Aims
To discuss
● the most appropriate management of peptic ulcer disease.
● to describe the role of surgery in peptic ulcer disease – primary treatment and complications.
● to present the indications for surgery in upper GI haemorrhage.
● To discuss the management of compli- cations of previous peptic ulcer surgery.
● to consider the role of gastric surgery in morbid obesity.
Introduction
Surgery for benign diseases of the stomach has undergone changes in the last 15 years as radical as those promoted by Billroth and Dragstedt, who popularised surgery for uncomplicated peptic ulcer. Operations such as highly selective vagotomy, selective and truncal vagotomy and drainage and gastric resection as primary treat- ment for peptic ulcer have been largely assigned to history by the discovery of Helicobacter pylori and the realisation that long-term cure of ulcers can be achieved by eradication therapy. This does not mean that there is no role for surgery in peptic ulcer disease. There is still a major role
in the treatment of complications, namely bleeding and perforation and rarely obstruc- tion. The role of surgery in the management of the complications of previous peptic ulcer surgery is ongoing.
Congenital Disorders of the Stomach (see also Chapter 2)
With the exception of hypertrophic pyloric stenosis, these are rare although cases of diver- ticula and reduplication are found in the litera- ture. Hypertrophic pyloric stenosis can present in adult life and may be treated by balloon dilatation or pyloromyotomy. Care must be taken to exclude pyloric canal cancer.
Peptic Ulcer Disease
Aetiology
It is now accepted that there are two main factors in the aetiology of peptic ulcers – non- steroidal anti-inflammatory drugs (NSAIDs) and H. pylori.
NSAIDs
The link between these drugs and peptic ulcers is well established [1]. This is a major problem in the elderly where the consumption of these 5
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Benign Diseases of the Stomach
Robert C. Mason BSc
drugs is associated with a two- to four-fold increase in the incidence of gastrointestinal haemorrhage. The probable mechanism by which NSAIDs cause peptic ulcers is by disrup- tion of the “mucosal barrier”. The effect is mediated via prostaglandins and the microcir- culation, which sweeps hydrogen ions away and buffers them with bicarbonate, rather than an effect on the mucus layer.
H. pylori
This organism lives in the epithelium and mucus of the stomach and duodenum. It is transmitted by the oral route and infection probably occurs in childhood.
The prevalence of H. pylori mirrors the preva- lence of peptic ulcer and accounts for at least 95% of non-NSAID peptic ulcers. The incidence of peptic ulcer in patients with H. pylori infec- tion is less than 10%. Once eradicated, the risk of reinfection in western countries is less than 0.5% per annum. The mechanism by which H.
pylori causes peptic ulceration is a combina- tion of a direct effect on epithelial cells due to cytokine release, and increased release of gastrin and pepsinogen as a result of antral gastritis [2].
Confirmation of infection can be obtained by gastric antral biopsy and histological examina- tion or CLO test for urease in biopsy tissue.
Non-invasive confirmation can be obtained by a carbon isotope urea breath test or by mea- surement of H. pylori antibodies in the blood.
This latter test can remain positive for up to one year post eradication. The accuracy of these tests exceeds 90%.
Diagnosis of Peptic Ulcers
The main means of diagnosis is endoscopy. This should be undertaken in all cases in suspected gastric ulcers along with biopsy to exclude malignancy. In young patients (<45 years) with symptoms of duodenal ulceration it is probably safe to treat expectantly and only endoscope if there is no response to medical treatment or recurrence of symptoms following a course of medical treatment. To treat on the basis of pos- itive serology or breath test alone is contentious, as only a minority of positive cases will have ulcers. As there is an association of H. pylori and antral cancer [3] it could be argued that this
would be preventative. This is, however, a “dis- appearing cancer” and it is recognised that eradication of H. pylori is associated with increased gastro-oesophageal reflux, which is a precursor of Barrett’s cancer at the gastro- oesophageal junction – an “increasing cancer”.
If the patient is symptomatic it is best to treat;
if not then eradication should probably be withheld.
Treatment of Peptic Ulcers
The mainstay of treatment of peptic ulcer is medical as outlined below. Surgery as primary treatment of uncomplicated disease has been consigned to history. The operations described for duodenal ulcer [4] together with mortality and recurrence rate are shown in Table 7.1. For comparison, the success of eradication therapy is also included.
The basis of these procedures is reduction of acid secretion by either vagotomy, resection of the antrum removing gastrin or resection of acid-secreting mucosa. As can be seen these procedures did not heal all ulcers and had a sig- nificant recurrence rate associated with them.
This compares with eradication therapy with a healing rate of >98% and recurrence rate at 7 years of <5% [5]. As similar rates of healing of gastric ulcers can be achieved medically, Billroth I gastrectomy has gone a similar route.
The complications of surgery are dealt with later in this chapter.
It is still important to modify lifestyle to max- imise success of treatment. Smoking should be stopped and diet adjusted. Any ingestion of NSAIDs should be stopped if at all possible. If
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Mortality Recurrence (%) rate (%) Bilroth I gastrectomy (GU) 1 1 Gastrojejunostomy (DU) <1 40 Truncal/selective vagotomy <1 8–10
and drainage(DU)
Highly selective vagotomy (DU) <1 10–20 Bilroth II Gastrectomy (DU) – 2 2
stomal ulcer
Truncal vagotomy and 2 0.5
antrectomy (DU)
Eradication therapy 0 <5
GU, gastric ulcer; Dll, duodenal ulcer.
this is not possible then lifetime treatment with either an H2receptor antagonist (ranitidine 150 mg twice daily) or proton pump inhibitor (lan- soprazole 15 mg daily) is indicated.
In all other cases a course of eradication therapy for H. pylori is indicated.
Many such regimens exist but a common one is “HeliClear” – a 7-day course of lansoprazole 30 mg twice daily, clarithromycin 500 mg twice daily, and amoxicillin 500 mg twice daily for 7 days. This eradicates H. pylori in over 90%
of cases. Eradication should be confirmed by breath test 6 weeks later. If eradication has not been achieved, a further course is given with the possible addition of metronidazole 400 mg twice daily.
The role for maintenance therapy with either H2 receptor antagonists or proton pump inhibitors is reserved for those with early recur- rence of symptoms or ulcers resistant to healing.
Care must be taken to ensure eradication and exclude Zollinger–Ellison syndrome although there are several causes of raised serum gastrin (Table 7.2) and other multiple endocrine adenopathies. Repeat biopsy to exclude malig- nancy is mandatory, especially in cases of gastric ulcer.
Recurrent Peptic Ulcers
These should be investigated as for primary ulcers to exclude H. pylori or NSAIDs and treated appropriately. There is a case for long- term low dose proton pump inhibitors in such cases.
Complications of Peptic Ulceration
Bleeding
This potentially is the most serious and com- mon complication of peptic ulcers. Bleeding can
be both overt, presenting with haematemesis, melaena or overt rectal bleeding, or occult blood loss, presenting with iron-deficient anaemia.
In the latter situation, it is vital also to investi- gate the lower gastrointestinal (GI) tract as a secound source of bleeding may be found in up to 20% of cases [6]. All common causes of upper GI haemorrhage are shown in Table 7.3 and peptic ulceration (acute and chronic) can be seen to be the major cause.
Management of Gastrointestinal Bleeding
This commences with full resuscitation, fol- lowed by investigation to determine the site of bleeding and then treatment to arrest haemor- rhage and prevent rebleeding and promote ulcer healing. Investigation is primarily upper GI endoscopy with rigid sigmoidoscopy if there is evidence of bleeding per rectum. If the source is not identified then further investigation with selective angiography and/or labelled red cell scan and colonoscopy is indicated.
The majority of bleeds are small and the patient stabilises rapidly. Such individuals should have endoscopy on the next available elective endoscopy list after a period of fasting to enable the stomach to empty. If the patient requires early endoscopy due to haemody- namic instability or continued haemorrhage or rebleeding, then the endoscopy should be undertaken in theatre under crash general anaesthesia to protect the airway and prevent aspiration. Such individuals are going to require an intervention either endoscopic or surgical to arrest bleeding and this is best achieved with an anaesthetised and stable patient. In all such patients, ingestion of NSAIDs should be stopped and a course of eradication therapy com- menced. There is no evidence that the acute administration of intravenous H2 receptor antagonists is beneficial although this may change with the advent of intravenous proton pump inhibitors.
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Table 7.2. Conditions resulting in increased levels of serum gastrin
• Pernicious anaemia
• Atrophic gastritis
• Medical treatment of peptic ulcers by acid supression
• Previous surgery for peptic ulcers
• Excluded gastric antrum
• G cell hyperplasia
Table 7.3. Causes of upper gastrointestinal bleeding 1. Peptic ulcers and erosions 80%
2. Oesophageal varices 8%
3. Oesophagitis 5%
4. Gastro-oesophageal cancer 5%
5. Angiodysplasia 2%
Arresting Haemorrhage from Peptic Ulcers
This can be achieved both endoscopically and surgically.
Endoscopic techniques [7] are based on injec- tion into and around the ulcer bed. This can be performed by the injection of adrenaline (epi- nephrine) 1 in 10 000 through a varices injec- tion needle. The main benefit is probably from the tamponading effect of the fluid rather than vasospasm induced by the adrenaline. This technique is also indicated in patients who are not actively bleeding but are at high risk of a rebleed – visible vessel or clot on the ulcer base.
Other endoscopic techniques include the use of a heater probe, laser, argon beam photocoagu- lation, or the placement of clips on the vessel.
As in all such cases, the simplest technique is the best and that is injection treatment, which requires no specialised equipment. Following cessation of bleeding, eradication therapy is administered as soon as oral intake can com- mence. There may be a role for parenteral proton pump inhibitors in the time between arrest of bleeding and commencement of oral intake.
The Role of Surgery in Bleeding Peptic Ulcers
Surgery is indicated when the patient is actively bleeding and the source cannot be seen or con- trolled endoscopically. Timing for surgery is contentious [8], but experience teaches us that we tend to intervene too late when the patient has had at least 6 units of blood, is unstable and is entering a state of coagulopathy. This proba- bly explains why the mortality from bleeding peptic ulcer has changed little in the past 20 years. Active intervention (endoscopic or surgi- cal) is required when the fourth unit of blood goes up and the threshold needs to be lower in older infirm patients, especially if they have a known chronic ulcer and are on NSAIDs.
Those on anticoagulation are a special case and need rapid reversal in cooperation with the haematologists.
Which operation should be undertaken [9]?
The principle is to do the quickest and safest procedure to arrest bleeding and then treat with appropriate eradication therapy. In the case of duodenal ulcers this is a duodenotomy and oversew of the vessel and if possible ulcer
exclusion with interrupted 2/0 vicryl sutures. If the pylorus is intact, the duodenotomy can be closed longitudinally. If it has been divided, then closure is in the form of a Heineke–
Mikulicz pyloroplasty. If there is significant pyloric scarring, an anterior gastrojejunostomy can be performed. There is probably now little role for adding a truncal vagotomy initially as this does not improve ulcer healing over medical treatment nor for performing a partial gastrectomy due to the high morbidity/mortal- ity associated with this operation. If rebleeding does occur, however, some form of resection will be required. Bleeding gastric ulcers are best treated by Billroth II gastrectomy if this can be performed quickly and safely. If not then over- sewing the bleeding vessel followed by medical therapy is indicated.
Other Gastric Causes of Bleeding
Oesophageal and gastric varices secondary to portal hypertension are dealt with elsewhere.
Bleeding gastric cancer should be treated as for all gastric cancer but if resection is not indicated and bleeding persists then external beam radio- therapy should be considered. A rare cause of upper gastrointestinal bleeding is Dieulafoy syndrome – a vascular malformation in which a jet of blood appears to come from normal epithelium. This can be controlled by either endoscopic injection or thermal ablation or simple suture if open surgery is indicated. Wide spread angiodysplasia can affect the distal stomach – watermelon stomach. This usually presents with chronic blood loss and anaemia and is treated with photocoagulation rather than resection. A rare cause of occult bleeding is leiomyoma which can ulcerate on its surface.
If small they may be snared but if larger they will require resection.
Perforation
As the incidence of bleeding peptic ulcer has increased, the incidence of perforation has decreased. It is now most commonly seen in elderly patients taking NSAIDs and/or steroids.
In such individuals such perforations may be occult and only diagnosed as the presence of free gas on a chest X-ray taken for other reasons.
It is important to recognise that up to a third of perforations, especially of duodenal ulcers, may not have free gas under the diaphragm due to
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the loss through the perforation being liquid only. This is rare in perforated gastric ulcer as this is a gas-filled organ. In patients with free gas the site of perforation will be colonic diver- ticular disease in a significant proportion.
Diagnosis of Perforation
This is a combination of history, clinical exam- ination revealing peritonitis and the presence of free gas on an erect chest X-ray or lateral decu- bitus abdominal X-ray. There is no role for endoscopy or barium study in such patients and the decision to operate is largely made on clinical grounds.
Treatment of Perforation
In those patients with occult perforation picked up on X-ray, who are stable with no physical signs, management is conservative.
This involves stopping NSAID ingestion and treatment with eradication therapy and mainte- nance therapy if the patient is on long-term steroids or requires NSAIDs for other pressing reasons. Such patients should be investigated at some stage to confirm the diagnosis, exclude gastric cancer and colonic diverticular disease.
For all other patients with a symptomatic presentation, the treatment is surgical after a short period of aggressive resuscitation. The approach can be by open surgery or laparo- scopically if appropriate skills exist. The basis of treatment of duodenal ulcer is closure of the perforation with an omental plug and thorough peritoneal lavage. If the ulcer is large with pyloric obstruction a gastrojejunostomy is advised. There is little role for gastric resection.
The patient should be given intravenous proton pump inhibitors or H2 receptor antagonists until oral intake can commence followed by eradication therapy. It is crucial in such patients to ensure eradication has been achieved. Future ingestion of NSAIDs and steroids should be reviewed.
In the case of gastric ulcer, care must be taken to exclude cancer. In fit patients with large per- forated lesser curve gastric ulcers, the treatment is Billroth II type gastric resection. If the patient is frail or the expertise does not exist, closure with sutures ± omental plug and biopsy of the ulcer margin should be undertaken. It is impor- tant to recognise that the base of such ulcers is frequently the pancreas with the splenic artery clearly visible.
It is vital to exclude at some stage gastric cancer. Such patients should have intravenous proton pump inhibitors or H2receptor antago- nists followed by eradication therapy as for duodenal ulcers. Emphasis is placed on the importance of thorough peritoneal toilet in all cases of perforation.
The advent of the laparoscope has led to experimental treatments gluing and plugging perforations. These should be treated with extreme caution and only performed with informed consent as patients do not suffer from a short midline incision and conventional suture.
Pyloric Stenosis
In all cases of gastric outlet obstruction secondary to presumed duodenal ulcer, every attempt must be made to exclude cancer either of the distal stomach or pancreas. If doubt exists on endoscopy and biopsy, CT scan, endoluminal ultrasound and even laparoscopy may need to be performed. This is now a rare complication. Such patients may if chronic have electrolyte disturbances, the classical picture being a hypokalaemic metabolic alkalo- sis. This needs correction before any therapy is given.
In cases where the diagnosis is made with confidence, the first-line treatment is with endoscopic or radiological balloon dilatation [10] associated with eradication therapy. In the few cases where this is not successful, surgery in the form of a gastrojejunostomy or pyloroplasty can be undertaken. It is now accepted that there is no need to perform a truncal vagotomy as medical treatment is so good and with eradication of H. pylori the risk of stomal ulceration is largely a thing of the past. In patients with chronic obstruction there may be some considerable delay before gastric emptying occurs. It is vital not to rush in with revisional surgery but to support with parenteral nutrition until emptying occurs.
To reassure the clinician a gentle endoscopy at 2 weeks will demonstrate a patent gastroje- junostomy.
There is no role for gastric resection in such cases unless there is obstruction of the gastric body by scarring from giant gastric ulcers.
These are now a thing of the past.
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Malignant Change in Peptic Ulcers
It is now accepted that malignant change never occurs in benign duodenal ulcers. If malignancy is detected on biopsy of a non-healing ulcer it is likely to be either a primary duodenal carci- noma or pancreatic cancer growing through the duodenal wall. These must be staged and treated appropriately.
If a risk occurs of malignant change in a benign non-healing gastric ulcer it is less than 1%. The likelihood is that it was primary gastric cancer all along as both are associated with infection with H. pylori. It emphasises the importance of multiple biopsies of non-healing gastric ulcers, and if doubt exists CT scanning and endoluminal ultrasound. Gastric ulcers sit- uated other than on the incisura of the lesser curve should be treated as cancer and treated by resection. Non-healing benign gastric ulcers on the incisura do occur. They are often associated with long-term steroid or NSAID ingestion and reflect a defect in the cytoprotective aspect of the gastric mucosa. Once malignancy and H.
pylori infection have been excluded by repeat biopsy and breath test, these ulcers are treated by long-term maintainance proton pump inhibitor therapy. If doubt exists or risk factors for haemorrhage are present they must be resected by either a Billroth I or II resection.
Complications of Previous Gastric Surgery
These can be classified as the six Ds: dumping, diarrhoea, deficiencies, delayed emptying, duo- denogastric reflux and dysplasia/cancer.
Any operation on the stomach whether it be a vagotomy, resection (partial or total) or even a gastrojejunostomy/pyloroplasty (bypass or damage the pylorus) exposes the patient to any or all of the above, the magnitude depending on the degree of insult. In general, surgery has little to offer any of these complications and should only be embarked upon when all medical ther- apies have been exhausted and the patient’s quality of life is unacceptable. Many of the com- plications post gastric surgery will improve with time and it is unwise to intervene in less than 1 year from the original surgery.
Dumping
This falls into two categories, early and late.
Early dumping results from early emptying of a hyperosmolar meal into the jejunum. This results in a shift of fluid into the gut lumen pro- ducing hypotension and feeling of lightheaded- ness. This can usually be controlled by eating smaller meals, separating liquids and solids.
Late dumping is due to hypoglycaemia sec- ondary to hyperinsulaemia resulting from a high glucose peak rather than the sustained rise seen in normal individuals. This occurs a few hours after eating and responds to oral glucose.
Diarrhoea
This was common following truncal vagotomy and drainage and is mainly due to rapid intesti- nal transit. It can be usually be managed by GI sedatives and dietary modification. Operations designed to slow transit by reversal of jejunal loops or reversed jejunal patches have been largely unsuccessful [11]. With the disappear- ance of vagotomy this complication, which can be disabling, is now a rare problem.
Deficiencies
These result from both the loss of gastric mucosa following resection and/or from intesti- nal hurry resulting in malabsorbtion.
The loss of a gastric reservoir following total gastric or high subtotal resection can restrict intake to such a degree that weight cannot be maintained. This is best treated by strict dietetic supervision with small regular high calorie/
protein intake. In rare cases nocturnal supple- mentation with a jejunostomy may be needed.
Similarly following Billroth II resection duode- nal secretions may never “catch up “ with gastric contents. If such an afferent loop syn- drome exists an enterostomy below the gastro- jejunostomy may help.
The usual means of reconstruction post total gastrectomy is by oesophagojejunostomy and Roux-en-Y. In a small group maintenance of weight can be a problem. Conversion to a jejunal pouch between the oesophagus and first part of the duodenum has been advocated as a preferred means of reconstruction [12]. It is, however, more complicated and should be reserved for rare cases of malnutrition resistant to all other means.
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The stomach is crucial for the absorption of vitamin B12 and all cases of total gastrectomy will require lifetime replacement therapy. The stomach is also important for the reabsorption of iron and calcium and all cases of total and high subtotal resection are advised to take regular mineral and vitamin supplements.
Delayed Gastric Emptying
Any case of truncal vagotomy is subject to delayed emptying. In one-third of cases this will be significant resulting in severe gastric stasis.
This was the reason why operations involving truncal vagotomy were combined with a drainage procedure – gastrojejunostomy or pyloroplasty. These additional procedures ame- liorate this problem in cases other than those with pre-existing pyloric stenosis when poor emptying can persist. The other operation asso- ciated with delayed gastric emptying is truncal vagotomy, antrectomy and Roux-en-Y recon- struction performed to combat severe duo- denogastric or gastro-oesophageal reflux when a fundoplication cannot be performed or has failed. It is not uncommon for patients having undergone this operation to fail to empty their stomachs for many weeks. They require pro- longed intravenous or enteral feeding. It is important to exclude a technical problem by gentle endoscopy but resist the temptation if all anastomoses are patent to reoperate. It will improve with time.
Truncal vagotomy will also influence gall bladder motility and is associated with an increased incidence of gallstones.
Duodenogastric Reflux
In any operation in which the pylorus is resected or bypassed, duodenogastric reflux will occur.
In most cases the patient is asymptomatic and requires no treatment. In a few however, there will be associated postprandial pain and bilious vomiting. Confirmation that this is due to duodenogastric reflux can be achieved by either a HIDA scan [13] or a provocation test. This involves the passage of a nasogastric tube into the afferent limb or duodenum.
Cholecystokinin is given and duodenal contents aspirated. The tube is withdrawn into the stomach and the patient given either saline, duodenal secretions or acid “blind”. If the
symptoms are reproduced only by the duodenal secretions then revisional surgery can be under- taken with some degree of success. In cases of pyloroplasty, this can be reversed, a gastroje- junostomy can be taken down and a Billroth II gastrectomy converted to a Roux-en-Y. In cases associated with a truncal vagotomy, at least 1 year should elapse before reversal to allow normal gastric emptying to occur.
Dysplasia and Carcinoma
There is now a well-established association between duodenogastric reflux consequent upon a gastrojejunostomy alone or associated with partial gastric resection and an increase incidence of gastric cancer [14]. These tumours are found at the site of the afferent limb and have a latent period of at least 20 years. The duo- denogastric reflux produces chronic irritation of the anastomosis leading to a hyperplasia/
dysplasia/carcinoma sequence. Although the prognosis for these so-called gastric stump car- cinomas is poor they should be staged and treated as for primary cancer of the stomach.
The only other significant complication of gastric surgery is an increased incidence of tuberculosis and fungal infection due to the loss of the gastric acid barrier.
Inflammation of the Stomach
Acute gastritis can follow any insult on the gastric mucosa by such things as drugs, spicey foods and acute infection with H. pylori. This will usually heal when the irritant is removed.
In patients on the intensive care unit, gas- trointestinal haemorrhage can occur from acute gastritis which can progress to superficial widespread gastric erosions. This is the result of mucosal ischaemia failing to sweep away the hydrogen ions which have penetrated the epithelial cells. Prevention of this complica- tion is achieved by maintaining a high intralu- minal pH by either intravenous H2 receptor antagonists, proton pump inhibitors, coating the mucosa with sucralfate or neutralising the gastric pH with antacids via a nasogastric tube. A total gastrectomy may be required if the bleeding becomes torrential although the mortality of this is in excess of 80%.
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In contrast, chronic gastritis is characterised by a mucosal infiltration with lymphocytes and plasma cells. It is usually persistent and pro- gressive to atrophic gastritis. In most cases this is associated with infection with H. pylori. If this progresses to intestinal metaplasia (type 3) in which differentiation is lost and which can be regarded as a form of dysplasia, an increased risk of gastric cancer appears.
The link between the immune system and chronic gastritis has been established in those patients with pernicious anaemia in whom anti- intrinsic factor and anti-parietal cell antibodies can be demonstrated. These patients have a fourfold increase in gastric cancer and should have regular surveillance by gastroscopy.
Other forms of gastritis include granuloma- tous gastritis from Crohn’s disease involving the stomach and hyperplastic gastritis in Ménétrier’s disease which may present with hypoproteinaemia.
Gastric Volvulus
This condition is frequently symptomless and is a chance finding on a barium meal examination.
When symptoms occur they are usually of sudden onset of vomiting and severe epigastric or retrosternal pain. It is invariably associated with a para-oesophageal hiatus hernia especially if of the organoaxial type. Treatment is surgical and involves repair of the diaphragmatic defect and fixing the greater curve of the stomach to the anterior abdominal wall by means of sutures or by performing a high greater curve gastros- tomy and posterior gastrojejunostomy.
Acute Gastric Dilatation
This usually presents as a complication of upper abdominal surgery especially splenectomy. The patient complains of shoulder tip pain and hiccoughs. If not recognised, the patient can rapidly become shocked and may die from a vomit and massive aspiration. Treatment is by passage of a wide bore nasogastric tube. This condition can occur in patients suffering from anorexia nervosa and other psychiatric condi- tions such as depression, especially when they are prescribed large doses of psychotropic drugs.
Gastric Bezoars
These can be composed of hair – trichobezoars, or vegetable matter – phytobezoars which can be precipitated by gastric stasis post vagotomy.
Attempts can be made to break them up endo- scopically or with pancreatic enzymes. If large, however, they will need removal by open surgery.
Trauma to the Stomach and Duodenum
These organs are at risk from both sharp and blunt injury, particularly when the stomach is full. In all cases of gastric and duodenal trauma, care must be taken to exclude injury to other organs, especially the pancreas.
Gastric Surgery for Morbid Obesity
Morbid obesity is defined as a body weight 100%
greater than the ideal weight. Before contem- plating surgery, endocrine disorders and hypo- thalamic lesions which cause obesity must be excluded. The need to reduce weight is based on the major increase in mortality associated with morbid obesity. There is a 14-fold increase if the patient is 100% above ideal weight.
The success of diet and psychological modi- fication of eating habits is disappointing in this group. Early surgical procedures to help weight loss are either disappointing (jaw wiring) or have an unacceptable morbidity and mortality (jejunoileal bypass). Current surgical approaches focus on the stomach and are based on suppressing appetite by producing early full- ness using a vertical banded gastroplasty or placement of an inflatable cuff. These can be performed using minimal access techniques. An alternative approach involves a combination of reduced gastric capacity with malabsorption produced by a Roux-en-Y gastric bypass and biliopancreatic bypass.
The importance of full medical and psycho- logical preparation cannot be overstated, and in the postoperative period the patients need careful monitoring as they are at high risk of respiratory and thromboembolic complica-
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tions. Patients often end up with a degree of mal- absorbtion, and the haemoglobin, iron, Vitamin B12and calcium should be regularly monitored.
Gastroplasty leads to weight reduction to within 50% of the ideal weight in 23% of cases com- pared with 55% for gastric bypass, although evidence from long-term follow-up is poor [15].
Questions
1. Is there a role for surgery in the primary treatment of peptic ulceration?
2. Should all patients with suspected pep- tic ulceration have endoscopy before commencing therapy? If not who should?
3. Should H. pylori be eradicated in the asymptomatic patient?
4. What are the indications for mainte- nance therapy in patients with peptic ulcer?
5. When should patients with upper GI haemorrhage be endoscoped?
6. What is the best means to control bleed- ing endoscopically?
7. What are the indications for surgery in upper GI bleeding and what operation should be performed?
8. How should chronic peptic ulcers be managed?
9. When considering revisional surgery for the complications of previous gastric surgery what factors should be consid- ered in the timing of such procedures?
10. What is the interval for the genesis of gastric stump cancer, and how should at-risk patients be followed up?
11. What are the indications for surgery for gastric volvulus and what operation should be undertaken?
12. What are the indications for surgery in morbid obesity and what are the risks associated with it?
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14. Clarke CG, Fresini A, Gledhill T. Cancer following gas- tric surgery. Br J Surg 1985;72:591–4.
15. Renquist KE, Cullen JJ, Barnes D et al. The effect of followup on reporting success for obesity surgery. Obes Surg 1995;5:285–92.
Further Reading
Burnand KG, Young AE (eds). The new Aird’s companion in surgical studies 2nd edn. London: Churchill Livingstone, 1998.
Griffin SM, Raimes SA (eds). Upper gastrointestinal surgery London: WB Saunders, 1997.
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