Gastroenterology and nutrition


Gastrointestinal symptoms are a common reason for attendance in primary care and hospital clinics. In developed countries they are often a manifesta-tion of functional bowel diseases. In developing countries infection is a more common diagnosis.


Dyspepsia and indigestion

Dyspepsia is a common complaint and describes a range of symptoms refer-able to the upper gastrointestinal tract, e.g. epigastric pain or burning, nausea, heartburn, fullness and belching. Patients are more likely to use the term ‘indigestion' for these symptoms. Dyspeptic symptoms are caused by disorders of the oesophagus, stomach, pancreas or hepatobiliary system but the most common cause is functional dyspepsia (p. 117). Other causes include peptic ulceration, gastro-oesophageal reflux disease or rarely a gastro-oesophageal cancer. Investigation and management of dyspepsia is discussed on page 84.


Dysphagia is difficulty in swallowing and suggests an abnormality in the passage of liquids or solids from the oral cavity through the oesophagus and into the stomach. The causes are listed in Table 3.1 and investigation dis-cussed on page 73.


Vomiting occurs as a result of stimulation of the vomiting centres in the lateral reticular formation of the medulla. This may result from stimulation of the chemoreceptor trigger zones in the floor of the fourth ventricle or from vagal

Table 3.1 Causes of dysphagia

Disorders of the mouth and tongue

Extrinsic pressure

E.g. tonsillitis

Mediastinal glands

Neuromuscular disorders


Pharyngeal disorders

Enlarged left atrium

Bulbar palsy

Myasthenia gravis

Intrinsic lesion

Benign stricture

Oesophageal motility disorders

Malignant stricture

Primary oesophageal disease


Other oesophageal dysmotility

Eosinophilic oesophagitis*

Oesophageal web or ring

Foreign body

Pharyngeal pouch

Systemic disease
Diabetes mellitus
Chagas’ disease

*Increasingly apparent cause of dysphagia (? due to discoordination of longitudinal
muscle of the oesophagus), characterized by eosinophil infiltration of the oesophagus and diagnosed on mucosal biopsies.

afferents from the gut. Vomiting is associated with many gastrointestinal conditions, but nausea and vomiting without abdominal pain are frequently non-gastrointestinal in origin, e.g. due to central nervous system (CNS) disease (e.g. raised intracranial pressure, migraine), excess alcohol, drugs (especially chemotherapeutic agents), metabolic conditions (e.g. uraemia, diabetic ketoacidosis) and pregnancy. Persistent nausea and vomiting without any other symptoms is often functional in origin (p. 117).


Flatulence describes excessive wind, presenting as belching, abdominal dis-tension and the passage of flatus per rectum. It is rarely indicative of serious underlying disease.

Diarrhoea and constipation

These are common complaints and not usually due to serious disease. Diarrhoea implies the passage of increased amounts of loose stool (stool weight >250 g/24 h) (p. 114). This must be differentiated from the frequent passage of small amounts of stool (that patients often refer to as diarrhoea), which is commonly seen in functional bowel disorders. Investigation and management are discussed on page 114. Constipation is difficult to define because there is considerable individual variation, but it is usually taken to mean infrequent passage of stool (< twice weekly) or the difficult passage of hard stools.


Steatorrhoea is the passage of pale bulky stools that contain fat (>17 mmol or 6 g per day) and indicates fat malabsorption as a result of small bowel, pancreatic disease (resulting in lipase deficiency), or cholestatic liver/biliary disease (resulting in intestinal bile salt deficiency). The stools are offensive, often float because of increased air content and are difficult to flush away.

Abdominal pain

Table 3.2 lists the common causes of abdominal pain based on the usual site of pain. Abdominal pain presenting as an acute abdomen is also discussed on page 118.


Other than blood tests, which will often include coeliac serology, endoscopy and radiological imaging are the common investigations in patients with gastrointestinal complaints. Faecal markers of intestinal inflammation and tissue damage, e.g. faecal calprotectin, are used in some centres. They are able to distinguish organic from non-inflammatory functional disease with high diagnostic accuracy.


Gastrointestinal endoscopy is usually performed as an outpatient procedure. These investigations require written informed consent. Mucosal biopsy is often an integral part of the examination; multiple biopsies (8-10) are taken in suspected cancer to reduce sampling error and a false-negative result.

Oesophagogastroduodenoscopy (OGD, ‘gastroscopy’)

A flexible endoscope is passed through the mouth into the oesophagus, stomach and duodenum following the administration of local anaesthetic spray to the pharynx and/or light sedation with intravenous midazolam. Patients fast for 6 hours prior to the procedure and must not drive for 24 hours after intravenous sedation. OGD is used in the investigation of dyspep-sia, dysphagia, weight loss and iron deficiency anaemia. Duodenal biopsies can be obtained to establish a diagnosis of coeliac disease, and therapeutic options include arresting upper gastrointestinal bleeding, dilatation of

Table 3.2 Causes of abdominal pain by location


Lower abdomen

Peptic ulceration

Functional pain

Functional dyspepsia


Gastric cancer



Gynaecological: salpingitis, ovarian cyst/cancer

Pancreatic cancer

Ectopic pregnancy

  Renal or urinary tract (p. 356)

Upper abdomen

Inflammatory bowel disease


Hepatic congestion

Diffuse or varied site



Biliary pain

Mesenteric ischaemia

Subdiaphragmatic abscess

Bowel obstruction

Functional pain


Splenic abscess or infarct

Ruptured aortic aneurysm

Cardiac (myocarditis, ischaemia)

Metabolic (DKA, porphyria)

Pneumonia Familial Mediterranean fever


Herpes zoster (pain precedes the rash)

DKA, diabetic ketoacidosis.

oesophageal strictures, and stent insertion for palliation of oesophageal malignancy.


This is performed with a rigid instrument to examine the rectum and distal sigmoid, or with a flexible instrument to examine the whole of the left colon. Bowel preparation is achieved with one or two phosphate enemas, and seda-tion is rarely required.


This allows visualization of the entire colon and terminal ileum. Bowel cleans-ing solutions (p. 132) are given in advance of the procedure to clear the bowel of solid contents. Intravenous analgesia (with pethidine) and sedation (with midazolam) is usually required. Colonoscopy is useful for the investigation of patients with altered bowel habit, rectal bleeding, or as a screening tool for colorectal cancer. Therapeutic options include removal of polyps (polypec-tomy) or diathermy of bleeding lesions such as angiodysplasia. Complications of colonoscopy (± polypectomy) are bowel perforation and bleeding, and respiratory depression and hypotension as a result of the sedation.

Small bowel examination


The length of the small intestine (6-7 m) limits passage of standard endo-scopes due to looping and patient discomfort.

■ Enteroscopy allows endoscopic visualization to about 80-100 cm beyond the duodenum. The whole of the small bowel can be visualized with balloon-assisted enteroscopy but this technique is limited to a few spe-cialized centres.

■ Video (wireless) capsule endoscopy is a non-invasive technique to image the small intestine. After an overnight fast the capsule is swallowed and images are recorded by sensors and a recorder worn on an abdominal belt.

These techniques are used in the investigation of suspected small bowel disease, e.g. obscure gastrointestinal bleeding, Crohn's disease and tumours.


Plain X-rays of the chest and abdomen are used in the investigation of the acute abdomen. They may show free gas with a perforated viscus, dilated loops of bowel with intestinal obstruction and colonic dilatation in a patient with severe ulcerative colitis (UC). Calcification in the pancreas (just to the left of L1) indicates chronic pancreatitis, and faecal loading is seen with constipation.


Transabdominalultrasound is useful for visualization of the liver, gall bladder and biliary tree, and kidneys. It is commonly used for investigation of abnormal liver blood tests, hepatomegaly and for characterization of abdominal masses. It is also used for the detection of bowel wall thickening and for determining the extent of involved segments in Crohn's disease, but is not disease specific. It is used to guide needle placement for biopsies of the liver and solid mass lesions, and for drainage of ascites and inflammatory collections.

Endoscopic ultrasound (EUS) combines endoscopy with an ultrasound probe at the scope tip.

It is used to visualize the walls of the upper and lower gastrointestinal tract and nearby organs such as the pancreas and gall bladder. It is used for tumour and nodal staging of oesophageal, gastric or pancreatic cancer or for non-invasive imaging of the bile ducts (with suspected stones) and pancreas.

Endoanal and endorectal ultrasonography involves the passage of an ultrasound transducer into the rectum. It is used to assess the anal sphinc-ters, particularly in patients with faecal incontinence and to stage rectal cancers.

Computed tomography (CT) scan

CT scanning (p. 822) is frequently used in the investigation of gastrointestinal disease, particularly in the staging of intra-abdominal malignancy and in the investigation and assessment of the acute abdomen (demonstrating perfo-rated viscus, inflammation, e.g. appendicitis, the site and cause of intestinal obstruction and renal calculi). CT colonography/CT pneumocolon (virtual colonoscopy) provides a computer-simulated intraluminal view of the air-filled colon. Like conventional colonoscopy it requires full bowel preparation (p. 132) and air distension of the colon. The images obtained can visualize colonic polyps (Fig. 3.1) and cancer, but biopsies cannot be taken or polyps removed. It is mainly used where conventional colonoscopy cannot be per-formed because of patient intolerance or technical difficulties. Unprepared abdominal and pelvic CT scanning is a good test for colon cancer in the frail or elderly patient who may not tolerate the necessary bowel preparation for conventional or CT colonography.

Fig. 3.1 Colon polyps seen at (Ai-iii) colonoscopy and (B) computed tomography (CT) colonography. Aii is after endoscopic resection of the polyps in Ai.

Risks associated with CT scanning are allergy to intravenous contrast and exposure to radiation. The effective radiation dose from abdominal and pelvic CT scan or CT colonography is 10 mSv and equivalent to about 3 years' natural background radiation. Multiple CT scans in an individual may increase cancer risk as a result of radiation exposure.

Magnetic resonance imaging (MRI)

MRI (p. 826) is particularly used to image the pelvis (assessment of perianal Crohn's disease and staging of rectal cancer) and in the assessment of small bowel, pancreatic and hepatobiliary disease (MR cholangiopancreatography).

Positron emission tomography (PET) scanning

PET scanning (p. 828) is used with other imaging modalities such as CT scan in the investigation of suspected malignancy and for detection of metastases in known malignancy.

Contrast studies

Ingestion of barium followed by X-rays allows examination of the oesophagus (barium swallow), stomach and duodenum (barium meal) and small intestine (barium follow-through). These techniques are less sensitive than endoscopy particularly for small mucosal lesions. However, unlike endoscopy, barium swallow will demonstrate motility problems in the investigation of dysphagia. Barium enema examines the colon by insufflation of barium and air per rectum after full bowel preparation (p. 132). Colonoscopy is usually the preferred method to examine the colon.

Oesophageal physiology testing

Insertion of probes into the lower oesophagus via the nose allows continual measurement over 24 hours of acid (pH monitoring) and volume (by imped-ance testing) reflux of gastric contents. Data are captured on a small device worn on a belt, and transferred to a computer at the end of the 24-hour period. These methods record the frequency and duration of reflux episodes and correlation with symptoms. They are performed prior to surgical treat-ment of reflux or in difficult diagnostic cases.

Oesophageal manometry involves the passage of a small tube containing several pressure transducers into the oesophagus via the nose. Oesophageal peristalsis and pressure are assessed on swallowing. Manometry is used in the investigation of suspected oesophageal motility disorders in patients with dysphagia (p. 73).


Problems in the mouth are common and often trivial, although they can cause severe symptoms.

Mouth ulcers Non-infective

■ Recurrent aphthous ulceration is the most common cause of mouth ulcers and affects at least 20% of the population; in most cases the aetiology is unknown. There are recurrent self-limiting episodes of painful oral ulcers (rarely on the palate). Topical corticosteroids are used for symp-tomatic relief but they have no effect on the natural history. In a few cases ulcers are associated with trauma or gastrointestinal and systemic dis-eases, e.g. anaemia, inflammatory bowel disease, coeliac disease, Behget's disease, Reiter's disease, systemic lupus erythematosus, pemphigus, pemphigoid and fixed drug reactions.

■ Squamous cell carcinoma presents as an indolent ulcer, usually on the lateral borders of the tongue or floor of the mouth. Aetiological factors include tobacco (smoking and chewing) and alcohol. Treatment is with surgery, radiotherapy or a combination of both.


Many infections can affect the mouth, though the most common are viral and


■ Herpes simplex virus type 1

■ Coxsackie A virus

■ Herpes zoster virus.

Oral white patches

Oral white patches are associated with smoking, Candida infection, lichen planus, trauma and syphilis. Leucoplakia is the term used to describe oral white patches or plaques for which no local cause can be found (i.e. a diagnosis of exclusion). Leucoplakia is occasionally a premalignant lesion and thus oral white patches must be biopsied to exclude malignancy. Hairy leuco-plakia is an Epstein-Barr-related white patch on the side of the tongue, which is almost pathognomonic of HIV infection; it is not premalignant.

Atrophic glossitis

A smooth, sore tongue with loss of filiform papillae may occur in patients with iron, vitamin B12 or folate deficiency.

Geographical tongue

This affects 1-2% of the population and describes discrete areas of depapil-lation on the dorsum of the tongue. This may be asymptomatic or produce a sore tongue. The aetiology is unknown and there is no specific treatment.

Periodontal disorders

Gum bleeding is most commonly caused by gingivitis, an inflammatory condi-tion of the gums associated with dental plaque. Bleeding may also be associ-ated with generalized conditions such as bleeding disorders and leukaemia. Acute ulcerative gingivitis (Vincent's infection) is characterized by the devel-opment of crater-like ulcers, with bleeding, involving the interdental papillae, followed by lateral spread along the gingival margins. It is thought to be the result of spirochaetal infection occurring in the malnourished and immuno-compromised. Treatment is with oral metronidazole and good oral hygiene.

Salivary gland disorders

Xerostomia (mouth dryness) may be caused by anxiety, drugs such as tricyclic antidepressants, Sjogren's syndrome and dehydration. Infection (parotitis) may be viral, i.e. mumps virus, or bacterial (staphylococci or streptococci). Calculus formation usually occurs in the duct of the sub-mandibular gland, and causes painful swelling of the gland before or during mastication. Among the salivary glands, tumours most commonly develop in the parotid gland and are usually benign, e.g. pleomorphic adenoma. Treat-ment is with surgical resection. Involvement of the VIIth cranial nerve raises the suspicion of malignancy.


Oesophageal symptoms are dysphagia, heartburn, regurgitation and painful swallowing:

■ Dysphagia (difficulty in swallowing) has mechanical and neuromuscular causes (Table 3.1). A short history of progressive dysphagia initially for solids and then liquids is suggestive of a mechanical stricture. Investiga-tion is with urgent OGD (p. 67) particularly to look for a malignant oesophageal stricture. A barium swallow is more appropriate as the first-line investigation when the history (slow onset of dysphagia for both solids and liquids) suggests a motility disorder such as achalasia. Oesophageal manometry may subsequently be necessary.

■ Heartburn is a retrosternal or epigastric burning sensation produced by the reflux of gastric acid into the oesophagus. The pain may radiate up to the throat and be confused with chest pain of cardiac origin (p. 408). It is often aggravated by bending or lying down and relieved by antacids.

■ Regurgitation is the effortless reflux of oesophageal contents into the mouth and pharynx. It occurs in reflux disease and oesophageal strictures.

■ Odynophagia is pain during swallowing particularly with alcohol and hot liquids. It suggests oesophageal inflammation (oesophagitis) due to gastro-oesophageal reflux disease, infections of the oesophagus (herpes simplex virus, Candida) or drugs such as slow release potassium or bisphosphonates.

Gastro-oesophageal reflux disease (GORD)

Reflux of gastric contents into the oesophagus is a normal event. Clinical symptoms only occur when there is prolonged contact of gastric contents with the oesophageal mucosa.


The lower oesophageal sphincter (LOS) tone is reduced, and there are fre-quent transient LOS relaxations. There is increased mucosal sensitivity to gastric acid and reduced oesophageal clearance of acid. Delayed gastric emptying and prolonged post-prandial and nocturnal reflux also contribute. Mechanical or functional aberrations associated with a hiatus hernia may contribute to GORD, but reflux disease can occur in the absence of a hiatus hernia. Other predisposing factors in GORD include obesity, pregnancy, sys-temic sclerosis and certain drugs (e.g. nitrates, tricyclics).

Clinical features

Heartburn (p. 73) is the major symptom. There may also be regurgitation and odynophagia (p. 73). Cough and nocturnal asthma can occur from aspiration of gastric contents into the lungs. Symptoms do not correlate well with the severity of oesophagitis.


The diagnosis is clinical and most patients are treated without investigation. OGD is indicated in patients with new-onset heartburn over 55 years of age or patients with alarm symptoms (weight loss, dysphagia, haematemesis, anaemia) suspicious for upper gastrointestinal malignancy. It is also per-formed to document complications of reflux (see Barrett's oesophagus, p. 75) and in patients who do not respond well to treatment.

OGD may show oesophagitis (mucosal erythema, erosions and ulcera-tion), a hiatus hernia or Barrett's oesophagus (p. 75). The oesophageal mucosa can be normal in patients with reflux.

24-hour intraluminal pH monitoring or impedance (p. 71) is usually reserved for the confirmation of GORD prior to surgery or where there is an inadequate response to standard doses of proton pump inhibitors (PPIs) (p. 129).


Conservative measures with lifestyle changes (weight loss, avoidance of excess alcohol and of aggravating foods, cessation of smoking) and simple antacids are often suf^icient for mild symptoms in the absence of oesoph-agitis. Patients with severe symptoms or with proven pathology (oesophagitis or complications) require PPIs.

■ Alginate-containing antacids (p. 126) are usually first-line treatments; they prevent reflux by forming a ‘foam raft' on gastric contents.

■ H2-receptor antagonists (e.g. ranitidine, p. 127) improve the symptoms of heartburn.

■ Prokinetic agents (p. 136) such as metoclopramide and domperidone, are occasionally helpful.

■ PPIs (e.g. omeprazole, esomeprazole, lansoprazole, pantoprazole, p. 129) inhibit gastric hydrogen/potassium-ATPase and block the luminal secre-tion of gastric acid. They are potent acid blockers and the drugs of choice for all but mild cases. Given the propensity of reflux symptoms to relapse, maintenance acid-suppressive therapy is often necessary. In these cases the aim is to reduce to the minimum dose necessary to control symptoms (‘step-down approach').

■ Surgery may be necessary for the few patients who continue to have symptoms in spite of full medical therapy, or in young people whose symptoms return rapidly on stopping treatment. Via a laparoscopic approach the fundus of the stomach is sutured around the lower oesopha-gus to produce an antireflux valve (Nissen fundoplication, ‘lap wrap'). Specific complications of this procedure are dysphagia and bloating.


Oesophageal stricture formation presents with gradually worsening dys-phagia. It is treated with endoscopic dilatation and long-term PPI therapy. Chronic GORD may also underlie the development of a Schaừki ring (localized mucosal stricture at the gastro-oesophageal junction), which also presents with dysphagia.

Barrett’s oesophagus, an abnormal columnar epithelium (specialized intestinal columnar metaplasia, SIM) replaces the squamous epithelium that normally lines the distal oesophagus. It develops in response to longstanding acid reflux and is irreversible. Diagnosis is based on endoscopic appearances (pale glossy squamous epithelium is replaced by red-coloured columnar epithelium) and biopsies from the columnar epithelium (showing SIM). Bar-rett's oesophagus is premalignant for adenocarcinoma of the oesophagus. Patients with this condition are treated with PPIs and undergo endoscopic surveillance every 2 years with multiple oesophageal biopsies to look for dysplasia or carcinoma. The detection and management of Barrett's oesoph-agus is controversial and a changing area. Endoscopic screening to initially detect Barrett's oesophagus is usually recommended in patients with long-standing (>10 years) heartburn. Definite high-grade dysplasia (confirmed by two pathologists) on follow-up endoscopic surveillance is a significant risk for an incident cancer and the management options include oesophagectomy (for a young fit patient), endoscopic mucosal resection (for a localized area of high-grade dysplasia) or endoscopic ablative therapies (photodynamic therapy, radiofrequency ablation) to ablate the dysplastic tissue. Patients with low-grade dysplasia undergo more intensive (6-12 monthly) endoscopic surveillance.


This is of unknown aetiology. Oesophageal aperistalsis and failure of relaxa-tion of the LOS impair oesophageal emptying.


There is a decrease in ganglionic cells in the nerve plexus of the oesophageal wall and degeneration in the vagus nerve.

Clinical features

It occurs at all ages but is rare in childhood. There is usually a long history of dysphagia for both liquids and solids, which may be associated with regurgitation. Retrosternal chest pain may occur and be misdiagnosed as cardiac pain.


■ Barium swallow is the initial investigation and shows a dilated oesophagus with a gradually tapering lower end (beak deformity). There is absence of peristalsis and sometimes asynchronous, purposeless, contractions of the oesophageal body.

■ Oesophageal manometry confirms the diagnosis. It demonstrates aperistalsis and failure of LOS relaxation on swallowing.

■ OGD (p. 67) may be necessary to exclude oesophageal cancer, which can produce similar symptoms and X-ray appearance (‘pseudoachalasia').

■ Chest X-ray is not necessary for diagnosis. It may show a dilated oesophagus with a fluid level behind the heart. The fundal gas shadow is absent.


There is no cure. Goals of treatment are relief of symptoms and improved oesophageal emptying. Endoscopic balloon dilatation (2% risk of oesophageal perforation) or surgical division of the LOS (Heller's cardiomyotomy) are the most effective treatments. Medical treatment to relax the LOS (oral nitrates or nifedipine, endoscopic injection of botulinum toxin into the LOS) is used in elderly or frail patients for whom the invasive methods of treatment pose unacceptable risks. However, they have limited efficacy. GORD is a complica-tion of all treatments, particularly surgery.


There is a slight increase in the incidence of squamous carcinoma of the oesophagus in both treated and untreated patients.

Systemic sclerosis

There is oesophageal involvement in most patients with systemic sclerosis. The smooth muscle layer is replaced by fibrous tissue and LOS pressure is reduced, thereby permitting gastro-oesophageal reflux. Symptoms are the result of reflux (leading to oesophagitis and strictures) and oesophageal hypomotility. Treatment is as for reflux and stricture formation.

Other oesophageal dysmotility disorders

Three types are characterized on oesophageal manometry: diftuse oesopha-geal spasm (simultaneous contractions in the distal oesophagus), nutcracker oesophagus (high-amplitude peristaltic waves), and hypertensive lower oesophageal sphincter (raised resting pressure). They present with dysphagia and chest pain and abnormalities may be seen on barium swallow (‘cork-screw' appearance in diffuse oesophageal spasm) and manometry. Nitrates and calcium-channel blockers, e.g. oral nifedipine, sometimes help symp-toms. Treatment of GORD may help.

Hiatus hernia

Part of the stomach herniates through the oesophageal hiatus of the diaphragm:

■ Sliding accounts for more than 95% of cases. The gastro-oesophageal junction slides through the hiatus and lies above the diaphragm. A sliding hiatus hernia does not cause any symptoms unless there is associated reflux.

■ Para-oesophageal hernias are uncommon. The gastric fundus rolls up through the hiatus alongside the oesophagus, the gastro-oesophageal junction remaining below the diaphragm. These pose a serious risk of complications including gastric volvulus (rotation and strangulation of the stomach), bleeding and respiratory complications. They should be treated surgically.

Benign oesophageal strictures

The causes vary geographically; benign peptic stricture secondary to long-standing GORD is the commonest cause in developed countries. Other causes are ingestion of corrosives, after radiotherapy or endoscopic treatment of oesophageal varices, and following prolonged nasogastric tube placement. Dysphagia is the main symptom and treatment is with endoscopic dilatation, PPIs and sometimes surgery.

Oesophageal perforation

latrogenic perforation occurs after endoscopic dilatation of oesophageal strictures (usually malignant) or achalasia, or rarely after passage of a nasogastric tube.

Traumatic or spontaneous oesophageal rupture occurs after blunt chest trauma or forceful vomiting (Boerhaave's syndrome). There is severe chest pain, fever, hypotension and surgical emphysema (crepitation).

Chest X-ray may be normal or show air in the mediastinum and neck, and a pleural effusion. Diagnosis is made with CT scan or water soluble contrast swallow.

Management should be in a surgical unit. Treatment is with intravenous antibiotics, nil by mouth and intravenous fluids. Surgical repair may be needed immediately or for patients who fail to settle with conservative management.

Malignant oesophageal tumours Pathology

■ Squamous cell, usually of the middle third of the oesophagus

■ Adenocarcinoma, lower third of oesophagus.

Epidemiology and aetiological factors

Squamous carcinoma The incidence is 5-10 per 100 000 in the UK, but world-wide it varies greatly, being particularly high in China and parts of Africa and Iran. It is most common in the 60-70-year age group. Major risk factors are smoking and excess alcohol consumption. Other risk factors are important in specific regions with a high incidence (high intake of salted fish and pickled vegetables and ingestion of very hot food and beverages). Pre-existing oesophageal disease (achalasia and caustic strictures) and coeliac disease also increase the risk.

Adenocarcinoma arises from Barrett's metaplasia (p. 75). Smoking and obesity are also risk factors.

Clinical features

There is progressive dysphagia (initially for solids and later for liquids) and weight loss. Bolus food impaction or local infiltration may cause chest pain. Physical signs are usually absent.


These are to confirm the diagnosis and stage the tumour (TNM system, p. 829).

■ Diagnosis is by OGD (p. 67) and tumour biopsy. A barium swallow will show the strictured area but biopsy specimens cannot be taken.

■ Staging is initially by CT scan of the chest and abdomen to look for distant metastases. Patients without evidence of metastatic disease and who are potentially curable, then undergo EUS (p. 69) to locally stage the tumour (depth of wall invasion and local lymph node involvement), PET scanning (more sensitive than CT to detect distant metastases) and sometimes laparoscopy to detect occult peritoneal disease.


Surgical resection provides the best chance of cure and is performed when the tumour has not infiltrated outside of the oesophageal wall. It is combined with pre-operative chemotherapy with or without radiotherapy (neo-adjuvant treatment). However, over half of patients present with incurable locally advanced or metastatic disease. Systemic chemotherapy may temporarily improve symptoms in patients with metastatic disease although local treat-ments may be necessary for relief of dysphagia. These include endoscopic insertion of an expanding metal stent across the tumour, or laser and alcohol injections to cause tumour necrosis. For patients with non-metastatic but locally unresectable disease, combined radiotherapy and chemotherapy may limit disease progression and increase survival.


The prognosis overall is poor with 10% 5-year survival.

Benign oesophageal tumours

See page 86 (gastrointestinal stromal tumour, GIST).


The major functions of the stomach are:

■ Emulsification of fat and mechanical breakup of food.

■ A reservoir for food.

■ Secretion of intrinsic factor (required for absorption of vitamin B12, p. 199) and gastric acid from parietal cells in the fundus. Gastric acid begins the process of protein digestion and has a protective role by destroying bacteria. Acid secretion is increased by vagal nerve stimula-tion, histamine and gastrin, and reduced by somatostatin from antral D cells.

■ Secretion of mucus and pepsinogen from chief cells in the fundus. Pepsinogen is converted by gastric acid to pepsin which breaks down protein.

Helicobacter pylori infection

H. pylori is a Gram-negative urease-producing spiral-shaped bacterium found predominantly in the gastric antrum and in areas of gastric metaplasia in the duodenum. It is closely associated with chronic active gastritis, peptic ulcer disease (gastric and duodenal ulcers), gastric cancer and gastric B cell lymphoma (p. 86). However, most patients with the infection are asymptomatic.


Infection is acquired in childhood and persists for life unless treated. The incidence increases with age probably due to acquisition in childhood when hygiene was poorer. Infection is associated with lower socio-economic status and is commoner in developing countries. Transmission is most likely via the oral-oral or faecal-oral routes.

Clinicopathological features

H. pylori infection produces a gastritis (p. 85) mainly in the antrum of the stomach. In some individuals gastritis can involve the body of the stomach, leading to atrophic gastritis and in some cases intestinal metaplasia, which is a premalignant condition.

Diagnosis of infection

This is by non-invasive or invasive (antral biopsy for patients undergoing an endoscopy) tests (Table 3.3).


Eradication of H. pylori is indicated for all patients with peptic ulcer disease, atrophic gastritis, gastric B cell lymphoma (p. 86), after gastric cancer resec-tion and in patients with dyspepsia (‘test and treat' strategy, p. 84). It is also indicated for individuals who have a first-degree relative with gastric cancer. Recurrence is rare after successful eradication. Several treatment regimens are available, although PPI-based triple therapy regimens for 7 days are favoured. Examples are:

■ Omeprazole 20 mg + metronidazole 400 mg + clarithromycin 500 mg - all twice daily

■ Omeprazole 20 mg + amoxicillin 1 g + clarithromycin 500 mg - all twice daily.

Table 3.3 Diagnosis of Helicobacter pylori infection


Main use


Non-invasive tests

13C-Urea breath

Hydrolysis of ingested
13C-Urea by H. pylori to
produce 13C in expired

Diagnosis of
infection Monitoring of
infection after

Highly sensitive
and specific False-negative
results after recent

Stool antigen tesst

Immunoassay using monoclonal antibodies


use of PPIs or


Serum antibody detection

Diagnosis of infection

Epidemiological studies

Inaccuracy limits use

Antibodies remain positive after infection cleared

Invasive tests (endoscopic gastric mucosal biopsy)

Rapid urease (cLo) test

Urease from H. pylori breaks down urea to produce ammonia causing a pH-dependent colour change in the indicator present

Diagnosis of infection in patients already undergoing endoscopy

Highly sensitive and speciíic False-negative results after recent upper

gastrointestinal bleeding and recent use of PPIs or antibiotics


Direct visualization of the organism

Subject to sampling error and observer variability

PP, proton pump inhibitors.

Peptic ulcer disease

A peptic ulcer (PU) is an ulcer of the mucosa in or adjacent to an acid-bearing area. Most occur in the stomach or proximal duodenum.


Duodenal ulcers (DUs) are two to three times more common than gastric ulcers (GUs) and occur in 15% of the population at some time. They are more common in the elderly and there is a significant geographical variation.


H. pylori and non-steroidal anti-inflammatory drugs (NSAIDs)/aspirin are the cause of most PUs. Co-administration of corticosteroids and NSAIDs further

increases the risk of an ulcer. Potential pathogenic mechanisms for H. pylori-induced ulcers are listed in Table 3.4; reduction of gastric mucosal resistance is thought to be the main factor in causation of GUs as, in contrast to DUs, gastric acid secretion is reduced. Aspirin and NSAIDs cause ulcers, at least in part, by reduced production of prostaglandins (through inhibition of cyclooxygenase-1) which provide mucosal protection in the upper gastroin-testinal tract. Less common causes of PUs are hyperparathyroidism, Zollinger-Ellison syndrome (p. 191), vascular insufficiency, sarcoidosis and Crohn's disease.

Clinical features

Burning epigastric pain is the most common presenting symptom, typically relieved by antacids and a variable relationship to food. DU pain often occurs when the patient is hungry and classically occurs at night. Other symptoms, such as nausea, heartburn and flatulence, may occur. Occasionally ulcers may present with the complications of perforation or painless haemorrhage.


Patients less than 55 years with ulcer-type symptoms should undergo non-invasive testing for H. pylori infection (Table 3.3); upper gastrointestinal endoscopy is not usually necessary (see management of dyspepsia, p. 84). In patients who undergo endoscopy and are found to have a GU, multiple biopsies from the centre and edge of the ulcer are taken because it is often impossible to distinguish by naked eye a benign from malignant ulcer. A barium meal is useful if gastric outlet obstruction is suspected.


Ulcers associated with H. pylori Treatment regimens (p. 80) that success-fully eradicate H. pylori result in ulcer healing rates of over 90% and prevent

Table 3.4 Proposed pathogenic mechanisms of H. pylori

Increased gastric acid secretion due to:

Increased gastrin secretion Increased parietal cell mass

Decreased somatostatin production due to antral gastritis Disruption of mucous protective layer Reduced duodenal bicarbonate production Production of virulence factors:

Vacuolating toxin (Vac A)

Cytotoxic associated protein (CagA)


Adherence factors

ulcer recurrence. There is usually no need to continue antisecretory treatment (with a PPI or H2-receptor antagonist) unless the ulcer is complicated by haemorrhage or perforation. This approach to treatment is indicated in all patients with H. pylori-associated peptic disease. Eradication is conữmed by either a urea breath test or faecal antigen testing in patients who remain symptomatic or who have had an ulcer complication.

H. pylori-negative peptic ulcers are usually associated with aspirin or NSAID ingestion. Treatment is with PPIs (p. 129) and stopping aspirin/NSAID if at all possible. After ulcer healing, NSAIDs can only be continued with PPI prophylaxis, or NSAID therapy is switched to a selective cyclo-oxygenase-2 inhibitor (p. 317).

Follow-up endoscopy plus biopsy is performed for all GUs to demonstrate healing and exclude malignancy (initial biopsies may be false negatives).

Surgery is now rarely necessary for PU but is reserved for the treatment of complications.


Pertoration is uncommon. DUs perforate more commonly than GUs, usually into the peritoneal cavity. Treatment is surgical closure of the perforation and drainage of the abdomen. H. pylori should subsequently be eradicated. Con-servative treatment with intravenous fluids and antibiotics may be indicated in elderly or very ill patients.

Gastric outlet obstruction Ulcer disease causing obstruction is now rare and carcinoma is the commonest cause. Outflow obstruction occurs because of surrounding oedema or scarring following healing. Copious projectile vom-iting is the main symptom, and a succussion splash may be detectable clini-cally. Metabolic alkalosis may develop as a result of loss of acid. In patients with PU disease the oedema will usually settle with conservative manage-ment with nasogastric suction, replacement of fluids and electrolytes and PPIs. Surgery is rarely required.

Haemorrhage See page 87.

Management of dyspepsia

Significant gastrointestinal pathology is uncommon in most young people with dyspepsia (p. 65). Furthermore, the close association of H. pylori with peptic ulcer disease and the ability to detect H. pylori by non-invasive methods means that investigation with endoscopy is unnecessary in most patients. An approach to the management of dyspepsia is outlined in Fig. 3.2.

Gastropathy and gastritis

Gastropathy is the term used when there is injury to the gastric mucosa associated with epithelial cell damage and regeneration. There is little or no


• Alarm symptoms or signs: dysphagia, weight loss, vomiting, gastrointestinal bleeding, epigastric mass.

• Think if pain could be originating from biliary tract (page xx) or pancreas (page xx) and patient needs US or CT scan.

Fig. 3.2 Approach to the investigation of patients with dyspepsia. GORD, gastro-oesophageal reflux disease; CLO, rapid urease test, OGD, oesophagogastroduodenoscopy; PPI, proton pump inhibitor; US, ultrasound; CT, computed tomography.

accompanying inflammation. Gastritis is inflammation of the gastric mucosa. This distinction has caused considerable confusion, since gastritis is often used to describe endoscopic or radiological characteristics of the gastric mucosa rather than specific histological findings.


The commonest cause of gastropathy is mucosal damage associated with the use of aspirin or other NSAIDs. These drugs deplete mucosal prostaglan-dins, by inhibiting the cyclo-oxygenase pathway, which leads to mucosal damage (p. 317). Other causes include infections, e.g. cytomegalovirus and herpes simplex virus, and alcohol in high concentrations. Gastric erosions can also be seen after severe stress (stress ulcer), burns (Curling's ulcer), and in renal and liver disease. Symptoms include indigestion, vomiting and haemorrhage, although these correlate poorly with endoscopic and pathologi-cal findings. Erosions (super^icial breaks in the mucosa <3 mm) and sub-epithelial haemorrhage are most commonly seen at endoscopy. Treatment is with a PPI with removal of the offending cause if possible. Prophylaxis is also given to prevent future damage in patients who continue to take aspirin or NSAIDs.


The commonest cause of gastritis is H. pylori infection (p. 80). Other causes are autoimmune gastritis (the cause of pernicious anaemia associated with antibodies to gastric parietal cells and intrinsic factor), viruses and duodeno-gastric reflux. Gastritis is a histological diagnosis and is usually discovered incidentally when a gastric mucosal biopsy is taken for histology at endos-copy. It is classified as acute or chronic. Acute inflammation is associated with neutrophilic infiltration, while chronic inflammation is characterized by mononuclear cells, chiefly lymphocytes, plasma cells and macrophages. Gastritis is usually asymptomatic; whether H. pylori gastritis itself produces functional dyspepsia is controversial (p. 117). At endoscopy the mucosa may appear reddened or normal. No specific treatment is required although eradi-cation treatment for H. pylori is often given.

Gastric cancer


Gastric cancer is the fourth most common cancer world-wide and the second leading cause of cancer-related mortality. Incidence increases with age and is more common in men. The frequency varies throughout the world, being more common in Japan and Chile, and relatively less common in the USA. Although the incidence overall is decreasing world-wide, proximal gastric cancers are increasing in frequency in the West.


This is unknown; H. pylori infection is implicated, causing chronic gastritis which in some individuals leads to atrophic gastritis and premalignant intes-tinal metaplasia. Other risk factors are lifestyle (tobacco smoking, diets low in fruits and vegetables or high in salted, smoked or preserved foods), pernicious anaemia, family history of gastric cancer, and after partial gastrectomy.


Tumours most commonly occur in the antrum and are almost always adeno-carcinomas. They are localized ulcerated lesions with rolled edges (intestinal, type 1), or diffuse with extensive submucosal spread, giving the picture of linitis plastica (diffuse, type 2).

Clinical features

Pain similar to peptic ulcer pain is the most common symptom. With more advanced disease, nausea, anorexia and weight loss are common. Tumours near the pylorus cause outflow obstruction and vomiting and dysphagia occurs with lesions in the cardia. Almost 50% have a palpable epigastric mass, and a lymph node is sometimes felt in the supraclavicular fossa (Virchow's node). Metastases in the peritoneum and liver cause ascites and hepatomegaly. Skin manifestations of malignancy, such as dermatomyo-sitis (p. 305) and acanthosis nigricans (p. 814), are occasionally associated.


Gastroscopy and biopsy is the initial investigation of choice. CT, EUS and laparoscopy are then used to stage the tumour in a similar manner to oesophageal cancer (p. 79).


Surgery is the most effective form of treatment if the tumour is operable. Adjuvant (postoperative) chemoradiotherapy is given for more advanced tumours. Palliative chemotherapy is sometimes used for unresectable lesions, with a modest improvement in survival.


The overall survival is poor (10% 5-year survival). Five-year survival after ‘curative' surgery is 50%. In Japan there is an active endoscopic screening programme, and earlier diagnosis and an aggressive surgical approach have resulted in a 5-year survival of 90%.

Other gastric tumours

GISTs are the most common type of stromal or mesenchymal tumour of the gastrointestinal tract and occur most commonly in the stomach and proximal small intestine. They were previously considered to be benign but on pro-longed follow-up, most have malignant potential. They are usually asympto-matic and discovered incidentally when an upper gastrointestinal endoscopy is performed for dyspepsia. They can ulcerate and bleed. Treatment is surgi-cal resection or with imatinib (p. 254) for advanced disease.

Gastric lymphoma arises from mucosal areas and is called mucosa-associated lymphoid tissue tumour (MALToma). Gastric lymphoma presents similarly to gastric carcinoma. Most are associated with H. pylori infection and some can be treated by eradication of H. pylori only. Other patients are treated with surgery or chemotherapy with or without radiotherapy.

Gastric polyps are uncommon and usually regenerative. Adenomatous polyps are rare.


Acute upper gastrointestinal bleeding

This is a common emergency admission with an overall mortality rate of 5-12%. Haematemesis is the vomiting of blood. Melaena is the passage of black tarry stools (the result of altered blood) and usually indicates bleeding from a site proximal to the jejunum. Acute massive upper gastrointestinal bleeding may present with fresh rectal bleeding, almost always in association with shock.


Peptic ulceration (PU) is the most common cause often associated with aspirin or NSAID ingestion (Fig. 3.3). Relative incidences vary according to patient population. Anticoagulants do not cause bleeding per se but bleeding from any cause is greater if the patient is anticoagulated.


This is summarized in Emergency Box 3.1.

Immediate management Two large-bore (16-gauge) intravenous can-nulas should be placed in a peripheral vein and blood taken for full blood count, liver biochemistry, urea and electrolytes, clotting screen and ‘group and save'; cross-match at least 4 units of blood if there is evidence of a large bleed (blood pressure <100 mmHg, pulse >100 beats per min, cool or cold extremities with slow capillary refill, Hb <10 g/dL). Intravenous fluids (0.9% saline) are started while the patient is assessed further, including a history and physical examination.

Risk assessment is made using a scoring system such as the ‘Rockall' Score (Table 3.5). It helps to identify those at high risk of recurrent or life-threatening haemorrhage and those at low risk who may be suitable for early hospital discharge (pre-endoscopy score 0, post-endoscopy <1).

Resuscitate In many patients no specific treatment is required, bleeding stops spontaneously and the patient remains well compensated. In patients with large bleeds (see above) or clinical signs of shock urgent blood transfu-sion is required (p. 576). Monitoring pulse rate and central venous pressure will guide transfusion requirements.

Pre-endoscopy drug therapy

■ Aspirin, NSAIDs and warfarin are stopped and the INR reversed if neces-sary (p. 246). Cardiology advice should be sought before stopping aspirin and clopidogrel in patients with low-risk bleeds.

■ PPIs (omeprazole 80 mg bolus i.v. followed by infusion of 8 mg/h) are given to high risk patients (Rockall score >4) in whom endoscopy cannot be performed immediately.

<img src="Causes of upper gastrointestinal haemorrhage. The approximate.jpg" width="525" height="702" />

Fig. 3.3 Causes of upper gastrointestinal haemorrhage. The approximate frequency is also given.

■ Antibiotics are given to patients with suspected variceal haemorrhage (p. 164). Consider also terlipressin in these patients.

Determine site of bleeding This may be evident from the history, e.g. bleeding from a PU is suggested by recent aspirin or NSAID ingestion or previous PU. A history of vomiting preceding the haematemesis suggests a Mallory-Weiss tear (linear mucosal tear at the oesophagogastric junction). Suspect variceal bleeding in patients with liver disease or known varices. After resuscitation, upper gastrointestinal endoscopy should be performed as soon as possible and preferably within 24 hours. More urgent endoscopy is

indicated in patients with shock, continued bleeding or suspected varices (e.g. signs of chronic liver disease).

Specitic management Varices are treated with banding or sclerotherapy (p. 165). Ulcers with high-risk stigmata for continued or re-bleeding (active bleeding, visible vessel, overlying clot) should undergo endoscopic haemo-stasis by injection of dilute adrenaline (epinephrine) together with coagulation of the vessel with thermal therapy (heater or bipolar probe), or application of

Table 3.5 Rockall score for upper gastrointestinal haemorrhage

Score 0

Score 1

Score 2

Score 3

Age (years)






Pulse >100

Pulse >100

Systolic BP >100

Systolic BP <100



Cardiac failure, HD,


Renal/liver failure, any other





None or dark spot seen

Blood in upper gastrointestinal tract

Adherent clot Visible or spurting vessel


M-W tear: no lesion seen and no SRH

All other diagnoses

Malignancy of upper gastrointestinal tract

Parameters indicated in bold calculate a pre-endoscopy Rockall score – maximum 7.
Final Rockall score – maximum 11.
M–W tear, Mallory–Weiss tear; SRH, stigmata of recent haemorrhage; IHD, ischaemic
heart disease.
Low risk patients (post-endoscopy score ≤1) 5% risk of re-bleeding, 0% risk of death.
High risk patients (post-endoscopy score 5–11), 11–41% risk of death.
Death and re-bleeding are particularly common in inpatients and patients with varices.

mechanical clips (endoclips) to the vessel. Intravenous PPIs (p. 129) are given for 72 hours following endoscopic therapy in PU bleeding; they reduce re-bleeding rates and transfusion requirements. Surgery is required for per-sistent or recurrent bleeding from ulcers.


In general, young patients with PU bleeding who are otherwise fit and haemo-dynamically stable and who have no stigmata of recent bleeding can be discharged from hospital within 24 hours (post-endoscopy Rockall Score <1). H. pylorieradication treatment is given (p. 80) and eradication conữmed by a urea breath test or faecal antigen testing. Assessment of ongoing need for antiplatelet therapy is made and essential treatment is co-prescribed with a PPI.

Lower gastrointestinal bleeding

Bright red or altered blood per rectum suggests bleeding from the colon or small intestine. Massive bleeding is rare and usually from diverticular disease or ischaemic colitis (Table 3.6). Minor bleeds from haemorrhoids and anal fissure are common.


Resuscitation with intravenous fluids or blood is necessary with large bleeds. The site of bleeding is determined from the history and physical examination including a rectal examination and the following investigations as appropriate:

■ Proctoscopy to look for anorectal disease e.g. haemorrhoids.

■ Sigmoidoscopy or colonoscopy for inflammatory bowel disease, polyps, colon cancer, diverticular disease, ischaemic colitis, vascular lesions.

■ Angiography for vascular abnormality, e.g. angiodysplasia.

In the non-emergency setting, bright red fresh rectal bleeding is likely to originate from a source distal to the splenic flexure and is usually investigated with a flexible sigmoidoscopy rather than full colonoscopy.

Specitic management Lesions are treated as appropriate.

Chronic gastrointestinal bleeding

Chronic gastrointestinal bleeding presents with iron deficiency anaemia. All such patients require investigation of the gastrointestinal tract particularly to

Table 3.6 Causes of lower gastrointestinal bleeding


Haemorrhoids Anal íissure

Neoplasms: benign and malignant

Colitis: ulcerative colitis, Crohn’s, infective, ischaemic

Angiodysplasia (abnormal collections of blood vessels)

Diverticular disease Small intestine Neoplasms

Ulcerative disease: Crohn’s disease, vasculitis, NSAIDs


Meckel’s diverticulum

NB: acute massive upper gastrointestinal bleeding may present with fresh rectal
bleeding usually with haemodynamic instability.
NSAIDs, non-steroidal anti-inflammatory drugs.

exclude a malignancy. The exception is menstruating women less than 50 years of age without gastrointestinal symptoms, in whom anaemia is assumed to be due to menstrual blood loss. Causes of chronic blood loss are those that cause acute bleeding (see Fig. 3.3, p. 88 and Table 3.6). However, oesophageal varices, duodenal ulcers and diverticular disease rarely bleed chronically. Malabsorption (most frequently from coeliac disease), previous gastrectomy and, rarely, poor dietary intake are causes of iron deficiency and will also present with anaemia.


Iron deficiency anaemia is investigated with OGD and colonoscopy ('top and tail') performed at the same endoscopic session; a distal duodenal biopsy is taken to look for coeliac disease. Further investigations, usually in the order listed, are only warranted in anaemia not responding to iron treatment or if there is abdominal pain or visible blood loss:

■ Small bowel barium follow-through or MRI (usually only helpful if there are symptoms to suggest Crohn's disease)

■ Video capsule endoscopy

■ Enteroscopy (push and/or balloon-assisted) is particularly useful for endo-scopic therapy of vascular lesions seen at capsule endoscopy

■ Coeliac axis and mesenteric angiography

■ Technetium-labelled red cell scan.


The cause of the bleeding is treated and oral iron (p. 240) is given to treat the anaemia.


The principal role of the small intestine is the digestion and absorption of nutrients. Vitamin B12 and bile salts have specific receptors in the terminal ileum but other nutrients are absorbed throughout the small intestine.

Presenting symptoms of small bowel disease are diarrhoea, steatorrhoea (p. 67), abdominal pain or discomfort, and anorexia causing weight loss. Small bowel disease may also be found after investigation for specific deficiencies such as vitamin B12. The two most common causes of small bowel disease in developed countries are coeliac disease and Crohn's disease. Disorders of the small intestine causing malabsorption are shown in Table 3.7. Investigation of suspected small bowel disease (e.g. in a symptomatic patient and/or folate/B12 deficiency) is initially with coeliac serology, small bowel barium follow or MRI, and endoscopic small bowel biopsy.

Table 3.7 Disorders of the small intestine causing malabsorption
Coeliac disease
Crohn’s disease
Dermatitis herpetiformis
Tropical sprue
Bacterial overgrowth
Intestinal resection
Whipple’s disease
Radiation enteritis
Parasite infection, e.g. Giardia intestinalis

Coeliac disease (gluten-sensitive enteropathy)

This is an autoimmune condition characterized by an abnormal jejunal mucosa that improves when gluten (contained in wheat, rye and barley) is withdrawn from the diet and relapses when gluten is reintroduced. About 1 in 100 individuals in European-derived populations have coeliac disease, most of whom are undiagnosed.


A strong association exists between coeliac disease and two human leuco-cyte antigen (HLA) class II molecules, HLA DQ2 and DQ8. The peptide a-gliadin is the toxic portion of gluten. Gliadin is resistant to proteases in the small intestinal lumen and passes through a damaged (as a result of an infection or possibly gliadin itself) epithelial barrier of the small intestine where it is deaminated by tissue transglutaminase so increasing its immu-nogenicity. Gliadin then interacts with antigen-presenting cells in the lamina propria via HLA DQ2 and DQ8 and activates gluten-sensitive T cells. The resultant inflammatory cascade and release of mediators contribute to the villous atrophy and crypt hyperplasia that are typical histological features of coeliac disease. There is an increase in intraepithelial lymphocytes but the pathogenic role of these lymphocytes, compared with lamina propria lym-phocytes, is controversial.

Clinical features

Presentation is at any age but there are two peaks in incidence: in infancy (after weaning on to gluten-containing foods) and in adults in the fifth decade. There may be non-specific symptoms of tiredness and malaise, or symptoms of small intestinal disease (see above). Physical signs are usually few and non-specific, and related to anaemia and nutritional deficiency. There is an increased incidence of atopy and autoimmune diseases (Table 3.8).

Table 3.8 Individuals who should be offered serological testing for coeliac disease

Autoimmune disease Type 1 diabetes mellitus Thyroid disease Autoimmune liver disease Addison’s disease Irritable bowel syndrome (symptoms may be similar to coeliac disease) Unexplained osteoporosis

Those with a first degree relative (10-fold increase compared to general population)

Down’s syndrome (20-fold increase)

Turner’s syndrome

Infertility and recurrent miscarriage


Serum antibodies IgA tissue transglutaminase (tTG) antibodies have a very high sensitivity and specificity for coeliac disease. False negatives occur in IgA deficiency (2% of coeliacs) when IgG based tests should be used. IgA endomysial (EMA) antibodies are less sensitive. Serological testing is offered to patients with signs or symptoms or in conditions where there is an increased risk of disease (Table 3.8). Patients with positive serology or if serology is negative but coeliac disease is strongly suspected are referred for intestinal biopsy.

Distal duodenal biopsies (obtained endoscopically) are required for a definitive diagnosis. Histological changes are of variable severity and show an increase in the number of intraepithelial lymphocytes, crypt hyper-plasia with chronic inflammatory cells in the lamina propria and villous atrophy. The latter is seen in other conditions (e.g. tropical sprue, Whipple's disease) but coeliac disease is the commonest cause of subtotal villous atrophy.

Blood count A mild anaemia is present in 50% of cases. There is almost always folate deficiency, commonly iron deficiency and, rarely, vitamin B12 deficiency.

Small bowel radiology or capsule endoscopy is usually only performed when a complication is suspected such as lymphoma.

Bone densitometry (dual energy X-ray absorptiometry [DXA] scan, p. 311) is performed at diagnosis because of the increased risk of osteoporosis.


Treatment is with a lifelong gluten-free diet and correction of any vitamin deficiencies. Pneumococcal vaccine is given as coeliac disease is associated with hyposplenism (p. 222). Symptoms and serologic testing (undetectable antibodies indicate a response) are used to monitor recovery and compliance with the diet; re-biopsy is reserved for patients who do not respond or in whom there is diagnostic uncertainty.


There is an increased incidence of malignancy, particularly intestinal T cell lymphoma, small bowel and oesophageal cancer. The incidence may be reduced by a gluten-free diet.

Dermatitis herpetiformis

Dermatitis herpetiformis is an itchy, symmetrical eruption of vesicles and crusts over the extensor surfaces of the body, with deposition of granular immunoglobulin (Ig) A at the dermoepidermal junction of the skin including areas not involved with the rash. Patients also have a gluten-sensitive enteropathy, which is usually asymptomatic. The skin condition responds to dapsone, but both the gut and the skin will improve on a gluten-free diet.

Tropical sprue

This is a Progressive small intestinal disorder presenting with diarrhoea, steatorrhoea and megaloblastic anaemia. It occurs in residents or visitors to endemic areas in the tropics (Asia, some Caribbean islands, Puerto Rico, parts of South America). The aetiology is unknown but likely to be infective. Diagnosis is based on demonstrating evidence of malabsorption (particularly of fat and vitamin B12) together with a small bowel mucosal biopsy showing features similar, but not identical, to those in untreated coeliac disease. Infective causes of diarrhoea, particularly Giardia intestinalis, should be excluded. Treatment is with folic acid and tetracycline for 3-6 months and correction of nutritional deficiencies.

Bacterial overgrowth

The upper small intestine is almost sterile. Bacterial overgrowth occurs when there is stasis of intestinal contents as a result of abnormal motility, e.g. systemic sclerosis, or a structural abnormality, e.g. previous small bowel surgery or a diverticulum.

Clinical features

The bacteria deconjugate bile salts causing diarrhoea and/or steatorrhoea, and metabolize vitamin B12, which may result in deficiency.


A therapeutic trial of antibiotics is given when clinical suspicion is high. Otherwise, diagnosis is usually by a hydrogen breath test in which hydrogen is measured in exhaled air after oral lactulose. With bacterial overgrowth an early peak is seen in the breath hydrogen followed by the later colonic peak (normally present due to metabolism of lactulose by colonic bacteria).


The underlying cause should be corrected if possible. Otherwise, rotating courses of antibiotics e.g. tetracycline and metronidazole, are given.

Intestinal resection

The effects of small intestinal resection depend on the extent and the area involved. Resection of the terminal ileum leads to malabsorption of:

■ Vitamin B12, leading to megaloblastic anaemia

■ Bile salts, which overflow into the colon. This causes secretion of water and electrolytes and diarrhoea, and increased oxalate absorption, which may result in renal oxalate stones (p. 377).

More extensive resection leaving less than 1 m of small bowel is followed by the short bowel syndrome. The majority of cases occur after resection due to Crohn's disease, mesenteric ischaemia, trauma, volvulus, or surgical com-plications. Parenteral nutrition is the mainstay of treatment for patients in whom absorptive function has failed. Intestinal transplantation is used in a few centres.

The ability of patients to cope without supplemental intravenous fluids or nutrition depends on the:

■ Amount of resected bowel - most patients with <100 cm of jejunum and no colon will require supplements.

■ Location of resected bowel (jejunal resection is better tolerated than ileal).

■ Colon intact which absorbs water and electrolytes.

■ Health of the residual intestine, i.e. there are fewer problems after resec-tion following trauma than in patients with Crohn's disease.

Whipple’s disease

This is a rare disease caused by the bacterium Tropheryma whipplei. Steatorrhoea, abdominal pain, fever, lymphadenopathy, arthritis and neurological involvement occur. Small bowel biopsy shows periodic acid-Schiff (PAS)-positive macrophages which on electron microscopy are seen to contain the causative bacteria. Treatment is with co-trimoxazole for 1 year.



This results from reactivation of the primary disease caused by Mycobact-erium tuberculosis (p. 541). In developed countries it is most commonly seen in ethnic minority groups or patients who are immunocompromised due to human immunodeficiency virus (HIV) infection or drugs. The ileocaecal valve is the most common site affected.

Clinical features

There is abdominal pain, diarrhoea, anorexia, weight loss and fever. A mass may be palpable. Presentation can be similar to Crohn's disease.


Imaging Chest X-ray shows evidence of pulmonary tuberculosis in 50% of cases. The small bowel follow-through may show features similar to those of Crohn's disease (p. 102). US or CT shows mesenteric thickening and lymphadenopathy.

Histology and culture of tissue is desirable but not always possible and treatment is started if there is a high degree of suspicion. Specimens can be obtained at laparoscopy; laparotomy is rarely required.


Treatment is similar to that for pulmonary tuberculosis (p. 544) but given for 1 year.

Protein-losing enteropathy

Increased protein loss across an abnormal intestinal mucosa occasionally leads to hypoalbuminaemia and oedema. Causes include Crohn's disease, Ménétrier's disease (thickening and enlargement of gastric folds), coeliac disease and lymphatic disorders, e.g. lymphangiectasia.

Meckel’s diverticulum

A diverticulum projects from the wall of the ileum approximately 60 cm from the ileocaecal valve. About 50% contain gastric mucosa which secretes acid, and peptic ulceration may occur. Presentation is with lower gastrointestinal bleeding (p. 91), perforation, inflammation (presents similarly to appendicitis) or with obstruction (due to an associated band). Treatment is surgical removal.

Intestinal ischaemia

Ischaemia is usually due to reduced arterial inflow as a result of atheroma, embolism (e.g. in atrial fibrillation), vasculitis (p. 307) or profound and pro-longed shock. It presents acutely with severe abdominal pain but often little to find on abdominal examination. Surgery is necessary to resect the gan-grenous bowel and the mortality is high. It may also present chronically with post-prandial abdominal pain and weight loss. Diagnosis is made by angiography.

Tumours of the small intestine

These are rare and present with abdominal pain, diarrhoea, anorexia and anaemia. Carcinoid tumours have additional clinical features, described below.

Malignant tumours

Adenocarcinoma accounts for 50% of malignant small bowel tumours; there is an increased incidence in coeliac disease and Crohn's disease. Non-Hodgkin's lymphoma constitutes 15% of malignant small bowel tumours and may be B cell or T cell in origin. The latter occur with increased frequency in coeliac disease. Treatment is surgical excision with or without chemo-therapy and radiotherapy.

Benign small bowel tumours

■ Peutz-Jeghers syndrome is an autosomal dominant condition with mucocutaneous pigmentation (circumoral, hands and feet) and hamar-tomatous gastrointestinal polyps. Polyps may occur anywhere in the gastrointestinal tract, but are most common in the small bowel. They may bleed or cause intussusception, and may undergo malignant change.

■ Adenomas, leiomyomas and lipomas are rare. They are usually asymp-tomatic and discovered incidentally.

■ Familial adenomatous polyposis (p. 111).

Carcinoid tumours


These originate from enterochromaffin cells (serotonin producing) of the intestine. Carcinoid syndrome is the term applied to the symptoms that arise as a result of serotonin (5-hydroxytryptamine, 5-HT), kinins, histamine and prostaglandins, released into the circulation by the tumour.

Clinical features

Patients with gastrointestinal carcinoid tumours have the carcinoid syndrome only if they have liver metastases. Tumour products are then able to drain directly into the hepatic vein (without being metabolized by the liver) and into the systemic circulation, where they cause flushing, wheezing, diarrhoea, abdominal pain, and right-sided cardiac valvular fibrosis causing stenosis and regurgitation.


A high level of 5-hydroxyindoleacetic acid (5-HIAA), the breakdown product of serotonin, is found in the urine in the carcinoid syndrome. A liver ultrasound confirms the presence of metastases.


Treatment of the carcinoid syndrome is symptomatic and aimed at:

■ Inhibition of tumour Products with the somatostatin analogue, octreotide, or with 5-HT antagonists, e.g. cyproheptadine

■ Reducing tumour mass through surgical resection, hepatic artery embo-lization, radiofrequency ablation or chemotherapy.


Inflammatory bowel diseases (IBD) are a group of chronic systemic diseases involving inflammation of the intestine and include: ulcerative colitis (UC), which only affects the colon; Crohn's disease (CD), which can affect the entire gastrointestinal tract; and indeterminate colitis, which shows features of both CD and UC.


IBD occurs world-wide but is most common in Northern Europe, the UK and North America. Presentation is usually in the teens and twenties. In the UK, there are about 400 IBD patients per 100 000 population.


IBD represents the outcome of three essential interacting co-factors: genetic susceptibility, the environment and host immune response.

Genetic susceptibility

■ Genetic association is stronger for CD than UC.

■ There is familial aggregation of disease.

■ Concordance rates are higher in monozygotic (58% for CD) than dizygotic twins (4%).

■ Disease susceptibility genes, e.g. mutations in the CARD15 (NOD2) gene on chromosome 16, confer susceptibility to stricturing small bowel CD.

■ Increased incidence of HLa-B27 in IBD with ankylosing spondylitis. Environment

■ Smoking is associated with a two-fold increased risk for CD. In contrast, current smoking is associated with a reduced risk for developing UC compared with non-smokers.

■ Stress and depression may precipitate relapses in IBD.

■ Enteric microflora is altered and the intestinal wall is contaminated by adherent and invading bacteria.

Host immune response IBD results from a defective mucosal immune system producing an abnormal response to luminal antigens such as bacteria which enter the intestine via a leaky epithelium. In the genetically predis-posed individual, there is an exaggerated immune response with effector T cells (T helper (Th)1, Th2 and Th17) predominating over regulatory T cells. Pro-inflammatory cytokines (interleukin (IL)-12, interferon (IFN)-Y, IL-5, IL-17) released by these activated T cells stimulate macrophages to produce tumour necrosis factor (TNF)-a, IL-1 and IL-6. There is also activation of other cells (neutrophils, mast cells and eosinophils) that together lead to increased production of a wide variety of inflammatory mediators, all of which can lead to cell damage.


CD and UC have some overlapping clinical and pathological features but also key differences at macroscopic and microscopic levels (Table 3.9).

Clinical features

Crohn’s disease Symptoms depend on the region(s) of involved bowel; the commonest site is ileocaecal, in 40% of patients. Small bowel disease causes abdominal pain, usually with weight loss. Less commonly, terminal ileal disease presents as an acute abdomen with right iliac fossa pain mimicking appendicitis. Colonic disease presents with diarrhoea, bleeding and pain related to defecation. In perianal disease there are anal tags, fissures, fistulae (p. 824) and abscess formation.

Ulcerative colitis presents with diarrhoea, often containing blood and mucus. The clinical course may be one of persistent diarrhoea, relapses and remissions, or severe fulminant colitis (Table 3.10). Patients with IBD may also have one or more extraintestinal manifestations (Table 3.11).


The purpose of investigations is to establish the diagnosis of IBD with dif-ferentiation between CD and UC, to define the extent and severity of bowel

Table 3.9 Differences between Crohn’s disease and ulcerative colitis
Macroscopic Crohn’s disease Ulcerative colitis
Affects any part of
gastrointestinal tract
Affects only the colon
Oral and perianal disease Begins in rectum and extends
proximally in varying degrees
Discontinuous involvement
(‘skip lesions’)
Continuous involvement
Deep ulcers and fissures in
mucosa: ‘cobblestone
Red mucosa, bleeds easily
Ulcers and pseudopolyps
(regenerating mucosa) in
severe disease
Microscopic Transmural inflammation Mucosal inflammation
Granulomas present in 50% No granulomata
Goblet cell depletion
Crypt abscesses
Table 3.10 Ulcerative colitis severity index
Bloody diarrhoea <4 per day >6 per day
Fever Absent >37.5 °C
Tachycardia Absent >90/min
Erythrocyte sedimentation rate <20 mm/h >30 mm/h
Anaemia Absent Hb <10 g/dL
Serum albumin normal <30 g/L
Severe colitis requires bloody diarrhoea plus any one of the systemic features.
Moderate colitis lies between these two definitions.

involvement, identify any extraintestinal manifestations and exclude other diseases that may present similarly.

Blood tests Anaemia is common and may be normochromic, normocytic anaemia of chronic disease or due to deficiency of iron, B12 or folate. The platelet count, erythrocyte sedimentation rate (ESR) and C-reactive protein are often raised in acute CD, and the serum albumin is low in severe disease. Liver biochemistry may be abnormal related to associated liver disease. Radiology and imaging

Rigid or ílexible sigmoidoscopy will establish the diagnosis of UC and CD (if the rectum and/or sigmoid colon is involved). A rectal biopsy is taken for histological examination to determine the nature of the inflammation.

Table 3.11 Extragastrointestinal manifestations of inflammatory bowel disease


Uveitis, episcleritis, conjunctivitis


Arthralgia*, small joint arthritis, monoarticular arthritis (knees and ankles), ankylosing spondylitis, nílammatory back pain


Erythema nodosum, pyoderma gangrenosum (necrotizing ulceration of the skin, commonly on lower egs)


Fatty liver*, sclerosing cholangitis, chronic hepatitis, cirrhosis, gallstones*

Renal calculi

Oxalate stones in patients with small bowel disease or after resection

Venous thrombosis

All uncommon, occur in less than 10% of patients other than those maiked*.

Colonoscopy allows the exact extent and severity of colonic and terminal ileal inflammation to be determined, and biopsies to be taken.

Smallbowelimaging is performed to determine the extent of small bowel involvement with CD. Specific imaging type depends on local expertise and includes small bowel barium follow-through or MR enteroclysis with oral contrast. Affected bowel shows an asymmetrical alteration in the mucosal pattern, with deep ulceration and areas of narrowing (‘string sign') commonly confined to the ileum. Skip lesions may be seen. Video capsule endoscopy is increasingly used to detect small bowel disease and is more sensitive than a barium follow-through. It is contraindicated in stricturing disease.

Perianal CD is usually assessed by MRI and sometimes by endoanal ultrasound.

Ultrasonography is particularly helpful in delineating abdominal and pelvic abscesses, and will show thickened bowel in involved areas. Abdomi-nal CT scanning is also used in patients with suspected abscesses.

Plain abdominal X-ray should be performed in all patients admitted to hospital with acute severe colitis. It helps to assess extent of colonic involve-ment and identifies toxic dilatation of the colon.

Radiolabelled white cell scanning is a safe, non-invasive investigation. It helps to identify small bowel and colonic disease but lacks specificity.

Differential diagnosis

CD must be differentiated from other causes of chronic diarrhoea, malabsorp-tion and malnutrition. In children it is a cause of short stature. Other causes of terminal ileitis are tuberculosis and Yersinia enterocolitica infection (causing an acute illness). IBD affecting the colon must be differentiated from other causes of colitis: infection (p. 32), ischaemia, radiation and microscopic colitis (p. 106).


Medical The aim of treatment is to induce and maintain a remission. Patients with CD who smoke should be advised to stop with help offered to achieve this (p. 513). Therapy for IBD is a rapidly evolving field and new drugs are likely to appear in the next decade. In general the treatments used have many anti-inflammatory and immunosuppressive properties combined with an antibacterial action in some cases (e.g. metronidazole).

Treatment of CD depends on the site and severity of disease, and also if the disease is stricturing or fistulating:

■ Oral 5-ASA is less efficacious than in UC and is used in mild disease only. It is generally well tolerated. Rare potentially serious side effects are bloody diarrhoea (resembling acute colitis), Stevens-Johnson syndrome, acute pancreatitis and renal impairment.

■ Steroids. Oral prednisolone (40 mg/day, p. 464) is used for moderate/ severe disease. It is reduced gradually according to severity and patient response, generally over 8 weeks. A few patients with severe disease require inpatient admission and intravenous hydrocortisone. Budesonide is a poorly absorbed oral corticosteroid with limited bioavailability and extensive first-pass metabolism that has therapeutic benefit with reduced systemic toxicity in ileocaecal CD.

■ Liquid enteral nutrition with an elemental (liquid preparation of amino acids, glucose and fatty acids) or polymeric diet induces a remission in active CD. The exact mode of action is not known. These diets are unpalatable and may have to be given via a nasogastric tube.

■ The thiopurine drugs, azathioprine (2.5 mg/kg/day) or its metabolite 6-mercaptopurine 1.5 mg/kg/day), are used to maintain a remission and are given to patients who require two or more corticosteroid courses per year. Major side-effects are bone marrow suppression (neutropenia, thrombocytopenia and anaemia), acute pancreatitis and allergic reac-tions. The enzyme, thiopurine methyltransferase (TPMT), is essential in metabolism of thiopurines and activity should be measured on a blood sample before treatment is given. Approximately 1 in 300 patients have absent TPMT activity and will not metabolize the drug. These patients are at high risk for pancytopenia and treatment is contraindicated. About 10% of patients have reduced TMPT activity and a lower drug dose is indicated (half to one third of normal dosing).

■ Metronidazole is useful in severe perianal CD as a result of both its antibacterial and immunosuppressive action.

■ Methotrexate (intramuscular) is used in a minority of patients with active CD that is resistant to conventional treatment with steroids. It is also used to maintain a remission in those refractory or intolerant to azathioprine/6-mercaptopurine.

■ Anti-TNF antibodies (infliximab, adalimumab, certolizumab) are used to induce a remission in patients resistant to corticosteroids/ immunosuppressives. Scheduled treatment at 8-weekly intervals is then given to maintain a remission.

Treatment of UC depends on severity (Table 3.10) and distribution of disease (Table 3.12). The management of acute, severe UC is summarized in Emer-gency Box 3.2.

Surgery In CD and UC, surgery is indicated for:

■ Failure of medical therapy with acute or chronic symptoms producing ill health

■ Complications (Table 3.13)

■ Failure to grow in children despite medical treatment.

Resections are kept to a minimum in CD as recurrence is almost inevitable in the remaining bowel. In some patients with small bowel disease, strictures can be widened (stricturoplasty) without resection.

The surgical options in UC are:

■ Colectomy with ileoanal anastomosis: the terminal ileum is used to form a reservoir (a ‘pouch'), and the patient is continent with a few bowel

Table 3.12 Summary of treatments used in ulcerative colitis

Disease severity




Oral 5-ASA

First line for left sided/extensive

Rectal 5-ASA/steroids

For proctitis or proctosigmoiditis

Oral prednisolone

Second line, if inadequate response to 5-ASA


Oral prednisolone

Severe with systemic features


See Emergency Box 3.2


Maintain remission


Most patients require maintenance treatment

Azathioprine/6- mercaptopurine

For patients who relapse frequently despite ASA or are ASa-intolerant

5-ASA, aminosaỉicyỉic acid; ỉett sided disease, up to spỉenic flexure; proctitis, rectaỉ iníbmmation.

Emergency Box 3.2
Management of acute severe colitis
Admit to hospital
• Joint inpatient management between gastroenterologist and colorectal surgeon
• FBC, CRP, liver biochemistry, serum albumin and electrolytes
• Blood cultures (Gram-negative sepsis occurs)
• Plain abdominal X-ray looking for colonic dilatation (transverse colon diameter >5 cm), and mucosal islands
• Stool cultures (× 3) and Cl. difficile toxin to exclude coincidental infection (do not delay steroids while awaiting result)
• Stop drugs that may precipitate colonic dilatation (anticholinergics, antidiarrhoeals, non-steroidal anti-inflammatory drugs, opioids)
• i.v. hydrocortisone 100 mg 6-hourly
• Correct electrolyte and fluid imbalance
• Low molecular weight heparin to reduce the risk of venous thrombosis
• Consider i.v. ciclosporin (2 mg/kg over 24 hours) or infliximab if no response after 4 days of i.v. hydrocortisone. Colectomy may be necessary.
• Stool chart: frequency, type and presence of blood
• Vital signs at least four times daily
• Daily bloods and abdominal X-ray if admitting film abnormal
Table 3.13 Complications of inflammatory bowel disease
Toxic dilatation of the colon + perforation
Stricture formation*
Abscess formation (Crohn’s disease)
Fistulae and fissures (Crohn’s)*
Colon cancer
*Surgical intervention only necessary if symptomatic and not responding to medical

motions per day. The pouch may become inflamed (‘pouchitis'), leading to bloody diarrhoea which is treated initially with metronidazole. Pro-biotics (live microorganisms that modify composition of enteric bacteria) are sometimes used to prevent and treat pouchitis.

■ Panproctocolectomy with ileostomy: the whole colon and rectum are removed and the ileum brought out on to the abdominal wall as a stoma.

Cancer in intlammatory bowel disease

Extensive UC and Crohn's colitis of more than 10 years' duration is associated with an increased risk of colorectal cancer (CRC, cumulative risk 12% after 25 years). Patients with colitis should undergo colonoscopy at 10 years from diagnosis and an assessment of cancer risk is made. High risk patients (extensive colitis with moderate/severe activity, primary sclerosing cholangi-tis or family history of CRC in first degree relative <50 years) are offered a further colonoscopy and multiple colonic biopsies (to look for dysplasia) one year later. Lower risk patients undergo colonoscopy 3-5 years later. Colec-tomy is recommended if high grade dysplasia is discovered and increased surveillance (6-12 monthly) with low-grade dysplasia.


Both diseases are characterized by relapses and remissions. Almost all patients with CD have a significant relapse over a 20-year period. The prog-nosis of UC is variable. Only 10% of patients with proctitis develop more extensive disease, but with severe fulminant disease there is a risk of colonic perforation and death.

Microscopic colitis

The colonic mucosa looks normal at endoscopy but histological examination of mucosal biopsies shows lamina propria inflammation and increased intraepithelial lymphocytes in lymphocytic colitis and thickening of the sub-epithelial collagen layer in collagenous colitis. Presentation is most commonly with chronic, watery diarrhoea in a middle-aged or elderly person. Micro-scopic colitis can be drug induced, e.g. NSAIDs, and occurs with increased frequency in coeliac disease. Treatment is symptomatic initially with anti-diarrhoeal drugs such as loperamide. Budesonide is the first-line therapy for both induction and maintenance of response in patients not controlled with symptomatic treatment. Aminosalicylates, bismuth subsalicylate, coles-tyramine and systemic steroids are used in resistant cases. Microscopic colitis does not progress to overt inflammatory bowel disease.


The main role of the colon is absorption of water and electrolytes and propul-sion of contents from the caecum to the anorectal region. About 9000 mL of water containing electrolytes enters the gastrointestinal tract each day; the majority from gastrointestinal secretions (stomach, pancreas, bile, intestinal secretion) and only a small amount from the diet. Most is absorbed in the small intestine and only about 1500 mL passes through the ileocaecal valve into the colon, of which about 1350 mL is normally absorbed.


This is a common problem in the general population, particularly in the elderly (associated with immobility and poor diet), and in young women (associated with slow colonic transit or post-partum pelvic floor abnormalities). Constipa-tion is a consistent difficulty in defecation. Specific definitions are infrequent passage of stools (<3/week), straining, passage of hard stools, incomplete evacuation and sensation of anorectal blockage. There is a long list of pos-sible causes (Table 3.14) but in many patients it is their perception that there is an abnormality and requires no more than dietary advice and reassurance. In many patients it is part of the irritable bowel syndrome (p. 117).


Initial evaluation is with a history and physical examination, including a rectal examination during which the patient is asked to strain. A patient with a defecatory disorder has paradoxical contraction rather than the normal relaxation of the puborectalis and external anal sphincter during straining, which may prevent defecation.

Routine blood tests, radiography and endoscopy are not usually indicated in the evaluation of patients with constipation without alarm symptoms; the latter includes rectal bleeding, anaemia or recent onset of constipation in the

Table 3.14 Causes of constipation General

Pregnancy, inadequate fibre intake, immobility Metabolic/endocrine

Diabetes mellitus, hypothyroidism, hypercalcaemia, porphyria Functional

Irritable bowel syndrome, idiopathic slow transit Drugs

Opiates, antimuscarinics, calcium channel blockers e.g. verapamil,

Antidepressants, e.g. tricyclics, iron


Spinal cord lesions, Parkinson’s disease Psychological

Depression, anorexia nervosa, depressed urge to defecate Gastrointestinal disease

Intestinal obstruction (e.g. by colon cancer) and pseudo-obstruction

Painful anal conditions, Hirschsprung’s disease

Defecatory disorders

Rectal prolapse, pelvic floor dyssynergia

Megarectum, large rectocele middle aged or elderly (>50 years) particularly if associated with a sense of incomplete evacuation.

A few patients with no obvious underlying cause (idiopathic constipation) may require studies of colonic transit (measured using radiopaque markers taken orally) and anorectal physiology to determine if they have normal colonic transit, slow transit, or a defecatory disorder.


Any underlying cause should be corrected. Patients with normal and slow transit constipation are treated with a high-fibre diet together with plenty of liquids. Long-term laxatives are only used in severe and unresponsive cases (p. 130). A wide variety of laxatives are available but many patients are not satisfied with their treatments. New therapeutic approaches are opioid antag-onists for the treatment of opiate-induced constipation, neurotrophins, chlo-ride channel activators which stimulate intestinal fluid secretion and selective serotonin receptor (5-HT4-receptor) agonists which regulate gut motility and intestinal secretion. Patients with defecatory disorders may require referral to a specialist centre.

Faecal incontinence

This is recurrent uncontrolled passage of flatus and/or stool. Continence depends on a number of factors including mental function, stool volume and consistency, structural and functional integrity of the anal sphincters, pubo-rectalis muscle, pudendal nerve function, rectal distensibility and anorectal sensation. Faecal impaction is a common cause of faecal incontinence in the elderly (overflow diarrhoea). Anal sphincter tears or trauma to the pudendal nerve can occur after childbirth or anal surgery (e.g. for haemorrhoids). Impaired rectal sensation occurs with diabetes mellitus, multiple sclerosis, dementia and spinal cord injuries. A detailed history and examination with digital rectal examination will help diagnose and exclude most common causes. Specific investigations include sigmoidoscopy to exclude mucosal disease, imaging of the anal sphincters (by anal endosonography, or MRI), anorectal manometry (to assess anal sphincter pressures), and sensory testing by rectal balloon distension to assess rectal sensation and compli-ance. Treatment depends on the cause.

Diverticular disease

Pouches of mucosa extrude through the colonic muscular wall via weakened areas near blood vessels to form diverticula. The term diverticulosis means the presence of diverticula. DiverticulHis implies inflammation, which occurs when faeces obstruct the neck of the diverticulum. Diverticula are common, affecting 50% of the population over 50 years of age.


The precise cause of diverticular disease is unknown, although it appears to be related to the low-fibre diet eaten in Western populations; insufficient dietary fibre leads to increased intracolonic pressure, which causes hernia-tion of the mucosa at sites of weakness.

Clinical features

It is asymptomatic in 95% and usually discovered incidentally when a barium enema or colonoscopy is performed for other reasons. Symptoms are the result of luminal narrowing (causing pain and constipation), bleeding which may be massive, or diverticulitis. The latter present with left iliac fossa pain, fever and nausea and may result in perforation (leading to abscess formation or peritonitis), fistula formation into the bladder or vagina, or intestinal obstruction. Acute diverticulitis is diagnosed by CT scan or in some cases by ultrasound.


Acute attacks are treated with antibiotics (cephalosporin and metronidazole). Surgery is indicated rarely for complications and for frequent attacks of diverticulitis.

Miscellaneous conditions


This term describes a number of conditions in which the colon is dilated. The most common cause is chronic constipation. Other causes are Chagas' disease (p. 821) and Hirschsprung's disease (congenital aganglionic segment in the rectum). Treatment is with laxatives, although Hirschsprung's disease responds to surgical resection.

Ischaemic colitis

Blood supply to the colon is from the superior and inferior mesenteric arteries. Watershed areas in the splenic flexure and caecum are most susceptible to ischaemia. Ischaemic colitis is most common in the elderly and related to underlying atherosclerosis and vessel occlusion. It also occurs in a younger population associated with use of contraceptives, thrombophilia (p. 229) and vasculitis (p. 306). Presentation is with abdominal pain and rectal bleeding, and occasionally shock. Sigmoidoscopy is often normal apart from blood. Treatment is symptomatic, although surgery may be required for gangrene, perforation or stricture formation.

Colon polyps and the polyposis syndromes

A polyp is an abnormal growth of tissue projecting into the intestinal lumen from the normally flat mucosal surface. Polyps may be single or multiple and are usually asymptomatic. Most polyps in the colon are adenomas, which are the precursor lesions of most colorectal cancer (CRC). Other types are hyper-plastic, inflammatory (in patients with IBD) and hamartomatous, of which only the latter carry a malignant potential.

Adenomatous polyps These are tumours of benign neoplastic epithelium and are more common with increasing age. The aetiology is unknown, although genetic and environmental factors are implicated. They rarely produce symptoms, although large polyps can bleed and cause anaemia, and large villous adenomas can occasionally present with diarrhoea and hypo-kalaemia. Although most adenomas do not become malignant during the patient's lifetime they are removed at endoscopy to reduce the risk of devel-oping CRC. The risk of malignant change in a polyp increases with:

■ Size >1 cm

■ Sessile polyps (base attached to colon wall) > pedunculated polyps (mucosal stalk is interposed between polyp and colon wall)

■ Severe dysplasia > mild dysplasia

■ Villous histology > tubular

■ Polyp number: multiple > single.

About 5% of CRCs occur on a background of a genetic syndrome associated with colonic polyps and an increased risk of colon cancer (Table 3.15). A family history suggestive of one of these syndromes may lower the threshold for investigation in a patient presenting with gastrointestinal symptoms. In addition, referral for genetic testing may be appropriate in a patient with colon polyps or cancer when one of these syndromes is suspected (e.g. young age at diagnosis <50 years, affected family members, other associated cancers).

Colorectal cancer

Most colorectal cancers occur sporadically. Family colon cancer syndromes (Table 3.15) or cancers occurring on a background of longstanding colitis (p. 106) account for a small percentage.


CRC is the third most common cancer world-wide and the second most common cause of cancer deaths in the UK. Increasing age is the greatest risk factor and the average age at diagnosis is 60-65 years. Family history, next to age, is the most significant risk factor. In the West, the lifetime risk of CRC is 1 in 50, increasing to 1 in 17 in those with one affected first-degree relative and greatly increased in the family cancer syndromes (Table 3.15).

Table 3.15 The family colon cancer syndromes


Mutated gene (s)


Cancer risk

HNPCC (Lynch's syndrome)


mismatch repair genes

Accelerated progression from adenoma to CRC. ncreased risk several extracolonic malignancies; endometrial is commonest.

Over half develop CRC, onset in fourth decade

Familial adenomatous polyposis (FAP)

APC gene

Numerous colorectal polyps (>100) develop in teenage years

increased risk of extracolonic malignancies. FAP variants are Turcot's (with brain tumours), Gardner's (with desmoid tumours, skull osteomas) and attenuated FAP (fewer polyps at a later age)

100% lifetime risk of CRC, onset in young adults



Base-excision repair gene

Multiple polyps (>15) at a young age (<50 years)

ncreased risk of CRC, onset in fourth decade



Numerous pigmented spots on lips and buccal mucosa. Multiple hamartomas, polyps. Small intestinal polyps may bleed, obstruct or cause

ncreased risk of non-gastrointestinal and gastrointestinal cancer (through adenomatous change in polyps)

All are autosomal dominant inheritance, other than MYH-associated polyposis.
HNPCC, hereditary non-polyposis colorectal cancer; CRC, colorectal cancer.

Colon cancer is rare in Africa and Asia, largely because of environmental differences. A diet high in meat and animal fat and low in fibre is thought to be one aetiological factor.


In sporadic CRC, a stepwise accumulation of abnormalities in a number of critical growth regulating genes drives the progression from normal mucosa to adenoma to invasive cancer. These include the activation of tumour-promoting genes or oncogenes, e.g. K-ras and the inactivation of tumour suppressor genes.


Spread is by direct invasion through the bowel wall, with later invasion of blood vessels and lymphatics and spread to the liver and lung. Mortality of CRC is related to the TNM stage at presentation (Table 3.16). Synchronous (i.e. more than one) tumours are present in 2% of cases.

Clinical features

Most tumours are in the left side of the colon. They cause rectal bleeding and stenosis, with symptoms of increasing intestinal obstruction such as an alteration in bowel habit and colicky abdominal pain. Carcinoma of the caecum and ascending colon often present with iron deficiency anaemia or a right iliac fossa mass. Clinical examination is usually unhelpful, although a

Table 3.16 TNM staging of colon cancer

TNM stage


5-year survival (%)

Stage 0

Tumour coníined to the mucosa


Stage 1

Tumour invades submucosa (T1) or muscularis propria (T2). No involved nodes (N0) or distant metastases (M0)


Stage II

Tumour invades into subserosa (T3) or directly into other organs (T4). No involved nodes (N0) or distant metastases (M0)


Stage IlIa

T1/T2 and 1-3 regional lymph nodes involved (N1).


Stage lllb

T3, N1 or T4, N1


Stage lllc

Any T ≥4 regional lymph nodes (N2)


Stage 4

Any T, any N + distant metastases


mass may be palpable transabdominally or in the rectum. Hepatomegaly may be present with liver metastases.


The purpose of investigation is to confirm the diagnosis and stage the tumour.

Colonic examination with colonoscopy, CT colonography or barium enema are all used to examine the colon in suspected CRC but colonoscopy and biopsy of lesions remains the gold standard.

Blood tests A full blood count may show anaemia, and abnormal serum liver biochemistry suggests the presence of liver secondaries. Serum levels of the tumour marker carcinoembryonic antigen (CEA) are often raised in CRC but are used in follow-up (rising levels suggest recurrence) rather than diagnosis.

Radiology CT scan of the chest, abdomen and pelvis is the initial staging investigation to look for local spread and metastatic disease. PET scanning is often used for evaluation of suspicious lesions found on CT. MRI and endoanal ultrasound are used to locally stage rectal cancer.

Faecal occult blood tests are used in population screening studies (see below) but are not of value diagnostically.


Treatment is surgical, with tumour resection and end-to-end anastomosis of bowel if possible. In very low rectal cancers abdominoperineal resection with permanent end colostomy is necessary. Post-operative (adjuvant) chemo-therapy increases survival in stage III and selected stage II tumours. Pre-operative radiotherapy improves survival in some patients with rectal cancer, and radiotherapy can also offer effective palliation in patients with locally advanced disease. Patients with up to two or three liver metastases confined to one lobe of the liver may be offered hepatic resection. Patients with unresectable metastatic disease are commonly offered palliative chemo-therapy, which increases median survival and improves quality of life.


This is related to tumour stage at presentation (Table 3.16).


High-risk individuals e.g. from family colon cancer syndromes or with a first-degree relative developing colon cancer aged <45 years are offered screening colonoscopy. Many countries now have population screening pro-grammes to detect early-stage cancer and hence improve outcome. In the UK, screening with biannual faecal occult blood tests (with colonoscopy when positive) for individuals 60-69 years is predicted to reduce CRC mortality by 16%.


Diarrhoea is a common complaint in clinical practice.

Acute diarrhoea This is usually due to infection or dietary indiscretion. Traveller's diarrhoea is discussed on page 35. Stool cultures (x 3 for ova, parasites and cysts) are sent and a flexible sigmoidoscopy with colonic biopsy is then performed if symptoms persist and no diagnosis has been made. Treatment is symptomatic to maintain hydration, with antidiarrhoeal agents (p. 133) for short-term relief and antibiotics for specific indications (p. 35).

Chronic diarrhoea This is defined as diarrhoea persisting for more than 14 days. Organic causes (resulting in stool weights >250g) have to be dis-tinguished from functional causes (frequent passage of small volume stools with stool weights <250g, p. 117) which can usually be done from the history (p. 115). Sometimes faecal markers of intestinal inflammation are used to differentiate functional disorders from organic disease (p. 67).

Mechanisms of diarrhoea

Osmotic diarrhoea

Large quantities of non-absorbed hypertonic substances in the bowel lumen draw fluid into the intestine. The diarrhoea stops when the patient stops eating or the malabsorptive substance is discontinued. The causes of osmotic diarrhoea are as follows:

■ Ingestion of non-absorbable substance, e.g. a laxative such as mag-nesium sulphate

■ Generalized malabsorption so that high concentrations of solute (e.g. glucose) remain in the lumen

■ Specific malabsorptive defect, e.g. disaccharidase deficiency.

Secretory diarrhoea

There is active intestinal secretion of fluid and electrolytes as well as decreased absorption. Secretory diarrhoea continues when the patient fasts. The causes are:

■ Enterotoxins, e.g. from Escherichia coli, cholera toxin

■ Hormone-secreting tumours, e.g. VIPoma (p. 191)

■ Bile salts (in the colon) following ileal disease, resection or idiopathic bile acid malabsorption

■ Fatty acids (in the colon) following ileal resection

■ Some laxatives.

Inflammatory diarrhoea (mucosal destruction)

Damage to the intestinal mucosal cell leads to loss of fluid and blood and defective absorption of fluid and electrolytes. Common causes are infective (e.g. Shigella, salmonella) and inflammatory conditions (e.g. UC and CD).

Motility related

Abnormal motility often produces frequency rather than true diarrhoea. Causes are thyrotoxicosis, diabetic autonomic neuropathy and post-vagotomy.

Approach to the patient with diarrhoea

An assessment of the likely cause of diarrhoea is initially made on the history:

Step 1: Determine if the diarrhoea is likely to have an organic or functional basis (p. 117). Frequent passage of small-volume stools (often formed) points to a functional cause; the exceptions are distal colon cancer and proctitis -organic causes that present with stool frequency and normal stool volumes. Symptoms suggestive of an organic cause include large-volume watery stools, nocturnal diarrhoea, bloody stools, weight loss or a stool description suggesting steatorrhoea (p. 67).

Step 2: Distinguish malabsorptive from colonic/inflammatory forms of diarrhoea. Colonic, inflammatory and secretory (see below) causes of diar-rhoea typically present with loose liquid or watery stools. Inflammatory diarrhoea is associated with blood or mucous discharge. Malabsorption is often accompanied by steatorrhoea (p. 67).

Step 3: Rarely, measurement of stool weight by a 3-day stool collection as a hospital inpatient may be necessary where differentiation between organic and functional bowel disease is difficult. Occasionally diarrhoea is factitious due to surreptitious laxative ingestion, or the patient deliberately dilutes the faeces by adding water or urine.


Chronic diarrhoea of likely organic origin always requires investigation. Fig. 3.4 outlines an approach to investigation. Laxative abuse, usually seen in young females, must be excluded as a cause. Patients taking anthra-quinone purgatives, e.g. senna, develop pigmentation of the colonic mucosa (melanosis coli) which may be seen at sigmoidoscopy. Other laxatives may be detected in the stool or urine. Treatment of chronic diarrhoea depends on the cause.


This is a large group of gastrointestinal disorders that are termed ‘functional' because symptoms occur in the absence of any demonstrable abnormalities in the digestion and absorption of nutrients, fluid and electrolytes, and no structural abnormality can be identified in the gastrointestinal tract. Func-tional bowel disorders are extremely common world-wide, accounting for up to 80% of patients seen in the gastroenterology clinic. Rather than a diagnosis of exclusion after normal investigations (as the definition would suggest), this

• Patients with presumed functional diarrhoea, based on history, age and normal baseline investigations (FBC, ESR coeliac serology) are excluded from this algorithm.

• High-risk patients (immunosuppressed, recent travel or antibiotics) should have multiple stool cultures including a search for unusual organisms.

Fig. 3.4 Approach to the investigation of chronic diarrhoea. FBC, full blood count; ESR, erythrocyte sedimentation rate; TFT, thyroid function test; SBFT, small bowel follow-through; HIAA, hydroxyindoleacetic acid; MCV, mean corpuscular volume; OGD, oesophagogastroduodenoscopy; MRCP, magnetic resonance cholangiopancreatography.

is frequently a positive diagnosis made in a patient with symptoms suggestive of a functional gastrointestinal disorder (Table 3.17). It is estimated that only 25% of persons with this condition seek medical care for it, and studies suggest that those who seek care are more likely to have behavioural and psychiatric problems than those who do not seek care.

Altered bowel motility, visceral hypersensitivity (they have a lower pain threshold when tested with balloon distension of the rectum), psychosocial factors, an imbalance in neurotransmitters and gastrointestinal infection have all been proposed as playing a part in the development of functional bowel disorders. Low-dose antidepressant treatment e.g. amitriptyline 10 mg daily, is frequently used for these disorders if initial symptom-based treatments do not prove beneficial. Common functional gastrointestinal disorders are listed below.

■ Functional oesophageal disorders occur in the absence of dysphagia, pathological gastrooesophageal reflux disease or other oesophageal dis-order. They include globus (a sensation of a lump in the throat persisting

Table 3.17 Chronic gastrointestinal symptoms suggestive of a functional gastrointestinal disorder

Nausea alone Vomiting alone Belching


Chest pain unrelated to exercise Postprandial fullness Abdominal bloating

Abdominal discomfort/pain (right or left iliac fossa)

Passage of mucus per rectum

Frequent bowel actions with urgency first thing in the morning

between meals), regurgitation and midline chest pain. Sometimes these symptoms will respond to high-dose acid suppression or antidepressants e.g. amitriptyline or citalopram.

■ Functional dyspepsia. Common symptoms include epigastric pain or dis-comfort, early satiety, bloating and nausea. Symptoms are sometimes similar to peptic ulceration. Investigation is frequently unnecessary in younger people (<55 years) but endoscopy is usually required in older people or in those with ‘alarm symptoms' (for management of dyspepsia, see p. 84). Management is mainly by reassurance and lifestyle changes (reducing intake of fat, coffee, alcohol and cigarette smoking). PPIs help some patients with epigastric pain. Prokinetic agents e.g. metoclopra-mide and domperidone (p. 136) are sometimes helpful, particularly in those with fullness and bloating. Eradication of H. pylori is helpful in some patients.

■ Irritable bowel syndrome (IBS). Crampy abdominal pain relieved by defecation or the passage of wind, altered bowel habit, a sensation of incomplete evacuation, abdominal bloating and distension are common symptoms. Subtypes of IBS can be identified according to the predomi-nant stool pattern: IBS with constipation, IBS with diarrhoea, and mixed IBS with alternating diarrhoea and constipation. In other patients with IBS, diarrhoea without pain (formed stools followed by loose mushy stools mainly in the morning) or abdominal pain without alteration in bowel habit are the major symptoms.

Symptoms are more common in women than men, and the history is usually prolonged. Characteristically the patient looks healthy. Examination is usually normal, although sigmoidoscopy and air insufflation may reproduce the pain. If frequency of defecation is a feature, a rectal biopsy should be performed to exclude IBD. Investigation depends on the individual patient. Young patients with classic symptoms need only simple blood tests (full blood count, C-reactive protein and coeliac serology) to look for evidence of other gastrointestinal diseases that present similarly, e.g. IBD and coeliac disease. Onset of symptoms in an older patient (>50 years) should be investigated further, e.g. colonoscopy, to exclude other pathology. The approach to inves-tigating a patient presenting with constipation or diarrhoea is discussed on pages 107 and 115, respectively. Management is reassurance, with a discus-sion of lifestyle and diet. Initial treatment is symptom based with soluble fibre supplements for constipation, e.g. ispaghula husk (p. 130) and antidiar-rhoeal drugs e.g. loperamide (p. 133) for bowel frequency. Smooth muscle relaxants, such as peppermint oil and mebeverine, are useful in some patients with abdominal pain. Second-line treatment is with low-dose amitriptyline or citalopram. Psychological interventions (hypnotherapy, cogni-tive behavioural therapy and psychotherapy) are used for patients with resist-ant symptoms.


This section deals with acute abdominal conditions that cause patients to be hospitalized within a few hours of the onset of their pain. Most are admitted under the care of the surgical team, and some will need a laparotomy. Medical conditions that present as an acute abdomen include diabetic ketoacidosis, myocardial infarction and pneumonia. IBS occasionally presents with acute severe abdominal pain. A leaking abdominal aortic aneurysm may present similarly to renal colic and should be considered in the over 50s presenting with apparent colic. Mesenteric ischaemia is easily missed and should be considered in a patient presenting with abdominal pain and prior weight loss. A plain abdominal X-ray and erect chest X-ray is usually per-formed in the acute abdomen but the most useful imaging investigations are ultrasound (for cholangitis, cholecystitis, appendicitis, gynaecological condi-tions) and CT (site and cause of intestinal obstruction, renal colic, acute pancreatitis).


The history, including gynaecological (vaginal discharge, last menstrual period) and urinary symptoms, will often point to the cause of the pain.

■ Onset of pain may be sudden or gradual. Sudden onset suggests perfora-tion of a viscus (e.g. duodenal ulcer), rupture of an organ (e.g. aortic aneurysm) or torsion (e.g. ovarian cyst). The pain of acute pancreatitis often begins suddenly. Ruptured ectopic pregnancy, rupture or torsion of ovarian cysts and acute salpingitis cause lower abdominal pain in women.

■ Site of pain and radiation must be noted. In general, upper abdominal pain is produced by pathology of either the upper abdominal viscera- e.g. acute cholecystitis, acute pancreatitis - or the stomach and duodenum. The pain of small bowel obstruction is often in the centre of the abdomen. A common cause of acute right iliac fossa pain is acute appendicitis. Pain

Table 3.18 Some causes of mechanical intestinal obstruction

Small intestinal obstruction


Adhesions (80% in adults)


Crohn’s disease Intussusception

Obstruction due to extrinsic involvement by cancer

Colonic obstruction

Carcinoma of the colon Sigmoid volvulus Diverticular disease

from acute pancreatitis, rupture of an aortic aneurysm or renal tract disease often radiates to the back.

■ Pain may be intermittent or continuous. Intermittent (colicky) pain describes pain that occurs for a short period (usually a few minutes) and is interspersed with pain-free periods lasting a few minutes or up to half an hour. This is characteristic of mechanical obstruction of a hollow viscus, e.g. ureteric calculus or bowel obstruction (Table 3.18). Additional symptoms of bowel obstruction, which may or may not be present, are abdominal distension, vomiting and absolute constipation (i.e. failure to pass flatus or stool). Biliary pain (previously called biliary colic) resulting from obstruction of the gall bladder or bile duct is not colicky but usually a constant upper abdominal pain.

■ Continuous pain is relentless with no periods of complete relief. It occurs in many abdominal conditions.


■ The presence of shock (pale, cool peripheries, tachycardia, hypotension) suggests rupture of an organ, e.g. aortic aneurysm, ruptured ectopic pregnancy. It also occurs in the later stages of generalized peritonitis resulting from bowel perforation (see below).

■ Fever is common in acute inflammatory conditions.

■ The signs of peritonitis are tenderness, guarding (involuntary contraction of the abdominal muscles when the abdomen is palpated) and rigidity on palpation. Bowel sounds are absent with generalized peritonitis.

■ Mechanical bowel obstruction produces distension and active ‘tinkling' bowel sounds. A strangulated hernia may produce obstruction, and the hernial orifices must always be examined.

A rectal and pelvic examination should be performed in most patients with an acute abdomen.


■ Blood tests. The white cell count is raised in inflammatory conditions. The serum amylase is raised in any acute abdomen, but levels greater than five times normal indicate acute pancreatitis.

■ Urinalysis may show evidence of infection or blood in renal colic. Women of childbearing age should have a pregnancy test.

■ Imaging. An erect chest X-ray may show air under the diaphragm with a perforated viscus, but its absence does not exclude pertoration. Plain abdominal X-ray shows dilated loops of bowel and fluid levels in obstruc-tion. Ultrasound examination is useful in the diagnosis of acute cholecys-titis, cholangitis, appendicitis and gynaecological conditions such as ruptured ovarian cyst and ectopic pregnancy. Spiral CT scan is the most accurate modality in the investigation of the acute abdomen but is usually reserved for patients with inconclusive or negative ultrasound results.

■ Surgery. Laparoscopy or laparotomy may be necessary depending on the diagnosis.

Acute appendicitis

Acute appendicitis occurs when the lumen of the appendix becomes obstructed by a faecolith.


It affects all age groups but is rare in the very young and very old.

Clinical features

The typical clinical presentation is the onset of central abdominal pain which then becomes localized to the right iliac fossa (RIF), accompanied by anorexia and sometimes vomiting and diarrhoea. The patient is pyrexial, with tender-ness and guarding in the RIF due to localized peritonitis. There may be a tender mass in the presence of an appendix abscess.


The white cell count, C-reactive protein and ESR are raised, but these are not specific. Ultrasonography may show an inflamed appendix and can also show an appendix mass. CT is highly sensitive and specific, and has reduced removal of histologically normal appendices by 90%.

Differential diagnosis

Non-specific mesenteric lymphadenitis, terminal ileitis due to Crohn's disease or Yersinia infection, acute salpingitis in women, inflamed Meckel's diverticu-lum and functional bowel disease can all mimic acute appendicitis.


The treatment is surgical, with removal of the appendix either by open surgery or laparoscopically. An appendix mass is treated conservatively initially with intravenous fluids and antibiotics and later appendicectomy.


These arise from gangrene and perforation, leading to localized abscess formation or generalized peritonitis.

Acute peritonitis

Localized peritonitis occurs with all acute inflammatory conditions of the gastrointestinal tract, and management depends on the underlying condition, e.g. acute appendicitis, acute cholecystitis.

Generalized peritonitis occurs as a result of rupture of an abdominal viscus, e.g. perforated duodenal ulcer, perforated appendix. There is a sudden onset of abdominal pain which rapidly becomes generalized. The patient is shocked and lies still, as movement exacerbates the pain. A plain abdominal X-ray may show air under the diaphragm; serum amylase must be checked to exclude acute pancreatitis.

Intestinal obstruction

Intestinal obstruction is either mechanical or functional.

Mechanical (Table 3.18) The bowel above the level of the obstruction is dilated, with increased secretion of fluid into the lumen. The patient com-plains of colicky abdominal pain, associated with vomiting (occurs earlier with small bowel than large bowel obstruction) and absolute constipation (occurs earlier with large bowel that small bowel obstruction). On examination there is distension and ‘tinkling' bowel sounds. Small bowel obstruction may settle with conservative management (i.e. nasogastric suction and intravenous fluids to maintain hydration). Large bowel obstruction is treated surgically.

Functional This occurs with a paralytic ileus, which is often seen in the post-operative stage of peritonitis or of major abdominal surgery, or in asso-ciation with opiate treatment (acute colonic pseudo-obstruction, Ogilvie's syndrome). It also occurs when the nerves or muscles of the intestine are damaged, causing intestinal pseudo-obstruction. Unlike mechanical obstruc-tion, pain is often not present and bowel sounds may be decreased. Gas is seen throughout the bowel on a plain abdominal X-ray. Management is conservative.


The peritoneal cavity is a closed sac lined by mesothelium. It contains a little fluid to allow the abdominal contents to move freely. Conditions which affect the peritoneum are:

■ Infective (peritonitis)

■ Secondary to gut disease, e.g. appendicitis, perforation

■ Chronic peritoneal dialysis

■ Spontaneous (associated with cirrhotic ascites)

■ Tuberculous

■ Neoplasia

■ Secondary deposits, e.g. from ovary

■ Primary mesothelioma

■ Vasculitis: connective tissue disease.


Dietary requirements

Food is necessary to provide the body with energy. The average daily require-ment (Table 3.19) of a middle-aged adult female in the UK is 8100 kJ (1940 kcal), and for a man is 10 600 kJ (2550 kcal). This is made up of 50% carbohydrate, 35% fat and 15% protein, plus or minus 5% alcohol. Energy requirements increase during periods of rapid growth, such as adolescence, pregnancy and lactation, and with sepsis.

Bodyweight is maintained at a ‘set point' by a precise balance of energy intake and total energy expenditure (the sum of the resting or basal metabolic rate, physical activity, and the thermic effect of food eaten). Weight gain is almost always due solely to an increase in energy intake which exceeds the total energy expenditure. Occasionally weight gain is due to a decrease in energy expenditure, e.g. hypothyroidism, or due to fluid retention, e.g. heart

Table 3.19 Protein, energy and water requirement of normal and hypercatabolic adults

Metabolic State

Nutritional requirements



Protein (g/kg)



Nitrogen (g/kg)



Energy (kcal/kg)



Water (mL/kg)



failure or ascites. On the other hand, weight loss associated with cancer and chronic diseases is due to a reduction in energy intake secondary to a loss of appetite (anorexia). In a few conditions, such as sepsis and severe trauma, there is an increase in energy requirements (hypercatabolic or hypermeta-bolic) which will result in a negative energy balance if there is no compensa-tory increase in energy intake.

A balanced diet also requires sufficient amounts of minerals and vitamins. In the Western world vitamin deficiency is rare except in specific groups, e.g. alcohol dependent and patients with small bowel disease, who may have multiple vitamin deficiencies, and patients with liver and biliary tract disease, who are susceptible to deficiency of the fat-soluble vitamins (A, D, E, K). Deficiencies of the B vitamins, riboflavin and biotin, are rare in all patient groups and are not discussed further. Dietary deficiency of vitamin B6 (pyri-doxine, pyridoxal and pyridoxamine) is also extremely rare, but drugs (e.g. isoniazid and penicillamine) that interact with pyridoxal phosphate may cause B6 deficiency and a polyneuropathy. Vitamin B12 and folate deficiency are discussed on pages 199 and 201, respectively, and vitamin D deficiency on page 315.


Patients should be screened for nutritional status on admission to hospital and during their hospital stay. Current recommendations suggest that:

■ Patients should be asked simple questions about recent weight loss, their usual weight and whether they have been eating less than usual.

■ Their weight and height should be recorded and body mass index (BMI) calculated (weight [kg]/height [m]2). The acceptable range of BMI is 20-25 kg/m2 for men and 19-24 kg/m2 for women.

Some form of nutritional supplementation is required in those patients who cannot eat, should not eat, will not eat or cannot eat enough. It is necessary to provide nutritional support for:

■ All severely malnourished patients on admission to hospital: severe mal-nutrition is indicated by a BMI of less than 15 kg/m2

■ Moderately malnourished patients (BMI 15-19 kg/m2) who, because of their physical illness, are not expected to eat for 3-5 days

■ Normally nourished patients not expected to eat for 7-10 days.

Enteral nutrition is cheaper, more physiological and has fewer complications than parenteral (intravenous) nutrition, and should be used if the gastroin-testinal tract is functioning normally. With both enteral and parenteral nutri-tion a complete feeding regimen consisting of fat, carbohydrates, protein, vitamins, minerals and trace elements can provide the nutritional require-ments of the individual (Table 3.17). Ideally a multidisciplinary nutrition support team should supervise the provision of artificial nutritional support.

Enteral nutrition

Foods can be given by:

■ Mouth

■ Fine-bore nasogastric tube for short-term enteral nutrition

■ Percutaneous endoscopic gastrostomy (PEG): this is useful for patients who need feeding for longer than 2 weeks

■ Percutaneous jejunostomy where a tube is inserted directly into the jejunum either endoscopically or at laparotomy.

A polymeric diet with whole protein, carbohydrate and fat is usually used; sometimes an elemental diet composed of amino acids, glucose and fatty acids is used for patients with CD (p. 103).

Total parenteral nutrition (TPN)

Parenteral nutrition may be given via a feeding catheter placed in a peripheral vein or a silicone catheter placed in the subclavian vein. Central catheters must only be placed by experienced clinicians under strict aseptic conditions in a sterile environment. The risk of introducing infection is reduced if these catheters are only used for feeding purposes, and not the administration of drugs or blood. Peripheral feeding lines usually only last for about 5 days and are reserved for when feeding is necessary for a short period. Central lines may last for months to years. Complications of TPN are given in Table 3.20.

Monitoring of artificial nutrition

Patients receiving nutritional support should be weighed twice weekly: they require regular clinical examination to check for evidence of fluid overload or depletion. Patients receiving nutritional support in hospital initially require daily measurements of urea and electrolytes and blood glucose. More fre-quent measurement of blood glucose with BM sticks is indicated in patients beginning TPN. Liver biochemistry, calcium and phosphate are measured twice weekly. Serum magnesium, zinc and nitrogen balance (see below) are measured weekly. The frequency of biochemical monitoring is adjusted according to the patient's clinical and metabolic status.

It is necessary to give 40-50 g of protein per 24 hours to maintain nitrogen balance, which represents the balance between protein breakdown and

Table 3.20 Complications of total parenteral nutrition
Catheter related: sepsis, thrombosis, embolism and pneumothorax
Metabolic, e.g. hyperglycaemia, hypercalcaemia
Electrolyte disturbances
Liver dysfunction

synthesis. The aim of any regimen is to achieve a positive nitrogen balance, which can usually be obtained by giving 3-5 g of nitrogen in excess of output. The amount of protein required to maintain nitrogen balance in a particular individual can be calculated from the amount of urinary nitrogen loss, using the formula:

N2 loss (g/24 h) = Urinary urea (mmol/24 h) X 0.028 + 2

Urinary nitrogen X 6.25 = grams of protein required (most proteins contain about 16% nitrogen)

Most patients require about 12 g of nitrogen per 24 hours, but hypercatabolic patients require more, about 15 g/day.

Refeeding syndrome

The refeeding syndrome occurs within the first few days of refeeding by the oral, enteral or parenteral route. It is underrecognized and can be fatal. It involves a shift from the use of fat as an energy source during starvation to the use of carbohydrate as an energy source during refeeding. With the introduction of artificial nutrition and carbohydrate by any source, insulin release is augmented and there is rapid intracellular passage of phosphate, magnesium and potassium resulting in hypophosphataemia (p. 654), hypo-magnesaemia (p. 342), and hypokalaemia (p. 338). Phosphate is an integral part of cellular machinery. Deficiency results in widespread organ dysfunction (muscle weakness, rhabdomyolysis, cardiac failure, immune suppression, haemolytic anaemia, thrombocytopenia, coma, hallucinations, fits). Thiamine deficiency can be precipitated. Patients at risk of refeeding are underweight (e.g. anorexia nervosa, alcohol dependent syndrome) or those with recent rapid weight loss (5% within preceding month), including patients after treat-ment for morbid obesity. These at-risk patients should receive high-dose vitamin B and C vitamins, e.g. Pabrinex® 1 pair twice daily, for 5-7 days beginning before feeding, and begin feeding at 25-50% of estimated calorie requirements, increasing by 100 calories per day. Serum phosphate, mag-nesium, calcium, potassium, urea and creatinine, bodyweight and evidence of fluid overload should be checked daily for the first week, and electrolyte deficiencies corrected as necessary.



Obesity, defined as an excess of body fat contributing to comorbidity, is a common problem in developed countries and is becoming more common in developing countries. A BMI of 30 kg/m2 or greater is a standard commonly used to define obesity. Overweight is defined as a BMI of 25-30 kg/m2 and is associated with a mildly increased risk of complications that have been identi-fied in obese patients (see below). In almost all obese individuals weight gain is as a result of increased energy intake and energy expenditure is normal or indeed increased. In a few conditions, of which hypothyroidism is the com-monest example, weight gain is due at least in part to reduced energy expendi-ture. Obese patients are at risk of a premature death, mainly from diabetes, ischaemic heart disease and cerebrovascular disease. Obesity is also associ-ated with an increased risk of hypertension, hyperlipidaemia, obstructive sleep apnoea, osteoarthritis of the knees and hips, fatty liver, gallstones and an increased cancer risk. Weight reduction can be achieved with a reduction in calorie intake and an increase in physical activity, although in practice this is difficult to achieve. The most common diets allow a daily energy intake of 4200 kJ (1000 kcal) which in a middle-aged woman would result in a daily energy deficit (expenditure vs intake) of about 4200 kJ. A week of dieting would result in a total energy deficit of 25-29 MJ (6000-7000 kcal) and weight loss of about 1 kg. A 10% loss of body weight (i.e. 10 kg in a 100 kg person) is associated with a fall in blood pressure and a reduced risk of diabetes and overall mortality. Drug treatment such as orlistat, an inhibitor of pancreatic lipase and hence fat digestion, is sometimes used in the severely obese patient. Surgical treatment is used in some patients with morbid obesity (BMI >40 kg/m2) or patients with a BMI >35 kg/m2 and obesity-related complica-tions, after conventional medical treatment has failed. The techniques used are restrictive, such as gastric banding (which restricts the ability to eat) or intestinal bypass (which reduces the ability to absorb nutrients).

Anorexia nervosa

Anorexia nervosa is a psychological illness, predominantly affecting young females and characterized by marked weight loss (BMI <17.5 kg/m2), intense fear of gaining weight, a distorted body image and amenorrhoea. Patients with anorexia nervosa control their body weight by a process of semi-starvation and/or self-induced vomiting (bulimia) and may develop conse-quences of undernutrition. Treatment is difficult and usually undertaken in a specialist eating disorders unit.


Drugs for dyspepsia and peptic ulceration


Mechanism of action

Main effect is to neutralize gastric acid. Alginate-containing antacids form a ‘raft' that floats on the surface of the stomach contents to reduce reflux and protect the gastro-oesophageal mucosa.


Symptomatic relief in dyspepsia, gastro-oesophageal reflux and peptic ulcer-ation. Healing of peptic ulcers is much less than with antisecretory drugs (see below) and antacids should not be used for this indication.


Preparations and dose

Aluminium hydroxide Tablets: 500 mg; Capsules (Alu-Cap®) 475 mg.

1-2 tablets chewed or 1 capsule four times daily and at bedtime, or as required.

Magnesium trisilicate mixture Oral suspension, 5% each of magnesium trisilicate, light magnesium carbonate, and sodium bicarbonate.

10-20 mL in water three times daily or as required.

Co-magaldrox (Mucogel®) Suspension. Mixture of aluminium hydroxide 220 mg, and magnesium hydroxide 195 mg/5 mL.

10-20 mL 20-60 minutes after meals and at bedtime, or as required. Alginate-containing antacid Tablets, suspension. Gaviscon® Advance contains potassium bicarbonate, sodium alginate.

1-2 tablets chewed or 10-20 mL four times daily after meals and at bedtime.


Magnesium-containing antacids tend to be laxative, whereas aluminium-containing antacids may be constipating; antacids containing both aluminium and magnesium may reduce these colonic side-effects.


Antacids may interfere with the absorption of other drugs and in general other drugs should be given at least 1 hour before or after each dose of antacid. The sodium content of preparations with a high sodium content, e.g. magnesium trisilicate mixture (6.3 mmol/10 mL) and Gaviscon® Advance (4.6 mmol/10 mL; 2.25 mmol/tablet) should be taken into account in patients on a ‘no added' salt diet (cardiac, renal or hepatic disease). Aluminium hydroxide is contraindicated in hypophosphataemia. Constipating antacids (i.e. those containing aluminium) should be avoided in liver disease.

H2-receptor antagonists

Mechanism of action

Reduce gastric acid secretion as a result of histamine H2-receptor blockade.


GORD, healing of benign gastric and duodenal ulcers, prevention of gastroduodenal damage in patients requiring intensive care, prevention of NSAID-induced DUs, and in high doses prevention of GUs. However, for all indications, PPIs are more effective and more commonly used in clinical practice.

Preparations and dose

Ranitidine Tablets: 150 mg, 300 mg;Syrup 75 mg/5 mL;Injection (Zantac®) 25 mg/mL.


■ Gastric and duodenal ulceration 150 mg twice daily or 300 mg at night for 4-8 weeks.

■ GORD: 150 mg twice daily or 300 mg at night, 150 mg four times daily in severe cases for up to 12 weeks. Reduce to lowest dose possible to relieve symptoms in maintenance treatment.

■ NSAID-associated ulceration: 150 mg twice daily or 300 mg at night, 300 mg twice daily can be given for higher healing rate.

■ Prophylaxis of NSAID-induced peptic ulceration, 300 mg twice daily.

IV 50 mg diluted to 20 mL and given over at least 2 minutes every 6-8 hours or infusion 25 mg/h for 2 hours repeated every 6-8 hours.

Cimetidine Tablets: 200 mg, 400 mg, 800 mg; Syrup 200 mg/5 mL.


■ GORD: 400 mg four times daily for 4-8 weeks; reduce down to lowest dose possible for maintenance treatment.

■ Peptic ulceration: 400 mg twice daily or 800 mg at night for at least 4 weeks, 8 weeks in NSAID-associated ulceration.


Diarrhoea, altered liver biochemistry, headache, dizziness, rash. Rarely, other side-effects (see national formulary).


Cimetidine retards oxidative hepatic drug metabolism by binding to microsomal cytochrome P450. It should be avoided in patients stabilized on warfarin, phenytoin, and theophylline (or aminophylline) but other interactions (see national formulary) may be of less clinical relevance.

Proton pump inhibitors Mechanism of action

Inhibit gastric acid secretion by blocking the hydrogen/potassium-adenosine triphosphate enzyme system (the ‘proton pump') of the gastric parietal cell.



GORD; healing of peptic ulcers; prevention of NSAID-induced peptic ulcers; in combination with antibacterials for eradication of H. pylori; intravenously and after endoscopic therapy to reduce re-bleeding rates in patients with bleeding peptic ulcers; inhibition of gastric acid in pathological hyper-secretory conditions, e.g. gastrinoma; prevention of peptic ulcers in critically ill patients; prophylaxis of acid aspiration during general anaesthesia; dyspepsia.

Preparations and dose

Omeprazole Capsules and tablets: 10 mg, 20 mg, 40 mg; Dispersible tablets: 10 mg, 20 mg, 40 mg; Intravenous intusion: 40 mg vial.

■ GORD: 20-40 mg once daily for 4-8 weeks, maintenance 10-20 mg once daily.

■ Healing of peptic ulcers (not H. pylori associated): 20 mg daily for 4 weeks.

■ Prevention of NSAID-induced ulcers: 20 mg daily.

■ Eradication of H. pylori (in combination with antibacterials): 20 mg twice daily for 1 week.

■ By i.v. injection in bleeding peptic ulcers: 80 mg over 5 minutes and then 8 mg/h (1 vial diluted in 100 mL 0.9% sodium chloride or 5% dextrose).

■ Gastrinoma: 60 mg once daily, usual range 20-120 mg daily.

■ Gastric acid reduction during general anaesthesia: 40 mg on preced-ing evening then 40 mg 2-6 hours before surgery.

Lansoprazole Capsules: 15 mg, 30 mg; Orodispersible tablet: 15 mg, 30 mg.

■ GORD: 30 mg once daily for 4-8 weeks, maintenance 15-30 mg once daily.

■ Healing of peptic ulcers (not H. pylori related): 30 mg daily for 4 weeks.

■ Prevention of NSAID-induced ulcers: 15-30 mg daily.

■ Eradication of H. pylori (in combination with antibacterials): 20 mg twice daily for one week.

■ Gastrinoma: 60 mg once daily, usual range 30-120mg daily.


Gastrointestinal disturbance (diarrhoea, nausea, vomiting), liver dysfunction, hypersensitivity reactions, headache, skin reactions, increased risk of gastrointestinal infections (due to reduced gastric acidity). Rarely, acute kidney injury, deficiency of vitamin B12, calcium (leading to hip fracture) and magnesium due to reduced intestinal absorption.


Omeprazole and esomeprazole competitively inhibit the CYP2C19 isoenzyme (which metabolises clopidogrel to its active metabolite) and may reduce the ability of clopidogrel to inhibit platelet aggregation. Omeprazole may decrease the effect of warfarin, phenytoin and diazepam. Lansoprazole may increase the effect of warfarin, phenytoin and theophylline. Reduce dose in severe liver disease.


Treatment of constipation is initially with lifestyle changes and drugs are reserved for use as second-line treatment. It may be necessary to use a combination of two different types of laxative, e.g. stimulant plus faecal softener. All laxatives are contraindicated in intestinal obstruction or perfora-tion, paralytic ileus, and severe inflammatory conditions of the gut such as CD and UC.

Bulk-forming laxatives Mechanism of action

Absorb water and increase faecal mass, which stimulates peristalsis.


Treatment of slow-transit constipation and bulking of stool in patients with a colostomy, diverticular disease and irritable bowel syndrome.

Preparations and dose

Unprocessed wheat bran is one of the most effective fibre laxatives, and patients can add it to meals, e.g. cereal (2-6 tablespoons per day).

Ispaghula husk Granules: 3.5 g sachet.

1 sachet or 2 level 5 mL spoonfuls in water twice daily after meals.

Methycellulose Tablets: 500 mg.

3-6 tablets twice daily with at least 300 mL of liquid.

Sterculia Granules: 7 g sachets.

1-2 sachets or 1-2 heaped 5 mL spoonfuls washed down with plenty of liquid once or twice daily after meals.


Flatulence, abdominal distension.


Maintain adequate fluid intake to prevent faecal impaction; contraindications (see above).

Stimulant laxatives

Mechanism of action

Increase colonic motor activity.


Short-term treatment of constipation.

Preparations and dose

Bisacodyl Tablets: 5 mg; Suppositories: 10 mg.

Oral 5-10 mg at night, occasionally increase to 15-20 mg.

By rectum in suppositories, 10 mg in the morning.

Docusate sodium Capsules: 100 mg; Solution: 50 mg/5 mL; Micro-enema: 120 mg in 10 g single-dose pack.

Oral 500 mg daily in two to three divided doses.

By rectum 10 g unit daily.

Glycerol (glycerin) Suppositories: glycerol 700 mg.

1 suppository moistened with water before use.

Senna Tablets: 7.5 mg; Syrup: 7.5 mg/5 mL.

2-4 tablets, 10-20 mL of syrup at night.


Abdominal cramps, diarrhoea and hypokalaemia.


Contraindications (see above).

Osmotic laxatives

Mechanism of action

Attract or retain water in the intestinal lumen, leading to softer stools and improved propulsion.


Treatment of constipation. Lactulose is used in the treatment of hepatic encephalopathy. Phosphate enemas are used to evacuate the bowel before radiological procedures, flexible sigmoidoscopy and surgery.

Preparations and dose

Lactulose Solution: 3.1-3.7g/5 mL.

Initially 15 mL twice daily; hepatic encephalopathy: 30-50 mL three times daily adjusted to produce two to three soft stools daily.

Macrogols (polyethylene glycol) Movico® (polyethylene glycol ‘3350’ with electrolytes).

1-3 sachets daily in divided doses; each sachet dissolved in 125 mL of water.

For smaller dosing, Movicol-Half® is also available.

Magnesium salts Magnesium hydroxide mixture; Magnesium sulphate (Epsom salts).

30-45 mL when required of magnesium hydroxide. 5-10 g of magnesium sulphate in a glass of warm water before breakfast.

Phosphates (rectal) Fleet® Ready-to-use Enema: 133 mL pack.

One enema inserted 30 minutes before evacuation required.

Sodium citrate (rectal) Micralax Micro-enema®: 5 mL.

One enema as required.


Abdominal distension, colic, nausea, local irritation after phosphate enema.


Contraindications (see above). May also cause electrolyte disturbance. Use with caution in hepatic and renal impairment. Although magnesium ions are absorbed poorly, similar to all osmotic ions some absorption does occur, which can cause problems in patients with abnormal renal function.

Bowel-cleansing solutions


Used before colonic surgery, colonoscopy or radiological examination to ensure the bowel is free of solid contents. They are not treatments for con-stipation. Bowel-cleansing agents are coupled with a low residue diet for at least 3 days before the procedure, copious intake of water or other clear fluids and cessation of all solid foods on the day before the procedure. All are contraindicated in bowel obstruction, perforated bowel or severe colitis and Moviprep® is contraindicated in glucose-6-phosphate dehydrogenase deficiency.

Mechanism of action

This is variable depending on the drug.

Preparations and dose

Citramag® Magnesium carbonate 11.57g and citric acid 17.79 g/sachet.

1 sachet at 8.00 a.m. and 1 sachet between 2 and 4 p.m. on day before procedure.

Fleet Phospho-soda® Sodium dihydrogen phosphate dehydrate 24.4 g, disodium phosphate dodecahydrate 10.8 g/45 mL.

45 mL diluted with 120 mL of water (half glass), followed by one full glass of water. For morning procedures, the first dose should be taken at 7 a.m. and the second dose at 7 p.m. the day before the procedure. For afternoon procedures, the first dose should be taken at 7 p.m. on the day before and the second dose at 7 a.m. on the day of the procedure.

Klean-prep® Macrogol ‘3350’ (polyethylene glycol ‘3350’ with electrolytes.

2 sachets diluted with water to 2 L, and 250 mL drunk rapidly every 10-15 minutes. 2 sachets on evening before examination, and 2 sachets on morning of examination.

Moviprep® Sachet A containing macrogol ‘3350’ (polyethylene glycol ‘3350’) with electrolytes and SachetB containing ascorbic acid 4.7 g and sodium ascorbate 5.9 g.

Dilute sachet A and B in 1 L of water. Drink 2 L of reconstituted solution on the evening before the procedure or 1 L on the evening before and 1 L early on the morning of the procedure.

Picolax® Sodium picosulfate 10 mg/sachet wih magnesium citrate.

Dosing as for Citramag®.


Nausea, vomiting, abdominal cramps. Occasionally dehydration and hypo-tension, electrolyte disturbance.


Most cases of acute diarrhoea are infective and will settle without treatment. Oral rehydration salts (Dioralyte®), 1 sachet after every loose motion, are often used especially in the elderly and children. Antidiarrhoeal agents relieve symptoms of acute diarrhoea but are not recommended routinely. Antidiar-rhoeal agents, e.g. loperamide, are sometimes used in the management of chronic diarrhoea.

Loperamide hydrochloride Capsules or tablets: 2 mg.

Mechanism of action

Antimotility agent.


Symptomatic treatment of acute diarrhoea; chronic diarrhoea in adults.


Constipation, abdominal cramps, dizziness.


Active ulcerative colitis or infective diarrhoea associated with bloody stools.

Nausea and vomiting

Antiemetics should be prescribed only when the cause of vomiting is known (e.g. drugs particularly cytotoxic chemotherapy, post-operative, motion sick-ness, pregnancy, and migraine) because otherwise they may delay diagnosis. If antiemetic drug treatment is indicated, the drug is chosen according to the aetiology of vomiting. Dexamethasone (p. 665) has antiemetic effects and is used in vomiting associated with cancer chemotherapy. It has additive effects when given with high-dose metoclopramide or with a 5-HT3-receptor antagonist such as ondansetron. The mechanism of action of dexamethasone as an antiemetic is unknown but may involve reduction of prostaglandin synthesis.



Motion sickness, drug-induced vomiting, vestibular disorders, such as vertigo and tinnitus.

Mechanism of action

Competitive antagonist at the histamine H1 receptor.

Preparations and dose

Cyclizine Valoid® tablets: 50 mg; Inịection 50 mg/mL.

Oral 50 mg up to three times daily.

IM/IV injection 50 mg three times daily.

Promethazine Phenergan® tablets: 10 mg, 25 mg; Elixir: 5 mg/mL; Inịection: 25 mg/mL.

Oral for motion sickness prevention, 20-25 mg (at bedtime the night before travel).

IM/IV 25-50 mg.


Drowsiness, antimuscarinic effects (urinary retention, dry mouth, blurred Vision), palpitations, arrhythmias and rashes.


Caution in prostatic hypertrophy, urinary retention, glaucoma and pyloro-duodenal obstruction (due to antimuscarinic effects). Drug interactions -see national formulary.


Mechanism of action

Dopamine antagonists. Act centrally by blocking the chemoreceptor trigger zone (CTZ) in the fourth ventricle. Many drugs produce vomiting by an action on the CTZ.


Phenothiazines are used for the prophylaxis and treatment of nausea and vomiting associated with diffuse neoplastic disease, radiation sickness and vomiting caused by drugs such as general anaesthetics, opioids and cytotox-ics. Chlorpromazine is associated with more sedation and is usually reserved for nausea and vomiting of terminal illness.

Preparations and dose

Chlorpromazine hydrochloride Tablets: 25 mg, 50 mg, 100 mg; Solution: 25 mg/5 mL, 100 mg/5 mL; Injection: 25 mg/mL; Suppositories: 25 mg and 100 mg.

Oral 10-25mg every 4-6 hours.

IM 25mg then 25-50mg every 3-4 hours.

By rectum In suppositories: 100 mg every 6-8 hours.

Prochlorperazine Tablets 5 mg; Stemeti® tablets and suppositories: 5 mg; Syrup: 5 mg/mL; Injection: 12.5 mg/mL.

Oral 20 mg initially, then 10 mg after 2 hours; prevention: 5-10 mg two to three times daily.

IM 12.5 mg followed if necessary after 6 hours by an oral dose.


See antipsychotics (p. 798).


See antipsychotics (p. 798).

Domperidone and metoclopramide

Mechanism of action

Block dopamine receptors and inhibit dopaminergic stimulation of the CTZ.


Domperidone is used particularly in post-operative nausea and vomiting and also gastro-oesophageal reflux disease and dyspepsia. Metoclopramide is particularly used in nausea and vomiting associated with cytotoxics or radiotherapy.

Preparations and dose

Metoclopramide Tablets: 10 mg; Syrup: 5 mg/mL; Injection: 5 mg/mL.

Oral/IM/IV (over 1-2 minutes): 10 mg three times daily.

Domperidone Tablets: 10 mg; Motilium® tablets: 10 mg; Suspension: 5 mg/mL; Suppositories: 30 mg.

Oral 10-20 mg three to four times daily; maximum 80 mg.

By rectum 60 mg twice daily.


Central nervous system effects are produced by metoclopramide and to a lesser extent by domperidone (due to limited passage across the blood-brain barrier). Extrapyramidal effects include acute dystonias (treated by drug cessation and procyclidine 5-10 mg i.m./i.v.), akathisia and a parkinsonism-like syndrome. Drowsiness with high doses of metoclopramide. Galactor-rhoea is caused by hyperprolactinaemia as a result of dopamine receptor blockade.


Contraindicated in gastrointestinal obstruction, 3-4 days after gastro-intestinal surgery where increased motility may be harmful, and phaeochromocytoma.

5-HT3-receptor antagonists

Mechanism of action

Block the 5-HT3-receptors in the CTZ (see phenothiazines, p. 135) and in the gut.


Particularly effective against vomiting induced by highly emetogenic chemo-therapeutic agents and radiotherapy used for treating malignancy and post-operative vomiting that is resistant to other agents.

Preparations and dose

Examples: dolasetron, granisetron, ondansetron, palonosetron.

Ondansetron Tablets: 4 mg; Inịection: 2 mg/mL; Zofran® syrup: 4 mg/5 mL; Suppositories: 16 mg.

■ Chemotherapy: 8mg by mouth, or 16 mg by rectum 1-2 hours before treatment; or by i.m./i.v. injection, 8 mg immediately before treat-ment, then by mouth, 8 mg every 12 hours; or by rectum, 16 mg daily. With severely emetogenic chemotherapy, treatment is given i.m./i.v. and continued by infusion 1 mg/h for up to 24 hours.

■ Prevention of post-operative nausea and vomiting: by mouth, 16 mg 1 hour before anaesthesia; or by i.m./i.v. injection, 4 mg at induction of anaesthesia.


Headache, constipation, hypersensitivity reactions. Following i.v. administra-tion: seizures, chest pain, arrhythmias, hypotension and bradycardia.


Caution with prolonged QT interval and cardiac conduction disorders.

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Ebook Essentials of Kumar and Clark's Clinical Medicine, 5e

1. Ethics and communication

Ethics and communication

2. Infectious diseases

Infectious diseases

3. Gastroenterology and nutrition

Gastroenterology and nutrition

4. Liver, biliary tract and pancreatic disease

Liver, biliary tract and pancreatic disease

5. Haematological disease

Haematological disease
Assessment and treatment of suspected neutropenic sepsis

6. Malignant disease

Malignant disease

7. Rheumatology

Clinical features, Investigations

8. Water, electrolytes and acid–base balance


9. Renal disease

Renal disease

10. Cardiovascular disease


11. Respiratory disease

Respiratory disease

12. Intensive care medicine

Intensive care medicine

13. Drug therapy, poisoning, and alcohol misuse

Drug therapy, poisoning, and alcohol misuse

14. Endocrine disease

Endocrine disease

15. Diabetes mellitus and other disorders of metabolism


16. The special senses


17. Neurology


18. Dermatology