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

History

• May be an obvious cause, e.g. foreign body, ingestion of caustic substance

• May be a previous history of oesophagitis suggesting an inflammatory stricture

• Younger patients with history of dysphagia, worse for fluids than solids and no weight loss suggests achalasia

• Rapid onset of dysphagia in the elderly with weight loss suggesting malignancy

• The patient may be able to accurately locate the site and point at which the foods sticks, e.g. sternal notch with Plummer–Vinson syndrome, lower sternum with carcinoma at the cardia.

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.

Treatment

Oesophageal dilatation

This is achieved using a pneumatic dilator introduced over a guide wire under radiological control. The success rate is over 50% but repeated dilatations are necessary.

Heller’s operation (i.e. cardiomyotomy)

The muscle layer is divided down to the mucosa over the lower end of the oesophagus and extended for about 1 cm on to the stomach. It is a similar principle to Ramstedt’s operation for pyloric stenosis in infancy.

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.

Treatment

Emergency

Dilute acid (vinegar) or alkali (sodium bicarbonate) may be used to neutralize the ingested substance. Never induce vomiting. It may rupture the already damaged oesophagus.

Medical

Broad-spectrum antibiotics. Steroids. TPN.

Endoscopic dilatation of strictures

Gentle dilatation may be undertaken at 3–4 weeks.

Surgery

If a severe stricture develops, oesophageal replacement by interposition of a segment of colon is required. Stomach may also be used if that has been spared from the effects of the caustic injury. Surgery is also required if perforation occurs.

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.

Plummer–vinson syndrome (syn. paterson–brown–kelly syndrome, sideropenic dysphagia)

This occurs in middle-aged females. It is an iron deficiency anaemia associated with a smooth tongue, koilonychia (spoon-shaped nails) and dysphagia. The dysphagia is due to the formation of a web in the upper oesophagus (postcricoid web). The condition is premalignant and carcinoma may develop in the upper oesophagus.

Treatment

Oesophageal dilatation if symptoms from web. Follow-up to check for developing carcinoma.

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).

Symptoms and signs

Duodenal ulcer (DU)

Epigastric pain. May radiate through to back. Relieved by eating. Worse at night. Symptoms are periodic and last about 14 days and recur at 3–4-monthly intervals. They are often worse in spring and autumn. Vomiting is rare. If it occurs, pyloric stenosis should be suspected. Examination may reveal tenderness in epigastrium.

Gastric ulcer (GU)

Epigastric pain. Not periodic. Food may precipitate pain. Pain may be relieved by vomiting. Patient may be afraid to eat and weight loss results. Examination reveals tenderness in epigastrium.

Investigations

• OGD and biopsy: risk of malignancy with GU; antral biopsy for mucosal urease test (CLO test)

• Serology for H. pylori

• Breath test

• Barium meal is rarely used nowadays but if a GU is diagnosed on a barium study, OGD and biopsy should be carried out

• Other routine investigations include Hb, FBC, U&Es, Ca, PO₄ and occasionally serum gastrin if Zollinger– Ellison syndrome is suspected.

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.

Treatment

This is surgical.

Attempt at cure

Wide excision of tumour usually with 5 cm margin and clearance of nodes. For distal tumours, partial gastrectomy (7/8) may suffice. For more proximal tumours, total gastrectomy. Over 60% are found to be incurable at laparotomy.

Palliative

Bypass gastrojejunostomy for antral tumours. Intubation via upper GI endoscopy with an expandable mesh stent.

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.

Dumping

Early

Fainting, sweating and dizziness shortly after eating. May be a reflex caused by osmotic effect of large volumes of food ‘dumped’ into the jejunum. Less common after highly selective vagotomy. Patient may need to lie down and rest for half an hour. Symptoms may be improved by eating small dry meals frequently and avoiding heavy carbohydrate meals. Early dumping may subside spontaneously with time.

Late

Due to hypoglycaemia and occurs 1–3 h after a meal. Responds to glucose (sucking barley sugars).

Diarrhoea

This may be disabling after vagotomy. Codeine phosphate and small dry meals may help. The incidence is less after highly selective vagotomy.

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.

Treatment

• Bed rest, pulse, BP, CVP line. Infusion of crystalloid, colloid, blood.

• Treat shock.

• Catheterize.

• Establish diagnosis by endoscopy.

• Control varices with Sengstaken tube or injection.

• Give intravenous proton pump inhibitor.

• Eradication of H. pylori.

Indications for surgical intervention:

• Massive uncontrolled bleeding

• Rebleeding, especially if bleeding vessel or clot on ulcer has been seen at endoscopy

• More than 4 unit bleed in 24 h unless the cause is varices.

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

Stomach

Gastrointestinal stromal tumour (GIST)

Vary from benign (leiomyoma) to high grade malignant. Epigastric discomfort, indigestion, haematemesis or melaena due to ulceration of mucosa overlying tumour. Investigations include OGD and CT scan. Barium meal shows space-occupying lesion. Surgical excision is required. Imatinib (tyrosine kinase inhibitor) for incomplete removal or recurrence.

Lymphoma

Symptoms are those of peptic ulcer or gastric carcinoma. OGD and biopsy to confirm diagnosis. Treatment is by surgical resection followed by radiotherapy or chemotherapy; 50% of patients survive 5 years or more.

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.

Symptoms and signs

Symptomless. Incidental finding at laparotomy. Symptoms typical of acute appendicitis may occur. Rectal bleeding (ectopic gastric mucosa). Rarely umbilical discharge (fistula), intestinal obstruction (due to entrapment around the band from the apex of the diverticulum to the back of the umbilicus), small bowel volvulus, or intussusception (ileo-ileal).

Investigations

• Technetium scan for GI bleeding may show gastric mucosa in a Meckel’s

• Laparotomy is required for complications of Meckel’s – the cause is not usually apparent until laparotomy is undertaken.

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.

Causes

Causes may be found:

• in the lumen: gallstone ileus, food bolus (following pylorus-destroying operations, i.e. gastrojejunostomy or pyloroplasty)

• in the wall: congenital atresia, Crohn’s disease, tumours, e.g. lymphoma or carcinoma

• outside the wall: herniae, adhesions, volvulus, intussusception.

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).

Figure 14.7 Small bowel obstruction. Distended loops of small bowel are visible in the central abdomen. These are identifiable as small bowel as the valvulae conniventes (arrows) cross the entire lumen.

Treatment

Conservative

• Intravenous fluids and nasogastric aspiration

• Nil orally

• 2-hourly temperature and pulse

• Abdominal examination 8-hourly.

Some cases of simple mechanical obstruction, e.g. due to adhesions, will settle on this regimen.

Indications for surgery

Strangulating obstruction, e.g. a tender irreducible hernia, requires urgent surgery. If a conservative ‘drip and suck’ regimen has been undertaken for obstruction, surgery is indicated for signs of incipient strangulation (pyrexia, tachycardia, localized tenderness). Surgery is also required for simple obstruction that fails to settle, e.g. adhesions, gallstone ileus. At surgery, the affected bowel is inspected for viability. Indications of non-viability include:

• Absence of peristalsis

• Loss of normal sheen

• Loss of pulsation in bowel mesentery

• Colour: green or black bowel is non-viable and resection is required. Plum-coloured bowel may respond to wrapping for a few minutes in warm saline-soaked packs. If colour returns and it will transmit a peristaltic wave, it is viable.

Prognosis

Small bowel obstruction has a very low mortality rate if it is simple. Strangulating obstruction increases the mortality and if small bowel resection is required, especially in the elderly, the mortality rate may reach 25%.

Appendicitis

This is the commonest cause of the acute abdomen in the UK. It usually occurs when there is an obstruction in the lumen of the appendix either by a faecolith or foreign body or by enlargement of lymphoid follicles in its wall. It most often affects children, teenagers and young adults. It is rare at the extremes of life. In the infant, the lumen of the appendix is wide in relation to the remainder of the bowel and the diet is soft and hence, obstruction within the lumen is less likely. In the elderly, the lumen tends to be obliterated. Rarer causes of appendicitis include carcinoma of the caecum obstructing the appendiceal lumen, carcinoid tumour and obstructing fibrous bands. Occasionally a carcinoma obstructing the lumen of the appendix will cause it to distend and fill with mucus, i.e. a mucocele of the appendix.

Symptoms and signs

Central abdominal cramping or colicky pain. Nausea. Vomiting is uncommon. Occasionally the patient may pass a loose stool. Frank diarrhoea is uncommon. Central abdominal pain lasts approximately 8 h. It is followed by the development of a sharp, stabbing somatic type of pain in the RIF made worse by coughing or moving. Low-grade pyrexia (37.2–37.8°C). Flushed. Characteristic fetor (sweet faecal smell to breath). White furred tongue. Tachycardia (100 in first 24 h). Tender with guarding in RIF over McBurney’s point. Examination PR: tender anteriorly in the rectovesical or rectouterine pouch.

In infants, diarrhoea and vomiting may be the only symptoms. This may lead to difficulty in diagnosis and confusion with gastroenteritis. In elderly patients there may be confusion and later, shock may develop.

Investigations

• WCC: usually >10 × 10⁹/L with neutrophil leukocytosis

• USS: may show a mass or abscess; usefulness in early appendicitis depends on the experience of the ultrasonographer

• Diagnostic laparoscopy.

Differential diagnosis

In the classical case of acute appendicitis there are few conditions that enter into the differential diagnosis. These include mesenteric adenitis, Meckel’s diverticulitis, Crohn’s disease (regional ileitis), mesenteric embolus and right-sided colonic diverticulitis. All these conditions will initially cause central abdominal cramping pain with subsequent tenderness in the RIF.

In the atypical case, other causes of intra-abdominal pathology, urinary tract disease, gynaecological problems (see Ch. 22) and extra-abdominal conditions must be considered.

Abdominal disease

Cholecystitis, gastroenteritis, pancreatitis, perforated DU, intestinal obstruction, diverticulitis, non-specific abdominal pain.

Urinary tract

Acute pyelonephritis, renal colic, cystitis. An inflamed appendix adherent to the bladder may cause frequency and pyuria. Organisms will be absent on urinary microscopy.

Gynaecological causes

Salpingitis. Ectopic pregnancy. Degeneration of a fibroid. Mittelschmerz. Pelvic inflammatory disease.

Extra-abdominal causes

Referred pain from nerve roots, e.g. herpes zoster, degenerative and malignant disease affecting roots T11, T12. Referred pain from right lower lobar pneumonia. Referred pain from a right-sided testicular torsion.

Treatment

The treatment of acute appendicitis is appendicectomy. Prophylactic metronidazole by suppository should be given 1 h preoperatively to reduce the risk of wound infection.

Complications

Appendicitis may resolve spontaneously. The appendix may become surrounded by adjacent small bowel and omentum and give rise to an appendix mass. It may perforate giving rise to generalized peritonitis or it may perforate amidst local adhesions giving rise to an appendix abscess. Often it is difficult to diagnose appendicitis. If the symptoms have been present for 48 h (‘48 h rule’) and the diagnosis is truly appendicitis, then the patient should either have developed an appendix mass or generalized peritonitis. If neither of these two is present, then the diagnosis of appendicitis should be reviewed.

Appendix mass

Omentum and small bowel adhere to the inflamed appendix. This usually happens 2–5 days after onset of initial symptoms. This should be initially treated conservatively. Mark out the size of the mass on the abdominal wall; i.v. fluids, analgesia, and antibiotics (cefuroxime and metronidazole) should be administered. If the mass resolves it is usual to carry out an interval appendicectomy after 3 months. If the mass gets bigger it is likely that an abscess is forming, i.e. the appendix has perforated within the appendix mass.

Appendix abscess

If an appendix mass enlarges and the temperature fails to settle, an appendix abscess is developing. The patient may appear toxic with a tachycardia. An appendix abscess requires either surgical drainage and appendicectomy, or percutaneous insertion of a drain under ultrasound control. Interval appendicectomy is required subsequently.

Other complications include subphrenic abscess, pelvic abscess, paralytic ileus, septicaemia, portal pyaemia (rare). Long-term complications may be due to adhesions resulting in intestinal obstruction in a small proportion of patients. Tubal adhesions with infertility may occur in females.

Appendicitis in pregnancy

This is no commoner than at other times. Pain and tenderness are higher because of displacement of the appendix by the enlarging uterus. Prompt assessment and intervention are essential. There is a risk of abortion in the first trimester but if treatment is delayed until perforation occurs the risk is considerably higher (approximately 25%).

Conditions of the colon, rectum and anus

Colonic polyps

A polyp is a sessile (broad-based) or pedunculated (on a stalk) protrusion from a body surface. In the colon, it is a lesion that projects into the lumen.

Hamartomas

Juvenile polyps

May occur in large or small bowel. Cause bleeding or obstruction. May auto-amputate in adolescence.

Peutz–Jeghers syndrome

Diffuse GI polyposis with mucocutaneous pigmentation of lips and gums. The polyps have no malignant potential. Surgery is indicated only for symptoms, i.e. obstruction or bleeding.

Neoplastic polyps

Adenomatous polyps and villous adenomas

These have malignant potential, especially the villous adenoma.

Familial polyposis coli

This is an autosomal dominant condition with multiple polyps involving colon and rectum. Duodenal adenomas may also occur and progress to malignancy. It first appears in adolescence. If untreated, malignancy will develop before the age of 40. Treatment is classically by subtotal colectomy with ileorectal anastomosis. However, now, most patients are offered restorative proctocolectomy with ileo-anal pouch. Ileorectal anastomosis is still a reasonable option. Occasionally, rectal polyps regress after this procedure. Regular (6-monthly) inspection of the rectum by sigmoidoscopy is undertaken and any polyps excised. Sulindac may reduce polyp formation. Recurrence is high with carcinoma developing in the rectum. Other operations include total colectomy with mucosal proctectomy, and ileo-anal anastomosis or in some cases panproctocolectomy with ileostomy. There is a need for upper GI surveillance as most of the mortality is from development of ampullary/duodenal carcinomas developing from duodenal adenomas.

Gardner’s syndrome

A variant of familial polyposis, it is associated with desmoid tumours, osteomas of the mandible and multiple sebaceous cysts.

Colorectal cancer

Commonest GI cancer. Usually presents after middle life but can occur earlier. The highest incidence of colorectal cancer is seen in Western Europe and North America; the lowest incidence occurs in Asia and South Africa. The precise cause is unknown but environmental and genetic factors are important. Lack of dietary fibre, increased fat, increased bile acids, have been implicated. Other predisposing factors include inflammatory bowel disease, familial polyposis coli, colorectal polyps, and previous irradiation. Apart from familial adenomatous polyposis, there are other groups of patients who have hereditary predisposition to develop large bowel cancer.

There are two types of autosomal dominant hereditary non-polyposis colorectal cancer (HNPCC):

• Cancer family syndrome (CFS), which occurs with early onset at around 20–30 years and is associated with other adenocarcinomas especially endometrial carcinoma and breast carcinoma

• Hereditary site-specific colonic cancer (HSSCC), which shows the same characteristics as CFS except for the extracolonic carcinomas.

It has also been demonstrated that the frequency of colorectal cancer developing in first-degree relatives of patients with large bowel carcinoma is significantly higher than expected. The relative sites of distribution of carcinoma in the colon are rectum, 40%; sigmoid colon, 25%;descending colon, 5%;transverse colon, 10%; caecum and ascending colon, 20%.

Symptoms and signs

Clinical features depend upon the sites. Right colon: anaemia, palpable mass, change in bowel habit. Left colon: change in bowel habit, lower abdominal colicky pain. Blood or mucus on or mixed with stool. With sigmoid cancers, spurious diarrhoea may occur. Rectal cancers present with frequency of defaecation because of tenesmus (a sense of incomplete evacuation). Blood and mucus PR. Patients may present with symptoms due to direct spread; sacral pain or sciatica due to direct invasion of the nerve. Jaundice due to liver or porta hepatis node metastases. Examination may reveal an abdominal mass or hepatomegaly. Examination PR may show blood on examining glove or mass may be palpable.

Some 25% of large bowel cancers present as emergencies. Obstruction may occur, e.g. small bowel obstruction with caecal cancers growing over the ileocaecal valve or obstruction occurring on the left side where the bowel lumen is narrow and the faeces more formed. Perforation may occur because of either direct perforation of the cancer or perforation of the caecum with a closed-loop obstruction where the ileocaecal valve is competent. Massive haemorrhage is rare.

Treatment

(→ Fig. 14.10)

Figure 14.10 Operations for colorectal cancer. The diagrams indicate the extent of resection and the method of re-establishing continuity. (A) Right hemicolectomy. (B) Extended right hemicolectomy. (C) Left hemicolectomy. (D) Sigmoid colectomy. (E) Anterior resection. (F) Abdominoperineal resection of the rectum with permanent colostomy. The shaded area is the area resected.

Elective

• Caecum and right colon: right hemicolectomy (see Procedures box, below)

• Transverse colon: extended right hemicolectomy

• Descending colon: left hemicolectomy

• Sigmoid colon: sigmoid colectomy.

• Rectum and rectosigmoid: anterior resection with primary anastomosis. If low rectal tumour, abdominoperineal excision of the rectum should be carried out with a permanent colostomy.

For any operation on the left side of the colon, the patient should be warned about a temporary defunctioning loop ileostomy until the primary anastomosis has healed.

Emergency

Correct fluid and electrolytes imbalance. In closed-loop obstruction a caecum of greater than 10 cm in diameter on AXR is an indication for urgent surgery, especially if it is tender. Right-sided tumours may be treated with right hemicolectomy with primary anastomosis. Lower left-sided tumours should be treated by resection of the tumour and Hartmann’s procedure, i.e. closure of the rectal stump and fashioning of an LIF end colostomy. Continuity of the bowel is re-established some weeks later. Some surgeons carry out an on-table colonic lavage with primary anastomosis covered by a loop ileostomy.

Prognosis

This is based on Dukes’ classification, originally described for rectal cancer but now applied to all colorectal adenocarcinomas (→ Table 14.2).

TABLE 14.2 Dukes’ Classification ^a

A	Confined to bowel wall; 80% 5-year survival
B	Through wall into surrounding tissue; 60% 5-year survival
C	Lymph node involvement; 30% 5-year survival

a If distant metastases are present, the 5-year survival is only 5%.

Screening

Populations at risk include asymptomatic relatives of patients with colorectal cancer and patients who have large bowel polyps. Screening methods include regular rigid sigmoidoscopy, flexible endoscopic screening or screening for faecal occult bloods. Serum markers such as carcinoembryonic antigen (CEA) may also be used for follow-up after resection. Ultrasound may be used for liver surveillance following successful resection. If an isolated secondary occurs, liver resection may be carried out.

Inflammatory bowel disease

The two main disorders are Crohn’s disease and ulcerative colitis.

Crohn’s disease

This is a chronic inflammatory disorder that may occur anywhere in the alimentary tract from the mouth to the anus. Common sites include the terminal ileum (regional ileitis), colon and rectum. Unlike ulcerative colitis the whole thickness of the bowel wall is involved. The aetiology is unknown. The disease occurs most commonly in the 15–35 age group. Familial clustering occurs. Malignancy may rarely occur in both the small and large bowel.

Symptoms and signs

Malaise, anorexia, fever, nausea, abdominal pain, weight loss, diarrhoea, rectal bleeding. Perianal inflammation with abscess, fissure, and fistulae formation may occur. Pallor, malnutrition, abdominal mass, perianal sepsis, fissures, fistulae, clubbing, erythema nodosum, pyoderma gangrenosum, uveitis.

Complications

Extra-alimentary manifestations (see above). Toxic dilatation. Stricture. Internal fistulae. Haemorrhage. Abscess formation. Perianal complications. Gallstones. Renal calculi. Psychological problems. Risk of carcinoma.

Treatment

Medical

Correction of fluid and electrolyte imbalance. Nutritional support. Steroids: 40 mg daily of prednisolone in acute exacerbations. Rectal disease may respond to Predsol enemas. Mesalazine may help colonic disease and may reduce the frequency of relapses. Other drug therapies include azathioprine (useful as steroid-sparing drug in some cases), ciclosporin, metronidazole (especially for colonic disease with perianal sepsis). Antidiarrhoeal agents may be used for symptomatic control but should be stopped if obstructed symptoms occur.

Surgical

Indicated for toxic dilatation, acute haemorrhage, perforation, obstruction, abscess formation, fistula formation, failure of medical treatment, uncertainty of diagnosis, development and prevention of carcinoma. Surgery involves segmental resection of bowel, sparing as much bowel as possible. For short strictures stricturoplasty may be carried out. Proctocolectomy with ileostomy may be required. Unlike ulcerative colitis, surgery in Crohn’s disease cannot be guaranteed to be curative.

Prognosis

Acute regional ileitis may be cured by right hemicolectomy. Colonic Crohn’s often responds well to medical treatment but at least 50% of patients will require surgery at some time. The mortality rate is about 14% over 30 years. The disease pursues a course of remissions and exacerbations.

Ulcerative colitis

This is a chronic inflammatory disease that involves the whole or part of the colon. The inflammation is confined to the mucosa and nearly always involves the rectum, extending to involve the distal or total colon. The aetiology is unknown but immunological, dietary and genetic factors may be involved. The majority of cases present between 25 and 30 years. Familial clustering occurs. Malignant change occurs in the colon with time.

Symptoms and signs

Diarrhoea, rectal bleeding, abdominal pain, fever, weight loss. The disease may be acute and fulminant, intermittent or chronic. Pallor, malnutrition, abdominal tenderness, abdominal distension, erythema nodosum, pyoderma gangrenosum, arthritis, uveitis, jaundice (sclerosing cholangitis).

Investigations

• Hb

• FBC

• U&Es: dehydration and electrolyte imbalance in severe cases

• LFTs: hypoproteinaemia or abnormal because of complications of sclerosing cholangitis

• AXR: acute toxic dilatation, perforation

• Barium enema – double contrast (→ Fig. 14.12): loss of haustrations, mucosal distortion, colonic shortening, stricture due to carcinoma. Barium enema should not be performed on ill patients with toxic dilatation in case of perforation

• Sigmoidoscopy: red, inflamed mucosa, contact bleeding, pseudopolyps

• Biopsy

• Colonoscopy: assess extent of disease, exclude carcinoma.

Figure 14.12 Ulcerative colitis. There is shortening of the colon with loss of haustrations (‘lead pipe’ appearance).

Complications

Local complications include toxic dilatation, haemorrhage, stricture, perforation, and carcinoma. Extracolonic complications include seronegative arthritis (sacroileitis, ankylosing spondylitis), sclerosing cholangitis, chronic active hepatitis, uveitis, and amyloid.

Treatment

Medical

Acute severe ulcerative colitis is treated with i.v. fluids, blood transfusion, parenteral nutrition and parenteral steroids. This regimen is instituted usually for 5 days. Regular examination of the patient is undertaken. If the patient deteriorates or toxic dilatation or perforation supervene, urgent surgery is required.

In the less ill patient, oral steroids may be given until the disease is controlled. Those who respond to the above regimens may be treated with sulphasalazine or mesalazine orally to maintain the remission. Distal colitis and proctitis may be controlled by Predsol retention enemas for relapses and sulphasalazine for maintenance.

Surgical

Indications for surgery include acute toxic dilatation, perforation, failure to respond to medical treatment, chronic disease, severe arthritic symptoms, carcinoma. Surgery usually involves panproctocolectomy with ileostomy but other procedures now available include retention of the rectum with mucosal proctectomy or fashioning of an ileal pouch with maintenance of anal sphincters.

Prognosis

The mortality rate with toxic dilatation or perforation is around 5%. The risk of colorectal cancer increases after 10 years’ duration of disease, being about 2% at 10 years and up to 30% at 30 years. The risk is greater in those with total colitis and severe disease. Dysplasia often precedes carcinoma. Colonoscopic surveillance should be carried out at least 2-yearly.

Diverticular disease

Diverticulae are outpouchings of mucosa through the bowel wall associated with increased intraluminal pressure (pulsion diverticulae). They occur between the taenia coli where vessels penetrate the bowel wall. They occur most commonly in the sigmoid colon and descending colon but may occur anywhere in the colon. They are rare before the age of 40 but thereafter there is an increase in incidence with age such that about 40% of patients over 70 have them. Diverticular disease is rare in countries where there is considerable roughage in the diet and is largely a condition occurring in western civilized societies where the diet is refined.

Symptoms and signs

Diverticular disease may be asymptomatic (diverticulosis).

Acute diverticulitis

Gives rise to lower abdominal colicky pain with localizing somatic pain usually in the LIF. Diarrhoea, constipation, and abdominal distension may occur. Fever. Tender in LIF.

Chronic diverticular disease

May cause lower abdominal colicky pain, alternating constipation and diarrhoea and excessive flatus together with abdominal distension. There may be little to find on abdominal examination.

Investigations

• Hb

• FBC (WCC raised in acute but normal in chronic)

• Sigmoidoscopy to exclude carcinoma

• Barium enema (→ Fig. 14.13) or colonoscopy.

Figure 14.13 Diverticular disease. A barium enema showing numerous diverticulae in the sigmoid colon.

Differential diagnosis

Carcinoma of the colon. Crohn’s disease. Ischaemic colitis.

Complications

Acute diverticulitis. Stricture formation. Perforation with either generalized peritonitis, paracolic abscess, or fistula formation (vesicocolic, vaginocolic, ileocolic). Haemorrhage. Large bowel obstruction.

Treatment

Uncomplicated, symptomatic diverticular disease

High-fibre diet. Antispasmodic, e.g. Colofac. Bulking agent, e.g. Fybogel.

Acute diverticulitis

Bed rest. Fluids only or nil orally. Analgesic. Antibiotics: cefuroxime and metronidazole i.v. When symptoms settle, treatment is as for uncomplicated symptomatic diverticular disease.

Perforation with generalized faecal peritonitis

Laparotomy. Peritoneal lavage. Resect perforated area. In case of sigmoid diverticulae treatment is by Hartmann’s procedure (see Procedures box at end of chapter). Drain peritoneal cavity. Antibiotics as for acute diverticulitis. In the elderly, perforated diverticulitis with faecal peritonitis carries a high mortality.

Perforation with paracolic abscess

Percutaneous drainage followed by elective resection.

Perforation with fistula formation

This involves bladder, vagina or small bowel. A vesicocolic fistula presents with dysuria and pneumaturia (passing wind in urine), a vaginocolic fistula presents with the passage of faeces PV and ileocolic fistula with diarrhoea. Vesicocolic fistulae show gas in the bladder on a plain radiograph. Barium enema may show the communication. Primary resection and anastomosis is the treatment of choice for ileocolic and vaginocolic fistulae. Vesicocolic fistulae may be treated by defunctioning loop ileostomy followed by resection, followed by closure of the loop ileostomy. In an adequately prepared bowel, primary resection with end-to-end anastomosis of colon and closure of bladder with interposition of omentum between colonic anastomosis and bladder may be more appropriate treatment.

Haemorrhage

Usually self-limiting. May be profuse and require transfusion. Exact site may be difficult to establish. Angiography may be required. If haemorrhage is life threatening, total colectomy with ileostomy and preservation of rectal stump may be required. Continuity of the bowel is re-established subsequently.

Intestinal obstruction

Progressive diverticular disease causes stricture. Treatment is by resection with either a Hartmann’s procedure followed by subsequent restorative surgery, or a primary anastomosis protected by a temporary defunctioning loop ileostomy.

Volvulus

This is a twisting of a loop of bowel around its mesenteric axis. Partial or complete obstruction may result. Occlusion of the arteries at the base of the involved mesentery leads to gangrene and perforation. The sigmoid colon and caecum may be involved, the sigmoid being the more common.

Sigmoid volvulus

Middle-aged and elderly males are more often affected. The twist is usually anticlockwise. A large redundant sigmoid colon and constipation are predisposing factors.

Symptoms and signs

Sudden onset of lower abdominal colicky pain associated with gross abdominal distension. May be history of recurrent mild attacks associated with partial volvulus relieved by passage of large amounts of faeces and flatus. Distended tympanitic abdomen.

Investigations

• AXR: distended loop of bowel the shape of a ‘coffee bean’ arising out of the pelvis on the left side

• Barium enema may be helpful in doubtful cases – the barium column resembles a ‘bird’s beak’ because of the way the lumen tapers towards the volvulus (→ Fig. 14.14).

Figure 14.14 Barium enema showing a sigmoid volvulus. A ‘bird’s beak’ deformity is seen (arrow). In this case, barium has passed into the volvulus – often it does not.

Treatment

Decompression by sigmoidoscopy. A rectal flatus tube should be left in situ for 48 h. If the patient is fit, elective resection of the sigmoid is carried out at a later date. If decompression is unsuccessful or there are signs of gangrene or perforation, laparotomy with resection is undertaken, the two ends of the colon being brought out as a double-barrelled colostomy (Paul–Mikulicz procedure), which is later closed.

Irradiation proctitis

This may complicate irradiation of pelvic lesions, e.g. cervix, uterus, bladder, prostate. Bleeding, diarrhoea and tenesmus may result. Later ulceration and stricture formation may also occur. Early symptoms appearing soon after irradiation may respond to steroid enemas. Diverting colostomy may be required for severe symptoms.

Large bowel obstruction

The major causes are carcinoma, diverticular disease and volvulus. In 20% of patients the ileocaecal valve is competent and decompression into the small bowel does not occur. Closed-loop obstruction therefore occurs, the caecum progressively distending. Ischaemia and perforation of the caecum may occur.

Symptoms and signs

Colicky abdominal pain, constipation, and vomiting (late). Constant severe pain suggests ischaemic bowel. Distended tympanitic abdomen. Obstructed bowel sounds. Rectum may be empty on examination PR.

Investigations

• Sigmoidoscopy: rectosigmoid lesions may be seen

• AXR: distended large bowel with air/fluid levels surrounding the abdomen like a picture frame (→ Fig. 14.15)

• Limited barium enema may show ‘apple core’ lesion

• Instant enema to exclude pseudo-obstruction.

Figure 14.15 A plain AXR showing large bowel obstruction. (A) Supine film. The left colon is distended down to the pelvis where there is sharp ‘cut-off’ of the gas shadow. (B) Erect film. This shows air/fluid levels in the large bowel. Again the sharp ‘cut-off’ is seen in the pelvis. This represents the point of the obstructing lesion, which in this case was in the lower sigmoid colon.

Treatment

Drip and suck. Correct electrolyte imbalance. A caecum 10 cm or greater in diameter on radiograph is an urgent indication for surgery, especially if tender to palpation. Laparotomy with decompression of the obstruction. Right-sided lesions are treated by right hemicolectomy. Left-sided lesions may be treated by left hemicolectomy with covering loop ileostomy. Low left-sided lesions are treated by resection of the tumour with Hartmann’s procedure. However, on-table lavage of the colon and primary anastomosis may be carried out in experienced hands with or without a defunctioning loop ileostomy. A carcinoma on the apex of the sigmoid loop may be treated by resection and a Paul–Mikulicz double-barrel colostomy. In a poorly patient a defunctioning colostomy or caecostomy may be carried out and elective resection delayed until a later date when the patient is fitter. Sigmoid volvulus may be treated by resection and a Paul–Mikulicz procedure. Colonic stenting may be carried out in those unfit for surgery.

Prognosis

The overall mortality rate approaches 15%. Perforation is the main cause of mortality.

Anal conditions

Haemorrhoids

These are enlarged vascular cushions in the lower rectum and anal canal. They are not simply varicosities. At least 10% of the population will have symptomatic haemorrhoids at some time in their life. The classical position of haemorrhoids corresponds to branches of the superior haemorrhoidal artery occurring at the 3 o’clock, 7 o’clock and 11 o’clock positions with the patient in the lithotomy position.

Symptoms and signs

Asymptomatic. Rectal bleeding (on toilet paper or drips into toilet on defaecation). Prolapse. Itching. Piles are not painful unless they thrombose. First-degree piles remain in the rectum and manifest only by bleeding. Second-degree piles prolapse on defaecation but reduce spontaneously. Third-degree piles prolapse and require manual reduction. Check Hb if bleeding is prolonged or heavy. Examine abdomen to exclude other lesions. Digital rectal examination.

Investigations

• Sigmoidoscopy to exclude other lesions

• Proctoscopy to confirm presence of piles. Remember at least 10% of population will have piles. Abdominal pain is not associated with piles

• If there is any doubt as to the cause of bleeding, carry out colonoscopy.

Treatment

• Injection treatment: inject 2–3 mL of phenol in almond oil into the submucosa above the pile. This is suitable for first-degree and small second-degree piles.

• Other non-operative approaches include rubber band ligation, cryosurgery and photocoagulation.

• Large second-degree piles and third-degree piles require haemorrhoidectomy.

• Thrombosed piles may be treated by bed rest, analgesia and ice packs. The piles may thrombose with cure or remain as skin tags, which require subsequent excision. Some surgeons advocate emergency haemorrhoidectomy. Whatever treatment is used, subsequent regulation of bowel habit with high-fibre diet and bulk laxatives is required.

Complications of haemorrhoidectomy

Acute retention of urine. Haemorrhage (slipped ligature in the early postoperative period or secondary haemorrhage 8–10 days postoperatively). Stricture may occur with anal stenosis if too much skin has been excised.

Differential diagnosis

Perianal haematoma, rectal prolapse, fissure-in-ano, inflammatory bowel disease, anal polyp, carcinoma, proctalgia fugax.

Rectal prolapse

This may be partial or complete. Partial prolapse involves the mucosa alone and prolapse is usually no more than a few centimetres. Complete prolapse involves all layers of the rectal wall and is most common in elderly females.

Symptoms and signs

Protruding mass from the anus, especially during defaecation. May reduce spontaneously. May need manual reduction and eventually becomes difficult to reduce. Blood and mucus PR from ulceration of exposed mucosa. Palpate prolapse between fingers. Mucosal prolapse reveals two layers of mucosa about 2–4 cm long with radial folds. Lax sphincter on examination PR. Complete prolapse is thick, up to 12 cm long and patient may be unable to contract sphincter muscles after prolapse reduced.

Differential diagnosis

Prolapsing haemorrhoids, polyps, intussusception.

Treatment

Mucosal prolapse usually responds to sclerosants injected submucosally as for piles. Excision of prolapsed mucosa may be necessary. Complete prolapse is treated by abdominal rectopexy. The rectum is mobilized and fixed to the sacrum usually by inserting a Teflon prosthesis to hold it in position (Ripstein procedure). Other procedures include excision of mucosa and longitudinal plication of the rectal muscle (Delorme procedure); and circumferential narrowing of the anus by inserting a suture subcutaneously around the anal orifice (Thiersch wire – although nylon rather than wire is used nowadays).

Complications

Abdominal rectopexy usually gives good results but residual incontinence due to chronic stretching of the sphincter may result. Thiersch wire procedure may result in infection and faecal impaction.

Rectal prolapse in children

Usually self-correcting. Parents require reassurance. Keep act of defaecation as short as possible and avoid straining. Repeat simple reduction is all that is required. A mild laxative may be necessary. In a few cases, subcutaneous injection of sclerosant may be required.

Perianal haematoma

Symptoms and signs

Acute perianal pain. Worse on sitting, walking and defaecation. Tense, smooth, tender blue lump at anal verge.

Treatment

Symptoms may subside spontaneously after 2–3 days during which time analgesia is given. If patient presents in acute phase, incision under LA should be carried out.

Fissure-in-ano

This is a tear at the anal margin due to passage of a constipated stool. The fissure is usually in the midline posteriorly but may occasionally be anterior. Multiple fissures may be due to Crohn’s disease.

Symptoms and signs

Acute anal pain, severe on defaecation. Blood on toilet paper. Part the buttocks and the fissure may be apparent. Acute sphincter spasm. Examination PR impossible. Occasionally ‘sentinel’ pile. This is a skin tag at the anal verge external to the fissure.

Differential diagnosis

Crohn’s disease, trauma (beware abuse in children), carcinoma, herpes, TB, syphilis and psoriasis.

Treatment

Conservative

If symptoms are relatively mild, LA gel or suppository may be applied. This is best applied some half hour before defaecation. Attention should be given to correcting constipation with a stool-softening laxative and high-fibre diet. An alternative treatment is to apply 0.2% GTN ointment locally, which relaxes the internal anal sphincter. This should be applied twice daily for 6 weeks. Many fissures heal with this regimen at the expense of headache due to absorption of GTN.

Surgical

Some 90% of acute anal fissures settle with conservative management. In those that do not, a lateral subcutaneous internal sphincterotomy should be carried out to relieve spasm and to allow the fissure to heal. A laxative and high-fibre diet should be taken in the postoperative period. Chronic fissures should be treated by lateral subcutaneous internal sphincterotomy. Recurrent fissures should be treated by excision of the fissure, which is sent for histological examination to exclude underlying causes, e.g. Crohn’s, anal carcinoma.

Anorectal abscesses

(→ Fig. 14.16)

Figure 14.16 The anatomy of anorectal abscesses.

These develop in tissue spaces adjacent to the anorectal area. They may be perianal (in a hair follicle, sebaceous gland or perianal haematoma), ischiorectal (in the ischiorectal fossa), intermuscular (between internal and external sphincters), or pelvirectal (spreading from a pelvic abscess – rare). In many cases, the infection may start in the anal crypt and spread along tissue planes.

Symptoms and signs

Constant, throbbing, perianal pain – worse on sitting. With pelvirectal abscesses, the pain may also be in the lower abdomen. Indurated tender mass perianally. Boggy mass on examination PR, in ischiorectal fossa or anteriorly if pelvirectal abscess. Fever.

Treatment

Prompt surgical drainage to prevent fistula formation. There is no role for antibiotics except in diabetics and the immunocompromised – and then only as an adjunct to surgery. Incision, curettage and packing are required.

Complications

Fistula-in-ano occurs in up to 30% of patients.

Fistula-in-ano

A fistula is an abnormal communication between two epithelial surfaces. In this instance, there is an internal opening in the anal canal and one or more external openings on the perianal skin. Most arise from delay in treatment, or inadequate treatment, of anorectal abscesses. Rarer causes include Crohn’s disease, tuberculosis and carcinoma. It may be difficult to locate the internal opening. Application of Goodsall’s rule (‘if the external opening lies anterior to a line drawn transversely through the centre of the anus, the track passes radially through a straight line towards the internal opening. If the external opening is behind this line the track curves in a horseshoe manner to open into the midline posteriorly’) (→ Fig. 14.17). Fistulae may be classified as subcutaneous, submucous, low anal (below puborectalis), high anal (opening in close relation to the anorectal junction) or pelvirectal (penetrating levator ani) (→ Fig. 14.18).

Figure 14.17 Goodsall’s rule.

Figure 14.18 The anatomy of fistula-in-ano.

Symptoms and signs

History of abscess, which drains spontaneously or was surgically drained. Persistent drainage of pus, mucus, blood or faecal matter associated with perianal irritation and discomfort. Drainage may be intermittent if the fistula heals and opens recurrently. Single opening near anus. Examination PR reveals indurated track, pressure on which may cause discharge. Proctoscopy or sigmoidoscopy to define internal opening.

Investigations

• Fistulogram

• Endoanal ultrasound

• MRI.

Differential diagnosis

Pilonidal sinus, hidradenitis suppurativa, incontinence, Crohn’s disease, trauma.

Treatment

The track is identified by probing and laid open under GA, so that it heals by granulation tissue from the base. With high fistulae or pelvirectal fistulae there is a danger to puborectalis when opening the track. Incontinence may result. Fortunately the latter types are rare but require specialist treatment, often by a two-stage operation.

Pruritus ani

This is itching in the perianal area. It is a symptom of various conditions. Local causes include poor hygiene, sweating, fistula, haemorrhoids, neoplasia, warts, fungal infections, contact dermatitis (deodorants), worms, antibiotics (possibly via the complication of diarrhoea or fungal infection). General causes include diabetes mellitus, obstructive jaundice, Hodgkin’s disease. Dermatological diseases include scabies, pediculosis, psoriasis and atopic eczema. The majority of causes are probably idiopathic or psychogenic. Often an ‘itch/scratch’ vicious circle is created and symptoms persist even after the initial cause has been eradicated.

Sexually transmitted diseases

Condylomata acuminata (anal warts)

Caused by human papilloma virus. Usually sexually transmitted. Over 50% of patients admit to anal intercourse. May be few or a continuous carpet of warts extending into the anal canal. Symptoms include bleeding and pruritus. Small groups may be treated with topical podophyllin. Widespread lesions require surgical excision or diathermy. Recurrence is common.

Gonorrhoea

Gonococcal proctitis presents with pain, bleeding and purulent rectal discharge. Proctoscopy reveals ulcerated friable mucosa and pus in the rectal lumen. Culture confirms diagnosis. Treatment is usually by i.m. procaine penicillin and probenecid.

Herpes

Severe perianal pain, constipation, discharge and ulceration. Examination reveals vesicles and ulcers. Treatment is by topical or oral aciclovir.

Syphilis

Perianal or anal ulcers. May resemble anal fissure. Often painless. Diagnosis is confirmed by dark field examination of discharge and serology. Penicillin is treatment of choice. Contact follow-up is important.

AIDS

Anorectal manifestations include fissure, perianal sepsis, ulceration, fungal or viral infections, rectal lymphoma and Kaposi’s sarcoma.

Anal malignancies

Anal tumours are rare and include epidermoid tumours, malignant melanoma, lymphoma (often in association with AIDS), and Kaposi’s sarcoma (associated with AIDS). Adenocarcinoma occurs in the upper part of the anal canal but may spread across the dentate line and appear at the anal margin. The most common of the tumours is the epidermoid carcinoma (squamous cell carcinoma). Patients should be checked for a history of homosexuality with penetrative anal sex.

Rectal bleeding

Bleeding PR is a common clinical problem. The commonest causes are haemorrhoids, fissure-in-ano and colorectal cancer. Massive rectal bleeding may be due to diverticular disease, angiodysplasia, or a cause in the upper GI tract, e.g. peptic ulcer or an aorto-enteric fistula. If bright red rectal haemorrhage is coming from the upper GI tract, the bleeding is massive with rapid gut transit time and the patient will always be shocked. (For causes of rectal bleeding → Table 14.3.)

TABLE 14.3 Causes of rectal bleeding

Haemorrhoids

Fissure-in-ano

Carcinoma of anus

Colorectal carcinoma

Colorectal polyps

Diverticular disease

Inflammatory bowel disease

• Crohn’s disease

• ulcerative colitis

Ischaemic colitis Angiodysplasia Irradiation colitis or proctitis Rectal prolapse Meckel’s diverticulum Intussusception Mesenteric infarction Aortoenteric fistula Massive upper GI haemorrhage Trauma Bleeding diathesis

Symptoms and signs

Check colour and amount of blood. Bright red bleeding in small amounts usually indicates that the source is in the anal canal or rectum. Large amounts suggest diverticular disease or angiodysplasia. Bleeding from haemorrhoids may occasionally be considerable. Blood on toilet paper suggests haemorrhoids or fissure-in-ano. Dripping into the toilet at defaecation suggests haemorrhoids. Blood streaked on stools suggests rectosigmoid or rectal carcinoma. Blood and mucus on defaecation suggest rectal carcinoma. Blood, mucus and pus associated with abdominal pain, diarrhoea and fever, suggest colitis. Bleeding associated with change in bowel habit and abdominal pain suggests colonic cancer. Bleeding associated with pain on defaecation suggests fissure-in-ano or carcinoma of the anal canal. Check for abdominal pain, anal pain, change in bowel habit, abdominal distension. Symptoms of anaemia, weight loss, jaundice. Abdominal mass, e.g. colonic tumour, hepatomegaly (metastases). Abdominal tenderness, distended abdomen – shifting dullness (ascites) – obstructed bowel sounds. Inspection PR for piles, warts, fissure, tumour. Rectal mass (90% of rectal cancers can be felt on examination PR).

Treatment

Principles of treatment include:

• Resuscitation if massive bleeding

• Diagnosis of the cause

• Definitive treatment of the cause.

The treatment of the various conditions is covered elsewhere in this book.

Liver

Diseases of the liver usually present to the surgeon as jaundice, hepatomegaly, or ascites. This section will deal only with liver disease as far as it concerns the surgeon. (For causes of hepatomegaly → Table 14.4.)

TABLE 14.4 Causes of hepatomegaly

Regular generalized enlargement without jaundice	Cirrhosis
	Congestive cardiac failure
	Reticuloses
	Budd–Chiari syndrome (hepatic vein obstruction)
	Amyloid
Regular generalized enlargement with jaundice	Viral hepatitis
	Biliary tract obstruction
	Cholangitis
Irregular generalized enlargement without jaundice	Secondary tumours
	Macronodular cirrhosis
	Polycystic disease
	Primary tumours
Irregular generalized enlargement with jaundice	Cirrhosis
Irregular generalized enlargement with jaundice	Widespread liver secondaries
Localized swellings	Riedel’s lobe
	Hydatid cyst
	Amoebic abscess
	Primary carcinoma

Infections in the liver

Abscess

This is rare and usually caused by pyogenic bacteria. Causes are due to the following:

• Portal pyelophlebitis secondary to acute abdominal infection, e.g. appendicitis, diverticulitis, peritonitis

• Biliary disease, e.g. cholecystitis, ascending cholangitis

• Trauma

• Direct extension from subphrenic abscess, empyema of gallbladder

• Septicaemia

• Infection of a liver cyst

• Rarely there is no cause, i.e. cryptogenic.

Hydatid disease

Due to infection with an Echinococcus granulosus (tapeworm). The tapeworm develops in the dog intestine and ova are shed in the faeces. These contaminate grass or vegetables and are ingested by sheep, cattle or humans. The ova then pass to the liver via the portal circulation where they develop into hydatid cysts. These may also enter the kidneys and lungs. The disease occurs in sheep- and cattle-rearing countries of the world, e.g. Australia, Africa and Wales.

Liver tumours

Secondary tumours are common arising from the GI tract, lung and breast. More than 25% of patients who die of malignant disease have liver secondaries. Primary tumours are rare. The commonest malignant primary tumours are hepatocellular carcinoma and cholangiocarcinoma. Benign tumours are rare and include adenoma and cavernous haemangioma.

Portal hypertension occurs when portal venous pressure equals or exceeds 15 mmHg (20 cm water). Collateral channels open up between the portal and systemic circulations, the clinically most important of these being at the gastro-oesophageal junction, leading to the development of oesophageal varices which may be responsible for torrential bleeding. Other consequences of portal hypertension include splenomegaly, ascites (in hepatic and posthepatic forms) and the manifestations of hepatic failure (encephalopathy).

Jaundice. Mental changes. Flapping tremor. Coma. Haematemesis and melaena. Ascites. Spider naevi, liver palms, clubbing, gynaecomastia, testicular atrophy, caput medusae. Peripheral oedema. Leukonychia. Dupuytren’s contracture. Xanthoma. Kayser–Fleischer rings. Bruising.

Investigations

Treatment of bleeding oesophageal varices

Acute bleed

Resuscitate. CVP monitoring. Blood transfusion. FFP. Platelets. Urgent endoscopy to confirm diagnosis. Inject the varices with sclerosant at the time of endoscopy. If a good view cannot be obtained because of gross bleeding, the following measures should be undertaken:

• Tamponade with a Sengstaken–Blakemore tube

• Administer vasopressin i.v. to lower portal venous pressure

• Administer i.v. metoclopramide – constricts lower oesophageal sphincter and empties stomach of blood

• Somatostatin may be beneficial by reducing portal venous pressure.

The control of bleeding by tamponade is temporary while the next stage of treatment is planned. Usually this is sclerotherapy, which is effective in 90% of patients. Patients who fail to respond should be considered for oesophageal transection or shunting.

Definitive treatment after bleeding

• Chronic injection sclerotherapy. The varices are injected at monthly intervals until they are obliterated. Endoscopic follow-up is carried out on a regular basis. Complications of this technique include ulceration, stricture, and dysphagia.

• Portosystemic shunting. Splenoportogram and CT are carried out to assess the patency of the portal vein. Shunts may be portocaval, mesocaval, or splenorenal. They may be carried out as an emergency to lower portal pressure but it is rare to do so since the advent of injection sclerotherapy. Shunting is usually carried out in the elective stage when there have been previous bleeding episodes. For a successful shunt operation, hepatic function needs to be reasonably good. Jaundice, hypoalbuminaemia, ascites, and encephalopathy indicate a bad prognosis with shunt operations. Liver transplantation is preferable except when the obstruction is prehepatic with good liver function.

Prophylaxis

Many patients with varices never bleed. If varices are known to be present, oral β-blockade with propranolol significantly decreases the incidence of bleeding and rebleeding.

Prognosis

Up to 40% of patients having their first variceal bleed will die. Long-term survival after portocaval shunt operations is poor. The 5-year survival after portocaval shunting for alcoholic liver disease is about 45%. Some degree of encephalopathy develops in 14–30% of patients.

Extrahepatic biliary system

Cholelithiasis (gallstones)

This is common and present in 10% of the population over 50. It is more common in females, especially in multiparous women. Obesity, drugs, contraceptive pill, clofibrate, haemolytic disorders, ileal disease (resection, Crohn’s disease) are aetiological factors. Factors that may produce lithogenic bile include increased cholesterol content, reduced bile acids, biliary stasis. Classically three types of stone are described:

• Cholesterol stones: (may be solitary), cholesterol ‘solitaire’ – radiolucent

• Pigment: occur with haemolysis – small, black, irregular and friable – radiolucent

• Mixed: often faceted – contain calcium, pigment, and cholesterol – 10% are radio-opaque (→ Fig. 14.20).

Figure 14.20 Gallstones. An incidental finding on barium enema. There are several radio-opaque gallstones in the right hypochondrium.

About 80% of stones are asymptomatic. Symptoms are related to the complications they cause.

Cholecystectomy. This may be by the open or laparoscopic technique. Unfit patients may be placed on a low-fat diet to control symptoms or treated by extracorporeal shock wave lithotripsy if suitable. Dissolution of stones which are small and non-radio-opaque in a functioning gallbladder may be attempted with chenodeoxycholic acid given orally.

Biliary colic

This is a symptom rather than a complication of gallstones. It is produced by impaction of a stone in the neck of the gallbladder or in the cystic duct. The stone may either fall back into the gallbladder or pass through the cystic duct into the CBD, whence the pain abates.

Symptoms and signs

Sudden onset of severe pain across the epigastrium (it is not confined to the RUQ). Severe spasms of colic against the background of continuous severe pain. The patient rolls around in agony and cannot get into a comfortable position. Tachycardia, sweating, and vomiting. Examination may reveal rigidity in the upper abdomen (beware making a diagnosis of peritonitis – in peritonitis the patient does not roll around but remains still). An attack may last 2–4 h. Following an attack, jaundice may occur owing to the passed stone impacting in the CBD.

This is rare and usually presents either as generalized biliary peritonitis or leakage of pus from a perforated empyema. Infected biliary peritonitis has a high mortality especially as this condition is most common in the elderly. Treatment involves laparotomy, peritoneal lavage, cholecystectomy and antibiotics (usually gentamicin and metronidazole).

Carcinoma

Associated with long-standing gallstone disease and is commoner in females. Local invasion of the liver and bile ducts occurs. Jaundice occurs owing to direct extension into the bile duct together with secondaries in the nodes at the porta hepatis. Small tumours may be an incidental finding at cholecystectomy for gallstones. In the latter case, long-term survival may be expected. Many cases present late when local spread and lymph node metastases have occurred. In this case, prognosis is poor – 90% of patients surviving less than 1 year.

Gallstone ileus

This results from a fistula occurring between the fundus of the gallbladder and the adjacent duodenum. A stone passes through the fistula and may impact in the terminal ileum causing obstruction to the small bowel.

Symptoms and signs

Colicky abdominal pain, vomiting and distension. History of flatulent dyspepsia. The diagnosis should be suspected in middle-aged to elderly females with symptoms of small bowel obstruction in the absence of a hernia or previous abdominal surgery to suggest adhesion formation.

Investigations

AXR: dilated loops of small bowel, air in the biliary tree (→ Fig. 14.21A). CT, dilated small bowel, gallstone in lumen, air in biliary tree (Fig. 14.21B).

Figure 14.21 (A) Plain AXR showing gallstone ileus. In this case, a large non-radio-opaque stone was obstructing the upper jejunum. Only one small loop of distended bowel is seen in the abdomen (large arrow). Gas is clearly seen in the biliary tree (small arrow) indicating the presence of a cholecystoduodenal fistula. (B) CT abdomen showing gallstone ileus. A large gallstone (large arrow) is seen in a dilated loop of small bowel. Gas is seen in the intrahepatic biliary tree (small arrow).

Treatment

Laparotomy. Removal of stone from small bowel lumen by ‘milking’ through ileocaecal valve or removal by enterotomy. Cholecystectomy at a later date if symptoms referable to gallbladder continue.

Acalculous cholecystitis

Acute cholecystitis without gallstones may occur in a variety of conditions. It may be due to infection, e.g. typhoid, or may occur following sepsis, burns, TPN, multiple injuries, in the puerperium and after unrelated surgery. Treatment is the same as for calculous acute cholecystitis.

Non-surgical treatment of gallstones

Oral dissolution therapy

Suitable for small radiolucent stones in a functioning gallbladder. A combination of chenodeoxycholic acid and ursodeoxycholic acid is given orally. Side-effects include diarrhoea, pruritus and transient rise in serum transaminases. Treatment must be continued for months. Recurrence rates are high.

Extracorporeal shock wave lithotripsy

Suitable for medium-sized, radiolucent stones in a functioning gallbladder. Concurrent treatment with chenodeoxycholic acid and ursodeoxycholic acid is required. Treatment by this method requires further evaluation. Biliary colic may occur as fragments are passed through the cystic duct.

Endoscopy

Stones in the CBD may be treated by endoscopic sphincterotomy and stone extraction. This treatment is suitable for the elderly, unfit patient with a gallstone impacted in the CBD. It allows jaundice to settle even if there are residual stones in the gallbladder; no further treatment is required if they remain asymptomatic. It is useful also for removing retained stones missed at cholecystectomy and exploration of the common bile duct, or recurrent stones forming in the CBD.

Treatment of asymptomatic gallstones

These may be seen on AXR or USS carried out for other conditions, or they may be discovered at laparotomy for another condition. In the younger patient, cholecystectomy is advisable to prevent the complications and to offset the long-term complication of carcinoma. In the elderly and unfit, no treatment is advised.

Previous history of cholecystectomy. Previous history of malignancy. Painless jaundice suggests malignancy. Jaundice preceded by severe upper abdominal pain suggests gallstones. Gradual onset of jaundice associated with dark urine and pale stools. Pruritus. Smooth palpable liver. Palpable gallbladder (carcinoma of pancreas or ampulla of Vater – Courvoisier’s law states that ‘if in the presence of jaundice the gallbladder is palpable, the cause of the jaundice is unlikely to be due to stones’). The reason for this is that with gallstone disease the gallbladder is usually fibrotic and unable to distend and thus become palpable.

Investigations

• LFTs: bilirubin and alkaline phosphatase markedly raised

• PT: may be clotting defect due to poor absorption of vitamin K

• USS: may show dilated ducts and site of obstruction, gallstones in gallbladder; the technique is poor for the lower end of the bile duct and head of pancreas as gas may obscure view

• CT: shows intrahepatic lesions, demonstrates invasion of adjacent structures

• MRCP

• ERCP (→ Fig. 14.22): possible to carry out biopsy, defines level of lesion, allows stenting and relief of jaundice

• PTC (→ Fig. 14.23) if ERCP impossible

• Liver biopsy.

Figure 14.22 ERCP. A gallstone (arrow) is seen in the dilated bile duct.

Figure 14.23 A percutaneous transhepatic cholangiogram. At least two stones (arrows) are seen within a grossly dilated bile duct. There is free flow of contrast into the duodenum.

Attempted curative resection may be carried out via a pancreaticoduodenectomy (Whipple’s operation). Relatively few tumours are curable. Recurrence rates are high. If the tumour is inoperable as judged by invasion of adjacent structures on CT, or because of liver metastases, stenting may be carried out. If the tumour is found to be inoperable at laparotomy a ‘triple bypass’ is carried out (→ section on pancreas).

Nodes at the porta hepatis

Stenting is the treatment of choice. Adjuvant radiotherapy may help depending upon the type of tumour invading the nodes.

Complications of surgery on the jaundiced patient

Coagulation disorders. Renal failure. GI tract haemorrhage (stress ulcers). Delayed wound healing.

Pancreas

Pancreatitis

Inflammation of the pancreas may be divided into acute and chronic. Acute pancreatitis is a condition presenting with acute onset of abdominal pain associated with raised levels of pancreatic enzymes in the blood and urine. The gland normally returns to functional and anatomical normality after the cause is treated. Recurrent attacks may occur (relapsing acute pancreatitis). Chronic pancreatitis is a continuing inflammatory disease characterized by irreversible functional and anatomical abnormalities in the gland, resulting in fibrosis of the gland and pancreatic insufficiency.

Acute pancreatitis

Aetiological factors include biliary tract disease (60%), alcohol (20%). Other causes include hyperlipidaemia, hyperparathyroidism, viral infections (mumps, Coxsackie virus), hypothermia, trauma, postoperative, drugs (steroids, oestrogen-containing contraceptives, azathioprine, thiazide diuretics), familial, scorpion bites, idiopathic, autoimmune (polyarteritis nodosa), post-ERCP, pancreatic carcinoma.

Symptoms and signs

Severe epigastric pain radiating through to back. Nausea, vomiting, shock. Tender in epigastrium initially spreading to whole abdomen. Abdominal distension. Absent bowel sounds. Bluish discoloration in flank (Grey Turner’s sign) or periumbilical area (Cullen’s sign) – due to haemorrhagic pancreatitis with spread of blood retroperitoneally to these areas.

• During first 48 h: PCV: fall >10%, urea >16 mmol/L, Ca²⁺ <2 mmol/L, PaO₂ <8 kPa, base deficit <4. The more criteria present the greater the mortality.

Treatment involves nil orally, NG suction; i.v. fluids (crystalloid, colloid, blood), catheterize and measure urine output hourly, analgesia (pethidine), antibiotics (i.v. cefuroxime and metronidazole or i.v. imipenem), early enteral feeding (in severe cases this may reduce mortality), peritoneal lavage (‘prune juice’ peritoneal fluid indicates severe haemorrhagic pancreatitis), H₂ receptor antagonists as prophylaxis against gastric erosions, inotropic support (dopamine, dobutamine), calcium gluconate for hypocalcaemia, O₂ by mask, ventilation if ARDS, dialysis if ARF. ERCP if common bile duct stones, i.e. jaundice with deranged liver function tests and dilated common bile duct.

Chronic alcoholism is responsible for most cases. A few cases result from hypercalcaemia, hyperlipidaemia or familial predisposition. Direct trauma with subsequent duct stricture is responsible for a few cases. Damage to acini occurs with destruction of the parenchyma, fibrosis and ductal stenoses with dilatation beyond.

Symptoms and signs

Upper abdominal pain often radiating through to the back. Weight loss. Nausea, vomiting, steatorrhoea. 30–40% develop diabetes. A few patients may become addicted to narcotic analgesics because of the severity of the pain. Upper abdominal tenderness. Occasionally jaundice if CBD obstructed.

Largely carried out for pain. Decompression of the duct by endoscopic sphincterotomy and insertion of pancreatic duct stent at ERCP. Longitudinal pancreaticojejunostomy may be carried out. Other operations include resection of the head, body and tail or whole gland. If total pancreatectomy is required, brittle diabetes results – consider isolating the islets cells from the pancreas and carrying out autotransplantation.

Prognosis

Depends upon ability to abstain from alcohol – 25% of patients die within 15 years. Some patients have a miserable life with narcotic addiction, diabetes mellitus and malnutrition.

Pancreatic cysts

True cysts are rare, and may be associated with congenital polycystic disease, retention cysts, hydatid disease and tumour (cystadenoma and cystadenocarcinoma). Pseudocysts are more common and are a consequence of acute pancreatitis, pancreatic trauma or, rarely, posterior perforation of a gastric ulcer.

Tumours of the pancreas

Carcinoma of the pancreas

Adenocarcinoma of the pancreas is increasing in frequency in the age range 40–60 years. It is rarely curable because of local invasion or lymph node metastases before it has been detected. Early diagnosis is difficult. Some 60% occur in the head of the pancreas, 25% in the body and the remainder in the tail. Risk factors include diabetes mellitus, alcoholism, cigarette smoking. It is more common in workers in the chemical industry.

Symptoms and signs

Epigastric pain. Deep, boring back pain. Jaundice (head of pancreas, secondaries in porta hepatis). Weight loss, fatigue, malaise, indigestion, pruritus. Palpable epigastric mass. Palpable gallbladder (Courvoisier’s law – ‘if in the presence of jaundice the gallbladder is palpable, the cause of the jaundice is unlikely to be stones’). Hepatomegaly. Thrombophlebitis migrans. Rarely splenomegaly due to splenic vein thrombosis from direct invasion of latter. Virchow’s node.

Investigations

• USS: often small mass obscured by bowel gas

• CT scan (→ Fig. 14.24) degree of invasion, metastases, guided biopsy

• PET scan: invasion, metastases

• MRCP/ERCP: duct obstruction and may show tumour.

Figure 14.24 CT scan of the upper abdomen. There is a carcinoma in the pancreas (arrow).

Treatment

• Pancreaticoduodenectomy (Whipple’s operation) for carcinoma of the head of the pancreas (→ Fig. 14.25). This involves a partial gastrectomy, partial pancreatectomy, and distal choledochectomy and cholecystectomy. Continuity is re-established via a Roux-en-Y choledochojejunostomy, pancreaticojejunostomy and gastroenterostomy. Operative mortality is high. Relatively few cases are suitable for this operation and the cure rate is very low.

• Total pancreatectomy for extensive tumour.

• Tumours in the tail may be treated by distal pancreatectomy.

• Palliative decompression and relief of jaundice can be treated by ‘triple bypass’, i.e. cholecystojejunostomy (to drain bile past the obstruction from gallbladder to jejunum), jejunojejunostomy (to prevent food passing up into the gallbladder), and gastrojejunostomy (to ensure adequate drainage of food from the stomach should the tumour invade the duodenum) (→ Fig. 14.26).

• As the prognosis is poor and many cases are inoperable at presentation, endoscopic stenting to relieve the jaundice is becoming the treatment of choice.

Figure 14.25 Pancreaticoduodenectomy (Whipple’s operation). The shaded area is excised.

Figure 14.26 Triple bypass for carcinoma of the head of the pancreas.

• Blood sugar is low during an attack

• Symptoms are relieved by the administration of glucose.

Investigations

• Fasting blood sugar

• Plasma insulin

• Glucagon provocation test: infuse glucagon i.v., an elevated insulin level is diagnostic

• CT scan to localize tumour

• Rarely, selective angiography may be required

• Intraoperative ultrasound.

Treatment

Because of malignant potential, treatment should be surgical exploration and excision.

Spleen

Splenomegaly

The spleen must be enlarged to about three times its normal size before it becomes clinically palpable. The lower margin may feel notched to palpation. It may become so large that it is palpable in the RIF. Massive splenomegaly in the UK is likely to be due to CML, myelofibrosis or lymphoma. Splenomegaly may lead to hypersplenism, i.e. pancytopenia as cells become trapped in an overactive spleen and are destroyed. Anaemia, infection, or haemorrhage may result. (For causes of splenomegaly → Table 14.5.)

TABLE 14.5 Causes of splenomegaly

Infective
Bacterial	Typhoid
	Typhus
	Tuberculosis
	Septicaemia
	Abscess
Viral	Glandular fever
Spirochaetal	Syphilis
Spirochaetal	Leptospirosis
Protozoal	Malaria
Parasitic	Hydatid cyst
Inflammatory	Rheumatoid arthritis
	Sarcoid
	Lupus
	Amyloid
Neoplastic	Leukaemia
	Lymphoma
	Polycythaemia vera
	Myelofibrosis
	Primary tumours
	Metastases
Haemolytic disease	Spherocytosis
	Acquired haemolytic anaemia
	Thrombocytopenic purpura
Storage diseases	Gaucher’s disease
Deficiency diseases	Pernicious anaemia
Deficiency diseases	Severe iron deficiency anaemia
Splenic vein hypertension	Cirrhosis
	Splenic vein thrombosis
	Portal vein thrombosis
Non-parasitic cysts