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 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

PPI The drugs sealed surgery’s fate

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Procedures

Vagotomy – eliminates cephalic phasePyloroplasty – prevents gastric atony

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Procedures

Vagotomy – eliminates cephalic phaseAntrectomy – eliminates gastric phase

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Procedures – Proximal gastric vagotomy

Divide vagal branchesTo body and fundus

Preserve antral innervation – normal solid emptying

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Vagotomy Truncal

Eliminates most basal acid secretion Abolishes receptive relaxation of the fundus

Liquids empty more rapidly Dennervates antrum

Solids empty more slowly

Parietal cell vagotomy Eliminates most basal acid secretion Abolishes receptive relaxation of the fundus Preserves antral innervation

Solids empty normally

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PyloroplastyHeineke-Mikulicz

Jaboulay

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PyloroplastyFinney

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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%

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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

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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

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Importance of H. Pylori Eradicationin prevention of re-bleeding

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Three point ligation Kocherize duodenum Longitudinal

duodenotomy Bimanual

Compression of Gastroduodenal a.

Simple suture above and below bleeding

Mattress suture to compress posterior artery

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Perforation Close the

perforation with a Graham Patch

No vagotomy

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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

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Gastric ulcer Peptic ulcer

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

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Gastric Ulcer Strong association with NSAID’s

and cigarettes Rx

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

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Postgastrectomy Syndromes Dumping

Dumping –

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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%

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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

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Alkaline Reflux Gastritis

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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

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Alkaline Reflux Gastritis Ursodeoxycholic acid – replaces bile salts

over 6-8 weeks some relief Roux-Y biliary diversion with 50-60 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

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Afferent Limb syndrome

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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

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Surgical therapy for Afferent Loop

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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

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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