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
Page 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 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)
Page 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
Page 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
Page 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
Page 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
Page 7
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
Page 8
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
Page 9
Duodenal Ulcer – 1st Portion
Duodenal bulb Postbulbar
Page 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 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
Page 11
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
Page 12
Procedures
Vagotomy – eliminates cephalic phasePyloroplasty – prevents gastric atony
Page 13
Procedures
Vagotomy – eliminates cephalic phaseAntrectomy – eliminates gastric phase
Page 14
Procedures – Proximal gastric vagotomy
Divide vagal branchesTo body and fundus
Preserve antral innervation – normal solid emptying
Page 15
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
Page 16
PyloroplastyHeineke-Mikulicz
Jaboulay
Page 17
PyloroplastyFinney
Page 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%
Page 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
Page 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
Page 21
Importance of H. Pylori Eradicationin prevention of re-bleeding
Page 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
Page 23
Perforation Close the
perforation with a Graham Patch
No vagotomy
Page 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
Page 25
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
Page 26
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
Page 27
Postgastrectomy Syndromes Dumping
Dumping –
Page 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%
Page 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
Page 30
Alkaline Reflux Gastritis
Page 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
Page 32
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
Page 33
Afferent Limb syndrome
Page 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
Page 35
Surgical therapy for Afferent Loop
Page 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
Page 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
Page 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