Consesus On Management Of Peptic Ulcer Disease
1. H.Pylori Related Peptic Ulcer Disease
Helicobacter Pylori and Its Role in peptic Ulcer Disease
How is H. Pylori Infection Diagnosed
Treatment Of H.Pylori
2. Non-H.Pylori Related Peptic Ulcer Disease
A. Non-Steroidal Anti-Inflammatory Drugs and peptic Ulcer Disease
Risk Factors for NSAID Induced Ulcers
Treatment of NSAID Induced Ulcers
Risk of Ulcer Complications Associated with Individual Non-Aspirin NSAID use
Relative risk of UGIB Associated with individual NSAID'S
B. Refractory Ulcer
C. Long Term Maintenance Therapy
D. Stress Ulcer
Aetiology and Risk Factors
2. Antisecretory agents
3. Role of Endoscopy in Peptic Ulcer Disease
Diagnosis of Peptic Ulcer
Medical Management of Bleeding peptic Ulcer
Prognostic Stigmata of Bleeding Peptic Ulcer
Endoscopic Haemostasis of Bleeding Peptic Ulcer
Endoscopic Management of Benign Peptic Pyloric Stricture
4. Role of Surgery in Peptic Ulcer Disease
A. Surgery for Uncomplicated Duodenal Ulcer
B. Surgery for Complication of Duodenal Ulcer
C. Surgery for Uncomplicated Gastric Ulcer
D. Surgery for Complications of Gastric Ulcer
E. Laparoscopic Surgery in peptic Ulcer Disease
6. Expert Commitee
7. Appendix 1
EXPERT COMMITTEE Chairperson: Dato Dr (Mrs) S T Kew Secretary : Dr Tan Soon Seng Dr Zainal Ariffin Hashim H.pylori Related Peptic Ulcer Disease A Prof K L Goh (Chairman) A Prof N Parasakthi A Prof Mahendra Raj A Prof Isa Ros A Prof Mazlam Mohd Zawawi Non-H.pylori Related Peptic Ulcer Disease Dato Dr (Mrs) S T Kew (Chairman) - NSAID & Peptic Ulcer Disease Dato Dr F K Chan - Refractory Ulcers Dr Andrew Chua - Long Term Maintenance Therapy Dr K Inbasegaran - Stress Ulcers Role of Endoscopy in Peptic Ulcer Disease Dr T P Yin (Chairman) A Prof Damien Wong Dr Anand Bhupalan Role of Surgery in Peptic Ulcer Disease Dato Dr J C Mehta (Chairman) Dato P Kandasami Mr Robert Jalleh Mr K T Ong Mr Ng Chuan Wai
1. H.Pylori related Peptic Ulcer Disease
Helicobacter Pylori and its Role in Peptic Ulcer Disease:
Evidence strongly suggests a causal relationship between H. pylori and peptic ulcer disease: H pylori is found in the majority of ulcer patients (>90% of duodenal ulcers and 70-90% of gastric ulcers), H. pylori causes chronic gastritis which is strongly correlated with peptic ulcer disease and H.pylori eradication results in marked reduction or abolition of ulcer recurrence. H.pylori eradication is recommended in H.pylori positive peptic ulcer patients.
There is no convincing data of an association between H.pylori and non ulcer dyspepsia at this point in time. H.pylori eradication cannot be routinely recommended in H.pylori positive NUD patients.
How is H.Pylori Infection Diagnosed?
Following the above recommendations, biopsy tests for H.pylori when ulcer disease is diagnosed at endoscopy should be performed.
For routine diagnosis, a rapid urease test and/or histological examination where expertise is available is recommended. H.pylori is invariably found in the gastric antrum. Sampling error due to uneven distribution of the bacteria is minimized if two biopsies from the antrum are taken.
Routine testing for successful H.pylori eradication is probably not necessary. Patients with complicated ulcers especially when discontinuation of acid-suppressing maintenance therapy is contemplated should be assessed for H.pylori eradication. Testing of eradication should be done not earlier than 4 weeks after completion of the eradication regime.
When assessing for H.pylori status following treatment, where endoscopy is not indicated (eg. uncomplicated duodenal ulcer), a radiolabelled carbon urea breath test is recommended where available. When endoscopy is indicated at follow-up (eg. to confirm gastric ulcer healing), an endoscopy biopsy test is recommended; both antral and body biopsies should be taken for testing.
A positive serological test for H.pylori reflects exposure to H.pylori. Laboratory based ELISA tests are acceptable methods of diagnosis but kits vary in their sensitivity and specificity. Furthermore, antibody titres decrease slowly over months after successful eradication. Post-treatment assessment of H.pylori status using serology is impractical and therefore not routinely recommended. Rapid qualitative blood tests (office based tests) may become useful tests in the future but need further evaluation.
At this present point in time, treatment to eradicate H.pylori is recommended in patients with peptic ulcers and proven H.pylori infection.
Treatment with any single agent is ineffective. Combination therapy with two or three drugs are needed.
Several treatment regimes are recommended: The bismuth triple therapy regime consisting of colloidal bismuth subcitrate and 2 antibiotics, metronidazole and tetracycline or amoxycillin for 2 weeks, is well established and gives consistent eradication rates of 80-90%. Side-effects have been reported in about 30% of patients in clinical trials and are normally minor.
Triple therapy with H2 antagonists and two antibiotics; metronidazole and amoxycillin or tetracycline have also been used: eradication rates of greater than 80% have been recorded. Similar side-effects as for the bismuth triple therapy are experienced by patients.
Omeprazole and amoxycillin or clarithomycin for 2 weeks achieves eradication rates of up to 80%; however, eradication rates have been inconsistent. Dual therapy regimes are well tolerated.
Recent studies indicate that a one week treatment with omeprazole 20mg daily or bd, with 2 of the following antibiotics: metronidazole or amoxycillin or clarithromycin achieves consistent eradication rates of greater than 90%. These regimes also appear to be well tolerated.
Newer drugs and regimes will constantly become available. Treatment regimes should not only be safe but simple to take and cheap.
Reinfection following successful eradication
appears to be low in our community and will not nullify the effect of successful
eradication. As with other bacterial infections, emergence of antibiotic resistance
particularly to nitroimidazoles may pose therapeutic problems. Indiscriminate use of
antibiotics to treat H.pylori may increase the problem of antibiotic resistance.
Therapeutic regimes that have
been used for eradication of H.pylori include:
|-Colloidal bismuth subcitrate 1 tablet (120mg)
qid or 2 (240mg) tablets bd
- Amoxycillin 500mg tds or
Tetracycline 500mg tds
- Metronidazole 400mg tds for 2 weeks
|-Omeprazole 40mg daily or 20mg bd
- Amoxycillin 500mg tds
or Clarithromycin 500mg tds for 2 weeks
|-Omeprazole 20mg daily or bd and 2 of the
- Metronidazole 400mg bd
- Amoxycillin 500mg bd
- Clarithromycin 250mg or 500mg bd for 1 week
|-Histamine - 2 receptor antagonist
(eg. Ranitidine 300mg daily or Famotidine 40mg daily)
- Amoxycillin 500mg tds
- Metronidazole 400 mg tds for 2 weeks
2. Non-H.pylori Related Peptic Ulcer
A. Non-steroidal Anti-inflammatory Drugs and Peptic Ulcer Disease
NSAIDs including Aspirin are among the most commonly prescribed drugs. The association of gastroduodenal mucosal damage and NSAID use is well documented, with relative risk of developing adverse gastrointestinal events approximately three times in users compared to non-users.
NSAID induced gastropathy may either take the form of acute mucosal petechiae, haemorrhages or erosions; or less acute, larger submucosal ulcers of the stomach or duodenum.
All NSAIDs are capable of inducing mucosal injury, and there is no consistent difference in the degree of mucosal damage among the various NSAIDs. In several case control studies, the odds ratios of some NSAIDs in causing upper gastrointestinal bleeding and perforation are lower than others (See Appendix 2 & 3).
Newer NSAIDs which are acid-insoluble, pro-drug, parenterally administered, or enteric coated formulation do not appear to reduce potential for causing gastrointestinal damage especially with long term use. With short term use, however, gastric mucosal injury from a topical effect is decreased with enteric coated formulations.
Risk Factors for NSAID Induced Ulcers
Include: Elderly persons (>65 years)
Severe co-morbid conditions
Past history of peptic ulcer disease or upper gastrointestinal bleeding
Arthritis related disability, the greater the disability the greater the risk
NSAID related risk factors
Dose dependence relationship - higher dosage of NSAID increases risk2 or more NSAIDsNSAID given with steroidNSAID given with anticoagulantHighest risk in the first month of therapy
The best approach of NSAID induced gastropathy is prevention. If the clinical situation only requires analgesia, then physical therapy, paracetamol or other non-opiate analgesics should suffice. NSAIDs are used only when they are absolutely indicated. The least ulcerogenic agent at the lowest therapeutically effective dose is recommended.
An agent for prophylaxis should be considered in persons at significantly increased risk of NSAID induced gastropathy. The only effective prophylaxis proven to protect against both gastric and duodenal ulcers is prostaglandin analogue (eg. Misoprostol). The dose recommended for prophylaxis is 400 - 800 ug/day in divided doses.
H2 receptor antagonists in standard doses reduces risks of NSAID induced duodenal ulcers but not gastric ulcers. Use of H2RA is reasonable as prophylaxis if such agent has previously healed NSAID induced duodenal ulcers in the same patients.
Proton pump inhibitor (eg. Omeprazole) used prophylactically reduces risks of NSAID induced gastropathy in the short term.
Treatment of NSAID induced ulcers
First step in the treatment of NSAID induced ulcers is the withdrawal or reduction of dose to the lowest minimum of NSAID. For NSAID induced duodenal ulcers and smaller gastric ulcers, full dose of H2RA should be prescribed for a minimum of 8 weeks. For larger gastric ulcers, proton pump inhibitor (eg. Omeprazole at 20 - 40 mg/day) for 8 weeks is recommended. Alternatively full dose of H2RA for up to 12 weeks is as effective in healing larger NSAID induced gastric ulcers. Prostaglandin analogue (eg. Misoprostol at 800 ug/day in divided doses) is also effective in healing NSAID induced GU and possibly DU.
If the clinical situation requires the continued administration of NSAID in the presence of healed ulcer, concurrent administration of anti-secretory drugs or prostaglandin analogue is recommended.
No. of Cases
Odds ratio (95% CI)*
31.5 (10.3-96 9)
|Any non-aspirin NSAID||
|Not on NSAID or aspirin||
*All odds ratios from unconditional logistic regression model with terms for aspirin use, smoking, alcohol, previous peptic ulcer, and history of dyspepsia. For azaproprazone, to obtain convergence, aspirin use was not included.
Risks of ulcer complications associated with individual non-aspirin NSAID use during previous 3 months
Ref : Langman MJS, Weil J, Wainwright P: Risks of bleeding peptic ulcer associated with individual non-steroidal anti-inflammatory drugs. Lancet 343:1075-78, 1994.
Cases (n= 862)
Controls (n= 9017)
Adjusted relative risk (95% CI)
|NSAID current use||.||.||.|
Only patients with no history of peptic ulcer were included.
Relative Risk of UGIB Associated with Individual NSAIDS
ef :Gatrcia Rodriguez LA, Jick H: Risk of upper gastrointestinal bleeding and perforation associated with individual non-steroidal anti-inflammatory drugs. Lancet 343:769-72, 1994.
Refractory ulcer, non-healing ulcer, resistant ulcer, and slow to heal ulcer are some of the terms used to describe ulcers that are difficult to heal. Though there is no consensus on the terminology, with current available therapies, truly non-healing ulcers are rare, the term "Slow-to-heal" ulcers may be a more accurate description of such ulcers.
Refractory ulcers are peptic ulcers that do not heal following at least 3 months of treatment with H2 receptor antagonist or proton pump inhibitor at standard doses recommended for ulcer healing.
Malignancy must be excluded conclusively in all ulcers that are slow to heal.
Certain factors have been known to be associated
with delay in healing of ulcers, attempts should be made to elucidate such factors in the
management of these patients.
2. Non-compliance with recommended therapies.
3. Usage (including surreptitious use) of NSAIDs, and steroid.
4. Gastrinoma, as Zollinger-Ellison syndrome or Multiple endocrine adenomatosis, typically manifests
as non-healing ulcers.
5. Non-peptic ulcers:
a. Crohns Disease.
c. Behcets disease.
d. Metastatic ulcerated lesions (to upper GIT)
e. ulcerated leiomyoma, leiomyosarcoma.
1. Where specific diagnosis has been made, appropriate therapies should be given.
2. Repeat upper GI endoscopy and multiple biopsies of ulcers (at least 6 biopsies at edges of ulcers)
must be obtained at each and every endoscopy until healing is complete and documented.
3. All patients should be advised to stop smoking.
4. Stop or reduce the use of NSAIDs and steroid when this is feasible. Consider alternative in place of
Options for treatment include:
1. Proton pump inhibitor offers the best option for treatment. A higher dose of proton pump inhibitor is
usually necessary and it may be necessary to continue treatment for at least 3 months. Surgical
option should be considered if ulcer remained unhealed after 6 months of therapy.
2. Should relapses occur following termination of treatment, maintenance therapy with proton pump
inhibitor at dosages comparable to that used for ulcer healing may be necessary to prevent relapses.
C. Long Term Maintenance Therapy
Long term maintenance therapy is desirable to prevent recurrence only in selected high risk patients:
1. Patients with known history of complicated ulcers which are non H pylori related or have failed
2. Patients with known history of ulcer disease on NSAID therapy
3. Patients with underlying conditions predisposing to ulcer recurrence.
With respect to complicated ulcers in patients who have H.Pylori eradicated the data is not clear. Long term maintenance therapy may be given until further results are available.
The most thoroughly investigated drugs which have been used in the long term maintenance therapy of ulcer disease are the H2-receptor antagonists. There is conclusive evidence that H2-receptor antagonists substantially reduce the frequency of symptomatic relapse, and reduce the recurrence of duodenal ulcer haemorrhage. The proton pump inhibitors have been shown to be an effective and safe alternative to the H2-receptor antagonists. Other substances such as sucralfate, prostaglandin analogues or antacids are not used to the same extent as the H2-receptor antagonists for long term therapy.
An alternative option which may be more cost effective to long term maintenance therapy is intermittent treatment. There is yet no evidence to prove that intermittent therapy is a safe and effective alternative to continuous maintenance therapy. Until more conclusive data is available, continuous therapy is preferred.
In patients with no contraindications, surgery is an alternative to long term maintenance therapy.
The term stress ulcers is used to describe a group of mucosal lesions of the oesophagus, stomach or duodenum that occur in the critically ill or otherwise stressed patient. The type of lesions that occur can vary from small petechial haemorrhages and erosions to deep ulcerations and occasional perforations. The true incidence of stress ulcers as diagnosed endoscopically varies from 20% to 50% in all intensive care patients not receiving prophylaxis for stress ulcers. However only about 2% of them develop clinically significant bleeding which requires active resuscitation and surgical or medical therapy.
and Risk Factors
The development of stress ulcers appears to be dependent on three factors: namely the presence of gastric acid and pepsin, reduction of mucosal blood flow from any cause such as hypotension and increased mucosal permeability brought about by lack or decreased local cytoprotection.
There are certain well known risk factors in the
critically ill that are closely associated with the development of stress ulcers. These
include the following:
1. Mechanical ventilation for more than 48 hours
2. Presence of sepsis
3. Hypotension or hypovolaemic shock
4. Acute respiratory failure, in particular ARDS
6. Steroid therapy
7. Multiple trauma
8. Severe head injury
9. Burns of more than 25% body surface area
11.Acute renal failure with sepsis.
The most significant risk factors are mechanical ventilation, sepsis, prolonged hypovolaemia and coagulopathy. In a number of patients multiple risk factors may be present.
The management of clinically significant bleeding will depend on the severity. The cause of the bleeding must be confirmed endoscopically as soon as possible and blood loss replaced appropriately. Other measures will include the administration of Oxygen, increasing intraluminal pH with H2 receptor antagonists or antacids and appropriate surgical and medical intervention described elsewhere in this document.
The most important prophylaxis is to ensure that the critically ill patient receives optimal supportive therapy. This includes adequate tissue oxygenation, maintenance of adequate intravascular volume and good perfusion pressures. These measures may require fluid loading, use of inotropes as well as vasodilators. Enteral feeding has been shown to reduce significantly the incidence of gastrointestinal bleeding and this should be started as soon as possible in the critically ill patients as long as there is no contraindication.Pharmacological prophylaxis should be used in patients with risk factors whether single or multiple.
In general, the pharmacological prophylaxis is directed towards the reduction of the volume of gastric acid secretion thereby reducing its acidity (ie increase in pH) or offering mucosal protection (cytoprotective effect).
Sucralfate is a non absorbable aluminium salt of sucrose octasulphate that has no effect on gastric secretion or acidity. Its mechanism of action is multiple including binding to pepsin and bile salts, cytoprotective effect, binding to exposed proteins among others. It has been shown to be as effective as Histamine-2 receptor antagonists in the prevention of stress ulcers and has no significant side effects. As it does not affect acidity, it does not increase the incidence of nosocomial pneumonia. The recommended dosage is 1 gm dissolved in 10 ml aliquots of water administered via a nasogastric tube every 6 hours. Currently it is the preferred choice for stress ulcer prophylaxis.
a. Histamine-2 receptor antagonists
The Histamine-2 receptor antagonists decrease gastric acid secretion as well as increase the pH. Long term use has been shown to produce bacterial overgrowth and a significantly increased incidence of nosocomial pneumonia. This is more common in intubated and ventilated patients. Bolus dosing of Histamine-2 receptor antagonists while effective in reducing acid secretion is not effective in maintaining the pH above 4 at all times. A continuous infusion will maintain the pH above 4 at all times, but may not be practical at most times.
Suggested dosages are as follows:
a. Cimetidine - 200 mg i.v. 6 hourly
b. Ranitidine - 50 mg i.v. 8 hourly
a. Cimetidine - 50-100 mg hourly after a bolus of 200 mg
b. Ranitidine - 6.25 - 12 mg hourly after a bolus of 50 mg
It would be preferable to monitor and maintain the intragastric pH at all times.
b. Proton pump inhibitors
Drugs belonging to this class of agents (eg. omeprazole) have been shown to reduce gastric secretions to very low levels. They have been shown to be effective in stress ulcer prophylaxis, but they also cause a higher than usual incidence of nosocomial pneumonia by the same mechanisms. The suggested dosage is 40 mg once daily.
Prophylactic therapy, though not totally
preventing the occurrence of stress ulcers, prevents the progression, reduces the severity
and expedites healing. In general, prophylactic therapy does not change the mortality of
the critically ill; the mortality is ultimately dependent on the underlying disease
process. Over the last two decades the incidence of stress ulcer related bleeding has
decreased dramatically independent of stress ulcer prophylaxis. This is attributed to
improvement in the management of the critically ill with inotropic drugs, vasodilators and
adequate intravascular volume replacement resulting in improved tissue oxygenation and
3. Role Of Endoscopy In Peptic Ulcer Disease
of Peptic Ulcer
Endoscopy is the investigation of choice in the evaluation of patients suspected of peptic ulcers. In the era of Helicobacter pylori infection this role is further enhanced as endoscopy allows direct proof of the infection to be made. Double contrast barium meal is an alternative investigation if endoscopy is not available. This investigation suffers from the inability to allow histological diagnosis when required and is unable to provide information on Helicobacter pylori status. Re-endoscopy is recommended for gastric ulcers to confirm healing.
Medical Management of Bleeding Peptic Ulcer
Acid suppression with H2 receptor antagonists and proton pump inhibitors are given in bleeding peptic ulcers to initiate ulcer healing. There is no evidence from clinical trials that these drugs are helpful in arresting ulcer bleeding, or in reducing transfusion requirement, emergency surgery and mortality.
Gastric lavage or the use of pharmacological agents like vasopressin, somatostatin and tranxenamic acid has not been proven to be effective as well.
80% of all bleeding peptic ulcers stop spontaneously. The reduction in morbidity and mortality in the small group of patients that continue to bleed or rebleed is the prime objective of current endoscopic and surgical approach.
Following resuscitation measures endoscopy is to be performed as soon as possible for actively bleeding patients. For the stable patient who appears to have stopped bleeding, the timing of endoscopy can vary considerably depending on the clinical situation. It is preferable to perform endoscopy within 24 hours if small lesions are not to be missed.
Prognostic Stigmata Of Bleeding Peptic Ulcer
The appearance of peptic ulcer at index bleed allows us to make prediction of its natural history and behaviour, and the indication for endoscopic haemostatic intervention. A clean base ulcer has a 5% rebleeding rate, and can be observed for a day and discharge without intervention in the majority of cases. A flat spot and adherant clot ulcers have a 10% and 20% rebleeding rates respectively and is advisable to be observed in a general ward for two to three days without endoscopic therapeutic intervention. The ulcer with non bleeding visible vessel and actively bleeding features have a rebleeding rate of 40 to 50% and will require active endoscopic haemostatic intervention, and where available, these patients are best observed in an intensive care unit or high dependency unit setting.
Endoscopic Haemostasis of Bleeding Peptic Ulcer
Injection of bleeding ulcer with dilute adrenaline (1:10,000), using aliquots of 0.5 ml each injection, around and into the bleeding spot, is efficacious in 84 - 94% of cases. This technique requires very little learning curve and is cost effective, with minimal complications. Other techniques like heater probe, bipolar and laser add little to reduction of mortality rate, although some trials suggested that heater probe has advantage over bipolar probe. Laser therapy suffers from high cost and immobility of the equipment. Haemoclip as a new method of endoscopic haemostasis may in future prove to be superior to other techniques. There is no agreement whether endoscopic haemostasis should be repeated if rebleeding occurs. The recommendation of the committee is that all such patients be offered surgical treatment except in specialised endoscopy unit.
Endoscopic Management of Benign Peptic Pyloric Stricture
According to published data, balloon dilatation through the endoscope achieved successful dilatation in the majority of cases with minimal complications. Improvement is however temporary and repeated dilatation may be required for long term relief. Endoscopic dilatation is recommended for patients who refuse surgery and for those whose general condition precludes surgery.
4. Role Of Surgery In Peptic Ulcer Disease
Despite the introduction of acid-reducing and Helicobacter pylori eradication therapies in the treatment of peptic ulcer disease, there remains a definite role for surgery in the management of peptic ulcer disease especially when dealing with its complications.
A. Surgery for Uncomplicated Duodenal
Where surgery is indicated, the recommended operations include truncal vagotomy and drainage (either posterior gastroenterostomy or pyloroplasty) with its acceptably low morbidity and recurrence rates.
Highly selective vagotomy (parietal cell vagotomy/proximal gastric vagotomy) is encouraged in those familiar with this procedure for its superior results if its completeness can be assured.
B. Surgery for Complications of
The common complications are bleeding, perforation and stenosis.
It is recommended that a joint approach between physician/gastroenterologist and surgeon be adopted in the management of bleeding duodenal ulcer. This is to reduce the morbidity and mortality associated with delayed surgical intervention.
Rigorous resuscitation with monitoring should be initiated immediately until haemodynamic stability is achieved.
Early endoscopic diagnosis preferably within 24 hours is essential. Those inappropriate for endoscopic techniques of haemostasis are then selected for surgery.
1.3 Surgical indications
Early surgery should be considered in the presence of any one of these criteria:
a. Hypovolaemic shock on admission (<90mmHg)
b. Age 65 or more
c. Resuscitation requirement of ³ 4 units blood in the first 24 hours
d. Signs of continuing haemorrhage
e. History of a previous admission for an ulcer complication
f. Ulcer size >2cm or with stigmata of recent haemorrhage (despite endoscopic haemostatic
g. Co-morbid factors
The majority of clinically significantly bleeding ulcers are posterior ulcers. Underruning of the bleeding ulcer alone or together with truncal vagotomy and pyloroplasty is a safe and expedient option in the poor risk patients. Anterior ulcer may be excised and incorporated into the pyloroplasty.
In the presence of a large duodenal ulcer, partial gastrectomy is recommended for its lower risk of rebleeding but there is an increased risk of duodenal leak compared to vagotomy and pyloroplasty. If vagotomy and pyloroplasty is inappropriate or has been performed previously, partial gastrectomy is the preferred option.
The first-choice operation is simple omental patch closure with meticulous peritoneal toilet. A definitive ulcer-treating procedure should only be considered in the haemodynamically stable patient and in the absence of gross contamination. Truncal vagotomy and drainage is recommended and highly selective vagotomy should be reserved for those familiar with the technique.
In cases where gross duodenal distortion or large perforation prevents satisfactory patch closure, partial gastrectomy is recommended.
Simple closure alone should be followed by long-term ulcer therapy or Helicobacter pylori eradication where indicated.
Duodenal stenosis not responding to medical or endoscopic therapy requires surgery. The recommended operation is truncal vagotomy with a drainage procedure.
C. Surgery for Uncomplicated Gastric Ulcer
Surgery is indicated in the presence of:
1. Refractory ulcer
2. Large gastric ulcers (>3cm)
3. Suspicion of malignancy
Gastrectomy incorporating the ulcer is the operation of choice. A prepyloric ulcer can be treated as a duodenal ulcer.
D. Surgery for Complications of Gastric Ulcer
The preferred option is partial gastrectomy including the ulcer. Other choices include ulcer excision or underrunning of the bleeding point with or without vagotomy (followed by ulcer therapy).
Gastric resection is ideal if feasible. If malignancy can be confidently excluded or the patient is too ill, ulcer excision with omental patch followed by ulcer therapy is acceptable.
E. Laparoscopic Surgery In Peptic
Major advances have been made in the application of laparoscopic techniques in both elective and emergency ulcer surgery. These include highly selective vagotomy, posterior truncal vagotomy with anterior seromyotomy, vagotomy and gastrojejunostomy or pyloroplasty, laparoscopic repair of perforated ulcer and gastrectomy. Although the feasibility of these procedures has been established, further considerations including efficacy, cost-effectiveness and training need to be made before they can be advocated in Malaysia.
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21st Jun 2000