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into a bolus and then propelled into the pharynx by elevation of the tongue against the palate.
of food comes into contact with pharyngeal mucosa. A
series of reflex actions take place carrying the food past
oro- and laryngopharynx into the oesophagus. The communications into nasopharynx, oral cavity and larynx are
cut off.
(a) Closure of nasopharynx. Soft palate contracts against
SECTION VII — Diseases of Oesophagus
Figure 67.2. Oesophagus and its sphincters.
2. PharyngeaL PhaSe. It is initiated when the bolus
the Passavant’s ridge on the posterior pharyngeal
wall and completely cuts off the nasopharynx from
the oropharynx.
(b) Closure of oropharyngeal isthmus. The entry of food
back into oral cavity is prevented by contraction of
tongue against the palate and sphincteric action of
palatoglossal muscles.
(c) Closure of larynx. Aspiration into the larynx is pre-
vented by temporary cessation of respiration, closure of laryngeal inlet by contraction of aryepiglottic
folds, closure of false and true cords, and rising of
larynx under the base of tongue. The role of epiglottis
in providing protection to larynx is not clear but it is
seen to deflect backwards when food passes into the
pyriform fossae.
(d) Contraction of pharyngeal muscles and relaxation of cri-
copharyngeus. Relaxation of cricopharyngeus muscles
is so timed and synchronous that food passes from
pharynx into the oesophagus during contraction of
pharyngeal muscles.
3. oeSoPhageaL PhaSe. After food enters the oesophagus, the cricopharyngeal sphincter closes and the peristaltic movements of oesophagus take the bolus down the
stomach. Gastro-oesophageal sphincter at the lower end
of oesophagus relaxes well before peristaltic wave reaches
and permits fluids to pass. Bolus of food is passed by contraction of peristaltic waves and then the sphincter closes.
Regurgitation of food back from stomach into oesoph-
agus is prevented by:
(i) tone of gastro-oesophageal sphincter,
(ii) negative intrathoracic pressure,
(iii) pinch-cock effect of diaphragm,
(iv) mucosal folds,
(v) oesophagogastric angle and
(vi) slightly positive intra-abdominal pressure.
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Disorders of Oesophagus
ACUTE OESOPHAGITIS
It is acute inflammation of the oesophagus and can be
due to (i) ingestion of hot liquids, (ii) ingestion of caustic or corrosive agents, (iii) laceration due to swallowed
foreign body, or trauma of oesophagoscopy, (iv) monilial
infection of oesophagus from thrush in the oral cavity
and (v) systemic disorder like pemphigus.
Patient complains of dysphagia, retrosternal burning
or haematemesis. Diagnosis can be made from history,
X-ray studies and oesophagoscopy.
PERFORATION OF OESOPHAGUS
AETIOLOGY
Perforation or the rupture of oesophagus results from:
1. Instrumental trauma, i.e. oesophagoscopy or dilata-
tion of strictures with bougies. The common site or
rupture in these cases is just above the upper sphincter;
sometimes it is the lower oesophagus near the hiatus.
2. Spontaneous rupture. This usually follows vomiting
and involves mostly the lower third of oesophagus.
Postemetic rupture of all the layers of oesophagus is
called Boerhaave syndrome.
DIAGNOSIS
Early diagnosis is imperative, as mediastinitis, resulting
from rupture, can rapidly prove fatal. All patients complaining of pain in the neck or interscapular region, following an oesophagoscopy, should be suspected of a perforation.
The features of cervical oesophageal rupture are pain, fever, difficulty to swallow and local tenderness, along with
signs of surgical emphysema in the neck.
The features of thoracic oesophageal rupture are pain, referred to the interscapular region, fever 102–104 °F (39–
40 °C), signs of shock, surgical emphysema in the neck,
crunching sound over the heart (Hamman’s sign, because
of air in the mediastinum) and pneumothorax.
X-rays of the chest and neck are essential. They may
reveal widening of the mediastinum and retrovisceral
space, surgical emphysema, pneumothorax, pleural effusion or gas under the diaphragm.
TREATMENT
All oral feeds are stopped immediately. Nutrition is maintained through i.v. route. Massive doses of antibiotics are
given i.v. to combat infection.
Early perforations of cervical oesophagus can be managed by conservative measures; drainage is required only
if suppuration develops. Retrovisceral space and/or upper
mediastinum can be drained through the neck.
Rupture of thoracic oesophagus is more serious and
conservative treatment rarely succeeds. If diagnosis is
made early (within 6 h), perforation is surgically repaired
and pleural cavity drained. If diagnosis is delayed, repair
is not possible; surgery is then restricted to drainage of
the infected area.
CORROSIVE BURNS OF OESOPHAGUS
AETIOLOGY
Acids, alkalies or other chemicals may be swallowed accidentally in children or taken with the purpose of suicide
in adults.
PATHOLOGY
Severity of oesophageal burns depends on the nature of
corrosive substance, its quantity and concentration and the
duration of its contact with the oesophageal wall. Alkalies
are more destructive and penetrate deep into the layers of
the oesophagus. With lye burns, entire oesophagus and
stomach may slough off causing fatal mediastinitis and
peritonitis.
Oesophageal burns run through three stages:
1. Stages of acute necrosis.
2. Stage of granulations: Slough separates leaving granu-
lating ulcer.
3. Stage of stricture: Stricture formation begins at 2 weeks
and continues for 2 months or longer.
EVALUATION OF PATIENTS
Evaluate the patient and determine the type of caustic
ingested, signs and symptoms of shock, upper airway obstruction, mediastinitis, peritonitis, acid-base imbalance,
and associated burns of face, lips and oral cavity. Take
X-ray of the chest and soft tissue lateral view of neck.
MANAGEMENT
1. Hospitalize the patient.
2. Treat shock and acid-base imbalance by i.v. fluids and
electrolytes. Monitor urine output for renal failure.
3. Relieve pain.
4. Relieve airway obstruction. Tracheostomy may be required.
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SECTION VII — Diseases of Oesophagus
5. Neutralization of the corrosive by appropriate weak
acid or alkali, given by mouth, can be done but is effective only if done within first 6 h.
6. Parenteral antibiotics should be started immediately
and continued for 3–6 weeks depending on the degree of burns.
7. Pass a nasogastric tube. It is useful to feed the patient
and to maintain oesophageal lumen.
8. Oesophagoscopy. Some advocate an early oesophagoscopy within 2 days to know if burns in the oesophagus have occurred and if so, their degree and extent
so as to plan further treatment. Oesophagoscope is
not passed beyond the first severe circumferential
burn.
9. Steroids should be started within 48–96 h and continued for 4–6 weeks to prevent stricture.
10. Follow the patient with oesophagogram and oesophagoscopy every 2 weeks, till healing is complete,
for the development of any stricture.
11. If stricture develops it can be treated by:
(a) Oesophagoscopy and prograde dilatations, if per-
meable.
(b) Gastrostomy and retrograde dilatation, if imper-
meable.
(c) Oesophageal reconstruction or by-pass, if dilata-
tions are impossible.
12. Patients of corrosive injuries of oesophagus may require life-long follow-up.
the stomach, and prograde or retrograde bouginage can
be done.
3. surgery. Excision of strictured segment and reconstruction of food passage using stomach, colon or jejunum.
HIATUS HERNIA
It is displacement of stomach into the chest through oesophageal opening of the diaphragm. Most patients are
elderly, past 40 years. This disorder is of two types:
1. Sliding. Stomach is pushed into the thorax, in line
with the oesophagus. Reflux oesophagitis is common
and may give rise to ulceration and stenosis. Haematemesis may occur. It is caused by raised intra-abdominal
pressure.
2. Paraoesophageal. A part of the stomach along with its
peritoneal covering passes up into the thorax by the
side of oesophagus. The gastro-oesophageal junction
still remains below the diaphragm and the angle between oesophagus and stomach is maintained. There
is no reflux oesophagitis in this type of hernia. The
main symptom is dyspnoea on exertion due to position of stomach in the thorax and sometimes bleeding.
Diagnosis of both types of hiatus hernia can be made
by barium swallow.
BENIGN STRICTURES OF OESOPHAGUS
AETIOLOGY
The strictures usually occur when muscular coat of the
oesophagus is damaged. The common causes are:
1. Burns due to corrosive substances or hot fluids.
2. Trauma to oesophageal wall due to impacted foreign
bodies or instrumentation or external injuries.
3. Ulcerations due to reflux oesophagitis.
4. Ulcerations due to diphtheria or typhoid.
5. Sites of surgical anastomosis.
6. Congenital, usually in the lower third.
CLINICAL FEATURES AND DIAGNOSIS
Dysphagia, first to solids and then to liquids, is the common complaint. When obstruction is complete, regurgitation and cough may occur. Patient is malnourished.
Barium swallow establishes the diagnosis. Oesophago-
scopy is required to exclude malignancy.
TREATMENT
1. prograde dilatation with bougies. It should be
done under direct vision through oesophagoscope. Dilatations may be required frequently.
2. gastrostomy. It helps to feed the patients and give
rest to the inflamed area above the strictures. After a few
days, when inflammation subsides, lumen may become
visible and prograde dilatation can be restored. Patient
can be given a thread to swallow, which is recovered from
TREATMENT
Mainly it is surgical; the hernia is reduced and diaphragmatic opening repaired. Early cases and those unfit for
surgery may be treated conservatively to reduce reflux
oesophagitis by measures such as (i) sleeping with head
and chest raised, (ii) avoidance of smoking, (iii) use of
drugs that reduce acidity (antacids and proton pump inhibitors), (iv) reduction of obesity and (v) attention to the
causes which raises intra-abdominal pressure.
PLUMMER–VINSON (PATTERSON–
BROWN–KELLY) SYNDROME
Classical features of this syndrome include dysphagia,
iron-deficiency anaemia, glossitis, angular stomatitis,
koilonychia (spooning of nails) and achlorhydria. There
is atrophy of the mucous membrane of the alimentary
tract.
Predominantly, it affects females past 40 years. Barium
swallow shows a web in the postcricoid region and the
same can be seen on oesophagoscopy. It is due to subepithelial fibrosis in this region.
About 10% of the cases with this syndrome will develop postcricoid carcinoma. It also predisposes to the
development of carcinoma in the tongue, buccal mucosa,
pharynx, oesophagus and the stomach.
TREATMENT
1. To correct anaemia by oral/parenteral iron. Serum
levels of iron are more important than haemoglobin
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389
level. Associated B12 and B6 deficiency should also be
corrected.
2. Dilatation of the webbed area by oesophageal bougies.
GLOBUS (HYSTERICUS) PHARYNGEUS
It is a functional disorder where the patient complains of
“lump” in the throat. There is no true dysphagia. In fact,
feeling of lump is more marked between the meals rather
than during a meal. Such a patient may have fear of cancer in the throat. Clinical examination of the pharynx,
larynx and base of tongue is normal.
Treatment is reassurance to the patient when no cause
has been found.
MOTILITY DISORDERS OF OESOPHAGUS
They can be divided into:
1. Hypermotility disorder, e.g. cricopharyngeal spasm,
diffuse oesophageal spasm, nut cracker oesophagus.
2. Hypomotility disorders, e.g. cardiac achalasia, gastrooesophageal reflux, scleroderma, amyotrophic lateral
sclerosis.
They may involve the upper sphincter, lower sphincter
or the body of oesophagus.
CRICOPHARYNGEAL SPASM
It is caused by failure of the upper oesophageal sphincter
to relax properly. There is incoordination between relaxation of the upper oesophageal sphincter and simultaneous contraction of the pharynx. The common causes are
cerebrovascular accidents, Parkinson’s disease, bulbar polio, multiple sclerosis and muscular dystrophies.
DIFFUSE OESOPHAGEAL SPASM
It is characterized by strong nonperistaltic contractions
of the body of oesophagus while sphincteric relaxation is
normal. The symptoms consist of dysphagia or odynophagia with substernal chest pain, simulating angina pectoris. Barium swallow may show segmented oesophageal
spasms giving a rosary bead or a cork-screw type of oesophagus, though it may be normal in some. Manometry shows
normal relaxation of the sphincter on swallowing. The
treatment is dilatation of lower oesophagus. Severe cases
may require myotomy of oesophagus from the arch of
aorta to lower sphincter.
NUT-CRACKER OESOPHAGUS
These are strong, high amplitude oesophageal contractions but the contractions remain peristaltic (compare
diffuse oesophageal spasm where contractions are nonperistaltic). It causes dysphagia and substernal pain.
CARDIAC ACHALASIA
It is characterized by the absence of peristalsis in the body
of oesophagus and high resting pressure in lower oesoph-
ageal sphincter; the latter also does not relax during swallowing.
The symptoms of cardiac achalasia include dysphagia,
which is more to liquids than solids (reverse of that seen
in malignancy or strictures) and regurgitation of swallowed food particularly at night.
The diagnosis is made by (i) radiography (barium swallow shows dilated oesophagus with narrowed rat tail
lower end), sometimes also called bird-beak appearance;
(ii) manometric studies (low pressure in the body of oesophagus and high pressure at lower sphincter and failure
of the sphincter to relax); (iii) endoscopy (to exclude benign stricture or any development of carcinoma which is
a common complication of this disorder.
The treatment of choice is the modified Heller’s op-
eration (myotomy of the narrowed lower portion of the
oesophagus). Forceful pneumatic dilatation of the lower
oesophagus can be done in those unfit for surgery.
GASTRO-OESOPHAGEAL REFLUX
It is due to decreased function of lower oesophageal
sphincter thus permitting regurgitation of gastric contents into oesophagus. Other causes of gastro-oesophageal reflux are pregnancy, hiatus hernia, scleroderma, excessive use of tobacco and alcohol, and drugs that relax the
smooth muscle (anticholinergic, beta-adrenergic drugs
and calcium-channel blockers).
The symptoms of oesophageal reflux include substernal
pain, heartburn and regurgitation.
The treatment consists of:
1. Elevation of the head of bed at night.
2. Avoiding food at least 3 h before bedtime.
3. Antacids.
4. Drugs that increase tone of lower oesophageal sphinc-
ter, e.g. metoclopramide.
5. H2 receptor antagonists, e.g. cimetidine and ranitidine.
6. Avoiding smoking, alcohol, caffeine, chocolates, mints
and carbonated drinks.
7. Antireflux surgery, e.g. Nissen’s fundoplication.
Complications of Gastro-oesophageal
Reflux
1. Oesophagus
• Oesophagitis, oesophageal mucosal erosion and
haemorrhage.
• Benign oesophageal stricture.
• Barrett’s oesophagus (normal squamous epithelium
of oesophagus is replaced by columnar epithelium
as a result of continuous inflammation). It is a precancerous condition.
2. Lung
• Aspiration pneumonia.
• Chronic cough.
• Asthma.
• Bronchiectasis.
3. Larynx
• Posterior laryngitis causing vague pain in throat,
hoarseness and repeated throat clearing.
• Pachydermia laryngis.
• Contact ulcers and granulomas.
• Posterior glottic stenosis.
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• Paroxysmal laryngospasm.
• Carcinoma larynx.
4. Ear
• Otitis media with effusion.
5. Miscellaneous
• Globus hystericus.
SCLERODERMA
It is a systemic collagen disorder primarily neural, but secondarily weakening the smooth muscles of the lower twothirds of oesophagus and the lower oesophageal sphincter. Dysphagia may precede cutaneous lesions. Barium
swallow shows absence of peristalsis in distal two-thirds
of the oesophagus. Many of these patients have hiatus
hernia, or reflux oesophagitis and may develop stricture
in distal part of the oesophagus due to recurrent inflammation.
SCHATZKI’S RING
It occurs at the junction of squamous and columnar
epithelium at the lower end of oesophagus and has also
been called lower oesophageal ring. Usually seen in patients
above 50 years of age. Cause is unknown. Symptomatic
patients complain of intermittent dysphagia and some
may even present with bolus obstruction. It may be associated with hiatus hernia. Treatment is oesophageal
dilatation.
NEOPLASMS OF OESOPHAGUS
BENIGN NEOPLASMS
Benign neoplasms are rare compared to malignant ones.
Leiomyoma is the most common and accounts for
two-thirds of all the benign neoplasms. It arises from the
smooth muscle and grows in the wall of oesophagus. Dysphagia is produced when tumour exceeds the diameter
of 5 cm. Barium swallow shows an ovoid filling defect.
Endoscopy reveals a submucosal swelling. Biopsy should
not be taken. Treatment is enucleation of the tumour by
thoracotomy.
Mucosal polyps, lipomas, fibromas and haemangiomas are other benign tumours. They are often peduncu-
lated and present in the oesophageal lumen. Endoscopic
removal is avoided because of the danger of oesophageal
perforation. Treatment is surgical excision by oesophagotomy.
CARCINOMA OESOPHAGUS
Incidence
Incidence of oesophageal carcinoma is high in China, Japan, USSR and South Africa. In India, it constitutes 3.6%
of all body cancers in the rich and 9.13% of those in the
poor.
Aetiology
Smoking and alcohol consumption are high-risk factors
and so are some particular dietary habits. In India, high incidence is associated with tobacco chewing and smoking.
About 5% of oesophageal cancers arise in the pre-existing pathological lesions, such as benign strictures, hiatus
hernia, cardiac achalasia and diverticula. Plummer–Vinson syndrome is another predisposing factor.
Pathology
Squamous cell carcinoma is the most common (93%).
Adenocarcinoma (3%) is also seen, but in the lower oesophagus, and may be an upward extension of the gastric
carcinoma. Other types are rare.
Spread of Carcinoma
1. Direct. The lesion may fill the lumen and infiltrate the
wall of oesophagus. It may also spread to the adjoining
structures which are contact with the oesophagus such
as the trachea, left bronchus, aorta or pericardium. In-
volvement of the recurrent laryngeal nerves causes as-
piration problems.
2. Lymphatic. Depending on the site involved, cervical,
mediastinal or coeliac nodes may be involved. Cervi-
cal and thoracic lesions also spread to supraclavicular
nodes. “Skip lesions” may also occur due to spread
through the submucosal lymphatics.
3. Blood borne. Metastases may develop in the liver,
lungs, bone and brain.
Clinical Features
1. Early symptoms. They include substernal discomfort
and preference for soft or liquid food.
2. Progressive dysphagia and emaciation. Dysphagia
first to solids and then to liquids. Patient loses weight
and becomes emaciated.
3. Pain. Usually signifies extension of tumour beyond
the walls of oesophagus. It is referred to the back.
4. Aspiration problem. Spread of cancer may cause la-
ryngeal paralysis or fistulae formation leading to
cough, hoarseness of voice, aspiration pneumonia and
mediastinitis.
Diagnosis
1. Barium swallow. It shows narrow and irregular oe-
sophageal lumen, without proximal dilatation of the
oesophagus.
2. Oesophagoscopy. Useful to see the site of involve-
ment, extent of the lesion and to take biopsy. Flexible
fibre-optic oesophagoscopy obviates the need for gen-
eral anaesthesia and gives a magnified view.
3. Bronchoscopy. It helps to evaluate any extension of
growth into the trachea and bronchi.
4. CT scan. It is useful to assess the extent of disease and
nodal metastases.
Treatment
Surgery of upper two-thirds of oesophagus is difficult due
to great vessels and involvement of mediastinal nodes.
Radiotherapy is the treatment of choice.
Surgery is the preferred method of treatment for cancer of lower one-third. The affected segment, with a wide
margin of oesophagus proximally and the fundus of
stomach distally, can be excised with primary reconstruction of the food channel.
In advanced lesions, only palliation is possible. An alternative food channel can be provided by:
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391
1. A by-pass operation.
2. Oesophageal intubation with Celestin or MousseauBarbin or a similar tube.
3. Permanent gastrostomy or a feeding jejunostomy.
4. Laser surgery: Oesophageal growth is burnt with Nd:
YAG laser to provide a food channel. Chemotherapy
is used only as a palliative measure in the locally advanced or disseminated disease.
Prognosis
Five-year survival is not more than 5–10%.
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Dysphagia
Dysphagia is difficulty in swallowing. The term
odynophagia is used when swallowing causes pain. The
latter is more marked in ulcerative and inflammatory
lesions of food passages-oral cavity, oropharynx and
oesophagus.
AETIOLOGY
The cause of dysphagia may be preoesophageal (i.e. due to
disturbance in the oral or pharyngeal phase of deglutition),
or oesophageal (when disturbance is in oesophageal phase).
This classification is clinically useful as most of the preoesophageal causes can be easily excluded by physical examination while oesophageal ones require investigation.
PREOESOPHAGEAL CAUSES
1. oral phase. Normally, food must be masticated,
lubricated with saliva, converted into a bolus by movements of tongue and then pushed into the pharynx by
elevation of the tongue against the hard palate. Any disturbance in these events will cause dysphagia. Thus cause
may be:
(a) Disturbance in mastication. Trismus, fractures of man-
dible, tumours of the upper or lower jaw and disorders of temporomandibular joints.
(b) Disturbance in lubrication. Xerostomia following ra-
diotherapy, Mikulicz’s disease, Sjogren’s disease.
(c) Disturbance in mobility of tongue. Paralysis of tongue,
painful ulcers, tumours of tongue, lingual abscess, to-
tal glossectomy.
(d) Defects of palate. Cleft palate, oronasal fistula.
(e) Lesions of buccal cavity and floor of mouth. Stomatitis,
ulcerative lesions, Ludwig’s angina.
2. pharyngeal phase. For a normal swallow, food
should enter the pharynx and then be directed towards
oesophageal opening. All unwanted communications
into the nasopharynx, larynx, oral cavity should be
closed. Disturbances in this phase can arise from:
(a) Obstructive lesions of pharynx, e.g. tumours of tonsil,
soft palate, pharynx, base of tongue, supraglottic larynx, or even obstructive hypertrophic tonsils.
(b) Inflammatory conditions, e.g. acute tonsillitis, periton-
sillar abscess, retro or parapharyngeal abscess, acute
epiglottitis, oedema larynx.
(c) Spasmodic conditions, e.g. tetanus, rabies.
(d) Paralytic conditions. Paralysis of soft palate due to
diphtheria, bulbar palsy, cerebrovascular accidents.
They cause regurgitation into the nose.
Paralysis of larynx, lesions of vagus and bilateral superior laryngeal nerves cause aspiration of food into the
larynx.
OESOPHAGEAL CAUSES
The lesions may lie in the lumen, in the wall or outside
the wall of oesophagus.
1. Lumen. Obstruction to lumen can occur in atresia, for-
eign body, strictures, benign or malignant tumours.
2. Wall. It can be acute or chronic oesophagitis, or motil-
ity disorders. The latter are:
(a) Hypomotility disorders, e.g. achalasia, scleroder-
ma, amyotrophic lateral sclerosis.
(b) Hypermotility disorders, e.g. cricopharyngeal
spasm, diffuse oesophageal spasm.
3. Outside the wall. The lesions cause obstruction by
pressing on the oesophagus from outside:
(a) Hypopharyngeal diverticulum (see p. 310).
(b) Hiatus hernia.
(c) Cervical osteophytes (Figure 69.1).
(d) Thyroid lesions, e.g. enlargement, tumours, Hashi-
moto thyroiditis.
(e) Mediastinal lesions, e.g. tumours of mediastinum,
lymph node enlargement, aortic aneurysm, cardiac enlargement.
(f) Vascular rings (dysphagia lusoria).
INVESTIGATIONS
1. history. A detailed history is of paramount importance. Ascertain, if dysphagia is of:
(a) Sudden onset: Foreign body or impaction of food on a
pre-existing stricture or malignancy, neurological dis-
orders.
(b) Progressive: Malignancy.
(c) Intermittent: Spasms or spasmodic episodes over an or-
ganic lesion.
(d) More to liquids: Paralytic lesions.
(e) More to solids and progressing even to liquids: Malig-
nancy or stricture.
(f) Intolerance to acid food or fruit juices: Ulcerative le-
sions.
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SECTION VII — Diseases of Oesophagus
Figure 69.1. (A & B) Cervical osteophytes causing dysphagia. Barium swallow shows pressure on oesophagus by large osteophytes.
Note any associated symptoms, e.g. regurgitation
and heart burn (hiatus hernia); regurgitation of undigested food while lying down, with cough at night (hypopharyngeal diverticulum); aspiration into lungs (laryngeal paralysis); aspiration into the nose (palatal paralysis).
2. clinical examination. Examination of oral cavity,
oropharynx, and larynx and hypopharynx can exclude
most of the pre-oesophageal causes of dysphagia. Examination of the neck, chest and nervous system, including
cranial nerves should also be undertaken.
3. blood examination. Haemogram is important in the
diagnosis and treatment of Plummer–Vinson syndrome
and to know the nutritional status of the patient.
4. radiography
(a) X-ray chest. To exclude cardiovascular, pulmonary and
mediastinal diseases.
(b) Lateral view neck. To exclude cervical osteophytes and
any soft tissue lesions of postcricoid or retropharyngeal space.
(c) Barium swallow. It is useful in the diagnosis of malig-
nancy, cardiac achalasia, strictures, diverticula, hiatus
hernia or oesophageal spasms. Combined with fluoroscopic control or cineradiography, it can help in the
diagnosis of motility disorders of oesophageal wall or
sphincters.
5. manometric and ph studies. A pressure transducer
along with a pH electrode and an open-tipped catheter is
introduced into the oesophagus to measure the pressures
in the oesophagus and at its sphincters. Acid reflux into
the oesophagus is measured by pH electrode. It also measures the effectiveness of oesophagus to clear the acid load
after acid solution is put in the oesophagus. These studies
help in motility disorders, gastro-oesophageal reflux and
to find whether oesophageal spasms are spontaneous or
acid induced.
6. oesophagoscopy. It gives direct examination of oesophageal mucosa and permits biopsy specimens. Flexible fibreoptic or rigid scopes can be used.
7. other inVestigations. Bronchoscopy (for bronchial
carcinoma), cardiac catheterization (for vascular anomalies), thyroid scan (for malignant thyroid) may be required, depending on the case.
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Foreign Bodies of Food Passage
An ingested foreign body (FB) may lodge in:
1. The tonsil.
2. The base of tongue/vallecula.
3. Posterior pharyngeal wall
4. The pyriform fossa.
5. The oesophagus.
1. tonsil. Usually, it is a sharp fish bone or a needle in
one of the tonsillar crypts. It can be easily observed by
oropharyngeal examination and removed.
2. base oF tongue or Vallecula. Here again it is
usually the fish bone or a needle. It can be observed
by mirror examination. It can be removed as an office
procedure by asking the patient to hold his own tongue
while examiner holds a large laryngeal mirror or an endoscope in one hand and a curved forceps in the other.
Sometimes a sharp needle in the base of tongue may get
totally embedded into its substance due to repeated attempts to feel. It can be diagnosed by radiology and may
require pharyngotomy to extract it. Once in muscular
layers, it has a chance to migrate and an early removal
is indicated.
3. posterior pharyngeal wall. A wire, a needle or a
staple can get transfixed to posterior pharyngeal wall. It
happens when these objects are accidentally taken with
food. Most of them can be seen with oropharyngeal examination under good illumination and removed with a
forceps.
4. pyriForm Fossa. Fish bone, chicken or a mutton
bone, needle or a denture may lodge in the pyriform fossa. Small foreign bodies can be removed under local anaesthetic with a curved forceps as described above. Large
impacted foreign bodies or those in children should be
removed by endoscopy under general anaesthesia.
5. oesophagus. Usual foreign bodies that get lodged in
the oesophagus are a coin, piece of meat, chicken bone,
denture, safety pin or a marble. Sometimes other object
like nails, screws, plastic objects or pieces of glass may also
be seen. Disc batteries are also becoming common these
days due to their wide spread usage. Most of oesophageal foreign bodies lodge just below the cricopharyngeal
sphincter. If they lodge lower down, an underlying condition such as congenital or acquired stricture or a malignancy (in adults) should be suspected and/or a follow-up
barium swallow should be done when oedema due to foreign body removal has subsided.
AETIOLOGY
1. Age. Children are most often affected. Nearly 80% are
below 5 years. They have a tendency to put anything
in the mouth. Playing while eating is another factor.
Education of parents is important to prevent such accidents in toddlers and young children.
2. Loss of protective mechanism. Use of upper denture
prevents tactile sensation and a foreign body is swallowed undetected. Loss of consciousness, epileptic
seizures, deep sleep or alcoholic intoxication are other
factors.
3. Carelessness. Poorly prepared food, improper mastication, hasty eating and drinking.
4. Narrowed oesophageal lumen. Pieces of food may be
held up in cases of oesophageal stricture or carcinoma.
The first symptom of carcinoma oesophagus may be
sudden obstruction from a foreign body such as a piece
of meat, fruit or vegetable.
5. Psychotics. Foreign body may be swallowed with an
attempt to commit suicide.
SITE OF LODGEMENT OF FOREIGN BODY
By far the commonest site is at or just below the cricopharyngeal sphincter. Flat objects like coins are held
up at the sphincter while others are held in the upper oesophagus just below the sphincter due to poor peristalsis.
Foreign bodies which pass the sphincter can be held up
at the next narrowing at bronchoaortic constriction or at
the cardiac end. Sharp or pointed objects lodge anywhere
in the oesophagus.
Once object passes the oesophagus it is likely to pass
per rectum but sometimes it gets obstructed at pylorus,
duodenum, terminal ileum, ileocaecal junction, caecum,
sigmoid colon or even at the rectum. Size and shape of the
object and its nature, sharp or pointed plays an important
part in its lodgement in oesophagus or lower down.
CLINICAL FEATURES
SYMPTOMS
1. History of initial choking or gagging.
2. Discomfort or pain located just above the clavicle on
the right or left of trachea. Discomfort increases on attempts to swallow. Local discomfort may point to the
site of FB in cervical oesophagus but not so in lower
oesophagus.
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