The comments by many surgeons are an important reminder, at the time when the bacterial (helicobacter) etiology of ulcers is (over) emphasized, that ulcers are the result of mulifaceted etiology, especially the socio-economic one.
That the incidence of complicated peptic ulcers is growing in what was the Soviet Union is not surprising in view of the post-communist socio-economic chaos there. A significant peak in the incidence of peptic ulceration was observed in the UK during world war II corresponding to the stress of war, change in nutrition and so forth.
Working in a few countries over a relatively short period I was impressed how the face of ulcer pathology varies between countries and within.
In urban South Africa we observed an epidemics of giant GU’s. In a public “white” hospital (end of Apartheid era) we operated on 2-3 bleeding or perforated GU’s a week. The ratio of complicated duodenal ulcer to GU was 2:1, while the corresponding ratio in series from the USA or UK was 4:1. All patients were whites from a low socioeconomic starta. Alcohol and NSAID were common. Professor George Decker (my Boss then) made the observation that most patients were toothless and that during the operations most had huge reactive perigastric lymphnodes. We did not know at that time (early 1980’s) about helicobacter and can only speculate in retrospect about any association. Those ulcers were GIANT: I remember cases in which both the splenic artery and left gastric artery were looking at your pumping from the same ulcer’s bed.
Moving to a nearby “black” hospital one stopped seeing GU’s. Instead pyloric and duodenal ulcers were extremely common. Going further out from town the incidence of peptic ulceration in the blacks was lower (and the ulcers were smaller). Message- urbanization or change in environment brings stress and ulcers.
Thinking that all ulcers bleed or perforate or obstruct and are huge I went to Leeds, UK and was surprised to see how “small” the DU’s and GU’s they operate upon are.
Note: Effective anti-ulcer therapy was widely available in South Africa at that time, albeit, only to those who bothered to see a doctor. Most presented ab initio with complications.
Moving then to Israel I hardly encountered a complicated ulcer. It appeared that anybody with the slightest dyspepsia was put by their GP’s on anti-H2 blockers (Jews like medications…) and this eliminated complicated ulcers almost completely. Until the Russian Jews arrived… medically neglected, stressed, heavy smoking, toothless, they did not differ much from the poor South African whites and had similar ulcers.
So far about etiology or its variation. During the years I have develop a structured approach to complicated peptic ulcers. I will share with you the one in the management of perforated GU.
The main goal: save life and prevent immediate morbidity. Secondary goal: long term cure of the ulcer. If possible (and safe) achieve both goals at the initial operation.
Back ground: a patient with a stomach is happier than the one with half a stomach. Therefore, I avoid resective surgery if possible. Gastric ulcer is not vne disease but comprises of: Johnson’s types:
GU type I: the classical lesser curvature ulcer.
GU type II: the prepyloric ulcer
GU type III: GU + DU
Lessons learned from elective operations for GU help us in the choice of the definitive procedures in the emergency situation:
Type I ulcer was classicaly treated with Bil I gastrectomy. Because excessive recurrence rate it was suggested that in younger patients or those consuming NSAID vagotomy should be added.
Highly selective vagotomy (HSV) plus excision of ulcer proved an good operation (Johnston). According the Oi Law (i.e, GU develops at the junction between the antrum and parietal cell mass) lesser curvature should be cleared from the ulcer and above (distal clearance not necessary).
Type II, III. Bil I gastrectomy is not enough. Vagotomy should be added. Alternatively, HSV plus pyloroplasty is an excellent procedure (Holle).
So what procedure for what patient with perforated GU. The decision is based on :
The ulcer. Is it possible and safe to close it without gastrectomy?
The patient. How sick he is? Can he tolerate a “big” procedure.
High risk or low risk is measured either by the Boey and Wong Method (shock on admission, associated medical risks, duration of > 48 hours) or using the APACHE II system in which APACHE II
The macroscopical appearance of the peritoneal cavity is a poor indicator to the duration and virulence of perforation, unless frank peritonitis with pus is present. Perforations operated within 12 hours do NOT represent an intraabdominal INFECTION but signify CONTAMINATION.
With the above in mind:
In good risk patients (i.e, APACHE II less than 10, duration of less than 48 hours) I would go for a definitive procedure. If the ulcer is amneable to a local excision with closure I add a HSV for type I, and HVS+pyloroplasty for type II or III. In the poor risk patient I opt for simple closure is possible.
Its common location along the lesser curvature and its usual larger size makes a perforation GU less amenable to simple closure. It is easy to wedge resect or close GU’s on the mobile greater curvature but the large, edematous crater, adherent to the left gastric artery is not easily locally exiced or closed. Thus, in such cases gastrectomy is indicated in both the good and high risk patients. Bilroth I PG would suffice in type I GU’s, in types II & III I would add a truncal vagotomy.
Surgeons who gained experience with complicated GU surgery have learned NOT to totally resect large adherent ulcers, but to “pinch them off”, leaving the crater adherent to adjacent vital structures.
The question of malignancy. It is extremely rare in series of perforated GU’s. It is not an argument for obligatory gastrectomy because the emergency partial gastrectomy is not a cancer operation. Obviously, the specimen is examined after partial resection or simple closure (edges and base of ulcer sampled). When malignancy is diagnosed an elective re-operation is planned on individual basis.