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6 Stomach
Research
189
Reference Findings
Kim J, Azagury D, Eisenberg D, Demaria E, Campos
GM.ASMBS position statement on prevention,
detection, and treatment of gastrointestinal leak after
gastric bypass and sleeve gastrectomy, including the
roles of imaging, surgical exploration, and
nonoperative management. Surg Obes Relat Dis.
2015;11(4):739–48
Rowland SP, Dharmarajah B, Moore HM, etal.
inferior vena cava lters for prevention of venous
thromboembolism in obese patients undergoing
bariatric surgery: a systematic review. Ann Surg.
2015;261(1):35–45
Peptic Ulcer Disease
Peptic ulcer disease
H. pylori infection, aspirin, NSAID, corticosteroids, cocaine, alcohol, cigarette smoking,
burns, Zollinger-Ellison syndrome, systemic mastocytosis, and selective serotonin reuptake
Risk factors
inhibitor use
H. pylori infection and the use of nonsteroidal anti-inammatory drugs (NSAIDS)➔most
common risk factors
Most commonly, postoperative gastric sleeve stenosis
occurs at the incisura angularis
A systematic review of IVC lter placement in bariatric
surgery patients found an overall higher risk of deep
venous thromboembolism and pulmonary embolism in
patients receiving a preoperative lter
190
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L. Amodu et al.
Peptic ulcer disease
Types Type Characteristics Figure Acid level
Type I Lesser curvature at
incisura angularis
Most common
Type II Gastric body and
in duodenum
Type III Prepyloric area
Normal acid
level
Type I
Increased acid
levels
Type II
Increased acid
levels
Type III
Type IV High on lesser
curvature
Type IV
Type V Anywhere
Induced by
NSAIDs
Type V
Normal acid
levels
Normal acid
6 Stomach
Peptic ulcer disease
191
High risk features
concerning for
malignancy
Pathophysiology
H. pylori testing
Giant ulcers (> 2cm), perforated ulcers, typically on the lesser curvature, intractable or
recurrent ulcers
Gastric ulcers are more concerning for malignancy than duodenal ulcers
Parietal cells secrete acid in response to three main stimuli: Acetylcholine (vagus nerve),
gastrin (G cells), and histamine (ECL cells)
Negative feedback involves somatostatin release from D cells➔inhibits parietal cell acid
secretion via inhibition of ECL cells and G cells
Helicobacter pylori (spiral or helical gram-negative rod with four to six agella, located within
or beneath mucosa
Noninvasive: Enzyme-linked immunosorbent assay (ELISA) H. pylori serology, stool antigen,
urea breath test
Invasive: Esophagogastroduodenoscopy with biopsies
H. pylori serology Lab-based ELISA
detection of IgG
antibodies to H.
pylori
➔diagnostic test
of choice
H. pylori stool
antigen
Detection of
bacterial antigen in
the stool
90% sensitivity and specicity
Not recommended in low prevalence areas
Does not reliably distinguish between past and
active infection
Indicates an active infection
Medical
management
Urea breath test
(rapid urease test)
Case Management
Uncomplicated
peptic ulcer
Uncomplicated
peptic ulcer with H.
pylori infection
Uncomplicated
peptic ulcer with H.
pylori infection+clarithyromycin resistance
Nonhealing or
recurrent duodenal
ulcer
Nonhealing or
recurrent gastric
ulcer
Based on
hydrolysis of urea
by H. pylori urease
to produce CO2
and NH3
PPI or H2 receptor blocker
PPI+clarithromycin+amoxicillin or metronidazole for 14days
PPI+bismuth+metronidazole+tetracycline for 14days
Retest for H. pylori and treat (after 4–6weeks)
Concern for malignancy➔EGD+biopsy
Best specicity (low false positive rate)
Best to conrm eradication of H. pylori
192
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Peptic ulcer disease
The goal of surgical therapy is to decrease gastric acid secretion
Antrectomy removal of G cells➔decrease acid secretion
Vagotomy➔reduced basal acid secretion and loss of receptive relaxation (loss of receptive
relaxation cause increased intragastric pressure➔early satiety, bloating, accelerated emptying
of liquids, and delay emptying of solids)
Surgical
management
Indications for operative intervention: Bleeding uncontrolled by endoscopic therapy and
bleeding in a hemodynamically unstable patient, transfusion requirement of >6units of blood;
perforation or obstruction; ulcer disease refractory to appropriate medical therapy
Medications used for peptic ulcer disease and their mechanism of action
Medication Mechanism of action
L. Amodu et al.
Proton pump inhibitor
H2 blocker
Sucralfate Coats and protects gastric mucosa
Prostanoids Inhibits gastric acid secretion by reducing parietal cell response to histamine
Bind to H, K- ATPase pump➔irreversibly inhibit parietal cell hydrogen
secretion
Antagonize H2 receptors on parietal cells➔prevent hydrogen secretion
Zollinger-Ellison syndrome
Characteristics Clinical triad of gastric acid hypersecretion, severe peptic ulcer disease, and non-beta-islet cell
tumors of the pancreas such as gastrinomas
Most gastrinomas are malignant (>50%)
More likely to be seen in young individuals
Presentation Gastric ulceration or complications of ulceration such as bleeding, perforation, strictures
May present with weight loss, diarrhea and ushing
Association with
MEN syndrome
Management
25% of patients have ZES as part of multiple endocrine neoplasia type 1
Medical management to reduce acid secretion (high-dose PPIs➔octreotide)
Gastrinomas in the absence of metastases should be resected via an exploratory laparotomy
6 Stomach
Gastroduodenal Ulcer- Complications
Bleeding peptic ulcer
Characteristics See upper gastrointestinal bleeding table
PPI/H. pylori treatment/stop anticoagulants
EGD for diagnosis and to achieve hemostasis: Epinephrine injection, clips, electrocoagulation
If endoscopy fails➔interventional radiology➔including angioembolization in selected
patients
Management
If endoscopy and IR fails➔ligation of the GDA or the left gastric artery, depending on the
location of the bleeding
Most bleeding duodenal ulcers represent posterior erosions into the GDA➔
Duodenum is opened longitudinally across pylorus
193
Key steps
Risk
stratication for
rebleeding
Prognosis
GDA is oversewn with a three-point U stitch (U stitch is intended to occlude any feeding
transverse pancreatic branch)
Perform a Heineke-Mikulicz pyloroplasty to close duodenum
• Blatchford score
• Forrest classication
Mortality is increased in patients >65years of age, patients with comorbidities, and in those with
hypotension
Greater magnitude of blood loss is also associated with increased morbidity and mortality
Gastric outlet obstruction
Risk factors Peptic ulcer disease, pancreatitis, gastrointestinal tumors, perigastric/duodenal
lymphadenopathy
Presentation Early satiety, abdominal pain, nausea, vomiting, oral intolerance
Management PPIs, H. pylori treatment/stop anticoagulation
UGI endoscopy with biopsy (to rule out cancer) and balloon dilation
Vagotomy+antrectomy with Roux-en-Y or BLII
194
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Gastroduodenal perforation
Gastric ulcers typically perforate along the anterior aspect of the lesser curvature
L. Amodu et al.
Characteristics
Presentation Contained perforation: Localized abdominal pain
Diagnosis
Duodenal ulcers tend to perforate through the anterior wall and bleed from the posterior wall
More than 95% of duodenal ulcers have been found in the rst portion of the duodenum
Free perforation: Diffuse peritonitis, fever, and tachycardia
X-ray: Free air under the diaphragm
CT abdomen and pelvis: Free air, uid collection, and a defect in the bowel wall
Spillage contained within the lesser sac may indicate posterior perforation
Refractory ulcers that have progressed to perforation➔check gastrin level to detect gastrinoma
(Gastrin >1000ng/mL➔diagnostic)
Small contained perforation➔observation and bowel rest instead of surgery
Peritonitis or free perforation➔surgical exploration and repair
All ulcers (in stomach) should be biopsied, because malignancy must be ruled out
Stable➔resection of the ulcer can be performed depending on the location
Unstable➔biopsy and source control with an omental patch
Gastric ulcers
Type Characteristics Management
Management
Type I Lesser curvature at incisura angularis
Most common
Type II Gastric body and in duodenum Distal gastrectomy+truncal
Type III Prepyloric area Distal gastrectomy+truncal
Type IV High on lesser curvature Distal gastrectomy, subtotal or
Type V Anywhere
Induced by NSAIDs
Perforated duodenal ulcer
Ulcer type Management
Anterior ulcer
Posterior ulcer Antrectomy+Billroth I/II or Roux-en-Y reconstruction
Small ulcer (1–3cm)➔Graham patch
Large ulcer (>3cm)➔jejunal serosal repair (Thal patch)+pyloric
exclusion (BLII or Roux-en-Y)+j-tube
If Billroth I is not possible,➔difcult duodenal stump closure
(Nissen-Bsteh) that attempt to reinforce the closure
Wedge resection or
antrectomy with BL I
vagotomy
vagotomy
total gastrectomy
Stop NSAIDs, cytoprotective
agents
Anterior
Right v
ve
Anterior
Posterior
Right
6 Stomach
Vagotomy andDrainage
Vagotomy and drainage procedures
Truncal
Procedure
Figure
vagotomy
+ drainage
Truncal vagotomy +
antrectomy Selective vagotomy
Posterior
Left vagus
agus
nerve
nerve
Celiac
branch
Pyloric
branch
Crow’s foot
Hepatic branch
Criminal ner
of grassi
Anterior nerve
of laterjet
Celiac
branch
Pyloric
branch
vagus
nerve
Left vagus
nerve
Crow’s foot
Hepatic branch
Criminal nerve
of grassi
Anterior nerve
of laterjet
Highly selective
vagotomy
Anterior
Posterior
Left vagus
Right vagus
nerve
nerve
Celiac branch
Pyloric branch
Crow’s foot
Hepatic branch
Criminal nerve
of grassi
Anterior nerve
of laterjet
195
Key steps Divide left and
Advantages Low
Disadvantages
right vagus
nerve proximal
to esophagogastric
junction +
drainage
procedure
(HeinekeMikulicz or
Finney
pyloroplasty or
a Jaboulay
gastroduodenostomy)
recurrence rate
Dumping,
diarrhea,
marginal ulcer
Impaired
pyloric
relaxation
Delayed
solid-phase
gastric
emptying
Accelerated
liquid phase
emptying
Antrectomy+gastrointestinal reconstruction
(Billroth I, Billroth II, or
Roux-en-Y)
Billroth I procedures are
preferred, when possible,
primarily due to avoidance
of duodenal stump and
gastrojejunal anastomosisrelated complications
Has the lowest recurrence
rates of available
denitive antiulcer
operations
Associated with higher
post-procedure
complication rates
Increased operative
mortality
Involves distal division
of vagus nerves distal to
the hepatic and celiac
branches
Requires a drainage
procedure
Avoidance of biliary
stasis and gallstones
Avoidance of
gastrointestinal
disturbances
Higher recurrence than
truncal vagotomy
Involves denervation of
parietal cells of the body
and fundus
Nerves of Latarjet that
innervate fundus and body
are divided, leaving antral
innervation (crow foot
branches) intact (divide
5cm distal to
esophagogastric junction to
7cm proximal to pylorus)
Criminal nerve of Grassi
should be divided
Lower incidence of
postoperative complications
Highest recurrence
196
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Case scenarios
L. Amodu et al.
Case scenario Management
Woman has an intractable ulcer and has failed
The best treatment option is truncal vagotomy and antrectomy
medical therapy for more than 12weeks
Recurrent ulcers after HSV Incomplete vagotomy is common after selective
vagotomies➔careful attention during a vagotomy to avoid
leaving criminal nerve of Grassi, a branch of the posterior vagus
nerve, has been frequently associated with recurrent ulcer
disease
Patient has recurrent abdominal pain after
Probably has ulcer recurrence. Please see above
highly selective vagotomy
Bilroth I versus Bilroth II
Billroth I Billroth II
Gastroduodenal
anastomosis
Billroth I
Billroth II
Advantages More closely resembles native anatomy
Decreased rates of postprandial dumping
Lower rate of bile reux gastritis
Lower rates of anastomotic stricture
Gastrojejunostomy
No risk of duodenal stump blow out or afferent
loop syndrome and has 1 suture line
Disadvantages Higher rates of gastritis and bile reux
Marginal ulcers
More feasible when extensive duodenal
pathology exists
Afferent loop syndrome
Higher risk of postprandial dumping
Risk of marginal ulcers
Duodenal stump blow out
Drainage procedure
Procedure Indications
Heineke-Mikulicz pyloroplasty Routine cases
Finney pyloroplasty In cases where the stomach lays in the longitudinal axis, where
ulcers are present in the second portion of the duodenum or with
chronic inammation displacing the pylorus
Jaboulay gastroduodenostomy In severe scarring or brosis, the Jaboulay gastroduodenostomy is
an option
6 Stomach
Postgastrectomy Syndromes
Postgastrectomy syndrome complications and their management
Complication Characteristics Management
197
Afferent loop
syndrome
Bile reux
Caused by long afferent limb or poor motility
of biliary limb and bacterial overgrowth (use
B12)
Partial or complete obstruction of afferent
limb/pancreatic, biliary secretions accumulate
➔Blind loop syndrome➔vitamin B12
deciency➔megaloblastic anemia
Most common after antecolic Billroth II loop
reconstructions with a long (>30cm) afferent
limb➔Retrocolic loop gastroenterostomy is
preferred
Acute: Complete mechanical obstruction; this
surgical emergency requires return to
operating room
Chronic: Partial mechanical obstruction
Diagnosis problematic: Failure to visualize
afferent limb on upper endoscopy
Reux of bile into stomach
More common after gastojejunostomy than
gastroduodenostomy
Most common after Billroth II
Diagnosed clinically or via scope or HIDA
Medium-chain triglyceride diets do not
require digestive enzymes and are more easily
absorbed; thus, they are more benecial in
situations of overgrowth than long-chain
triglyceride diets
Surgical correction
Conversion of Billroth II➔Roux-en-Y
construction or enteroenteostomy below the
stoma
Conversion to Roux-en-Y gastrojejunostomy
with a Roux limb of at least 40cm is
associated with symptomatic relief in up to
85% of patients
Distal Braun enteroenterostomy has been
shown to improve symptoms of bile reux
gastritis in 53% of patients
Efferent loop
obstruction
Usually, a diagnosis of exclusion because of
low specicity of ndings
50% in rst month postop
Symptoms: LUQ pain, biliary vomiting,
abdominal distention
Diagnosis: GI contrast study with failure of
barium to enter efferent limb
Reducing retroanastomotic hernia and
closing retroanastomotic space
198
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Postgastrectomy syndrome complications and their management
Complication Characteristics Management
L. Amodu et al.
Dumping
Marginal ulcer
Metabolic
disturbances and
anemia:
Most commonly seen after Billroth II
Distention, nausea, vomiting, abdominal pain
palpitations, and tachycardia
Early symptoms 30–60min postprandial
secondary to rapid entry of high osmotic
chyme into jejunum
Late dumping 2–3h postprandial(after
delivery of carbohydrates to small intestine)➔hyperinsulinemia➔hypoglycemia
(mediated by glucose-dependent insulinotropic peptide-1)
Result from exposure of gastric G cells to
alkaline duodenal secretions causing acid
hypersecretion (NSAIDS, ethanol, diabetes,
smoking, and steroids)
Avoid large carbohydrate-heavy meals
Minimize the consumption of liquids during
meals, decrease carbohydrate intake, eat
multiple small meals
Acarbose or octreotide
In refractory cases: Conversion of Bl
II➔Roux-en-Y reconstruction
PPI
Surgical resection for refractory or
complicated disease can involve local
resection and redo of the anastomosis, with or
without additional resection of gastric remnant
to reduce G-cell or parietal cell mass
Vagotomy can be considered if not previously
done
Use of supplements as needed (iron, vitamin
B12, fat-soluble vitamins)
Delayed gastric
emptying
Incomplete
vagotomy
Failure of
adequate drainage
Anastomotic leak Peritonitis Reoperation
Most commonly after truncal or selective
vagotomies
Result in recurrent ulceration Medical management
Result in persistent vomiting, dyspepsia and
fullness
Metoclopramide and erythromycin
Reoperation with vagotomy and antrectomy
Intractable symptoms➔reoperation
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