Julianne Steiner, MS, RD, CDE Endocrine/Diabetes Clinic
McKay-Dee Hospital Center Slide 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. Slide 3 Normal
Gastric Function Fundic relaxation to accommodate food Contractions
for breaking large food particles Pyloric relaxation to allow food
to exit Slide 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 90-120
minutes after eating Slide 5 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 Slide
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
Slide 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. Slide 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 Slide 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 Slide 10 Gastroparesis majority of patients are women
(82%) Associated with increased BMI Not universal or inevitable
Slide 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 55:1463-1469, 2006 Slide 12 Clinical
Consequences Gastrointestinal symptoms Alteration in oral drug
absorption Glipizide Poor glycemic control Slide 13 Symptoms
(nonspecific) Nausea (92%) Vomiting (84%) Bloating (75%) Early
satiety Upper abdominal discomfort Reflux Unexplained weight loss
Erratic blood glucose levels Slide 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 Slide 15 Blood Glucose Effects Hyperglycemia slows
gastric emptying Causes pyloric value to contract Decreases
motility Induces gastric dysrhythmias Slide 16 Vicious Cycle
Hyperglycemia Delayed gastric emptying Initial hypoglycemia Late
hyperglycemia Slide 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. Slide 18
Pathogenesis Combination of factors Vagal neuropathy Hyperglycemia
Unknown factors Slide 19 Diagnosis Consider medications that may
cause gastric stasis: Anticholinergic agents Antidepressants
Calcium-channel blockers Upper endoscopy to rule out obstruction
Slide 20 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 Slide 21 Nutrition Management Treatment
goals: Alleviate symptoms Improve gastric emptying Enhance glycemic
control Delay progression of other complications Slide 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. Slide 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. Slide 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 patients tolerance based on postprandial glucose
results Slide 25 Nutrition Management Avoid alcohol and tobacco
Chew sugar-free gum for 1 hr after meal Slide 26 Nutrition
Management Add nutrition supplements High nutrient liquids Enteral
feedings via jejunostomy tube TPN seldom indicated Slide 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: 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 Slide 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 Slide 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
97:420-422, 1997. Slide 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
97:420-422, 1997. Slide 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 Slide 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 Slide 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
Slide 34 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 Slide 35
Pharmacotherapy Erythromycin Increases stomach contractions Given
IV in acutely ill Less effective when given orally or long term ?
transdermally Slide 36 Pharmacotherapy Botulinum toxin (Botox)
Intrapyloric injection Relaxes pyloric muscle in some Benefits are
temporary No efficacy in controlled studies Slide 37
Pharmacotherapy Domperidone (Motilium) Used to suppress
nausea/vomiting Used as a prokinetic Stimulates lactation *Not
approved for use in the U. S. Slide 38 Electrical Gastric
Stimulation Uses electrical current to cause stomach contractions
Surgically placed in a pocket on outer edge of stomach Slide 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 Slide 40
Medtronic Enterra 2.2 X 2.4 X 0.4 Slide 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.
Slide 42 Surgical Treatment Rarely used Increase the size of
opening between stomach and intestine Gastrectomy Slide 43
Long-term Management Multidisciplinary approach Patients
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 Slide 44 Thank
You!
