Benign ulceration of the stomach and duodenum and the complications of previous ulcer surgery

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Benign ulceration of the stomach and duodenum and the complications of previous ulcer surgery

Management of refractory peptic ulceration

Endoscopic confirmation

Gastric and duodenal ulcers may be considered ‘refractory’ to medical treatment if there is no sign of significant healing by 12 and 8 weeks, respectively. Gastric ulcers must be carefully re-biopsied as there is a risk that an apparently benign gastric ulcer is in fact an early malignancy. Direct endoscopic inspection, adequate tissue biopsy and expert histological interpretation are essential to identify dysplasia, neoplasia or other more uncommon mucosal disease. Repeat endoscopy to confirm healing and re-biopsy are mandatory for all gastric ulcers but probably unnecessary for duodenal ulcers if symptoms have resolved. Persistent duodenal ulceration should be re-biopsied for similar, albeit less likely, reasons given above to identify the several neoplastic, infectious and inflammatory conditions that can mimic peptic ulcer disease. Assuming that the diagnosis of peptic ulcer is correct, there are three main causes to consider: that HP has not been eradicated, that there are other factors inhibiting ulcer healing or that there is a state of acid hypersecretion (Zollinger–Ellison syndrome). Having examined all of these factors, true ‘refractory’ ulcers have become rare.

Confirmation of persistent Helicobacter infection

Multiple non-invasive diagnostic tests for Helicobacter are available, including carbon isotope (13C or 14C) urea breath test, serological enzyme-linked immunosorbent assay or the monoclonal antibody faecal antigen test. At endoscopy, biopsy material can be analysed by a rapid functional assay of urease activity as well as histological analysis. Several drugs, including proton-pump inhibitors, bismuth and antibiotics, temporarily suppress HP and may render functional assays falsely negative. The sensitivity of any test may be less following treatment when the inoculum is reduced. For tests relying on functional assay of endoscopic biopsy tissue, the sensitivity may be enhanced post-treatment by using more than one biopsy and, since there may be proximal migration of the infection, analysis of biopsies from both the antrum and body of the stomach. More elaborate immunohistochemistry using polyclonal antisera to HP can improve sensitivity and the polymerase chain reaction allows detection of the presence of HP DNA in the absence of viable bacteria.

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In clinical practice, the urea breath test is considered the most reliable tool for assessing HP status post-treatment.1

Failure of HP eradication may be due to antibiotic resistance or non-compliance. The former may be overcome by appropriate modification of the antibiotic regimen, occasionally even using bacteriological culture to help direct treatment.

Non-HP-related refractory ulceration

Ingestion of non-steroidal anti-inflammatory drugs (NSAIDs) should be re-evaluated. Surreptitious aspirin ingestion has been observed and if suspected can be established by assay of plasma salicylate levels. Any other factor that may be facilitating ulceration and impairing healing, such as intercurrent disease and smoking, should be sought and eliminated where possible. Diseases associated with peptic ulceration are chronic liver disease, hyperparathyroidism and chronic renal failure, particularly during dialysis and after successful transplantation. Smokers are more likely to fail both medical and, indeed, surgical ulcer treatment. Smoking impairs the therapeutic effects of antisecretories, may stimulate pepsin secretion and promotes reflux of duodenal contents into the stomach. Smoking increases the harmful effects of HP, and increases the production of free radicals, endothelin and platelet-activating factor. Smoking also affects the mucosal protective mechanisms by decreasing gastric mucosal blood flow and inhibiting gastric prostaglandin generation and the secretion of gastric mucous, salivary epidermal growth factor, duodenal mucosal bicarbonate and pancreatic bicarbonate.2 Stopping smoking is an important, yet often ignored, first step to allow effective ulcer treatment.

A diagnosis of Zollinger–Ellison should be suspected in cases of Helicobacter-negative, non-NSAID-induced refractory ulceration and especially where there is ulceration of the second part of the duodenum or large confluent ulcers in the duodenum. Hypergastrinaemia should be excluded prior to a decision to treat a refractory ulcer.

Where no cause for persistent ulceration can be found it may be necessary for the patient to take long-term antisecretory drugs. Alternatively, elective surgery may be considered in this group of patients. The risks of complications of persistent ulcer disease, the degree of disability experienced by patients and their fitness for surgery should all be considered in the decision of whether or not to operate.

Elective surgery for peptic ulceration

Surgery for peptic ulcer disease evolved around the concept of acid reduction either by resection of most of the parietal cell mass, vagal denervation of the parietal cells or resection of the antral gastrin-producing cells. The balance lay in minimising the chance of ulcer recurrence while at the same time trying to avoid the symptomatic and metabolic sequelae of the procedure that would affect patients for the rest of their life.

The trend by the mid-1970s was towards highly selective vagotomy (HSV) or proximal gastric vagotomy, which denervated the parietal cell mass but left the antrum and pylorus innervated and so allowed a gastric-emptying pattern that, while not completely normal, did not require a drainage procedure. This was the first ulcer procedure that did not involve bypass, destruction or removal of the pylorus, and as a result has significantly fewer side-effects than other ulcer operations. The main concern with this operation, whether for duodenal or gastric ulcer, has been the recurrence rate. In the best hands recurrence rates of 5–10% have been achieved.

Anterior seromyotomy with posterior truncal vagotomy probably denervates the proximal stomach more consistently. This proved that the posterior vagal trunk can be divided and the patient not experience significant diarrhoea, provided the pylorus is intact and innervated. Some surgeons advocated the use of truncal vagotomy and antrectomy, suggesting that this operation is the most effective for reducing acid secretion and has a very low recurrence rate of about 1%. The procedure was subsequently modified to a selective vagotomy and antrectomy, leaving the hepatic and coeliac fibres of the vagi intact. This did reduce the incidence of side-effects, especially diarrhoea, though dumping was still a problem. Bile gastritis and oesophagitis were also troublesome side-effects unless a Roux-en-Y reconstruction was used, though recurrent stomal ulceration was then more frequent unless a more extensive gastric resection was performed. The perfect ulcer operation has remained elusive and there is none that has no side-effects or risks.

Operations for refractory duodenal ulcers: There is no good evidence on which to base the decision of operation in cases of resistant ulceration in the modern era. Intuitively, one might predict a poor result with HSV alone since its success rate historically was less than that of modern medical treatment. It seems likely that resection of the antral gastrin-producing mucosa and either resection or vagal denervation of the parietal cell mass is necessary. The operations that could be considered include the following:

• Selective vagotomy and antrectomy. Selective denervation is preferred because of a lower incidence of side-effects. It is not an easy procedure; in particular, the dissection around the lower oesophagus and cardia has to be done very carefully. The vagotomy should be performed before the resection and tested intraoperatively. The reconstruction should either be a gastroduodenal (Billroth I) anastomosis or a Roux-en-Y gastrojejunostomy. The latter is associated with fewer problems with bile reflux into the gastric remnant and oesophagus, but a higher risk of stomal ulceration and so at least a two-thirds gastrectomy is advised.

• Subtotal gastrectomy. Removal of a large part of the parietal cell mass is sound in theory and indeed ulcer recurrence after this operation is unusual. However, there is an incidence of postprandial symptoms, and in particular epigastric discomfort and fullness that can limit calorie intake. Importantly, there is a high incidence of long-term nutritional and metabolic sequelae that require lifelong surveillance and can be difficult to prevent, although this is mainly in women.

• Pylorus-preserving gastrectomy. This operation involves highly selective vagotomy with resection of about 50% of the parietal cell mass and the antral mucosa, but preserving the pyloric mechanism and the vagus nerves to the distal antrum and pylorus. There is some evidence that this may be a superior technique with fewer sequelae compared to the traditional approaches.3 Comparable results of the technique used in the context of treatment of early gastric cancer confirm a good long-term functional result.4

Zollinger–Ellison syndrome (ZES)

Refractory peptic ulceration should raise the suspicion of ZES. Alternatively, the syndrome may present with diarrhoea and weight loss and a third present with oesophagitis only. The disease may present more dramatically with perforation, haemorrhage, oesophageal stricture, jejunal or anastomotic ulceration. The condition should be suspected particularly when a duodenal ulcer coexists with primary hyperparathyroidism or metastatic adenocarcinoma of unknown origin. The aims of treatment are control of gastric acid hypersecretion and, where possible, removal of the underlying tumour itself to prevent metastatic disease. Since the introduction of adequate medical acid suppression the former aim is no longer the primary concern of the surgeon.

Pathology

Although originally described as a pancreatic endocrine tumour, the definition has also come to include extrapancreatic gastrin-secreting tumours. The majority of tumours lie within an area defined by the junction of the cystic and common bile ducts superiorly, the junction of the second and third portions of the duodenum inferiorly, and the junction of the neck and body of the pancreas medially: the ‘gastrinoma triangle of Stabile’5 (Fig. 18.1). Where the condition is due to a pancreatic tumour, in two-thirds of cases the tumour will be multifocal within the pancreas.6 At least two-thirds will be histologically malignant. One-third will already have demonstrable metastases by the time of diagnosis.7 The most common extrapancreatic site is in the wall of the duodenum. Less frequently (6–11% of cases) ectopic gastrinoma tissue has been identified in the liver, common bile duct, jejunum, omentum, pylorus, ovary and heart.8 These extrapancreatic tumours rarely metastasise to the liver and, even though they do metastasise just as frequently to regional lymph nodes, they tend to have a better prognosis than primary pancreatic tumours.

One-quarter of patients with ZES have other endocrine tumours as part of a familial multiple endocrine neoplasia (MEN-1) syndrome, particularly hyperparathyroidism.7 This group of patients has a much worse prognosis than sporadic ZES, in part due to the multifocal nature of the disease.

Diagnosis

Diagnosis may be confirmed by paradoxical fasting hypergastrinaemia associated with gastric acid hypersecretion. Hypergastrinaemia may be expected to occur in cases of achlorhydria such as ingestion of antisecretory drugs, postvagotomy, pernicious anaemia, atrophic gastritis, antral G-cell hyperplasia or gastric outlet obstruction. Hypergastrinaemia is also associated with a retained antrum after a Billroth II/Polya-type gastrectomy where a small cuff of antrum has been included in the ‘duodenal’ closure (if a retained antrum is suspected, technetium pertechnetate scan may be useful in identifying the antral mucosa). If there is diagnostic uncertainty or the basal serum gastrin level is marginal, dynamic assay of serum gastrin following secretin (or alternatively calcium or glucagon) provocation may be required. Gastrin response to a standard meal helps to differentiate hypergastrinaemia due to antral G-cell hyperplasia, which will result in an increase in serum gastrin levels, while no response would be expected in cases of gastrinoma. Serum chromogranin A, a non-specific marker for neuroendocrine tumours, should also be measured.9

Tumour localisation

Tumours may be localised initially by computed tomography (CT). This may also identify metastatic disease. Endoscopic ultrasound (EUS) is highly accurate in the localisation of pancreatic tumours and gastrinomas in the duodenal wall as small as 4 mm. Octreotide scan and selective arterial secretagogue injection (SASI) testing are the most reliable approaches to localising gastrinomas. Liver metastases can frequently be detected by conventional imaging, but octreotide scan has proved a more sensitive investigation that may prevent unnecessary surgical exploration. SASI involves selective catheterisation of the feeding arteries of the duodenum and pancreas and the hepatic veins. Secretin is injected in turn into the splenic, gastroduodenal (GDA) and superior mesenteric (SMA) arteries. Corresponding hepatic venous gastrin levels are measured and allow identification of the main feeding vessel. More precise localisation can be achieved by more peripheral cannulation of the SMA and GDA or different points along the splenic artery. The test has greater than 90% sensitivity and specificity for preoperative tumour localisation.10

Surgery for ZES

The surgical management of ZES is characterised by controversy and little evidence. Historically, the debate centred around the radicality of surgical approaches to eliminate end organ acid production such as total gastrectomy. This is generally accepted, as unnecessary given that adequate acid suppression can usually be achieved with proton-pump inhibitors (PPIs), albeit at much higher doses than those usually recommended. How aggressively surgery should be pursued for the gastrinoma itself became the next area of controversy. With adequate acid suppression, patients may be rendered asymptomatic and the natural history of the gastrinoma tended to one of only very slow progression. Nevertheless, 60–90% of gastrinomas are reported to be malignant and some do have a more aggressive course. It became more acceptable to consider resection, as 30–50% with sporadic disease may be cured or at least have a reduced rate of development of liver metastases. Whether that should be local enucleation or a wider resection remains controversial. In the past many would say that patients with MEN-1 and those with liver metastases should not be treated surgically. Nevertheless, impressive results have been reported even in the former group and there is evidence that surgical resection of metastatic liver disease does offer long-term survival, even where resection may be incomplete. One of the largest series has shown that surgical exploration and resection resulted in excellent long-term results, with a 15-year disease-related survival rate of 98% compared to 74% for non-operated cases.11

Surgical exploration when preoperative investigations have failed to precisely localise a tumour is now a less frequent problem, particularly in specialist centres with access to SASI and octreotide scan. Nevertheless, a laparotomy will detect a third more gastrinomas than even octreotide scan. If surgical exploration is performed then the pancreas must be mobilised along its entire length, inspected, palpated and if the facilities are available re-scanned intraoperatively by endoluminal or standard ultrasound. Palpation of the duodenal wall will identify 61% of duodenal gastrinomas. Duodenal transillumination by endoscopy will improve detection to 84% and duodenotomy identifies the remaining cases.12 If no gastrinoma is found in the usual locations, other ectopic sites should be examined carefully. Resection of these primary ectopic tumours can sometimes lead to durable biochemical cures. Gastrinomas may be identified in 96% of surgical explorations if these approaches are adopted.11 With the use of SASI in particular, though a tumour cannot be precisely localised, it may be sufficiently ‘narrowed down’ to allow a limited pancreatic and/or duodenal resection.10 The intraoperative secretin test in which gastrin levels in response to secretin are measured before and after resection can be useful in assessing the effectiveness of resection.

Emergency management of complicated peptic ulcer disease

Although very few patients now require elective surgery, the number who require surgery for the complications of peptic ulcer disease has remained constant for many years.

Perforation

A number of factors associated with poor outcome in perforated peptic ulcer have been identified: delay in diagnosis, coexistent medical illness, shock on admission, leucocytosis and age over 75. A delay in treatment of greater than 24 hours is associated with a sevenfold increase in mortality, threefold risk of morbidity and a twofold increase in hospital stay. The elderly are particularly vulnerable and often more difficult to diagnose because of poorly localised symptoms and signs and fewer preceding symptoms. The principles of treatment of peptic ulcer perforation involve resuscitation, control of contamination and prevention of recurrence.

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Careful resuscitation and perioperative optimisation play a significant role in reducing morbidity and mortality associated with perforated peptic ulcer disease.13

Conservative management

Study of the natural history of perforated peptic ulcers suggests that they frequently seal spontaneously by omentum or adjacent organs and that, particularly when this occurs rapidly, contamination can be minimal. Taylor showed that the mortality in his series of patients with peptic ulcer disease was half that of the contemporary (pre-1946) reported mortality for perforation treated surgically.14 Conservative treatment today consists of parenteral broad-spectrum antibiotics, intravenous acid antisecretories, intravenous fluid resuscitation and nasogastric aspiration. In addition, water-soluble meal and limited follow-through is recommended to confirm that the leak has sealed. CT is becoming increasingly used in the diagnosis of acute abdominal pain and the degree of fluid contamination may also serve as a useful guide as to whether peritoneal lavage or drainage is necessary.

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The conservative approach may be particularly appropriate in patients under 70, whose comorbidity (recent myocardial infarction, severe chronic obstructive pulmonary disease, etc.) place them at high operative risk. Sometimes, where there is some delay in presentation and patients exhibit an already improving clinical picture with minimal abdominal signs, conservative treatment is likely to be successful. Such an approach, however, requires careful interval assessment by an experienced surgeon with a low threshold for performing surgery if clinical improvement is not apparent, both to confirm the diagnosis and oversew an unsealed perforation. Small series have demonstrated low, comparable mortality for the conservative approach with conversion to operation of around 20–30%. Those that failed conservative treatment were more often over 70 years of age.15–17

Surgery

In most cases the treatment of choice for patients with perforation of the duodenum is still laparotomy, peritoneal lavage and simple closure of perforation, usually by pedicled omental patch repair (Fig. 18.2). The routine use of drains is unnecessary and may in fact increase morbidity. This simple treatment is safe and effective in the long term, when combined with pharmacological acid suppression. Ninety per cent of perforations are associated with HP infection,18 and HP eradication further significantly reduces the risk of ulcer recurrence.19

In cases of ‘giant’ perforation, where the defect measures 2.5 cm or more, partial gastrectomy with closure of the duodenal stump should be considered (see also management of bleeding from giant duodenal ulcer below). Alternatively, in situations where the clinical situation or expertise dictates more expeditious surgery, the duodenal perforation should be closed as well as possible around a large Foley or T-tube catheter to create a controlled fistula. This can be combined with venting gastrototomy and feeding jejunostomy.20 The advances in understanding of the medical treatment of peptic ulcer disease together with the decrease in experience of elective antiulcer surgery have made the argument for definitive ulcer surgery in the emergency setting almost untenable.

Although laparoscopic treatment of peptic ulcer perforation was first reported in 199021 and many excellent series have been reported since, a European population study demonstrated that the proportion of cases performed laparoscopically is as low as 6%,22 and even in centres with a specialist interest in laparoscopic surgery the proportion of cases completed laparoscopically is less than 50%.23

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There are several series that show favourable results with the laparoscopic approach,24 but there are very few prospective studies.25 Shock, delayed presentation, confounding medical condition, age greater than 70 years, poor laparoscopic expertise and ASA grade are risk factors for open conversion and for poorer outcome.26 In ‘low-risk’ patients the laparoscopic approach may have significant advantages. For higher-risk patients (prolonged perforation for > 24 h, shock on admission and confounding medical conditions) there is no evidence that the laparoscopic approach is advantageous.

Whatever the approach, basic surgical tenets must be observed: careful preparation for theatre with timely expeditious operation involves thorough peritoneal lavage and secure closure of the defect. Any marginal benefit of the minimally invasive approach is lost if any of these tenets are compromised.

Bleeding

Management of acute haemorrhage from peptic ulceration of the stomach and duodenum has been revolutionised by rapidly developing endoscopic technology and expertise. The principle of successful management is by prompt resuscitation, accurate endoscopic diagnosis and the timely application of appropriate therapy.

Medical therapy

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Although there is evidence that proton-pump inhibitors given pre-endoscopy reduce the incidence of endoscopic findings of stigmata of recent haemorrhage and the need for endoscopic intervention, there is no evidence that this or any other specific pre-endoscopy medical intervention has any effect on overall morbidity, mortality, or specifically the risk of re-bleeding or need for surgery.27

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There is compelling evidence that proton-pump inhibitors given after endoscopic control of bleeding are beneficial. A randomised controlled study (n = 240) from Hong Kong has demonstrated a significant reduction in re-bleeding following endoscopic treatment with a protocol of intravenous omeprazole (omeprazole 80 mg i.v. bolus followed by 8 mg/h infusion for 72 hours).28 This is supported by meta-analysis of subsequent studies.29

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Meta-analysis of randomised, double-blinded trials with tranexamic acid reveals no significant difference in the incidence of re-bleeding but an increase in complications related to therapy such as stroke, myocardial infarction, deep vein thrombosis and pulmonary embolism.30

Somatostatin decreases gastric acid and pepsin secretion. Nevertheless, there is no proven benefit of somatostatin or its analogue (octreotide) in the management of active non-variceal upper gastrointestinal bleeding. Prostaglandin E2 and its analogue (misoprostol) inhibit gastric acid production, stimulate mucosal perfusion, and promote bicarbonate and mucus secretion. Small studies to date have demonstrated no benefit of stopping acute bleeding or preventing re-bleeding.

Endoscopic therapy

The various techniques of endoscopic haemostasis have dramatically reduced the need for emergency surgery for bleeding due to peptic ulceration.

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Meta-analysis suggests that endoscopic therapy reduces the mortality of acute upper gastrointestinal bleed in patients’ active bleeding or non-bleeding visible vessel by avoiding the often considerable morbidity or mortality of emergency surgery.31

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Ulcers with a clean base or non-protuberant pigmented dot in an ulcer bed, which are at low risk of re-bleeding, do not require endoscopic treatment. For all others, including those who have active bleeding or non-bleeding visible vessels or have adherent blood clot, endoscopic treatment should be given.32

Injection with 4–16 mL 1:10 000 adrenaline around the bleeding point and then into the bleeding vessel achieves haemostasis in up to 95% of cases. Additional injection with sclerosants (sodium tetradecyl sulphate, polidoconal, ethanolamine) or absolute alcohol does not confer additional benefit and may cause perforation. Fibrin glue and thrombin may be more effective, but they are not widely available.

Techniques used commonly are the heater probe, multipolar coagulation (BICAP) and argon plasma coagulation. There is no strong evidence to recommend one thermal haemostasis technique over another.

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