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

Introduction

The role of the surgeon in the management of peptic ulcer disease has changed in the last few decades. Since the introduction of effective acid antisecretories and greater understanding of Helicobacter pylori (HP), the role of the surgeon has become limited to the management of occasional resistant ulcers, emergency management of complicated ulcer disease and management of the consequences 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.

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.

Figure 18.1 Gastrinoma triangle of Stabile et al.⁵

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.

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.

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

Figure 18.2 Closure of duodenal perforation with pedicled omental patch.

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 1990 ²¹ 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

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.