stomach and duodenum

STOMACH AND DUODENUM د.زياد شنشل

INTRODUCTION
The function of the stomach is to act as a reservoir for ingested food.
It also serves to break down food stuffs mechanically and commence the processes of digestion before these products are passed into the duodenum.

HELICOBACTER PYLORI

Over the last 20 years this organism has proved to be of overwhelming importance in the aetiology of a number of common gastroduodenal diseases, such as chronic gastritis, peptic ulceration and gastric cancer.

The organism is spirally shaped and is fastidious in its requirements, being difficult to culture outside the mucus layer of the stomach.

One of the characteristics of the organism is its ability to hydrolyse urea, resulting in the production of ammonia, a strong alkali.

The effect of ammonia on the antral G cells is to cause the release of gastrin this is probably responsible for the modest, but inappropriate, hypergastrinaemia in patients with peptic ulcer disease, which, in turn, may result in gastric acid hypersecretion.

It appears that most infection is acquired in childhood and the probability of infection is inversely related to socio-economic group.

Helicobacter infection is amenable to treatment with antibiotics. Commonly used eradication regimes include a proton pump inhibitor and two antibiotics, such as clarithromycin or metronidazole and amoxycillin.


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GASTRITIS

The understanding of gastritis has increased markedly following elucidation of the role of H. pylori in chronic gastritis.

Type A gastritis

This is an autoimmune condition in which there are circulating antibodies to the parietal cell.
This results in the atrophy of the parietal cell[Hcl secreation] mass, resulting in hypochlorhydria and ultimately achlorhydria.[decres acid]

As intrinsic factor is also produced by the parietal cell there is malabsorption of vitamin B12, which, if untreated, may result in pernicious anaemia.

In type A gastritis, the antrum is not affected and the hypochlorhydria leads to the production of high levels of gastrin from the antral G cells. This results in chronic hypergastrinaemia. Patients with type A gastritis are predisposed to the development of gastric cancer, and screening such patients endoscopically may be appropriate.

Type B gastritis

There are abundant epidemiological data to support the association of this type of gastritis with H. pylori infection.

Most commonly, type B gastritis affects the antrum, and it is these patients who are prone to peptic ulcer disease.

Patients with pangastritis seem to be most prone to the development of gastric cancer. Intestinal metaplasia is associated with chronic pangastritis with atrophy. Although intestinal metaplasia per se is common, intestinal metaplasia associated with dysplasia has significant malignant potential.

Reflux gastritis

This is caused by enterogastric reflux and is particularly common after gastric surgery.

Its histological features are distinct from those of other types of gastritis. Bile-chelating agents may be useful in treatment.

Erosive gastritis

This is caused by agents that disturb the gastric mucosal barrier; NSAIDs and alcohol are common causes.

The NSAID-induced gastric lesion is associated with inhibition of the cyclo-oxygenase type 1 (COX-1) enzyme, hence reducing the production of cytoprotective prostaglandins in the stomach.

Many of the beneficial anti-inflammatory activities of NSAIDs are mediated by COX-2, and the use of specific COX-2 inhibitors reduces the incidence of these side-effects.

Stress gastritis [IMP]

This is a common sequel of serious illness or injury and is characterized by a reduction in the blood supply to superficial mucosa of the stomach.

Although common, it is not usually recognized unless stress ulceration and bleeding supervene, in which case treatment can be extremely difficult.

Prevention of the stress bleeding from the stomach is much easier than treating it, hence the routine use of H2-receptor antagonists, with or without barrier agents such as Sucralfate, in patients who are in intensive care.

PEPTIC ULCERS

Although the name ‘peptic’ ulcer suggests an association with pepsin, this is essentially unimportant as in the absence of acid, for instance in type A gastritis with atrophy, peptic ulcers do not occur. All peptic ulcers can be healed by using proton pump inhibitors, which can render a patient virtually achlorhydric.


Common sites for peptic ulcers are the first part of the duodenum and the lesser curve of the stomach, but they also occur on the stoma following gastric surgery, the oesophagus and even in a Meckel’s diverticulum, which contains ectopic gastric epithelium.

As with many diseases, genetic factors may be involved to a limited degree and social stress has also been implicated. It is now widely accepted that infection with H. pylori is the most important factor in the development of peptic ulceration. The other factor of major importance at present is ingestion of NSAIDs.

Duodenal ulceration

Incidence
There have been marked changes in the demography of patients presenting with duodenal ulceration in the west. This may relate to the widespread use of gastric antisecretory agents and eradication therapy for patients with dyspepsia.
The peak incidence is now in a much older age group than previously and, although it is still more common in men, the difference is less marked.

Pathology

Most duodenal ulcers occur in the first part of the duodenum. A chronic ulcer penetrates the mucosa and into the muscle coat, leading to fibrosis. The fibrosis causes deformities such as pyloric stenosis. When an ulcer heals, a scar can be observed in the mucosa. Sometimes there may be more than one duodenal ulcer. The situation in which there is both a posterior and an anterior duodenal ulcer is referred to as ‘kissing ulcers’. Anteriorly placed ulcers tend to perforate and, in contrast, posterior duodenal ulcers tend to bleed, sometimes by eroding a large vessel such as the gastroduodenal artery. Occasionally, the ulceration may be so extensive that the entire duodenal cap is ulcerated and devoid of mucosa. Malignancy in this region is so uncommon.

Gastric ulceration

Incidence
As with duodenal ulceration, H. pylori and NSAIDs are the important aetiological factors in gastric ulceration. Gastric ulceration is also associated with smoking and are more prevalent in low socioeconomic groups and considerably more common in the developing world than in the west.

Pathology

The pathology of gastric ulcers is essentially similar to that of duodenal ulcers, except that gastric ulcers tend to be larger. Fibrosis, when it occurs, may result in the now rarely seen hourglass[ساعه رملية ] contraction of the stomach.

Large chronic ulcers may erode posteriorly into the pancreas and, on other occasions, into major vessels such as the splenic artery. Less commonly, they may erode into other organs such as the transverse colon.


Chronic gastric ulcers are much more common on the lesser curve (especially at the incisura angularis) than on the greater curve.

Malignancy in gastric ulcers

Chronic duodenal ulcers are not associated with malignancy but, in contrast, gastric ulcers are. It is fundamental that any gastric ulcer should be regarded as being malignant, no matter how classically it resembles a benign gastric ulcer. Multiple biopsies should always be taken, perhaps as many as 10 well-targeted biopsies, before an ulcer can be accepted as being benign. Even then it is important that further biopsies are taken while the ulcer is healing and when healed.

Clinical features of peptic ulcers

Although many textbooks try to create differences in the clinical features of gastric and duodenal ulceration, detailed analysis has shown that they cannot be differentiated on the basis of symptoms.

Pain

The pain is epigastric, often described as gnawing, and may radiate to the back. Eating may sometimes relieve the discomfort. The pain is normally intermittent rather than intractable.

Periodicity[most important]

One of the classic features of untreated peptic ulceration is periodicity. Symptoms may disappear for weeks or months to return again.

This periodicity may be related to the spontaneous healing of the ulcer.

Vomiting
Although this occurs, it is not a notable feature unless stenosis has occurred.

Alteration in weight

Weight loss or, sometimes, weight gain may occur..DU….
Patients with gastric ulceration are often underweight.


Bleeding
All peptic ulcers may bleed. The bleeding may be chronic and presentation with anaemia or presented acutely with haematemesis and melaena.

Clinical examination

Examination of the patient may reveal epigastric tenderness but, except in extreme cases (for instance gastric outlet obstruction), there is unlikely to be much else to find.

Investigation of the patient with suspected peptic ulcer

Gastroduodenoscopy[OGD]
This is the investigation of choice in the management of suspected peptic ulceration and, in the hands of a well-trained operator, is highly accurate. In the stomach, any abnormal lesion should be multiply biopsied to exclude malignancy.

Commonly, biopsies of the antrum will be taken to see whether there is histological evidence of gastritis and test performed to determine the presence of H. pylori [difficult to cutler out side the mucosa]. In the duodenum, care must be taken to view all of the first part.

Treatment of peptic ulceration

Medical treatment[uncomplicated]
The vast majority of uncomplicated peptic ulcers are treated medically. Surgical treatment of uncomplicated peptic ulceration has decreased markedly.

It is reasonable that a doctor managing a patient with an uncomplicated peptic ulcer should suggest modifications to the patient’s lifestyle, particularly the cessation of cigarette smoking.
H2-receptor antagonists and proton pump inhibitors revolutionised the management of peptic ulceration;

most duodenal ulcers and gastric ulcers can be healed by a few weeks of treatment with these drugs provided that they are taken and absorbed. Symptom relief is impressively rapid, most patients being asymptomatic within a few days. The problem with all gastric anti-secretory agents is that, following cessation of therapy, relapse is almost universal.


Eradication therapy
Eradication therapy is now routinely given to patients with peptic ulceration.

Evidence suggests that if a patient has a peptic ulcer and H. pylori is the principal aetiological factor (essentially the patient not taking NSAIDs), complete eradication of the organism will cure the disease and reinfection as an adult is uncommon.

There are some patients with peptic ulcers in whom eradication therapy may not be appropriate and this includes

patients with NSAID-associated ulcers. Such patients should avoid these drugs if possible and, if not, they should be co-prescribed with a potent anti-secretory agent.
Similarly,

patients with stomal ulceration are not effectively treated with eradication therapy and require a prolonged course of anti-secretory agents.

Patients with Zollinger–Ellison syndrome should be treated in the long term with proton pump inhibitors unless the tumour can be adequately managed by surgery.

Surgical treatment of uncomplicated peptic ulceration

From its peak in the 1960s, the incidence of surgery for uncomplicated peptic ulceration has fallen markedly, to the extent that peptic ulcer surgery is now of little more than historical interest.

Operations for duodenal ulceration[not imp]

Billroth II gastrectomy: The use of gastrojejunal anastomosis after gastric resection could be safer and easier than the Billroth I procedure, and it became popular and effective in the surgical treatment of duodenal ulcer. Its disadvantages include higher operative mortality and morbidity. A common cause of morbidity is leakage from the duodenal stump, which is particularly associated with kinking of the afferent loop.
Truncal vagotomy and drainage
The principle of the operation is that section of the vagus nerves, which are critically involved in the secretion of gastric acid, reduces the maximal acid output by approximately 50%. Because the vagal nerves are conductors of motor impulses to the stomach, denervation of the antropyloroduodenal segment results in gastric stasis in a substantial proportion of patients on whom truncal vagotomy alone is performed so drainage procedure is required.
Highly selective vagotomy
In which only the parietal cell mass of the stomach was denervated. This proved to be the most satisfactory operation for duodenal ulceration, with a low incidence of side-effects and acceptable recurrence rates when performed to a high technical standard.


Operations for gastric ulcer
In contrast to duodenal ulcer surgery, in which the principal objective was to reduce duodenal acid exposure, in gastric ulceration, the diseased tissue is usually removed as well. This has the advantage that malignancy can then be confidently excluded.

Sequelae of peptic ulcer surgery[imp]

Recurrent ulceration

Although mentioned first, this is by far the easiest problem to treat by potent anti-secretory agents.

Gastrojejunal colic fistula

In this rare condition, the anastomotic ulcer penetrates into the transverse colon.

Patients suffer from diarrhea that is severe and follows every meal. They have foul breath and may vomit formed faeces.

Severe weight loss and dehydration are rapid in onset and, for this reason, the condition may be mistaken for malignancy.

The major factor producing the nutritional disturbance is the severe contamination of the jejunum with colonic bacteria.

CT with oral contrast or a barium enema can be used to detect the fistula. The treatment of gastrocolic fistula consists of first correcting the dehydration and malnutrition and then performing revisional surgery.


Small stomach syndrome
Early satiety follows most ulcer operations to some degree, including highly selective vagotomy,

in which, although there is no anatomical disturbance of the stomach, there is a loss of receptive relaxation.

Fortunately, this problem does tend to get better with time and revisional surgery is not necessary.

Bile vomiting

Bile vomiting can occur after any form of vagotomy with drainage or gastrectomy. Bile-chelating agents can be tried but are usually ineffective. In intractable cases, revisional surgery may be indicated.
Early and late dumping

Early dumping

Early dumping consists of abdominal and vasomotor symptoms, which are found in about 5–10% of patients following gastrectomy or vagotomy and drainage.

It also affects a small percentage of patients following highly selective vagotomy because of the loss of receptive relaxation of the stomach.

The small bowel is filled with foodstuffs from the stomach, which have a high osmotic load, and this leads to the sequestration of fluid from the circulation into the gastrointestinal tract.

Treatment The principal treatment is dietary manipulation.

Small, dry meals are best, and avoiding fluids with a high carbohydrate content also helps.


Fortunately, following operation, the syndrome tends to improve with time. For some reason, however, there is a group of patients who suffer intractable dumping regardless of any of these measures.

The Somatostatin analogue Octreotide, given before meals, has been shown to be useful in some individuals. However, this treatment can lead to the development of gallstones and it does not help the diarrhoea from which many patients with dumping also suffer.

Revisional surgery may be occasionally required.

Late dumping
This is reactive hypoglycaemia.

The carbohydrate load in the small bowel causes a rise in the plasma glucose level, which, in turn, causes insulin levels to rise, causing a secondary hypoglycaemia.

The treatment is essentially the same as for early dumping. Octreotide is very effective in dealing with this problem.

Post-vagotomy diarrhoea

This can be the most devastating symptom to afflict patients having peptic ulcer surgery.

Most patients will suffer looseness of bowel action to some degree (with the exception of highly selective vagotomy) but, in about 5%, it may be intractable.

Despite much investigation, the precise aetiology of the problem is uncertain. It is partly related to rapid gastric emptying.
The condition is difficult to treat.


The patient should be managed as for early dumping and anti-diarrhoeal preparations may be of some value.

Malignant transformation

Many large studies now confirm that operations such as gastrectomy or vagotomy and drainage are independent risk factors for the development of gastric cancer.

The increased risk appears to be approximately four times that of the control population.

The lag phase between operation and the development of malignancy is at least 10 years.

Highly selective vagotomy does not seem to be associated with an increased incidence.

Nutritional consequences
Nutritional disorders are more common after gastrectomy than after vagotomy and drainage.

Weight loss is common after gastrectomy and the patient may never return to their original weight.

Eating small meals often may help.

Anaemia may result from either iron or vitamin B12 deficiency.


Iron-deficiency anaemia is multifactorial in origin. Reduced iron absorption is probably the most important factor, although the loss of blood from the gastric mucosa may also be important.

Vitamin B12 deficiency is prone to occur after total gastrectomy. However, because of the very large vitamin B12 stores, this may be very late in occurring. Vitamin B12 supplementation after total gastrectomy is essential.

The cause is a combination of reduced intrinsic factor production and, in some patients, bacterial colonisation, which results in the destruction of vitamin B12. Bone disease is seen principally after gastrectomy and mainly in women.

Treatment is through dietary supplementation with calcium and vitamin D, and with exercise.

Gallstones

The development of gallstones is strongly associated with truncal vagotomy,

in which the biliary tree as well as the stomach is denervated, leading to stasis and, hence, stone formation.

Patients developing symptomatic gallstones will require cholecystectomy.

Complications of peptic ulceration
The common complications of peptic ulcer are perforation, bleeding and stenosis.

Perforated peptic ulcer

Epidemiology
There has been a steady increase in the age of the patients suffering from this complication and an increase in the number of women affected, such that perforations now occur most commonly in elderly female patients. NSAIDs appear to be responsible for most of these perforations.


Clinical features
The classic presentation is instantly recognizable.

The patient, who may have a history of peptic ulceration, develops sudden-onset, severe, generalized abdominal pain as a result of the irritant effect of gastric acid on the peritoneum.

Although the contents of an acid-producing stomach are relatively low in bacterial load, bacterial peritonitis supervenes over a few hours, usually accompanied by a deterioration in the patient’s condition.

Initially, the patient may be shocked with a tachycardia but a pyrexia is not usually observed until some hours after the event.

The abdomen exhibits a board-like rigidity and the patient is disinclined to move because of the pain.

The abdomen does not move with respiration. Patients with this form of presentation need an operation, without which they will deteriorate with a septic peritonitis.

This classic presentation of the perforated peptic ulcer is observed less commonly than in the past.

Very frequently, the elderly patient who is taking NSAIDs will have a less dramatic presentation, perhaps because of the use of potent anti-inflammatory drugs.

The board-like rigidity seen in the abdomen of younger patients may not be observed and a higher index of suspicion is necessary to make the correct diagnosis.

In other patients, the leak from the ulcer may not be massive. They may present only with pain in the epigastrium and right iliac fossa as the fluid may track down the right paracolic gutter.


Sometimes perforations will seal as a result of the inflammatory response and adhesion within the abdominal cavity, and so the perforation may be self-limiting.

By far the most common site of perforation is the anterior aspect of the duodenum.

However, the anterior or incisural gastric ulcer may perforate and, in addition, gastric ulcers may perforate into the lesser sac, which can be particularly difficult to diagnose.
These patients may not have obvious peritonitis.

Investigations

An erect plain chest radiograph will reveal free gas under the diaphragm in more than 50% of cases but CT imaging is more accurate.

All patients should have serum amylase levels tested, as distinguishing between peptic ulcer perforation and pancreatitis can be difficult. Measuring the serum amylase, however, may not remove the diagnostic difficulty; it can be elevated following perforation of a peptic ulcer although, fortunately, the levels are not usually as high as the levels commonly seen in acute pancreatitis.

Treatment

The initial priorities are resuscitation and analgesia.

Analgesia should not be withheld for fear of removing the signs of an intra-abdominal catastrophe.

In fact, adequate analgesia makes the clinical signs more obvious. Following resuscitation, the treatment is principally surgical.

All patients should be treated with systemic antibiotics in addition to a thorough peritoneal lavage.


Following operation, gastric anti-secretory agents should be started immediately. It is important that the stomach is kept empty postoperatively by nasogastric suction.
Patients who have suffered one perforation may suffer another one. In patients with Helicobacter associated ulcers, eradication therapy is appropriate.
Lifelong treatment with proton pump inhibitors is a reasonable option, especially in those who have to continue with NSAID treatment.
HAEMATEMESIS AND MELAENA
Upper gastrointestinal haemorrhage remains a major medical problem. Despite improvements in diagnosis and the proliferation in treatment modalities an in-hospital mortality rate of 5% can be expected. In patients in whom the cause of bleeding can be found, the most common causes are bleeding peptic ulcer, erosions, Mallory–Weiss tear and bleeding oesophageal varices.

Whatever the cause, the principles of management are identical. The patient should be first resuscitated and then investigated urgently to determine the cause of the bleeding.

Only then should definitive treatment be instituted. For any significant gastrointestinal bleed, intravenous access should be established and, for those with severe bleeding, central venous pressure monitoring should be set up and bladder catheterization performed.

Blood should be cross-matched and the patient transfused as clinically indicated. As a general rule, most gastrointestinal bleeding will stop, albeit temporarily, but there are sometimes instances when this is not the case. In these circumstances, resuscitation, diagnosis and treatment should be carried out in quick succession.

There are occasions when life-saving manoeuvres have to be undertaken without the benefit of an absolute diagnosis.

For instance, in patients with known oesophageal varices and uncontrollable bleeding, a Sengstaken– Blakemore tube may be inserted before an endoscopy has been carried out.

This practice is not to be encouraged, except in extremis. In some patients bleeding is secondary to a coagulopathy.

The most important current causes of this are liver disease and inadequately controlled warfarin therapy.

In these circumstances, the coagulopathy should be corrected, if possible, with fresh frozen plasma.
Upper gastrointestinal endoscopy should be carried out by an experienced operator as soon as practicable after the patient has been stabilized.
In patients in whom the bleeding is relatively mild, endoscopy may be carried out on the morning after admission. In all cases of severe bleeding it should be carried out immediately.


Bleeding peptic ulcers
The epidemiology of bleeding peptic ulcers exactly mirrors that of perforated ulcers.

In recent years, the population affected has become much older and the bleeding is commonly associated with the ingestion of NSAIDs. Diagnosis can normally be made endoscopically.

Medical and minimally interventional treatments

Medical treatment has limited efficacy.

All patients are commonly started on a proton pump antagonist. Numerous endoscopic devices are now available that can be used to achieve haemostasis.

Surgical treatment

Criteria for surgery are well worked out.

A patient who continues to bleed requires surgical treatment.

The same applies to a significant rebleed.

Patients with a visible vessel in the ulcer base, a spurting vessel or an ulcer with a clot in the base are likely to require surgical treatment.

Elderly and unfit patients are more likely to die as a result of bleeding than younger patients; ironically, they should have early surgery.


In general, a patient who has required more than 6 units of blood needs surgery.
The aim of the operation is to stop the bleeding.

The most common site of bleeding from a peptic ulcer is the duodenum and the gastroduodenal artery is commonly the source of major bleeding.

Acid can be inhibited by pharmacological means and appropriate eradication therapy will prevent ulcer recurrence.

Stress ulceration

This commonly occurs in patients who have a major injury or illness, who have undergone major surgery or who have a major comorbidity.

Many such patients are found in intensive care units.

Acid inhibition and the nasogastric or oral administration of sucralfate has been shown to reduce the incidence of stress ulceration.

There is no doubt that it is far better to prevent this condition than to try to treat it.

Gastric erosions

Erosive gastritis has a variety of causes, especially the use of NSAIDs.

Fortunately, most such bleeding settles spontaneously but when it does not it can be a major problem to treat and should be dealt with endoscopically, although sometimes surgery is necessary.


Mallory–Weiss tear
This is a longitudinal tear below the gastro-oesophageal junction, which is induced by repetitive and strenuous vomiting.

Dieulafoy’s disease

This is essentially a gastric arterial venous malformation that has a characteristic histological appearance.

Bleeding as a result of this malformation is one of the most difficult types of upper gastrointestinal bleeding to treat. The lesion itself is covered by normal mucosa and, when not bleeding, it may be invisible.

If the lesion can be identified endoscopically there are various means of dealing with it, including the injection of sclerosant.

If it is identified at operation then only a local excision is necessary.

Tumours
All of the gastric tumours may present with chronic or acute upper gastrointestinal bleeding.

Gastric stromal tumours commonly present with bleeding and have a characteristic appearance, as the mucosa breaks down over the tumour in the gastric wall

Whatever the nature, the tumours should be dealt with as appropriate.

Portal hypertension and portal gastropathy
The management of bleeding gastric varices is very challenging.


Fortunately, most bleeding from varices is oesophageal and this is much more amenable to sclerotherapy, banding and balloon tamponade.

Gastric varices may also be injected, although this is technically more difficult. Banding can also be used, again with difficulty.

The gastric balloon of the Sengastaken–Blakemore tube can be used to arrest the haemorrhage if it is occurring from the fundus of the stomach.

Octreotide reduces portal pressure in patients with varices, and it is of value in arresting haemorrhage.

Most surgeons prefer to avoid acute surgery on bleeding varices as, in contrast with elective operations for portal hypertension, acute shunts are attended by considerable operative mortality.

Portal gastropathy is essentially the same disease process as above. The mucosa is affected by the increased portal pressure and may exude blood, even in the absence of well developed visible varices.

The treatment is as above.

Aortic enteric fistula
Contrary to expectation, the bleeding from such patients is not always massive, although it can be.

The vast majority of patients will have had an aortic graft and, in the absence of this, the diagnosis is unlikely.

However, it is occasionally seen in patients with an untreated aortic aneurysm.

A well-performed CT scan will commonly allow the diagnosis to be made.

The condition should be managed by an expert vascular surgeon as the morbidity and mortality rates are high.

GASTRIC OUTLET OBSTRUCTION

The two common causes of gastric outlet obstruction are gastric cancer and pyloric stenosis secondary to peptic ulceration.

Previously, the latter was more common. Now, with the decrease in the incidence of peptic ulceration and the advent of potent medical treatments, gastric outlet obstruction should be considered malignant until proven otherwise.

Commonly, when the condition is due to underlying peptic ulcer disease the stenosis is found in the first part of the duodenum, the most common site for a peptic ulcer.

In gastric cancer the metabolic consequences may be somewhat different from those of benign pyloric stenosis because of the relative hypochlorhydria found in patients with gastric cancer.

Clinical features

In benign gastric outlet obstruction there is usually a long history of peptic ulcer disease.

In some patients the pain may become unremitting and in other cases it may largely disappear.

The vomitus is characteristically unpleasant in nature and is totally lacking in bile.

Very often it is possible to recognise foodstuff taken several days previously.


The patient commonly loses weight, and appears unwell and dehydrated. On examination it may be possible to see the distended stomach and a succussion splash may be audible on shaking the patient’s abdomen.

Metabolic effects

These are most interesting as the metabolic consequences of benign pyloric stenosis are unique.

The vomiting of hydrochloric acid results in hypochloraemic alkalosis but, initially, sodium and potassium levels may be relatively normal.

However, as dehydration progresses, more profound metabolic abnormalities arise, partly related to renal dysfunction.

Initially, the urine has a low chloride and high bicarbonate content, reflecting the primary metabolic abnormality.

This bicarbonate is excreted along with sodium and so, with time, the patient becomes progressively hyponatraemic and more profoundly dehydrated. Because of the dehydration, a phase of sodium retention follows and potassium and hydrogen are excreted in preference.

This results in the urine becoming paradoxically acidic and hypokalaemia ensues. Alkalosis leads to a lowering of the circulating ionised calcium, and tetany can occur.

Management

Treating the patient involves correcting the metabolic abnormality and dealing with the mechanical problem.

The patient should be rehydrated with intravenous isotonic saline with potassium supplementation.

Replacing the sodium chloride and water allows the kidney to correct the acid–base abnormality.


It is notable that the metabolic abnormalities may be less if the obstruction is due to malignancy, as the acid–base disturbance is less pronounced.

The stomach should be emptied using a gastric tube.

This allows investigation of the patient with endoscopy and contrast radiology.

Biopsy of the area around the pylorus is essential to exclude malignancy. The patient should also have an anti-secretory agent, initially given intravenously to ensure absorption.

Early cases may settle with conservative treatment, presumably as the oedema around the ulcer diminishes as the ulcer is healed.

Severe cases are treated surgically, usually with a gastroenterostomy rather than a pyloroplasty.

GASTRIC CANCER

Carcinoma of the stomach is a major cause of cancer mortality worldwide. Its prognosis tends to be poor with cure rates little better than 5–10%.

Early diagnosis is the key to success. Unfortunately, the late presentation of many cases is the cause of the poor overall survival figures.

The only treatment modality able to cure the disease is resectional surgery.

Incidence
There are variations in the incidence of gastric cancer worldwide.


In the UK the incidence is approximately 15 cases per 100 000 population per year, in the USA 10 cases per 100 000 population per year. In Japan the disease is much more common, with an incidence of approximately 70 cases per 100 000 population per year.

These underlying epidemiological data make it clear that this is an environmental disease.

In general, men are more affected than women and the incidence increases with age.

The incidence of gastric cancer is continuing to fall with the reduction exclusively affecting carcinomas arising in the body of the stomach and the distal stomach.

In contrast, the incidence of carcinoma in the proximal stomach, particularly the oesophagogastric junction, appears to be increasing. Carcinoma of the distal stomach and body of the stomach is most common in low socio-economic groups and seems to be associated with H. pylori infection, whereas the proximal gastric cancer seems to affect higher socio-economic groups.

Aetiology

Gastric cancer is a multifactorial disease. Epidemiological studies point to a role for H. pylori in the incidence of gastric cancer .

H. pylori seems to be principally associated with carcinoma of the body of the stomach and the distal stomach rather than the proximal stomach.

Several other risk factors have been identified as patients with pernicious anaemia and gastric atrophy are at increased risk, as are those with gastric polyps.

Patients who have had peptic ulcer surgery, particularly drainage procedures are at approximately 4 times the average risk due to duodenogastric reflux and reflux gastritis.

Intestinal metaplasia is a risk factor. Carcinoma is associated with cigarette smoking and dust ingestion from a variety of industrial processes. Diet appears to be important, as illustrated by the change in the incidence of gastric cancer in Japanese families living in the USA.


The ingestion of substances such as spirits may induce gastritis and, in the long term, cancer.

Excessive salt intake, deficiency of antioxidants and exposure to N-nitroso compounds are also implicated.

The aetiology of proximal gastric cancer is not associated with Helicobacter but is associated with obesity and higher socio-economic status. Genetic factors are also important but imperfectly understood.

Clinical features

The features of advanced gastric cancer are usually obvious.

However, curable gastric cancer has no specific features to distinguish it symptomatically from benign dyspepsia.

The key to improving the outcome of gastric cancer is early diagnosis and, although in Japan there is a screening program, most curable cases are picked up by the liberal use of gastroscopy in patients with dyspepsia. It is important to note that gastric anti-secretory agents will improve the symptoms of gastric cancer so the disease should be excluded before therapy is started.

In advanced cancer, early satiety, bloating, distension and vomiting may occur. The tumour frequently bleeds, resulting in iron-deficiency anaemia. Obstruction leads to dysphagia, epigastric fullness or vomiting.

With pyloric involvement the presentation may be of gastric outlet obstruction, although the alkalosis is usually less pronounced.

Metastatic lymph nodes may be palpable, most notably in the left supraclavicular fossa (Virchow’s node, Troisier’s sign).

Non-metastatic effects of malignancy are seen, particularly thrombophlebitis (Trousseau’s sign) and deep venous thrombosis.


These features result from the effects of the tumour on thrombotic and haemostatic mechanisms.

Pathology

There are principally two forms of gastric cancer: intestinal gastric cancer and diffuse gastric cancer.

In intestinal gastric cancer, the tumour resembles carcinomas found elsewhere in the gastrointestinal tract and forms polypoid tumours or ulcers.

In contrast, diffuse gastric cancer infiltrates deeply into the stomach without forming obvious mass lesions but spreading widely in the gastric wall so this has a much worse prognosis.

A small proportion of gastric cancers are of mixed morphology.

Gastric cancer can be divided into early gastric cancer and advanced gastric cancer.

Early gastric cancer can be defined as cancer limited to the mucosa and submucosa with or without lymph node involvement.

Early gastric cancer is eminently curable, and even when associated with lymph node involvement have 5-year survival rates of 90%.

Unfortunately this is not the case usually. Advanced gastric cancer involves the muscularis.

Spread of carcinoma of the stomach

No better example of the various modes by which carcinoma spreads can be given than the case of stomach cancer.


It is important to note that distant spread is unusual before the disease spreads locally.

Direct spread

The tumour penetrates the muscularis, serosa and ultimately adjacent organs such as the pancreas, colon and liver.

Lymphatic spread

This may be extensive, with the tumour even appearing in the supraclavicular nodes. Unlike malignancies such as breast cancer, nodal involvement does not imply systemic dissemination.

Blood-borne metastases

Blood-borne metastases occur first to the liver and subsequently to other organs, including lung and bone.

Transperitoneal spread

This is a common mode of spread once the tumour has reached the serosa of the stomach and indicates incurability.

Tumours can manifest anywhere in the peritoneal cavity and commonly give rise to ascites. Advanced peritoneal disease may be palpated either abdominally or rectally as a tumour ‘shelf’.

The ovaries may sometimes be the sole site of transcoelomic spread (Krukenberg’s tumours). Tumour may spread via the abdominal cavity to the umbilicus (Sister Joseph’s nodule).

Operability

It is important that patients with incurable disease are not subjected to radical surgery that cannot help them.


Evidence of incurability is haematogenous metastases, involvement of the distant peritoneum and fixation to structures that cannot be removed.

It is important to note that involvement of another organ per se does not imply incurability, provided that it can be removed.

Curative resection should be considered on the remaining patients. Most operable patients should have neoadjuvant chemotherapy as this improves survival.

Palliative surgery

In patients suffering from significant symptoms of either obstruction or bleeding, palliative resection is appropriate.
A palliative gastrectomy need not be radical and it is sufficient to remove the tumour and reconstruct the gastrointestinal tract.

Sometimes it is impossible to resect an obstructing tumour in the distal stomach and other palliative bypass procedures needed although the prognosis in such patients, even in the short term, is poor.

For inoperable tumours situated in the cardia, either palliative intubation, stenting or recanalisation can be used.

Postoperative complications of gastrectomy

Radical gastrectomy is complex major surgery and predictably there are a large number of potential complications.

Leakage of the oesophagojejunostomy should be uncommon in experienced hands. When it does occur it can often be managed conservatively as it is mainly saliva and ingested food that leaks.

Some patients may establish a fistula from the wound or drain site and others may need radiological or surgically placed drains.


As with any gastrectomy, leakage from the duodenal stump can occur. This is usually due to a degree of distal obstruction and care must be taken when performing the anastomosis that there is no kinking. Paraduodenal collections can be drained radiologicall , which will often convert the collection into an external fistula. If there is no distal obstruction then with time the fistula will close.

Long-term complications of surgery

Considering the radical nature of the total gastrectomy it is surprising that many patients, particularly younger ones, have good functional results.

However, most patients will have a reduced capacity, particularly in the short term. They need to be given detailed nutritional advice while the jejunum or small gastric remnant adapts. In fact, there is very little functional difference between patients who have a total gastrectomy and those who have a subtotal gastrectomy.

Nutritional deficiencies may occur and the patient should be monitored for vitamin B12 deficiency and replacement should be given routinely.

Other treatment modalities

Because of the failure of radical surgery to cure advanced gastric cancer, there has been interest in the use of radiotherapy and chemotherapy.

Radiotherapy

The routine use of radiotherapy is controversial as the results of clinical trials are inconclusive.

There are a number of radiosensitive tissues in the region of the gastric bed, which limits the dose that can be given.

Radiotherapy has a role in the palliative treatment of painful bony metastases.

Chemotherapy
Gastric cancer may respond well to combination neoadjuvant chemotherapy and cytotoxic chemotherapy to improve the outcome following surgery.


There are a number of regimes but the best results are obtained using a combination of epirubicin, cis-platinum and 5-fluorouracil. Chemotherapy for advanced disease is palliative.

GASTROINTESTINAL STROMAL TUMOURS

Gastrointestinal stromal tumours (GISTs) commonly occur in the stomach and duodenum.

Previously named leiomyoma and leiomyosarcoma. The tumours are universally associated with a mutation in the tyrosine kinase oncogene so these tumours are sensitive to the tyrosine kinase antagonist imatinib.

The biological behaviour of these tumours is unpredictable but size and mitotic index are the best predictors of metastasis.

Peritoneal and liver metastases are most common. Spread to lymph nodes is extremely rare. The only way that many stromal tumours are recognised is either that the mucosa overlying the tumour ulcerates, leading to bleeding, or that they are noticed incidentally at endoscopy.

Because the mucosa overlying the tumour is normal, endoscopic biopsy can be uninformative unless the tumour has ulcerated.

Larger tumours present with non-specific gastric symptoms and, in many instances, it may initially be thought that they are gastric cancers.
If easily resectable, surgery is the primary mode of treatment.

Smaller tumours can be treated by wedge excision. Larger tumours may require a gastrectomy or duodenectomy but lymphadenectomy is not required.

Larger tumours may be better treated for 3–6 months with imatinib before operation as this will usually radically reduce their size and vascularity.

GASTRIC LYMPHOMA

It is important to distinguish primary gastric lymphoma from involvement of the stomach in a generalised lymphomatous process, the latter situation is more common.


Unlike gastric carcinoma, the incidence of lymphoma seems to be increasing. Primary gastric lymphoma accounts for approximately 5% of all gastric neoplasms.

The presentation is no different from gastric cancer, the common symptoms being pain, weight loss and bleeding.

Acute presentations of gastric lymphoma such as haematemesis, perforation or obstruction are not common.

Primary gastric lymphomas are B cell-derived, the tumour arising from the mucosa-associated lymphoid tissue (MALT).

Primary gastric lymphoma remains in the stomach for a prolonged period before involving the lymph nodes. At an early stage, the disease takes the form of a diffuse mucosal thickening, which may ulcerate.

Diagnosis is made as a result of the endoscopic biopsy. Following diagnosis, adequate staging is necessary, primarily to establish whether the lesion is a primary gastric lymphoma or part of a more generalised process. CT scans of the chest and abdomen and bone marrow aspirate are required, as well as a full blood count.

Although the treatment of primary gastric lymphoma is somewhat controversial, it seems most appropriate to use surgery alone for the localised disease process.

In gastric involvement with the diffuse lymphoma, the treatment is chemotherapy, sometimes with dramatic and rapid responses.

Surgeons are frequently asked to deal with the complications of gastric involvement.

The two common complications are bleeding and perforation; both may occur at presentation, but more usually they may follow chemotherapy when there is rapid regression and necrosis of the tumour.

NEUROENDOCRINE TUMOURS

Duodenum is a common site for primary gastrinoma (Zollinger– Ellison syndrome).


Non-functioning neuroendocrine tumours (usually called carcinoid tumours) also occur but uncommonly in comparison with the ileum.

Zollinger–Ellison syndrome

This syndrome is mentioned here because the gastrin-producing endocrine tumour is often found in the duodenal loop, although it also occurs in the pancreas, especially the head. It is a cause of persistent peptic ulceration.

The advent of proton pump inhibitors has rendered this extreme endocrine condition fully controllable, but also less easily recognized. Gastrinomas may be either sporadic or associated with the autosomal dominantly inherited multiple endocrine neoplasia (MEN) type I (in which a parathyroid adenoma is almost invariably present).

The tumours are most commonly found in the ‘gastrinoma triangle’ (Passaro) defined by the junction of the cystic duct and common bile duct superiorly, the junction of the second and third parts of the duodenum inferiorly, and the junction of the neck and body of the pancreas medially (essentially the superior mesenteric artery).

Many are found in the duodenal loop, presumably arising in the G cells. It is extremely important that the duodenal wall is very carefully inspected endoscopically and also at operation.

Very often all that can be detected is a small nodule that projects into the medial wall of the duodenum. However, the minority of tumours that are found to the left of the superior mesenteric artery (outside the ‘triangle’) seem to have a worse prognosis, with more having liver metastases at presentation.

In MEN type I, the tumours may be multiple and the condition is incurable. Even in this situation, as with sporadic gastrinoma, surgical treatment should be employed to remove any obvious tumours and associated lymphatic metastases, as the palliation achieved may be good.

OTHER GASTRIC CONDITIONS

Acute gastric dilatation
This condition usually occurs in association with pyloroduodenal disorders or after surgery without nasogastric suction.

The stomach, which may also be atonic, dilates enormously. Often the patient is also dehydrated and has electrolyte disturbances.


Failure to treat this condition can result in a sudden massive vomit with aspiration into the lungs.

The treatment is nasogastric suction with a large-bore tube, fluid replacement and treatment of the underlying condition.

Trichobezoar and phytobezoar

Trichobezoars (hair balls) are unusual and are almost exclusively found in female psychiatric patients, often young.

They are caused by the pathological ingestion of hair, which remains undigested in the stomach.

The hair ball can lead to ulceration and gastrointestinal bleeding, perforation or obstruction.

The diagnosis is made easily at endoscopy or, indeed, from a plain radiograph.

Treatment consists of removal of the trichobezoar, which may require open surgical treatment.

Phytobezoars are made of vegetable matter and are found principally in patients who have gastric stasis. Often this follows gastric surgery.