Nutrition Diagnosis Nutrition diagnoses com-

Figure 14.8 Hiatal Hernia

mon for achalasia would also be similar to dysphagia

and may include diculty swallowing; inadequate oral
food/beverage intake; and involuntary weight loss.

Gastroesophageal
junction

Nutrition Intervention Prior to treatment, patients with achalasia will need to have texture-modied
diets with increased caloric and protein density. Foods
that are extreme in temperature or very spicy should
also be avoided in order to prevent damage to esophageal mucosa. Smaller, more frequent feedings will be
tolerated best. After myotomy or dilatation, patients
should receive a texture-modied diet such as the
NDD-3 outlined in Table 14.11. A regular diet can be
resumed within 5 to 7 days of the procedure.

Pleura
Peritoneum
Peritoneal sac
Diaphragm

Hiatal Hernia
A - type 1 (sliding)
B - type 2 (rolling)
Hiatal hernia is a condition where the upper portion of the stomach protrudes through the esophageal
Reprinted from Price and Wilson: Pathophysiology: Clinical Concepts of Disease Processes, 6e
hiatus into the thoracic cavity. Most cases of hiatal
2006 Mosby with permission from Elsevier.
hernia are designated as type 1 (sliding) where both the
LES and some portion of the upper stomach protrude
considered together because they are controlled through the
through the esophageal hiatus or diaphragm into the chest (see
same neural pathways. Neural signals are sent to the vomiting
Figure 14.8). In type 2 (rolling hiatal hernia) the LES remains
center located in the medulla. As a result of these stimuli, the
below the diaphragm. Incidence of hiatal hernia increases with
steps of vomiting or emesis occur. In this sequence of events,
age. Any factor that increases intra-abdominal pressure, such
gastric contents are pushed upward by the constriction of the
as obesity or pregnancy, will also increase the risk of hiatal
respiratory muscles, the esophageal sphincter opens, the glottis
hernia.
closes (to prevent aspiration), and gastric contents are expelled
Symptoms of hiatal hernia are consistent with those of GERD.
through the mouth. Additionally, chemoreceptor zones in the
First-line interventions, both medically and nutritionally, are
medullary nucleus can also trigger the vomiting center. Drugs,
the same as those previously discussed for GERD. Some patoxins, metabolic conditions (such as renal failure or acid-base
tients do require surgical repair of the hernia. In this procedure,
imbalances), and motion aect chemoreceptor zones, which
which may be performed conventionally or laparoscopically,
can lead to nausea and emesis. Vomiting may also occur as a
the surgeon retracts the hernia and repairs the hole in the diaresult of stress or extreme emotions.
phragm. Fundoplication (previously described in the section on
Nausea and vomiting occur with many dierent medical condiGERD) can also be done at this time, if needed. The combinations. These may include infection, pain, pregnancy, syncope,
tion of surgical repair with fundoplication provides additional
headache, metabolic disorders, motion sickness, kidney failure,
support of the LES, which prevents the stomach from sliding
myocardial infarction, and a host of other possibilities. Thereback through the diaphragm.6, 31
fore, treatment of the underlying cause is the most important
step in treating nausea and vomiting. The patients history and
physical examination will assist in determining the cause of
nausea and vomiting. The etiology may be further claried after
Disease and clinical disorders that aect the stomach can cerassessment of the symptoms the patient experiences prior to
tainly inuence normal nutritional status. Some disorders, such
and after vomiting. For example, if vomiting occurs within a
as indigestion, are mild and temporary conditions that resolve
very short time after eating, it may be indicative of an obstruceasily. Others, such as peptic ulcer disease, are chronic and
tion.
Abdominal pain is symptomatic of an inammatory prorequire aggressive medical intervention.
cess. Simple regurgitation of food occurs when gastric contents
move easily from stomach to the mouth and is not a forceful
Indigestion
expulsion like that seen in vomiting.
Indigestion, or dyspepsia, is not considered to be a specic
After determining the etiology of nausea and vomiting, the
condition. Most people use the term indigestion to refer to
next step for treatment is use of medications or antiemeta wide range of symptoms that may include abdominal pain,
ics. Table 14.13 provides a summary of antiemetics used to
abdominal fullness, gas, bloating, belching, nausea, or even
treat nausea and vomiting. Medication action may decrease
gastroesophageal reux.
the sensitivity of the chemoreceptor trigger zones. In many
situations, such as in the use of chemotherapy, antiemetics
Nausea and Vomiting
are prescribed at the onset of treatment to prevent nausea.
Nausea is the unpleasant sensation that there is a need to
Controlling nausea from the very beginning of treatment
vomit; vomiting is the expulsion of gastric contents. Even
prevents anticipatory nausea and/or vomiting, which can octhough nausea does not always lead to vomiting, they are often
cur when there is a direct association between the nausea and

Pathophysiology of the Stomach

Chapter 14

Diseases of the Upper Gastrointestinal Tract

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359

Table 14.13 Antiemetic Agents Used in the Treatment of Nausea and/or Vomiting
Generic and/or Trade Name
H1 antihistamines

Dimenhydrinate (Dramamine )
Diphenhydramine (Benadryl)
Hydroxyzine (Atarax)

Uses/Mechanism
Work by blocking histaminemay treat mild nausea such as motion
sickness; also provide benefit of mild relaxation. Not effective for severe
nausea and vomiting.

Benzamides

Metoclopramide (Reglan)

This medication blocks dopamine and therefore affects the vomiting center
in the brain. Side benefit of increasing gastric emptying.

Benzodiazepines

Diazepam (Valium)

Primarily used as tranquilizers, but can also increase the effectiveness of

other antiemetics.

Lorazepam (Ativan)
Butyrophenones

Droperidol (Inapsine)

This medication blocks dopamine and therefore affects the vomiting center
in the brain.

Phenothiazines

Prochlorperazine (Compazine)

This medication blocks dopamine and therefore affects the vomiting center
in the brain.

Corticosteroids

Dexamethasone
Methylprednisolone

Reduces the effect of prostaglandins and can also improve the effectiveness
of other antiemetics.

Dronabinol (Marinol)

Mechanism unclear but produces feelings of euphoria and antiemetic effect.

Cannabinoids

NK1-receptor antagonists

Aprepitant (Emend )

Blocks Substance P in the brain, which appears to have direct affect on

vomiting center.

5-HT3 receptor antagonists/

serotonin antagonists

Ondansetron (Zofran)

Blocks serotoninusually given in combination with dexamethasone.

Tropisetron (Navoban)
Granisetron (Kytril)
Dolasetron (Anzemet)

vomiting and a specic event, food, or smell. For instance, an

individual who has gotten sick after eating a specic food may
experience similar symptoms when faced with that food again,
because it continues to remind the person of how sick he/
she was previously. Complementary and alternative medicine
(CAM) may provide some additional avenues for controlling
and treating symptoms experienced with nausea as well as
other symptoms experienced with diagnoses involving the
upper gastrointestinal tract (see Appendix F.1). These may
include the use of ginger and peppermint oil in treatment of
nausea. Acupuncture, yoga, meditation, and guided imagery have also been successfully used to assist with control of
nausea.6668
Prolonged nausea and vomiting can have signicant clinical consequences. Forceful vomiting can either rupture the
esophagus (Boerhaaves syndrome) or tear the lower esophageal
sphincter (Mallory-Weiss tear). Bleeding or hematemesis is a
serious outcome of these injuries. Continued vomiting also can
result in dehydration and acid-base imbalances. Malnutrition
can be a long-term consequence for the patient if he or she is
not able to ingest an
adequate diet for a
prolonged amount
Sample PES statement: Inadequate oral
food/beverage intake related to nausea
of time. If gastric
and vomiting as evidenced by <300 kcal
contents are aspirated
ingestion for previous 48 hours reported
into the lungs, aspiraby patient and nursing records.
tion pneumonia is a
likely result.

Nutrition Therapy for Nausea and Vomiting

Nutritional Implications Nausea and vomiting can
result in inadequate nutrient intake, dehydration, and acid-base
imbalances, and over time can lead to learned food aversions.
This is similar to anticipatory nausea and vomiting. When
360

a negative consequence is linked to a particular food, most

people choose to avoid eating that food.

Nutrition Diagnosis Nutrition diagnoses secondary to

nausea and vomiting may include altered GI function; involuntary weight loss; inadequate uid intake; and inadequate food/
beverage oral intake.
Nutrition Intervention Nutrition therapy does not necessarily treat nausea and vomiting but can minimize symptoms and
discomfort. Appropriate nutrition therapy can assist in maintaining nutritional status during periods of nausea and vomiting. If
patients can manage oral intake, foods that are cold and have
minimal smell usually are best tolerated. Table 14.14 outlines
suggestions for foods and food-related activities that may reduce
nausea and vomiting. Close monitoring of hydration status and
length of time that the patient is without adequate oral intake
will be crucial in preventing long-term nutritional consequences.
Nutritional support will be necessary for those individuals who
are unable to meet their nutritional needs orally.

Gastritis
Gastritis is inammation of the gastric mucosa. This condition is not a single disorder and may be a result of numerous
conditions. Under normal conditions, the gastric mucosa is
protected against injury. The production of mucus provides a
barrier that prevents damage to the cells, and their high turnover rate allows for ecient recovery from injury. Prostaglandins also assist in support of the mucosal defense by stimulating
mucus production, inhibiting acid production and release,
and regulating blood ow to the mucosal cells. Acute gastritis
is due to local irritation of the gastric mucosa. This irritation
can result from infections, such as with Helicobacter pylori
(H. pylori), food poisoning, alcohol ingestion, or medications
such as nonsteroidal anti-inammatory drugs (NSAIDs). By

Part 4 Nutrition Therapy

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Table 14.14 Nutrition Interventions to Reduce

Nausea and Vomiting

1. Liquids
q
to try
y after vomiting
g has stopped
pp
Water
Apple juice
Sports drink
Warm or cold tea
Lemonade
Instructions
First suck on ice chips if over 3 years of age. If tolerated, start with
1 teaspoon (5 g) every 10 minutes. Increase to 1 tablespoon (15 g)
every 20 minutes. Double the amount of fluid every hour. Progress to
the other liquids as tolerated. If diarrhea is present, use only rehydration
beverage.
2. Solid Food Introduction

Peptic Ulcer Disease

When there has been no vomiting for at least eight hours, start
oral intake slowly by adding one solid food at a time in very small
increments. Avoid food that high in fat or fiber as well as food that has a
strong odor or is gas producing. The use of ginger to treat nausea and
vomiting may help. Take medications after eating.

Source: Atlas of Gastrointestinal Endoscopy www.EndoAtlas.com

Foods Recommended for Initial Introduction of Solid Food

Grains

Dry toast, crackers, pretzels, rice or rice

cereal, potato

Milk and Dairy Products

Yogurt, sherbet

Meat, Poultry, and Fish

Clear broths, baked chicken, eggs

blocking prostaglandin release, NSAIDs assist in control of

inammation but may also inhibit their protective function for
the gastric mucosa. Generally, gastritis caused by NSAIDs is
short lived and causes no long-term problems. Symptoms of
gastritis can include belching, anorexia, abdominal pain, vomiting, and, in the more severe cases, bleeding and hematemesis.
Chronic gastritis is usually classied by either the etiology or
the region of the stomach involved. Type A chronic gastritis
involves the fundus and is associated with an autoimmune process, which results in the formation of antibodies against the
parietal cells. Type A chronic gastritis also occurs with pernicious anemia. Type B chronic gastritis results in atrophy of the
gastric mucosa and is most frequently associated with infection from H. pylori.31 Incidence of chronic gastritis increases
with age and is often seen with achlorhydria. Achlorhydria is
associated with nutritional implications including B12, iron, and
calcium malabsorption.54, 55, 69, 70 Treatment for gastritis includes
identifying and treating the cause of the gastritis; for example,
an antibiotic and medication regimen may be used to treat
infections caused by H. pylori that are responsible for gastritis.

Peptic Ulcer Disease

Peptic ulcer disease (PUD) involves ulcerations of the gastric
or duodenal mucosa that penetrate the submucosa. They
usually occur in the antrum of the stomach or in the rst few
centimeters of the duodenum. Erosion may proceed to other
levels of tissue and can eventually perforate. Breakdown in the
tissue allows for continued insult by the highly acidic environment of the stomach as well as damage from other secretions of
the stomach, such as pepsin.
Peptic ulcer disease has been redened over the last decade
because H. pylori is now recognized as a pivotal factor in devel-

opment of gastric and duodenal ulcers. It is estimated that 92%

of duodenal ulcers and 70% of gastric ulcers are caused by
H. pylori. Recent research indicates that there is also an increased risk of gastric cancer associated with H. pylori infection.71, 72 Nonetheless, even with this progress in research on
PUD, there are still quite a large number of individuals who suffer from ulcer disease and are not infected with H. pylori. This
section will describe the role of H. pylori and other factors that
have been correlated to the development of PUD (see Box 14.5.)
Helicobacter pylori is a spiral-shaped, agellated, Gramnegative rod that lives under the mucous layer of the stomach
and attaches to mucus-secreting cells lining the stomach. These
organisms break down urea to produce ammonia, which helps
neutralize acid in the immediate vicinity of these bacteria and
enhances their survival. The H. pylori organisms subsequently
produce various proteins that damage mucosal cells, attracting
lymphocytes and causing persistent inammation.7173 Byproducts released by the organism result in damage to the epithelium and impair the mucous barrier within the stomach.
The etiology of PUD also involves factors that may decrease
mucosal integrity, such as a reduction of protective prostaglandins through the use of NSAIDs (e.g., ibuprofen) or alcohol, excessive glucocorticoid secretion or steroid medication, and factors that decrease the blood supply, such as smoking, stress, or
shock. Factors that increase acid secretions, including certain
foods, rapid gastric emptying, or increased gastrin secretions,
also contribute to the development of PUD. The genetic link
to PUD has also been explored; ulcers are approximately three
times more common in rst-degree relatives than in the general
population. This may be related to an increased susceptibility to
infection from H. pylori.74
The most common symptom related to PUD is epigastric
pain, but this pattern is not consistent. In general, patients will
complain of abdominal pain and a burning sensation, which may
be precipitated by certain types of foods or accentuated by food
intake. For others, epigastric pain may be relieved by food intake
due to its ability to dilute any irritants. For a duodenal ulcer,
pain characteristically occurs from 90 minutes to 3 hours after
eating, and is usually relieved within minutes either by eating
or by use of antacids. Unfortunately, partial neutralization of
gastric acid is followed by a rebound of gastrin release, causing
additional stimulation of HCl and probably more pain.75, 76
Chapter 14

Diseases of the Upper Gastrointestinal Tract

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361

BOX 14.5 Historical Perspectives

History of Ulcer Diagnosis and Treatment

The road to a cure for ulcers has been a long and bumpy
one. Research over the previous decade that indicates that
ulcers are caused by a bacterium and can be cured with
antibiotics has changed traditional thinking.

Early Twentieth Century

Ulcers are believed to be caused by stress and dietary
factors. Treatment focuses on hospitalization, bed rest,
and prescription of special bland foods. Later, gastric acid
is blamed for ulcer disease. Antacids and medications that
block acid production become the standard of therapy. Despite this treatment, there is a high recurrence of ulcers.

1982
Australian physicians Robin Warren and Barry Marshall rst
identify the link between Helicobacter pylorii (H. pylori) and
ulcers, concluding that the bacterium, not stress or diet,
causes ulcers. The medical community is slow to accept
their ndings.

1994
A National Institutes of Health Consensus Development
Conference concludes that there is a strong association
between H. pylorii and ulcer disease and recommends that
ulcer patients with H. pylorii infection be treated with antibiotics.

1995
Data show that about 75% of ulcer patients are still treated
primarily with antisecretory medications, and only 5% receive antibiotic therapy. Consumer research by the American Digestive Health Foundation nds that nearly 90% of
ulcer sufferers are unaware that H. pylorii causes ulcers. In
fact, nearly 90% of those with ulcers blame their ulcers on
stress or worry, and 60% point to diet.

The presence of blood in stool or vomit may be indicative

of active bleeding from the ulcer. Changes in hematological
indices such as hemoglobin or hematocrit will also be indicative of active bleeding. If there is an active infection, changes in
white blood cell count will be consistent with the inammatory
process.
The same diagnostic procedures that have been discussed earlier in this chapter will allow for a denitive diagnosis. Endoscopy coupled with a tissue biopsy will allow for visualization of
the ulcer and conrmation of H. pylori infection. Less invasive
testing for H. pylori includes the urea breath test, stool antigen
test, and serum testing for antibodies. At present, the most accurate and reliable test for both diagnosis and follow-up is the
urea breath test.71, 73
Treatment of peptic ulcer disease associated with H. pylori
infections includes regimens of three to four medications
362

1996
The Food and Drug Administration approves the rst antibiotic for treatment of ulcer disease.

1997
The Centers for Disease Control and Prevention (CDC), with
other government agencies, academic institutions, and industry, launches a national education campaign to inform health
care providers and consumers about the link between H. pylorii and ulcers. This campaign reinforces the news that ulcers
are a curable infection and the fact that health can be greatly
improved and money saved by disseminating information
about H. pylori. Medical researchers sequence the H. pylori
genome. This discovery can help scientists better understand
the bacterium and design more effective drugs to ght it.

2005
Nobel Prize for physiology or medicine awarded to Drs.
Barry J. Marshall and Robin Warren for proving that bacteria and not stress was the main cause of painful ulcers of
the stomach and intestine.
Sources:
Centers for Disease Control and Prevention [homepage on the Internet].
Atlanta: Centers for Disease Control and Prevention; 2001 Feb 2. History
of Ulcer Disease and Treatment. Available at http://www.cdc.gov/ulcer/
history.htm
Helicobacter pylori in Peptic Ulcer Disease, National Institutes of Health
Consensus Development Panel on Helicobacter pylori in Peptic Ulcer Disease, Journal of the American Medical Association. 1994 July 6;272(1):
6569. Source: Centers for Disease Control and Prevention [homepage on
the Internet]. Atlanta: Centers for Disease Control and Prevention; 2001
Feb 2. History of Ulcer Disease and Treatment. Available at http://www.cdc
.gov/ulcer/history.htm
Marshall BJ, ed. Helicobacter pioneers: rsthand accounts from the
scientists who discovered helicobacters, 18921982. Victoria, Australia:
Blackwell; 2002.
Munnangi S., Sonnenberg A. Time trends of physician visits and treatment
patterns of peptic ulcer disease in the United States. Arch Intern Med. 1997
July 14;175:148994.
Parsonnet J Clinician-discoverersMarshall, Warren, and H. pylori. N Engl
J Med. 2005 Dec 8;353(23):242123.

(triple/quadruple therapy). The recommended therapy involves a 7- to 14-day course of two antibiotics with bismuth
and one of the proton pump inhibitors.71, 73, 77, 78 Eradication
rates associated with triple/quadruple therapy range from
86% to 98% if patients comply with triple/quadruple therapy
treatment regimens (see Table 14.15). However, frequently
occurring adverse eects such as nausea, vomiting, and
abdominal pain associated with these regimens signicantly
hinder patient compliance and most often the 7-day treatment is recommended.71, 73, 7779
Other treatment for PUD focuses on use of medications to
suppress acid secretion, which will ultimately promote healing of the ulceration (see Table 14.16). These medications,
as discussed in the section on treatment for GERD, include
antacids, proton pump inhibitors, histamine blocking agents,
prokinetic agents, and mucosal protectants. Because salicylates (aspirin) and NSAIDs are linked to increased gastric

Part 4 Nutrition Therapy

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Table 14.15 FDA-Approved Treatment Options

for Eradication of H. pylori Infection
Omeprazole
p
20 mg
g bid clarithromycin
y
500 mg
g bid amoxicillin 1 g
bid 714 days
OR
Omeprazole 20 mg bid clarithromycin 500 mg bid Metronidazole
(500 mg bid) 714 days
OR
Omeprazole 20 mg bid bismuth subsalicylate (2 tabs qid)
tetracycline HCL (500 mg qid) Metronidazole (500 mg bid) 714
days
Sources: Malfertheiner P, Megraud F, OMorain C, et al. Current concepts in the
management of Helicobacter pylori infection: the Maastricht III Consensus
Report. Gut 2007;56:77281.
Atherton John C, Blaser Martin J, Chapter 144. Helicobacter pylori Infections
(Chapter). Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL,
Loscalzo J: Harrisons Principles of Internal Medicine, 17th ed. Available at http://
www.accessmedicine.com/content.aspx?aID2894613

Table 14.16 Drugs Used in Treatment

of Peptic Ulcer Disease
Antibiotics

Metronidazole; tetracycline;
y
clarithromycin;
y
amoxicillin

Antacids

Mylanta, Maalox; Tums; Gaviscon

H2 blockers

Cimetidine; ranitidine; famotidine;

nizatidine

Proton pump inhibitors

Lansoprazole; rabeprazole; esomeprazole;

omeprazole; pantoprozole

Cytoprotective agents

Sucralfate; prostaglandin analogue

(Misoprostol); bismuth subsalicylate

irritation, these medications should not be taken by someone

with PUD.
For those patients who are refractory to treatment or who
suer from complications such as hemorrhage, perforation, or
gastric outlet obstruction, surgical resection may be necessary
(this will be discussed later in this chapter).

Nutrition Therapy for Peptic Ulcer Disease

Nutritional Implications and Assessment For patients with PUD, symptomatic abdominal pain can impair oral
intake and result in weight loss and/or nutrient imbalances.
Therefore it is important to obtain as much information as possible regarding weight and dietary intake changes and to evaluate this data in the context of the medical history of abdominal
pain and symptoms.

Nutrition Diagnosis Nutrition diagnoses associated with

peptic ulcer disease include inadequate oral/food beverage intake; altered GI function; involuntary weight loss; and food and
nutrition-related knowledge decit.
Nutrition Intervention For several decades, dietary factors have gained and lost favor as a signicant component in
both the cause and treatment of peptic ulcers. Currently, goals
for nutrition therapy include supporting medical treatment,
maintaining or improving nutritional status, and providing a
diet that minimizes symptoms of PUD. There are no data indicating that diet is a causative factor for PUD.73
Current nutrition therapy for PUD (see Table 14.17) recommends a trial of restricting foods that may increase acid
secretion or cause direct irritation to gastric mucosa. These
foods include black and red pepper, caeine, coee (including
decaeinated), and alcohol. Additionally, it is recommended
that patients avoid any foods they do not individually tolerate.
Historically, milk and cream were used to treat PUD, but it is
now known that their consumption increases both gastrin and
pepsin secretion. Furthermore, pH of a food prior to its consumption has little eect after it is consumed. Restricting acidic
juices or other foods is not consistently warranted unless the
patient identies intolerance to them.34, 4244, 55
Other components of NT will include timing and size of meals.
Patients should not lie down after eating and avoid eating large
meals close to bedtime.80 Smaller, more frequent meals may be
better tolerated.
Micronutrients of concern may include iron, calcium, and
B12, as previously discussed in this chapter. The need for

Table 14.17 Nutrition Therapy for Peptic Ulcer

Food Groups

Foods Recommended

Food Not Recommended if Symptomatic

Beverages

Non-cola carbonated beverages, Postum, herbal teas

Cola, coffee, tea, cocoa, alcohol

Milk and milk products

Skim, 1%, buttermilk, low-fat yogurt

2% or whole milk, cream, high-fat yogurt, chocolate milk

Eggs

Poached, hard-cooked, or scrambled using low-fat

cooking methods

Fried or scrambled using high-fat cooking methods

Cereals

All ready-to-eat or cooked

None

Meats and Protein Sources

Baked, roasted, broiled, grilled, stewed; trimmed of visible

fat; beef, veal, Iamb, pork, poultry, fish, low-fat cottage
cheese, low-fat cheese, peanut butter

Fried meats, bacon, sausage, pepperoni, salami, bologna,

frankfurters/hot dogs

Potatoes/Rice/Pasta

All except fried

None except fried

Vegetables

All

Only individual intolerance

Fruits

All

Only individual intolerance

Fat

As tolerated consistent with current dietary guidelines

As tolerated consistent with current dietary guidelines

Dessert

All except those considered high fat or those fried such as

pastries, doughnuts

Those considered high fat or those fried such as pastries,

doughnuts

Miscellaneous

All except pepper

Pepper
Chapter 14 Diseases of the Upper Gastrointestinal Tract

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363

additional supplementation should be evaluated for each client individually.

cells, resulting in decreased acid production and a decreased

response to gastrin. Other functions of the vagus nerve remain
intact, and the normal pathway for gastric emptying and
peristalsis continues. In many patients, total vagotomy with pyloroplasty is chosen. In this procedure, innervations to parietal
cells are severed, and the portion of the vagus nerve controlling
gastric emptying is also eliminated. Pyloroplasty enlarges the
pyloric sphincter. Gastric resection is also an option depending
on location of the ulcer and extent of the stomach that requires
removal. Reconstruction after pyloroplasty or gastric resection
will generally use one of three procedures: a gastroduodenostomy (Billroth I), gastrojejunostomy (Billroth II), or Roux-en-Y
procedure (see Figure 14.9).

Monitoring and Evaluation Follow-up for the patient

with PUD will focus on adequacy of the patients nutritional
intake and tolerance to the oral diet. Normal nutrition assessment indices will be monitored to ensure maintenance of
nutritional status.

Gastric Surgery
When peptic ulcer disease does not respond adequately to
medical treatment, or when the patient experiences a complication of PUD, surgery is often the next step. Complications
from PUD may include hemorrhage, perforation, or obstruction of the pyloric sphincter. These surgical procedures
are based on the patients current medical status and prior
surgical history. The same procedures are used for surgical resections required for other diagnoses such as gastric
malignancy.

Gastroduodenostomy (Billroth I); Gastrojejunostomy (Billroth II); Roux-en-Y Procedure Figure 14.9
illustrates these types of surgery. In the procedure gastroduodenostomy, or Billroth I, a partial gastrectomyy or pyloroplasty
is performed with a reconstruction that consists of an anastomosis of the proximal end of the duodenum to the distal end
of the stomach. A gastrojejunostomy, or Billroth II, is a partial
gastrectomy with a reconstruction that consists of an anastomosis of the proximal end of the jejunum to the distal end

Vagotomy The purpose of the vagotomy is to eliminate the

cholinergic stimulation of the stomach. Selective vagotomy
eliminates innervations from the vagus nerve to parietal

Figure 14.9 Gastric Surgeries

(a) Roux-en-Y gastric bypass; (b) Billroth I; (c) Billroth II
Billroth I (after)

Liver

Top half of the

stomach is reconnected
to the duodenum

Surgical
staples

Esophagus
Small stomach
pouch

Gallbladder

Duodenum
Stomach
(b)

Jejunum

This operation removes part of the stomach

Billroth II (after)

Large intestine

Liver

In gastric bypass, the surgeon constructs a

small stomach pouch and creates an outlet
directly to the jejunum.
(a)
Gallbladder

Top half of the

stomach is
reconnected
to the small bowel

Sewn up
end of
duodenum
(c)

This operation removes part of the stomach

Sources: (a) John E. Pandolno, Brintha Krishnamoorthy, Thomas J. Lee. Gastrointestinal Complications of Obesity Surgery, Medscape General Medicine 6(2), 2004.
http://www.medscape.com/viewarticle/471952; (b, c) Diagrams reproduced with permission from CancerHelp UK, a free information service about cancer and cancer care
for people with cancer and their families. It is brought to you by Cancer Research UK. www.cancerhelp.org.uk

364

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