STOMACH AND DUODENUM

BENIGN GASTRIC ULCER

Modified Johnson Classification:
TYPE I: incisura or lesser curvature; most
common benign gastric ulcer; not acid-
hypersecretor
BENIGN GASTRIC ULCER
Modified Johnson Classification:
TYPE II: body of stomach, incisura +
duodenal ulcer (active or healed); acid
hypersecretor
BENIGN GASTRIC ULCER
Modified Johnson Classification:
TYPE III: prepyloric; acid hypersecretor
BENIGN GASTRIC ULCER
Modified Johnson Classification:
TYPE IV: uncommon (5%); high on lesser
curvature, near GE junction; not acid-
hypersecretor
BENIGN GASTRIC ULCER
Modified Johnson Classification:
TYPE V: anywhere; medication-induced;
not acid-hypersecretor
BENIGN GASTRIC ULCER
GIANT GASTRIC ULCER:
 Ulcer larger than 3 cm.
 Increased rate of malignancy (30%)
BENIGN GASTRIC ULCER
 The initial approach to a patient with a
benign gastric ulcer should be medical
therapy.
 Treatment with either an H2-receptor
antagonist, proton pump inhibitor, or
double antibiotic and proton pump
inhibitor regimen for H. pylori.
BENIGN GASTRIC ULCER
 With effective medical therapy, most
uncomplicated ulcers will heal within 12
weeks.
 A change of medication with additional
12-week observation before ulcer is
declared refractory to medical therapy.
BENIGN GASTRIC ULCER
Indications for surgical therapy:
 Hemorrhage
 Perforation
 Obstruction
 Intractabilily
DUODENAL ULCER
 First documented case of perforated PUD
– 167 B.C.

 1892 – first successful operation for

perforated gastric ulcer (Ludwig Huesner of
Wuppertal, Germany)

 1894 – first successful operation for

perforated duodenal ulcer (Henry Percy
Dean, London)
DUODENAL ULCER
 Early 1970’s – antacids; NSAIDs
 1974 – H2-receptor antagonist
 1982 – proton pump inhibitors
 1982 – H. pylori identified (Warren and
Marshall)

Frequency: M = F
Duodenal ulcer younger than gastric ulcer.
DUODENAL ULCER
Etiology:
 Helicobacter pylori
◦ approximately 90% of duodenal ulcers and 80% of
gastric ulcers are associated with H. pylori
infection.
 Hyperacidity and duodenal defense
 Non-steroidal anti-inflammatory drugs
◦ daily use of NSAIDs increases the risk of ulcer
disease by 10- to 20-fold, and they are now the
second most common cause of PUD.
◦ Mechanism: topical damage to mucosal barrier;
reduction in mucosal prostaglandins
DUODENAL ULCER
Pathophysiology:
◦ first portion of duodenum (1-2 cm of pyloric
sphincter)
◦ anterior vs. posterior wall – equal frequency
◦ rarely malignant
◦ other ulcer location, consider: Zollinger-
Ellison syndrome, drug-induced ulcers,
malignancy, or Crohn’s disease
DUODENAL ULCER
Signs & symptoms:
◦ gnawing or burning epigastric pain
◦ nausea, vomiting, anorexia, anemia
DUODENAL ULCER
Diagnostic Studies:
 Endoscopy
◦ provides access for biopsy
 Radiology - UGIS
 Gastric analysis
◦ normal BAO = 2 mEq acid/hr
◦ duodenal ulcer = 4 mEq/hr
◦ Z-E syndrome = 10 mEq/hr
◦ vagotomy alone – 50% dec. in MAO
◦ antrectomy alone – 40% dec. in MAO
◦ vagotomy + antrectomy – 90% dec. in MAO
◦ Note: abstain from H2-receptor antagonists 48 hrs. or
from PPIs 5 days prior to gastric analysis.
DUODENAL ULCER
Diagnostic Studies:
 Serum gastrin
◦ normal = 100 pg/ml
 H. pylori detection
◦ serologic test
◦ urea breath test
◦ histologic test
◦ rapid urease test
◦ culture
DUODENAL ULCER
Treatment:
Medical:
 Antisecretory agents
◦ Histamine H2-receptor antagonists
(cimetidine, ranitidine, famotidine, nizatidine)
◦ Proton-pump inhibitors (omeprazole,
lansoprazole, esomeprazole)
 DUODENAL ULCER
Treatment:
Medical:
 Antibiotics:
◦ Omeprazole 40 mg/d + clarithromycin 500 mg TID x 2 wks, then
omeprazole 20 mg/d x 2 wks
◦ Ranitidine bismuth citrate (RBC) 400 mg BID + clarithromycin 500
mg TID x 2 wks, then RBC 400 mg BID x 2 wks
◦ Bismuth salicylate 525 mg QID + metronidazole 250 mg QID +
tetracycline 500 mg QID x 2 wks, then H2-receptor antagonist AD x
4 wks
◦ Lansoprazole 30 mg BID + amoxicillin 1 g BID + clarithromycin 500
mg TID x 10 days
◦ Lansoprozole 30 mg TID + amoxicillin 1 g TID x 2 wks
◦ RBC 400 mg BID + clarithromycin 500 mg BID x 2 wks, then RBC
400 mg BID x 2 wks
◦ Omeprazole 20 mg BID + clarithromycin 500 mg BID + amoxicillin
1 g BID x 10 days
◦ Lansoprazole 30 mg BID + clarithromycin 500 mg BID + amoxicillin
1 g BID x 10 days
 DUODENAL ULCER
Treatment:
Medical:
 Protective barrier drugs
◦ Sucralfate – act by coating and forming
protective barrier

 Prostaglandins
◦ PGE1 - misoprostol
Indications for surgical therapy:
 Hemorrhage
 Perforation
 Obstruction
 Intractabilily
SURGICAL THERAPY: (Elective)
ULCER TYPE OPERATION
TYPE I Distal gastrectomy w/ Billroth I
TYPES II & III Antrectomy, BTV, Billroth II or
Billroth I
Parietal cell vagotomy w/ ulcer
excision
TYPE IV Ulcers 2-5 cm from cardia: Pauchet,
Shoemaker procedure (distal
gastrectomy w/ extension along lesser
curvature & Billroth I)
Less than 2 cm from GEJ: Csendes’
procedure (tounge-like resection to
lesser curvature + Roux-en-Y
reconstruction)
SURGICAL THERAPY: (Emergent)
HEMORRHAGE:
Forrest Classification
CLASSIFICATION REBLEEDING
RATE
GRADE Ia: active, pulsatile bleeding High (50-80%)
GRADE Ib: active, non-pulsatile bleeding Low
GRADE IIa: non-bleeding, visible vessel High (50-80%)
GRADE IIb: adherent clot Low
GRADE III: no signs of recent bleeding Low
(hematemesis / melena in the past 48
hours)
SURGICAL THERAPY: (Emergent)
HEMORRHAGE:
 Risk of initial hemorrhage in patient w/ H.
pylori – 1% per year
 Mortality w/ bleeding gastric ulcer – 10%
 Re-bleeding risk for non-arterial hemorrhage
from gastric ulcer – 10% - 53%
 Over 75% of patients with bleeding duodenal
ulcers will be treated successfully by non-
operative therapy.
SURGICAL THERAPY: (Emergent)
HEMORRHAGE:
 Indications for surgery:
◦ Massive blood loss with shock
◦ Chronic or repeated hemorrhage exceeding 6 units
of blood over 24-hour period
◦ Recurrent hemorrhage during a course of non-
operative therapy
◦ Repeat hospitalization for bleeding
SURGICAL THERAPY: (Emergent)
PERFORATION:
 Presents as acute abdomen
 Marked involuntary
guarding and rebound
tenderness
 Pneumoperitoneum – 80%
of patients in upright CXR
SURGICAL THERAPY: (Emergent)
OBSTRUCTION:
 Pyloroduodenal inflammation & edema
 Abdominal pain, nausea, vomitting
 Succusion splash, barium study, saline-load test
 May resolve NGT suction & anti-ulcer therapy
Clinical results of surgery for duodenal
ulcer:
Complication PCV TV, pyloroplasty TV, antrectomy
Operative mortality (%) 0 <1 1
Ulcer recurrence (%) 5-15 5-15 <2
Dumping syndrome (%)
Mild <5 10 10-15
Severe 0 1 1-2
Diarrhea (%)
Mild <5 25 20
Severe 0 2 1-2
Indications & procedures in duodenal ulcer
surgery:
Indication Procedure of Choice
Bleeding (Acute) TV w/ pyloroplasty & oversewing of ulcer
Bleeding (Chronic) Truncal vagotomy & antrectomy
Obstruction Truncal vagotomy & antrectomy
Perforation Plication w/ omental patch closure + PGV
Intractability Proximal gastric vagotomy
Complications:
 Ulcer recurrence
 Dumping syndrome
 Gastroparesis
 Post-vagotomy diarrhea
 ZOLLINGER-ELLISON
SYNDROME
 1955, Robert Zollinger & Edwin Ellison
 Gastrinoma  gastrin: acid hypersecretion &
peptic ulceration
 Incidence: 0.2 to 2 / million population
 Genetic alterations: p16/MST1, Her-2-Neu
mutation
 ¾ sporadic; ¼ MEN 1 syndrome
 ½ have solitary tumors
 ZOLLINGER-ELLISON
SYNDROME
 Multiple tumors more common with MEN 1
 50% metastasize to lymph nodes or liver
 Clinical presentation:
◦ Abdominal pain
◦ Peptic ulcer disease
◦ Severe esophagitis
 Serum gastrin level >1,000 pg/ml
 Secretin stimulation test
Aspects of Peptic Ulcer Disease That Raise Suspicion for Zollinger-
Ellison Syndrome
1. Ulcers in atypical locations, e.g., distal duodenum or jejunum
2. Multiple ulcers
3. Ulcers that fail to respond to conventional treatment
4. Ulcers that recur after conventional treatment
5. Peptic ulcer disease in association with diarrhea
6. Ulcers in association with hyperparathyroidism
Conditions other than Z-E Syndrome Associated with Elevated
Gastrin Levels
1. Pernicious anemia
2. Treatment with proton pump inhibitors
3. Renal failure
4. G-cell hyperplasia
5. Atrophic gastritis
6. Retained or excluded antrum
Gastric outlet obstruction
 ZOLLINGER-ELLISON
SYNDROME
TUMOR LOCALIZATION:
 70-90% in Passaro’s triangle
◦ Junction of cystic & CBD
◦ 2nd & 3rd portion of duodenum
◦ Neck & body of pancreas
 Test of choice: somatostatin receptor
scintigraphy combined with CT
◦ More sensitive than CT
◦ Locate 85% of gastrinomas
◦ Detects tumors <1cm
 Endoscopic ultrasound (EUS)
 ZOLLINGER-ELLISON
SYNDROME
TREATMENT:
 Proton pump inhibitors
 Most gastrinomas are malignant 
exploration, removal of tumor
 Suspicious portal, perigastric, or celiac LN
biopsied
 Inoperable disease: chemotherapy w/
streptozocin, doxorubicin, & 5-FU
 ZOLLINGER-ELLISON
SYNDROME
PROGNOSIS:
 Histology is not a reliable method for
predicting whether the tumor is malignant;
only the presence of LN or liver metastases
proves the malignant nature of these
disease.
 ZOLLINGER-ELLISON
SYNDROME
PROGNOSIS:
 Without liver metastases: 80% 15-yr survival
rate
 With liver metastases: 20%-50% 5-yr survival
rate
 In gastrinomas, liver metastases decreases
survival rates, but lymph node metastases
donot.
 MALLORY-WEISS
SYNDROME
 1929, G. Kenneth Mallory & Soma Weiss
 5%-15% as cause of UGIB
 M:F = 2-7:1; 39-62 y/o
 Common factor: increased abdominal
pressure
◦ Retching, vomiting
◦ Hiatal hernia
 MALLORY-WEISS
SYNDROME
Diagnosis:
 Hematemesis (80%-90%)
 Melena (10%)
 Triad: (30%-80%) retching & vomiting
followed by hematemesis
 50% have no history of vomiting/hematemesis
 25% have no identifiable risk factor
 Hemodynamic instability & shock (10%)
 MALLORY-WEISS
SYNDROME
Diagnosis:
 Current standard for evaluation: flexible
endoscopy
◦ Linear ulcerations of the mucosa
 Gastric cardia
 GE junction
 Distal esophagus
 Water-soluble contrast radiography
 Tagged RBC scanning & selective mesenteric
arteriography
 MALLORY-WEISS
SYNDROME
Management:
 90% are self-limited
 Endoscopic therapy
◦ Injection therapy
◦ Multifocal electrocoagulation (MPEC)
◦ Band ligation
◦ Hemoclipping
 Interventional radiology
◦ Intraarterial infusion of vasopressin
◦ Trans-catheter embolization
◦ Sengstaken-Blakemore tube (use is controvertial)
 MALLORY-WEISS
SYNDROME
Management:
 Factors associated with recurrent
hemorrhage & poor outcome from
conservative therapy:
◦ Bleeding at endoscopy
◦ Initial hematocrit <30%
◦ Presence of non-bleeding visible vessel
◦ Coagulopathy
◦ Presence of liver dysfunction
 MALLORY-WEISS
SYNDROME
Management:
 Surgery
◦ Oversewing the tear

Outcome:
 Rebleeding – 10%
 Overall mortality - <1.5%
BENIGN GASTRIC TUMORS
 Uncommon
 5% to 10% of all tumors of stomach
 Arise from:
◦ Mucosa
◦ Submucosa
◦ Muscle layer
BENIGN GASTRIC TUMORS
Leiomyomas
 Most common
 Develop in antrum, pylorus, or distal
stomach
 Asymptomatic
 Endoscopy or contrast study: smooth,
well-circumscribed
 Bleed from central ulcerations & mucosal
sloughing
 Treatment: excision
BENIGN GASTRIC TUMORS
Leiomyomas
Gastric polyps
Fibromas, fibromyomas
Neurogenic tumors
Ectopic pancreas
Lipomas
Vascular tumors
GASTRIC ADENOCARCINOMA
 2ndor 3rd most common cancer globally
 75-100/100,000 men in Korea, Japan, South &
Central America
 8-15/100,000 men in US, Western Europe
 95% of all gastric cancers
 Most were found in antrum
 More common along lesser curvature than
greater curveture
 10% involve entire stomach (linitis plastica)
GASTRIC ADENOCARCINOMA
Risk factors:
 Diets high in salt, cured & smoked foods
 Diets low in fresh fruits & vegetables,
antioxidants
 Smoking, alcohol (less clear)
 Low socio-economic status; metal, miners,
rubber workers
 Infection with H. pylori
 Epstein Barr virus
 Pernicious anemia
GASTRIC ADENOCARCINOMA
Risk factors:
 Chronic atrophic gastritis
 Intestinal metaplasia
 Gastric villous adenomas
 Operations for benign peptic ulcers
 Heritable risk
◦ HNPCC
◦ E-cadherin mutations
 Usually aggressive & metastasizes early via both
lymphatic & hematogenous routes.
GASTRIC ADENOCARCINOMA
GASTRIC ADENOCARCINOMA
Borrman’s classification
 Type I – fungating
 Type II – ulcerating
 Type III – combined ulcerating and polypoid
 Type IV – infiltrating
 Type V – superficial spreading carcinoma
GASTRIC ADENOCARCINOMA
Laureen classification
INTESTINAL TYPE DIFFUSE TYPE
Glandular Invasive growth pattern
Arise from gastric mucosa Arise from lamina propria,
transmural extension through
lymphatic invasion
Older patients Younger patients
More common in distal stomach More common in proximal
stomach
Associated w/ H. pylori infection
Chronic atrophic gastritis
Intestinal metaplasia
GASTRIC ADENOCARCINOMA
Clinical presentation:
 Abdominal pain & weight loss
 Anemia secondary to blood loss
 Dysphagia
 Nausea, vomiting, symptoms of GOO
 Early satiety (w/ linitis plastica)
 Palpable mass
 Signs of metastasis:
◦ Blummer’s shelf tumors
◦ Krukenberg tumors
◦ Sister Mary Joseph’s node
◦ Virchow’s node
GASTRIC ADENOCARCINOMA
Diagnosis:
 UGI endoscopy w/ biopsy – modality of
choice
 Endoscopic ultrasound (EUS)
 CT scan of abdomen & pelvis
 Laparoscopic ultrasound
 Cytologic analysis of peritoneal washings
 AJCC/UICC Staging System
GASTRIC ADENOCARCINOMA
Surgical Treatment:
 Wide resection (6 cm. gross margin), en bloc
resection of lymph nodes & any adherent
organs
◦ Total gastrectomy
◦ Distal subtotal gastrectomy
GASTRIC ADENOCARCINOMA
Surgical Treatment:
 Reconstruction after gastrectomy
◦ Gastroduodenostomy (Billroth I)
◦ Gastrojejunostomy (Billroth II)
◦ Roux-en-Y reconstruction
 Gastrojejunostomy
 Esophagojejunostomy
GASTRIC ADENOCARCINOMA
Surgical Treatment:
GASTRIC ADENOCARCINOMA
Surgical Treatment:
GASTRIC ADENOCARCINOMA
Lymphadenectomy:
 D1 dissection
◦ Perigastric lymph nodes
 D2 dissection
◦ Along hepatic, left gastric, celiac & splenic aa.
◦ Splenic hilum
◦ Perigastric LN greater than 3 cm from primary
tumor
 D3 dissection
◦ Along porta hepatis, retropancreatic & peri-
aortic regions
GASTRIC ADENOCARCINOMA
Lymphadenectomy:
 For an adequate curative resection, it is
recommended that the level of dissection be one
level greater than the highest echelon of lymph
node involved.
GASTRIC ADENOCARCINOMA
Lymphadenectomy:
GASTRIC ADENOCARCINOMA
Adjuvant therapy:
 Chemotherapy
◦ Not recommended because of disappointing
results
 Adjuvant intra-peritoneal therapy
◦ Mitomycin, 5-FU
 Adjuvant chemo-radiotherapy
◦ Considered standard of care for curatively
resected patients
◦ 5-FU, folinic acid, 45 Gy XRT
GASTRIC ADENOCARCINOMA
Neoadjuvant therapy:
 Neoadjuvant chemotherapy
◦ Improved patient tolerance
◦ Early initiation of systemic therapy
◦ Potential downstaging of primary tumor
◦ Evaluation of response to therapy
◦ Combination of etoposide, cisplatinum, & 5-FU or
doxorubicin
◦ Randomized prospective trial needed before
recommendation.
GASTRIC ADENOCARCINOMA
Neoadjuvant therapy:
 Pre-operative chemo-radiotherapy
◦ On-going trials with 5-FU, folinic acid, & cisplatin
followed by 5-FU potentiated 45 Gy XRT
◦ Safe, rate of complete pathologic responses 20%
◦ Awaits long-term survival data
◦ Need larger randomized trials
 GASTROINTESTINAL
STROMAL TUMORS
 Most common sarcoma of the alimentary tract
 1% of all GI neoplasms
 Originate from intestinal cell of Cajal
 Median age: 60 yrs.; slight male predominance
 Arise at:
◦ Stomach (65%)
◦ Small intestine (25%)
◦ colon, rectum, esophagus
◦ Mesentery, omentum, retroperitoneum
 GASTROINTESTINAL
STROMAL TUMORS
Clinical presentation
 Asymptomatic
 Displacement of adjacent organs
 Vague abdominal discomfort
 Bleeding (25%)
 Rupture into peritoneal cavity
 Obstruction from tumor – rare
 Lead point of intussusception
 GASTROINTESTINAL
STROMAL TUMORS
Diagnosis:
 CT scan of pelvis & abdomen
 Chest x-ray
 Pre-operative percutaneous biopsy
◦ Not recommended – highly vascular & friable
◦ Tumor rupture, hemorrhage, tumor
dissemination
 H-E staining
 KIT receptor tyrosine kinase protein
 GASTROINTESTINAL
STROMAL TUMORS
Treatment:
 Primary GIST
◦ Without metastasis – surgical resection (1-2 cm
margin)
◦ Lymphadenectomy not indicated – rarely
metastasize to LN
◦ Predictors of outcome:
 Tumor size (most important predictor)
 Mitotic rate
 Tumor location
 GASTROINTESTINAL
STROMAL TUMORS
Treatment:
 Primary GIST
◦ Majority develop recurrence after resection
◦ STI571 – effective in eradicating or stabilizing
occult, residual, microscopic disease
 Approved by USFDA only for patients w/ metastatic or
recurrent GIST
 GASTROINTESTINAL
STROMAL TUMORS
Recurrent GIST
 Median time after resection: 2 yrs
 Peritoneum, liver, or both
 Distant metastasis: lung, bone
 Initially treated w/ STI571
◦ 60% partial response
◦ Complete response – rare
 Progression of disease: chemotherapy
 Radiation therapy rarely indicated
 Hepatic artery embolization: tumor confined
to liver
 GASTRIC LYMPHOMAS
 Stomach – most common site of GI
lymphomas
 5% of all gastric malignancies
 95% are non-Hodgkin’s type
 Mucosa-associated lymphoid tissue
(MALT)
 Response to chronic infection
 GASTRIC LYMPHOMAS
Treatment:
 Low-grade:
◦ Antibiotic irradication of H. pylori
 High grade:
◦ Primary chemotherapy & radiation
 Comp: bleeding, perforation
◦ Radical subtotal gastrectomy