Surgery for peptic ulcers is performed less often since the advent of the H2 antagonists. Subsequently proton pump inhibitors (PPIs) and the treatments to eradicate Helicobacter pylori have further reduced the requirement for surgery. Nevertheless, there are still some complications that require surgical interventions and many patients still alive who have had surgery for peptic ulcers. Surgery for uncomplicated peptic ulcer disease has become less common but problems related to medication are relatively more important (NSAIDs and even COX-2 inhibitors). It should be remembered that although the frequency of PUD is decreasing in the developed world it is increasing in developing countries.
Complications of peptic ulceration
Since recurrent ulceration is a complication following peptic ulcer surgery the complications of peptic ulceration should be borne in mind. Briefly these are:
- Malignant change
Indications for surgery
There are still indications for surgical interventions:
- Intractable ulcers
- Obstruction, usually pyloric stenosis
The options for malignant ulcers are discussed in Gastric Cancer. The mortality associated with haemorrhage and perforation is still in excess of 10%. There are a variety of procedures that have been assessed.
The operations that have been used traditionally are:
- Billroth I gastrectomy
- Billroth II or Polya gastrectomy
- Truncal vagotomy and pyloroplasty
- Highly selective vagotomy
Gastric ulcers were in the past best removed together with the gastrin secreting zone of the antrum (achieved by the Billroth I gastrectomy).
Duodenal ulcers were treated by either removing the body and lesser curve of the stomach (where acid secretion mainly occurs) or by dividing the vagi. As this could interfere with gastric emptying it was performed with either gastro-jejunostomy or pyloroplasty. Gastro-jejunostomy alone was used occasionally in elderly patients but this was often complicated by stomal ulcers. In theory this achieved ulcer healing by introducing alkali secretions from the jejunum. Partial gastrectomy with a gastrojejunal anastamosis is called a Polya gastrectomy.
The partial gastrectomies are largely superseded by the vagotomy operations but many patients may be found who had such operations many years ago. Nowadays even operations to repair perforated ulcers are often performed via the laparoscope and there may be a lower risk of immediate complications in low risk patients. Gastric resection can also be achieved via the laparoscope.
Complications after surgery
Complications can occur soon after surgery. Early complications usually occur whilst the patient is still in hospital and include wound infections, anastomotic leaks, or recurrence of bleeding. However the later complications are worthy of closer consideration as they produce more unusual syndromes which present in the community, often with more insidious symptoms. These late complications vary according to the precise technique but generally they are more marked after partial gastrectomy than vagotomy. Simple truncal vagotomy would lead to failure of gastric emptying and so a drainage procedure such as pyloroplasty is performed but this leads to poor control of gastric outflow. Highly selective vagotomy is supposed to overcome the problem in that it does not require a drainage procedure. It requires great skill to get enough denervation to heal the ulcer but not too much to cause delayed gastric emptying. Highly selective vagotomy has a much lower incidence of complications but a significantly higher incidence of recurrence. Between 25 and 50% of patients have some problems after surgery for peptic ulcer but in only 1 to 5% are they disabling.
- Recurrent ulceration- 2% (probably rather more with highly selective vagotomy)
- Diarrhoea - 16%
- Dumping syndrome rates are as follows:
- Partial gastrectomy - 14 to 20%
- Truncal vagotomy and drainage - 6 to 14%
- Highly selective vagotomy - 2%
- Bilious vomiting - 10%
- Iron deficiency - 12%
- Vitamin B12 deficiency - 14%
- Folate deficiency - 34%
The stomach transforms the intermittent intake of food into a more gradual release into the duodenum and small intestine as well as initiating the process of digestion. The control of gastric emptying is both neural and hormonal. The post gastrectomy syndromes include:
- Small capacity or 'small stomach' syndrome is associated with fullness after only moderate sized meals and may be associated with weight loss and reduced appetite.
- Dumping syndrome can be early or late as set out in more detail below.
- Bile gastritis and bilious vomiting can occur particularly after emptying of the afferent loop of a Polya gastrectomy into the stomach remnant.
- Blind loop syndrome (sometimes called stasis syndrome or stagnant loop syndrome) affects digestion and absorption causing:
- Bloating, loss of appetite, abdominal pain and nausea
- Fatty stools (steatorrhea)
- Diarrhea with weight loss
- Food unable to move through the bypassed section of bowel produces a bacterial overgrowth syndrome. The bacteria may produce toxins as well as interfere with the absorption of nutrients.
- Anaemia usually results from iron deficiency from failure of iron absorption. It can also occur with loss of intrinsic factor and less B12 absorption (typically about 2 years after total gastrectomy).
- Steatorrhoea occurs particularly with a long afferent loop when fatty food is less well absorbed.
- Stomal ulceration complicates about 2% of gastrectomies for duodenal ulcer.
- Metabolic bone disease.
Highly selective vagotomy aims to maintain the nerves of Latarjet (branches of the vagus nerve which supply the pyloric sphincter) and obviate the need for an accompanying drainage procedure (usually pyloroplasty). Complications afterwards include:
- Steatorrhoea and diarrhoea are common after vagotomy (although this is less of a problem after highly selective vagotomy). Often such symptoms are transient or episodic. However, in about 2% of cases symptoms are severe or persistent.
- Stomal ulceration can occur particularly if the vagotomy is incomplete.
This is the most troublesome of the syndromes after surgery to eradicate peptic ulcer. It can be divided into early dumping and late dumping depending upon how soon after a meal the symptoms occur. After partial gastrectomy or vagotomy there is a tendency to expel the gastric contents into the duodenum too fast. Vagotomy increases the tone of the stomach, decreasing capacity and operations such as pyloroplasty reduce the ability to control the release of gastric contents.
Early dumping causes symptoms 30 to 60 minutes after a meal.
- Symptoms include:
- Desire to lie down (with fatigue, faintness and possibly syncope)
- Epigastric fullness
- Nausea, vomiting and diarrhoea
- Abdominal cramps and borborygmi
- Possible mechanisms for these symptoms include:
- Uncontrolled release of food into the duodenum leading to an increase in osmotic pressure so that water is drawn into the bowel. This may cause dilatation which then creates the symptoms of cramping pain, bloating and diarrhoea.
- Plasma volume is reduced (producing fatigue and faintness).
- This may be over simplistic and there is evidence that some of the enteric hormones have role to play. Both dumping syndrome and gastro-oesophageal reflux disease may be related to gastric hormones.
Late dumping occurs between 1 and 3 hours after a meal.
- Symptoms include:
- Sweating and tremor
- Difficulty concentrating and even reduced level of consciousness
- Possible mechanisms for these symptoms include:
- The rapid delivery of a large load of carbohydrate leads to an increase in secretion of insulin.
- This can be excessive and cause hypoglycaemia with associated symptoms.
Failure to absorb essential nutrients may be caused by a combination of factors:
- Poor dietary intake (as a result, for example, of bloating and decreased appetite)
- Intestinal hurry (with for example changes in the gut flora in blind loop syndromes
- Reduced intrinsic factor (for example after gastrectomy)
- Reduced acid secretion (after gastrectomy)
These may be vague and the onset is usually slow:
- Iron deficiency anaemia may be accompanied by fatigue. FBC will show a microcytic, hypochromic anaemia and ferritin will be low.
- Folate deficiency will cause macrocytosis and macrocytic anaemia. Poor intake and blind loop syndromes are probably to blame for this common problem.
- Pernicious anaemia occurs after partial gastrectomy. Production of intrinsic factor is reduced (and hence absorption of B12). This produces a macrocytic anaemia.
- A mixed picture results from a combination of iron, B12 and folate deficiency.
- Chronic intake of an inadequate number of calories will cause weight loss and even muscle wasting.
Patients who have had such surgery need long term follow up with periodic weighing, FBC, ferritin, folate and B12 levels.
- Small, frequent meals may enable an adequate intake of nutrients and reduce dumping syndrome. Avoid simple sugars and reduce fluid intake with meals.
- Iron and folic acid supplements may be required.
- Hydroxocobalamin injection, 1 mg every 3 months will prevent vitamin B12 deficiency.
- Acarabose can reduce the absorption of glucose and help prevent late dumping but it may also aggravate bloating and diarrhoea
- Octreotide is a somatostatin antagonist that can inhibit the release of insulin and various gut peptide hormones. Trials have shown benefit in severe dumping syndrome but it is not licensed for this purpose and may be prohibitively expensive as well as needing 3 or 4 injections a day.
- A number of surgical reconstructions are possible of which the best known is the Roux-en-Y gastrojejunostomy. Symptoms may improve with time and so remedial surgery should not be undertaken without giving time.
Further reading & references
- Padda SP; Dumping syndrome. eMedicine, 2005.
- Sawyer MAJ; Afferent loop syndrome. eMedicine, January 2006.
- Angel CA; Peptic Ulcer - Surgical perspective. eMedicine, 2005.; Orientated to paediatric surgery.
- Peptic ulcer disease, Surgical-tutor.org.uk
- Peptic ulcer is rare without H pylori or NSAID, Bandolier
- Dyspepsia - proven peptic ulcer, Clinical Knowledge Summaries (June 2008)
- Lanas A; Prevention and treatment of NSAID-induced gastroduodenal injury. Curr Treat Options Gastroenterol. 2006 Apr;9(2):147-56.
- Rostom A, Dube C, Wells G, et al; Prevention of NSAID-induced gastroduodenal ulcers. Cochrane Database Syst Rev. 2002;(4):CD002296.
- Chan FK, Graham DY; Review article: prevention of non-steroidal anti-inflammatory drug gastrointestinal complications--review and recommendations based on risk assessment. Aliment Pharmacol Ther. 2004 May 15;19(10):1051-61.
- Quan C, Talley NJ; Management of peptic ulcer disease not related to Helicobacter pylori or NSAIDs. Am J Gastroenterol. 2002 Dec;97(12):2950-61.
- Bardhan KD, Williamson M, Royston C, et al; Admission rates for peptic ulcer in the trent region, UK, 1972--2000. changing pattern, a changing disease? Dig Liver Dis. 2004 Sep;36(9):577-88.
- de Boer WA, Tytgat GNJ; Treatment of Helicobacter pylori infection (Regular review) BMJ 2000 320: 31-34.
- Silverstein FE, Faich G, Goldstein JL, et al; Gastrointestinal toxicity with celecoxib vs nonsteroidal anti-inflammatory drugs for osteoarthritis and rheumatoid arthritis: the CLASS study: A randomized controlled trial. Celecoxib Long-term Arthritis Safety Study. JAMA. 2000 Sep 13;284(10):1247-55.
- Malhotra S, Shafiq N, Pandhi P; COX-2 inhibitors: a CLASS act or Just VIGORously promoted. MedGenMed. 2004 Mar 23;6(1):6.
- Shayne P; Gastritis and PU Disease. eMedicine, 2002.
- Millat B, Fingerhut A, Borie F; Surgical treatment of complicated duodenal ulcers: controlled trials. World J Surg. 2000 Mar;24(3):299-306.
- Sanabria AE, Morales CH, Villegas MI; Laparoscopic repair for perforated peptic ulcer disease. Cochrane Database Syst Rev. 2005 Oct 19;(4):CD004778.
- Lunevicius R, Morkevicius M; Systematic review comparing laparoscopic and open repair for perforated peptic ulcer. Br J Surg. 2005 Oct;92(10):1195-207.
- Rivera RE, Eagon JC, Soper NJ, et al; Experience with laparoscopic gastric resection: results and outcomes for 37 cases. Surg Endosc. 2005 Dec;19(12):1622-6. Epub 2005 Oct 12.
- Chan VM, Reznick RK, O'Rourke K, et al; Chan VM, Reznick RK, O'Rourke K, et al; Meta-analysis of highly selective vagotomy versus truncal vagotomy and pyloroplasty in the surgical treatment of uncomplicated duodenal ulcer. Can J Surg. 1994 Dec;37(6):457-64.
- Filipponi P, Gregorio F, Cristallini S, et al; Partial gastrectomy and mineral metabolism: effects on gastrin-calcitonin release. Bone Miner. 1990 Nov;11(2):199-208.
- Ralphs DN, Thomson JP, Haynes S, et al; The relationship between the rate of gastric emptying and the dumping syndrome. Br J Surg. 1978 Sep;65(9):637-41.
- Yamashita Y, Toge T, Adrian TE; Gastrointestinal hormone in dumping syndrome and reflux esophagitis after gastric surgery. J Smooth Muscle Res. 1997 Apr;33(2):37-48.
- Gray JL, Debas HT, Mulvihill SJ; Control of dumping symptoms by somatostatin analogue in patients after gastric surgery. Arch Surg. 1991 Oct;126(10):1231-5; discussion 1235-6.
|Original Author: Dr Richard Draper||Current Version: Dr Richard Draper|
|Last Checked: 17/07/2009||Document ID: 2897 Version: 21||© EMIS|
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