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The Problem. 300,000 new peptic ulcer cases per year in the US4M are on some treatment for PUDAttributable mortality as high as 10,000 / yAcute perforation in 5-10%; median age 40-55y (18-90)Long-standing clinical history of PUD in 60-75% even w. symptoms < 3 mo (
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1. Perforated Duodenal Ulcer:Acid Reduction Surgery Still Has a Role
Thomas Genuit, MD, MBA, FACS
Sinai Hospital of Baltimore
2. The Problem 300,000 new peptic ulcer cases per year in the US
4M are on some treatment for PUD
Attributable mortality as high as 10,000 / y
Acute perforation in 5-10%; median age 40-55y (18-90)
Long-standing clinical history of PUD in 60-75%even w. symptoms < 3 mo (acute ulcers) 30-35% have changes c/w. chronic ulceration (i.e. scarring)
3. Goals of Treatment / Operation Treat the complication [perforation] effectively / safely
Alter the ulcer diathesis - accelerate healing - minimize recurrence
Provide freedom of undesirable chronic side effects
Be cost effective
4. Acid-secretion & defects in mucosal defense are crucial in DU Increased capacity for gastric acid secretion (BAO, MAO); prolonged acid output after stimulation
Accelerated gastric emptying & reduced feedback = increased duodenal acid exposure
Lower basal HCO3 secretion & response to acid exposure
HP & antral gastritis in 70 to > 80% of DU patients; HP also found in gastric metaplasia surrounding ulcers
Other risk factors (NSAIDS, ETOH, Smoking) in -> 55 %
5. HP works through hyperchlorhydria Earliest stages of HP colonization = decreased acid output;chronically HP causes increased acid output
HP causes increase in basal gastrin levels and gastrin response to mixed meal stimulation
HP produces N?-methylhistamine, a histamine analogue
HP decreases mucosal PGE2 and somatostatin production (diminished duodenal HCO3 production & mucosal defense)
6. Perforated Ulcer: What type of acid-reduction? Truncal Vagotomy + Antrectomy vs. Pyloroplasty
Posterior [truncal] Vagotomy + anterior Seromyotomy
Proximal Gastric Vagotomy +/- Pyloroplasty
[Highly] Selective Vagotomy: transection vs. chemical
Medical therapy: H2B vs. PPI alone vs. HP eradication + PPI (gastrin inhibitors, sucralfate, PGE2 analogues, )
7. Acid reduction surgery works
8. Yet what do we do today ? > 80% of operations for perforated DU in US: primary closure or Graham patch +/- ulcer biopsy or resection + post-op PPI therapy alone for variable duration +/- HP testing and/or therapy
Short- results are encouraging > 80-90% ulcer healing in some seriesunless high risk patient (malnutrition, large ulcer, shock, )
9. Problems with closure alone Satisfactory long-term results in < 30%
> 2/3 develop recurrent DU symptoms
45 50% develop recurrent ulcer complicationand/or need additional operation(s)
10. Problems with med. acid reduction H2B alone: < 80% ulcer healing at 4-6 wks in uncomplicated DU -> 60% short-term ulcer recurrence after cessation
PPI -> 100% initial healing uncomplicated DU; also suppress growth of HP; -> 45% short-term ulcer recurrence
Initially both thought to have minimal side effects PPI long-term: ? B12 absorption / anemia (8-15%) ? Ca absorption / ? fracture risk older females ? C. difficile colitis risk (5-10%) ? Increased risk of asp. Pneumonia
COST: $800 2000 /y for PPI - $ 200- 600 /y for H2B; Insurers shifting reimbursement to patient w. OTC PPIs available
11. Problems w. HP eradication 60-80 % initial success w. triple or quadruple Tx (> 20% initial eradication failure rate under best circumstances )
Relapse rates from 15 - 25% after 18-24 months (inadequate long-term follow-up in past 10 y studies)
Ulcer recurrence 10-20% with therapy compliance >30% with non-completion of therapy or primary failure70% with no initial therapy or [rapid] HP recurrence
Emerging primary resistance of HP: 5-10%
12. Problems with HP eradication Majority of patients w. perorated DU had Sx of chronic DU [under-treated, treatment failure?] prone to ? recurrence
Not well defined who needs long-term H2B or PPI therapy(cost $ 500 2000/y)
Not well defined what to do with HP eradication failures(re-treatment ?, frequency of surveillance ?)
13. Problems w. Acid-reduction Surgery Still taught as standard of care [textbooks], but
Surgeons no longer [routinely] treat ulcer disease- lack of expertise with gastric surgery / vagotomy among surgeons likely to encounter perforated ulcer- lack of [long-term] follow-up
Wide-spread acceptance of Medical adjunct therapy: - lack of good quality [US] studies comparing [newer] operative approaches w. medical therapy in the last decade
14. For the past decade its all around us
15. Perforated Ulcer Surgery considerations: Predictors of morbidity / mortality (for more extensive surgery)- age > 65-70- [multiple] co-morbid conditions- perforation > 12-24 h; severe [purulent] peritonitis- shock at presentation; need for ICU post-op- resection vs. closure or drainage
In patients w/o. significant operative risk factors,acid reduction component can be added w/o. increase in short-term morbidity and mortality
16. Patients who should be considered for Acid-reduction Surgery < 65- 70 years of age
Difficult to alter risk factors (NSAIDS, Smoking, ETOH, ) /patients that are likely to be non-compliant
Patients with healthcare access problems
Patients with long standing / therapy refractive or complicated ulcer disease pre-op
17. Summary If a chronic duodenal ulcer perforates, the choice of operation will depend on the patients condition
The patient without contraindication to a definitive operation should have PGV in addition to an omental patch closure. The addition of this procedure [ in experienced hands ] does not change the operative mortality in properly selected patients, does not cause the gastrointestinal sequelae associated with TV & P or A, and has a low rate of ulcer recurrence.
D. Feliciano. Do perforated duodenal ulcers need an acid-decreasing surgical procedure now that Omeprazole is available? Surg Clin N Am 1992.72920;369-80