Dietary Interventions for the Patient with Gastropathy
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Transcript Dietary Interventions for the Patient with Gastropathy
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!