CHAPTER 14 Alimentary tract

Oesophagus

Most conditions of the oesophagus have dysphagia as a symptom. Dysphagia is difficulty in swallowing. It may result from local or general causes (→ Table 14.1).

TABLE 14.1 Causes of dysphagia

Local
In the lumen	Foreign body
In the wall	Congenital atresia
	Inflammatory stricture – reflux oesophagitis
	Caustic stricture
	Achalasia
	Carcinoma
	Plummer–Vinson syndrome (oesophageal web)
	Scleroderma
	Irradiation
Outside the wall	Mediastinal lymphadenopathy
	Bronchial carcinoma
	Retrosternal goitre
	Pharyngeal pouch
	Para-oesophageal (rolling) hiatus hernia
	Thoracic aortic aneurysm
	Dysphagia lusoria (vascular ring)
General	Myasthenia gravis
	Bulbar palsy
	Bulbar poliomyelitis
	Hysteria

Investigation of dysphagia

Examination

There may be little to find. There may be evidence of weight loss and anaemia with malignant strictures. Koilonychia is associated with Plummer–Vinson syndrome. Glands may be palpable in the neck with carcinoma. The abdomen should be palpated to exclude liver secondaries. A lump may be palpable in the posterior triangle of the neck with pharyngeal pouch. This may gurgle when full of food.

Foreign body

This is usually accidental in children (small toys and coins), housewives (safety pins) and the elderly (false teeth). Deliberate swallowing occurs in the psychiatrically disturbed. Foreign bodies often impact at the narrowest parts of the oesophagus, i.e. at its commencement, where it is crossed by the left bronchus, and where it passes through the diaphragm. Smooth objects will usually pass into the stomach. Sharp and irregular objects impact.

Oesophageal perforation

This may be caused by swallowed foreign bodies or corrosives; rupture at oesophagoscopy, dilatation or biopsy; penetrating wound, or following a violent vomit after a large meal (Boerhaave’s syndrome).

Inflammatory stricture

This may result from prolonged acid reflux with oesophagitis. Reflux occurs through an incompetent lower oesophageal sphincter. It is often associated with a sliding hiatus hernia. Other causes of reflux oesophagitis include: prolonged vomiting, prolonged nasogastric intubation, operations which destroy the cardio-oesophageal area, e.g. resection with gastro-oesophageal anastomosis, cardiomyotomy for achalasia. As a result of long-standing reflux, the lower oesophagus may come to be lined by columnar mucosa, an appearance known as Barrett’s oesophagus.

Treatment

Medical

Lose weight, loosen corset. Sleep propped up. Antacids. Proton pump inhibitors: omeprazole or lansoprazole are now the most effective treatment. Many patients obtain relief with this regimen.

Surgical

Indicated for failed medical treatment or complications, e.g. anaemia or severe dysphagia due to stricture. Surgery may also be indicated for young patients who do not want to take long-term acid-suppressant agents. There are several operations but a Nissen fundoplication (→ Fig. 14.3) is the most commonly performed. The hernial defect is repaired and the mobilized fundus of the stomach is wrapped around the lower end of the oesophagus to provide an antireflux mechanism. This may be done by the ‘open’ or laparoscopic method.

Figure 14.3 Nissen fundoplication. The fundus of the stomach is mobilized, wrapped around the lower oesophagus, and held with seromuscular sutures.

Achalasia

This is due to failure of relaxation of the lower oesophageal ‘sphincter’. It presents between 30 and 50 years and affects sexes equally. The cause is unknown but degeneration of Auerbach’s plexus occurs.

Symptoms and signs

Intermittent dysphagia. Gets progressively worse. May be worse for liquids than for solids. Fluid regurgitation especially at night with aspiration pneumonitis. Retrosternal pain.

Investigations

• Barium swallow: dilated tortuous oesophagus above smooth tapering stricture (‘rat’s tail’ appearance → Fig. 14.2)

• Oesophagoscopy: needs aspiration of stagnant food initially, exclude benign stricture or carcinoma.

Complications

Aspiration pneumonitis, oesophageal erosions. Carcinoma may develop even after treatment.

Carcinoma of the oesophagus

This occurs most commonly in males. The commonest site is the lower third of the oesophagus followed by the middle third and upper third. Postcricoid carcinoma usually occurs in females and is part of the Plummer–Vinson syndrome. Achalasia of the cardia is also a predisposing cause. Squamous cell carcinoma occurs in the upper and middle thirds but adenocarcinoma may occur in the lower third associated with areas of gastric mucosa (Barrett’s oesophagus) or by growth of a carcinoma of the cardiac area of the stomach into the oesophagus. Spread occurs by the following:

• Local invasion into surrounding structures, trachea, lung and aorta (massive haemorrhage may be terminal event)

• Lymphatic to paraoesophageal nodes, supraclavicular and abdominal nodes

• The blood stream to liver and lung.

Symptoms and signs

Dysphagia, usually rapid onset. Initially for solids then fluids. Weight loss, anorexia, anaemia. Palpable supraclavicular nodes, palpable irregular liver (secondaries).

Treatment

Resection. The stomach is mobilized and brought up into the chest and anastomosed to the remaining oesophagus in either the chest or neck. If the tumour is inoperable, an expandable metal stent may be placed through the tumour using a fibreoptic endoscope. Other methods of relieving dysphagia include laser therapy. Radiotherapy may be used for primary or palliative treatment of both squamous cell carcinomas and adenocarcinomas, the latter responding nearly as well as the squamous cell carcinomas. The best response is now with a combination of chemotherapy (cisplatin and 5-FU) and radiotherapy.

Prognosis

Prognosis is poor. Most patients survive less than 6 months if the primary is non-resectable. The 5-year survival following resection is less than 20%.

Barrett’s oesophagus

Barrett’s oesophagus refers to metaplasia of the cells in the lower oesophagus from squamous to columnar epithelium as a result of long standing acid reflux. OGD reveals areas of pink columnar mucosa replacing pearly white squamous epithelium. It occurs in 5–15% of patients with GORD. The risk of malignancy in patients with Barrett’s oesophagus is 100 times higher than in the general population. Endoscopic surveillance with biopsy to identify dysplasia is required. Prevention involves treatment of GORD with proton pump inhibitors and anti-reflux surgery. Treatment of established dysplasia involves photodynamic therapy, radiofrequency ablation or endoscopic mucosal resection.

Corrosive oesophagitis

The accidental or deliberate ingestion of corrosives causes severe oesophagitis. Common substances include caustic soda, bleach and sulphuric acid. Extensive damage occurs to the mouth, pharynx, larynx and stomach as well as to the oesophagus.

Symptoms and signs

History of ingestion. Burning pain from mouth to stomach. Fever. Shock. Respiratory distress if aspiration. Oedema of lips, lung, pharynx.

Investigations

Early endoscopy with fine fibreoptic endoscope to assess degree of damage.

Complications

Bleeding. Perforation. Stricture is a late complication.

Prognosis

Appropriate early treatment of caustic burns usually gives good results. Extensive burns with strong acid or strong alkali progress to stricture formation and require surgery.

Stomach and duodenum

Peptic ulceration

This occurs anywhere where pepsin and acid occur together. It is caused by an imbalance between secretion of acid and pepsin, and mucosal defence mechanisms. An acid environment and reduced mucosal defences provide ideal circumstances for pepsin to cause mucosal ulceration. If there is no acid, peptic ulceration cannot occur. Oversecretion of acid is associated with duodenal ulceration. Breakdown of the mucosal defences occurs in gastric ulceration. Exacerbating factors in peptic ulceration include stress, smoking, alcohol, NSAIDs, steroids, hyperparathyroidism, Zollinger–Ellison syndrome. Infection with Helicobacter pylori may impair mucosal defences and is associated with duodenal ulcer and gastritis and to a lesser extent, gastric ulcers. Common sites for peptic ulcer are the stomach and duodenum, the anterior and posterior walls of the first part of the duodenum and the lesser curve of the stomach being the most common sites. Less common sites include the oesophagus (Barrett’s oesophagus), Meckel’s diverticulum containing ectopic gastric mucosa and gastrojejunal anastomosis (after ulcer surgery).

Treatment

Medical

• Antacids, e.g. Mist. Mag. Trisil., relieve pain but are of limited value.

• Proton pump inhibitors reduce acid secretion by inhibiting the proton pump in parietal cells. Results in greater inhibition of acid than H₂ receptor antagonists. Omeprazole and lansoprazole may be used. First-line treatment is acid suppression with proton pump inhibitor plus eradication therapy for H. pylori, i.e. triple therapy with omeprazole 20 mg b.d. plus two of the following three antibiotics: amoxicillin, clarithromycin, metronidazole. Check for eradication 6 weeks later by re-endoscopy and biopsy or breath test.

In addition to the above specific therapies, advice should be given regarding stopping smoking, stopping NSAIDs, and dealing with a stressful lifestyle.

Surgical

Indications are the following:

• Failed medical treatment (unusual nowadays).

• Complications – haemorrhage, perforation, pyloric obstruction. Operations in the past have included vagotomy and drainage and highly selective vagotomy. These operations are used rarely nowadays and the most common operation is pyloroplasty (Fig. 14.4) with oversewing of bleeding duodenal ulcer. Partial gastrectomy (Fig. 14.5) may be required for bleeding gastric ulcer.

Figure 14.4 (A) Truncal vagotomy and gastrojejunostomy. (B) Truncal vagotomy and pyloroplasty. The pylorus is opened longitudinally and sutured transversely thus destroying the pyloric sphincter.

Figure 14.5 Types of partial gastrectomy. (A) Billroth I. The gastric remnant is anastomosed directly to the first part of the duodenum. (B) Billroth II (Polya). The duodenal stump is oversewn and continuity re-established by gastrojejunostomy.

Complications of peptic ulceration

Haemorrhage

Posterior duodenal ulcers erode the gastroduodenal artery. Lesser curve gastric ulcers erode the left gastric artery. OGD to locate the site of the ulcer. A bleeding ulcer can be treated by injection, diathermy or laser coagulation at OGD. If the ulcer is not actively bleeding, a course of medical treatment may be given. The majority of patients stop bleeding spontaneously. If bleeding is massive or recurrent, surgery is required. The bleeding vessel in the base of the ulcer is oversewn to stop the bleeding. A GU is best excised or at least a biopsy should be taken to exclude malignancy. The pylorus is opened for treating a bleeding DU and is closed as a pyloroplasty. The patient is treated with long-term proton-pump inhibitors.

Perforation

Anterior DUs and GUs may perforate causing generalized chemical peritonitis. Surgery involves simple suture of the ulcer with reinforcement with an omental patch. A biopsy should be taken from the edge of a GU as there is a risk of malignancy. Check H. pylori status and eradicate if necessary. Long-term proton-pump inhibitors if chronic ulceration.

Pyloric obstruction

Late complication. Rare nowadays. Vomiting of large amounts of foul-smelling vomit often containing food eaten several days previously. Eructations of foul gas. Gastric succussion splash on examination. Empty stomach with wide-bore nasogastric tube. Confirm by OGD or contrast study. Surgical treatment is by gastrojejunostomy. Hypokalaemia and metabolic alkalosis may be present and require correction prior to surgery.

Obstruction of the mid-stomach may occur because of fibrosis of a large saddle-shaped ulcer astride the lesser curve. This gives rise to the ‘hourglass’ appearance on a barium study. It is largely of historical interest from the days when patients kept their ulcers a long time prior to consideration of surgery.

Zollinger–Ellison syndrome

Peptic ulcer disease caused by excessive production of gastrin. Peptic ulcers may occur in unusual sites, e.g. the third part of the duodenum. There is usually a gastrin-secreting pancreatic tumour (gastrinoma); 60% are malignant; 30% associated with MEN (Type I).

Carcinoma of the stomach

The incidence is declining but it remains a common tumour with a poor prognosis. Widespread geographical variations occur, the incidence being high in Japan and certain coastal countries where the intake of dietary nitrate is high. Eating smoked fish and highly spiced foods has been implicated. Other associations include blood group A (suggesting a genetic factor), pernicious anaemia, atrophic gastritis, previous gastric surgery and benign gastric ulcer.

Symptoms and signs

Onset silent and insidious. Vague dyspepsia, epigastric pain, weight loss, dysphagia (cardiac area), vomiting (pyloric area), anaemia, lassitude. Epigastric mass, hepatomegaly, ascites, left supraclavicular gland palpable (Virchow’s node, Troisier’s sign), gastric succussion splash, acanthosis nigricans.

Prognosis

In Japan, where screening programmes are undertaken because of the high incidence, the 5-year survival for early gastric cancer is around 90%. In the UK at least 60% of cases present too late for curative surgery. Overall about 20% survive 5 years. Radiotherapy is of no value.

Gastric surgery and its complications

Carcinoma and complications of peptic ulcer are the commonest indications for gastric surgery. The operations of vagotomy, vagotomy and pyloroplasty, vagotomy and gastrojejunostomy and highly selective vagotomy are described but are largely of historical interest. Patients are still seen who have had these operations and have suffered the complications of them. Vagotomy is rarely, if ever, carried out nowadays.

Operations

Vagotomy (Fig. 14.4)

This reduces acid secretion from the stomach. It reduces gastric motility and therefore interferes with gastric emptying. A drainage procedure is therefore required.

Pyloroplasty (Fig. 14.4)

The pylorus is cut longitudinally and sewn up transversely. In this operation, vagotomy is designed to reduce acid secretion and thus allow the ulcer to heal. The pyloroplasty is performed to allow gastric drainage.

Gastroenterostomy (Fig. 14.4)

The most dependent part of the stomach is anastomosed to a loop of jejunum. This diverts acid away from the duodenum and allows the ulcer to heal. Vagotomy is carried out to reduce acid secretion and thus prevent stomal ulceration.

Highly selective vagotomy

The vagus is sectioned such that only the body of the stomach is denervated. The nerve of Latarjet to the pylorus is left intact, thus preserving motility of this region and allowing the stomach to empty without need for a pyloroplasty.

Gastrectomy (Fig. 14.5)

This may be partial or total. Partial gastrectomy usually involves removal of about {7/8} of the stomach. The gastric remnant may be reanastomosed directly to the first part of the duodenum (Billroth I) or the duodenal stump oversewn and the continuity re-established by a gastrojejunostomy (Billroth II or Polya gastrectomy. If partial gastrectomy is used for GU, the ulcer is removed together with the segment of stomach. For DU, removal of the bulk of the acid-secreting area of the stomach allows the ulcer to heal. The ulcer is not usually removed.

Complications

Recurrent ulceration

Epigastric fullness

Particularly after partial gastrectomy. Treatment is to take small meals frequently. The symptom tends to improve with time.

Bilious vomiting

Sudden emptying of the afferent loop with Billroth II. Associated biliary gastritis. May respond to metoclopramide. Severe cases need revisional surgery, e.g. Roux-en-Y anastomosis so that bile enters the GI tract lower down in the jejunum (→ Fig. 14.6).

Figure 14.6 Roux-en-Y conversion for bilious vomiting. The afferent loop is detached and reanastomosed lower down the jejunum.

Nutritional disturbances

Weight loss

May be due to reduced caloric intake or poor absorption.

Steatorrhoea

Due to poor mixing of food and enzymes, e.g. long afferent loop where food passes into the jejunum before it is adequately mixed with digestive enzymes coming from the afferent loop. Blind loop syndrome may be responsible, i.e. stasis in the long afferent loop with colonization with abnormal bacteria, which restricts digestion and absorption of food. Surgical correction of the afferent loop may be necessary.

Anaemia

Iron deficiency anaemia due to reduced hydrochloric acid, which is required for iron absorption. With total gastrectomy, megaloblastic anaemia may occur, owing to loss of intrinsic factor and subsequent B₁₂ deficiency. Vitamin B₁₂ injections are required.

Bolus obstruction

Destruction of the pylorus allows unmasticated food to pass into the small intestine. This may swell and lodge in the terminal ileum. This occurs particularly with orange pith and dried fruits. Patients should be warned not to eat these foods if the pylorus is not intact.

Carcinoma

May occur in the gastric remnant. This is rare.

Upper gastrointestinal tract bleeding

This causes either haematemesis (vomiting of blood), melaena (passage of altered blood PR – usually black and tarry with a characteristic smell), or both. Causes include peptic ulceration, acute gastric erosions, oesophageal varices, oesophagitis, Mallory–Weiss syndrome, and carcinoma. Rarer causes include GIST, angiomatous malformations, haemobilia and bleeding disorders. Drugs that may precipitate bleeding include steroids, NSAIDs, and anticoagulants. Principles of treatment include replacement of blood loss, diagnosis of the cause and treatment of the condition.

Symptoms and signs

Clinically anaemic. With severe bleed, shock will occur. History of aspirin, NSAIDs, steroid or anticoagulant. Stigmata of liver failure. Abdominal mass.

Investigations

• Angiography if source of bleeding is obscure.

Prognosis

The overall mortality for an upper GI bleed is 10%. Adverse prognostic factors include old age, shock at presentation, rebleeding and oesophageal varices.

Other conditions of the stomach and duodenum

Duodenum

Other than peptic ulcer, conditions of the duodenum are rare. A duodenal diverticulum may occur on the medial wall near the ampulla of Vater. Most are asymptomatic. Rarely bleeding and perforation may occur. Symptomatic diverticulae should be excised. Tumours of the duodenum are rare. Adenocarcinoma does not occur in duodenal ulcers. Rarely, it may occur in other parts of the duodenum and if it arises near the bile ducts, may cause obstructive jaundice.

Conditions of the small bowel

Meckel’s diverticulum

A remnant of the vitellointestinal duct of the embryo. Classically it occurs in 2% of patients, is 2 inches long, and 2 feet from the ileocaecal junction (‘rule of 2 s’). It occurs on the antimesenteric border of the terminal ileum.

Crohn’s disease

This is dealt with in the section on inflammatory bowel disease.

Typhoid

Caused by Salmonella typhi. About 200 cases occur in the UK annually. It may occur in the immigrant population and in those who have travelled in countries where the disease is endemic. The organism enters Peyer’s patches and may result in perforation or bleeding usually involving the ileum. This usually occurs during the third week of the disease. The patient shows signs of perforation with peritonitis. Surgical closure of the perforation is required. The bowel is very friable. Chloramphenicol i.v. is given for 2 weeks’ postoperatively.

Tumours of the small intestine

These form less than 5% of all tumours of the GI tract. Obstruction and bleeding are the usual symptoms.

Benign

These include adenomas, leiomyomas and lipomas. Obstruction, intussusception, or bleeding may occur. Polyposis of the small bowel (mainly jejunum) may occur in association with pigmentation of the lips and mouth (Peutz–Jeghers syndrome). Bleeding or intussusception may occur.

Malignant

Adenocarcinoma is rare and usually affects the jejunum. Bleeding and obstruction may occur. Lymphoma may present as intestinal obstruction or a palpable mass. Consider lymphoma in patients with coeliac disease. Palliation of these tumours is by radiotherapy or chemotherapy.

Carcinoid tumour

These occur most commonly in the appendix but can occur anywhere in the GI tract and occasionally in the lung. Those in the small bowel grow slowly but most of those greater than 2 cm have metastasized at the time of surgery. The tumours arise from argentaffin cells.

Small bowel obstruction

Mechanical obstruction of the small bowel may be simple (one point of obstruction) or closed loop (obstruction at two points enclosing a segment of bowel). If the bowel is viable, the obstruction is termed non-strangulating. If the blood supply is compromised, strangulating obstruction occurs with subsequent infarction of bowel. Strangulation occurs when the obstructing mechanism cuts off the mesenteric arterial blood flow, e.g. the neck of the sac with a loop of bowel trapped in a hernial sac, or the twist of a volvulus. Mechanical obstruction is more common in the small bowel than in the large bowel.

Symptoms and signs

Colicky abdominal pain. The patient cannot get into a comfortable position. Vomiting. Constipation. Symptoms depend on whether the obstruction is high or low. High obstruction is characterized by early vomiting (bilious), and late constipation. Low obstruction is characterized by early constipation, and late vomiting (faeculent). Distension, marked with low obstruction, tympanitic abdomen, high-pitched tinkling bowel sounds. Hernial orifices should be carefully examined. Pyrexia, tachycardia, continuous pain and localized tenderness suggest actual or impending strangulation.

Investigations

• Hb

• FBC

• WCC with neutrophilia may indicate strangulation

• U&Es

• AXR: distended loops of small bowel in central abdomen (→ Fig. 14.7). Erect films show air/fluid levels. Absent or diminished colonic gas. Dilated proximal small bowel shows lines close together (valvulae conniventes) crossing completely the lumen of the bowel. These get progressively fewer the more distal the distended loop and are absent in the terminal ileum. Look for gas in the biliary tree (gallstone ileus with cholecystoduodenal fistula).