Gecompliceerd Ulcuslijden Bloedingen en Perforaties H.W. Tilanus 31 Januari 2006, Delft.
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Transcript of Gecompliceerd Ulcuslijden Bloedingen en Perforaties H.W. Tilanus 31 Januari 2006, Delft.
Gecompliceerd Ulcuslijden
Bloedingen en Perforaties
H.W. Tilanus
31 Januari 2006, Delft
“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
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)
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
Ivan Pavlov (1849-1936) performing an experimental vagotomy
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
Stomach surgery in the Netherlands.1908
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
1881:Billroth performing a stomach resection (A.Seligmann)
von Eiselsberg at work in University Hospital, Utrecht 1898
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.
Lester Dragstedt (l)with brother Carl in 1918
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;53:152Dragsted L Ann Surg 1947; 126:687
Dragsted LR, Am J Surg 1974;128:344
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
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
Various teDevelopment of vagotomy 1814-
1979of the
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 yrsSvanes C et al.Gut,1997;41:177
NSAID’s contributes one-fifth to one-third to
perforationsSvanes C et al. 1996;
Major role of H.pylori in perforations not confirmedReinbach DH et al, Gut,1993;34:1344
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
Incidence of ulcer perforationSvanes et al.
Am J Epidemiol 1995;141:836
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
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
Numbers and time of perforations:A: GastricB: Duodenal
“Once the perforation has occurred, the case must be considered hopeless…….
In surgery’s present state the idea of cutting openthe abdomen and closing the opening would be too
quixotic to mention…”
Edward Crisp, 1842
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
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
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, 1982Hay et al. World.J.Surg.12:705,1988Tanphiphat et al. Br.J.Surg.72:370,1985
Een maagoperatie in het Zuiderziekenhuis,
Rotterdam
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
Lethality and complications after perforation according to treatment delay during periods ’35-50, ’51-’70, ’71-’90
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
.
“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
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