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Gecompliceerd Ulcuslijden Bloedingen en Perforaties H.W. Tilanus 31 Januari 2006, Delft
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“If Anyone should consider removing half of my stomach to cure a small ulcer in my duodenum I would run faster than he” Charles E. Mayo, 1927
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History of Vagal Pioneers Ivan Pavlov : acid secretion in dogs (1904) Andre Latarjet : vagotomy inhibits emptying (1921) Lester Dragstedt : vagotomy and pyloroplasty (1945) Farmer and Smith : recurrence after VT+A: < 16%(1952)
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Ivan Petrovic Pavlov Surgical diversion of the esophagus of the dog Production of 700 ml “gastric juice” after sham feeding Dramatically reduced after bilateral vagotomy Production restored after electric vagal stimulation “The effect of feeding is transmitted by nervous channels to the gastric glands” Pavlov IP. The work of the digestive glands London, Griffin 1902,48
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Ivan Pavlov (1849-1936) performing an experimental vagotomy
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Andre Latarjet (1876-1947) First human vagotomy 1921 All extrinsic nerves to stomach and duodenum severed 24 patients presented to the “Academy de Chirurgie” Delayed gastric emptying Failed to gain widespread support By 1940 fewer than 100 operations performed Latarjet A.: Bull Acad Natl Med 1922;87:681
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Stomach surgery in the Netherlands.1908
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Predominance of “Gastrectomists” Billroth, von Eiselsberg, Moynihan advocated resection Diminished interest in vagotomy Resection controls the ‘three factors in ulcerogenesis’: 1: the specific ulcer gastritis 2: existence of free hydrochloric acid in stomach 3: secondary infection with green streptococcus Vagotomy “was not practiced for the next 20 years” Klein E. Ann Surg 1929; 90:65 Berg A. Ann Surg 1930; 92:340
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1881: Billroth performing a stomach resection (A.Seligmann)
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von Eiselsberg at work in University Hospital, Utrecht 1898
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Lester Reynolds Dragstedt 1893-1975 Born 22 october 1893 Modest background and minimal education. Rose to the pinnacle of American surgery and science Internationally known for research on gastric physiology Introduced vagotomy as safe procedure for peptic ulcer disease. Honored by numerous national and international surgical societies. Loved by his patients and students.
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Lester Dragstedt (l) with brother Carl in 1918
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Dragstedt’s first vagotomies Abnormally secretion at night during empty stomach Neural stimulation causes increased output of juice: Fasting hypersecretion by neural or ‘hormonal’ stimulation Hormone: gastric secretine or gastrine First vagotomy in 35 year old patient refusing resection Followed by 200 thoracic vagotomies in next 4 years ‘Gastrostasis’ only ‘temporary’ Dragsted L Owens F Proc Soc Exp Biol Med 1943;53:152 Dragsted L Ann Surg 1947; 126:687
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Dragsted LR, Am J Surg 1974;128:344
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Vagotomy and hemigastrectomy Farmer and Smith (1952): Vagotomy with hemigastrectomy superior. 93% gastric pH < 3.5 Farmer and Smith N Engl J Med 1952:247:1071 Edwards and Herrington (1953): 200 vagotomies with 40% gastrectomy Excellent results in 93.4% Edwards LW and Herrington JL Ann Surg 1953:137;873
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Refinements in Vagotomy Single layer pyloroplasty (n=500) Weinberg et al, Am J Surg 1956;92:202 More selective vagotomy Griffith C et al, Gastroenterology 1957;32: Parietal cell vagotomy Holle F, Hart W, Med Clin, 1967;62:441 Maintaining the antral innervation Johnston D et al’ Br.J Surg 1969;69:626 Superficial seromyotomy, truncal left vagotomy (Taylor II) Taylor T, Br J Surg, 1979;66:733
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Various teDevelopment of vagotomy 1814-1979of the
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Etiology of ulcer perforation Smokers have 3 fold higher mortality Doll R et al. Br Med J,1994;309:901 Accounts for perforation in >70% in patients <70 yrs Svanes C et al.Gut,1997;41:177 NSAID’s contributes one-fifth to one-third to perforations Svanes C et al. 1996; Major role of H.pylori in perforations not confirmed Reinbach DH et al, Gut,1993;34:1344
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Incidence of Perforated Ulcer Disease Rare during 19th century Sharp increase at turn of twentieth century Since then epidemic of duodenal perforations is waning In men: increase until 1950 and declined thereafter In women: slow increase after 1950 Increasing age among ulcer perforation patients Svanes C et al.,Am J Epidmiol. 1995;141:836
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Incidence of ulcer perforation Svanes et al. Am J Epidemiol 1995;141:836
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Incidence of Perforated Ulcer Disease No fall of complications after H2-blocker Alalgaratnam et al. J Clin Gastroenterol. 10:25, 1988 No fall in era of H.Pylori eradication Liu et al. Asian J Surg 20:305, 1997 Significant reduction in only one study Hermansson et al. Scand j Gastroenterol 32:523, 1997 Conservative management warrants consideration
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Bio-rhythms of Ulcer Perforation Typical and dramatic onset: time can be assessed Consistent daily variation is reported Greater incidence during the day, decreasing during night No change since first report in 1903 Duodenal perforations: peak: afternoon and evening Gastric perforations: peak: midday and night Jamieson RA, Br.Med. J. 1955;2:222 Hennessy E,Aust N.Z.J.Surg.1969;38:243 Svanes C et al. Int J Chronobiol 1998;15:241
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Numbers and time of perforations: A: Gastric B:Duodenal
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“Once the perforation has occurred, the case must be considered hopeless……. In surgery’s present state the idea of cutting open the abdomen and closing the opening would be too quixotic to mention…” Edward Crisp, 1842
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Non-surgical approach of perforated ulcer Mortality rate of surgical treatment: close to 20% Resuscitation with intravenous fluids Intravenous antibiotics Nasogastric suction Taylor, H.: Lancet 1956,14;270:397
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Perforated ulcers-controlled trials Conservative management vs emergency surgery: Surgical group: n=43 24 omental patch; 15 V+P; 4 partial gastrectomies Conservative group: n=40 11 patients (27%) underwent surgery after 12 hours No difference in morbidity or death (2 vs 2) Conclusion: place for conservative treatment Crofts et al. N.Engl. J. Med. 320:970,1989
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Perforated ulcers- controlled trials Simple closure vs. definitive surgery: 3 Trials: Patients with risk factors excluded: 328 patients included, one death overall Morbidity equal in groups: 11% chest infections Difference in recurrence: 61% after simple closure 6% after definitive surgery Boey et al. Ann.Surg.196:338, 1982 Hay et al. World.J.Surg.12:705,1988 Tanphiphat et al. Br.J.Surg.72:370,1985
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Een maagoperatie in het Zuiderziekenhuis, Rotterdam
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Risk factors and operative mortality Operative mortality for perforated ulcer is about 5% 30% or higher has been reported Co-morbidity: cardiac; COPD Delay of presentation > 24 hrs. Shock on admission Boey.J.et al. Ann. Surg. 205:22,1987 Blomgren L. et al. World J.Surg.21:412,1997 Irvin T. et al. Br.J.Surg.77:1006,1990
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Lethality and complications after perforation according to treatment delay during periods ’35-50, ’51-’70, ’71-’90
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H.pylori and perforated ulcer H.pylori is positive in 70-80% of operated patients H.pylori 55% prevalence in population Urea breath test positive in 24 of 29 of patients Urease test on biopsy positive in 12 of 14 patients In NSAID- patients no association with H.pylori Matskura N. et al. J.Clin.Gastroenterol. S235,1997 Ng.E. et al. Br.J.Surg. 83: 1779,1996 Sebastian M. et al. Br.J.Surg.82:360,1995 Reinbach D. et al. Gut 34:1344, 1993 .
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“If Anyone should consider removing half of my stomach to cure a small ulcer in my duodenum I would run faster than he”. Charles E. Mayo, 1927
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Conclusions High recurrence rate after simple closure <40 yrs. NSAID neg. may benefit from conservative R/ >40 yrs.: (laparoscopic) surgery NSAID neg. patients: H.pylori-eradication Intractable DU adequate R/: definitive surgery Patients with risk factors: simple closure Millat B,et al. World J. Surg. 24,299,2000
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