabetes Care 1993;6:463-67.
10. Horowitz MB, Harding PE, Chatterton BE, et al. Acute and chronic effects of domperidone on gastric emptying in diabetic autonomic neuropathy. Dig Dis Sci 1985;30:1-9. 11. Janssens J, Peeters TL, Vantrappen G, et al. Improvement of gastric emptying in diabetic gastroparesis by erythromycin. N Engl J Med
1990;332:1028-31. References
13. Holt S, Heading RC, Carter DC, et al. Effect of gel fibre on gastric emptying and absorption of glucose and paracetamol. Lancet 1979;1(8117):
12. Bury KD, Jambunathan G. Effects of elemental diets on gastric emptying and gastric secretion in
man. Am J Surg 1974;127:59-64.
14. Nompleggi D, Bell S, Blackburn G, et al. Overview of gastrointestinal disorders due to diabetes mellitus: emphasis on nutritional support J Parentr Enteral Nutr 1989;13:84-91. 15. Peters AL. Enteral and parenteral nutrition in patients with diabetes. Diabetes Professional 1990;Spring:1-16. 16. Jacober SJ, Narayan A, Strodel WE, et al. Jejunostomy feeding in the management of gasDiabetes
Care
17. Wade JE. Practical aspects of tube Clin Consult Nutr Supp 1982;2:12-14.
feeding.
troparesis
diabeticorum.
1986;9:217-19.
18. Dietary fiber and bowel function in tube-fed patients. J Am Diet Assoc 1991;91:590-96,599. 19. Bell SJ. Nutrition support in diabetes mellitus. In: Shronte EP, ed. Nutrition support dietetics core curriculum. Silver Spring, Md: American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.), 1990:175-80.
20. Ogbonnaya KI, Arem R. Diabetic diarrhea. Pathophysiology and management. Arch Intern Med 1990;150:262-67. 21. Michaels PE, Cameron RB. Ocreotide is costeffective therapy in diabetic diarrhea. Arch Intern Med 1991:151:2469,2473. 22. Kim CH.
Managing GI complications of diabetes. Contemp Intern Med 1992;00:77-86. 23.
Exchange lists for meal planning. Alexandria, Va, and Chicago: American Diabetes Association and American Dietetic Association,1989.
Downloaded from tde.sagepub.com at UNIVERSITY OF SASKATCHEWAN LIBRARY on June 21, 2015
