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
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All Things Gastric and Duodenal Gastric Cancer, Carcinoid, Lymphoma, Gastric Polyps, Gastric Ulcer, Peptic Ulcer, Gastrectomy (Partial, Total), Vagotomy.
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(Partial, Total), Vagotomy and Drainage, Postgastrectomy Syndromes
Foregut Grab BagJames W. Maher M.D.Professor, Department of Surgery
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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 elderly @ 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)
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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
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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
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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
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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
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NSAIDS Linked to
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
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Diagnosis Epigastric pain
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
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Duodenal Ulcer – 1st Portion
Duodenal bulb Postbulbar
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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 20-30 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
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Operative Rx of Ulcers Reserved for complications
Bleeding, perforation, obstruction No indication for uncomplicated ulcer surgery
Goal1. Treat the complication
2. 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
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
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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
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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