Many gastrointestinal (and non-gastrointestinal) conditions are associated with vomiting (Table 6.1). This is controlled by a complex reflex involving central neural control centres located in the lateral reticular formation of the medulla which are stimulated by the chemoreceptor trigger zones (CTZs) in the floor of the fourth ventricle, and also by vagal afferents from the gut. The central zones are directly stimulated by toxins, drugs, motion sickness and metabolic disturbances. Raised intracranial pressure has a direct effect on the vomiting centre leading to vomiting. Luminal toxins, inflammation and mechanical obstruction are local GI causes of vomiting.

Table 6.1 Causes of vomiting: some examples

Diabetic ketoacidosis

Drugs

Antibiotics

Chemotherapy

Digoxin

Immunosuppressives such as azathioprine

Levodopa

Opiates

Reflex

Myocardial infarction

Nausea is a feeling of wanting to vomit, often associated with autonomic effects including salivation, pallor and sweating. It often precedes actual vomiting. Retching is a strong involuntary unproductive effort to vomit associated with abdominal muscle contraction but without expulsion of gastric contents through the mouth.

Faeculent vomit suggests low intestinal obstruction or the presence of a gastrocolic fistula.

Haematemesis is vomiting fresh or altered blood (‘coffee-grounds’) (see p. 254).

Early-morning nausea and vomiting is seen in pregnancy, alcohol dependence and some metabolic disorders (e.g. uraemia).

Persistent nausea alone is often stress-related and is not due to gastrointestinal disease.

Flatulence

This term describes excessive wind. It is used to indicate belching, abdominal distension, gurgling and the passage of flatus per rectum. Swallowing air (aerophagia) is described on page 296. Some of the swallowed air passes into the intestine where most of it is absorbed, but some remains to be passed rectally. Colonic bacterial breakdown of non-absorbed carbohydrate also produces gas. Rectal flatus thus consists of nitrogen, carbon dioxide, hydrogen and methane. It is normal to pass rectal flatus up to 20 times/day. Causes of increased gas production and intake include high-fibre diet and carbonated drinks.

Diarrhoea and constipation

These are common complaints and in the community are not usually due to serious disease. They are described in detail on pages 291 and 282, respectively. Some general rules concerning the aetiology and investigation of diarrhoea are shown in Box 6.1.

Box 6.1

Simple rules in diarrhoea

A single episode of diarrhoea is commonly due to dietary indiscretion or anxiety.

Large volume watery stools always have an organic cause.

Bloody diarrhoea implies colonic and/or rectal disease.

Acute diarrhoea lasting 2–5 days is most often due to an infective cause.

– Stool cultures should be taken to exclude an infective cause.

Patients often consider themselves constipated if their bowels are not open on most days, though normal stool frequency is very variable, from 3 times daily to 3 times a week. The difficult passage of hard stool is also regarded as constipation, irrespective of stool frequency. Constipation with hard stools is rarely due to organic colonic disease.

Abdominal pain

Pain is stimulated mainly by the stretching of smooth muscle or organ capsules. Severe acute abdominal pain can be due to a large number of gastrointestinal conditions, and normally presents as an emergency (see p. 298). An apparent ‘acute abdomen’ can occasionally be due to referred pain from the chest, as in pneumonia or to metabolic causes, such as diabetic ketoacidosis or porphyria.

Check:

Site (Fig. 6.2), intensity, character, duration and frequency of the pain

Aggravating and relieving factors

Associated symptoms, including non-gastrointestinal symptoms.

Figure 6.2 The abdominal quadrants.

Anorexia and weight loss

Anorexia describes reduced appetite. It is common in systemic disease and may be seen in psychiatric disorders. Anorexia often accompanies cancer but is usually a late symptom and not of diagnostic help. Weight loss is almost always due to reduced food intake and is a frequent accompaniment of gastrointestinal diseases. Weight loss in malabsorption disorders is primarily due to anorexia. Weight loss with a normal or increased dietary intake only occurs with hyperthyroidism and other catabolic states. Weight loss should always be assessed objectively as patients’ impressions are unreliable.

Examination of the abdomen

Inspection

Look for abdominal distension. Common causes (the five Fs) are: flatus, fat, fetus, fluid and faeces. Intermittent distension is most commonly a feature of functional bowel disorders.

Palpation

Look for palpable masses or abdominal tenderness. All abdominal quadrants should be palpated in turn followed by deeper palpations; remember to watch the patient’s face for signs of pain or discomfort. Evaluate any palpable mass and note its size, shape and consistency and whether it moves with respiration, to decide which organ is involved. Some abdominal organs may be just palpable normally, usually in thin people (Fig. 6.3). Reidel’s lobe is an anatomical variant consisting of a palpable enlargement of the lateral portion of the right lobe of the liver. The hernial orifices should be examined if intestinal obstruction is suspected.

Figure 6.3 The organs sometimes palpable in thin subjects.

Percussion

Abdominal percussion detects the areas of dullness caused by the liver and spleen, ascites or over masses. It can also detect a full bladder. Ascites is a term for excess fluid in the peritoneal cavity. It is detected clinically by central abdominal resonance due to gas within small bowel loops with dullness in the flanks which shifts when the patient lies on their side. This ‘shifting dullness’ is a reliable physical sign, if 1–2 L of fluid are present.

Auscultation

Auscultation is not of great value in abdominal disease, except for evaluation of bowel sounds in the acute abdomen (see p. 299). Abdominal bruits are often present in normal subjects and are rarely clinically significant.

A succussion splash suggests gastric outlet obstruction if the patient has not drunk for 2–3 hours. The splash of fluid in the stomach can be heard with a stethoscope laid on the abdomen when the patient is moved.

Examination of the rectum and sigmoid colon

A digital examination of the rectum should be performed in all patients with a change in bowel habit, rectal bleeding and prior to proctoscopy or sigmoidoscopy.

Proctoscopy (see Practical Box 6.1) is performed in all patients with a history of bright red rectal bleeding to look for anorectal pathology such as haemorrhoids; a rigid sigmoidoscope is too narrow and long to enable adequate examination of the anal canal.

Sigmoidoscopy is part of the routine hospital examination in cases of diarrhoea and in patients with lower abdominal symptoms such as a change in bowel habit or rectal bleeding. The rigid sigmoidoscope allows inspection of a maximum of 20–25 cm of distal colon.

Flexible sigmoidoscopy (FS) (60 cm) can reach up to the splenic flexure, and can be performed in the outpatient department or endoscopy unit after evacuation of the distal colon using an enema or suppository. FS can be used in patients with increased stool frequency or looseness or rectal bleeding to diagnose colitis or polyps. Most rectal bleeding is due to benign anorectal disease (haemorrhoids or fissure-in-ano) and an otherwise normal FS can be reassuring to avoid over-investigation. Up to 60% of colonic neoplasms occur within the range of FS (see Fig. 6.45) and it has therefore been proposed as screening test for colorectal cancer in asymptomatic individuals.

Practical Box 6.1

Sigmoidoscopy and proctoscopy

Proctoscopy

1. The proctoscope is passed into the anus and the obturator is removed.

2. The patient strains down as the proctoscope is removed.

3. Haemorrhoids are seen as purplish veins in the left lateral, right posterior or right anterior positions.

4. Fissures may also be seen, but pain often prevents the procedure from being performed.

Stool examination

It is useful to confirm a patient’s account (e.g. passing of blood or steatorrhoea). The shape and size may be helpful (e.g. ‘rabbit dropping’ or ribbon-like stools in the irritable bowel syndrome). Stool charts for recording consistency and frequency of defecation are useful in inpatients to follow the progress of diarrhoea, particularly in the management of severe colitis. The Bristol Stool Chart is commonly used in the UK (Fig. 6.4).

Figure 6.4 The Bristol Stool Chart.

Investigations

Routine haematology and biochemistry, followed by endoscopy and radiology, are the principal investigations. The investigation of small bowel disease is discussed in more detail on page 267. Manometry is mainly used in oesophageal disease (see p. 237) and anorectal disorders (see p. 286).

Endoscopy

Video endoscopes have replaced fibreoptic instruments and relay colour images to a high definition television monitor. The tip of the endoscope can be angulated in all directions. Channels in the instrument are used for air insufflation, water injection, suction, and for the passage of accessories such as biopsy forceps or brushes for obtaining tissue, snares for polypectomy and needles for injection therapies. Permanent photographic or video records of the procedure can be obtained.

Oesophagogastroduodenoscopy (OGD, ‘gastroscopy’) is the investigation of choice for upper GI disorders with the possibility of therapy and mucosal biopsy. Findings include reflux oesophagitis, gastritis, ulcers and cancer. Therapeutic OGD is used to treat upper GI haemorrhage and both benign and malignant obstruction. Relative contraindications include severe chronic obstructive pulmonary disease, a recent myocardial infarction, or severe instability of the atlantoaxial joints. The mortality for diagnostic endoscopy is 0.001% with significant complications in 1 : 10 000, usually when performed as an emergency (e.g. GI haemorrhage).

Colonoscopy allows good visualization of the whole colon and terminal ileum. Biopsies can be obtained and polyps removed. Benign strictures can be dilated and malignant strictures stented. The success rate for reaching the caecum should be at least 90% after training. Cancer, polyps and diverticular disease are the commonest significant findings. Perforation occurs in 1 : 1000 examinations but this is higher (up to 2%) after polypectomy (see Practical Box 6.2).

Balloon enteroscopy, either double or single balloon, can examine the small bowel from the duodenum to the ileum using specialized enteroscopes in expert centres.

Capsule endoscopy is used for the evaluation of obscure GI bleeding (after negative gastroscopy and colonoscopy) and for the detection of small bowel tumours and occult inflammatory bowel disease. It should be avoided if strictures are suspected.

Practical Box 6.2

Gastroscopy and colonoscopy

Explain the procedure to the patient, including benefits and risks.

Discuss the need for sedation.

Obtain written informed consent.

Colonoscopy

1. Stop oral iron a week before the procedure.

2. Restrict diet to low residue foods for 48 hours; clear fluids only for 24 hours.

3. Use local bowel cleansing regime, usually starting 24 hours beforehand (e.g. two sachets of sodium picosulfate with magnesium citrate and 2–4 bisacodyl tablets, or macrogols 2–4 L, or local alternative; more if constipated).

4. Give oxygen and monitor O₂ levels.

5. Give sedation (midazolam ± opiate) if required by patient.

6. Pass the colonoscope to the caecum or ileum under direct vision.

7. Examine in detail during withdrawal.

8. Colonoscopy takes 15–30 min, depending on the colon anatomy, indication and findings.

9. Withhold fluid and food until sedation wears off.

10. Observe patient for at least an hour after sedation given.

11. Complications are rare: beware of over-sedation, perforation and aspiration.

12. Patient must be accompanied home if sedation given.

Imaging

Full clinical information must be provided before the examination, and ideally, the images obtained should be reviewed with the radiologist to aid interpretation. The optimal technique to be used will depend on local expertise.

Plain X-rays of the chest and abdomen are chiefly used in the investigation of an acute abdomen. Interpretation depends on analysis of gas shadows inside and outside the bowel. Plain films are particularly useful where obstruction or perforation is suspected, to exclude toxic megacolon in colitis and to assess faecal loading in constipation. Calcification may be seen with gall bladder stones and in chronic pancreatitis, though CT is more sensitive for both.

Ultrasound involves no radiation and is the first-line investigation for abdominal distension, e.g. ascites, mass or suspected inflammatory conditions. It can show dilated fluid-filled loops of bowel in obstruction, and thickening of the bowel wall. It can be used to guide biopsies or percutaneous drainage. In an acute abdomen, ultrasound can diagnose cholecystitis, appendicitis, enlarged mesenteric glands and other inflammatory conditions.

Endoscopic ultrasound (EUS) is performed with a gastroscope incorporating an ultrasound probe at the tip. It is used diagnostically for lesions in the oesophageal or gastric wall, including the detailed TNM staging (see p. 245) of oesophageal/gastric cancer and for the detection and biopsy of pancreatic tumours and cysts.

Endoanal and endorectal ultrasonography are performed to define the anatomy of the anal sphincters (see p. 285), to detect perianal disease and to stage superficial rectal tumours.

Computed tomography involves a significant dose of radiation (approximately 10 millisieverts). Modern multislice fast scanners and techniques involving intraluminal and intravenous contrast enhance diagnostic capability. Intraluminal contrast may be positive (Gastrografin or Omnipaque) or negative (usually water). The bowel wall and mesentery are well seen after intravenous contrast especially with negative intraluminal contrast. Clinically unsuspected diseases of other abdominal organs are quite often also revealed (Fig. 6.5a).

CT is widely used as a first-line investigation for the acute abdomen. CT is sensitive for small volumes of gas from a perforated viscus as well as leakage of contrast from the gut lumen.

Inflammatory conditions such as abscesses, appendicitis, diverticulitis, Crohn’s disease and its complications are well demonstrated. In high-grade bowel obstruction, CT is usually diagnostic of both the presence and the cause of the obstruction.

CT is widely used in cancer staging and as guidance for biopsy of tumour or lymph nodes.

CT pneumocolon/CT colonography (virtual colonoscopy) after CO₂ insufflation into a previously cleansed colon provides an alternative to colonoscopy for diagnosis of colon mass lesions (Fig. 6.5b). It is being evaluated as a screening test for colon pathology with sensitivities of over 90% for >10 mm polyps.

Unprepared CT is a good test for colon cancer in the frail (often elderly) patient who would have problems with bowel preparation.

Figure 6.5 (a) CT scan of the normal abdomen at the level of T12. (1) Aorta; (2) spine; (3) top of right kidney; (4) liver; (5) gall bladder; (6) stomach (containing air); (7) pancreas; (8) spleen. (b) CT cross-sectional (2-dimensional) image of a colonic polyp on a long stalk. The colon has been emptied as for visual colonoscopy. The pedunculated polyp and its stalk show enhancement after intravenous contrast. (c) 3D reconstruction of part of the colon (false colour) generated by a computer program from multiple axial CT images. A sessile polypoid lesion is shown.

(b and c: Courtesy of Dr Paul Jenkins.)

Magnetic resonance imaging. MRI uses no radiation and is particularly useful in the evaluation of rectal cancers and abscesses and fistulae in the perianal region. It is also useful in small bowel disease and in hepatobiliary and pancreatic disease.

Positron emission tomography (PET) relies on detection of the metabolism of fluorodeoxyglucose. It is used for staging oesophageal, gastric and colorectal cancer and in the detection of metastatic and recurrent disease. PET/CT adds additional anatomical information.

Contrast studies

Barium swallow examines the oesophagus and proximal stomach. Its main use is for investigating dysphagia.

Double-contrast barium meal examines the oesophagus, stomach and duodenum. Barium is given to produce mucosal coating and effervescent granules producing carbon dioxide in the stomach create a double contrast between gas and barium. This test has a high accuracy for the detection of significant pathology – ulcers and cancer – but requires good technique. Gastroscopy is a more sensitive test and enables biopsy of suspicious areas.

Small bowel meal or follow-through specifically examines the small bowel. Ingested barium passes through the small bowel into the right colon. The fold pattern and calibre of the small bowel are assessed. Specific views of the terminal ileum can be obtained and are used to identify early changes in patients with suspected Crohn’s disease.

Small bowel enema (enteroclysis) is an alternative specific technique for small bowel examination. A tube is passed into the duodenum and a large volume of dilute barium is introduced. It is particularly used to demonstrate strictures or adhesions when there is suspicion of intermittent obstruction. Generally, this has been replaced by MR enteroclysis.

Barium enema examines the colon and is used for altered bowel habit. Colonoscopy and CT colonography have largely replaced this examination for rectal bleeding, polyps and inflammatory bowel disease.

Absorbable water-soluble (Gastrografin or Omnipaque) contrast agents should be used in preference to barium when perforation is suspected anywhere in the gut.

Radioisotopes

Radionuclides are used to a varying degree depending on availability and expertise. Some more common indications and techniques:

Detect urease activity of Helicobacter pylori – ¹³C urea breath test (see p. 249)

Assess oesophageal reflux – gamma camera scan after oral [^99mTc]technetium-sulphur colloid

Measure rate of gastric emptying – sequential gamma camera scans after oral [^99mTc]technetium-sulphur colloid or ¹¹¹In-DTPA (indium-labelled diethylene triamine penta-acetic acid)

Demonstrate a Meckel’s diverticulum – gamma camera scan after i.v. [^99mTc]pertechnetate, which has affinity for gastric mucosa

Assess extent of inflammation and presence of inflammatory collections in inflammatory bowel disease – gamma camera scan after i.v. ^99mTc-HMPAO (hexamethylpropylene amine oxime) labelled white cells

Evaluate neuroendocrine tumours and their metastases – gamma camera scan after i.v. radiolabelled octreotide or MIBG (meta-iodobenzylguanidine)

Assess obscure gastrointestinal bleeding – gamma camera abdominal scan after i.v. injection of red cells labelled with ^99mTc (only useful if the bleeding is >2 mL/min)

Measure albumin loss in the stools (in protein-losing enteropathy) – following albumin labelled in vivo with i.v. ⁵¹CrCl₃. This test has been replaced by the measurement of the intestinal clearance of α₁ antitrypsin

Assess bile salt malabsorption (in patients with unexplained diarrhoea) – gamma camera scan to measure both isotope retention and faecal loss of orally administered ⁷⁵selenium-homocholic acid taurine (SeHCAT) (see p. 293)

Detect bacterial overgrowth in the small bowel – measure ¹⁴CO₂ in breath following oral ¹⁴C glycocholic acid.

The mouth

The oral cavity extends from the lips to the pharynx and contains the tongue, teeth and gums. Its primary functions are mastication, swallowing and speech. Problems in the mouth are extremely common and, although they may be trivial, they can produce severe symptoms. Poor dental hygiene is often a factor.

Recurrent aphthous ulceration

Idiopathic aphthous ulceration is common and affects up to 25% of the population. Recurrent painful round or ovoid mouth ulcers are seen with inflammatory halos. They are commoner in females and non-smokers, usually appear first in childhood and tend to reduce in number and frequency before age 40. Other family members may be affected. There is no sign of systemic disease.

Minor aphthous ulcers are the most common, are <10 mm diameter, have a grey/white centre with a thin erythematous halo and heal within 14 days without scarring. They rarely affect the dorsum of the tongue or hard palate.

Major aphthous ulcers (>10 mm diameter) often persist for weeks or months and heal with scarring.

The cause is not known. Deficiencies of iron, folic acid or vitamin B₁₂ (with or without gastrointestinal disorders) are sometimes found but are not causally linked. Secondary causes, e.g. Crohn’s disease, should be excluded.

There are no specific effective therapies. Sufferers should avoid oral trauma and acidic foods or drinks which cause pain. Topical (1% triamcinolone) or systemic corticosteroids may lessen the duration and severity of the attacks. Chlorhexidine gluconate or tetracycline mouthwash, dapsone, colchicine, thalidomide and azathioprine have all been used with variable effect.

Neoplasia (squamous cell carcinoma)

Malignant tumours of the mouth account for 1% of all malignant tumours in the UK. The majority develop on the floor of the mouth or lateral borders of the tongue. Early lesions may be painless, but advanced tumours are easily recognizable as hard indurated ulcers with raised and rolled edges. Aetiological agents include tobacco, heavy alcohol consumption and the areca nut. Human papillomavirus 16 causes some oral cancers. Premalignant lesions include leucoplakia (single adherent white patch), lichen planus, submucous fibrosis and erythroplakia (a red patch).

Treatment is by surgical excision which may require extensive neck dissection to remove involved lymph nodes and/or radiotherapy. Ablative treatment with photodynamic therapy is being pioneered for early lesions.

Oral white patches

Transient white patches are either due to Candida infection or are very occasionally seen in systemic lupus erythematosus. Local causes include mechanical, irritative or chemical trauma from drugs (e.g. ill fitting dentures or aspirin). Oral candidiasis in adults is seen following therapy with broad-spectrum antibiotics or inhaled steroids and in people with diabetes, patients who are seriously ill or immunocompromised.

Persistent white patches can be due to leucoplakia, which is associated with alcohol and (particularly) smoking, and is premalignant. A biopsy should always be taken; histology shows alteration in the keratinization and dysplasia of the epithelium. Treatment is unsatisfactory. Isotretinoin possibly reduces disease progression. Oral lichen planus presents as white striae, which can rarely extend into the oesophagus.

Oral pigmented lesions

Non-neoplastic lesions

Racial pigmentation is scattered and symmetrically distributed. Amalgam tattoo is the most common form of localized oral pigmentation and consists of blue-black macules involving the gingivae and results from dental amalgam sequestering into the tissues. Diseases causing pigmentation include Peutz–Jeghers syndrome and Addison’s disease. Heavy metals, such as lead, bismuth and mercury, and drugs (e.g. phenothiazines and antimalarials) all cause pigmentation of the gums.

Neoplastic lesions

These include melanotic naevi on the hard palate and buccal mucosa. These are rarer in the mouth than on the skin. Malignant melanomas are rare, more common in males and occur mainly on the upper jaw. The 5-year survival is only 5%.

The tongue

The tongue may be affected by inflammatory or malignant processes with similar lesions to those described above.

Glossitis is a red, smooth, sore tongue associated with B₁₂, folate or iron deficiency. It is also seen in infections due to Candida and in riboflavin and nicotinic acid deficiency.

A black hairy tongue is due to a proliferation of chromogenic microorganisms causing brown staining of elongated filiform papillae. The causes are unknown, but heavy smoking and the use of antiseptic mouthwashes have been implicated.

A geographic tongue is an idiopathic condition occurring in 1–2% of the population and may be familial. There are erythematous areas surrounded by well-defined, slightly raised irregular margins. The lesions are usually painless and the patient should be reassured.

The gums

The gums (gingivae) are the mucous membranes covering the alveolar processes of the mandible and the maxilla.

Chronic gingivitis follows the accumulation of bacterial plaque. It resolves when the plaque is removed. It is the most common cause of bleeding gums.

Acute (necrotizing) ulcerative gingivitis (‘Vincent’s angina’) is characterized by the proliferation of spirochaete and fusiform bacteria associated with poor oral hygiene and smoking. Treatment is with oral metronidazole 200 mg three times daily for 3 days, improved oral hygiene and chlorhexidine gluconate mouthwash.

Desquamative gingivitis is a clinical description of smooth, red atrophic gingivae caused by lichen planus or mucous membrane pemphigoid. The diagnosis is confirmed by biopsy.

Gingival swelling may be due to inflammation or fibrous hyperplasia. The latter may be hereditary (gingival fibromatosis) or associated with drugs (e.g. phenytoin, ciclosporin, nifedipine). Inflammatory swellings are seen in pregnancy, gingivitis and scurvy. Swelling due to infiltration is seen in acute leukaemia and Wegener’s granulomatosis.

The teeth

Dental caries occur as a result of bacterial damage to tooth structures leading to tooth decay and ‘cavities’. The main cause in man is Streptococcus mutans, which is cariogenic only in the presence of dietary sugar. Dental caries can progress to pulpitis and pulp necrosis, and spreading infection can cause dentoalveolar abscesses. If there is soft tissue swelling, antibiotics (e.g. amoxicillin or metronidazole) should be prescribed prior to dental intervention.

Erosion of the teeth can result from exposure to acid (e.g. in bulimia nervosa) or, very occasionally, in patients with gastro-oesophageal reflux disease.

Oral manifestations of HIV infection

HIV-infected patients often have characteristic oral lesions. Lesions strongly associated with HIV infection include candidiasis (with erythema and/or white exudates), erythematous candidiasis, oral hairy leucoplakia, Kaposi’s sarcoma, non-Hodgkin’s lymphoma, necrotizing ulcerative gingivitis and necrotizing ulcerative periodontitis and are described elsewhere.

All oral lesions are much less common since the introduction of HAART (in Chapter 4).

The salivary glands

Excessive salivation (ptyalism) may occur prior to vomiting or be secondary to other intraoral pathology. It can be psychogenic.

Dry mouth (xerostomia) can result from a variety of causes:

Sjögren’s syndrome

Drugs (e.g. antimuscarinic, antiparkinsonian, antihistamines, lithium, monoamine oxidase inhibitors, tricyclic and related antidepressants, and clonidine)

Radiotherapy

Psychogenic

Dehydration, shock and chronic kidney disease.

The principles of management are to preserve what flow remains, stimulate flow and replace saliva (glycerine and lemon mouthwash and artificial saliva).

Sialadenitis

Acute sialadenitis is viral (mumps, p. 110) or bacterial. Bacterial sialadenitis is a painful ascending infection with Staphylococcus aureus, Streptococcus pyogenes and Strep. pneumoniae, usually secondary to secretory failure. Pus can be expressed from the affected duct.

Salivary duct obstruction due to calculus

Obstruction to salivary flow is usually due to a calculus. There is a painful swelling of the submandibular gland after eating and stones can sometimes be felt in the floor of the mouth. Plain X-ray films and sialography will show the calculus; removal of the obstruction by sialoendoscopy gives complete relief.

Sarcoidosis (see also p. 845)

Sarcoidosis can involve the major salivary glands as part of Heerfordt’s syndrome (uveoparotid fever).

Neoplasms

Salivary gland neoplasms account for 3% of all tumours worldwide. The majority occur in the parotid gland. The pleomorphic adenoma is the most common and 15% of these undergo malignant transformation. Malignant tumours classically result in lower motor neurone 7th cranial nerve signs. Recurrence following surgical excision is common.

The pharynx and oesophagus

Structure and physiology

The oesophagus is a muscular tube approximately 20 cm long that connects the pharynx to the stomach just below the diaphragm. Its only function is to transport food from the mouth to the stomach. In the upper portion of the oesophagus, both the outer longitudinal layer and inner circular muscle layers are striated. In the lower two-thirds of the oesophagus, including the thoracic and abdominal parts containing the lower oesophageal sphincter, both layers are composed of smooth muscle.

The oesophagus is lined by stratified squamous epithelium, which extends distally to the squamocolumnar junction where the oesophagus joins the stomach, recognized endoscopically by a zig-zag (‘Z’) line, just above the most proximal gastric folds.

The oesophagus is separated from the pharynx by the upper oesophageal sphincter (UOS), which is normally closed due to tonic activity of the nerves supplying the cricopharyngeus. The lower oesophageal sphincter (LOS) consists of a 2–4 cm zone in the distal end of the oesophagus that has a high resting tone and, assisted by the diaphragmatic sphincter, is largely responsible for the prevention of gastric reflux.

Swallowing

During swallowing, the bolus of food is voluntarily moved from the mouth to the pharynx. This process is mediated by a complex reflex involving a swallowing centre in the dorsal motor nucleus of the vagus in the brainstem. Once activated, the swallowing centre neurones send pre-programmed discharges of inhibition followed by excitation to the motor nuclei of the cranial nerves. This results in initial relaxation, followed by distally progressive activation of neurones to the oesophageal smooth muscle and LOS. Pharyngeal and oesophageal peristalsis mediated by this swallowing reflex causes primary peristalsis. Secondary peristalsis arises as a result of stimulation by a food bolus in the lumen, mediated by a local intra-oesophageal reflex. Tertiary contractions indicate pathological non-propulsive contractions resulting from aberrant activation of local reflexes within the myenteric plexus.

The smooth muscle of the thoracic oesophagus and lower oesophageal sphincter is supplied by vagal autonomic motor nerves consisting of extrinsic preganglionic fibres and intramural postganglionic neurones in the myenteric plexus (Fig. 6.6). There are parallel excitatory and inhibitory pathways.

Figure 6.6 Innervation of the oesophagus. The excitatory pathway consists of vagal preganglionic neurones releasing acetylcholine (ACh), connecting to postganglionic neurones that release ACh and substance P. The inhibitory pathway consists of vagal preganglionic neurones releasing ACh, connecting to postganglionic neurones that release nitric oxide (NO), vasoactive intestinal peptide (VIP), adenosine triphosphate (ATP) and substance P (SP).

Symptoms of oesophageal disorders

Major oesophageal symptoms are:

Dysphagia, or difficulty in swallowing, is defined as a sensation of obstruction during the passage of liquid or solid through the pharynx or oesophagus, i.e. within 15 s of food leaving the mouth. The characteristics of the progression of dysphagia to solids can be helpful, e.g. intermittent slow progression with a history of heartburn suggests a benign peptic stricture; relentless progression over a few weeks suggests a malignant stricture. The slow onset of dysphagia for solids and liquids at the same time suggests a motility disorder, e.g. achalasia (see p. 237). The causes are shown in Table 6.3.

Odynophagia is pain during the act of swallowing and is suggestive of oesophagitis. Causes include reflux, infection, chemical oesophagitis due to drugs such as bisphosphonates or slow-release potassium or associated with oesophageal stenosis.

Substernal discomfort, heartburn. This is a common symptom of reflux of gastric contents into the oesophagus. It is usually a retrosternal burning pain that can spread to the neck, across the chest, and when severe can be difficult to distinguish from the pain of ischaemic heart disease. It is often worst lying down at night when gravity promotes reflux or on bending or stooping.

Regurgitation is the effortless reflux of oesophageal contents into the mouth and pharynx. Uncommon in normal subjects, it occurs frequently in patients with gastro-oesophageal reflux disease or organic stenosis.

Table 6.3 Causes of dysphagia

Signs of oesophageal disorders

The main sign of oesophageal disease is weight loss due to reduced food intake. Cervical lymphadenopathy with cancer is uncommon. Rarely a pharyngeal pouch may be seen to swell the neck during drinking.

Investigations available for oesophageal disorders

Barium swallow and meal.

Oesophagoscopy.

Manometry (Fig. 6.7) is performed by passing a catheter through the nose into the oesophagus and measuring the pressures generated within the oesophagus. It is used to assess oesophageal motor activity. It is not a primary investigation and should be performed only when the diagnosis has not been achieved by history, barium radiology or endoscopy. Recordings are usually made over a short time period, or much more rarely for up to 24 h. High resolution manometry has superseded conventional manometry and the greater concentration of pressure sensors enables the identification of a wider range of abnormalities of oesophageal function with a greater diagnostic accuracy.