1. Dietary Interventions for the Patient with Gastropathy
Julianne Steiner, MS, RD, CDE
Endocrine/Diabetes Clinic
McKay-Dee Hospital Center

2. Objectives
The participant will be able to: 1. Describe neuropathic complications of diabetes that can impact the GI tract. 2. Describe nutritional therapies that can be utilized in treating diabetic gastropathy.

3. Normal Gastric Function
Fundic relaxation to accommodate food
Contractions for breaking large food particles
Pyloric relaxation to allow food to exit

4. Normal Gastric Emptying
Coordinated effort between different regions of the stomach and the duodenum
Extrinsic modulation by CNS and distal gut factors
“Pacemaker” located on upper, outer portion of stomach. Electrical waves cause muscles to contract.
Normally contracts 3 X/min.
Stomach empties in minutes after eating

5. Gastric Emptying Rate Physical nature of food Particle size
Liquid vs. solid
Particle size
2 mm in diameter
Fat content
Caloric content
High calorie liquids empty at a constant rate

6. Gastroparesis
Characterized by delayed gastric emptying in the absence of mechanical obstruction
Vagal nerve conduction is diminished
Reduced smooth muscle contractility
Compromised myoelectrical activity
Results in erratic blood glucose control

7. Gastroparesis
Estimated that up to 75% of individuals with diabetes develop some gastrointestinal symptoms
Many patients do not report symptoms to doctor
Patients do not realize that symptoms are related to diabetes.

8. Gastroparesis Symptoms can last days to months or occur in cycles
Poor correlation between symptoms and actual diagnosis
Little evidence of a time interval between diabetes diagnosis and development of gastroparesis

9. Gastroparesis 11%- 18% of individuals with diabetes report symptoms
25%-50% of patients with Type 1 diabetes (not correlated with nongastrointestinal complications)
About 30%of patients with Type 2 diabetes

10. Gastroparesis majority of patients are women (82%)
Associated with increased BMI
Not universal or inevitable

11. Pittsburgh Epidemiology of Diabetes Complications
A: Proliferative retinopathy, B: Overt nephropathy,
C: Symptomatic automatic neuropathy, D: Distal symmetric polyneuropathy
Pambianco, G., et al. The 30 –Year Natural History of Type 1 Diabetes Complications
Diabetes 55: , 2006

12. Clinical Consequences
Gastrointestinal symptoms
Alteration in oral drug absorption
Glipizide
Poor glycemic control

13. Symptoms (nonspecific)
Nausea (92%)
Vomiting (84%)
Bloating (75%)
Early satiety
Upper abdominal discomfort
Reflux
Unexplained weight loss
Erratic blood glucose levels

14. Delayed Gastric Emptying
First sign: erratic blood glucose levels
Other symptoms may be mild to severe
Unexplained weight loss
Prone to bezoar formation / obstruction

15. Blood Glucose Effects Hyperglycemia slows gastric emptying
Causes pyloric value to contract
Decreases motility
Induces gastric dysrhythmias

16. Delayed gastric emptying
Vicious Cycle
Hyperglycemia
Delayed gastric emptying
Initial hypoglycemia
Late hyperglycemia

17. Blood Glucose Effects Hyperglycemia slows gastric emptying
Causes pyloric value to contract
decreases motility
Hypoglycemia accelerates gastric emptying
Important in counter-regulation of hypoglycemia
Continuous inverse relationship between blood glucose levels and rate of gastric emptying.

18. Pathogenesis Combination of factors Vagal neuropathy Hyperglycemia
Unknown factors

19. Diagnosis Consider medications that may cause gastric stasis:
Anticholinergic agents
Antidepressants
Calcium-channel blockers
Upper endoscopy to rule out obstruction

20. Diagnosis Scintigraphy (gold standard) Isotope breath tests
Calculates time to empty 50% of meal and percentage remaining after 2 and 4 hours
Isotope breath tests
Measures amount of CO2 in breath samples
Ultrasonography
Measures flow of food through pyloric sphincter
Magnetic resonance imaging

21. Nutrition Management Treatment goals: Alleviate symptoms
Improve gastric emptying
Enhance glycemic control
Delay progression of other complications

22. Gastroparesis Emptying of solid food is delayed
Emptying of liquids remains unchanged until condition becomes more advanced
Prone to development of bezoars
Severity of symptoms does not correlate with degree of gastric emptying.

23. Nutrition Management Eat smaller meals more frequently.
Eat low-fiber forms of high-fiber foods, such as well-cooked fruits and vegetables rather than raw fruits and vegetables.
Choose mostly low-fat foods, add small servings of higher fat foods if tolerated
Avoid fibrous fruits and vegetables, such as oranges and broccoli, that are likely to cause bezoars.

24. Nutrition Management
Choose soft or liquid foods such as soups and pureed foods
Drink water throughout each meal.
Try mild exercise after eating, such as going for a walk.
Individualize to patient’s tolerance based on postprandial glucose results

25. Nutrition Management Avoid alcohol and tobacco
Chew sugar-free gum for 1 hr after meal

26. Nutrition Management Add nutrition supplements High nutrient liquids
Enteral feedings via jejunostomy tube
TPN – seldom indicated

27. Case Study
“Carol”
2/3/2011
52 yo female
Type 1
Ht: 62”
Wt: 140 (down 3 lbs. in 3 mo.)
A1c 7.3
Blood glucose:
High BG spikes after meal
Eats one meal a day
Gives bolus after eating
Counseled on diet for gastroparesis: -6 small meals - low fat, fiber -avoid carbonation and gas producing foods -Advised to give part of bolus before meal

28. Case Study “Carol” 7/19/11 Wt: 141 ( up 1 pound)
A1c (7/19/11): 6.8 (down 0.5)
Blood glucose: majority within target range on cgms
Tries to eat something for breakfast and lunch, but still skips meals
?? Nutrition adequacy

29. Dietary Adequacy 10 Type 1 patients Mean age 44 yrs BMI 25.4 A1c 10.4
Common symptoms
Bloating, nausea, halitosis, acid reflux, belching, abdominal pain, flatulence, diarrhea, anorexia, heartburn, vomiting
Symptom severity did not correlate with A1c
Goldberg K.B. JADA 97: , 1997.

30. Dietary Adequacy Mean energy intake: 63% of recommended levels
Carbohydrate and fat reduced proportionately more than protein
Calcium: 70% of recommended amount
Recommend nutrition supplements to this population
Goldberg K.B. JADA 97: , 1997.

31. Nutrition Management Factors which influence postprandial glucose
Fasting blood glucose level
Meal composition (carbohydrate)
Rate of absorption from small intestine
Insulin secretion/timing
Hepatic glucose metabolism
Peripheral insulin sensitivity

32. Insulin Therapy
Mismatch between insulin action and glucose absorption from meal
Insulin peaks before glucose is absorbed
Causes early hypoglycemia
Later, glucose is absorbed, but no insulin
Causes late hyperglycemia

33. Insulin Treatment Strategies
Rapid acting- adjust timing of injection
Regular insulin before meal
Delayed or extended bolus delivery with pump
Monitor blood glucose frequently or use CGMS

34. Pharmacotherapy Metoclopramide (Reglan)
Stimulates stomach muscle contractions
Helps reduce nausea and vomiting
Taken minutes before meals and at bedtime
Long-term use is limited by development of:
Tolerance
Restlessness
prolactinemia

35. Pharmacotherapy Erythromycin Increases stomach contractions
Given IV in acutely ill
Less effective when given orally or long term
? transdermally

36. Pharmacotherapy Botulinum toxin (Botox) Intrapyloric injection
Relaxes pyloric muscle in some
Benefits are temporary
No efficacy in controlled studies

37. Pharmacotherapy Domperidone (Motilium)
Used to suppress nausea/vomiting
Used as a prokinetic
Stimulates lactation
*Not approved for use in the U. S.

38. Electrical Gastric Stimulation
Uses electrical current to cause stomach contractions
Surgically placed in a pocket on outer edge of stomach

39. Enterra Therapy Pacemaker-like device Produced by Medtronic
Battery operated (battery life 5-10 yrs)
Implanted in abdomen
Electrode connected to the stomach muscle
Releases low-voltage electrical shocks every 6 seconds, causing stomach to contract

40. Medtronic Enterra
2.2” X 2.4” X 0.4”

41. Enterra Therapy
Approved by U.S. FDA April, 2000 as humanitarian device Authorized by Federal law for use in the treatment of chronic intractable (drug refractory) nausea and vomiting secondary to gastroparesis of diabetic or idiopathic etiology. The effectiveness of this device for this use has not been demonstrated.
Because of the HDE status, the system must be implanted in a medical center whose institutional review board (IRB) has approved use of the device.

42. Surgical Treatment Rarely used
Increase the size of opening between stomach and intestine
Gastrectomy

43. Long-term Management Multidisciplinary approach
Patient’s understanding of how food and medicines work together
Frequent blood glucose monitoring (4-8 /day) and/or use of CGMS
Individualized diet according to patient tolerance
Normal life expectancy after adjustments for other disorders

44. Thank You!