Presentation on theme: "Dietary Interventions for the Patient with Gastropathy"— Presentation transcript:
1Dietary Interventions for the Patient with Gastropathy Julianne Steiner, MS, RD, CDEEndocrine/Diabetes ClinicMcKay-Dee Hospital Center
2ObjectivesThe 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.
3Normal Gastric Function Fundic relaxation to accommodate foodContractions for breaking large food particlesPyloric relaxation to allow food to exit
4Normal Gastric Emptying Coordinated effort between different regions of the stomach and the duodenumExtrinsic 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
5Gastric Emptying Rate Physical nature of food Particle size Liquid vs. solidParticle size2 mm in diameterFat contentCaloric contentHigh calorie liquids empty at a constant rate
6GastroparesisCharacterized by delayed gastric emptying in the absence of mechanical obstructionVagal nerve conduction is diminishedReduced smooth muscle contractilityCompromised myoelectrical activityResults in erratic blood glucose control
7GastroparesisEstimated that up to 75% of individuals with diabetes develop some gastrointestinal symptomsMany patients do not report symptoms to doctorPatients do not realize that symptoms are related to diabetes.
8Gastroparesis Symptoms can last days to months or occur in cycles Poor correlation between symptoms and actual diagnosisLittle evidence of a time interval between diabetes diagnosis and development of gastroparesis
9Gastroparesis 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
10Gastroparesis majority of patients are women (82%) Associated with increased BMINot universal or inevitable
11Pittsburgh Epidemiology of Diabetes Complications A: Proliferative retinopathy, B: Overt nephropathy,C: Symptomatic automatic neuropathy, D: Distal symmetric polyneuropathyPambianco, G., et al. The 30 –Year Natural History of Type 1 Diabetes ComplicationsDiabetes 55: , 2006
12Clinical Consequences Gastrointestinal symptomsAlteration in oral drug absorptionGlipizidePoor glycemic control
17Blood Glucose Effects Hyperglycemia slows gastric emptying Causes pyloric value to contractdecreases motilityHypoglycemia accelerates gastric emptyingImportant in counter-regulation of hypoglycemiaContinuous inverse relationship between blood glucose levels and rate of gastric emptying.
18Pathogenesis Combination of factors Vagal neuropathy Hyperglycemia Unknown factors
19Diagnosis Consider medications that may cause gastric stasis: Anticholinergic agentsAntidepressantsCalcium-channel blockersUpper endoscopy to rule out obstruction
20Diagnosis Scintigraphy (gold standard) Isotope breath tests Calculates time to empty 50% of meal and percentage remaining after 2 and 4 hoursIsotope breath testsMeasures amount of CO2 in breath samplesUltrasonographyMeasures flow of food through pyloric sphincterMagnetic resonance imaging
21Nutrition Management Treatment goals: Alleviate symptoms Improve gastric emptyingEnhance glycemic controlDelay progression of other complications
22Gastroparesis Emptying of solid food is delayed Emptying of liquids remains unchanged until condition becomes more advancedProne to development of bezoarsSeverity of symptoms does not correlate with degree of gastric emptying.
23Nutrition 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 toleratedAvoid fibrous fruits and vegetables, such as oranges and broccoli, that are likely to cause bezoars.
24Nutrition ManagementChoose soft or liquid foods such as soups and pureed foodsDrink 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
25Nutrition Management Avoid alcohol and tobacco Chew sugar-free gum for 1 hr after meal
26Nutrition Management Add nutrition supplements High nutrient liquids Enteral feedings via jejunostomy tubeTPN – seldom indicated
27Case Study“Carol”2/3/201152 yo femaleType 1Ht: 62”Wt: 140 (down 3 lbs. in 3 mo.)A1c 7.3Blood glucose:High BG spikes after mealEats one meal a dayGives bolus after eatingCounseled on diet for gastroparesis: -6 small meals - low fat, fiber -avoid carbonation and gas producing foods -Advised to give part of bolus before meal
28Case 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 cgmsTries to eat something for breakfast and lunch, but still skips meals?? Nutrition adequacy
29Dietary Adequacy 10 Type 1 patients Mean age 44 yrs BMI 25.4 A1c 10.4 Common symptomsBloating, nausea, halitosis, acid reflux, belching, abdominal pain, flatulence, diarrhea, anorexia, heartburn, vomitingSymptom severity did not correlate with A1cGoldberg K.B. JADA 97: , 1997.
30Dietary Adequacy Mean energy intake: 63% of recommended levels Carbohydrate and fat reduced proportionately more than proteinCalcium: 70% of recommended amountRecommend nutrition supplements to this populationGoldberg K.B. JADA 97: , 1997.
31Nutrition Management Factors which influence postprandial glucose Fasting blood glucose levelMeal composition (carbohydrate)Rate of absorption from small intestineInsulin secretion/timingHepatic glucose metabolismPeripheral insulin sensitivity
32Insulin TherapyMismatch between insulin action and glucose absorption from mealInsulin peaks before glucose is absorbedCauses early hypoglycemiaLater, glucose is absorbed, but no insulinCauses late hyperglycemia
33Insulin Treatment Strategies Rapid acting- adjust timing of injectionRegular insulin before mealDelayed or extended bolus delivery with pumpMonitor blood glucose frequently or use CGMS
34Pharmacotherapy Metoclopramide (Reglan) Stimulates stomach muscle contractionsHelps reduce nausea and vomitingTaken minutes before meals and at bedtimeLong-term use is limited by development of:ToleranceRestlessnessprolactinemia
35Pharmacotherapy Erythromycin Increases stomach contractions Given IV in acutely illLess effective when given orally or long term? transdermally
36Pharmacotherapy Botulinum toxin (Botox) Intrapyloric injection Relaxes pyloric muscle in someBenefits are temporaryNo efficacy in controlled studies
37Pharmacotherapy Domperidone (Motilium) Used to suppress nausea/vomitingUsed as a prokineticStimulates lactation*Not approved for use in the U. S.
38Electrical Gastric Stimulation Uses electrical current to cause stomach contractionsSurgically placed in a pocket on outer edge of stomach
39Enterra Therapy Pacemaker-like device Produced by Medtronic Battery operated (battery life 5-10 yrs)Implanted in abdomenElectrode connected to the stomach muscleReleases low-voltage electrical shocks every 6 seconds, causing stomach to contract
41Enterra TherapyApproved 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.
42Surgical Treatment Rarely used Increase the size of opening between stomach and intestineGastrectomy
43Long-term Management Multidisciplinary approach Patient’s understanding of how food and medicines work togetherFrequent blood glucose monitoring (4-8 /day) and/or use of CGMSIndividualized diet according to patient toleranceNormal life expectancy after adjustments for other disorders