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