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.

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.

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

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.

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.

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

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.

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 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).