Surgical resection is the principal therapy for gastric cancer, as it offers the only potential for cure. A subtotal gastrectomy is usually performed for tumours of the distal stomach. Subtotal gastrectomy is the treatment of choice for middle and distal-third gastric cancer as it provides similar survival rates and better functional outcome compared to total gastrectomy, especially in early-stage disease with favourable prognosis. D2 dissections are recommended by the National Comprehensive Cancer Network over D1 dissections. A pancreas-and spleen-preserving D2 lymphadenectomy is suggested, as it provides greater staging information, and may provide a survival benefit while avoiding its excess morbidity when possible. Patients that undergo D2 lymphadenectomy as a standard part of surgical resection of gastric adenocarcinoma generally have better stage-for-stage overall survival figures compared to patients undergoing less extensive lymphadenectomies.
After partial gastrectomy, some patients report disorders such as reflux esophagitis and alkaline gastritis, as well as dumping syndrome, delayed gastric emptying and malabsorption, which are defined as functional dyspepsia. Duodenogastric reflux is recognized to be a major cause of clinical symptoms after resection.
Roux-Y reconstruction seems to be effective in reducing bile reflux into the stomach, compared to Billroth I and II procedure, and conversion to this procedure has been reported in patients with symptomatic uncontrolled reflux disease.

Achalasia is a failure of the lower oesophageal sphincter (LES) to relax that is caused by the degeneration of inhibitory neurons within the oesophageal wall. It is classified as either primary (idiopathic) or secondary (in the context of another disease). In patients with achalasia, the chief complaint is dysphagia to both solids and liquids, although regurgitation, retrosternal pain, and weight loss may also occur. Upper endoscopy, barium esophagram, and oesophageal manometry play complementary roles in the diagnosis of achalasia. While upper endoscopy and/or barium esophagram are often obtained initially, manometry usually confirms the diagnosis, and upper endoscopy is indicated to rule out a malignant underlying cause. In good surgical candidates, achalasia is usually treated with pneumatic dilation or myotomy. In most other cases, an injection of botulinum toxin is attempted. If these measures fail to provide relief, medical therapy (e.g., nifedipine) is indicated.

Dumping syndrome is the effect of altered gastric reservoir function, abnormal postoperative gastric motor function, and/or pyloric emptying mechanism. Clinically significant dumping syndrome occurs in approximately 10% of patients after any type of gastric surgery and in up to 50% of patients after laparoscopic Roux-en-Y gastric bypass. Dumping syndrome has characteristic alimentary and systemic manifestations. It is a frequent complication observed after a variety of gastric surgical procedures, such as vagotomy, pyloroplasty, gastrojejunostomy, and laparoscopic Nissan fundoplication. Dumping syndrome can be separated into early and late forms, depending on the occurrence of symptoms in relation to the time elapsed after a meal.
Postprandially, the function of the body of the stomach is to store food and to allow the initial chemical digestion by acid and proteases before transferring food to the gastric antrum. In the antrum, high-amplitude contractions triturate the solids, reducing the particle size to 1-2 mm. Once solids have been reduced to this desired size, they are able to pass through the pylorus. An intact pylorus prevents the passage of larger particles into the duodenum. Gastric emptying is controlled by the fundic tone, antropyloric mechanisms, and duodenal feedback. Gastric surgery alters each of these mechanisms in several ways.

The late dumping syndrome is suspected in the person who has symptoms of hypoglycaemia in the setting of previous gastric surgery, and this late dumping can be proven with an oral glucose tolerance test (hyperinsulinemic hypoglycaemia), as well as gastric emptying scintigraphy, which shows the abnormal pattern of initially delayed and then accelerated gastric emptying.

The clinical presentation of dumping syndrome can be divided into GI symptoms and vasomotor symptoms. GI symptoms include early satiety, crampy abdominal pain, nausea, vomiting, and explosive diarrhoea. Vasomotor symptoms include diaphoresis, flushing, dizziness, palpitations, and an intense desire to lie down.

The expression of these symptoms varies in different individuals. Most patients with early dumping have both GI and vasomotor symptoms, while patients with late dumping have mostly vasomotor symptoms. Patients with severe dumping often limit their food intake to avoid symptoms. This leads to weight loss and, over time, malnutrition.

Early dumping syndrome generally occurs within 15 minutes of ingesting a meal and is attributable to the rapid transit of food into the small intestine, whereas late dumping syndrome occurs later and may be attributed to hypoglycaemia with tremors, cold sweats, difficulty in concentrating, and loss of consciousness.

Early dumping systemic symptoms are as follows:
Desire to lie down
Palpitations
Fatigue
Faintness
Syncope
Diaphoresis
Headache
Flushing

Early dumping abdominal symptoms are as follows:
Epigastric fullness
Diarrhoea
Nausea
Abdominal cramps
Borborygmi

Late dumping symptoms are as follows:
Perspiration
Shakiness
Difficulty to concentrate
Decreased consciousness
Hunger

Iatrogenic perforation of the gastrointestinal tract
related to diagnostic or therapeutic endoscopy is
a rare but severe adverse event, associated with
significant morbidity and mortality

Conservative treatment may be suitable for patients with limited oesophageal injury and contained leakage. Such patients include those suffering endoscopic iatrogenic perforation, as the patient is likely to be fasted and the diagnosis made promptly. They must remain nil by mouth, with appropriate antibiotic cover, and proton pump inhibitor therapy, total parenteral nutrition, and continued observation. Similarly, medical treatment might be suitable for cases of inoperable malignant stricture, that is, palliation.

The intragastric balloon aids weight loss by slowing the rate at which food enters the stomach and by stimulating gastric stretch receptors. But lifestyle changes, including behaviour modification, exercise and a healthy diet, are crucial for maintaining weight loss once the device is removed. Intragastric balloon is really only suitable as a bridge to a more definitive surgical solution and is associated with a high failure rates and complications.

Gastric banding: band applied to upper stomach which can be inflated or deflated with normal saline. This affects satiety. Over a 5 year period complications requiring further surgery occur in up to 15% cases.

Roux-en-Y gastric bypass: a gastric pouch is formed and connected to the jejunum. Patients achieve greater and more long-term weight loss than gastric banding.

Sleeve gastrectomy: body and fundus resected to leave a small section of stomach

This patient had endoscopy and biopsy done by different doctors and proton pump inhibitor therapy followed by repeat endoscopy and biopsy six months later which had no definite evidence of dysplasia.

British Society of Gastroenterology (BSG) guidelines state that for patients with Barrett’s oesophagus (BO) but without dysplasia, the recommended surveillance protocols are two yearly, four quadrant biopsies every 2 cm, but jumbo biopsies are not required.

A gastrinoma is a gastrin-secreting tumour that can occur in the pancreas, although it is most commonly found in the duodenum. Duodenal wall gastrinomas have been identified in 40-50% of patients. These duodenal wall tumours are frequently small and multiple. Sporadic tumours occurring in the pancreas tend to be solitary and have a greater malignant potential as compared to duodenal gastrinomas.

Primary tumours also occur in a variety of ectopic sites, including the body of the stomach, jejunum, peripancreatic lymph nodes, splenic hilum, omentum, liver, gallbladder, common bile duct, and the ovary. Over 50% of gastrinomas are malignant and can metastasize to the regional lymph nodes and the liver. One fourth of gastrinomas are related to multiple endocrine neoplasia (MEN) type I and are associated with hyperparathyroidism and pituitary adenomas.

The symptoms in 90-95% of patients with gastrinomas are similar to the symptoms of common peptic ulcer disease. Usually, persistent abdominal pain exists that is less responsive to medical treatment.
Sometimes, symptoms may relate to a complication of peptic ulcer disease, such as bleeding (e.g., melena, hematemesis), gastric outlet obstruction (e.g., vomiting), and perforation (e.g., peritoneal irritation).
Other symptoms include gastroesophageal reflux, diarrhoea, steatorrhea, and weight loss, all of which are secondary to acid hypersecretion. Vitamin B-12 malabsorption, which is not correctable by oral intrinsic factor, may also be observed.

Somatostatin receptor scintigraphy (SRS) is very useful to identify the primary lesions preoperatively. SRS is the most sensitive non-invasive method for localizing the primary tumours and metastases. It also is helpful for detecting the presence of liver or bone metastasis.

Peptic ulcer disease can involve the stomach or duodenum. Gastric and duodenal ulcers usually cannot be differentiated based on history alone, although some findings may be suggestive. Epigastric pain is the most common symptom of both gastric and duodenal ulcers, characterized by a gnawing or burning sensation and that occurs after meals—classically, shortly after meals with gastric ulcers and 2-3 hours afterward with duodenal ulcers.

Upper gastrointestinal (GI) endoscopy is the preferred diagnostic test in the evaluation of patients with suspected peptic ulcer disease. At endoscopy, gastric ulcers appear as discrete mucosal lesions with a punched-out smooth ulcer base, which often is filled with whitish fibrinoid exudate. Ulcers tend to be solitary and well circumscribed and usually are 0.5-2.5 cm in diameter.
Treatment of peptic ulcers varies depending on the aetiology and clinical presentation. The initial management of a stable patient with dyspepsia differs from the management of an unstable patient with upper gastrointestinal (GI) haemorrhage. In the latter scenario, failure of medical management not uncommonly leads to surgical intervention.

Treatment options include empiric antisecretory therapy, empiric triple therapy for H pylori infection, endoscopy followed by appropriate therapy based on findings, and H pylori serology followed by triple therapy for patients who are infected. Breath testing for active H pylori infection may be used.

Dysphagia that is episodic and nonprogressive and varies between solids and liquids is more likely to represent a motility disorder. It may also associated with retrosternal chest pain.

Motility disorder is a condition where the nerves and muscles in the gastrointestinal tract are not working together correctly, which cause difficulty in the digestive process. These conditions include chronic intractable constipation, gastroesophageal reflux disease (GERD), chronic intestinal pseudo-obstruction, gastroparesis, Hirschsprung’s disease, and oesophageal achalasia, among other disorders.

In addition to imaging studies, these conditions are usually evaluated with manometry studies which measure the pressure in different areas of the gastrointestinal tract.

Achalasia is a rare neurological deficit of the oesophagus that produces an impaired relaxation of the lower oesophageal sphincter and decreased motility of the oesophageal body. Achalasia is generally accepted to be a pre-malignant disorder, since, particularly in the mega-oesophagus, chronic irritation by foods and bacterial overgrowth may contribute to the development of dysplasia and carcinoma.
When oesophageal cancer develops in patients with underlying achalasia, diagnosis tends to be in the more advanced stages of cancer, compared to cases with no achalasia, because both physicians and patients often regard symptoms such as dysphagia and chest discomfort as attributable to the achalasia, rather than to other causes. Therefore, additional approaches that would lead to earlier diagnosis might be pursued less aggressively.
Achalasia is a predisposing factor for oesophageal squamous cell carcinoma.

Upper gastrointestinal (GI) bleeding is usually defined by a bleeding source proximal to the ligament of Treitz although some may also include a bleeding source in the proximal jejunum. Upper GI bleeding emergencies are characterized by hematemesis, melena, haematochezia (if the bleeding is massive and brisk) and evidence of hemodynamic compromise such as dizziness, syncope episodes and shock. The most commonly used endoscopic haemostatic interventions include epinephrine (adrenaline) injection, thermal coagulation and endoscopic clipping at the ulcer site to constrict, compress and/or destroy the bleeding vessel. Injection of 30 mL diluted epinephrine (1:10 000) can effectively prevent recurrent bleeding with a low rate of complications. The optimal injection volume of epinephrine for endoscopic treatment of an actively bleeding ulcer (spurting or oozing) is 30 mL.

Achalasia is an oesophageal motor disorder characterized by aperistalsis of the oesophageal body and lack of relaxation of the lower sphincter in response to swallows.
Achalasia cardia is one of the common causes of motor dysphagia. Pathophysiologically, achalasia cardia is caused by loss of inhibitory ganglion in the myenteric plexus of the oesophagus. In the initial stage, degeneration of inhibitory nerves in the oesophagus results in unopposed action of excitatory neurotransmitters such as acetylcholine, resulting in high amplitude non-peristaltic contractions (vigorous achalasia); progressive loss of cholinergic neurons over time results in dilation and low amplitude simultaneous contractions in the oesophageal body (classic achalasia).

Iron deficiency anaemia (IDA) is the most common form of anaemia worldwide and can be due to inadequate intake, decreased absorption (e.g., atrophic gastritis, inflammatory bowel disease), increased demand (e.g., during pregnancy), or increased loss (e.g., gastrointestinal bleeding, menorrhagia) of iron. Prolonged deficiency depletes the iron stores in the body, resulting in decreased erythropoiesis and anaemia.
Symptoms are nonspecific and include fatigue, pallor, lethargy, hair loss, brittle nails, and pica. Diagnostic lab values include low haemoglobin, microcytic, hypochromic red blood cells on peripheral smear, and low ferritin and iron levels. Once diagnosed, the underlying cause should be determined. Patients at risk for underlying gastrointestinal malignancy should also undergo a colonoscopy.
Iron deficiency anaemia is treated with oral (most common) or parenteral iron supplementation. Severe anaemia or those with concomitant cardiac conditions may also require blood transfusions. The underlying cause of IDA should also be corrected. IDA may manifest as Plummer-Vinson syndrome (PVS): triad of postcricoid dysphagia, upper oesophageal webs, and iron deficiency anaemia

Boerhaave syndrome refers to an oesophageal rupture secondary to forceful vomiting and retching. They are often associated with the clinical triad (Mackler’s triad) of vomiting, chest pain and subcutaneous emphysema. Other symptoms include epigastric pain, back pain, dyspnoea and shock. This condition was universally fatal before the age of surgery.

Ideal management for Boerhaave syndrome involves a combination of both conservative and surgical interventions.

Mainstays of therapy include the following:
– Intravenous volume resuscitation
– Administration of broad-spectrum antibiotics
– Prompt endoscopic and/or surgical intervention

Duodenal ulcers are more common than gastric ulcers and unlike gastric ulcers, are caused by increased gastric acid secretion. Duodenal ulcers are commonly located anteriorly, and rarely posteriorly. Anterior ulcers can be complicated by perforation, while the posterior ones bleed. The reason for that is explained by their location. The peritoneal or abdominal cavity is located anterior to the duodenum. Therefore, if the ulcer grows deep enough, it will perforate, whereas if a posterior ulcer grows deep enough, it will perforate the gastroduodenal artery and bleed.
Patients with duodenal ulcers will usually have a history of epigastric pain that occurs several hours after eating. The pain is often improved by eating food.

Oesophageal dysphagia occurs when there is a difficulty with the passage of solid or liquid material through the oesophagus, specifically the region between the upper and lower oesophageal sphincter. It results from either abnormal motility of this segment of the oesophagus or obstruction.
Common causes of dysphagia:
Gastro-oesophageal reflux—waterbrash, regurgitation, due to dysmotility or stricture
Achalasia—classically hold-up relieved by carbonated beverages
Motility disorders—may be associated with central chest pain, systemic disease (scleroderma, dermatomyositis)
Oesophageal cancer—progressive, weight loss
Head and neck cancer—pain, dysphagia, otalgia, >90% smokers, often excess alcohol consumption
Pharyngeal pouch—slowly progressive, regurgitation, gurgling
Web—able to swallow only small amounts, “can’t swallow tablets”
Stroke
Neurodegenerative disorders—parkinsonism, motor neurone disease, multiple sclerosis, myasthenia gravis
Presbyphagia

Endoscopy has the advantage of potentially yielding a histological diagnosis. The overall rate of oesophageal perforation after flexible endoscopy involving oesophageal instrumentation, biopsy, or dilatation is 2.6%

Oesophageal manometry remains the investigation of choice in suspected motility disorders. Manometry can classify oesophageal dysmotility into rare specific disorders such as achalasia and diffuse oesophageal spasm or more common non-specific motility disorders that do not respond directly to drug treatment but may improve if related reflux or psychiatric disturbances are treated. The symptoms of non-specific motility disorders may have an uncertain relation to the manometric abnormalities

Management is based on the history, findings of the clinical investigations, and prognosis for the individual patient. The underlying disorder is treated, but the impact of dysphagia on nutrition and hydration will compromise any intervention unless managed effectively. Poor physical condition from malnutrition or dehydration will lead to a suboptimal rehabilitation process, in both duration and completeness of recovery and inadequate management of dysphagia contributes to this. A malnourished person is at risk of decompensation of the swallow, leading to dysphagia. The clinical swallow assessment is used to determine safely modified diets that reduce malnutrition and dehydration. This may range from nil by mouth with total enteral support to full oral route or a balance of the two. Enteral feeding is essential to maintain nutritional status when oral feeding is suspended, even if only for a short time. Prompt involvement of a dietitian is thus essential.

Ulcer bleeding stops spontaneously in about 80% of patients. Only a small percentage require specific measures to stop bleeding. surgery remains the most definitive method of controlling ulcer haemorrhage, and is indicated when endoscopic haemostasis fails to control the bleeding, or when rebleeding occurs. The morbidity and mortality of emergency surgery for ulcer bleeding is high. In principle, the operation performed should be the minimum compatible with permanent haemostasis. The choice of operations is determined by the site and size of the ulcer as well as the experience and preference of the surgeon. Most bleeding duodenal ulcers may be managed by underrunning the bleeding vessel together with vagotomy and pyloroplasty.