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The Mouth 73
self-limiting episodes of painful oral ulcers (rarely on the palate). Topical
corticosteroids are used for symptomatic relief, but they have no effect on
the natural history. In a few cases ulcers are associated with trauma or
gastrointestinal and systemic diseases, e.g. anaemia, inflammatory bowel
disease, coeliac disease, Behçet’s disease, Reiter’s disease, systemic lupus
erythematosus (SLE), 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.
Infective
Many infections can affect the mouth, though the most common are viral
and include herpes simplex virus type 1, Coxsackie A virus and herpes zoster
virus.
Oral white patches
Transient white patches are commonly due to Candida infection, but very
occasionally may be due to SLE. 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. Local
causes of white patches include mechanical, irritative or chemical trauma
from drugs (e.g. ill-fitting dentures or aspirin).
Persistent white patches may be due to leucoplakia, which is premalignant and associated with alcohol and (particularly) smoking. 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.
The tongue
The tongue may be affected by inflammatory or malignant processes with
similar lesions to those described above.
• Glossitis is a red, smooth, painful tongue associated with deficiencies
of vitamin B12, folate, iron, riboflavin and nicotinic acid. It is also seen in
infections due to Candida.
• 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
74 Gastroenterology and nutrition
are usually painless and may persist for days, months or years. The
symptoms often resolve but may reoccur at a later date. No specific
management is required other than reassurance.
Periodontal disorders
Gum bleeding is most commonly caused by gingivitis, an inflammatory
condition of the gums associated with dental plaque. Bleeding may also
be associated with generalized conditions such as bleeding disorders and
leukaemia. Acute ulcerative gingivitis (Vincent’s infection) is characterized by
the development 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 malnourished and
immunocompromised patients. Treatment is with oral metronidazole and
good oral hygiene.
Salivary gland disorders
Xerostomia (mouth dryness) may be caused by anxiety, drugs (e.g. tricyclic
antidepressants), Sjögren’s syndrome and dehydration. Infection (parotitis)
may be viral (e.g. mumps) or bacterial (e.g. staphylococci or streptococci).
Calculus formation usually occurs in the duct of the submandibular 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. Treatment is with surgical resection. Involvement of the VIIth cranial nerve raises the suspicion of malignancy.
THE OESOPHAGUS
Symptoms of oesophageal disorders
• Dysphagia (difficulty in swallowing) has mechanical and neuromuscular
causes (see Table 3.1). A short history of progressive dysphagia initially
for solids and then liquids is suggestive of a mechanical stricture.
Investigation is with an urgent OGD particularly to look for a malignant
oesophageal stricture. A barium swallow is more appropriate as the
first-line investigation when the history suggests a motility disorder
such as achalasia (slow onset of dysphagia for both solids and liquids).
Oesophageal manometry may also 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. 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.
The Oesophagus 75
• 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)
Pathophysiology
The reflux of gastric acid, pepsin, bile and duodenal contents back in to the
oesophagus can be influenced by many factors which overcome the innate
defence mechanisms, primarily the lower oesophageal sphincter. Between
swallows, the muscles of the oesophagus are relaxed except for those of the
two sphincters. The lower oesophageal sphincter (LOS) in the distal oesophagus remains closed due to the unique property of the muscle and relaxes when
swallowing is initiated. Transient lower oesophageal sphincter relaxations
(TLESRs) are part of normal physiology, but occur more frequently in patients
with GORD, allowing gastric acid to flow back in to the oesophagus. Increased
abdominal pressure (e.g. pregnancy) and low LOS pressure also predispose to
GORD. 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,
systemic sclerosis and drugs (e.g. nitrates, tricyclic antidepressants).
Clinical features
Heartburn is the major symptom. There may also be regurgitation and odynophagia. Cough and nocturnal asthma can occur from aspiration of gastric
contents into the lungs. The correlation between heartburn and the severity
of oesophagitis is poor.
Investigations
GORD is a clinical diagnosis and most patients are treated without investigation. OGD is indicated in patients with new-onset heartburn over 55 years of
age or patients with ‘red-flag’ symptoms which may suggest an underlying
upper gastrointestinal malignancy (e.g. weight loss, dysphagia, haematemesis, anaemia). It is also performed to document complications of reflux (e.g.
Barrett’s oesophagus) and in patients who do not respond well to treatment.
The OGD may show oesophagitis (e.g. mucosal erythema, erosions and
ulceration), a hiatus hernia with or without Barrett’s oesophagus (p. 77) or, in
fact, it may be normal. In some patients 24-hour intraluminal pH monitoring
or impedance (p. 72) is used for the confirmation of GORD prior to surgery
or where there is an inadequate response to standard doses of proton pump
inhibitors (PPIs) (p. 130).
76 Gastroenterology and nutrition
Management
Conservative measures with lifestyle changes (e.g. weight loss, avoidance
of excess alcohol or aggravating foods, smoking cessation) and simple antacids are often sufficient for mild symptoms in the absence of oesophagitis.
Patients with severe symptoms or with proven pathology (e.g. oesophagitis)
require PPIs. Alginate-containing antacids are the most frequently used ‘over
the counter’ agents for GORD. They form a gel or ‘foam raft’ with gastric
contents to reduce reflux. Magnesium-containing antacids tend to cause
diarrhoea while aluminium-containing compounds may cause constipation.
Proton pump inhibitors (PPIs; e.g. omeprazole, lansoprazole, pantoprazole,
esomeprazole) inhibit gastric hydrogen/potassium-ATPase. PPIs reduce
gastric acid secretion by up to 90% and are the drugs of choice for all but
mild cases. Most patients with GORD will respond well, with approximately
60% symptom free after 4 weeks of a once-daily PPI. Patients with severe
symptoms may need twice-daily PPIs and prolonged treatment, often for
years. Once oesophageal sensitivity has normalized, a lower dose may be
sufficient for maintenance. Long-term PPI prescription is not uncommon
although recent evidence has suggested an increased risk of osteoporosis
and an association with Clostridium difficile infection. Patients who do not
respond to a PPI and have continuing symptoms with a normal endoscopy
are described as having non-erosive reflux disease (NERD).
H2-receptor antagonists (e.g. cimetidine, ranitidine, famotidine and
nizatidine) are frequently used for acid suppression if antacids fail, as they
can easily be obtained. They can be used in conjunction with PPIs for patients
with more severe GORD.
Dopamine antagonist prokinetic agents (e.g. metoclopramide,
domperidone) may be helpful as they enhance peristalsis and speed gastric
emptying, but there is little data to substantiate this. The role of domperidone
has been limited still further following reports of serious cardiac side effects.
Endoluminal gastroplication is an endoscopic procedure where multiple
plications or pleats are made below the gastro-oesophageal junction with the
aim of decreasing reflux of stomach acid into the oesophagus. Randomized
controlled trials have shown benefit with reduction in heartburn, acid reflux
episodes and PPI usage, but not sustained improvements in the oesophageal
pH measurements.
In more severe cases surgery may be required. This is performed
laparoscopically with the fundus of the stomach being sutured around the
lower oesophagus to produce an antireflux valve (Nissen fundoplication, ‘lap
wrap’). The indications for the operation are not clearly elucidated but include
intolerance to medication, the desire for freedom from medication, the expense
of therapy and the concern of long-term side effects. The best predictors of a
good surgical result are typical reflux symptoms with documented acid reflux,
which correlates with symptoms and response to PPI. The most common cause
of mechanical fundoplication failure is recurrent hiatus hernia.
The Oesophagus 77
The Linx Reflux Management System is a device with a row of magnets
which increase LOS closure pressure, allowing food passage during
swallowing. Patients with oesophageal dysmotility unrelated to acid reflux,
patients with no response to PPIs and those with underlying functional bowel
disease should rarely have surgery.
Complications
Peptic stricture
Since the advent of PPIs peptic strictures have become far less common.
They usually occur in patients over the age of 60 and present with intermittent dysphagia for solids which worsens gradually over a long period. Mild
cases may respond to PPI alone. More severe cases need endoscopic dilatation and long-term PPI therapy. Surgery is required if medical treatment fails.
Barrett’s oesophagus
Barrett’s oesophagus describes a condition in which part of the normal
oesophageal squamous epithelium is replaced by metaplastic columnar
mucosa to form a segment of ‘columnar-lined oesophagus’ (CLO). It is a
complication of GORD and there is almost always a hiatus hernia present. It is
diagnosed at endoscopy where proximal displacement of the squamocolumnar mucosal junction can be seen and biopsies demonstrate columnar lining
above the proximal gastric folds. Intestinal metaplasia is no longer a requirement of the British Society of Gastroenterology definition, but is central to the
American College of Gastroenterology guidelines.
Central obesity increases the risk of Barrett’s by 4.3 times. Long-segment
(>3 cm) and short-segment (<3 cm) Barrett’s is found, respectively, in 5%
and 15% of patients undergoing endoscopy for reflux symptoms. It is also
often found incidentally in endoscoped patients without reflux symptoms.
The major concern is that up to 0.5% of patients with Barrett’s oesophagus
develop oesophageal adenocarcinoma per year, likely through gradual
transformation from intestinal metaplasia to low-grade then high-grade
dysplasia, before invasive adenocarcinoma. A typical patient with Barrett’s
oesophagus has a lifetime risk of developing oesophageal carcinoma of 1%.
Although there is an absence of high-quality evidence, endoscopic
surveillance of Barrett’s oesophagus is recommended by some. This involves
use of a high-definition gastroscope and targeted biopsies taken of any
focally abnormal tissue in addition to random biopsies. Chromo-endoscopy
(topical application of stains or pigments via the endoscope), narrow band, and
autofluorescence imaging may aid the diagnosis of dysplasia and carcinoma.
Endoscopic technology has improved the detection of pre-malignant lesions,
enabling removal with either endoscopic mucosal resection (EMR) or endoscopic
submucosal dissection, therefore preventing surgical oesophagectomy.
If low-grade dysplasia is found on endoscopic surveillance, a repeat
endoscopy with quadrantic biopsies every 1 cm is usually performed within
78 Gastroenterology and nutrition
6months, while on high-dose PPI. Recent guidelines now suggest that if lowgrade dysplasia persists then patients should be offered endoscopic ablation
therapy or 6-monthly surveillance.
If high-grade dysplasia is found, it is usually in the context of an
endoscopically visible lesion which, if nodular, is removed by EMR for
more accurate histological staging. If high-grade dysplasia is detected in
the absence of any endoscopically visible lesion, high-dose proton pump
inhibition is started and repeat biopsies taken within 3 months. Endoscopic
ultrasound is frequently used to more accurately stage this patient group to
exclude cancer and associated significant lymphadenopathy.
Radiofrequency ablation (RFA) has superseded photodynamic therapy as
the technique of choice for endoscopic treatment of dysplasia within Barrett’s
segments following removal of any nodular lesions, returning the oesophagus
to squamous lining. The benefit of RFA in low-grade dysplasia is currently
under evaluation.
Achalasia
Achalasia is a condition of unknown aetiology characterized by oesophageal
aperistalsis and impaired relaxation of the lower oesophageal sphincter. The
lower oesophageal pressure is elevated in more than half of patients.
Clinical features
The incidence of achalasia is 1:100 000 with an equal male to female ratio.
It occurs at all ages although 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.
Investigations
• Chest X-ray shows a dilated oesophagus, sometimes with a fluid level
seen behind the heart. The fundal gas shadow is absent.
• Barium swallow shows lack of peristalsis and often synchronous
contractions in the body of the oesophagus, sometimes with dilatation. The
lower end shows a ‘bird’s beak’ due to failure of the sphincter to relax.
• Oesophagogastroduodenoscopy is performed to exclude a carcinoma at
the lower end of the oesophagus, as this can produce a similar X-ray
appearance. When there is marked dilatation, a 24-hour liquid-only diet
and a washout, prior to endoscopy, is useful to remove food debris. In
true achalasia, the endoscope passes through the lower oesophageal
sphincter with little resistance.
• CT scan excludes distal oesophageal cancer.
• Manometry shows aperistalsis of the oesophagus and failure of
relaxation of the lower oesophageal sphincter.
The Oesophagus 79
Management
All current forms of treatment for achalasia are for symptom relief. Drug
therapy rarely produces satisfactory or durable relief; nifedipine, nitrates or
sildenafil can be tried.
Endoscopic and surgical therapies are equally effective. Endoscopic dilation
of the LOS weakens the sphincter and is initially successful in around 80% of
cases although 50% of patients require a second or third dilation in the first
5 years. There is a 2% risk of oesophageal perforation. Surgical division of
the LOS (Heller’s cardiomyotomy) is the surgical treatment of choice. Per oral
endoscopic myotomy (POEM) is a novel technique, which is a division of the LOS
using a gastroscope. The early results show great promise. Reflux oesophagitis
complicates all procedures and the aperistalsis of the oesophagus remains.
Complications
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 the 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: diffuse oesophageal 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
(‘corkscrew’ appearance in diffuse oesophageal spasm) and manometry.
Nitrates and calcium channel blockers, e.g. oral nifedipine, sometimes help
symptoms. Treatment of GORD may help.
Hiatus hernia
Part of the stomach herniates through the oesophageal hiatus of the
diaphragm:
• Sliding hernias account 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.
80 Gastroenterology and nutrition
• 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 and should be treated surgically.
Benign oesophageal strictures
In developed countries, benign peptic stricture is most commonly secondary
to long-standing GORD. They also occur after ingestion of corrosives, radiotherapy, sclerotherapy of oesophageal varices, and prolonged nasogastric
tube placement. Dysphagia is the predominant symptom and treatment is
with endoscopic dilatation, PPIs and sometimes surgery.
Oesophageal infection
Infection is a cause of painful swallowing and is seen particularly in immunosuppressed patients (e.g. patients with acquired immunodeficiency syndrome
(AIDS) or during chemotherapy). Infection can occur with Candida, herpes
simplex, cytomegalovirus and Mycobacterium tuberculosis. It is occasionally difficult to distinguish between these disorders on oesophagoscopy, as
only widespread ulceration is seen. In candidiasis, the characteristic white
plaques are frequently found; oral candidiasis is not always present. The
diagnosis of Candida infection can be confirmed by examining a direct smear
taken at endoscopy, but often infections are mixed, and cultures and biopsies
must be performed. Tuberculosis causes deep ulceration with associated
mediastinal lymphadenopathy.
Eosinophilic oesophagitis
Eosinophilic oesophagitis is increasingly recognized, but its pathogenesis is
unknown. There may be a personal or family history of allergic disorders, such
as food allergy, eczema or asthma. Patients may present with a long history
of dysphagia, food impaction, ‘heartburn’ and oesophageal pain caused by the
eosinophil-induced oesophageal inflammation. Usually, the patient is male and
white, and has an average age at diagnosis of 35, but eosinophilic oesophagitis is becoming more common in children. Typical endoscopic abnormalities
include mucosal furrowing, loss of vascular pattern due to a thickened mucosa,
plaques of eosinophilic surface exudate and prominent circular folds, but the
oesophagus may appear macroscopically normal. Eosinophilic infiltration of
the oesophagus seen in reflux disease tends to have a different microscopic
appearance and fewer eosinophils. First-line treatment is with topical steroids,
such as swallowing fluticasone spray or budesonide syrup. If this is not effective, systemic steroids or empirical elimination diets may also be used. A cohort
of patients respond to PPIs in the absence of GORD.
The Oesophagus 81
Oesophageal perforation
Iatrogenic perforation occurs after endoscopic dilatation of oesophageal
strictures (usually malignant) or achalasia, or rarely after passage of a
nasogastric tube. Management involves placement of an expanding covered
oesophageal stent, which usually seals the hole. A water-soluble contrast
X-ray is performed after 2–3 days to check the perforation has sealed.
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. The chest X-ray may
be normal or show air in the mediastinum and neck, and a pleural effusion.
Diagnosis is made with a CT scan or water-soluble contrast swallow. The
best outcomes are associated with early diagnosis and definitive surgical
management within 12 hours of rupture.
Malignant oesophageal tumours
Pathology
Oesophageal cancer is the sixth most common cancer worldwide. Squamous
cancers occurring in the middle third account for 40% of tumours, and in the
upper third, 15%. Adenocarcinomas occur in the lower third of the oesophagus and at the cardia and represent approximately 45%. Primary small cell
cancer of the oesophagus is extremely rare.
Epidemiology and aetiological factors
Squamous carcinoma The incidence of squamous carcinoma is 5–10
per 100 000 in the UK, but there is great international variation, 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 increase the risk.
Adenocarcinoma Adenocarcinoma arises from Barrett’s metaplasia
(p. 78). Smoking and obesity are also risk factors.
Clinical features
Patients report progressive dysphagia (initially for solids and later for liquids)
and weight loss. Bolus food impaction or local infiltration may cause chest
pain. Physical signs may be absent.
Investigations
These are performed to confirm the diagnosis and stage the tumour (TNM
system, p. 829).
82 Gastroenterology and nutrition
• Diagnosis is by oesophagogastroscopy and tumour biopsy. Barium
swallow can be useful where the differential diagnosis of dysphagia
includes a motility disorder such as achalasia.
• Tumour staging is performed initially by CT scan of the chest and
abdomen. Patients without evidence of metastatic disease and who are
potentially curable, then undergo EUS (p. 70) 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.
Management
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). Unfortunately, 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 treatments 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.
Prognosis
The overall prognosis is poor with a 10% 5-year survival.
Benign oesophageal tumours
See page 89 (gastrointestinal stromal tumour, GIST).
THE STOMACH AND DUODENUM
Acid secretion is central to the functionality of the stomach. Acid is not essential for digestion but does prevent some food-borne infections. It is under
neural and hormonal control, and both act to stimulate acid secretion through
the direct action of histamine on the gastric parietal cell. Acetylcholine and
gastrin also release histamine via enterochromaffin cells. Somatostatin
inhibits both histamine and gastrin release and therefore acid secretion. The
stomach plays a minimal role in absorption of food.
Other major functions are:
• Reservoir for food
• Emulsification of fat and mixing of gastric contents
• Secretion of intrinsic factor.