Perforated Peptic Ulcer 17 Moshe Schein

Perforated Peptic Ulcer 17 Moshe Schein – There’s a hole in my bucket…How should I mend it? – Just patch it! (a folk song) “Every doctor, faced with a perforated ulcer of the stomach or intestine, must consider opening the abdomen, sewing up the hole, and averting a possible or actual inflammation by careful cleansing of the abdominal cavity.” (Johan Mikulicz-Radecki, 1850–1905) Thanks to effective, modern anti-ulcer drug management the incidence of perforated peptic ulcers has decreased drastically, but not everywhere. Perforated ulcers are still common in the socio-economically disadvantaged or stressed popu- lations worldwide. Usually perforations develop against the background of chronic symptomatic ulceration but de novo presentation without previous history is not uncommon.In the Western World perforated duodenal ulcers (DU) are much more common than perforated gastric ulcers (GU), which are seen more in lower socio- economic groups. Natural History Classically, the abdominal pain caused by a peptic perforation develops very suddenly in the upper abdomen. Most patients can accurately time the dramatic onset of symptoms.The natural history of such an episode can be divided into three phases: Chemical peritonitis/contamination. Initially, the perforation leads to chemical peritonitis,with or without contamination with micro-organisms.(Note that the presence of acid sterilizes gastroduodenal contents; it is when gastric acid is reduced by treatment or disease (e.g. gastric cancer) that bacteria and fungi are present in the stomach and duodenum).Spillage of gastroduodenal contents is usually diffuse but may be localized in the upper abdomen by adhesions or the omentum. Spillage along the right gutter into the right lower quadrant, mimicking acute appendicitis, is mentioned in every textbook but almost never seen in clinical practice. Intermediate stage. After 6 to 12 hours many patients obtain some spontaneous relief of the pain. This is probably due to the dilution of the irritating gastroduodenal contents by the ensuing peritoneal exudate. Intra-abdominal infection.Should the patient escape the scalpel initially,after 12 to 24 hours intra-abdominal infection supervenes.The exact point in time in the individual patient when contaminating micro-organisms become invasive-infective, 144 Moshe Schein is unknown. Therefore, you should consider any perforation operated upon with a delay of more than 12 hours as infection rather than contamination. This bears on your postoperative antibiotic therapy as discussed below. Neglected patients may present a few days after the perforation in septic shock. Shock in the earlier stages is very rare although quoted commonly by medical students, but when confronted with a combination of shock and abdominal pain think about ruptured aortic aneurysm,mesenteric ischemia or severe acute pancreatitis. Untreated perforation can lead eventually to an early “septic”death from peritonitis or the development of an intra-abdominal abscess. Diagnosis The vast majority of patients present with signs of diffuse or localized peritoneal irritation; most lie still, groaning, and have a board-like abdomen as in the textbook. Spontaneous “sealing off”of the perforation or localization of the spill or leakage into the lesser sac causes atypical and delayed presentation. We had a patient who re-perforated his duodenal ulcer a few years after receiving an omental patch. The second perforation was thus diverted backwards into the retroperi- toneum – behind the pancreas, the left colon and into the scrotum – while the abdomen remained soft. In a patient with an abrupt onset of upper abdominal pain and diffuse peritonitis the diagnosis is simple. It can be summarized in the following formulas: Sudden onset peritonitis + free gas = perforated viscus Sudden onset peritonitis + no free gas + normal amylase = perforated viscus There is free gas under the diaphragm in about two-thirds of perforated patients. Remember, free gas is visualized better on upright chest X-ray than on plain abdominal radiographs (> Chaps. 4 and 5). If your patient can’t stand, or sit up, order a left lateral decubitus abdominal film. Free gas is diagnostic, although it is not always due to a perforated peptic ulcer. But so what? It signifies a perforated viscus, and a laparotomy is almost always indicated. But “almost always” means not “always”: free gas without clinical peritonitis is NOT an absolute indication for an emergency laparotomy. As mentioned in > Chap. 4 there is a long list of “non-operative” conditions that may produce free intra-peritoneal gas. Free gas in a “soft” abdomen may also mean that the perforation has been spontaneously sealed and is amenable to non-operative therapy as discussed below. In the absence of free air, acute pancreatitis – the “great simulator” – should be considered and excluded (> Chap. 18). Normal serum amylase levels support 17 Perforated Peptic Ulcer 145 a diagnosis of a perforation, while very elevated amylase levels in a “susceptible” patient (e.g.,alcohol,gallstones) suggest acute pancreatitis.The “border line”patient with atypical presentation and marginal elevation of amylase remains a problem because perforated ulcer may cause hyperamylasemia. In the good old days, before imaging techniques replaced clinical skills,our decision to operate or observe would have depended on the whole clinical picture. Rarely, a gastrografin contrast study was performed to demonstrate or exclude leakage. Faced with such a patient today we would advise you to obtain a CT scan of the abdomen,looking for free gas,extra- luminal gastrografin and free peritoneal fluid. CT is excellent at picking up minute amounts of free intraperitoneal gas and is thus a valuable tool in clarifying the diagnosis in patients with an ambiguous clinical picture. Philosophy of Treatment The primary goal of treatment is to save the patient’s life by eliminating the source of infection and cleaning the abdominal cavity. The secondary goal is to cure, if possible, the ulcer diathesis. The former goal may be achieved by simple closure of the ulcer; the latter requires a definitive ulcer operation.When to do what? Before telling you what to do we must answer a few other questions. Who Are the Patients who Require a Definitive Procedure? Twenty years ago the reply was simpler. The “law of thirds” maintained that after a simple closure of perforation one-third of the patients are cured permanently, another third would require long-term medical anti-ulcer therapy,and the last third would require definitive ulcer surgery because of intractability or further compli- cations. This provided us with a rationale to add a definitive procedure in order to cure the ulcer in two-thirds of the patients.With the emergence of modern anti- ulcer agents we were told that definitive ulcer procedures are not necessary as all perforated patients could be maintained indefinitely and effectively on proper anti- ulcer drugs. Our counter-argument was then that an ulcer operation is more cost- effective than a life-long commitment to drugs; that patients often are not compliant with the latter, and, in fact perforate while taking anti-ulcer drugs. Now, with the availability of anti-Helicobacter pylori treatment of peptic ulcers we are told: “why do you want to add an anti-ulcer procedure? Close the perforation and give a course of anti-Helicobacter antibiotics – the ulcer will be cured and never recur”.This may be true, but in patients acutely operated for a perforated ulcer we do not know whether Helicobacter is or is not involved. Furthermore, the very patients who are susceptible to perforation also suffer from substandard access to medical care and 146 Moshe Schein reduced compliance, both adversely affecting successful medical anti-ulcer thera- pies. Consequently, if the operation for a perforated ulcer can kill two birds using one bullet (especially if the environment around you cannot ensure optimal medical management and follow up of your patient) why not do it? This appears initially to be a reasonable argument, but after a few moments’ thought one realizes that it is obviously just the ravings of a committed peptic ulcer surgeon who laments the passing of interesting anti-ulcer surgery.Modern surgeons know that duodenal ulcers are due to acid hypersecretion and H. pylori infection and that elimination of this infection will cure the disease. Thus, definitive anti-ulcer surgery is nowadays indicated in only the most unusual of situations and should not even be considered in the routine perforation. [Paul Rogers, Co-editor]. Rebuttal: I agree with this comment in the Western World settings but there are places where follow-up and effective anti-ulcer therapy are not available. And there are patients who perforate while allegedly on such “effective” therapy and those whose ulcers are associated with non-steroidal anti-inflammatory drug intake. Thus, while I agree that the role of definitive surgery for perforated and bleeding (see > Chap. 16) ulcers has drastically declined,surgeons still need to know how to do these procedures and when.[Moshe Schein] In What Patients is a Definitive Procedure Safe? Surely you do not want to embark on a lengthy definitive procedure in a critically ill and “septic”patient.Over the years we encountered surgeons who omit- ted a definitive procedure because of “severe contamination”, often quoting a myth that vagotomy in a perforated patient may “spread the infection into the mediastinum”.The Hong Kong group showed that when the following three factors are present an anti-ulcer procedure can be safely performed: blood pressure >90 mmHg, operation within 48 hours of perforation, and lack of associated medical illnesses.We found the APACHE II scoring system (p. 57) useful in this situation as patients with perforated ulcers with scores less than 11 can tolerate a definitive procedure of any magnitude. Conversely, in patients with higher APACHE II scores the simplest operation should be performed.

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