Nutrition Intervention for the Patient with Gastroparesis: An Update

PRACTICAL GASTROENTEROLOGY • AUGUST 2005

INTRODUCTION

alua

tion of nutritional status and the treatment of

malnutrition are important factors in the manage-

ment of pa

tients with g

astr

opar

esis. Symptoms of

gastroparesis (Table 1) may be severely debilitating

and the resultant aberrations in nutritional status can

be lif

e thr

tening

. Once a pa

tient de

elops pr

otracted

nausea and vomiting, providing adequate nutrition,

hydration and access to therapeutics such as prokinet-

ics and antiemetics can pr

esent a unique c

hallenge to

clinicians.

Gastroparesis has many origins and its clinical pre-

senta

tion ma

y w

ax and w

ane de

pending on the under

lying etiology (see Table 2 for conditions associated

with gastroparesis). Many patients (and some clini-

cians) assume that a diagnosis of gastroparesis means

continuous clinical deterioration until an end-stage is

reached. Research to date, however, supports that early

utrition support can reverse significant malnutrition

hile g

astric function returns over time. In truth, many

patients with refractory gastroparesis who initially

equir

e jejunal f

eeding tube placement f

or n

utrition

support often eventually eat again on their own (1–5).

Nutrition Intervention for

the Patient with Gastroparesis:

An Update

NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #30

Carol Rees Parrish, RD, MS, Series Editor

Carol Rees Parrish R.D., M.S., Nutrition Support

Specialist, University of Virginia Health System,

Digestive Health Center of Excellence, Charlottesville,

VA.Cynthia M. Yoshida, M.D., Gastroenterologist,

Charlottesville, VA.

Gastroparesis, or dela

yed gastric emptying, has many origins. The clinical presentation

may wax and wane depending on the under

lying etiology. However, once a patient

develops protracted nausea and vomiting, providing adequate nutrition, hydration and

access to therapeutics such as prokinetics and antiemetics can present a unique chal-

lenge to c

linicians. This article provides suggested guidelines to assess the nutritional

status of patients with gastroparesis and strategies to treat the nutritional issues that

arise in this patient population.

Carol Rees Parrish

(continued on page 33)

Cynthia M. Yoshida

Although prokinetic agents and antiemetics are

front line therapy in the treatment of gastroparesis (6),

the purpose of this article is to provide strategies to

maintain or restore nutritional status in this patient

popula

tion. There is a scar

city of clinical trials in the

area of nutrition intervention for patients with gastro-

paresis. Review articles and textbooks are available,

however, evidence-based nutrition recommendations

are lacking. Most of the current dietary guidelines and

restrictions have been developed from studies evaluat-

ing the effect of a single parameter on gastric empty-

ing in normal subjects (7).

This artic

le pr

ovides practical guidelines to assess

the nutritional status of patients with gastroparesis and

strategies to treat nutritional issues that arise in this

tient popula

tion. Mor

e detailed r

vie

ws of all facets

of gastroparesis are available elsewhere (8,9).

NUTRITION ASSESSMENT

The purpose of nutritional screening and evaluation in

the pa

tient with g

astr

opar

esis is to objectively distin-

guish the adequately nourished patient who can pursue

further gastrointestinal (GI) evaluation and/or proki-

netic tr

ials, fr

om a malnour

ished pa

tient w

ho r

equir

immediate nutritional support.

Weight Change Over Time

Unintentional weight loss over time is probably the

most important, nonin

asive parameter to assess over-

all nutritional status in the pa

tient with gastroparesis.

(continued from page 29)

PRACTICAL GASTROENTEROLOGY • AUGUST 2005

Nutrition Intervention for the Patient with Gastroparesis: An Update

NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #30

Table 1

linical Symptoms of Gastroparesis

• Decreased appetite / anorexia

• Nausea and vomiting

•

Bloating

• Fullness (especially in the morning after an overnight fast)

• Early satiety

• Halitosis

• Post-prandial hypoglycemia, or fluctuating glucose levels in

an otherwise well-controlled patient with diabetes mellitus

Used with permission from the University of Virginia Health System

Nutrition Support Traineeship Syllabus (31)

Table 2

Clinical Conditions Associated with Gastroparesis (53,54)

Mechanical obstruction

Duodenal ulcer

Pancreatic carcinoma or pseudocyst

Gastric carcinoma

Superior mesenteric artery syndrome

Metabolic/endocrine disorders

Diabetes Mellitus

Hypothyroidism

Hyperthyroidism

Hyperparathyroidism

Adrenal insufficiency (Addison’s disease)

Acid-peptic disease

Gastric ulcer

Gastroesophageal reflux disease

Gastritis

Atrophic gastritis

Viral gastroenteritis

Post-gastric surgery

Vagotomy

Antrectomy

Subtotal gastrectomy

Roux-en-y gastrojejunostomy

Fundoplication

Disorders of gastric smooth muscle

Scleroderma

Polymyositis

Muscular dystrophy

Amyloidosis

Chronic idiopathic pseudoobstruction

Dermatomyositis

Systemic lupus erythematosus (SLE)

Psychogenic disorders

Anorexia

Bulimia

Depression

Neuropathic disorders

Parkinson’s disease

Paraneoplastic syndrome

CNS disorders

High cervical cord lesions (C4 and above)

PRACTICAL GASTROENTEROLOGY • AUGUST 2005

Nutrition Intervention for the Patient with Gastroparesis: An Update

NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #30

When an accurate weight can be obtained, this para-

meter is a simple

, reliable indicator of nutritional sta-

tus. An unintentional

≥7.5% loss of usual body weight

over a three-month period signals significant malnutri-

tion and should be a cause f

or concer

It is impor

tant to compare a patient’s current

actual weight (A

W) to their

usual body weight

(UBW) to deter

mine nutr

itional r

isk and/or whether

significant weight loss has occurred. To compare the

patient’s actual weight to an

ideal body weight might

either g

rossly over- or underestimate the true weight

loss, and therefore the severity of malnutrition.

Another essential principle is to assure that the patient’s

actual weight represents a “euvolemic” weight, neither

dehydrated, nor edematous. As an example, a patient

with diabetes mellitus (DM) who presents with vomit-

ing, diarrhea and poor glucose control may have a

falsely low actual weight due to dehydration. Failure to

use a euvolemic actual weight might overestimate the

amount of weight loss over time and suggest signifi-

cant malnutrition instead of the fact that the patient is

merely dehydrated. Finally, it is also imperative to

remember that those patients who are clinically over-

weight or obese, yet have unintentionally lost a signif-

icant amount of weight over a short time interval, may

carry the same risk profile as a chronically undernour-

ished patient.

The time course of weight loss is also important.

Table 3 demonstrates that both a 2% loss over 1 week

and a

≥10% loss o

ver 6 months both constitutes severe

malnutrition, w

hich is associated with increased mor-

bidity and mortality (10). Beware of the hemodialysis

patient who experiences serial drops in their target

weight over time; 50% of patients on dialysis are a

result of long-standing DM, which is commonly asso-

cia

ted with g

astropar

esis.

Although unintentional w

eight loss over time is the

best indicator of the severity of malnutrition, some

investigators utilize weight alone as a measure of a

patient’s nutritional status. Patients may be deemed mal-

(continued on page 39)

Table 3

valuation of Weight Change Over Time

% Weight Change = Usual Weight – Actual Weight* (×100)

sual Weight

Significant Severe

Malnutrition Malnutrition

1 week 1%–2% >2%

1 month 5% >5%

3 months 7.5% >7.5%

6 months 10% >10%

*Compare the patient’s UBW to their euvolemic current actual weight.

Adapted from Shopbell JM, Hopkins B, Shronts EP. Nutrition screening

and assessment. In: Gottschlich M, ed. The Science and Practice of Nutri-

tion Support: A Case-Based Core Curriculum.

Dubuque, IA: Kendall/Hunt

Publishing Company, 2001:119, with permission from the American

Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). A.S.P.E.N. does

not endorse the use of this material in any form other than its entirety.

Table 4

Risk of Associated Disease According to BMI and Waist Size

Waist less than or equal to

Waist greater than

BMI* Category 40 in. (men) or 35 in. (women) 40 in. (men) or 35 in. (women)

18.5 or less

Underweight —- N/A

18.5–24.9 Normal —- N/A

25.0–29.9

Overweight Increased High

30.0–34.9 Obese High Very High

35.0– 39.9

Obese

Very High Very High

40 or greater Extremely Obese Extremely High Extremely High

*These values may underestimate the degree of malnutrition in some patients. An overweight or obese patient may be malnourished if significant weight

loss has occurred, but not fall into the category of malnutrition based on BMI alone.

Obtained from http://www.consumer.gov/weightloss/bmi.htm (Accessed 7-1-05).

nourished based on a stable weight below normal, loss

of an arbitrary amount of weight, or loss of a significant

percentage of baseline weight. Commonly, ideal body

weight for an individual is determined based on weight

relative to height. The Body Mass Index (BMI) is deter-

mined as weight (kg)/ height (m)

(see Table 4 or go to:

http://nhlbisupport.com/bmi/bmicalc.htm) (11). A BMI

of 20 to 25 is considered to be normal. Most guidelines

identify patients at nutritional risk if they:

• Are <80% of ideal weight

• Have a body mass index less than 20

• Have lost 5% of baseline weight or 5 pounds in one

month

• Have lost 10 pounds or 10% of usual body weight in

6 months.

Diet History

A diet histor

y can be very helpful in identifying

patients who might benef

it from nutrition support and

to determine the level of nutrition support required. As

an example, a patient who develops nausea while eat-

ing the usual, three large meals per day, may not require

supplemental calories, but may benefit by simply insti-

tuting smaller

, mor

e frequent meals. In contr

ast, the

tient with sever

e gastr

oparesis who has significant

vomiting after the ingestion of water may require gas-

tric decompression and enteral jejunal feeding to pro-

vide symptom relief, nutrients, fluids, and medications.

hen obtaining a diet histor

y, be sure to evaluate for:

•

Changes in appetite, nausea/vomiting/diarrhea.

•

oblems chewing and/or swallowing which can

affect their ability to ingest certain foods.

•

he pa

tient’

s typical dail

y dietary intake.

• The use of supplemental nutrition (oral, enteral or

parenteral).

•

ood intoler

ances or aller

ies.

• Use of supplements, such as vitamins, minerals,

herbs or protein powders.

• Use of stool bulking agents or laxatives.

•

Medications known to slow gastric emptying (Table 5).

Laboratory Data

Intolerance to various foods/food groups and malab-

sorption can lead to n

utr

ient def

iciencies, w

hic

h can

fur

ther a

ggravate clinical morbidity. Intolerances can

often be mana

ged with dietary manipula

tion and close

nutrition follow-up. Nutrient deficiencies, particularly

those resulting in anemia and metabolic bone disease,

require ongoing monitoring and supplementation. Lab-

oratory values are a useful adjunct in the initial evalu-

ation and continued management, of the patient with

gastroparesis. Initial assessment of a patient with gas-

oparesis should inc

lude:

• Glucose and glycosylated hemoglobin (HgbA1C) if

the patient has DM

• Ferritin

• Vitamin B

• 25-OH vitamin D (particularly with longstanding

gastroparesis or in the post- gastrectomy patient)

Serum glucose and HgbA

C. Glycemic control is crit-

ical in the management of diabetic gastroparesis. Hyper-

ycemia (>200 mg %) can cause tr

ansient g

astroparesis

in some patients and this delayed gastric emptying can

respond quickly to normalization of serum glucose lev-

els (12,13). Ad

ditionall

, h

yper

ycemia has been shown

to attenuate the prokinetic effect of erythromycin.

Finally, hyperglycemia is a catabolic process, which ulti-

mately thwarts the efforts of nutrition repletion.

Glycemic control must therefore be carefully evaluated

at the initial nutritional assessment and monitored regu-

lar

ly during the repletion process.

An ele

ted glycosylated hemoglobin at initial eval-

uation may suggest that improved glycemic control might

tten

te the g

astr

oparesis, and that the gastroparesis is

PRACTICAL GASTROENTEROLOGY • AUGUST 2005

Nutrition Intervention for the Patient with Gastroparesis: An Update

NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #30

(continued from page 34)

Table 5

edications Known to Delay Gastric Emptying (6,53)

• Aluminum-containing

antacids

•

Anticholinergics

• Atropine

• Beta agonists

• Calcitonin

• Calcium channel blockers

• Dexfenfluramine

• Diphenhydramine

• Ethanol

• Glucagon

• Interleukin-1

•

L-dopa

•

Lithium

• Octreotide

• Ondansetron

• Narcotics

• Nicotine

• Potassium salts

• Progesterone

• Sucralfate

• Tricyclic antidepressants

• Selective serotonin reuptake

inhibitors (SSRI)

PRACTICAL GASTROENTEROLOGY • AUGUST 2005

the likely culprit causing poor glycemic control. Subse-

quent monitoring of the glycosylated hemoglobin assures

that optimal glucose control is maintained.

Ferritin. Iron-deficiency anemia is common in this

patient population. The etiology is likely multifactorial.

Serum iron levels may be marginal especially in men-

struating women who are unable or prefer not to con-

sume red meat. At our institution, we have anecdotally

noted that many patients with gastroparesis report intol-

erance to red meat and voluntarily remove it from their

diet.

Iron absorption is significantly enhanced by gas-

tric acid. Reduced gastric acidity impairs the conver-

sion of dietary ferric iron to the more absorbable fer-

rous form (14). Gastroparesis symptoms, especially

concomitant acid reflux, are often treated with acid

suppressive medications such as proton pump

inhibitor

s. Vagotomy also reduces acid production,

which is necessar

y for efficient iron absorption. Ele-

vated gastric pH and poor motility can also increase

the patient’s risk of developing small bowel bacterial

overgrowth, which can significantly decrease duodenal

iron absorption. Iron deficiency should be carefully

monitor

ed in pa

tients recei

ving jejunal enter

al nutri-

tion as the duoden

um (primar

y site f

or iron a

bsorption)

is bypassed. Similarly, iron deficiency is also of partic-

ular concern in patients whose gastroparesis results

from post-vagotomy syndrome, especially those with a

astr

ojejunostomy anastomosis (15). Low gastric acid-

ity

, combined with duodenal exclusion, results in

impair

ed ir

on uptake. Iron deficiency may manifest

more quickly following Billroth II than in Billroth I

ocedur

es, f

or this same r

eason (16). A decade f

ol-

lowing gastrectomy, iron deficiency is the most fre-

quently reported nutrient deficiency (17).

A f

itin le

el is an accur

te indica

tor of iron

stores over time (18). However, ferritin is an acute

phase reactant, therefore it should be checked in the

non-acute setting (absence of infection, inflammation,

etc

.). Ferritin levels may be low even in the setting of

a normal hematocrit, as the body utilizes iron stores

while preserving hemo

globin and hematocrit. In one

small study, 67% of pa

tients with g

astr

oparesis were

found to have a low ferritin level despite low-normal

hemoglobin and hema

tocr

it le

els (2).

al ir

on supplementation is the preferred method

of replacement (19) and is available as ferrous sulfate,

gluconate or fumarate. Optimal dosing is approxi-

mately 200 mg of elemental iron daily (18). Iron

replacement therapy is typically administered three

times daily, preferably 6 hours apart. The addition of

very small amounts of vitamin C (25–50 mg) can

enhance iron absorption (20). Patients can obtain this

amount of vitamin C with 3 ounces of a vitamin C con

taining juice or beverage, either orally or via a feeding

tube (given with the iron dose). Chewable or liquid

iron is the preferred iron replacement in post-gastrec-

tomy patients as solubilization of iron tablets may not

be complete, resulting in poor absorption of the sup-

plement (21).

Gastrointestinal side effects (nausea, abdominal

pain, constipation or diarrhea) often decrease patient

compliance to ir

on ther

. Ad

vising patients to take

iron with food can reduce these GI symptoms. Because

the body increases its avidity for iron uptake (up to

20%–30%) in deficient states, even modest iron intake

is better than none at all (18). Reducing the dosage or

Nutrition Intervention for the Patient with Gastroparesis: An Update

NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #30

(continued on page 42)

Table 6

uidelines for Iron Replacement in Adults (24)

1. 150–300 mg of elemental iron per day should be given in

three divided doses.

. Four to six months of oral iron therapy is needed to reverse

uncomplicated iron deficiency anemia.

3. Sustained released preparations should not be crushed or

chewed.

4. Absorption is enhanced when iron is taken on an empty

stomach but GI intolerance may necessitate administration

with food.

5. GI discomfort may be minimized with slow increase to goal

dosage. Start with 1/4 to 1/2 dose two to four times daily if

necessary; some replacement is better than none.

6. Do not take iron supplements within two hours of taking a

dose of tetracycline or fluoroquinolone.

7. Drink liquid iron via a straw to minimize dental enamel stains.

8. Following Billroth II and total gastrectomy, sustained release

or enteric-coated iron preparations may not be optimal as

available iron is delivered past the duodenum following

these surgeries.

Adapted with permission from Drug Facts and Comparisons

www.efactsweb.com

PRACTICAL GASTROENTEROLOGY • AUGUST 2005

Nutrition Intervention for the Patient with Gastroparesis: An Update

NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #30

decreasing the frequency of administration may pre-

vent patients from completely discontinuing their iron

supplementation. Patients should also be encouraged

to increase their intake of iron-rich foods. Meats (heme

on sources) are the most readily absorbed form of

dietar

y ir

on.

Parenteral iron replacement is often unnecessary

and should be reserved for patients with severe iron

deficiency who cannot tolerate oral replacement. Par-

enteral replacement is expen-

sive and its risks include ana-

phylactic shock. See Tables 6

and 7 for further information

on iron supplementation.

Vitamin B

. Vitamin B

deficiency is common in

patients following partial or

total gastrectomy. Intrinsic

factor is synthesized in the

stomach and is complexed to

vitamin B

to facilitate

absorption in the terminal

ileum. Reduced levels of

intrinsic factor and gastric

acid following gastrectomy

impairs the cleavage of pro-

tein bound B

resulting in little or no intestinal

absorption. Bacter

ial overgrowth and reduced intake of

vitamin B

rich foods also contribute to a deficiency

(22). The resulting anemia can be severe and often pre-

sents as a late complication of gastric resection. Lassi-

tude, fatigue, chills, numbness in the extremities,

dizziness and neur

olo

gical symptoms ar

e also com

mon symptoms of vitamin B

def

iciency (23). Clini

cal features are non-specific and often absent in defi-

cient patients. Baseline and periodic monitoring of vit-

amin B

levels are therefore important.

itamin B

supplements ar

e a

vailable in oral,

ansnasal or intramuscular (IM) preparations. Follow-

ing total g

astr

ectomy, enteral vitamin B

ther

py will

increase serum B

levels (24). Symptom resolution is

compar

le in pa

tients w

ho receive enteral versus par-

enteral supplementation. Table 8 outlines guidelines

for monitoring and replacing vitamin B

. The deci-

sion to supplement B

via or

al, intr

anasal or intr

muscular approach should be based on patient compli-

ance. Table 9 provides a cost comparison for various

vitamin B

supplements.

25-OH vitamin D. The literature has shown that

tients with g

astr

ectomies (sub-total or total) can

e acceler

ted bone loss, ther

efore increasing the

risk for osteoporosis. A percentage of patients who

under

o subtotal g

astr

ectom

y subsequentl

y de

velop

(continued from page 40)

able 7

Elemental Iron Content of Various Iron Formulations (24)

Elemental Iron

Product Dose Content (mg) Comments

Tablets

Ferrous Sulfate 325 mg 65

Ferrous Gluconate 325 mg 36

Ferrous Fumarate 325 mg 106

Suspension

Ferrous Sulfate Elixir 220 mg/5 mL 44 mg/5 mL May contain sorbitol

Ferrous Sulfate Drops 75 mg/0.6 mL 15 mg/0.6 mL May contain sorbitol

Feostat (ferrous fumarate) 100 mg/5 mL 33 mg/5 mL Butterscotch flavor

Chewable tablets

Feostat (ferrous fumarate) 100 mg 33 Chocolate flavor

Adapted with permission from Drug Facts and Comparisons www.efactsweb.com

Table 8

Guidelines for Vitamin B

Supplementation (24)

Mild deficiency

—over the counter oral vitamin B

(500–1000 mcg/day).

• The amount absorbed decreases with higher doses.

Severe deficiency—vitamin B

intramuscular (IM) or

subcutaneous (SC) 100–200 mcg/month

•

1000 mcg dose is often used, however, the percentage of

vitamin B

retained decreases with larger doses.

Intranasal B

should be limited to patients in remission

following IM B

injection.

• Recommended dose is 500 mcg once weekly.

Monitor B

levels at baseline and then every 3 months until

normalized, then annually.

Adapted with permission from Drug Facts and Comparisons

www.efactsweb.com

gastr

oparesis. Osteopenia and osteomalacia are also

not uncommon in this popula

tion (25). Lo

w bone min-

eral density has been reported in 27%–44% of these

patients (25), many of whom had normal serum cal-

cium and alkaline phosphatase levels. Klein, et al

found that vertebral compression fractures were three

times as common in men who had undergone Billroth

II sur

gery compar

ed with controls (26). Age of the

patient and bone mineral density (BMD) at the time of

surgery play a significant role in the development of

bone disease

, independent of the type of gastric resec-

tion. The etiology of bone disease in this population is

thought to be due to decreased intake of calcium, vita-

min D and lactose-containing foods coupled with

altered absorption and metabolism (14,26,27). Evalua-

tion of 25-OH vitamin D levels (

not 1, 25-OH

vitamin

D) and bone mineral density may also be beneficial in

patients with gastroparesis. Dual energy x-ray absorp-

tiometry (DXA) provides an inexpensive, reproducible

method to determine BMD (28). Given the frequency

of bone disease in these patients, it is reasonable to

monitor BMD (even in the setting of normal laboratory

values), at baseline and then every one to two years. It

is imperative to identify and treat high-risk patients

early (i.e., young women with amenorrhea due to sig-

nificant weight loss from debilitating gastroparesis) in

order to reduce incident fractures.

Currently, there are no accepted calcium and vita-

min D supplementation guidelines for gastroparesis

or post-g

astrectomy patients. Multivitamin/mineral

tablets contain v

arying amounts of calcium and vita-

min D; therefore additional supplementation is often

required. Patients with bone disease are recommended

to take 1500 mg calcium and 800 IU of vitamin D

PRACTICAL GASTROENTEROLOGY • AUGUST 2005

Nutrition Intervention for the Patient with Gastroparesis: An Update

NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #30

(continued on page 47)

Table 9

ost Comparison of Vitamin B

upplements

# Doses/ Average Cost

Formulation month Per Month*

Intranasal Nascobal

4 $34.80 (500 mcg dose)

IM injection (cost of

syringes not included) 1 $0.79 (1000 mcg dose)

Capsule 30 $0.76 (1000 mcg dose)

*Prices from Wal-Mart 2003

Used with permission from the University of Virginia Health System

Nutrition Support Traineeship Syllabus (31)

Table 10

Common Calcium Supplements

Calcium Carbonate: 40% elemental calcium

Elemental Calcium

Approximate

Brand

(mg) per tablet

cost per tablet Comments

Tums

200 $.02

Extra Strength Tums

300 $.04

Oscal

500

$.10 Also available with 200 IU vitamin D

Also available in 250 mg dose

Caltrate

600 Plus

600 $.11 Contains 200 IU vitamin D plus additional minerals

Viactiv

500

$.10

Contains 100 IU vitamin D and 40 mcg vitamin K

Contains <0.5 g lactose per dose

20 calories per piece

Calcium Citrate: 21% elemental calcium (25)

Citrical

200 $ .07

Citrical

+ D

315 $.11 Contains 200 IU vitamin D

Used with permission from the University of Virginia Health System Nutrition Support Traineeship Syllabus (31)

daily (29). To maximize absorption, calcium should be

administered in single doses no greater than 500 mg.

Patients should also be encouraged to include calcium

rich foods in their diet along with calcium supplements

as tolerated (Table 10).

Anti-resorptive agents (calcium, vitamin D, calci-

tonin and bisphosphonates) and bone-formation agents

(recombinant hormone PTH) may all be considered to

treat bone loss.

Albumin, prealbumin and/or transferrin were often

used in the past as markers of a patient’s nutritional

status. Today we know that levels of these proteins can

be significantly altered by a multitude of factors, thus

eliminating their validity as markers of nutritional sta-

tus (30).

Albumin. Serum albumin levels are a poor measure of

a patient’s nutritional status and they can be especially

misleading in pa

tients with gastroparesis. Patients may

have signif

icant malnutrition, yet maintain intact vis-

ceral protein stores (31). Serum albumin levels can

also appear to be normal due to extravasation of albu-

min from the interstitium into the vascular space with

starvation. Low serum albumin levels can be caused by

many conditions other than malnutrition such as uri-

nary wasting due to nephrotic syndrome; it is also a

negative acute phase reactant. See Table 11 for other

factors that alter serum albumin levels.

Prealbumin. In healthy individuals, prealbumin levels

decline during periods of decreased intake and nor-

malize within two days upon resumption of nutrition.

Thus prealbumin is primarily utilized to monitor the

effectiveness of nutritional intervention. Prealbumin

levels can decrease with hyperglycemia or in other

catabolic states (e.g. inflammation/infection). Patients

with poorly controlled DM may have low values that

do not reflect the patient’s true nutritional status; in

addition, prealbumin is lost via the kidney in the set-

ting of ne

phritic syndrome, common in patients with

long-standing DM. Other factors tha

t affect prealbu-

min levels are presented in Table 12.

Transferrin. In the past, serum transferrin levels were

used to assess visceral protein status. Due to the many

factor

s that af

fect these levels and the eight-day half-life,

PRACTICAL GASTROENTEROLOGY • AUGUST 2005

Nutrition Intervention for the Patient with Gastroparesis: An Update

NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #30

(continued from page 43)

Table 11

Factors Affecting Serum Albumin Levels

Increased in:

• Dehydration

• Marasmus

• Blood transfusion

• Exogenous albumin

Decreased in:

• Overhydration/ascites/eclampsia

• Hepatic failure

• Inflammation/infection/metabolic stress

• Nephrotic syndrome

•

Protein-losing states

•

Burns

• Trauma/postoperative states

• Kwashiorkor

•

Collagen diseases

• Cancer

•

Corticosteroid use

• Bedrest

• Pregnancy

• Zinc deficiency

Used with permission from the University of Virginia Health System

Nutrition Support Traineeship Syllabus (31)

Table 12

Factors Affecting Serum Prealbumin Levels

Increased in:

• Severe renal failure

•

Corticosteroid use

• Oral contraceptive use

Decreased in:

• Acute catabolic states

• Post-surgery

•

Liver disease/hepatitis

• Infection/stress/inflammation

• Dialysis

•

Hyperthyroidism

• Sudden demand for protein synthesis

•

Nephrotic syndrome

• Significant hyperglycemia (catabolic state)

• Pregnancy

Used with permission from the University of Virginia Health System

Nutrition Support Traineeship Syllabus (31)

PRACTICAL GASTROENTEROLOGY • AUGUST 2005

ser

um tr

ansf

in is not a g

ood indicator of protein sta-

tus. See Table 13 for factors that affect transferrin levels.

KEY FACTORS AFFECTING GASTRIC EMPTYING

The key factors affecting gastric emptying are pre-

sented in or

der of clinical importance below. These

actor

s are reported to slow gastric emptying, however,

their clinical significance has yet to be proven in

ospecti

, r

andomized, controlled trials. Physicians

and dietitians may successfully manipulate them in an

effort to improve gastric emptying.

The patient’s diet history will help determine which

factors may be integral to dietary tolerance for a particu-

lar patient. As an example, if a patient with gastroparesis

has better tolerance of liquids than solids, convert the

vast majority of nutrients and calories to a more liquid

form. Provide medications, specifically prokinetics, in a

liquid form also. It may behoove the clinician to start

prokinetic therapy and change only one or two parame-

ters at a time. This technique often allows patients to tol-

erate their diet and medications, and ultimately restore

nutritional status. Avoid overzealous intervention of all

of these factors at one time (i.e. “the shotgun approach”)

because it often results in unnecessary limitations of the

patient’s dietary and caloric needs, which can further

aggravate the nutritional decline.

Volume

The primary influence on gastric emptying is vol-

ume—the greater the volume, the slower the emptying.

Early satiety is one of the hallmarks of gastroparesis.

Because larger volumes slow emptying, smaller, more

equent meals may enable patients to tolerate their

diet and achieve adequate caloric intake (32).

Liquids Versus Solids

Functionally, the stomach can discern between liquids

and solids. In nor

mal subjects, antr

al peristaltic w

aves

occur

ring thr

ee times per min

ute can deliver approxi-

mately 30 mL to the small bowel with each contrac-

tion. Patients with gastroparesis will often have pre-

served emptying of liquids even when they have a clin-

icall

y documented dela

y in the emptying of solids.

Liquids empty b

y gravity and do not require antral

contr

action to lea

ve the stomach (32). Liquids, even

those that are highly caloric, will empty from the stom-

h. Pur

eed f

oods become liquif

ied after mixing with

saliva and gastric secretions, and may be more easily

tolerated than solid foods. A trial diet primarily of

pur

eed f

ood or liquids can be designed to meet a

patient’s nutritional requirements.

Patients with gastroparesis often report increased

fullness and bloating with subsequent meals over the

cour

se of the day. As a result, patients often avoid eat-

ing later in the day and this can exacerbate malnutri-

tion. T

ansitioning to mor

e liquid calor

ies towards the

end of the da

y ma

y be useful to alle

via

te these symp

toms while continuing to provide appropriate nutrition.

Nutrition Intervention for the Patient with Gastroparesis: An Update

NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #30

(continued on page 50)

Table 13

actors Affecting Serum Transferrin Levels

Increased in:

• Iron deficiency

•

Dehydration

• Pregnancy (third trimester)

• Oral contraception/ Estrogens

• Chronic blood loss

• Hepatitis

• Hypoxia

• Chronic renal failure

Decreased in:

• Pernicious anemia (B

deficiency)

• Anemia of chronic disease

• Folate deficiency anemia

• Overhydration

• Chronic infection

• Iron overload/iron dextran therapy

• Acute catabolic states

• Uremia

• Nephrotic syndrome (permeability of glomerulus)

• Severe liver disease/hepatic congestion

• Kwashiorkor

• Age

• Zinc deficiency

• Corticosteroids

• Cancer

• Protein

Used with permission from the University of Virginia Health System

Nutrition Support Traineeship Syllabus (31)

PRACTICAL GASTROENTEROLOGY • AUGUST 2005

Medications

Many medications can delay gastric emptying, and

their use can significantly exacerbate idiopathic or dia-

betic gastroparesis (Table 5). The patient’s medication

list should be reviewed regularly and avoid prescribing

drugs that aggravate gastroparesis.

Hyperglycemia

Hyperglycemia (glucose >200 mg %) is known to

worsen the symptoms of gastroparesis. In the patient

with DM, it is not often clear whether the gastropare-

sis is negatively affecting the glucose control or vice

versa. Wide fluctuations in blood glucose impair gas-

tric emptying more so than contin

uously elevated glu-

cose levels. In addition, hyperglycemia can diminish

the prokinetic effects of erythromycin (33,34). Mainte-

nance of glycemic control is imperative to maximize

utilization of the nutrition that is provided.

Fiber

Fiber, particularly pectin, can slow gastric emptying.

Fiber is also poorly digestible and increases a patient’s

risk of forming a bezoar (35). Although the avoidance of

high fiber foods is recommended in patients with gastro-

paresis, what is not known is the type of fiber and the

quantity of fiber that should be withheld. Over-the-

counter fiber/bulking laxatives (Table 14) should proba-

bly be discontinued (36). Fiber-containing jejunal enteral

feedings are generally well tolerated, unless small bowel

bacterial overgrowth is present as unabsorbable fiber may

theoretically aggravate symptoms due to fermentation.

Fat

Fat is a potent inhibitor of gastric emptying (32), how-

ever, many patients are not affected by dietary fat if it is

present in liquid form (e.g. whole milk, milkshakes,

nutritional supplements, etc.) Avoid manipulating fat

calories as a fir

st line endeavor because fat in liquid

for

m is often well tolerated (and pleasur

able), and it pro-

vides high-density calories in a smaller volume.

Osmolality

Osmolality has been shown to slow gastric emptying in

various study populations, however it is overrated in

terms of its clinical significance (37). Most patients

with g

astroparesis can easily tolerate a clear liquid diet.

he standar

d c

lear liquid diet has an osmolality range

from 500–1200 mOsm (isotonic = 300 mOsm). Sherbet

has an osmolality of a

ppr

oximately 1225 mOsm; juices

are 700–950 mOsm. Liquid metoclopramide, a com-

monly used prokinetic agent in this patient population,

has an osmolality of 5400 mOsm. Ov

all, osmolality is

believed to be a non-issue (versus volume or fiber) to

manipulate when attempting to nourish these patients.

IMPORTANT FACTORS THAT CAN AFFECT ORAL

INTAKE IN THE PATIENT WITH GASTROPARESIS

Nausea and Vomiting

Treatment of nausea and vomiting is paramount to pro-

viding successful oral nutrition and in preventing elec-

trolyte and acid-base abnormalities. Antiemetics and

Nutrition Intervention for the Patient with Gastroparesis: An Update

NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #30

(continued from page 48)

(continued on page 52)

Table 14

High Fiber Foods/Medications and Foods Associated

with Bezoar Formation*

High Fiber Foods

• Legumes/Dried Beans. Refried beans, baked beans, black-

eyed peas, lentils, black, pinto, northern, fava, navy,

kidney, and garbanzo beans, soy beans

•

Bran /Whole Grain Cereals. Bran cereals, Grape nuts,

shredded wheat type, granolas

•

Nuts and Seeds. Pumpkin seeds, soy nuts, chunky nut

butters

•

Fruits. Dried fruits (apricots, dates, figs,* prunes, raisins),

blackberries* blueberries* raspberries* strawberries*

oranges, apples* kiwi, coconuts* persimmons*

•

Vegetables. Green peas, broccoli, Brussels sprouts* green

beans* corn* potato peels* sauerkraut* tomato skins*

High Fiber Medications/Bulking Agents

• Acacia fiber

• Benefiber

• Citrucel

•

FiberChoice

•

Fibercon

• Konsyl

• Metamucil

• Perdiem

*Foods Associated with Bezoar Formation

Used with permission from the University of Virginia Health System

Nutrition Support Traineeship Syllabus (31)

PRACTICAL GASTROENTEROLOGY • AUGUST 2005

prokinetic agents are the mainstay of treatment in gas-

troparesis. When administering these useful medica-

tions, regular, scheduled dosing and the use of liquid

preparations provide the most consistent symptom

control. Scheduled dosing (versus “as needed” dosing)

assures that continuous, consistent levels of medica-

tion are provided to the patient. Provision of liquid

forms of these drugs in patients with delayed gastric

emptying also assures more accurate and consistent

drug delivery as liquids empty readily via gravity with-

out the need for antral peristalsis. From a clinical per-

spective, if the patient does not respond to this therapy,

intravenous medications, or more distal enteral deliv-

ery will be required. In the patient who requires gastric

decompression concurrent with jejunal nutrient infu-

sion, all medications should be delivered via the jeju-

nal port to promote maximal absorption. Tablet or pill

forms of medications should be crushed into a fine

wder with careful flushing of the tube before and

after dosing to keep the jejunal tube pa

tent.

Note: Medications should be checked from a phar-

macological standpoint to assure that they may be

crushed and that they are efficacious when delivered

into the jejunum.

Small Bowel Bacterial Overgrowth

Patients with gastroparesis are at high risk of develop-

ing small bowel bacterial overgrowth (SBBO). Peri-

stalsis and nor

mal g

astric acid production typically

events the colonization of bacteria within the small

el. In the setting of gastric dysmotility, bacteria

colonize the relatively sterile small bowel. Because

man

y pa

tients with g

astr

opar

esis are concurrently

treated with potent acid inhibitors to reduce reflux

symptoms, the resultant hypochlorhydria also signifi-

cantl

y pr

edisposes these pa

tients to de

elop SBBO

Bacterial colonization of the small bowel results in

a mucosal inflammatory process that impairs nutrient

absorption. Intestinal bacteria also compete with the

host f

or available nutrients. They deconjugate bile

salts, altering micelle formation, which results in fat

malabsorption. Bacter

ial meta

bolism also produces

short chain fatty acids tha

t are poorly absorbed in the

small bowel. These decrease luminal pH, hindering

intestinal enzymes and incr

easing the o

all osmotic

load. The endpoint is increased gut transit, maldiges-

tion and malabsorption.

Symptoms of SBBO include gas, bloating, abdomi-

nal distension, nausea, diarrhea, weight loss and an over-

all decline in nutritional status. These symptoms may

mimic those of gastroparesis, thus it is imperative to con-

sider SBBO in every patient with gastroparesis (38,39).

Enterally provided antibiotics are generally the treatment

of choice. The most frequently utilized antibiotics are

metronidazole, ciprofloxacin, amoxicillin/clavulanate or

doxycycline. However, rifaximin is being used with

increasing frequency (40). For persistent SBBO,

monthly rotating antibiotics may be necessary.

Ileal Brake

The ileal brake is the primary inhibitory feedback

mechanism that acts to control the transit of a meal

thr

ough the gastrointestinal tract. This distal gut

inhibitory feedbac

k system slows the speed of gas-

trointestinal transit in response to a meal. Nutrients,

particularly fatty acids, are believed to be the main

activator of the ileal brake. Teleologically, this gut

“traffic brake” regulates the speed of luminal peristal-

sis in the GI tr

act to maximiz

e the absor

ption of n

utri-

ents (41). Clinicall

y, the ileal br

e may pla

y a role in

increased GI symptoms that develop when jejunal tube

feedings are initiated. Exacerbation of nausea and

vomiting may be attributed to stimulation of the ileal

e by fats that have escaped more proximal absorp-

tion in the small bo

wel. This phenomenon should not

be confused with intoler

ance to jejunal f

eeding or

abnormal small bowel dysmotility. It is conceivable

tha

t SBBO can a

avate the ileal brake due to the

resultant malabsorption. Treatment should be aimed at

slowing the rate of tube feeding for a short period of

time and tr

ting SBBO if pr

esent.

Bezoar Formation

Bez

oars are retained concretions of indigestible for-

eign material that accumulate in the stomach. Patients

with alter

ed g

astr

ointestinal ana

tomy and/or motility

e a

t incr

eased r

isk f

or developing bezoars, thus

patients with gastroparesis are particularly predisposed

Nutrition Intervention for the Patient with Gastroparesis: An Update

NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #30

(continued from page 50)

(continued on page 55)

toward this complication (35). Clinicians should be

mindful of bezoar formation because when present, the

symptoms often mimic that of gastroparesis. Patients

may present with early satiety, nausea and vomiting.

Failure to recognize the presence of a bezoar may fur-

ther compromise the patient’s nutritional status.

Phytobezoars are composed of nondigestible food

material including cellulose, hemicellulose, lignin, and

fruit tannins (leucoanthocyanins and catechins). These

are found in celery, pumpkins, grapes, prunes, raisins,

and persimmons. In high concentrations, fruit tannins

may form a coagulum upon exposure to an acidic envi-

ronment initiating the formation of a phytobezoar.

Some medications can also cause pharmacobezoars.

Common culprits include: cholestyramine, sucralfate,

enteric-coated aspirin, antacids (e.g. aluminum

hydroxide) (42) and bulk forming laxatives (Table 14).

Additionally, extended-release nifedipine or verapamil

can cause bez

oars as the tablets are coated with poorly

digestible cellulose

Treatment of gastric phytobezoars includes enzy-

matic therapies such as papain or cellulose or lavage

with or without endoscopic therapy to mechanically

disrupt the bezoar. Patients with gastroparesis also

benef

it fr

om long-term pr

okinetic ther

apy to treat and

event bez

oar for

mation. Metoclopramide (43), ery-

thromycin or domperidone may be efficacious given

their effect on gastrointestinal motility. Avoiding high

fiber foods (especially citrus fruits and raw vegetables)

is necessar

y to pr

event recurrent phytobezoar forma-

tion (T

able 14).

NUTRITION SUPPORT

Oral Nutrition Guidelines

tients, dietitians and c

linicians fundamentall

y pr

to provide nutrition by the oral route. If the patient’s

nutritional status and symptoms allow, then a trial of

oral nutrition is indicated.

Ask the pa

tient to keep a food diary to provide a

more objective determination of actual oral intake (we

generally do not recommend a specific caloric intake

per day but rather look a

t overall trends over the ensuing

1–2 weeks). During this time, we look for improve-

ments in caloric intak

e and g

astr

ointestinal symptoms.

At the start, it is prudent for the physician, patient and

dietitian to define a target weight goal and the time

period over which this weight must be reached. If the

patient begins to gain weight, we stay the course and

continue the oral nutrition trial. If they fail to gain

weight or continue to lose weight, we proceed to enteral

nutrition support. Table 15 summarizes an approach to

oral nutrition support in the patient with gastroparesis.

In addition, oral dietary guidelines can be found at:

http://www.healthsystem.virginia.edu/internet/diges-

tive-health/nutrition.cfm. Look under patient education

materials and find three different diets for patients with

gastroparesis: gastroparesis, gastroparesis and diabetes

mellitus, and gastroparesis and kidney disease.

Enteral Nutrition (EN)

When significant malnutrition or poor control of gas-

oparesis symptoms prevails, a trial of enteral nutri-

tion should be initiated. Enter

al nutrition can keep

patients out of the hospital, reducing their risk of noso-

comial infection while concomitantly allowing for pro-

vision of nutrients, hydration and medication. EN is

less expensive and is associated with fewer infectious

complica

tions than total par

enteral n

utr

ition (TPN)

(44). It is also less la

bor intensive for the patient and

the caregiver in the home setting. See Table 16 for cri-

teria for enteral nutrition support.

Patients may be resistant to the idea of enteral

utr

ition, especially regarding nasal or endoscopically

placed tubes. W

e stress to patients that:

•

Enter

al access provides reliable delivery of nutrition

and hydration, as well as medications.

•

Enter

al access pr

vides better deli

very and thus

more consistent absorption of prokinetic and

antiemetic medications.

•

Mor

e consistent deli

y of n

utr

ients enhances glu

cose control.

• Enteral nutrition is optimal in that it utilizes the gut.

• Even endoscopically placed tubes can be easily

emoved when symptoms resolve and they return to

an oral diet.

•

Our g

oal is to ultima

tel

y get the patient back on the

oad to or

al f

eedings.

• If necessary, gastric venting can alleviate many of

the de

bilita

ting symptoms of g

astr

opar

esis.

PRACTICAL GASTROENTEROLOGY • AUGUST 2005

Nutrition Intervention for the Patient with Gastroparesis: An Update

NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #30

(continued from page 52)

PRACTICAL GASTROENTEROLOGY • AUGUST 2005

Nutrition Intervention for the Patient with Gastroparesis: An Update

NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #30

1. Decrease the volume of meals.

• Advise patients to eat smaller, more frequent meals.

2. Use more liquid calories.

• If solid foods cause increased symptoms, begin with a

liquid/pureed diet to promote gastric emptying.

• If symptoms increase over the course of the day, try solid

food meals in the morning, switching to more liquid meals

later in the day.

• Chew foods well.

• Suggest that the patient sit up during and for 1–2 hours

after meals.

3. Glucose control

• If gastroparesis is a result of diabetes mellitus, maximize

glucose control.

• Monitor the need to change the timing of, or the overall

requirements for insulin in order to have consistent delivery

of nutrients with optimal total calories ingested.

• Expect an increase in insulin requirements as improved

symptom control will likely result in an increase in total

calories ingested.

• In general, dietary restrictions (e.g. diabetic or heart healthy

diets) should be lifted during the trial.

4. Medications

• Prokinetics and antiemetics should be given in regular

scheduled doses (rather than “as needed” doses) and

may be best tolerated in liquid form.

• Avoid use of medications that affect gastric motility if

possible (Table 5).

• Review and delete any “unnecessary” meds (they can

always be added back later).

5. Fat

• Fat in liquids should be tolerated; implement #1–4 above

before restricting.

6. Fiber

• Fiber can be fermented in a “slow” gut by bacteria poten-

tially causing gas, cramping and bloating, and can

ultimately aggravate gastroparesis.

• If bezoar formation is a concern, the patient should avoid

the following high-fiber foods and medications:

– Oranges, persimmons, coconuts, berries, green beans,

figs, apples, sauerkraut, Brussels sprouts, potato peels,

and legumes.

– Fiber supplements such as: Metamucil, Perdiem,

Benefiber, Fibercon, Citrucel, etc.

7. Treat bacterial overgrowth if suspected/symptomatic.

8. Monitor and replace as needed: Iron, vitamin B

, vitamin D,

and calcium.

• If the patient is significantly malnourished, a daily standard

vitamin/mineral elixir can be used for one month or longer

or until stores are replete.

• If patient has gastric intolerance to iron, try smaller doses;

some is better than none. Liquid iron may be a better

choice in some patients. Consider giving iron with

vitamin C.

Used with permission from the University of Virginia Health System

Nutrition Support Traineeship Syllabus (31)

able 15

ummary of Oral Nutrition Intervention in the Patient with Gastroparesis

Enteral Access

The type of enteral access required depends on

patient/physician preference, estimated time that EN

will be needed, and the ability of the patient to toler-

ate endoscopy or surgery for enteral tube placement.

In the ideal situation, patients should be given a

short-term (48 hour) trial of nasojejunal feeding prior

to endoscopicall

y or sur

ically placed enteral access.

This allows clinicians to determine if the patient will

tolerate small bowel feedings. The major drawback of

the nasojejunal tube is tha

t it can mig

te bac

k into the

stomach or become dislodged during a bout of emesis.

Some clinicians favor the use of nasogastric/jejunal

(NG-J) tubes, which allow gastric venting concomi-

tantly with jejunal feedings. In our clinical experience,

patient acceptance of these tubes is poor because of

discomf

t due to their lar

e outer diameter

. Multiple

nasoenteric tube replacements with the burden of rein-

serting tubes along with radiation risks from repeated

fluoroscopy should prompt placement of more perma-

nent endoscopic or surgical enteral access. Endoscop-

ically placed feeding tubes do not require general

anesthesia and the

y ar

e typically associated with lower

costs w

hen compar

ed to sur

gically placed tubes.

If the pa

tient toler

tes jejunal f

eeding

, endoscopic

laparoscopic or surgical jejunostomy may be the best

approach. Oftentimes, patients with gastroparesis also

benefit from concurrent gastric venting to prevent nau-

sea and v

omiting. There is no consensus regarding the

need for gastric venting or the method by which it is

accomplished. Percutaneous endoscopic gastrostomy-

(continued on page 58)

PRACTICAL GASTROENTEROLOGY • AUGUST 2005

jejunostomy (also known as Jet-PEG or PEG-J) is ben-

eficial in that it can provide gastric decompression with

concurrent infusion of jejunal feedings utilizing only

one abdominal insertion site. Some clinicians prefer a

separate percutaneous endoscopic gastrostomy (PEG)

for g

astric venting plus a per

cutaneous endoscopic

jejunostomy (PEJ) for enteral nutrition. Those advocat-

ing the latter option claim that the gastric venting is

insufficient with the “tube within a tube” approach.

They also describe excessive retrograde migration of the

jejunal tube (J-tube) to the stomach with the PEG-J, thus

increasing the risk for aspiration pneumonia. Other

experts refute the benefit of gastric venting asserting

that it may delay the recovery of gastric motility. Clini-

cal tr

ials ar

e greatly needed in this area to determine if

one technique is better than others with regard to patient

preference, symptom improvement and complications.

At our institution, we prefer the PEG-J approach.

wer tubes have larger lumens that provide adequate

gastric tube (G-tube) venting and consistent jejunal

eeding without e

xcessi

e clogging of the tube. J-tubes

e also long

er in length, allo

wing f

or mor

e distal

placement and significantly less retrograde migration.

One per

cutaneous site theor

eticall

y r

esults in f

total site infections and less enteral/wound drainage

than two separate abdominal sites. The University of

Virginia’s Digestive Health Center of Excellence uti-

lizes a 24 French (Fr) Wilson Cook PEG tube with a 12

Fr J-tube passed fluoroscopically beyond the ligament

of Treitz. Anecdotally, patients who have a PEG

placed in the mid- to lower antrum facing the pylorus

experience easier placement of the j-arm and less

migration of the j-arm back into the stomach.

Direct percutaneous endoscopic jejunostomy

(PEJ) (45) and surgical jejunostomy tubes do not allow

for gastric venting and are used less often than PEG-J

tubes. Care must be taken to avoid distal placement of

a surgical jejunostomy, which can result in malabsorp-

tion due to a short bowel syndrome-like state. Surgical

J-tubes also often have internal balloons, which if

over-inflated, can obstruct the small bowel.

Fluoroscopically placed or computer tomography

(CT) guided gastric tubes should be avoided. Their

small diameter (12–16 Fr) makes them significantly

more prone to clogging and they do not allow place-

ment of a J-tube for jejunal feeding. If endoscopic tube

placement cannot be performed, surgical jejunostomy

with or without g

astrostomy is preferred.

Initiating Feeding After Tube Placement

If the pa

tient is significantly malnourished, special care

should be tak

en to start nutr

ition support at the lower

end of the calorie range at 20–25 kcal per kilogram of

actual, euvolemic weight to avoid refeeding syndrome

(46). Overfeeding the diabetic patient can also aggravate

glucose contr

ol and hence nutritional rehabilitation.

he f

ollowing are the UVAHS Nutrition Support

Team protocols for initiating EN in patients with gas-

troparesis after feeding tube placement (Table 17):

•

p pa

tient NPO dur

ing initia

tion of tube f

eeding

until tolerance is established: Avoids clouding the issue

of gastric intolerance versus tube feeding intolerance.

•

If feeding tube trial is desired prior to permanent

access, soft, small bor

e f

eeding tubes, nasojejunal (not

nasoduodenal), orojejunal: radiographic confirmation

of tube placement f

ollo

ed b

y immediate use.

• PEJ or PEG with jejunal extension (PEG-J): Tube

feeding may begin immediately via the jejunal port.

her

e is no need to c

hec

k f

or r

esidual v

olumes with

jejunal tubes, as there is no “reservoir” to collect tube

feeding. In patients who continue to vomit, the gas-

tric port can be placed to gravity drainage (e.g. leg

g or standard urinary drainage bag). If the gastric

output is greater that 500 mL over a twenty-four hour

Nutrition Intervention for the Patient with Gastroparesis: An Update

NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #30

(continued from page 56)

Table 16

riteria to Determine Candidacy for Enteral Nutrition

• Severe weight loss, e.g. unintentional weight loss >5%–10%

of UBW over 3–6 months respectively.

• Repeated hospitalizations for refractory gastroparesis

equiring intravenous hydration and/or medication delivery.

• Patient would benefit from gastric decompression.

• Patient has maintained usual body weight, but experiences

significant clinical manifestations such as:

– Diabetic ketoacidosis

– Cyclic nausea and vomiting

– Overall poor quality of life due to gastroparesis symptoms.

• Inability to meet weight goals set by physician, dietitian and

patient.

Used with permission from the University of Virginia Health System

Nutrition Support Traineeship Syllabus (31)

period, patients should re-infuse the gastric contents

(see reinfusion section) via the jejunostomy.

• Sur

gically placed tubes: Initiation and advancement

per the surgeon.

Formula Selection

Man

y practitioners believe that small bowel feeding

requires special enteral formulas; however the major-

ity of pa

tients toler

te standard, polymeric formulas. In

general, we use the least expensive formula that meets

their indi

vidual needs.

A fiber containing formula may be useful due to its

benef

its on gut inte

ity

. However, if the patient has

concomitant small bowel dysmotility, indigestible

fiber may aggravate symptoms if bacterial overgrowth

is a c

onic pr

lem (47,48). F

or jejunall

y f

ed pa

tients,

the remaining absorptive area of the small bowel com-

bined with intact pancreatic enzyme and bile salt

secretions, further supports the use of standard formu-

las (consider the pa

tient who has undergone a total

gastrectomy that is discharged eating a regular diet). In

patients with pancr

tic e

xocrine insufficiency, pow-

dered pancreatic enzymes can be added to enteral feed-

ings or dosed periodically during infusion.

For patients with DM, ther

e ar

e no da

ta to w

rant

the use of the more expensive diabetic formulas (49).

Formulas to control glucose levels have not been

shown by clinical trials to be efficacious or cost effec-

tive. One longitudinal study demonstrated no differ-

ence in HgbA

C levels when utilizing a standard, poly-

meric versus a lower carbohydrate formula in a nurs-

ing home population (50). The studies that have been

done are small, of short duration, mostly in relatively

healthy, non-hospitalized subjects, or in acute head

injury patients without a documented history of DM. If

glucose control is suboptimal and insulin therapy is

undesirable, then it may be worthwhile to try one of

the lower carbohydrate formulas.

Patients with end-stage renal disease are allowed a

reasonable level of potassium, sodium, phosphorus,

and volume. Often these patients can tolerate standard

products and still stay within the guidelines of their

renal diet prescription.

In the rare patient that can tolerate gastric tube

feedings, volume is the most important factor. Chang-

ing to a calorically dense f

ormula will provide more

calories at a lower flow rate. Decreasing the total vol-

ume needed to meet nutrient needs may be all that is

needed to allow continued gastric feeding.

Delivery Methods

Jejunal feeding commits the patient to cycled pump or

ravity infusion typically over 8 to 14 hours, depend-

ing on symptoms. The small bowel is volume sensitive

and does not tolerate intermittent bolus feeding to any

ppr

ecia

ble extent. Enteral feedings do not need to be

diluted, and the flow rate can be increased from 125

mL to 160 mL per hour or g

ter if toler

ted.

Hydration

Patients that are enterally fed do not get enough hydra-

tion with tube f

eeding alone

, thus it is imper

tive to

provide supplemental water. As a rule of thumb, most

tube feeding products are approximately 80% water.

Cur

ent r

ecommenda

tions sug

est tha

t pa

tients receive

1 mL of fluid (combined tube feeding and supplemen-

tal water) for every kcal of tube feeding. Patients typi-

cally require at least 1800–2000 mL of fluid each day.

hus if a patient is taking in only 1500 kcal of tube

feeding per day (80% = 1200 mL), we provide an extra

500–700 mL of w

ter to ensur

e they receive adequate

PRACTICAL GASTROENTEROLOGY • AUGUST 2005

Nutrition Intervention for the Patient with Gastroparesis: An Update

NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #30

Table 17

rotocol for Initiation of Enteral Nutrition

Following PEG-J Placement

1. NPO except 8 ounces of ice chips per day

. Enteral nutrition to start via the J-port upon return to the

unit per Nutrition Support Team recommendations

3. G-port to gravity for the first 24 hours after PEG-J placed

• If <500 mL drainage, clamp G-port and monitor for nau-

sea/vomiting

• If >500 mL drainage, continue gravity drainage and

assess need for jejunal re-infusion

4. Start liquid PPI via J-port q HS same day PEG-J was placed

5. Check gastric pH (via G-port) Day #2 (or after patient has

received 3 doses of PPI

6. If patient is hyperglycemic on nocturnal tube feedings, add

accucheks at 1800, 2200 and 0600.

Used with permission from the University of Virginia Health System

Nutrition Support Traineeship Syllabus (31)

PRACTICAL GASTROENTEROLOGY • AUGUST 2005

hydration over the course of the day. In patients who

take in more than 1800 kcal of tube feeding, we adjust

to provide an additional 1 mL of water for every 1 kcal

over 1800. Patients with DM are at increased risk of

dehydration, hence an additional 200–400 mL of water

during the day may prove beneficial.

Because water is h

ypotonic

, it is generally toler-

ated in bolus infusions (even in the jejunum) or it can

be mixed with TF. Water can be delivered via syringe,

gravity drip or pump. One convenient way to ensure

adequate water delivery is to recommend that patients

measure their daily water allotment every morning into

a quart or similar container. Instruct them to use the

water from this container over the course of the day;

emphasize that

ALL of it needs to be used before bed-

time. They can infuse water through their enteral tube,

use it as medication flushes, or drink it (if tolerated).

Advise them to take in more water if they are thirsty, if

their urine appears concentrated or if their urine output

declines.

Re-infusion of Gastric Output

Gastric venting can be extremely beneficial to the

patient with gastroparesis by decreasing nausea and

preventing most episodes of vomiting. Patients with

intractable nausea and vomiting can place their G-tube

to gravity drainage using a leg bag or a standard uri-

nar

y collection bag. If their G-tube output is g

reater

than 500 mL over 24 hour

s, deh

ydration and meta

bolic

disarray (hypochloremic, hypokalemic metabolic alka-

losis) can occur if the fluid and electrolytes are not

replaced. Re

placement can be accomplished using a

saline solution given via the jejunal port (e.g. 1/2 nor-

mal saline = 3/4 teaspoon salt in a liter of water

replaced 1:1 for losses—this is in addition to their

water and

medication flushes!!). A more physiologic

method in

olves re-infusion of the gastric secretions.

To further minimize the volume of gastric output, it

is often beneficial to treat patients with acid reducing

ents suc

h as the pr

oton pump inhibitor

s (PPI):

omeprazole, lansoprazole, pantoprazole, etc., which

also act to decrease the sheer volume of gastric secre-

tions. Liquid PPI pr

eparations are available; however,

most PPIs in pills or ca

psule f

orm may also be made

into liquid forms that can be given via the enteral tube.

ysicians should be cautioned

, ho

ever that continued

inhibition of gastric acid may increase the patient’s risk

to develop small bowel bacterial overgrowth.

Problem Solving

ue intoler

ance of jejunal tube f

eeding is uncommon

in patients with gastroparesis. More often, the side

Nutrition Intervention for the Patient with Gastroparesis: An Update

NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #30

Table 18

nteral Nutrition Summary and Problem-Solving Suggestions

for the Patient with Gastroparesis

1. If needed, use enteral (rather than parenteral) nutrition;

referably jejunal feedings.

2. Use standard, polymeric formulas.

3. If there is a high suspicion of oral intake, we ask our

patients to tell us what, rather than “if”, they are eating and

drinking on a daily basis.

4. Reiterate periods of strict NPO status (except for a few ice

chips) during initiation of EN to avoid confusing oral intol-

erance with EN intolerance, until tube feeding tolerance is

established.

5. If the patient experiences increased nausea/vomiting after

initiating EN, try decreasing the rate of infusion for a few

days (this could be from the ileal brake).

6. Maximize the use of liquid prokinetic agents and anti-emet-

ics with delivery via the J-tube (scheduled versus “prn”

dosing and liquid preparations may be beneficial). Gastric

delivery of medications in a patient requiring gastric

decompression will be ineffective.

7. Consider enteral treatment of bacterial overgrowth utilizing

antibiotics given via the J-tube.

8. If bacterial overgrowth is a chronic problem, try a non-

fiber-containing formula.

9. Check tube placement—specifically for backward migration

of a J-tube into the stomach. Seek to reposition the tube.

10. If nausea and vomiting increase after the placement of a

surgical J-tube and ileus is ruled out, a fluoroscopic study

with oral contrast (swallowed, not via the J-tube) can

determine if the internal balloon is obstructing the lumen.

Decreasing the volume of saline in the balloon will alleviate

the mechanical obstruction.

11.

Use a more calorically dense formula to decrease total vol

ume of EN required to meet calorie needs. Note: be sure

to increase hydration with more calorically dense tube

feeding formulas.

12.

Maximize glucose control (glucose levels >200 mg/dl may

aggravate gastroparesis).

Used with permission from the University of Virginia Health System

Nutrition Support Traineeship Syllabus (31)

(continued on page 63)

effects associated with enteral nutrition can be

xplained physiologically and are relatively simple to

resolve. In some patients, the ileal brake may be the

culprit (38,39,41). In our experience, this feedback

inhibition generally resolves within a few weeks. Prox-

imal migration of the J-tube can also result in a sudden

increase in v

omiting in the pa

tient who has previously

toler

ated small bowel f

eedings. If the J-tube is not at,

or beyond the ligament of Treitz, tube feeding can

reflux back into the stomach. Surgical jejunostomy

tubes can also cause nausea and vomiting due to par-

tial mechanical obstruction caused by over-inflation of

the internal balloon. A barium fluoroscopic study,

all

y or via the g-por

t, can confir

m the obstr

uction;

minor deflation of the balloon generally resolves the

oblem. Finally, it is imperative to ascertain if the

nausea and v

omiting are resulting from covert oral

intak

e of f

oods. See T

able 18 for summary and prob-

lem-solving guidelines for enteral intervention.

Total Parenteral Nutrition (TPN)

Total parenteral nutrition is rarely necessary for the

patient with gastroparesis. TPN should be considered a

last r

esor

t in pa

tients w

ho ha

e a functional GI tr

act

distal to the stomach. If TPN is required, close clinical

and laboratory monitoring is imperative to prevent

metabolic disarray and significant complications.

ransition to enteral nutrition should be undertaken

when clinically feasible and should be a priority.

ipher

al parenteral nutrition (PPN) is often con-

sidered to be easier than TPN, primarily because it is

delivered via a peripheral vein. Its use, however, is lim-

ited by the sensitivity of per

ipher

al v

eins to h

yper

tonic

solutions (51,52). The primary complication associ-

ated with PPN is thrombophlebitis (Table 19). This

limits the caloric density of fluids that may be used and

limits the length of time that PPN can be given. Thus,

it is often impossib

le to meet full calorie and protein

needs with PPN.

CONCLUSION

Gastroparesis can be very debilitating. Nausea and vom-

iting impact the pa

tient’

s quality-of-lif

e and can r

esult in

significant medical problems, most notably malnutri-

tion. Accurate nutrition assessment is vital in the initial

evaluation of a patient with gastroparesis as malnutrition

contributes to significant morbidity and mortality in this

patient population. Providing nutrition support, assuring

xcellent glucose control and treating nutrient deficien-

cies can be e

xtr

emely challenging in the patient with

gastroparesis. Nutrition intervention can decrease symp-

toms, r

plenish n

utr

ient stores and improve an individu-

al’s overall quality of life. As with any chronic condi-

tion, support groups provide an invaluable resource for

these pa

tients. T

le 20 pr

vides a list of w

bsites avail-

able for patients with gastroparesis or other gastroin-

PRACTICAL GASTROENTEROLOGY • AUGUST 2005

Nutrition Intervention for the Patient with Gastroparesis: An Update

NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #30

(continued from page 60)

Table 19

reparation to Prevent Thrombophlebitis Associated with

Peripheral Parenteral Nutrition (51)

Add directly to each liter of intravenous PPN solution:

•

Hydrocortisone, 15 mg

• Heparin, 1500 units

• AND place transdermal nitroglycerin (NTG) patch,

0.1 mg/hour proximal to catheter

Table 20

ther Resources

GI Motility Web Sites

• Gastroparesis and Dysmotilities Association (GPDA):

ttp://digestivedistress.com

• American Motility Society

www.motilitysociety.org

• Association of Gastrointestinal Motility Disorders, Inc.

www.agmd-gimotility.org

• Cyclic Vomiting Association

www.cvsaonline.org

• International Foundation for Functional Gastrointestinal

Disorders

www.iffgd.org

Nutrition Support Web Sites

• American Society of Parenteral and Enteral Nutrition (ASPEN)

www.nutritioncare.org

• Oley Foundation (Support Organization for patients on home

nutrition support)

www.oley.org

PRACTICAL GASTROENTEROLOGY • AUGUST 2005

testinal dysmotility disorders and for those patients who

require nutrition support.

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