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Postgastrectomy Nutrition
Nutr Clin Pract 2011 26: 126
DOI: 10.1177/0884533611400070

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Invited Review
Postgastrectomy Nutrition
Christie Rogers, MS, RD, CNSC
Financial disclosure: none declared.
Gastric resection, whether partial or total gastrectomy, often
results in nutrition-related complications including weight loss,
diet intolerances, and micronutrient deficiencies. The physiol-
ogy of normal and postgastrectomy digestion is the basis for
most of the current diet recommendations after gastric surgery.
A careful review reveals that there is not sufficient literature to
support a standard postgastrectomy diet. Rather, individualized
T
he prevalence of gastric resection has decreased
with improved medical management of peptic ulcer
disease. Gastrectomy remains a treatment option
for patients with refractory peptic ulcer disease and is the
primary treatment for localized gastric cancer. Clinicians
will continue to encounter patients with partial or total
gastrectomies. The most common nutrition-related postgas-
trectomy complications include weight loss, gastric stasis,
dumping syndrome, fat maldigestion, and nutrient deficien-
cies. Appropriate nutrition interventions can reduce or
prevent these complications. Therefore, it is important for
clinicians to recognize nutrition complications associated
with this surgery and be knowledgeable of dietary modifica-
tions that may alleviate these complications. The traditional
postgastrectomy diet, with its many restrictions, is based on
well-studied physiology of anatomical changes postopera-
tively. A careful review of the literature reveals there is no
consensus as to the optimal way to feed postgastrectomy
patients. Nutrition management of these patients may need
to be individualized and will require careful monitoring and
adjusting based on the patient’s symptoms.
Overview of Gastric Surgeries
Partial Gastrectomy
A partial gastrectomy involves removal of the gastric
antrum and the gastrin-producing G cells that promote
hydrochloric acid secretion.1 The resultant decrease in
From the University of Virginia Health System, Nutrition
Support Services, Charlottesville, Virginia
Address correspondence to: Christie Rogers, University of
Virginia Health System, Nutrition Support Services, PO Box
800673, Charlottesville, VA 22908; e-mail: cr8db@virginia.edu.
126
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Nutrition in Clinical Practice
Volume 26 Number 2
April 2011 126-136
© 2011 American Society for
Parenteral and Enteral Nutrition
10.1177/0884533611400070
http://ncp.sagepub.com
hosted at
http://online.sagepub.com
diet manipulation for symptom relief is recommended. This
review highlights the physiology behind common postgastrec-
tomy complications, provides guidelines for the medical and
nutrition management of these complications, and presents a
basic approach to postgastrectomy gastrointestinal symptoms.
Keywords:   gastrectomy; nutrition therapy; nutrition support
acid production makes this surgery an option for patients
with peptic ulcers that do not respond to acid-suppressing
medications.1 Partial gastrectomy is also a treatment
option for those with localized gastric cancer. A Billroth I
or II procedure will reestablish continuity of the gastroin-
testinal (GI) tract. A Billroth I reconstruction, or gastro-
duodenostomy, involves creating an anastomosis between
the distal gastric segment and the proximal duodenum
(Figure 1). A Billroth II reconstruction, or gastrojejunos-
tomy, involves making an anastomosis between the distal
gastric segment and the proximal jejunum. A “blind loop”
of duodenum is created to maintain the flow of bile salts
and pancreatic enzymes2 (Figure 2).
Vagotomy
Vagotomy, or resection of the vagus nerve, may be com-
pleted in conjunction with a Billroth I or Billroth II
reconstruction, or as a stand-alone procedure. A vagot-
omy eliminates cholinergic stimulation of acid-producing
gastric cells.3 In a total vagotomy, the innervations to both
the parietal cells and the portion of the vagus nerve that
control gastric emptying are eliminated.2 This results in
decreased acid production but also leads to gastric stasis
and poor gastric emptying.4 To improve gastric emptying,
a pyloroplasty (enlarging of the pyloric sphincter) or gas-
trojejunostomy may also be performed.4 In a selective, or
partial, vagotomy, only the vagal nerve innervations to the
parietal cells are severed, preserving the functions of the
antrum and pylorus.2,4 In a partial vagotomy, acid produc-
tion is decreased whereas gastric emptying and peristalsis
remain functional.2
Total Gastrectomy
A total gastrectomy involves the removal of the entire
stomach with a Roux-en-Y reconstruction to establish GI

Figure 1.   Billroth I.
Figure 2.   Billroth II. Figures courtesy of CancerHelp UK:
www.cancerhelp.org.uk.
Figure 3.   Total gastrectomy.
tract continuity. With a Roux-en-Y, the jejunum is pulled
up and anastomosed to the esophagus. The duodenum is
connected to the small bowel so that bile and pancreatic
secretions can flow into the intestine (Figure 3). In some
instances, the Roux limb is doubled over to create an
artificial “stomach pouch.”4 Loss of the entire stomach
results in a functional vagotomy and consequently elimi-
nates acid production.
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Postgastrectomy Nutrition / Rogers   127
Postgastrectomy Nutrition-Related
Complications
Weight Loss
Weight loss after partial or total gastrectomy is well docu-
mented.5-9 Pedrazzani et al8 evaluated 195 patients, over a
5-year period, who had undergone subtotal gastrectomy
with Billroth II reconstruction. The authors demon-
strated that the majority of weight loss occurred within
the first 3 months after gastric surgery.8 Weight then sta-
bilized and a small amount of weight gain was observed,
although few patients attained preoperative weight.8
Postprandial fullness appears to contribute to weight loss,
especially during the first 3-6 months after operation.8
Weight loss may also result from inadequate food intake
due to dumping syndrome symptoms or due to nutrient
malabsorption.10 Because the majority of weight loss
appears to occur within the first 3 months postopera-
tively, it is important that early nutrition interventions
aim to curtail this trend.8,11,12 The following sections will
address the hypothesized reasons for weight loss, includ-
ing gastric stasis, dumping syndrome, and fat maldiges-
tion. Dietary modifications that may alleviate these
postgastrectomy nutrition complications will be addressed.
In addition, a basic approach to postgastrectomy GI com-
plications is provided in Figure 4.
Gastric Stasis
Patients with gastric stasis, or delayed gastric emptying,
often present with nausea and vomiting, loss of appetite,
bloating and fullness, or early satiety.4 Incidence of gas-
tric stasis following gastrectomy ranges from 0.4% to
13%.4,13,14 Total vagotomy often causes gastric stasis since
the loss of the vagus nerve inhibits normal gastric empty-
ing. However, even in Billroth II procedures without
vagotomy, patients have experienced gastric stasis, possi-
bly due to hypomotility of the gastric remnant.15,16 Motor
disturbances in the jejunal limb following distal and total
gastrectomy may also lead to gastric stasis.16,17
Once mechanical obstruction and ulcer disease have
been excluded via upper endoscopy or radiographic imag-
ing, a gastric emptying test can be used to diagnose gas-
tric stasis.18 Several methods exist to evaluate gastric
emptying, including scintigraphy, stable isotope breath
test, and ultrasonography. Gastric emptying by scintigra-
phy is considered the gold standard because it evaluates
the emptying of a standard meal.18 This meal typically
includes 2 eggs, 2 pieces of white toast, and water, so that
the procedure analyzes the emptying of both liquids and
solids with approximately the same distribution of calo-
ries, fat, protein, and carbohydrates.18,19 Gastric emptying
is abnormal when greater than 50% of the meal is
retained after 2 hours of study or when greater than 10%
128   Nutrition in Clinical Practice / Vol. 26, No. 2, April 2011

I. Procedure Partial Gastrectomy or Total Gastrectomy

II. Symptoms Diarrhea Nausea/Vomiting Early Satiety

Fat Dumping Gastric

III. Differential Malabsorption Syndrome Stasis

-72 hr fecal fat -Symptom Evaluation -Gastric Emptying by Scintigraphy

IV. Evaluation -OGTT

V. Management
-If SBBO suspected,
empirically treat
with antibiotics
-If SBBO not
suspected, initiate a
trial of pancreatic
enzymes
-Dietary modifications -Trial of prokinetic and/or
(see article for details) antiemetic agents
-If symptoms continue -If symptoms continue,
despite diet initiate dietary modifications
manipulation, consider (see article for details)
the following
medications:
-acarbose (most effective
with late dumping
syndrome)
-octreotide (use only
after exhausting all other
options)

This algorithm is intended to aid in the evaluation and management of common symptoms that
occur after partial or total gastrectomy. After identifying symptoms (II), fat malabsorption,
dumping syndrome, and gastric stasis can be confirmed (III) using diagnostic tools provided (IV).
Guidelines for management are also included (V).
Abbreviations: SBBO, small bowel bacterial overgrowth; OGTT, oral glucose tolerance test

Figure 4.   Approach to postgastrectomy GI symptoms.

of the meal is retained after 4 hours.19 During isotope
breath tests, patients typically ingest eggs labeled with 13C
or 14C octanoic acid.18,19 After passage into the small
bowel, the labeled solid is metabolized to the labeled
CO2, which is then excreted by the lungs.18,19 Breath sam-
ples are obtained every 10-15 minutes after egg ingestion
to determine the time it takes for food to pass into the
small bowel.18,19 Isotope breath tests have not been vali-
dated in patients with abnormal small bowel, pancreas,
liver, or pulmonary function.18,19 Ultrasonography is not
ideal because of operator dependence and its inability to
assess the emptying of solid materials.18,19 Although
breath testing and ultrasonography are not recommended
as the gold standard to assess gastric emptying, they are
less invasive and do not involve ionizing radiation expo-
sure.19
Medication management of gastric stasis typically
involves the use of prokinetic and antiemetic agents.20
Metoclopramide has an antiemetic and a prokinetic
effect.20 Onset of action is typically 60 minutes after an
oral dose and 30 minutes after an intravenous dose.20 A
usual dose of metoclopramide is 5-20 mg orally 4 times
per day or 10 mg intravenously every 2-3 hours. 20
Erythromycin, both orally and intravenously, has been
used to promote gastric emptying.20 Since erythromycin is
typically used to address acute symptom flares, intrave-
nous administration of 1-2 mg per kg every 8 hours is
usually recommended.20 Oral dosing of 50-250 mg 4
times per day is also an option.20 Although nausea and
vomiting secondary to gastric stasis typically resolve with
prokinetic agents alone, antiemetics can also be used if
nausea persists. Promethazine can be given orally, intra-
muscularly, or per rectum at a dosage of 12.5-50.0 mg
every 4 to 6 hours.20 Both prokinetic and antiemetic
agents are best provided in regularly scheduled doses
rather than on an as-needed basis.4,20
Patients with gastric stasis have an increased risk for
small bowel bacterial overgrowth (SBBO). Although

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healthy bowel contains a certain amount of bacteria, the
presence of an excess number of bacteria in an atypical
location represents SBBO.21 Symptoms occur when the
human host competes with the excessive bacteria for
ingested nutrients or when the excessive bacteria cause
injury to the small bowel epithelium.21 Ironically, the
symptoms of SBBO can be similar to those of gastric sta-
sis: nausea, vomiting, bloating, or early satiety.4 SBBO
can be diagnosed by obtaining a small bowel aspirate dur-
ing endoscopy.21 Although this is the gold standard, limi-
tations exist.21 This process will not detect SBBO
occurring in the distal small intestine. Furthermore, more
than 50% of the bacterial species of the GI tract cannot
be cultured, making identification of the microorganisms
difficult.21 Hydrogen breath testing is an alternative and
more commonly used method to diagnose SBBO.21
However, false-positive hydrogen breath tests have been
seen in patients with a history of gastric resection.21
Given discrepancies and difficulties with testing and diag-
nosis of SBBO, it is common to empirically treat with
enteral antibiotics that cover both aerobic and anaerobic
bacteria. The use of probiotics for the prevention or treat-
ment of SBBO has been postulated, but human studies
are minimal and inconsistent.22-25 Additional research in
this area would be beneficial. If gastric stasis is not
responding to dietary and medical interventions, the pres-
ence of SBBO should be investigated and treated.
Gastric stasis can also increase the incidence of bez-
oar formation. These accumulations of undigested mate-
rial or medications within the GI tract can cause
obstructions that may require surgical intervention. Like
SBBO, the presence of a bezoar can mimic the classic
symptoms of gastric stasis.4 Although plain abdominal
radiographs and barium studies may identify a bezoar,
endoscopy is the preferred method for diagnosing bez-
oars.26 Removal of the bezoar alone may eliminate the
symptoms that were once attributed to gastric stasis. If,
however, the patient developed a bezoar because of gas-
tric stasis, dietary modifications can reduce the incidence
of additional bezoars. Details regarding these modifica-
tions are discussed below.
There are several dietary modifications that may alle-
viate the symptoms associated with gastric stasis. Prior to
deciding which modification to recommend, the clinician
should obtain a thorough diet history from the patient.
Only 1 or 2 aspects of the diet should be changed at a
time so that symptom relief can be achieved without
unnecessary dietary restrictions.4 These recommenda-
tions have not been validated by controlled trials but are
derived from the idea that certain foods enhance gastric
emptying. Additionally, most gastric emptying studies
involve nonsurgical, healthy patients. More research eval-
uating postgastrectomy gastroparesis and diet manipula-
tion would be beneficial.
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Postgastrectomy Nutrition / Rogers   129
Nutrition Interventions for Gastric Stasis
Symptoms include nausea and/or vomiting after meals.
Begin by advising patient to eat smaller, more frequent
meals throughout the day.
Symptoms are exacerbated after eating solid foods but
minimal after consuming liquids. Encourage patient to
increase calories from liquids or pureed foods. Pureed
foods usually empty from a gastroparetic stomach even
when larger particles are retained.4,20,27
Symptoms continue despite medications and previous diet
modifications. Initiate a trial of a low-fat/low-fiber diet.
Lipids and indigestible fibers have been reported to delay
gastric emptying.4,20,28 Liquid fats do not pose a problem
and therefore should not be avoided.4
Patient with a history of bezoar formation. Encourage
patients to avoid foods high in fiber, especially citrus
fruits and raw vegetables. Patients should also eliminate
bulk-forming laxatives, such as psyllium.26,29
Dumping Syndrome
Dumping syndrome occurs when food rapidly empties
into the small bowel resulting in GI and/or vasomotor
symptoms. After gastric surgery, 25%-50% of patients
experience dumping syndrome. Of these patients, 5%-10%
experience symptoms that are clinically significant.22
Symptoms of dumping syndrome present during the first
3 months after surgery and can resolve within 1 year post-
operatively.8 Although the symptoms were identified and
the term dumping was coined nearly a century ago, the
pathophysiology of dumping syndrome continues to be
contested.30
Two forms of dumping syndrome have been observed:
early and late. Early dumping syndrome occurs 10-30
minutes post prandial with a combination of GI and vaso-
motor symptoms.31 These may include abdominal pain,
bloating, nausea, vomiting, diarrhea, headache, flushing,
fatigue, and hypotension.22,31 Late dumping syndrome
occurs 1-3 hours post prandial with predominantly vaso-
motor symptoms. Symptoms of late dumping syndrome
include perspiration, weakness, confusion, shakiness,
hunger, and hypoglycemia.22,31
The decreased gastric reservoir and loss of the pyloric
sphincter after gastric surgery mean that food passage
into the small intestine is accelerated. Typically, the
antrum grinds food particles into 1-2 mm fragments
before delivery into the small intestine.31 Without the
stomach sieving or grinding, large, difficult-to-digest par-
ticles are funneled into the small intestine.32 Early dump-
ing syndrome GI symptoms most likely occur because of
130   Nutrition in Clinical Practice / Vol. 26, No. 2, April 2011
the rapid influx of hyperosmolar contents into the duode-
num or small intestine.22,31 A subsequent fluid shift from
the intravascular compartment to the intestinal lumen is
observed. This results in small intestine distention, which
may cause cramps and bloating.22,31 The vasomotor symp-
toms of early dumping have been attributed to elevated
serotonin levels.10,33 Serotonin as a neurotransmitter
causes vasodilation manifested as flushing, hypotension,
and increased gastric motility, the symptoms associated
with early dumping.
Late dumping syndrome is most likely the result of
reactive hypoglycemia. Because of the surgical changes
previously explained, large amounts of carbohydrate are
delivered rapidly into the small intestine. This causes an
accelerated absorption of glucose into the blood.22
Subsequently, excessive insulin is released and a reactive
hypoglycemic response is observed.22,34,35 Glucagon-like
peptide-1 (GLP-1) is also involved in late dumping syn-
drome. The secretion of GLP-1 from the small intestine
and colon results in insulin release.22,36 Several studies
have demonstrated an increase in GLP-1 secretion fol-
lowing an oral glucose challenge in patients who have had
gastric resection.22,37-39
Dumping syndrome is typically confirmed by the pres-
ence of the previously mentioned symptoms in a patient
with a history of upper abdominal surgery.22,31 Hypoglycemia
combined with several GI symptoms is strongly indicative
of dumping syndrome.31 An oral glucose tolerance test
using a 50-75 g glucose solution after an overnight fast can
be used to confirm dumping syndrome.31 Blood glucose,
hematocrit, pulse rate, and blood pressure are measured
immediately before glucose ingestion and every 30 minutes
for up to 180 minutes after ingestion.31 The test is consid-
ered positive if hypoglycemia occurs at 120-180 minutes, if
hematocrit increases by more than 3% at 30 minutes, or if
pulse rate increases by more than 10 beats per minute at
30 minutes.
Patients with refractory dumping syndrome, despite
diet manipulation, may benefit from pharmacologic ther-
apy. Acarbose has been used in the treatment of late
dumping syndrome because of its effect on postprandial
hypoglycemia.22 Acarbose minimizes reactive hypoglyc-
emia by delaying the conversion of polysaccharides to
monosaccharides and thereby decreasing postprandial
glucose and insulin release.22 A few small studies, giving
50-100 mg of acarbose to patients with late dumping
syndrome, have demonstrated conflicting results.31,40-44
In a double-blind study of 9 gastric surgery patients,
Speth et al42 showed improved symptoms of postprandial
hypoglycemia when 50 mg of acarbose was given after
a carbohydrate-rich meal. In contrast, Lyons et al43
showed no significant improvement in symptoms when
13 patients were given 50 mg of acarbose both before 1
meal and also 3 times daily before meals for 1 month.
Hasegawa et al44 gave 6 gastric surgery patients with late
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dumping syndrome and non–insulin-dependent diabetes
mellitus 50 mg of acarbose 3 times daily before meals for
1 month. All patients demonstrated a resolution of symp-
toms.44 Larger, long-term prospective studies are neces-
sary to evaluate the effect of acarbose on late dumping
syndrome symptoms. Additionally, as the unabsorbed car-
bohydrates reach the small intestine, bacterial fermenta-
tion causes diarrhea, bloating, and flatulence.31 These
side effects of acarbose may decrease patient compliance.
Octreotide, a somatostatin synthetic analog, has been
used in the treatment of both early and late severe dump-
ing syndrome.22 Somatostatin analogs can delay gastric
emptying and small bowel transit time, inhibit GI hor-
mone and insulin secretion, decrease postprandial vasodi-
lation, and increase the absorption of water and sodium
in the intestine.22,31 Short-acting and long-acting repeat-
able (LAR) octreotide formulations have been used in the
management of severe or refractory dumping syndrome.
An initial dose of the short-acting formulation is a 25-50
mcg subcutaneous injection given 15-30 minutes before
meals.22 If ineffective, this dose can be increased to 100
mcg.22,31 Given its slow release, the LAR octreotide for-
mulation can be given monthly via a 20 mg intramuscular
injection.31 A systematic review of randomized controlled
trials evaluating the effectiveness of short-acting octre-
otide confirmed that octreotide, both short term and long
term, improves dumping syndrome symptoms.45 However,
the studies evaluated were small: 7 studies with a com-
bined total of 63 patients.45 Several studies reported
increased diarrhea with short-acting octreotide,46-48 and 2
reported steatorrhea.48,49 Despite steatorrhea, Geer et al48
reported an 11% increase in mean body weight and Vecht
et al49 reported an average weight gain of 2.4 kg.22 Two
studies, both open-label and uncontrolled, evaluated LAR
octreotide for the treatment of dumping syndrome.50,51
Penning et al51 gave 12 patients, who previously required
daily short-acting octreotide, 10-20 mg of the LAR for-
mulation, monthly, for 6 months.51 Significant improve-
ment in quality of life, specifically in the GI symptoms
subscale, was observed in patients receiving the 10 mg
dose.51 It is important to note that the 10 mg dose of LAR
octreotide is not available in most countries.31 Arts et al50
gave 30 patients 50 mcg injections of short-acting octre-
otide 3 times daily for 3 days. On the evening of day 3,
the patients were started on 20 mg of LAR octreotide
intramuscularly, monthly, for 3 months.50 Both the short-
acting and LAR formulations improved both early and
late dumping syndrome symptoms, but the short-acting
formulation alleviated late dumping symptoms better
than the LAR formulation.50 The LAR formulation was
associated with an improvement in quality of life.50
Further study, including large, long-term randomized
controlled trials, is required to evaluate the efficacy of
both short-acting and LAR octreotide in the management
of dumping syndrome. The adverse effects of pain at the

site of injection, gallstone formation, increased diarrhea,
and steatorrhea along with the increased cost of octre-
otide should all be considered before initiating this medi-
cation for dumping syndrome.31
Patients should be advised of the following dietary
modifications, which may alleviate the symptoms associ-
ated with both early and late dumping syndrome. Similar
to the recommendations for gastric stasis, most guidelines
for the dietary management of dumping syndrome are not
validated by controlled trials. Recommendations are
based on the physiology of digestion and on results from
gastric emptying studies. More research evaluating post-
gastrectomy dumping syndrome and diet manipulation
would be beneficial.
Nutrition Interventions for Dumping Syndrome
Eat smaller, more frequent meals. Because gastric empty-
ing is accelerated and the gastric reservoir is smaller, food
passes more quickly from the stomach to the small intes-
tine. Eating smaller meals decreases the likelihood that
large amounts of food will reach the small bowel too
quickly.
Chew all foods thoroughly and eat slowly. With the antrum
removed, the stomach can no longer grind large particles
of food before passing food into the small intestine.
Chewing food into smaller particles can stop the flow of
large, difficult-to-digest particles into the small intestine.
By decreasing the rate of food intake, one can consciously
slow the passage of food to the small bowel, similar to the
unconscious approach that was once managed by the
pylorus.
Limit fluid consumption with meals and wait at least 30
minutes after meals to drink fluid. After vagotomy, diar-
rhea can be increased with liquid meals, and intestinal
motility can be decreased with dry meals.52 Normally, the
gastric fundus creates a pressure gradient that helps con-
trol liquid emptying. Gastrointestinal scintigraphy has
shown that liquids empty more quickly than solids, even
in patients who have not undergone gastrectomy.19
Therefore, in a postsurgical patient, liquid passage to the
small bowel may be accelerated, causing diarrhea.19 Maes
et al53 evaluated the emptying of the liquid, solid, and oil
phases of a meal in 7 Billroth II subjects compared with
10 normal subjects. This small study found that the solid
phase emptied concurrently with the liquid phase in
Billroth II subjects, whereas the solid phase emptied sig-
nificantly later than the liquid phase in normal subjects.53
Limit high-sugar foods and beverages. Simple carbohy-
drates are hydrolyzed into osmotically active substances
more quickly than are proteins and fats.10 Decreasing the
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Postgastrectomy Nutrition / Rogers   131
intake of simple sugars decreases the delivery of hyper-
tonic solutions to the small intestine.
Eat protein at each meal. Decreasing carbohydrate intake
tends to lead to a net loss of overall caloric intake.
Increasing protein can offset this imbalance and help
avoid unintentional weight loss.
Increase intake of fiber. Gastrointestinal scintigraphy has
shown that indigestible residue empties slower than both
liquids and solids.19 Supplemental fibers such as guar
gum, pectin, and glucomannan increase food viscosity
and bind with carbohydrates to both increase transit time
and slow glucose absorption.27,22,54,55
Fat Maldigestion
After partial or total gastrectomy, patients may experience
increased fecal fat excretion. About 10% of these patients
exhibit clinically significant steatorrhea.4,10,56 Symptoms
of fat malabsorption are typically cramping, abdominal
pain, and a greasy, foul-smelling diarrhea.2 Several mech-
anisms have been explored to account for fat maldigestion
after gastrectomy, including decreased gastric lipase, exo-
crine pancreatic insufficiency, pancreatocibal asynchrony,
altered cholecystokinin release, and SBBO.10,56,57 Diagnosis
of steatorrhea involves the ingestion of 100 g of fat per
day for 72 hours with a concurrent analysis of fecal fat
excretion. A quantitative fecal fat ≤ 7 g is expected with
normal fat absorption.10
In a normal stomach, chief cells in the fundus secrete
gastric lipase. Lipase initiates preliminary lipid diges-
tion.1,10 Additionally, with an intact digestive tract, gastric
lipase activity increases to compensate for inadequate
pancreatic lipase, thus ensuring functional lipid diges-
tion.1 Decreased gastric lipase after subtotal or total gas-
trectomy results in fat malabsorption because both
preliminary and compensatory lipid digestion are altered.
Controversy exists regarding exocrine pancreatic insuf-
ficiency and fat malabsorption after gastrectomy. Several
studies report increased fecal fat excretion following
gastrectomy,5,56,58 and additional studies report decreased
exocrine pancreatic function following total gastrec-
tomy.59,60 However, studies are lacking that correlate
decreased exocrine pancreatic function with steatorrhea.
In a small, double-blind, crossover trial with 15 patients,
Armbrecht et al61 demonstrated a statistically significant
improvement in fecal fat excretion following pancreatic
enzyme therapy. However, this improvement was only seen
in patients who originally presented with severe steator-
rhea. A follow-up prospective, double-blind, randomized,
parallel, placebo-controlled, multicenter trial found that
high-dose pancreatic enzyme supplementation did not sig-
nificantly improve fat malabsorption in patients with total
132   Nutrition in Clinical Practice / Vol. 26, No. 2, April 2011
gastrectomy.62 Not entirely consistent with the first study,
all participants in the follow-up study had symptoms that
were mild.62 Another study reported improvement in fecal
fat excretion after adding exogenous pancreatic enzymes
but only in 2 study participants with severe diarrhea.58
Sufficient evidence does not exist linking exogenous pan-
creatic enzymes with a specific patient benefit.63 However,
from these studies a common thread emerges. Participants
with severe diarrhea benefit from exogenous pancreatic
enzymes, but those with minimal diarrhea do not respond
to exogenous pancreatic enzymes. Additional research in
this area would be beneficial to determine the utility of
pancreatic enzyme supplementation in postgastrectomy
patients.
Another complication of gastrectomy is pancreatoci-
bal asynchrony. The rapid transit of food through the
small intestine or the bypass of the duodenum causes
insufficient mixing of food with enzymes, or pancreatoci-
bal asynchrony.56,62 With an intact GI tract, lipids empty
into the small intestine more slowly than other contents.
Fats leave the body of the stomach last because they form
an oily layer that sits atop other gastric contents. Also, as
fat reaches the duodenum, cholecystokinin is released,
significantly decreasing the rate of gastric emptying.1
Maes et al53 compared gastric emptying rates of the liq-
uid, solid, and oil phases of a meal in both normal sub-
jects and subjects with Billroth II gastrojejunostomies.
The investigators found that in normal subjects, the oil
phase emptied much more slowly than the liquid phase,
but in subjects with Billroth II gastrojejunostomies, in the
presence of liquids the oil phase emptied extremely
quickly.53 With high-calorie lipids emptying too quickly,
the pancreatic enzymes released are not given sufficient
time to mix with the lipids, resulting in fat malabsorption.
In patients in whom this is suspected, exogenous pancre-
atic enzymes would be beneficial.56
As previously mentioned, SBBO can result from gas-
tric stasis, but it can also be present in surgical blind
loops.4 Stasis in these areas can lead to infection.56 Fat
malabsorption occurs in patients with SBBO primarily
because excess bacteria in the small bowel deconjugate
bile salts and alter micelle formation.4 If fat maldigestion
is the result of SBBO, deficiency of fat-soluble vitamins
A, D, and E may be present.21 Vitamin K deficiency is rare
in SBBO because enteric microbiota produce some
micronutrients, including vitamin K, biotin, and folate.21
Patients with surgical blind loops who present with steat-
orrhea should be evaluated for SBBO. Diagnosis and
treatment of SBBO was discussed in the section address-
ing gastric stasis.
Nutrition Interventions for Fat Maldigestion
After confirming steatorrhea with a quantitative fecal fat
test and ensuring that SBBO is not to blame for fat mal-
absorption, the following interventions may be initiated.
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Monitor and replace fat-soluble vitamins, A, D, E, and K as
needed
Concurrently, initiate a trial of exogenous pancreatic
enzymes. Start with 500 units of lipase per kg of body
weight with each meal and titrate up to desired effect.
Typically, half the dosage given with meals should be
taken with snacks.
If steatorrhea continues, initiate a low-fat diet with
medium-chain triglyceride (MCT) oil. When all possible
causes of fat malabsorption have been addressed and the
use of exogenous pancreatic enzymes has failed, this can
be used as a last resort. The increased cost and decreased
palatability of MCT oil may result in patient noncompli-
ance.3 MCT oil contains 8.3 kcal/g, so that 15 mL, or 1
tablespoon, provides 115 kcal.64 Too much MCT oil may
increase GI distress; therefore, doses of 4-5 tablespoons,
administered throughout the day, are recommended.64 If
a patient’s only fat source is MCT oil, essential fatty acid
deficiency (EFAD) can develop. Providing 2%-4% of the
patient’s total caloric intake via linoleic acid will deter
EFAD.64 For example, on a 2,000-kcal diet, 40-80 kcal of
linoleic acid should be recommended.64 Examples of oils
containing linoleic acid include safflower oil, sunflower
oil, and corn oil.64
Nutrient Deficiencies
Anemia
Anemia arises after partial or total gastrectomy due to
vitamin B12, folate, and/or iron deficiencies. These defi-
ciencies can result from both inadequate intake and mal-
absorption. It is essential to continually monitor for
anemia as it can present several years after gastrectomy.
Two components necessary for vitamin B12 absorption
are lost with the removal of part or all of the stomach: gas-
tric acid and intrinsic factor. Gastric acid cleaves B12 from
protein whereas intrinsic factor forms a necessary complex
with B12 before its absorption in the terminal ileum.65 In
some cases, the duodenum and jejunum begin to produce
intrinsic factor, but supplementation of B12 may still be
necessary.66 Vitamin B12 deficiency also occurs in the pres-
ence of SBBO. It is postulated that bacterial use of B12
results in an insufficient amount of B12 available for
absorption. Another theory suggests that bacteria produce
a toxin that inhibits the transfer of B12 across the small
bowel mucosa.56 Traditionally, vitamin B12 deficiency is
treated with intramuscular injections. However, Adachi
et al66 compared oral and intramuscular administration of
supplemental B12 and found that enteral administration
rapidly increased serum B12 concentration. The decision
whether to supplement via oral or intramuscular route

should be based on patient comfort and compliance.
Parenteral B12 supplementation begins with 1,000 mcg
every day for 1 week, followed by 1,000 mcg every week for
4 weeks. To maintain normal B12 levels, monthly 1,000
mcg injections may be required for life. Oral B12 supple-
mentation requires 1,000-2,000 mcg daily.67
Little information exists regarding folate deficiency
after partial or total gastrectomy. Although folate is
absorbed in the proximal small bowel and rapid transit
through this area is possible after gastrectomy, folate defi-
ciency due to malabsorption has not been documented. If
suspected, folate deficiency should be diagnosed with red
blood cell folate, not serum folate.4 To correct folate defi-
ciency, 5 mg of folate should be given daily.4 Vitamin B12
is needed to activate folate, so supplementing folate
with a concurrent B12 deficit will only exacerbate the B12
deficiency.68
Tovey et al5 found that 10 years after gastrectomy,
iron deficiency was the most common nutrient deficiency.
Iron deficiency usually occurs 10 years before the onset
of B12 deficiency.5 Most iron absorption occurs along the
duodenal and upper jejunum mucosa.69 After gastrec-
tomy, bypass of the duodenum and/or rapid transit of food
particles through the intestine can lead to iron defi-
ciency.65 Additionally, gastric acid aids the conversion of
ferric ions to ferrous ions, which are more easily
absorbed.69 The decreased acid production following gas-
trectomy impedes this process. Serum ferritin, a storage
protein for iron, will accurately reflect iron stores in a
nonacute phase setting.3,70 Iron deficiency is best treated
with 200 mg of oral elemental iron daily. A 200-mg tablet
of ferrous sulfate provides 67 mg of elemental iron.
Therefore, it should be given 3 times per day, 6 hours
apart, and with the addition of vitamin C to enhance
absorption.3,68 One case report revealed villi flattening on
jejunal biopsies in a patient with anemia unresponsive to
oral iron therapy. After the administration of parental iron
over 4 weeks, the villous atrophy resolved and the
patient’s anemia continued to improve with the use of
oral iron supplementation.69
Patient compliance is often an issue with iron therapy
because of side effects including nausea, abdominal pain,
constipation, or diarrhea.3 Consequently, frequent
encouragement to increase intake of iron-rich foods may
be necessary. The heme form of iron is more available
than the nonheme form of iron. Absorption of nonheme
iron is enhanced by ascorbic acid (vitamin C) and amino
acids and inhibited by phosphates, phytates, oxalates, and
tannates.69 Heme and nonheme iron are found in meat,
fish, and poultry. However, only nonheme iron exists in
eggs, grains, vegetables, and fruits.71
Bone Disease
The incidence and cause of bone disease after subtotal or
total gastrectomy are not clear. Zittel et al72 reported
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Postgastrectomy Nutrition / Rogers   133
osteopenia in 44% of Billroth I patients, 27% of Billroth
II patients, and 44% of total gastrectomy patients. Bisballe
et al73 found that 18% of postgastrectomy patients had
osteomalacia. However, when Liedman et al74 compared
total gastrectomy patients with age- and sex-matched
controls, they could not demonstrate any divergence.
Even though 25% of the total gastrectomy patients had
osteoporosis approximately 8 years after surgery, the
results indicate that this is more likely due to aging rather
than a consequence of postsurgical sequelae.74
Although the cause of bone disease following gastrec-
tomy is also unclear, several mechanisms have been sug-
gested. Decreased dietary intake of calcium and vitamin
D may play a role.3,10 Malabsorption of calcium may also
be a factor because calcium is primarily absorbed in the
duodenum, which may be bypassed because of surgical
reconstruction or rapid transit.75 Additionally, fat malab-
sorption may lead to the formation of insoluble calcium
soaps.75 Alterations in bone-related hormones may lead to
bone disease although serum parathyroid hormone levels
in postgastrectomy patients have ranged from subnormal
to normal.75 Malabsorption of vitamin D has been dis-
cussed as a possible mechanism, but neither calcium nor
vitamin D malabsorption has been proven in postgastrec-
tomy patients.75 In fact, when Bisballe et al73 found osteo-
malacia in 18% of postgastrectomy patients, the majority
if the patients had normal serum calcium and 25-hydrox-
yvitamin D levels (25-OHD).3
Despite the contradictions regarding incidence and
cause of bone disease post gastrectomy, monitoring bone
mineral density via dual-emission X-ray absorptiometry scans
and ensuring that postgastrectomy patients consume ade-
quate amounts of calcium rich foods is beneficial. This is
especially true given that the majority of these surgical
patients are elderly. For patients with confirmed bone dis-
ease, 1,500 mg of calcium daily is recommended.3 Additionally,
as more information emerges regarding suboptimal 25-OHD
levels in the healthy population, monitoring serum 25-OHD
post gastrectomy seems reasonable. The current guidelines
from the Institute of Medicine recommend a 25-OHD level
of 20 ng/mL to maintain good bone health.76 For men and
women under the age of 51, 600 international units of vita-
min D daily should be sufficient to meet this goal.76 For those
over the age of 71, 800 international units of vitamin D daily
is recommended.76 The Institute of Medicine cautions that
the risk for harm increases in doses of vitamin D beyond
4,000 international units daily.76
Implications for Clinical Practice
Most studies analyzing patients post gastrectomy, including
those cited in this review, have a small sample size, and
few involve randomized controlled trials.* Additionally,
*5, 9, 16, 53, 62, 66, 74, 77, 78
134   Nutrition in Clinical Practice / Vol. 26, No. 2, April 2011
most recent studies that evaluate postgastrectomy out-
comes compare different surgical procedures, not different
diet approaches.11,79-81 To my knowledge, no study has com-
pared weight loss, GI symptoms, or nutrient deficiencies in
patients on a specific postgastrectomy diet versus a regular
diet. Before a standard postgastrectomy diet can be pro-
posed, more research comparing the effects of a regular
diet versus a postgastrectomy diet is needed.
In general, diet restrictions can increase weight loss and
even make weight gain difficult. As clinicians, we must
acknowledge our limitations regarding postsurgical weight
gain. Copland et al77 had a registered dietitian follow post-
gastrectomy patients for 1 year, during which time the
patients did not realize significant weight gain. Patients had
difficulty increasing energy intake because they were follow-
ing earlier diet restrictions. Furthermore, the patients stated
that multiple diet manipulations proved burdensome.77
Given that weight loss, especially in the first 3 months after
surgery, is a well-documented outcome following partial or
total gastrectomy, it seems advantageous to avoid nutrition
advice that may accelerate this process.5-9
Overall, there is limited evidence supporting a stand-
ard postgastrectomy diet, short-term or long-term. Diet
manipulation should be individualized for symptom relief.
Food restrictions should be minimal to avoid an unneces-
sary calorie deficit. Nutrient deficiencies should be mon-
itored and supplemented accordingly, but excess vitamin
and mineral recommendations beyond those of a stand-
ard multivitamin are not required for all postgastrectomy
patients. Regular follow-up with a registered dietitian,
especially during the first year after surgery, would be
advantageous. However, clinicians must recognize that
too many recommendations may be burdensome to the
patient. As GI symptoms change or improve, appropriate
diet modifications should be suggested and evaluated for
effectiveness. This could avoid unnecessary diet restric-
tion, which may exacerbate nutrient deficiencies, weight
loss, and overall frustration.
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