Julianne Steiner, MS, RD, CDE
Endocrine/Diabetes Clinic
McKay-Dee Hospital Center
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.
Normal Gastric Function
 Fundic relaxation to
accommodate food
 Contractions for
breaking large food
particles
 Pyloric relaxation to
allow food to exit
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 90-120 minutes after eating
Gastric Emptying Rate
 Physical nature of food
 Liquid vs. solid
 Particle size
 2 mm in diameter
 Fat content
 Caloric content
 High calorie liquids empty at a constant rate
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
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.
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
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
Gastroparesis
 majority of patients are women (82%)
 Associated with increased BMI
 Not universal or inevitable
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 55:1463-1469, 2006
Clinical Consequences
 Gastrointestinal symptoms
 Alteration in oral drug absorption
 Glipizide
 Poor glycemic control
Symptoms (nonspecific)





Nausea (92%)
Vomiting (84%)
Bloating (75%)
Early satiety
Upper abdominal
discomfort
 Reflux
 Unexplained weight loss
 Erratic blood glucose
levels
Delayed Gastric Emptying
 First sign: erratic blood glucose levels
 Other symptoms may be mild to severe
 Unexplained weight loss
 Prone to bezoar formation / obstruction
Blood Glucose Effects
 Hyperglycemia slows gastric emptying
 Causes pyloric value to contract
 Decreases motility
 Induces gastric dysrhythmias
Vicious Cycle
Hyperglycemia
Late
hyperglycemia
Delayed gastric
emptying
Initial
hypoglycemia
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.
Pathogenesis
 Combination of factors
 Vagal neuropathy
 Hyperglycemia
 Unknown factors
Diagnosis
 Consider medications that may cause gastric stasis:
 Anticholinergic agents
 Antidepressants
 Calcium-channel blockers
 Upper endoscopy to rule out obstruction
Diagnosis
 Scintigraphy (gold standard)
 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
Nutrition Management
 Treatment goals:
 Alleviate symptoms
 Improve gastric emptying
 Enhance glycemic control
 Delay progression of other complications
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.
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.
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
Nutrition Management
 Avoid alcohol and tobacco
 Chew sugar-free gum for 1 hr after meal
Nutrition Management
 Add nutrition supplements
 High nutrient liquids
 Enteral feedings via jejunostomy tube
 TPN – seldom indicated
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: 150-200
 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
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
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 97:420-422, 1997.
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 97:420-422, 1997.
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
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
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
Pharmacotherapy
 Metoclopramide (Reglan)
 Stimulates stomach muscle contractions
 Helps reduce nausea and vomiting
 Taken 20-30 minutes before meals and at bedtime
 Long-term use is limited by development of:



Tolerance
Restlessness
prolactinemia
Pharmacotherapy
 Erythromycin
 Increases stomach contractions
 Given IV in acutely ill
 Less effective when given orally or long term
 ? transdermally
Pharmacotherapy
 Botulinum toxin (Botox)
 Intrapyloric injection
 Relaxes pyloric muscle in some
 Benefits are temporary

No efficacy in controlled studies
Pharmacotherapy
 Domperidone (Motilium)
 Used to suppress nausea/vomiting
 Used as a prokinetic
 Stimulates lactation
*Not approved for use in the U. S.
Electrical Gastric Stimulation
 Uses electrical current to cause stomach contractions
 Surgically placed in a pocket on outer edge of stomach
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
Medtronic Enterra
 2.2” X 2.4” X 0.4”
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.
Surgical Treatment
 Rarely used
 Increase the size of opening between stomach and
intestine
 Gastrectomy
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
Thank You!