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The salivary glands 205
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(which resembles bronchiectasis in the lung), associated with a stricture of the duct or a stone. These
changes are best demonstrated by performing a
sialogram.
Treatment
An associated stricture is treated by dilation, and if
stones are present these must be removed. Massage
of the gland several times a day, and the use of
sialogogues (such as ‘acid drops’), encourage drainage. Sialoendoscopy can be used to help with diagnosis and treatment of stenoses and stones.
Occasionally, in severe and refractory cases, excision of the gland with preservation of the facial
nerve is required.
Sjögren’s syndrome
Sjögren’s syndrome3 is an autoimmune disease characterized by periductal lymphocytes in multiple
organs. The salivary glands are affected in approximately 40% of cases and one in six patients will progress to lymphoma. It is associated with dry eyes
(xerophthalmia), leading to conjunctivokeratitis, and
dry mouth (xerostomia). If there is no connective tissue component, it is described as primary and if there
is a connective tissue disorder, usually rheumatoid
arthritis, it is secondary.
Clinical features
There is painful swelling of the affected gland, aggravated
by food (classically, by sucking a lemon), and there
may be an unpleasant taste in the mouth due to the
purulent discharge. On examination, the obstructed
gland is enlarged and tender. The orifice of the submandibular duct, visible in the floor of the mouth, is
red and swollen and the calculus may be visible or
palpable on bimanual examination of the duct.
Gentle pressure on the gland may produce a purulent
exudate from the orifice of the duct.
Special investigations
• X- rays invariably confirm the presence of the
stone.
•
A sialogram, in which contrast material is injected
into the duct, may be necessary if no stone is visible. This may reveal stenosis of the ostium of the
duct, which mimics the symptoms of a stone, or
sialectasis.
• Sialoendoscopy.
Treatment
If the stone lies within the submandibular duct, it can
be removed from within the mouth, with the duct
being marsupialized at the site of extraction. It can
also be removed via sialoendoscopy. If one or more
stones are impacted in the gland substance, excision
of the whole gland is required.
Calculi
Stone formation is common in the submandibular
gland and its duct, rare in the parotid and rarer still in
the sublingual. The different composition of the saliva
from each gland probably explains this difference.
Stasis of the more viscid secretion of the submandibular gland in its long duct, changes in composition of
the saliva, trauma to the duct, infection, and stricture
may predispose to stone formation. Calcium phosphate is the predominant salt of the calculi and the
majority are radio- opaque particularly in the submandibular gland or duct.
3
Henrik Sjogren (1899–1986) a Swedish Ophthalmologist.
Salivary tumours
There are over 35 variants of salivary gland
tumours and a simplified classification is shown
below. A good approximation is that 80% of all
salivary gland tumours are in the parotid, 80% of
parotid tumours are benign and 80% of the benign
parotid tumours are pleomorphic adenomas. One
in three tumours arising in the submandibular
gland and one in two arising in the minor salivary
glands are malignant.
Benign
• Pleomorphic adenoma (mixed salivary tumour).
• Adenolymphoma (Warthin’s tumour).
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Malignant
• Primary: carcinoma – adenoid cystic, acinic,
mucoepidermoid, carcinoma exadenoma.
•
Secondary: secondarily involved intraparotid
lymph nodes, usually from primary skin squamous cell carcinomas.
pleomorphic
Pleomorphic adenoma
These account for 70–80% of all salivary gland neoplasms with 80% appearing in the parotid gland.
Mean age of presentation is 46 years although any age
may be affected. Sex distribution is roughly equal.
Pathology
Macroscopic appearance
The tumour is lobulated and lies within a capsule of
varying thickness. In minor salivary gland sites, the
capsule may be completely absent. The outer surface
is bosselated with finger like processes extending into
and occasionally through the capsule.
Microscopic appearance
Epithelial and modified myoepithelial elements
intermingle most commonly with tissue of mucoid,
myxoid or chondroid appearance hence the synonym
of ‘mixed tumour’.
Clinical features
The patient presents with a slow- growing swelling
anywhere within the parotid gland, but usually in the
lower pole and in the region of the angle of the jaw.
The lump is wellsometimes cystic in consistency. It is usually placed
in the superficial part of the gland but may occasionally be in its deep lobe in the parapha ryngeal space
and indeed may project into the pharynx. The facial
nerve is never involved, except by frankly malignant
tumours. Its integrity should be confirmed.
defined, usually firm or hard but
Surgical considerations
Complete surgical excision is the treatment of choice
as, although pleomorphic adenoma is a benign
tumour, there is a risk of recurrence and malignant
transformation. Because of the variability of the capsule and protuberances through it, excision with a
cuff of normal salivary gland tissue is recommended
to reduce the chance of recurrence.
Removal of the tumour with an appropriate part of
the superficial part of the gland (superficial parotidectomy) is adequate treatment for the majority of
tumours. If the tumour involves the deep lobe, a total
conservative parotidectomy may be required with
removal of all or nearly all of the parotid tissue with
preservation of the facial nerve.
Prognosis
Providing the tumour is completely excised, the prognosis is excellent but inadequate surgery is followed
by a recurrence in a high percentage of cases.
Adenolymphoma
Adenolymphoma (Warthin’s tumour4) accounts for
about 10% of parotid tumours and 10% present bilaterally. Adenolymphomas usually occur in men over
the age of 50 years, and there is a strong association
with cigarette smoking.
Macroscopically, the tumour is soft and cystic.
Microscopically, it consists of columnar cells forming
papillary fringes, which project into cystic spaces and
are supported by a lymphoid stroma. These tumours
probably arise from ectopic salivary duct epithelium
within intraof the lymphoid tissue may lead to confusion with
lymphoproliferative disorders. Prognosis is excellent
after local removal.
or para- parotid lymph nodes. Presence
Carcinoma
Clinical features
There is a significant correlation between tumour stage
and survival. Sex distribution is equal, and the patients
are usually over the age of 50 years. All ages, however,
can be affected with mucoepidermoid tumours being
the commonest salivary neoplasm in children. The
tumour is hard and infiltrating. Clinically, malignancy
should be suspected if there is rapid growth, pain and
4
Aldred Scott Warthin (1866–1931), Professor of Pathology,
University of Michigan, Ann Arbor, MI, USA.
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involvement of the facial nerve and regional lymph
nodes. Eventually, surrounding tissues are infiltrated
and the overlying skin becomes ulcerated.
Adenoid cystic, acinic and mucoepidermoid carcinomas are the commonest primary salivary gland
malignancies. Growth rates may be variable as is spread
to regional lymph nodes. Adenoid cystic tumours tend
to spread along nerve sheaths and acinic and mucoepidermoid tumours are more likely to spread to cervical
lymph nodes. All may metastasize distantly.
Treatment
Treatment of these tumours is primarily surgical if
there has been no distant spread. Wide local excision
with clear surgical margins is preferred with or without an associated neck dissection to remove the cervical lymph nodes. Preservation of the facial nerve in
parotid tumours may be possible if it is not involved
preoperatively. However, it may need to be sacrificed
if involved or to achieve adequate clearance.
Postoperative radiotherapy may be considered in
some cases.
Additional resources
Case 45: A painful submandibular swelling
Case 46: A lump over the angle of the jaw
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The oesophagus
Peter Safranek
Learning objectives
✓ To know the common causes of dysphagia.
✓ To know the presentation and management of oesophageal perforation.
✓ To know the presentation and management of oesophageal carcinoma.
Dysphagia
Dysphagia is difficulty in swallowing. The causes
may be local or general. The local causes of obstruction of any tube in the body can be subdivided into
those in the lumen, those in the wall and those outside the wall.
Local causes
In thelumen
• Foreign body.
In thewall
• Congenital atresia.
• Inflammatory stricture, secondary to reflux
oesophagitis.
• Caustic stricture.
• Achalasia.
• Eosinophilic oesophagitis causing dysmotility
and/or stricture.
• Plummer–Vinson syndrome with oesophageal web.
• Pharyngeal pouch.
• Epiphrenic diverticulum.
Schatzki’s ring.
•
• Tumour of oesophagus or cardia.
• Systemic sclerosis (scleroderma).
1
Outside thewall
• Pressure of enlarged lymph nodes (secondary
cancer or lymphoma).
•
Thoracic aortic aneurysm.
• Bronchial carcinoma.
• Retrosternal goitre.
• Hiatus hernia.
General causes
• Myasthenia gravis.
•
Bulbar palsy.
• Bulbar poliomyelitis.
• Diphtheria.
• Hysteria.
Investigations
History
The subjective site of obstruction is not always exact;
the patient often merely points vaguely to behind the
sternum. The diagnosis may be given by a history of
Ellis and Calne’s Lecture Notes in General Surgery, Fourteenth Edition.
Edited by Christopher Watson and Justin Davies.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/Watson/GeneralSurgery14
1
Richard Schatzki (1901–1992), Radiologist, Boston, MA,
USA. Described a circumferential ring of mucosal tissue in
the distal oesophagus.
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swallowed caustic in the past. A previous story of
reflux oesophagitis may suggest peptic stricture.
Patients with achalasia tend to be younger and the
history may be longer.
Malignant stricture has a short history, occurs usually in older people and tends to be associated with
significant weight loss.
Examination
Often this is negative, but search is made for
clinical evidence of Plummer–Vinson syndrome (a
smooth tongue, anaemia and koilonychia; see later
in this chapter), secondary nodes from a
carcinoma of the oesophagus which may be felt in
the neck and supraclavicular fossae, and the upper
abdomen is carefully palpated, as a carcinoma of
the cardia is also a common cause of dysphagia in
older patients.
Special investigations
• Fibreoptic endoscopy enables biopsies to be taken
to confirm malignancy, and permits therapeutic
dilation of benign strictures and palliative stenting
of incurable malignant obstruction.
• Barium swallow, with cine- radiography, may
demonstrate the characteristic appearances of a
cervical web, extrinsic compression and the
dilated oesophagus of achalasia (Figure22.1).
(a) Pharyngeal
pouch
(d) Caustic
stricture
(b) Achalasia (c) Carcinoma
(e) Extrinsic
compression
from bronchial
carcinoma
Figure22.1 (a–e) Barium swallow
appearances of common causes of
dysphagia.
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Endoscopy is the primary investigation but they are
complementary and a barium swallow may add useful information.
Swallowed foreign bodies
Foreign bodies are swallowed either accidentally,
usually by children, or deliberately by those with
psychiatric illness, and prison inmates. Button batteries, which can generate sodium hydroxide when in
contact with body fluids, are a particular hazard
in children, since they can stick in the oesophagus
and cause caustic ulceration and perforation or
haemorrhage.
Obstruction of the oropharynx and tracheal opening by a large portion of meat can rapidly become
fatal. A sharp blow just below the xiphoid, Heimlich’s
manoeuvre,
abdominal pressure, may dislodge the plug and save
the patient’s life.
Unless they are sharp or irregular, amazingly large
foreign bodies will pass into the stomach. If a
smooth object such as a bolus of food impacts in the
oesophagus, one must suspect the presence of a
stricture or dysmotility such as that caused by eosinophilic oesophagitis. Occasionally, a carcinoma of
the oesophagus presents with acute dysphagia
when a morsel of food lodges above it. Absolute dysphagia, with failure to swallow even saliva, is then
characteristic and needs urgent treatment.
The presenting feature is painful dysphagia. The
danger depends on the nature of the foreign body.
Perforation may occur with resultant mediastinitis;
rarely, perforation of the aorta occurs with fatal haematemesis. The diagnosis is usually made with a
computed tomography (CT) scan often with the addition of oral contrast medium if perforation is
suspected.
2
causing a sudden rise in intra-
rectum. Occasionally, a sharp foreign body penetrates
the wall of the bowel (there is a particular tendency
for it to lodge in, and pierce, a Meckel’s diverticulum;
see Chapter25).
The treatment of a foreign body that has passed the
cardia is initially conservative. The patient is watched
and serial Xprogress if it is radioif a sharp object fails to progress or if abdominal pain
or tenderness develop.
If the foreign body is potentially toxic when
ingested, emetics or laxatives may be indicated.
rays can be taken to observe the object’s
opaque. Operation is performed
Perforations ofthe
oesophagus
Classication
From within
• Swallowed foreign body– may occur anywhere in
the oesophagus.
Rupture at rigid oesophagoscopy– usually at the
•
level of cricopharyngeus or above a stricture.
•
Rupture during dilation or biopsy– usually at the
lower end of the oesophagus and especially likely
in the presence of oesophageal disease (carcinoma or stricture).
Rupture during oesophageal echocardiography–
•
again usually at the lower end, often in the presence of a hitherto unknown stricture or pharyngeal
pouch.
•
Rupture during endoscopic retrograde cholangiopan-
creatography (ERCP) - the side viewing endoscope
inadvertently enters an undiagnosed pharyngeal
pouch which is thin and perforates easily.
Treatment
Endoscopic removal is indicated when the foreign
body is stuck in the oesophagus. With advances in
flexible endoscopy, surgery for removal of foreign
bodies is seldom necessary in the absence of perforation. The great majority of foreign bodies, once they
have passed into the stomach, proceed uneventfully
along the gastrointestinal tract and are passed per
2
Henry J. Heimlich (1920–2016), oracic Surgeon, Xavier
University, Cincinnati, OH, USA.
From without
• Perforating wounds (rare).
Spontaneous
• Lower thoracic oesophagus (Boerhaave’s syndrome3).
3
Hermann Boerhaave (1668–1738), Physician, Leiden,
the Netherlands. Diagnosed spontaneous rupture of the
oesophagus at postmortem on the Grand Admiral of the
Dutch Fleet.
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Clinical features
After instrumentation, perforation is suspected if the
patient complains of pain in the neck, chest or upper
abdomen, together with dysphagia and pyrexia.
Diagnosis is certain if subcutaneous emphysema is
felt in the supraclavicular area.
Spontaneous rupture of the oesophagus occurs
rarely and is associated with vomiting after a large
meal (Boerhaave’s syndrome) where perforation
occurs when luminal pressure is increased and cricopharyngeus fails to relax. There is severe pain in the
chest, the dorsal region of the spine or the upper
abdomen (acute mediastinitis). The patient shows
signs of sepsis (fever/tachycardia/raised inflammatory markers). The abdomen may be rigid if perforation extends below the diaphragm. Surgical
emphysema (subcutaneous crepitation) can be palpable in the neck owing to gas escaping into the
mediastinum.
Special investigations
• Chest X- ray shows gas in the neck and mediasti-
num and there may be fluid and gas in the pleural
cavity.
•
Thoraco- abdominal computed tomography (CT),
combined with oral gastrografin (a water- soluble
contrast medium), will confirm the perforation
and define its position.
Treatment
Cervical perforation is managed conservatively with
parenteral antibiotics, nil by mouth and intravenous
fluids. Abscess formation in the superior mediastinum requires drainage via a thoracoscopic or radiological approach.
Thoracic rupture is treated by immediate surgical
repair (with or without a Tnoma may potentially be resected. The prognosis
from spontaneous rupture is inversely related to the
time to surgery, and after 12 hours can be very poor
with rapid progression from systemic sepsis to multiorgan failure.
A novel therapy which has gained popularity in the
treatment of both iatrogenic and spontaneous
oesophageal perforation is Endoluminal Vacuum
Therapy. This involves endoscopic placement of a
vacuum device through the perforation to control any
leak, collapse the mediastinal or pleural cavity and
tube). A perforated carci-
promote healing. This can be used successfully in
patients who would not survive the major surgery that
conventional treatment entails.
Caustic stricture ofthe
oesophagus
This follows accidental or suicidal ingestion of strong
acids or alkalis (particularly, caustic soda and ammonia). It occurs more commonly in children.
In the acute phase, there are associated burns of
the mouth and pharynx. The mid- and lower oesophagus are usually affected, as these are the sites of temporary holdoesophagus is crossed by the aortic arch and at the
cardiac sphincter.
up of the caustic material where the
Treatment
In the acute phase, treatment aims to neutralize the
cause, so alkali ingestion may be neutralized with vinegar and acid ingestion with bicarbonate of soda. The
damaged oesophagus is rested by instituting feeding
via a gastrostomy or jejunostomy, nil being given by
mouth. Systemic steroids are given to reduce scar formation. If a stricture develops, gentle balloon dilation
is commenced after 3 or 4 weeks. An established,
impassable stricture is treated by resection and
reconstruction with either stomach (if this remains
healthy) or a colonic conduit if not.
Achalasia ofthe cardia
This is a neuromuscular condition of the oesophagus
where there is failure of both peristalsis and relaxation of
the lower oesophageal sphincter, resulting in progressive
dilation and tortuosity. The pathological process
involves loss of inhibitory ganglion cells from the wall of
the oesophagus. It is thought that the cause of the neurone loss may relate to a viral infection or autoimmune
response to infection in susceptible individuals. The
condition is indistinguishable from Chagas’ disease,
which occurs in South America secondary to
4
Carlos Chagas (1879–1934), Professor of Tropical Medicine,
Rio de Janeiro, Brazil.
4
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Trypanosoma cruzi infection. The parasite destroys the
intermuscular ganglion cells of the oesophagus.
Clinical features
Achalasia may occur at any age but particularly in the
third decade. The ratio of women to men is 3:2.
There is progressive dysphagia (particularly to fluids) over months to years, sometimes associated with
a spasmthe dilated oesophagus may cause an aspiration
pneumonia. The failure of clearance of fluid and food
can sometimes lead to symptoms which can be mistaken for reflux in the early stages. Occasionally,
malignant change occurs in the oesophagus.
like chest pain. Regurgitation of fluids from
Special investigations
• Chest X- ray may reveal the dilated oesophagus as a
mediastinal mass, with an air–fluid level, and pneumonitis from aspiration of oesophageal contents.
(Note that there are three other ‘pseudotumours’:
scoliosis, tuberculous paravertebral abscess and
thoracic aortic aneurysm, all of which may simulate
a mediastinal tumour on a chest X-
• Barium swallow shows gross dilation and tortuos-
ity of the oesophagus leading to an unrelaxing narrowed segment at the lower end (said to resemble
a bird’s beak) (see Figure22.1).
• Endoscopy demonstrates a dilated and tortuous
oesophagus containing food and fluid residue
despite a period of fasting.
•
Oesophageal high resolution manometry is the
gold standard investigation and shows failure of
peristalsis with impaired lower oesophageal
sphincter relaxation.
ray.)
Treatment
Good relief of symptoms is obtained by Heller’s
operation,
muscle of the lower end of the oesophagus and the
upper stomach down to the mucosa in a similar
manner to Ramstedt’s operation (see Chapter23) for
congenital pyloric hypertrophy. This procedure can be
performed laparoscopically, thus reducing morbidity.
It is often combined with an anterior fundoplication
which reduces the risk of postoperative reflux.
5
Ernst Heller (1877–1964), Surgeon, Leipzig, Germany.
5
which is a cardiomyotomy dividing the
The same effect may be achieved by forcible
dilation of the oesophagogastric junction by means of
an endoscopic balloon that is inflated under
fluoroscopic (X- ray) control. Although this avoids an
operation, there is a risk of rupture of the oesophagus.
A temporary non endoscopic injection of botulinum toxin (Botox) to
paralyse the lower oesophageal sphincter. This can be
useful for frail patients unsuitable for surgery or as a
temporary means of relieving symptoms.
There is a new endoscopic therapy, perscopic myotomy (POEM) which is gaining some popularity. In this technique, the myotomy is performed
from the oesophageal lumen using an endoscope.
invasive approach involves
oral endo-
Plummer–Vinson
syndrome
A syndrome actually described by Paterson and Kelly
before Plummer and Vinson, and which sometimes
rejoices in all four names, comprising dysphagia and
iron deficiency anaemia (with its associated smooth
tongue and koilonychia – spoon- shaped nails) usually in middle- aged or elderly women.
The dysphagia is associated with hyperkeratinization of the oesophagus and often with the formation
of a web in the upper part of the oesophagus. The
condition is premalignant and is associated with the
development of a carcinoma in the cricopharyngeal
region.
Treatment
The dysphagia responds to treatment with iron,
although the web may require endoscopic dilatation.
6
Oesophageal diverticula
The only common diverticulum of the oesophagus is
the pharyngeal pouch.
6
Henry S. Plummer (1874–1937) and Porter Paisley Vinson
(1890–1959), Physicians, Mayo Clinic, Rochester, MN, USA.
Donald Ross Paterson (1863–1939), ENT Surgeon, Royal
Inrmary, Cardi, UK. Adam Brown- Kelly (1865–1914), ENT
Surgeon, Victoria Inrmary, Glasgow, UK.
Thyropharyngeus
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Thyroid cartilage
Cricopharyngeus
Cricoid cartilage
Pharyngeal pouch
The oesophagus 213
Figure22.2 A pharyngeal pouch
emerging between the two
components of the inferior constrictor
muscle.
Other oesophageal diverticula
Other oesophageal diverticula are very rare.
•
Traction diverticula may occur in association with
fixation to tuberculous nodes or to pleural
adhesions.
•
Pulsion or epiphrenic diverticula may be associ-
ated with cardiospasm and occur at the lower end
of the oesophagus.
• Congenital diverticula are occasionally found.
These are usually X- ray findings only, although
they may occasionally produce dysphagia.
Pharyngeal pouch
This is a mucosal protrusion between the two parts of
the inferior pharyngeal constrictor– the thyropharyngeus and cricopharyngeus (Figure22.2). The weak area
between these portions of the muscle is situated posteriorly (Killian’s dehiscence
7
Gustav Killian (1860–1921), Professor of
Otorhinolaryngology, Freiburg and Berlin, Germany.
7
). The pouch is believed to
originate above the cricopharyngeus muscle which is
in spasm; it develops first posteriorly but cannot then
expand in this direction and protrudes to one or the
other side, usually the left. As the pouch enlarges, it displaces the oesophagus laterally. It is an example of a
pulsion diverticulum, forming as a result of increased
intraluminal pressure.
Clinical features
It occurs more often in men and usually in the elderly.
There is dysphagia, regurgitation of the food that has
collected in the pouch, and often a palpable swelling
in the neck, which gurgles. Food retained in the pouch
leads to a foetor, and late regurgitation may lead to
aspiration pneumonia and lung abscess. Diagnosis is
confirmed by a barium swallow.
Treatment
Traditional surgery involved a cervical incision with
excision of the pouch combined with a posterior
myotomy of the cricopharyngeus. More commonly
now, the pouch can be treated by division of the wall
between pouch and oesophagus using an endoscopic
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stapling device (endoscopic diverticulotomy), leaving
the pouch in situ and avoiding the risk of fistula
formation and leaks associated with the open
operation.
Reflux oesophagitis
This is produced by the reflux of peptic juice through
the incompetent cardiac sphincter into the lower
oesophagus, resulting in ulceration and inflammation and eventually in stricture formation. The exact
mechanism of the cardio- oesophageal sphincter is
not understood; it is sufficient to prevent regurgitation into the oesophagus when standing on one’s
head or in forced inspiration, when there is a pressure
difference of some 80mmHg between the intragastric
and intraoesophageal pressure, yet it can relax readily
to allow vomiting or belching to occur. The mechanism is probably a complex affair comprising the
following:
•
Positive intra- abdominal pressure acting on the
lower (intra- abdominal) oesophagus, maintaining a high- pressure zone at the cardia.
•
Physiological muscle sphincter at the lower end of
the oesophagus.
Valve- like effect of the obliquity of the oesophago-
•
gastric angle.
Pinch- cock effect on the lower oesophagus of the
•
diaphragmatic sling when the diaphragm contracts in full inspiration.
•
Plug- like action of the mucosal folds at the cardia.
The diaphragm is an important but not essential part
of the cardiac sphincter mechanism, as sliding hiatus
hernias are not necessarily accompanied by regurgitation. Similarly, free regurgitation occurs in some
subjects with a normal oesophageal hiatus, presumably because of some defect in the function of the
physiological sphincter.
Reflux oesophagitis may also occur in association
with the following:
• Repeated vomiting, especially in the presence of a
duodenal ulcer with high acid content of gastric
juice.
•
Long- standing nasogastric intubation.
• Resections of the cardia with gastro- oesophageal
anastomosis.
• Most commonly, in association with hiatal hernia
and a weak lower oesophageal sphincter.
Special investigations
• Endoscopy demonstrates the presence of
oesophagitis and hiatus hernia, and facilitates
biopsy to exclude carcinoma, or the presence of
Barrett’s metaplasia or dysplasia.
Twenty- four- hour oesophageal pH and Impedance
•
studies: a probe in the oesophagus will demonstrate reflux of gastric acid, intestinal fluid and gas
and their temporal relation to symptoms.
•
Barium swallow: this will demonstrate the outline
of a hernia and the presence of any associated
stricture. Tilting the patient head down will demonstrate reflux, but does not necessarily confirm
that the symptoms are due to reflux.
Differential diagnosis
The pain of oesophagitis may be confused with cholecystitis, peptic ulcer or angina pectoris; indeed,
these conditions often co-
The obstructive symptoms of an associated stricture must be differentiated from carcinoma of the
oesophagus or of the cardia.
exist.
Treatment
Medical treatment comprises weight loss, stopping
smoking and dietary manipulation. Regurgitation is
discouraged by avoiding stooping or lying and by
sleeping propped up in bed. Alginate antacids
(e.g.Gaviscon) taken after meals neutralize the acidity as well as lining the oesophagus. The mainstay of
medical treatment is proton pump inhibitors
(e.g.omeprazole), which directly block acid production. H
- receptor antagonist drugs (e.g. cimetidine)
2
are less effective. Prokinetic drugs to increase gastric
emptying, such as metoclopramide, are occasionally
used. Many patients with mild symptoms obtain relief
of their symptoms with medical treatment.
Laparoscopic surgery for reflux is undertaken when
medical treatment fails, if there is significant volume
reflux, or if medical therapy cannot be tolerated due to
side effects. It usually consists of repair of any hiatal hernia combined with a complete (360 degree, Nissen
partial (270 degree, Toupet
8
Rudolph Nissen (1896–1981), Professor of Surgery, Berlin,
Turkey, USA and Switzerland.
9
André Toupet (1915–2015) Surgeon, St Cloud Hospital
Paris, France.
9
) fundoplication which
8
), or
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