En bloc resection is required to evaluate margins for confirma-
tion of complete resection. The development of endoscopic
submucosal dissection (ESD) allows en bloc resection of larger
tumors. This has increased the feasibility of endoscopic resec-
tion of larger lesions (<3 cm) at experienced centers. If patho-
logic evaluation of the resected specimen does not demonstrate
ulceration, penetration of the muscularis mucosae, or lymphatic
invasion, the risk of lymph node metastases is less than 1%.
Even the occasional patient with higher risk stigmata may be
managed endoscopically, particularly in the presence of comor-
bidities that preclude safe operation.
Screening for Gastric Cancer. In Japan, it clearly has been
shown that patients participating in gastric cancer screening pro-
grams have a significantly decreased risk of dying from gastric
cancer. Thus, screening is effective in a high-risk population.
Screening the general population in the United States (a low-
risk country) is probably not justified, but patients clearly at
risk for gastric cancer probably should have periodic endoscopy
and biopsy. This includes patients with familial adenomatous
polyposis, hereditary nonpolyposis colorectal cancer, gastric
adenomas, Ménétrier’s disease, intestinal metaplasia or dyspla-
sia, and remote gastrectomy or gastrojejunostomy.
Gastric Lymphoma
Gastric lymphomas generally account for about 4% of gastric
malignancies. Over half of patients with non-Hodgkin’s lym-
phoma have involvement of the GI tract. The stomach is the
most common site of primary GI lymphoma, and over 95% are
non-Hodgkin’s type. Most are B-cell type, thought to arise in
mucosa associated lymphoid tissue (MALT), although most
high-grade gastric lymphomas are without any characteristics
of the low-grade MALT neoplasm.183 About half of gastric lym-
phomas are histologically low grade, and about half are high
grade. Interestingly, the normal stomach is relatively devoid of
lymphoid tissue. However, in the setting of chronic gastritis, the
stomach acquires MALT, which can undergo malignant degen-
eration. Again, H pylori is thought to be the culprit. In popula-
tions with a high incidence of gastric lymphoma, there is a high
incidence of H pylori infection; patients with gastric lymphoma
also usually have H pylori infection.184
Low-grade MALT lymphoma, essentially a monoclonal
proliferation of B cells, presumably arises from a background
of chronic gastritis associated with H pylori. These relatively
innocuous tumors then undergo degeneration to high-grade
lymphoma, which is the usual variety seen by the surgeon.
Remarkably, when the H pylori is eradicated and the gastritis
improves, the low-grade MALT lymphoma often disappears.
Thus, low-grade MALT lymphoma is not a surgical lesion.
Careful follow-up is necessary particularly in those lesions
with a t(11:18) translocation, thought to be a risk factor for a
more aggressive MALT lesion. If low-grade lymphoma per-
sists after H pylori eradication, radiation should be consid-
ered for disease clinically confined to the stomach (stage I),
while chemotherapy with or without radiation is used for more
advanced lesions (Fig. 26-58).
Patients with high-grade gastric lymphoma require aggres-
sive oncologic treatment for cure and present with many of the
same symptoms as gastric cancer patients. However, systemic
symptoms such as fever, weight loss, and night sweats occur in
about 50% of patients with gastric lymphoma. The tumors may
bleed and/or obstruct. Lymphadenopathy and/or organomegaly
suggest systemic disease. Diagnosis is by endoscopy and biopsy.
Much of the tumor may be submucosal, and an assiduous 1149
attempt at biopsy is necessary. Primary lymphoma is usually
nodular with enlarged gastric folds. A diffusely infiltrative pro-
cess akin to linitis plastica is more suggestive of secondary gas-
tric involvement by lymphoma. A diligent search for extragastric
disease is necessary before the diagnosis of localized primary
gastric lymphoma is made. This includes EUS; CT scanning of
the chest, abdomen, and pelvis; and bone marrow biopsy. Most
patients with high-grade gastric lymphoma are currently
7 treated with chemotherapy and radiation, without surgical
CHAPTER 26 STOMACH
resection. Treatment-related perforation or bleeding is an
unusual but recognized complication. For disease limited to the
stomach and regional nodes, radical subtotal D2 gastrectomy
may be performed, especially for bulky tumors with bleeding
and/or obstruction. Palliative gastrectomy for tumor complica-
tions also has a role. Certainly, a multidisciplinary team should
be involved in managing patients with primary gastric
lymphoma.
Gastrointestinal Stromal Tumor
GISTs arise from interstitial cells of Cajal (ICC) and are dis-
tinct from leiomyoma and leiomyosarcoma, which arise from
smooth muscle.185,186 Prognosis in patients with GIST tumors
depends on tumor size, location, and mitotic count. Metasta-
sis, when it occurs, is typically by the hematogenous route.
Virtually all GISTs should be resected along with a margin
of normal tissue. Most GISTs (and almost no smooth muscle
tumors) express c-KIT (CD117) or the related PDGF receptor A,
as well as CD34; almost all smooth muscle tumors (and
almost no GISTs) express actin and desmin. These markers
can often be detected on specimens obtained by fine-needle
aspiration187 and are useful in differentiating between GIST
and smooth muscle tumor histopathologically. Lesions that
are definitively leiomyoma by histopathologic criteria can be
observed if small and asymptomatic. Larger or symptomatic
gastric leiomyomas are adequately treated by enucleation or
wedge resection. Lesions that are definitively GIST or leio-
myosarcoma are best treated by resection with negative mar-
gins. Most equivocal lesions should be resected provided that
the patient has a reasonable operative risk.
Two-thirds of all GISTs occur in the stomach and have
a more favorable prognosis than do GISTs occurring in other
locations. Epithelial cell stromal GIST is the most common cell
type arising in the stomach, and cellular spindle type is the next
most common. The glomus tumor type is seen only in the stom-
ach. Smaller lesions are usually found incidentally, although
they occasionally may ulcerate and cause bleeding. Larger
lesions may produce symptoms of weight loss, abdominal pain,
fullness, early satiety, and bleeding. An abdominal mass may be
palpable. Metastasis is by the hematogenous route, most often
to liver.
Diagnosis is by endoscopy and biopsy, although the inter-
pretation of the latter may be problematic. When performed, a
transluminal (i.e., endoscopic) approach to biopsy is preferred
to a percutaneous one, to avoid to the potential for fragmenta-
tion and peritoneal seeding. A nondiagnostic biopsy does not
preclude resection of a suspicious appearing lesion. Metastatic
workup entails CT of the abdomen, and pelvis (chest X-ray suf-
fices in lieu of CT of the chest for most patients). Most GISTs
are solitary. Local resection with clear margins is adequate sur-
gical treatment but is sometimes impractical for larger prepy-
loric or pyloric channel tumors, or those near the GE junction.
1150
Low-grade (indolent) MALT

Confined to gastric wall Lymph node involvement

Stage III or IV
No t(11:18) translocation t(11:18) translocation

H pylori eradication therapy H pylori eradication therapy H pylori eradication therapy

Re-evaluate at 12 months Re-evaluate at 3–6 months and chemo** +/– XRT*
PART II

Lymphoma regression Lymphoma persists

SPECIFIC CONSIDERATIONS

Stage I Stage II
Close follow-up
XRT* Chemo** + XRT*

*XRT: external beam radiation therapy, approximately 30 Gy with 10 Gy boost

**Chemo: chemotherapy regimens include chlorambucil, fludarabinel,
and cyclosphosphamide, vincristine, prednisone (COP) +/– rituximab

High-grade (aggressive)

Stage I, II, III Stage IV

Chemo* + XRT** Chemo* +/– XRT**

No residual disease Residual disease

Follow-up Further chemotherapy Surgery

*Chemo: chemotherapy regimen usually cyclophosphamide,

doxorobicin, vincristine, prednisone (CHOP) +/– rituximab
**XRT: external beam radiation, approximately 30 Gy with 10 Gy boost

Figure 26-58. Algorithm for the treatment of gastric lymphoma. MALT = mucosa-associated lymphoid tissue. (Reproduced with permission from
Yoon SS, Coit DG, Portlock CS, et al. The diminishing role of surgery in the treatment of gastric lymphoma, Ann Surg. 2004 Jul;240(1):28-37.)

True invasion of adjacent structures by the primary tumor is
occasionally seen with larger more aggressive lesions. If safe,
en bloc resection of involved surrounding organs is appropriate
to remove all tumor.
The risk of tumor recurrence or metastasis behavior has
been stratified into four groups according to the tumor size and
mitotic count.110 Very low risk is defined by size <2 cm and
<5 mitoses/50 HPF (high-power field). Low risk is defined
by size 2 to 5 cm and <5 mitoses/50 cm. Intermediate risk is
defined by size <5 cm and 6 to 10 mitoses/50 HPF or size
5 to 10 cm and >5 mitoses/50 HPF. High risk is defined by size
>5 cm and >5 mitoses/50HPF, size >10 cm regardless of mitotic
rate or >10 mitoses/50 HPF regardless of size. As mentioned,
stomach lesions are associated with lower risk than are tumors
in other locations. Classification based on tumor location, size,
and mitotic rate have been proposed to evaluate the risk of
recurrence and metastasis and role for adjuvant therapy.188 In
an effort to further refine risk stratification, a number of nomo-
grams have been introduced incorporating tumor features. These
tools draw upon and are subject to the limitations of the institu-
tional data from which they are derived, but they are sometimes
helpful in counseling patients.
Mutations in the oncodriver c-kit and PDGFRA are pres-
ent in a majority of GISTs. This has been exploited through
the use of imatinib (Gleevec), a tyrosine kinase inhibitor. Sev-
eral clinical trials in a metastatic disease setting demonstrated
marked improvements in median survival from 9 months to
greater than 5 years.189 These striking results not only estab-
lished imatinib as the primary therapy for metastatic GIST,
but they also compelled broader efforts to target solid tumors
with small molecule inhibitors. Notably, up to 50% of treated
patients develop resistance to imatinib by 2 years, and several
second-line agents have been utilized for patients with refrac-
tory disease, most notable sunitinib.
The efficacy of imatinib as adjuvant therapy for high risk
GIST has been demonstrated in two randomized clinical
8 trials, ACOSOG Z9001 and SSG XVIII.190,191 The former
trial randomized patients to 1 year of adjuvant imatinib or pla-
cebo and showed an improvement in recurrence-free survival
with imatinib. The latter trial demonstrated an overall survival
advantage with 3 years compared to 1 year of therapy. Imatinib
is now recommended in high risk groups as an adjuvant therapy,
Nomenclature remains a point of confusion; carcinoid and 1151
well-differentiated neuroendocrine tumor (NET) are synony-
mous according to WHO classification.
Gastric neuroendocrine tumors are classified into one
of three different types. Type I is the most common, account-
ing for about 75% of cases. Type I lesions occur in patients
with chronic hypergastrinemia secondary to pernicious anemia
or atrophic gastritis. These lesions occur more frequently in
women, are often multiple and small, and have low malignant
potential (<5% metastasize). The role of long-term acid sup-

for three years or longer. Preoperative therapy with imatinib
may be indicated in selected patients with larger lesions that
may be more difficult to completely resect or require multivis-
ceral resection.
Molecular profiling has been embraced with growing rec-
ognition that specific tumor subtypes are insensitive to imatinib.
Patients with PDGFRA D842V mutations, for example, do not
respond to imatinib.192 Management of metastatic GIST is prin-
cipally medical, but surgery has a selected role. An algorithm
for the treatment of patients with metastatic GIST is shown in
Fig. 26-59.
Gastric Neuroendocrine Tumors193,194
Compared to neuroendocrine tumors of the midgut and hind-
gut, neuroendcorine tumors of the stomach are rare. Gastric
neuroendocrine tumors comprise about 1% of all neuroen-
docrine tumors and less than 2% of gastric neoplasms. They
arise from gastric enterochromaffin-like (ECL) cells and
may have malignant potential. The apparent incidence of
gastric neuroendocrine tumors is increasing, perhaps related
to increased detection or the increasing use of acid suppres-
sive medication. The latter may cause hypergastrinemia, and
gastrin has a recognized trophic effect on gastric ECL cells.
CHAPTER 26 STOMACH
pression with resultant hypergastrinemia in the pathogenesis of
type I gastric carcinoids is unclear. Type II gastric neuroendo-
crine tumors are associated with MEN1 and ZES. These lesions
also tend to be small and multiple, but they have a somewhat
higher malignant potential than type I lesions (10% metasta-
size). Type II lesions are more common in the setting of MEN1;
they are quite uncommon in patients with sporadic ZES. The
constellation of gastric acidity, hypergastrinemia, and gastric
neuroendocrine tumors suggests gastrinoma until proven other-
wise. Type III gastric neuroendocrine tumors are sporadic. They
are most often solitary (usually >2 cm) and occur more com-
monly in men. They are not associated with hypergastrinemia.
Most patients have regional nodal or distant metastases at the
time of diagnosis, and some present with symptoms of carcinoid
syndrome.
Gastric neuroendocrine tumors are usually diagnosed with
endoscopy and biopsy. The type can be determined based upon
clinical context, patient history, the presence or absence of atro-
phic gastric mucosa, gastric pH and gastrin level. Some tumors
are submucosal and may be quite small. They are often confused
with heterotopic pancreas or small leiomyomas. Biopsy may
be difficult because of the submucosal location, and EUS can
be helpful in defining the size and depth of the lesion. Plasma

Metastatic or recurrent GIST

Imatinib 400 mg four times a day in all KIT, non-D842V PDGFRA mutations,
and WT GIST Consider 400 mg twice a day in exon 9 KIT mutations
Consider clinical trial in PDGFRA D842V mutations

Repeat imaging in 1 to 3 months

Responsive/Stable disease Progressive disease

Resectable Unresectable Unifocal Multifocal

Consider Continue Consider Dose escalation to

surgery imatinib surgery imatinib 400 mg bid

Sunitinib
Regorafenib
Clinical trial

Figure 26-59. Algorithm for the treatment of malignant gastrointestinal stromal tumor. (Reproduced with permission from Balachandran
VP, DeMatteo RP: Gastrointestinal stromal tumors: who should get imatinib and for how long? Adv Surg. 2014;48:165-183.)
1152 chromogranin A levels are frequently elevated. CT scan and
Table 26-22
octreotide or gallium dotatate scans are useful for staging.
Type I and II patients with numerous diminutive lesions Etiology of gastroparesis
can be followed with serial endoscopy. Small lesions con- Idiopathic
9 fined to the mucosa (typically type I or type II lesions) less Endocrine or metabolic
than 1 cm may be treated endoscopically with EMR if there are Diabetes mellitus
only a few lesions (<5). Occasionally a slightly larger lesion Thyroid disease
(1–2 cm) necessitate local surgical excision. Larger lesions and Renal insufficiency
type III lesions should be removed by D1 or D2 gastrectomy. After gastric surgery
Antrectomy to mitigate gastric secretion in type I patients with After resection
refractory growing lesions was invoked as a viable treatment After vagotomy
PART II

strategy in the past, but it is rarely indicated. Central nervous system disorders
Survival is excellent for node-negative patients (>90% Brain stem lesions
5-year survival); node-positive patients have a 50% 5-year sur- Parkinson’s disease
vival. Gastrinoma should be resected if located in patients with Peripheral neuromuscular disorders
type II carcinoid. The 5-year survival for patients with type I Myotonia dystrophica
gastric carcinoid is close to 100%; for patients with type III
SPECIFIC CONSIDERATIONS

Duchenne muscular dystrophy

lesions, the 5-year survival is less than 50%. Somatostatin ana- Connective tissue disorders
logue therapy may delay progression of metastatic disease. Sur- Scleroderma
gical debulking may have a role in selected patients with limited Polymyositis/dermatomyositis
metastatic disease. Infiltrative disorders
Lymphoma
Amyloidosis
BENIGN GASTRIC NEOPLASMS Diffuse gastrointestinal motility disorder
Leiomyoma Chronic intestinal pseudo-obstruction
The typical leiomyoma is submucosal and firm. If ulcerated, it Medication-induced
has an umbilicated appearance and may bleed. Histologically, Electrolyte imbalance
these lesions appear to be of smooth muscle origin. Lesions Potassium, calcium, magnesium
<2 cm are usually asymptomatic and benign. Larger lesions may Miscellaneous conditions
cause symptoms such as bleeding, obstruction, or pain. Asymp- Infections (especially viral)
tomatic lesions <2 cm may be carefully observed or enucleated Paraneoplastic syndrome
if fine-needle aspiration and immune markers confirm smooth Ischemic conditions
muscle tumor; larger lesions and symptomatic lesions should be Gastric ulcer
removed by wedge resection (often possible laparoscopically). Reproduced with permission from Parkman HP, Harris AD, Krevsky B,
et al: Gastroduodenal motility and dysmotility: an update on techniques
When lesions thought to be leiomyoma are observed rather than
available for evaluation, Am J Gastroenterol. 1995 Jun;90(6):869-892.
resected, the patient should be made aware of their presence and
the small possibility for malignancy.

Lipoma
Lipomas are benign submucosal fatty tumors that are usually
asymptomatic, found incidentally on upper GI series or EGD.
Endoscopically, they have a characteristic appearance; there
also is a characteristic appearance on EUS. Excision is unnec-
essary unless the patient is symptomatic.
Gastroparesis
Gastric motility disorders include delayed gastric emptying
(gastroparesis), rapid gastric emptying, and motor and sensory
abnormalities (e.g., functional dyspepsia). Surgically relevant
secondary disorders of gastric motility (e.g., dumping, gastric
stasis, and Roux syndrome) are discussed under Postgastrec-
tomy Problems. Gastroparesis is the most surgically relevant
primary disorder of gastric motility.195,196
Most patients with primary gastroparesis present with
nausea, vomiting, bloating, early satiety, and/or abdominal
pain. Eighty percent of these patients are women; some are
diabetic. Postprandial vomiting significantly complicates the
management of blood glucose in the latter group, predispos-
ing to hypoglycemia following preprandial insulin. In patients
with gastroparesis, it is important to rule out mechanical gastric
outlet obstruction, and small-bowel obstruction. An upper GI
series may suggest slow gastric emptying and relative atony,
or it may be normal. EGD may show bezoars or retained food
but is frequently normal. Gastric emptying scintigraphy shows
delayed solid emptying, and often delayed liquid emptying.
Gastroparesis can be a manifestation of a variety of problems
(Table 26-22). Medical treatment includes promotility agents,
antiemetics, and, perhaps, botulinum injection into the pylorus.
If the diabetic gastroparetic patient is not a candidate for
pancreas transplant, both gastrostomy (for decompression)
and jejunostomy tubes (for feeding and prevention of hypo-
glycemia) can be helpful in managing these patients. Other
surgical options include implantation of a gastric pacemaker,
pyloroplasty or peroral endoscopic pyloromyotmy (particularly
in patients responsive to pyloric Botox injection), and gastric
resection.197 Generally, gastric resection should be done only
after other therapeutic options have been exhausted.
Massive Upper Gastrointestinal Bleeding
Although there are arbitrary definitions of “massive” upper GI
bleeding put forth, perhaps the most practical definition in the
current era would be acute GI bleeding proximal to the ligament
of Treitz, which requires blood transfusion. In multiple series,
the stomach and proximal duodenum are by far the most com-
mon sources of pathology associated with this diagnosis.109,198
The most common causes of acute upper GI bleeding in emer-
gency department or hospitalized patients are peptic ulcer, gastri-
tis, Mallory-Weiss syndrome, and esophagogastric varices. Less
common causes include benign or malignant neoplasm, angio-
dysplasia, Dieulafoy’s lesion, portal gastropathy, Ménétrier’s
disease, and watermelon stomach. Arterioenteric fistula should
always be considered in the patient who has an aortic graft or
who has undergone repair of a visceral artery aneurysm.
The most important issues in the early hospital manage-
ment of patients with acute upper GI bleeding are resuscita-
tion and risk stratification. Large-bore IV access and Foley
catheterization is accomplished, and nasogastric intubation is
considered. Risk stratification is essentially accomplished by
answering the following questions:
a. What is the magnitude and acuity of the hemorrhage? Hy-
potension, tachycardia, oliguria, low hematocrit, pallor, al-
tered mentation, and/or hematemesis suggest a large blood
loss that has occurred over a short period of time. This is a
high-risk situation.
b. Does the patient have significant chronic disease, particu-
larly lung, liver, kidney, and/or heart disease, which com-
promises physiologic reserve? If yes, this is a high-risk
situation.
c. Is the patient anticoagulated, or immunosuppressed? If
yes, this is a high-risk situation.
d. On endoscopy, is the patient bleeding from varices, or is
there active bleeding, or is there a visible vessel, or is there
a deep ulcer overlying a large vessel (e.g., posterior duode-
nal ulcer overlying the gastroduodenal artery)? Could the
patient be bleeding from an arterio-enteric fistula? If yes,
this is a high-risk situation.
When judged to be low risk, most patients will stop bleed-
ing with supportive treatment and IV PPI. Selected patients may
be discharged from the emergency department and managed on
an outpatient basis.
If the patient is deemed to be high risk based on one
or more of the aforementioned questions, then the following
should be done immediately:
1. Type and cross-match for transfusion of blood products.
2. Admit to ICU or monitored bed in specialized unit.
3. Consult surgeon.
4. Consult gastroenterologist.
5. Start intravenous PPI.
6. Perform upper endoscopy within 12 hours, after resuscita-
tion and correction of coagulopathy. Endoscopic hemosta-
sis should be considered in most high-risk patients with
acute upper GI bleeding.
Although the surgeon should be involved early in the hos-
pital course of all high-risk patients with acute upper GI bleed-
ing, most of these patients will be adequately managed without
operation. Mucosal lesions can usually be controlled with endo-
scopic hemotherapy and medical management. Occasionally,
arteriography can be helpful.199 Operation for bleeding ulcer is
discussed previously (see “Operation for Bleeding Peptic Ulcer”
and Fig. 26-43).
Isolated Gastric Varices
Isolated gastric varices are those that occur in the absence
of esophageal varices and are classified as type I (fundic) or
type II (distal to fundus including proximal duodenum). 200
The presence of isolated gastric varices is usually associated 1153
with portal hyper-tension or splenic vein thrombosis. Although
there is a significant bleeding risk from isolated gastric varices
on long-term follow-up, there is no indication for the routine
application of prophylactic measures.
Patients with acute upper GI bleeding from isolated gas-
tric varices should be considered high risk. Although data are
limited, octreotide and/or vasopressin infusion may decease
bleeding, if tolerated. Balloon tamponade with a Sengstaken-
Blakemore tube may provide temporary control of exsanguinat-
CHAPTER 26 STOMACH
ing hemorrhage from type isolated gastric varices, but if this is
used, endotracheal intubation for airway protection is prudent.
Endoscopic treatment with sclerotherapy or varix ligation is
less successful than in esophageal varices but should be con-
sidered. Interventional radiology should be consulted and bal-
loon-occluded retrograde transvenous obliteration considered.
A transjugular intrahepatic portosystemic shunt (TIPSS) may
be useful if there is nonsegmental portal hypertension. If the
patient has splenic vein thrombosis and left-sided (sinistral) or
segmental portal hypertension, splenectomy is quite effective in
controlling bleeding from isolated gastric varices. The operative
mortality is 5%. Liver transplantation should always be consid-
ered in the cirrhotic patient.
Hypertrophic Gastropathy
(Ménétrier’s Disease)
There are two clinical syndromes characterized by epithelial
hyperplasia and giant gastric folds: ZES and Ménétrier’s dis-
ease. The latter is characteristically associated with protein-
losing gastropathy and hypochlorhydria. There are large
rugal folds in the proximal stomach, and the antrum is usu-
ally spared. Mucosal biopsy shows diffuse hyperplasia of the
surface mucus-secreting cells and usually decreased parietal
cells (Fig. 26-60). It has recently been suggested that Méné-
trier’s disease is caused by local overexpression of transform-
ing growth factor-α in the gastric mucosa, which stimulates
the epidermal growth factor receptor, a receptor tyrosine
kinase, on gastric SECs. This results in the selective expan-
sion of surface mucous cells in the gastric body and fundus.
A few patients with this unusual disease have been successfully
Figure 26-60. Mucosal biopsy in Ménétrier’s disease. (Repro-
duced with permission from Ming S-C, Goldman H: Pathology
of the Gastrointestinal Tract, 2nd ed. Baltimore, MD: Williams &
Wilkins; 1998.)
1154 treated with the epidermal growth factor receptor blocking
monoclonal antibody cetuximab.201
Most patients with Ménétrier’s disease are middle-aged
men who present with epigastric pain, weight loss, diarrhea,
and hypoproteinemia. There may be an increased risk of gastric
cancer. Sometimes, the disease regresses spontaneously. Occa-
sionally it is associated with H pylori infection, and the disease
improves with helicobacter eradication. Total gastrectomy may
be indicated for bleeding, severe hypoproteinemia, or cancer.

Watermelon Stomach (Gastric Antral

Vascular Ectasia)
PART II

The parallel red stripes atop the mucosal folds of the distal
stomach give this rare entity its sobriquet. Histologically, gas-
tric antral vascular ectasia (GAVE) is characterized by dilated
mucosal blood vessels that often contain thrombi, in the lamina
SPECIFIC CONSIDERATIONS

propria. Mucosal fibromuscular hyperplasia and hyalinization

often are present (Fig. 26-61). The histologic appearance can
resemble portal hypertensive gastropathy, but the latter usually
affects the proximal stomach, whereas watermelon stomach pre-
dominantly affects the distal stomach. β-Blockers and nitrates,
useful in the treatment of portal hypertensive gastropathy,
are ineffective in patients with gastric antral vascular ectasia.
Patients with GAVE are usually elderly women with chronic
GI blood loss requiring transfusion. Most have an associated
autoimmune connective tissue disorder, and at least 25% have
chronic liver disease. Nonsurgical treatment options include
estrogen and progesterone, and endoscopic treatment with the
neodymium yttrium-aluminum garnet (Nd:YAG) laser or argon
plasma coagulator.202 Antrectomy may be required to control
blood loss, and this operation is quite effective but carries
increased morbidity in this elderly patient group. Patients with
portal hypertension and antral vascular ectasia should be consid-
ered for transjugular intrahepatic portosystemic shunt (TIPSS).
Dieulafoy’s Lesion
Dieulafoy’s lesion is a congenital arteriovenous malformation
characterized by an unusually large tortuous submucosal artery.
If this artery is eroded, impressive pulsatile bleeding may occur.
To the endoscopist or surgeon, this appears as a stream of arte-
rial blood emanating from what appears grossly to be a normal
gastric mucosa. The lesion typically occurs in middle-aged or
Figure 26-61. Gastric antral vascular ectasia (watermelon stom-
ach). (Reproduced with permission from Godlman H, Hayek J,
Federman M: Gastrointestinal Mucosal Biopsy. New York, NY:
Churchill Livingstone; 1996.)
Figure 26-62. Trichobezoar forming cast of stomach and duode-
num; removed from 15-year-old girl. (Reproduced with permission
from DeBakey M, Ochsner A: Bezoars and concretions, Surgery.
1938;Dec;4:934.)
elderly men and may be more common in patients with liver
disease.203 Patients typically present with upper GI bleeding,
which may be intermittent, and endoscopy can miss the lesion if
it is not actively bleeding. Treatment options include endoscopic
hemostatic therapy, angiographic embolization, or operation. At
surgery, the lesion may be oversewn or resected.
Bezoars/Diverticula
Bezoars are concretions of indigestible matter that accumulate
in the stomach. Trichobezoars are composed of swallowed hair
(Fig. 26-62). Phytobezoars are composed of vegetable matter
and, in the United States, are usually seen in association with
gastroparesis or gastric outlet obstruction. They also are asso-
ciated with persimmon ingestion. Most commonly, bezoars
produce obstructive symptoms, but they may cause ulceration
and bleeding. Diagnosis is suggested by upper GI series and
confirmed by endoscopy. Treatment options include enzyme
therapy (papain, cellulase, or acetylcysteine), endoscopic dis-
ruption and removal, or surgical removal.
Gastric diverticula are usually solitary and may be con-
genital or acquired. Congenital diverticula are true diverticula
and contain a full coat of muscularis propria, whereas acquired
diverticula (perhaps caused by pulsion) usually have a negli-
gible outer muscle layer. Most gastric diverticula occur in the
posterior cardia or fundus (Fig. 26-63) and are usually asymp-
tomatic. However, they can become inflamed and may produce
pain or bleeding. Perforation is rare. Asymptomatic diverticula
do not require treatment, but symptomatic lesions should be
removed. This can often be done laparoscopically.
Foreign Bodies
Ingested foreign bodies are usually asymptomatic. Small coins
usually pass through the GI tract without difficulty. Sharp or

Figure 26-63. Upper GI contrast study showing a diverticulum of
the stomach. (Used with permission from Marc Levine, MD.)
large objects in the stomach should be removed. This can usu-
ally be done endoscopically, with an overtube technique. Rec-
ognized dangers include aspiration of the foreign body during
removal and rupture of drug-containing bags in “body packers.”
Both complications can be fatal. Surgical removal is recom-
mended in body packers who ingest drug parcels for smuggling
and in patients with large jagged objects that cannot be safely
removed endoscopically. Corrosive objects (i.e., batteries)
should be removed promptly usually endoscopically. Ingested
magnets should be removed unless they are small and singular
and without other ingested metal objects.
Mallory-Weiss Syndrome
The Mallory-Weiss lesion is a longitudinal tear in the mucosa
of the GE junction.204 It is presumably caused by forceful vom-
iting and/or retching, and it is commonly seen in alcoholics.
It presents with upper GI bleeding, often with hematemesis.
Endoscopy confirms the diagnosis and may be useful in con-
trolling the bleeding, but 90% of patients stop bleeding sponta-
neously. Other options to control the bleeding include balloon
tamponade, angiographic embolization, or selective infusion of
vasopressin, systemic vasopressin, and operation. Surgical treat-
ment consists of oversewing the bleeding lesion through a long
gastrotomy.
A B
Figure 26-64. A through C. Gastric volvulus. (Reproduced with permission from Buchanan J: Volvulus of the stomach, Br J Surg.
1930;July;18(69):99-112.)
Volvulus 1155
Gastric volvulus is a twist of the stomach that usually occurs
in association with a large hiatal hernia. It also can occur in
patients with an unusually mobile stomach without hiatal hernia.
Typically, the stomach twists along its long axis (organoaxial
volvulus), and the greater curvature flips up (Fig. 26-64C). If the
stomach twists around the transverse axis, it is called mesentero-
axial rotation (Fig. 26-64A and Fig. 26-64B). Often, volvulus
is a chronic condition that can be surprisingly asymptomatic.
In these instances, expectant nonoperative management is typi-
CHAPTER 26 STOMACH
cally advised, especially in the elderly. The risk of strangulation
and infarction has been overestimated in asymptomatic patients.
Symptomatic patients should be considered for operation, espe-
cially if the symptoms are severe and/or progressive. Patients
may present with symptoms of pain and pressure related to the
intermittently distending and poorly emptying twisted stomach.
Pressure on the lung may produce dyspnea, pressure on the peri-
cardium may produce palpitations, and pressure on the esopha-
gus may produce dysphagia. Symptoms are often relieved with
vomiting or passage of a nasogastric tube. Gastric infarction is
a surgical emergency, and the patient can be moribund. Gastric
necrosis may be extensive or focal. Elective operation for gas-
tric volvulus usually involves reduction of the stomach and gas-
tropexy with or without repair of hiatal hernia. Gastropexy alone
should be considered for high-risk patients since it can nearly
always be performed laparoscopically and may be surprisingly
effective in relieving mechanical symptoms.
GASTROSTOMY
A gastrostomy is performed either for alimentation or for gastric
drainage/decompression. Gastrostomy may be done percutane-
ously, laparoscopically, or via open technique.205,206 Currently,
percutaneous endoscopic gastrostomy is the most common
method used. The open techniques include the Stamm method
(Fig. 26-65), the Witzel method (Fig. 26-66), and the Janeway
method. The Janeway gastrostomy, designed to create a per-
manent nondraining gastric stoma that can be intermittently
intubated, is more complicated than the other open techniques,
and is rarely necessary. By far the most common surgical tech-
nique is the Stamm gastrostomy, which can be performed open
or laparoscopically.
Complications of gastrostomy include infection, dis-
lodgment, leakage with peritonitis, and aspiration pneumonia.
Although gastrostomy tubes usually do prevent tense gastric dil-
atation, they may not adequately drain the stomach, especially
when the patient is bedridden, and they cannot always be relied
upon to prevent pulmonary aspiration of gastric contents.
C
1156 POSTGASTRECTOMY PROBLEMS207
Dumping Syndrome
Dumping is a phenomenon caused by the destruction or bypass
of the pyloric sphincter.208 However, other factors undoubtedly
play a role because dumping can occur after operations that pre-
serve the pylorus, such as parietal cell vagotomy. Also, an appro-
priate stimulus may provoke dumping symptoms, even in some
patients who have not undergone surgery. Clinically significant
dumping occurs in 5% to 10% of patients after pyloroplasty,
pyloromyotomy, or gastrectomy, and consists of a constellation
of postprandial symptoms ranging in severity from annoying
PART II

to disabling. The symptoms are thought to be the result of the

abrupt delivery of a hyperosmolar load into the small bowel due
to ablation of the pylorus or decreased gastric compliance. Typi-
cally, 15 to 30 minutes after a meal, the patient becomes dia-
phoretic, weak, light-headed, and tachycardic. These symptoms
SPECIFIC CONSIDERATIONS

may be ameliorated by recumbence or saline infusion. Crampy

abdominal pain is not uncommon, and diarrhea often follows.
This is referred to as early dumping and should be distinguished
Figure 26-65. Stamm gastrostomy. (Reproduced with permission
from postprandial (reactive) hypoglycemia, also called late
from Zuidema GD, Yeo CJ: Shackelford’s Surgery of the Alimentary
dumping, which usually occurs later (2–3 hours following a
Tract, 5th ed. Vol. II. Philadelphia, PA: Elsevier/Saunders; 2002.)
meal) and is relieved by the administration of sugar. A variety

Figure 26-66. A through F. Witzel gastros-

tomy. (Reproduced with permission from
Zuidema GD, Yeo CJ: Shackelford’s Sur-
gery of the Alimentary Tract, 5th ed. Vol. II.
Philadelphia, PA: Elsevier/Saunders; 2002.)
of hormonal aberrations have been observed in early dumping,
including increased serum levels of VIP, CCK, neurotensin,
peripheral hormone peptide YY, renin-angiotensin-aldosterone,
and decreased atrial natriuretic peptide. Late dumping is associ-
ated with hypoglycemia and hyperinsulinemia.
Medical therapy for the dumping syndrome consists of
dietary modification and somatostatin analogue (octreotide).
Often, symptoms improve if the patient avoids liquids during
meals. Hyperosmolar liquids (e.g., milk shakes) may be particu-
larly troublesome. There is some evidence that adding dietary
fiber compounds at mealtime may improve the syndrome. If
dietary manipulation fails, the patient is started on octreotide,
100 μg subcutaneously twice daily. This can be increased up to
500 μg twice daily if necessary. The long-acting depot octreo-
tide preparation is useful. Octreotide not only ameliorates the
abnormal hormonal pattern seen in patients with dumping
symptoms, but it also promotes restoration of a fasting motility
pattern in the small intestine (i.e., restoration of the MMC). The
α-glucosidase inhibitor acarbose may be particularly helpful in
ameliorating the symptoms of late dumping.
Only a very small percentage of patients with dumping
symptoms ultimately require surgery. Most patients improve
with time (months and even years), dietary management, and
medication. Therefore, the surgeon should not rush to reoper-
ate on the patient with dumping symptoms. Multidisciplinary
nonsurgical management must be optimized first. Before reop-
eration, a period of inhospital observation is useful to define the
severity of the patient’s symptoms and patient compliance with
prescribed dietary and medical therapy.
The results of remedial operation for dumping are
variable and unpredictable. There are a variety of surgical
approaches, none of which work consistently well. Addition-
ally, there is not a great deal of experience reported in the
literature with any of these methods and long-term follow-up
is rare. Patients with disabling refractory dumping after gas-
trojejunostomy can be considered for simple takedown of this
anastomosis provided that the pyloric channel is patent. The
reversed intestinal segment is rarely used today—and rightly
so. This operation interposes a 10-cm reversed segment of
intestine between the stomach and the proximal small bowel.
This slows gastric emptying, but often leads to obstruction,
requiring reoperation. Isoperistaltic interposition (Henley
loop) has not been successful in ameliorating severe dumping
over the long term. The Roux-en-Y gastrojejunostomy is asso-
ciated with delayed gastric emptying, probably on the basis
of disordered motility in the Roux limb. Taking advantage of
this disordered physiology, surgeons have used this operation
successfully in the management of the dumping syndrome.
Although this is probably the procedure of choice in the small
group of patients requiring operation for severe dumping fol-
lowing gastric resection, gastric stasis may result, particularly
if a large gastric remnant is left. In the presence of significant
gastric acid secretion, marginal ulceration is common after
both jejunal interposition and Roux-en-Y procedures; thus,
concomitant vagotomy and hemigastrectomy should be con-
sidered. The theoretical possibility of treating postpyloroplasty
dumping with a Roux-en-Y to the proximal duodenum (the
duodenal switch, a potentially reversible operation) has not yet
been reported (Fig. 26-67). Because pyloric ablation seems to
be the dominant factor in the etiology of dumping, it is not sur-
prising that conversion of Billroth II to Billroth I anastomosis
has not been successful in the treatment of dumping.
1157
CHAPTER 26 STOMACH
Figure 26-67. Duodenal switch operation. (Reproduced with per-
mission from Hinder RA: Duodenal switch: a new form of pancreati-
cobiliary diversion, Surg Clin North Am. 1992 Apr;72(2):487-499.)
Diarrhea
Diarrhea following gastric surgery may be the result of trun-
cal vagotomy, dumping, or malabsorption. Truncal vagotomy is
associated with clinically significant diarrhea in 5% to 10% of
patients. It occurs soon after surgery and usually is not associ-
ated with other symptoms, a fact that helps to distinguish it from
dumping. The diarrhea may be a daily occurrence, or there may
be significant periods of relatively normal bowel function. The
symptoms tend to improve over the months and years after the
index operation. The cause of postvagotomy diarrhea is unclear.
Possible mechanisms include intestinal dysmotility and accel-
erated transit, bile acid malabsorption, rapid gastric emptying,
and bacterial overgrowth. The latter problem is facilitated by
decreased gastric acid secretion and (even small) blind loops.
Although bacterial overgrowth can be confirmed with the
hydrogen breath test, a simpler test is an empirical trial of oral
antibiotics. Some patients with postvagotomy diarrhea respond
to cholestyramine, while in others codeine or loperamide may
be useful. Octreotide should also be tried. Another theoretical
cause of diarrhea following gastric surgery is fat malabsorption
due to acid inactivation of pancreatic enzymes or poorly coor-
dinated mixing of food and digestive juices. This can be con-
firmed with a qualitative test for fecal fat and treated with acid
suppression. Postvagotomy diarrhea usually does not respond
to treatment with pancreatic enzymes. In the rare patient who is
debilitated by postvagotomy diarrhea unresponsive to medical
management, operation might be considered, but outcomes can
be problematic. The operation of choice is probably a 10-cm
reversed jejunal interposition placed in continuity 100 cm distal
to the ligament of Treitz. Another option is the onlay antiperi-
staltic distal ileal graft. Both operations can cause obstructive
symptoms and/or bacterial overgrowth.209
Gastric Stasis210,211
Gastric stasis following surgery on the stomach may be due to
a problem with gastric motor function or caused by an obstruc-
tion. The gastric motility abnormality could have been preexist-
ing and unrecognized by the operating surgeon. Alternatively,
1158 it may be secondary to deliberate or unintentional vagotomy,
or resection of the dominant gastric pacemaker. An obstruction
may be mechanical (e.g., anastomotic stricture, efferent limb
kink from adhesions or constricting mesocolon, or a proximal
small-bowel obstruction) or functional (e.g., retrograde peristal-
sis in a Roux limb). Gastric stasis presents with vomiting (often
of undigested food), bloating, epigastric pain, and weight loss.
The evaluation of a patient with suspected postoperative
gastric stasis includes EGD, upper GI and small bowel series,
gastric emptying scan, and gastric motor testing. Endoscopy
shows gastritis and retained food or bezoar. The anastomosis
PART II
and efferent limb should be evaluated for stricture or narrow-
ing. A dilated efferent limb suggests chronic stasis, either from
a motor abnormality (e.g., Roux syndrome) or mechanical
small bowel obstruction (e.g., chronic adhesion). If the problem
is thought to be primarily a disorder of intrinsic motor func-
tion, newer techniques such as EGG and GI manometry should
SPECIFIC CONSIDERATIONS
be considered, but chronic distal mechanical obstruction may
result in disordered motility in the proximal organ confounding
interpretation.
Once mechanical obstruction has been ruled out, medi-
cal treatment is successful in most cases of motor dysfunction
following previous gastric surgery. This consists of dietary
modification and promotility agents. Intermittent oral antibiotic
therapy may be helpful in treating bacterial overgrowth, with its
attendant symptoms of bloating, flatulence, and diarrhea.
Gastroparesis following V + D may be treated with subto-
tal gastrectomy but simple loop gastrojejunoctomy (GJ) should
be tried if previous drainage was pyloroplasty. Billroth II anas-
tomosis with Braun enteroenterostomy may be preferable to
Roux-en-Y reconstruction after subtotal gastrectomy for gas-
tric stasis, but bile reflux can still occur. Initial operation for
gastric stasis is often associated with persistent gastric empty-
ing problems that may subsequently require near-total or total
gastrectomy, a nutritionally unattractive option. Delayed gastric
emptying following ulcer surgery (V + D or V + A) may rep-
resent an anastomotic stricture (often due to recurrent ulcer) or
proximal small bowel obstruction. Recurrent ulcer may respond
to medical therapy with PPI and abstinence from NSAIDs, aspi-
rin, and smoking. And if necessary, endoscopic dilation is occa-
sionally helpful. However, when associated with symptomatic
gastric stasis, reoperation is often necessary. Gastroparesis fol-
lowing subtotal gastric resection is best treated with near-total
(95%) or total gastric resection and Roux-en-Y reconstruction.
If total gastrectomy is performed, a jejunal reservoir should be
considered. Gastric pacing is promising, but it has not achieved
widespread clinical usefulness in the treatment of postoperative
gastric atony.
Bile Reflux Gastritis and Esophagitis
Most patients who have undergone ablation or resection of the
pylorus have bile in the stomach on endoscopic examination,
along with some degree of gross or microscopic gastric inflam-
mation. Therefore, attributing postoperative symptoms to bile
reflux is problematic because most asymptomatic patients have
bile reflux too. However, it is generally accepted that a small
subset of patients have bile reflux gastritis syndrome. These
patients present with nausea, bilious vomiting, and epigastric
pain, and quantitative evidence of excess enterogastric reflux.
Curiously, symptoms often develop months or years after the
index operation. The differential diagnosis includes afferent
or efferent loop obstruction, gastric stasis, and small-bowel
obstruction. Plain abdominal X-rays, upper endoscopy, upper
GI series, abdominal CT scan, and gastric emptying scans are
helpful in evaluating these possibilities.
Bile reflux may be quantified with gastric analysis or
esophageal impedance testing or with scintigraphy (bile reflux
scan). Typically, enterogastric reflux is greatest after Billroth II
gastrectomy or gastrojejunostomy, and least after vagotomy and
pyloroplasty, with Billroth I gastrectomy giving intermediate
values. Patients who are well into the abnormal range of bile
reflux may be considered for remedial surgery if symptoms are
severe. Remedial surgery will eliminate the bile from the vomi-
tus and may improve the patient’s pain, but it is quite unusual
to render these patients completely asymptomatic, especially if
they are narcotic dependent.
Bile reflux gastritis after distal gastric resection may be
treated by one of the following options: Roux-en-Y gastroje-
junostomy; interposition of a 40-cm isoperistaltic jejunal loop
between the gastric remnant and the duodenum (Henley loop);
Billroth II gastro jejunostomy with Braun enteroenterostomy;
total gastrectomy with Roux esophagojejunostomy. To mini-
mize reflux of bile into the stomach or the esophagus, the Roux
limb should be at least 45 cm long (preferably 60 cm). The
Braun enteroenterostomy should be placed at a similar distance
from the stomach. Excessively long limbs may be associated
with obstruction or malabsorption. All of these operations can
result in marginal ulceration on the jejunal side of the gastrojeju-
nostomy and thus are combined with a generous distal gastrec-
tomy. If this has already been done at a previous operation, the
Roux or Braun operations may be attractively simple. Whether
truncal vagotomy should be considered to decrease the risk of
marginal ulceration is controversial because acid-suppressing
medications may be equally effective. In addition, the benefits
of decreased acid secretion following vagotomy may be out-
weighed by problems with vagotomy-associated dysmotility
in the gastric remnant. The Roux operation may be associated
with an increased risk of emptying problems compared to the
other two options, but controlled data are lacking. Patients with
debilitating bile reflux after gastrojejunostomy can be consid-
ered for simple takedown of this anastomosis provided that the
pyloric channel is open.
Primary bile reflux gastritis (i.e., no previous operation)
is rare, and may be treated with the duodenal switch operation,
essentially an end-to-end Roux-en-Y to the proximal duodenum
(see Fig. 26-68). The Achilles’ heel of this operation is, not sur-
prisingly, marginal ulceration. Thus, it should be combined with
highly selective vagotomy, and/or long-term acid suppressive
medication.
Bile gastritis or esophagitis is a recognized complication
after esophagogastrectomy with or without pyloroplasty. This
can be effectively treated by division of the duodenum immedi-
ately distal to the pylorus with drainage of the prepyloric antrum
into a Roux limb. Preservation of the right gastroepiploic pedi-
cal is important. Proximal subtotal gastrectomy with esophago-
antral anastomosis should be avoided, but when performed, the
pylorus should be left intact.
Roux Syndrome
A subset of patients who have had distal gastrectomy and
Roux-en-Y gastrojejunostomy will have great difficulty
with gastric emptying in the absence of mechanical obstruc-
tion. These patients present with vomiting, epigastric pain,
and weight loss. This clinical scenario has been labeled the
Roux syndrome. Endoscopy may show retained food or
bezoars, dilation of the gastric remnant, and/or dilation of the
Roux limb. Anastomotic inflammation and stricture from mar-
ginal ulceration is a confounding finding. An upper GI series
confirms these findings and may show delayed gastric empty-
ing. This is better quantified by a gastric emptying scan, which
always shows delayed solid emptying and may show delayed
liquid emptying as well.
GI motility testing shows abnormal motility in the Roux
limb, with much of the propulsive activity toward, rather than
away from, the stomach.212 Gastric motility also may be abnor-
mal. Presumably, the disordered motility in the Roux limb
occurs in all patients with this operation. Why only a subset
develops the Roux syndrome is unclear. Perhaps patients with
disordered gastric motility are at most risk. The disorder seems
to be more common in patients with a generous gastric
10 remnant. Truncal vagotomy also has been implicated.
Medical treatment consists of promotility agents. Surgi-
cal treatment consists of paring down the gastric remnant. Care
should be taken to preserve adequate blood supply to the new
gastric pouch. If the left gastric artery is intact, a vertically ori-
ented lesser curvature based pouch (similar to gastric bypass)
with excision of the fundus can be considered. If gastric motility
is severely disordered, 95% gastrectomy or total gastrectomy
should be considered. The Roux limb should be resected if it is
dilated and flaccid, unless doing so puts the patient at risk for
short bowel.
Gallstones
Gallstone formation following gastric surgery generally is
thought to be secondary to vagal denervation of the gallblad-
der with attendant gallbladder dysmotility and stasis. Although
prophylactic cholecystectomy is not justified with most gas-
tric surgery, it should be considered if the gallbladder appears
abnormal, especially if subsequent cholecystectomy is likely to
be difficult. If preoperative evaluation reveals sludge or gall-
stones, or if intraoperative evaluation reveals stones, incidental
cholecystectomy should be considered.
Weight Loss
Weight loss is common in patients who have had a vagotomy
and/or gastric resection. The degree of weight loss tends to par-
allel the magnitude of the operation. It may be insignificant in
the obese but devastating in the asthenic patient. The surgeon
should always consider the possible nutritional consequences
before performing a gastric resection for benign disease in a
thin patient. The causes of weight loss after gastric surgery
generally fall into one of two categories: altered dietary intake
or malabsorption. If a stool stain for fecal fat is negative, it is
likely that decreased caloric intake is the cause. This is the most
common cause of weight loss after gastric surgery, and it may
be due to small stomach syndrome, postoperative gastroparesis,
anorexia due to loss of ghrelin, or self-imposed dietary modifi-
cation because of dumping and/or diarrhea. Consultation with
an experienced dietitian may prove invaluable.
Anemia
Iron absorption takes place primarily in the proximal GI tract,
and it is facilitated by an acidic environment. Intrinsic factor,
essential for the enteric absorption of vitamin B12, is made by
the parietal cells of the stomach. Vitamin B12 bioavailability also
is facilitated by an acidic environment. Folate-rich vegetables
may be poorly tolerated if gastric emptying is delayed or if
gastric capacity is limited. Since iron, B12, and folate play vital 1159
roles in hematopoiesis, it is easy to understand why patients
who have had a gastric operation are at risk for anemia. Ane-
mia is the most common metabolic side effect in patients who
have had a gastric bypass for morbid obesity. It also occurs in
up to one-third of patients who have had a vagotomy and/or
gastric resection. Iron deficiency is the most common cause, but
vitamin B12 or folate deficiency also occurs, even in patients who
have not had total gastrectomy. Of course, patients who have
had a total gastrectomy will all develop B12 deficiency with-
CHAPTER 26 STOMACH
out some type of regular nonenteral vitamin B12 administration.
Gastric bypass patients should be given oral iron supplements
and monitored for iron, B12, and folate deficiency. Patients who
have had a vagotomy and/or gastrectomy should be similarly
monitored with periodic determination of hematocrit, red blood
cell indices, iron and transferrin levels, B12, and folate levels.
Marginal nutrient status should be corrected with oral and/or
parenteral supplementation.
Bone Disease
Gastric surgery sometimes disturbs calcium and vitamin D
metabolism. Calcium absorption occurs primarily in the duo-
denum, which is bypassed with gastrojejunostomy. Fat mal-
absorption may occur because of blind loop syndrome and
bacterial overgrowth or because of inefficient mixing of food
and digestive enzymes. This can significantly affect the absorp-
tion of vitamin D, a fat-soluble vitamin. Both abnormalities of
calcium and vitamin D metabolism can contribute to metabolic
bone disease in patients following gastric surgery. The prob-
lems usually manifest as pain and/or fractures many years after
the index operation. Musculoskeletal symptoms should prompt
a study of bone density. Dietary supplementation of calcium
and vitamin D may be useful in preventing these complications.
Routine skeletal monitoring of patients at high-risk (e.g., elderly
males and females and postmenopausal females) may prove
useful in identifying skeletal deterioration that may be slowed
or stopped with appropriate treatment after gastric surgery.
LAPAROSCOPIC GASTRIC OPERATIONS
The most common laparoscopic gastric operations performed
today are for GERD and obesity. However, all conventional
gastric operations can be performed with minimal access
techniques.213 Some are more technically challenging (e.g.,
partial or total gastric resection) are of debatable advantage
over conventional open approaches. Certainly, highly selective
vagotomy, vagotomy and gastrojejunostomy, and gastrostomy
lend themselves to a minimal access approach. Laparoscopic
local excision is often feasible for GI stromal tumors, leiomyo-
mas, or gastric diverticula. Difficult to access lesions near the
GE junction or pylorus may be removed through an anterior
gastrotomy; more recent approaches utilizing transgastric ports
or combined laparoscopic and endoscopic approaches show
promise in allowing removal of practically any small gastric
lesion with limited incisions.
In Japan and Korea, laparoscopic and robotic assisted
approaches have been applied increasingly in the manage-
ment of gastric cancer.214,215 Indeed, laparoscopic subtotal gas-
trectomy has supplanted the traditional open operation as the
preferred operation for patients with earlier stage tumors, and
laparocopic total gastrectomy for proximal tumors is performed
with regularity and excellent outcomes. The Asian experience
1160 has firmly established the feasibility of safe laparoscopic D2
gastrectomy. Translation of this experience to the United States,
however, is not easily accomplished. Studies from Asia suggest
that expertise in the laparoscopic approach require upwards of
40 cases, a challenging baseline given the much lower incidence
of gastric cancer in the United States.216-219 A more advanced
spectrum of disease and higher mean BMI in Western coun-
tries are additional barriers to widespread implementation of
laparoscopic resection for gastric cancer. Notwithstanding,
several high volume centers in the United States have reported
excellent outcomes after laparoscopic gastrectomy. As robotic
PART II
technology that facilitates dissection and anastomosis with
articulated instrumentation and enhanced visualization becomes
increasingly ubiquitous, the pendulum will likely swing toward
increasing utilization of minimal access approaches for all gas-
tric operations.220
SPECIFIC CONSIDERATIONS
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