1. James W. Maher M.D. Professor, Department of Surgery
All Things Gastric and Duodenal Gastric Cancer, Carcinoid, Lymphoma, Gastric Polyps, Gastric Ulcer, Peptic Ulcer, Gastrectomy (Partial, Total), Vagotomy and Drainage, Postgastrectomy Syndromes Foregut Grab Bag
James W. Maher M.D.
Professor, Department of Surgery

2. Key Points Most Ulcers produced by Helicobacter pylori
NSAID’s responsible for the rest
As a group, DU pts have increased H+ secretion
Therapy
PPI
Antibiotics
Hemorrhage leading cause of death
Pts w recurrent hemorrhage and greatest risk
Perforation – omental patch closure and anti-H.pylori Rx
Minimally Invasive approach becoming standard
Trauma, shock sepsis, MSOF accompanied by Stress Gastritis (the canary in the coal mine)

3. Gastroduodenal Ulcer 300,000 cases US/year
4 million people under treatment
Cause of death in 10,000 cases/year
Antibiotics are front-line treatment
Development of Ulcers balance between
Inflammatory injury
Acid-peptic secretion and
Mucosal defense
H pylori only binds to gastric mucosa
Gastric metaplasia common in duodenal ulcer
Only infection, no colonization – gastritis
H. pylori eradication – ulcer healing
Relapse of DU after antibiotics preceded by reinfection
Most common bacterial infection worldwide
20-30% USA

4. Pathogenesis Increased basal acid output
Lots of other abnormalities but acid foremost
These abnormalities are a consequence of Helicobacter
Early decrease H+, antral gastritis and then fundic inflammation
With eradication of H.pylori acid returns to normal within 4w to 6 mo.
H.pylori increases gastrin

5. Patterns of H. pylori infection
Always produces inflammation – three patterns
Mild to moderate pangastritis most common
Normal acid, asymptomatic, no ulcers
15% - antral predominant gastritis
Intense inflammation antrum, gastrin high, acid high
Duodenal and peptic ulcer common
1% corpus predominant, hypochlorhydria and gastric atrophy
Precursor for gastric cancer

6. Environmental etiologys
Cigarettes
Impairs healing and increases recurrence
Smoking attenuates effectiveness of ulcer Rx
Increases both risk of requiring surgery and risk of surgery itself
NSAIDs
Ulcers in both duodenum and stomach
Hemorrhage, superficial erosions, deeper ulcerations
Systemic suppression of prostaglandin production
Clinically important ulceration – 2 – 4% per year

7. NSAIDS Linked to Increases risk of bleeding 3x for those under 65 yoa
50 – 75% of bleeding ulcers
1/3 of deaths due to hemorrhage
30% of hospitalizations
Increases risk of bleeding 3x for those under 65 yoa
8x for people over 75 yoa
13x people with prior bleeding ulcer
Cox2 inhibitors – some improvement, not complete

8. Diagnosis Epigastric pain Usually 1st portion duodenum Upper
Burning, stabbing, gnawing
Food or antacid prompt relief
PE – WNL unless perforated
Differential Dx – broad (dyspepsia, gastric ca, gallstones, pancreatitis, pancreatic cancer)
Usually 1st portion duodenum
3rd or 4th – think gastrinoma

9. Duodenal Ulcer – 1st Portion
Duodenal bulb
Postbulbar

10. Treatment In the absence of treatment H.pylori infection is life-long
Anti-secretory drug (usually PPI) and two antibiotics (usually clarithromycin and flagyl or amoxicillin x 14 days
Eradication > 90%
Resistance approx 5%
Omeprazole mg nearly complete inhibition of acid at 6 hours.
Sucralfate – Aluminum salt of sulfated sucrose.
Adheres to ulcerated areas
binds bile salts
inhibits pepsin, stimulates mucus,
increases prostaglandin E2

11. Operative Rx of Ulcers Reserved for complications Goal
Bleeding, perforation, obstruction
No indication for uncomplicated ulcer surgery
Goal
Treat the complication
Patient safety and minimize long-term side effects of operation
70s Golden Age of Ulcer Surgery
Incidence began to drop prior to H2 blockers and PPI
The drugs sealed surgery’s fate

12. Procedures Vagotomy – eliminates cephalic phase
Pyloroplasty – prevents gastric atony

13. Procedures Vagotomy – eliminates cephalic phase
Antrectomy – eliminates gastric phase

14. Procedures – Proximal gastric vagotomy
Divide vagal branches
To body and fundus
Preserve antral innervation – normal solid emptying

15. Vagotomy Truncal Parietal cell vagotomy
Eliminates most basal acid secretion
Abolishes receptive relaxation of the fundus
Liquids empty more rapidly
Dennervates antrum
Solids empty more slowly
Parietal cell vagotomy
Preserves antral innervation
Solids empty normally

16. Pyloroplasty
Heineke-Mikulicz
Jaboulay

17. Pyloroplasty
Finney

18. Consequences of Surgery
Dumping, Diarrhea, weight loss and altered lifestyle
PGV superior to other operations in reducing these complications
Vagotomy and Antrectomy – best ulcer recurrence but highest mortality (1.5%)
Dumping 15%, disabling in 1-2%

19. Hemorrhage Leading cause of death associated with peptic ulcer
Incidence unchanged by therapy
Risk 15% at five years
Previous hemorrhage – higher risk of bleeding again
Rebleeding 20-30%
Mortality 10-40%
Risk of mortality increased by
Shock at admission, recurrent bleeding, delay in operative intervention or comorbidity

20. Hemorrhage Initial therapy – UGI Endoscopy
Active hemorrhage – arterial jet, oozing or oozing beneath clot.
Recent hemorrhage – adherent clot wo oozing, adherent slough in base or visible vessel
30% with recent hemorrhage require surgery
PPI therapy doesn’t reduce rebleed
Endoscopic control – thermal coagulation, injection of epinephrine
Reduces rebleeding and surgery

21. Importance of H. Pylori Eradication in prevention of re-bleeding

22. Three point ligation Kocherize duodenum Longitudinal duodenotomy
Bimanual Compression of Gastroduodenal a.
Simple suture above and below bleeding
Mattress suture to compress posterior artery

23. Perforation
Close the perforation with a Graham Patch
No vagotomy

24. Obstruction Edema and inflammation in pyloric channel and duodenum
Sx – recurrent vomiting, dehydration, hypochloremic alkalosis
Tx – nasogastric suction, rehydration, iv PPI – most will resolve wi 72 hrs
Hydrostatic balloon dilatation – successful 85%
40% sustained
Some use antrectomy
IMHO – overkill
Pyloroplasty more than sufficient

25. Gastric ulcer Peptic ulcer Etiology H. pylori – treatment same
Less common than DU
Older patients
Ulcer base smooth and flat, gray exudate
Margin slightly raised and friable
Differentiation from Cancer – endoscopy
All multiple biopsies and brushings
95% accuracy
60% lesser curve proximal to incisura
<10% greater curve
All within 2 cm of antral-body junction
Etiology H. pylori – treatment same
Recurrence implies re-infection

26. Gastric Ulcer Strong association with NSAID’s Rx and cigarettes
Antimicrobial treatment
Surgery – hemorrhage, perforation, failure to heal, ? Malignancy
Distal gastrectomy with Billroth I anastamosis
Include ulcer in specimen
2-3% mortality
No vagotomy necessary
Near GE junction – resect ulcer if possible, extend margin to include ulcer
Vagotomy and pyloroplasty with ulcer excision also works

27. Postgastrectomy Syndromes
Dumping
Dumping –

28. Postgastrectomy Syndromes
Dumping
Dumping –
postprandial abdominal discomfort,
weakness
sweating
dizziness
borborygmi
Palpitations
Late- dizziness or syncope d/t late dumping (1-3 Hours pc)
occurs in 10% to 15% of patients with truncal vagotomy and antrectomy
Disabling in 1-2%

29. Postgastrectomy Syndromes
Etiology – rapid emptying of hyperosmolar meal into small bowel draws fluid into sm bowel
Sx are hypovolemia
Treatment
Avoid hyperosmolar liquids
Don’t drink 1-2 hours postprandial
Somatostatin analogue – administered before meal

30. Alkaline Reflux Gastritis

31. Alkaline Reflux Gastritis
Constant epigastric pain, nausea and vomiting of bile
No relief with vomiting
All gastrectomy patients have bile reflux and gastritis but 1-2% have pain so it’s a clinical diagnosis for the most part
Differential – recurrent ulcer, afferent loop obstruction, esophagitis, biliary or pancreatic disease
Serum gastrin to r/o ZE
Endo – r/o recurrent ulcer

32. Alkaline Reflux Gastritis
Ursodeoxycholic acid – replaces bile salts over 6-8 weeks some relief
Roux-Y biliary diversion with cm alimentary limb
Nearly 100% effective
20-40% terrible gastric atony
d/t disruption of pacesetter potential and alimentary limb dysrrhthmias
Some need total or near-total gastrectomy which is only 50% effective

33. Afferent Limb syndrome

34. Afferent Limb syndrome
30-45’ crescendo postprandial cramping pain
relieved by projectile bilious emesis without food
Weight loss d/t “food fear”
Roux Y or uncut Roux Y

35. Surgical therapy for Afferent Loop

36. Stress gastritis
Common with Burns, Trauma, MSOF, ARDS, SIRS, “DaNang Lung”, abdominal sepsis, Cushings ulcers
Superficial ulcerations – proximal stomach
Progressive during first 72 hours post-injury
Mucosal ischemia
Major manifestation is hemorrhage
Control of pH – if above 3.5 can effectively prevent this
H2 blockers, PPI or Antacids
Very few need surgery but if they do – total gastrectomy

37. Gastric Cancer Geographic variability
Japan and China, Central and S America, Eastern Europe and Middle East
2nd leading cause of cancer death world wide
Reductions - ? Improvement in refrigeration and reduced intake of pickled, smoked and chemically preserved food
Males > females
Peak 7th decade
Ranks 13th as cause of death USA
Poor survival – 23% 5 year
Advanced stage
IA 78%, IB 58%, II 34%, IIIA 20%, IIIB 8%, IV 7%
Site shifting proximal – now 52% proximal

38. Gastric Cancer Histologic
Intestinal – distal stomach, associated with atrophic gastritis and nitrates
Glandlike structures
Develops in H. pylori + patients
Diffuse – younger patients, no precursor, any part of the stomach, cells infiltrate and thicken stomach wo discrete ulcer. Worse prognosis
Familial diffuse gastric cancer
average age of 38 years
autosomal dominant with 70% penetrance