Esophagus : Benign and Malignant diseases

 Neuromuscular disorders :
 Motility disorders - Achalasia
 Diverticulum
 Benign Neoplasms
 Malignant Neoplasms
 Perforation
 Injury : Corrosive, Drug induced
 Reflux : GERD, Barret’s
 Hernia : Hiatus
 Congenital abnormalities
 Foreign bodies in esophagus
 Infections
 Strictures : Schatzki’s rings
 Syndromes : Mallory Weiss, Plummer Vinson

 Motility disorders of the esophagus run on a
continuum from hypomotile to hypermotile
dysfunction, with intermediate types in between.
 There are both primary and secondary motor
disorders of the esophagus.
 Most esophageal motility disorders fall into one of
five primary motor disorders: achalasia, DES,
nutcracker esophagus, hypertensive LES, and
ineffective esophageal motility (IEM).
 Secondary motor disorders of the esophagus
result from progression of other diseases such as
collagen vascular and neuromuscular diseases.

 Esophageal manometry is the most accurate method
to assess the coordination and pressure of the lower
esophageal sphincter (LES) and the esophageal body.
 Patients with GERD may have manometric findings of
a defective LES or impaired esophageal motility.
Manometry is an important component in the
preoperative workup of patients who are candidates
for antireflux surgery.
 First, this form of testing excludes achalasia that
may be occasionally misdiagnosed as GERD.
 Second, esophageal manometry characterizes the
esophageal motility, and this information will be used
to determine the surgical approach (Nissen or partial
fundoplication).
 Finally, manometry enables measurement of the
precise location of the LES for accurate pH probe
placement

 Usually a train of five pressure transducers
are bound together with the transducers
placed at 5 cm intervals from the tip and
oriented radially at 72 degrees from each
other around the circumference of the
catheter.
 Recent introduction and clinical application
of high-resolution manometry (HRM) has
made esophageal manometry simple, fast,
and accurate

 The literal meaning of achalasia is “failure to relax,” which is said
of any sphincter that remains in a constant state of tone with
periods of relaxation.
 The incidence is 6 per 100,000 persons per year and is seen in
young women and middle-aged men and women alike.
 Its pathogenesis is presumed to be idiopathic or infectious
neurogenic degeneration.
 Severe emotional stress, trauma, drastic weight reduction, and
Chagas' disease (parasitic infection with Trypanosoma cruzi) have
also been implicated.
 Prevailing theories support the model that the destruction of the
nerves to the LES is the primary pathology and that degeneration
of the neuromuscular function of the body of the esophagus is
secondary.

 This degeneration results in both hypertension of the LES and
failure of the LES to relax on pharyngeal swallowing, as well as
pressurization of the esophagus, esophageal dilation, and a
resultant loss of progressive peristalsis.
 Vigorous achalasia is seen in a subset of patients presenting with
dysphagia. In these patients, the LES is hypertensive and fails to
relax, as seen in achalasia.
 Achalasia is also known to be a premalignant condition of the
esophagus. Over a 20-year period, a patient will have up to an 8%
chance of developing carcinoma.

 The classic triad of presenting symptoms consists of dysphagia,
regurgitation, and weight loss.
 The dysphagia that patients experience begins with liquids and
progresses to solids.
 They eat slowly and use large volumes of water to help wash the
food down into the stomach.
 As the water builds up pressure, retrosternal chest pain is
experienced and can be quite severe until the LES opens and is
quickly relieving. Regurgitation of undigested, foul-smelling foods
is common, and with progressive disease, aspiration can become
life-threatening. Pneumonia, lung abscess, and bronchiectasis
often result from long-standing achalasia.
 The diagnosis of achalasia is usually made from an esophagram
and a motility study.

 The esophagram will show a dilated esophagus with a distal
narrowing referred to as the classic “bird's beak” appearance of
the barium-filled esophagus .
 Sphincter spasm and delayed emptying through the LES, as well
as dilation of the esophageal body, are observed.
 A lack of peristaltic waves in the body and failure of relaxation of
the LES are observed. Lack of a gastric air bubble is a common
finding on the upright portion of the esophagram

 Manometry is the gold standard test for diagnosis and will
help eliminate other potential esophageal motility
disorders.
 In typical achalasia, the manometry tracings show five
classic findings: two abnormalities of the LES and three of
the esophageal body.
 The LES will be hypertensive with pressures usually above
35 mm Hg, but more importantly, it will fail to relax with
deglutition.
 The body of the esophagus will have a pressure above
baseline (pressurization of the esophagus) from incomplete
air evacuation, simultaneous contractions with no evidence
of progressive peristalsis, and low-amplitude waveforms
indicating a lack of muscular tone.
 These five findings provide a diagnosis of achalasia.
 An endoscopy is performed to evaluate the mucosa for
evidence of esophagitis or cancer. It otherwise contributes
little to the diagnosis of achalasia.

•Medical therapy : Calcium ChannelBlocker ,
Botulinum toxin injection
•Modified Heller’s operation (Heller—German, 1913):
Oesophagocardiomyotomy.
Success rate is 85%.
•Either through thoracic or through abdominal
approach,thickened circular muscle fibres are cut longitudinally
for about 8-10 cm, 2 cm proximal to the thickened muscle to 1
cm distal to OG junction. Care should be taken not to open the
mucosa
(Anterior myotomy is done now. Original Heller’s is both anterior
and posterior myotomies).
Nissen’s or Toupet’s fundoplication is done along with the
above procedure to prevent reflux.

Forcible dilatation
 It stretches the spasmodic segment and gradual repeated
dilatations are required. Dilatation up to 54 French bougie
can be done.
 Two types of dilatations are used—
1. Pneumatic and
2. Hydrostatic.
 Plummer’s pneumatic dilatation is done using balloons of
30-40 mm diameters. It is inserted over a guidewire.
 Negus hydrostatic dilatation is done to dilate O-G
junction.
 30 mm diameter balloon is inflated for 3 minutes.
 Laparoscopic/thoracoscopic cardiomyotomy—ideal
 A transhiatal esophagectomy with or without preservation
of the vagus nerve offers a good long-term result.

 Peroral endoscopic myotomy (POEM) is the
endoscopic equivalent of surgical myotomy
and a newer technique for the management
of achalasia.
 POEM utilizes the principles of submucosal
endoscopy to transform the submucosal layer
in the esophagus and proximal stomach into
a tunnel, through which esophageal and
gastric myotomy are carried out using a
flexible endoscope
 Because POEM is performed perorally
without any incisions in the chest or
abdomen, it is a form of natural orifice
transluminal endoscopic surgery (NOTES).

Types
1. Pulsion diverticulum:
 Pulsion diverticula are false type containing mucosa and
submucosa only; is due to high abnormal intraluminal
oesophageal pressure developed due to various motility
disorders.
 a. Pharyngeal pouch through Zenker’s or Killian’s dehiscence
 b. Epiphrenic pulsion diverticulum occurs in lower oesophagus,
usually towards right side, due to obstruction in the distal
oesophagus or due to incoordinated LOS relaxation.
 – Site is within 10 cm of OG junction. It is false type.
 – It is common on right side with wide mouth.
 – Features are of motility disorders like dysphagia, regurgitation,
cough, weight loss, chest pain.
 – Barium study, CT chest are diagnostic; endoscopic evaluation
with EUS, manometry is a must.

Treatment: Diverticulopexy/diverticulectomy (excision)+
oesophageal myotomy (Heller’s) + repair of
associated hiatus hernia/antirefl ux procedure.
2. Traction diverticulum:
 Occurs in mid-oesophagus or in parabronchial region, is due to
mediastinal granulomatous disease like tuberculosis.
 Traction diverticulum is a true type containing all layers in its
wall and is due to traction by the healing fibrosing mediastinal
lymph nodes.
 It is seen commonly towards right side. It has got wide mouth
and it rests on the spine.
 Presentation is dysphagia, chest pain and regurgitation.
 CT scan (chest), barium study, manometry, endoscopy to assess
mucosa with EUS, blood test for tuberculosis
 (ESR, peripheral smear) are the investigations.
 Treatment: Treating the cause like tuberculosis, histoplasmosis.
 Diverticulum less than 2 cm is observed; progressive symptoms,
size > 2 cm needs surgery.
 Surgeries are—diverticulopexy, long oesophageal myotomy.

 Benign tumours of the oesophagus are rare (0.5-1% of all
oesophageal tumours).
 It grows slowly by expansion, compressing surrounding
structures. It never infiltrates or spreads.
 It can be solid, cystic, polypoid.
 It is usually in submucosal plane.
 It can cause obstruction/regurgitation/aspiration/
mediastinal compression.
 It can be squamous papilloma/polyp/inflammatory pseudo
tumour/leiomyoma (commonest benign tumour of
oesophagus— 65%)/neurofibroma/rhabdomyoma/ lipoma.
True adenoma in oesophagus is very rare.
 Features may be asymptomatic (85%—identified
incidentally during contrast X-ray/endoscopy);
dysphagia/airway obstruction/pneumonia/spluttering
during swallowing; stridor/regurgitation.

 Leiomyoma (commonest—65%) is smooth, sessile, lobulated, firm, with
grey-white whorled appearance.
 Only when leiomyoma reaches 5 cm in size it causes obstruction.
 Multiple localised leiomyomas can occur which can be enucleated
independently.
 True diffuse leiomyomas can occur occasionally in females (4%) in lower
oesophagus, as diffuse hyperplasia
 and thickening of both muscular layers; often as part of the Alport’s
syndrome which needs total oesophagectomy
 with gastric pull up, even though benign. Benign leiomyoma of
oesophagus rarely turns into
 leiomyosarcoma. 90% of oesophageal leiomyomas occur in lower third
 of the oesophagus. Leiomyomas are common in men in 5th decade.
 Leiomyoma which expresses the c-kit oncogene (CD117) is considered
as GIST.
 Investigations—barium swallow X-ray (smooth circular outline/eccentric
fi lling defect)/oesophagoscopy/endosonography/
 CT scan.

 Treatment—if tumour is more than 5 cm/symptomatic
 tumour/intraluminal tumour/when diagnosis is doubtful
surgical enucleation is indicated. Enucleation is the therapy
of choice. Ideally it should be done through right-sided
thoracotomy. Occasionally oesophageal resection is needed
 If tumour is very large/tumour with mucosal ulceration/if
tumour is near OG junction. Thoracoscopic resection can be
done. Leak, empyema, sepsis and stricture are the
occasionalComplications
 Unlike in the stomach and intestine (gastric leiomyoma
more than 6 cm/intestinal leiomyoma more than 4 cm are
potentially malignant)
 increased size of the oesophageal leiomyoma does not
predispose the malignant transformation.

 It is 2nd commonest benign tumour of oesophagus.
 It can be congenital or acquired. Congenital is derived
from foregut. It contains mucous. It is lined by ciliated
columnar epithelium. In infants it is common in upper third
of oesophagus; often with a fistula into airway. It can
cause obstruction.
 Acquired cyst is from obstruction of the excretory ducts of
oesophageal glands.
 Treatment: Enucleation or resection

 In the presence of a large sliding hiatus
hernia, the oesophagus is short, but this does
not necessarily mean that, with mobilisation
from the mediastinum, it cannot easily be
restored to its normal length.
 If a good segment of intra-abdominal
oesophagus cannot be restored without
tension, a Collis gastroplasty should be
performed .This produces a neo-oesophagus
around which a fundoplication can be done
(Collis–Nissen operation).

Investigations
 Plain X-ray—lateral and PA erect view showing
retrocardiac air-fluid level.
 Barium meal study very useful.
 ECG.
 3D CT scan is useful.
Treatment
 Treatment is always surgical.
 Excision of sac and repair of the defect.
 If it is gangrenous, gastrectomy is required.
 Either abdominal or thoracic or laparoscopic approach can
be used in treating rolling hernia surgically.
 Mesh reinforcement to hiatus to close the defect may be
needed.

Types
 1. Acute: Following burns, trauma, infection, peptic
ulcer.
 2. Chronic: Reflux of acid in sliding hernia, after gastric
surgery.
 Reflux is quite common in pregnancy.
 Site is always in lower oesophagus.
Pathology
 There is bleeding granulation tissue in lower oesophageal
mucosa with spasm of longitudinal muscle which pulls the
adjacent gastric area upwards into the oesophagus causing
sliding hernia.

Grading
1. Mucosal erythema
2. Mucosal erythema + superficial ulceration
3. Mucosal erythema + superficial ulceration + submucosal
fibrosis
4. Mucosal erythema + extensive ulceration +para mural fi
brosis

Clinical Features
 It is a part of GORD.
 Pain and burning sensation in retrosternal area often
referred to shoulder, neck, arm.
 Heart burn is common.
 Dysphagia.
 Anaemia.
Diagnosis
 Barium meal X-ray.
 Gastroscopy and biopsy.
 Barrett’s ulcer is an ulcer with gastric (columnar)
metaplasia in lower oesophagus.

Treatment
Antacids
H2 blockers
Proton pump inhibitors—Main method and more effective.
Omeprazole 20 mg BD one hour before food (Morning) for 6
months
 Lansoprazole 30 mg
 Pantoprazole 40 mg
 Esomeprazole 20 mg
 Rabeprazole 20 mg (can be given with food).
Prokinetic drugs like metochlopramide, domperi
done,cisapride, mosapride.
 Treating GORD and associated causes. By fundoplication
and other surgeries.
 Resection in severe cases.

 Described by Norman Barrett, British in 1950
 It is the metaplastic changes in the mucosa of the oesophagus as
the result of GORD.
 Squamous epithelium of lower end of the oesophagus is
replaced by diseased columnar epithelium (columnar
metaplasia).
 There is macroscopic visible length of columnar mucosa with
microscopic features of intestinal metaplasia.
 It affects lower oesophagus commonly often middle oesophagus
also.

Types (Based on Length)
a. If the length of metaplasia is more than 3
cm, it is called as long segment Barrett’s
oesophagus—classic Barrett type.
b. If the length is less than 3 cm, it is called as
short segment
Barrett’s oesophagus.
 Histological Types
a. Gastric type: Contains chief and parietal
cells.
b. Intestinal type: Contains goblet cells.
c. Junctional type: Contains mucous glands
alike of gastric cardia.

Clinical Features
 Features of GORD.
 Haematemesis.
 Common in men; common in whites.
Complications of Barrett’s oesophagus
 Ulcerations and stricture
 Dysphagia
 Bleeding
 Perforation
 Adeno carcinoma of O-G junction (25 times more
common)

 Regular endoscopic biopsy and surveillance for low grade
dysplasia.
 Ablation of Barrett’s oesophagus by laser.
 Photodynamic therapy—through endoscopy.
 Argon beam coagulation.
 Proton pump inhibitors—high dose for 3-6 months.
 Antireflux treatment by surgery.
 Resection—Always better choice—for high grade dysplasia.
 Transhiatal oesophagectomy is preferred.
 Endoscopic mucosal resection.

Causes
 Instrumental injuries—commonest cause, 75% commonest
site is just above the level of crico pharyngeus.
 Foreign bodies.
 Alkali injuries.
 Carcinoma oesophagus 1%.
 Boerhaave’s syndrome 15%.
 Trauma 9%.
 Surgical trauma (Vagotomy, thyroidectomy, Heller’s
operation,pneumonectomy, spine surgery).

 Clinical Features
 Chest pain, vomiting, shock, subcutaneous emphysema.
 Investigations
 Chest X-ray—shows pneumomediastinum.
 CT scan.
 Complications
 Mediastinitis.
 Septicaemia.
 Empyema, ARDS.

 Conservative treatment: It is advocated in small
perforations due to instrument where there is minimal
air leak and contamination of mediastinum with less
septic load. Crepitus should be absent; pleura should
be clear and without any obstruction.
 Treatment is—antibiotics, nutrition (TPN/enteral
through tube), fluid management, proper observation
and monitoring the patient by repeated blood counts,
and imaging. Biodegradable removable self expanding
stents also can be used.
 Thoracotomy, proper saline wash to pleura,
mediastinum and repair with buttressing the area
using pedicled intercostal musculopleural flap is done.
Nasogastric tube for long duration, jejunostomy tube
for feeding, ICT for drainage is essential. Often in late
cases decortication of lung is needed to achieve full
expansion of the lung.

 Repair over T tube so as to create a controlled fistula
along with feeding jejunostomy
 Intraluminal stents/mediastinal irrigation and drainage.
 Resection of oesophagus with gastric pull up. As condition
is an emergency situation and with sepsis it carries high
mortality.
 Oesophageal exclusion with cervical oesophagostomy
above and feeding jejunostomy below.
 Diversion surgeries using colon/stomach/jejunum.

Common Foreign Bodies
 Coins, metals, plastics.
 Dentures.
 Pins, toothpicks, batteries.
 Fish or meat bones—dangerous—40%.
 Food (meat—common/vegetables) impaction—45%.
Sites of Impaction in Oesophagus
 Cervical constriction—C6.
 Broncho-aortic constriction—T4.
 Diaphragmatic constriction—T10.
 Pre-existing malignancy or infl ammatory stricture site.

Features
 Sudden dysphagia with chest pain and breathlessn ess.
 Later features of shock, sepsis, mediastinitis, empyema.
Management
 X-ray shows site and level of the F/B.
 Endoscopic removal can be tried.
 Impacted large F/B should be removed by thoracotomy.
 Antibiotics, jejunostomy, TPN are required.

 Here oesophageal webs are seen in uppermost portion of the
oesophagus with spasm of circular muscle fibres.
 Common in patients with long standing iron deficiency anaemia.
 Common in females.
 Superficial glossitis, cheilitis, koilonychia commonly seen.
 Splenomegaly may be present.
 In oesophageal webs, mucosa is hyperkeratotic, friable,
desquamated.
 It is a premalignant condition and presents with severe
dysphagia.
 Oesophagoscopy and biopsy is required to rule out malignancy.

 Oral iron—ferrous sulphate 300 mg TDS with vitamins.
 Blood transfusion is given when there is severe anaemia
 (Transfusion of packed cells).
 IV or IM iron therapy.
 Once anaemia comes under control, webs will clear and
 patient can swallow.
 Follow-up endoscopy is a must.
 Dilatation of web may be required.

 Corrosives are commonest cause of oesophageal stricture.
 Mainly due to ingestion of alkali (sodium hydroxide),
occasionally due to acid (sulphuric acid, nitric acid).
 Acid commonly damages the stomach.
 It causes extensive inflammation of the mucosa with
perioesophagitis which, if not treated leads to multiple
strictures in oesophagus.
 Acute phase lasts for 3 weeks.
 Damage is more in lower 1/3rd of oesophagus.
 Alkali is odourless and tasteless and so large volume is
ingested.
 Alkali causes liquefaction, saponification and thrombosis of
vessels and later leading to fibrosis and stricture.
 Acid causes intense pylorospasm, antral pooling of acid,
coagulation necrosis and eschar formation.
 Severity depends on type of agent, its concentration and
volume.

Features of oesophageal corrosive lesion
Acute/immediate
 – Severe pain, shock, laryngeal oedema
 – Mediastinitis, septicaemia, haemorrhage,
perforation
Late/chronic
 – Dysphagia
 – Stricture—50%
 – Severe malnutrition
 – Recurrent respiratory infection
 – Oesophageal shortening
 – Malignant changes
 – Tracheo-oesophageal fi stula formation
 Corrosive strictures can be multiple. Damage is more
in lower 1/3rdof oesophagus

 Acute phase management: Neutralisation with vinegar or citrus
food if it is alkali ingestion (If pH of the solution is less than 11.5
then damage is less); it is with antacids, milk, egg whites if it is
acid ingestion. Early endoscopy is needed to assess the severity
and extent.
 Emetics and NaHCO3 are avoided as they may precipitate
perforation.
 In 1st degree burns: 48 hours observation; oral feeds are started
once patient swallows saliva painlessly. Regular follow-up
endoscopy at 1st, 2nd and 8th months.
 2nd and 3rd degree burns: They are treated with fluid therapy,
antibiotics, nutrition, resuscitation, PPIs, aerosolised steroids,
fiberoptic guided airway intubation if needed / tracheostomy;
endoscopic oesophageal stenting, feeding jejunostomy,
laparoscopy for evaluation.

 Unstable patients have high mortality. Laparotomy is done
in such patients. If oesophagus and stomach shows full
thickness necrosis, resection of these parts is done and end
cervical oesophagostomy with jejunostomy is done.
 When in doubt re-exploration for second look is done after
36-48 hours to assess the stomach.
 Careful early gentle repeated endoscopy is mandatory.
 Though advocated often for 2-3 weeks, use of steroids is
controversial and under debate.

 Antibiotics if there are chances of aspiration or
perforation.
 Regular oesophageal dilatation is done for stricture.
Stricture is dilated endoscopically using guidewire.
 Dilators are solid type with gradual increase in diameters.
Often radiologic C-ARM guidance is needed to pass the
guide wire into the stomach.
 Dilatation should be done up to minimum 16 mm
diameter. Pneumatic or balloon dilatation is also
practiced.
 Gum elastic dilators, mercury weighted dilators, Eder-
Puestow dilators, Savary-Gilliard dilators, balloon dilators
are other dilators used.
 Earlier, blind dilatation using oesophageal bougies of
increased diameters was the practice, which is followed
even now in many places, but chances of perforation is
more.

 Oesophageal resection in corrosive strictures is technically
diffi cult and may be hazardous. Oesophageal bypass is
better and easier, and following later by regular
endoscopic surveillance for malignant transformation (5%).
Colon is used as replacing conduit as stomach itself may be
diseased in corrosive pathology.
 In multiple strictures oesophageal resection and colonic
transposition may be advocated if risk of malignancy is
 considered.
 Malignancy can develop in corrosive strictures—5%. It is
1000 fold greater than general population.

 Peptic stricture (oesophagitis induced)
 Foreign body
 Postsurgical, radiotherapy
 Congenital
 Infection like tuberculosis
 Drugs like tetracycline, vitamin C

 They are semicircular protrusion of lower oesophageal mucosa
located at or just above the oesophagogastric junction
(squamocolumnar junction). Its under-surface is lined by
columnar gastric epithelium.
 They involve only the mucosa and submucosa of the
oesophagus, not the muscle.
 They present with dysphagia and reflux.
 Episodic aphagia can occur causing, food bolus or meat bone to
get impacted which requires emergency rigid oesophagoscopy to
remove the food.
 5 ml of 2.5% oral papain every 30 minutes to digest food protein
along with 50 mg meperidine IV to dislodge the impacted food
bolus can be tried initially.
 Treatment
 Intermittent oesophageal bougienage.
 Antireflux drugs.
 Ring should not be excised.

 It is a tear in the lower third of the oesophagus which occurs
when a person vomits against a closed glottis, causing leak into
the mediastinum, pleural cavity and peritoneum.
 Site :2-10 cm of posterolateral part of lower oesophagus.
Investigations
 Chest X-ray—shows pneumomediastinum (‘V’ sign of Naclerio).
 MRI/CT chest.
 Total count.
Treatment
 Nil by mouth.
 Antibiotics, IV fl uids, TPN.
 Feeding by jejunostomy.
 Most often surgery with resection may be required (thoracotomy
and repair).
 When severe mediastinitis occurs, condition has high mortality.

 It is seen in adults with severe prolonged vomiting, causing
 longitudinal tear in the mucosa of stomach at and just
below
 the cardia, leading to severe haematemesis.
 Violent vomiting often may be due to migraine or vertigo
 or following a bout of alcohol.
 Presents with severe vomiting and later haemate mesis,
with
 features of shock.
 It is common in one o’clock position.
 Only 10% of cases involve lower oesophageal mucosa.

Investigations
 Gastroscopy, Hb%, PCV, blood grouping.
 During gastroscopy, if stomach is not inflated
properly, 50% cases may be missed.
Differential diagnosis
 Bleeding peptic ulcer
 Oesophageal varices
 Erosive gastritis
 Carcinoma stomach
 Treatment
 Conservative, as it is only a mucosal tear.
 Blood transfusion.
 IV fluids.
 Sedation.
 Haemostatic agents like vasopressin.
 Endoscopic injection therapy

 Carcinoma oesophagus is common in China,South Africa
and Asian countries.
 It is 6th most common cancer in the world.
 It is less than 1% of all cancers. It is 7% of all GI
malignancies.
 It is less common in America and European countries.
 In India, it is common in Karnataka and Orissa.
 When patient presents with dysphagia, often it is fairly
advanced and inoperable and only palliation is the
possibility.
 S urgery is the treatment of choice in early growths.

 Common in:
Middle third—50%.
Lower third—33%.
Upper third—17%.
 Lower 3 cm of oesophagus is lined by columnar
epithelium,and so adenocarcinoma is common here.
 Barrett’s columnar metaplasia which occurs in lower third of
oesophagus is also more prone for adeno carcinoma.
 Squamous cell carcinoma is commonest type in India and
Asian countries.
 • In India 90% are squamous cell carcinomas.
 • In western countries, adenocarcinoma is becoming more
common.
 Adenocarcinoma arises from submucosal oesophageal glands/
heterotrophic columnar epithelium/Barrett’s oesophagus.

 Gross Types
Annular (15%).
Ulcerative (20%).
Fungating—cauliflower like (60%).
Polypoid.
Varicoid—diffuse submucosal type.

 Direct
 Lack of serosal layer in oesophagus favours local extension. In
upper third it spreads through muscular layer and get adherent to
left main bronchus, trachea, and left recurrent laryngeal nerve
(causes hoarseness), aorta or its branches (causes fatal
haemorrhage, but rare).
 It may perforate and cause mediastinitis.It may get adherent to
pleura also.
 Lymphatic spread
 It spreads both by lymphatic permeation and lymphatic
embolisation.
 It can cause satellite nodules elsewhere in the oesophagus,away
from the main tumour.
 Above in the neck, it spreads to supraclavicular lymph nodes.
 In thorax, it spreads to paraoesophageal, tracheobronchial
lymph nodes to sub diaphrag matic lymph nodes.
 In abdomen, it spreads to coeliac lymph nodes.
 Blood spread
occurs to liver, lungs, brain and bones.

 Recent onset of dysphagia is the commonest feature
 Regurgitation.
 Anorexia and loss of weight
 Pain-substernal or in the abdomen.
 Liver secondaries, ascites.
 Bronchopneumonia, melaena.
 Features of broncho-oesophageal fi stula in carcinoma of
upper third oesophagus (30%).
 Left supraclavicular lymph nodes may be palpable.
 Hoarseness of voice due to involvement of recurrent
laryngeal nerve.
 Hiccough, due to phrenic nerve involvement.
 Back pain—due to nodal spread (paraoesophageal/coeliac
 nodes).
 Male to female ratio is 3:1. In adenocarcinoma it is 15:1.

 Barium swallow: Shouldering sign and irregular filling
defect.
 Oesophagoscopy
 Biopsy—
 Chest X-ray—to look for aspiration pneumonia, to see
vocal cord palsy, to identify fistula.
 Bronchoscopy—to see invasion in upper third growth.
 Oesophageal endosonography—to look for the
involvement of layers of oesophagus, nodes, cardia and
left lobe of the liver.
 EUS guided transmucosal nodal needle aspiration cytology
can also be done.
 CT scan (95% accuracy)—to look for local extension, nodal
status, perioesophageal/diaphragmatic/pericardial (1%)/
vascular infi ltration, obliteration of mediastinal fat and
status of tracheobronchial tree in case of upper third
growth.

 Endoscopic oesophageal staining with labelled
iodine results in normal mucosa being stained
brown, but remains pale in carcinoma
 Blood tests: Haematocrit; ESR; Liver function
tests
 Laparoscopy: It is useful to see peritoneal
spread, liver spread and nodal spread..
 PET scan using 18 F-fl uorodeoxyglucose
(FDG):
 Video assisted thoracoscopic approach—to
stage oesophageal carcinoma.
 Endoscopic mucosal resection (EMR) is done
using double channeled endoscope with tip
having a soft plastic cap.
 Endoscopic submucosal dissection (ESD, Japan)
is now devised using hook cautery and scissors
to remove the lesion up to muscularis propria.

 Only 20% of oesophageal cancers present early and becomes
curable. In such early growths confirmed with absence of nodal
spread, curative surgery is the main approach—radical
oesophagectomy.
 Proximal extent of resection should be 10 cm above the
macroscopic tumour and distal extent of resection is 5 cm from
macroscopic distal end of tumour. Proximal stomach has to be
removed commonly especially in lower 1/3rd of tumour.
 If nodes are present, then multimodal approach should be used
like—curative resection; radiotherapy and chemotherapy.
 Outcome of surgery depends on location of tumour; number,
location and size of nodes; tumour grading.
 Neoadjuvant therapy by chemotherapy and/or radiotherapy
prior to surgery may improve the survival.
 In remaining patients (80%) palliation is the main modality of
treatment..

 Indications for Curative Treatment
1. Early growth when patient is fit.
2. When there is no involvement of adjacent perioesophageal
structures, bronchus, liver or distant organs.

Post cricoid tumour (Squamous cell carcinoma):
• Treated mainly by radiotherapy. Radical radiotherapy— 5000-6000
rads.
• Often pharyngolaryngectomy is done along with gastric or colonic
transposition. Free jejunal transfer is the other option.
Upper third growth (Squamous cell carcinoma):
• Treated mainly by radiotherapy.
•Commonly it is advanced with left recurrent laryngeal nerve palsy and
bronchial invasion.If it is early and operable, McKeown three phased
oesophagectomy and anastomosis is done in the neck.
•Initially laparotomy is done to mobilise the stomach. Then
thoracotomy through right 5th space is done and oesophagus is
mobilised. Through right side neck approach, oesophagus with growth
is removed. Anastomosis between pharynx and stomach is done in the
neck.
•Split sternum approach oesophagectomy is also practiced.

Middle third growth (Squamous cell carcinoma):
Ivor Lewis operation (Lewis-Tanner two-phased
oesophagectomy):
•After laparotomy stomach is mobilised. Pyloroplasty is done.
Through right 5th space thoracotomy is done and
growth with tumour is mobilised. Partial oesophagectomy
and oesophagogastric anastomosis is done in the thorax.
•Intercostal tube drainage is placed during closure. Right
gastroepiploic vessels should be retained safely. Azygos vein
should be ligated securely. Mediastinal nodes should be
dissected. Thoracic duct should be ligated if needed. Feeding
jejunostomy is better to maintain nutrition.
•If the growth is inoperable, palliative radiotherapy is given.

Lower third growth (Squamous cell
carcinoma + adenocarcinoma):
1) Orringer approach, i.e. transhiatal blind total oesophagectomy
with anastomosis in the left side of the neck.
•Through laparotomy, stomach and lower part of the oesophagus are
mobilised.
•Through left sided neck approach, upper part of
the oesophagus is mobilised using finger.
•Blind dissection is completed by meeting both fingers above and below in
the thorax. Later oesophagus is pulled up out above through the neck
wound and removed. Continuity is maintained in the neck.
2) Here through Left Thoracoabdominal approach, partial
oesophagogastrectomy is done with oesophagogastric anastomosis.
Often jejunal Roux-en-Y loop anastomosis is done.

Mc- keown esophagectomy combines the attractive
aspects of both trans-thoracic and trans-hiatal
approaches.

 Thoracoscopic oesophagectomy and lymphadenectomy is
becoming popular, safer and effective.
 Robotic surgery is also used.
 Radical oesophagectomy with 3-field clearance of
abdominal/ thoracic and cervical nodes is also practiced in
many centres.
 3-Field clearance (coeliac, thoracic and neck) is done for
mainly squamous cell carcinoma as spread in SCC is
upwards. In adenocarcinoma 2-field clearance is sufficient
 (abdominal—coeliac and thoracic) as spread is downwards.
 Lymphadenectomy in carcinoma oesophagus:
Standard: Nodes removed are—paratracheal,
parabronchial,
carinal, paraoesophageal, posterior mediastinal,
paracardial, left gastric, along lesser curve of stomach.

•When oesophagus is removed totally or subtotally an
interposition is required between cervical oesophagus/pharynx
and distal stomach.
Different parts of GI is used for the same.
•Oesophageal substitutes:
1. Stomach: It is preferred one and is based on right gastric
and right gastroepiploic arteries. It needs only one
anastomosis and take up is well due to good vascularity.
But it can cause postprandial fullness with bile or acid
regurgitation (> 50%). It also needs a pyloroplasty for
gastric drainage as vagotomy is done.
2. Colon: It is better as there is less postprandial problems.
But technique is more with the need of three anastomoses.
Right colon is used with middle colic artery based
as isoperistaltic loop. Left colon is used with ascending
branch of left colic artery as antiperistaltic loop.

3 . Jejunum: Isolated required length of pedicled jejunum
is transposed. Jejunal free transfer is also tried; vessels
are sutured to internal mammary vessels or to the vessels
available the neck. It is used as a last option only.
Transposition is done through posterior mediastinum
(shortest route), right pleural space (transpleural),
retrosternal or subcutaneous route.

Terminal Events in Carcinoma Oesophagus
• Cancer cachexia.
• Sepsis, mediastinitis.
• Immunosuppression.
• Malignant tracheo-oesophageal fi stula (causes severe respiratory
infection and death. Here expansile (self-expandable) endoluminal
stents are used at the site of fistula to have temporary benefi t).
• Erosion into major blood vessel—bleeding.
Prognosis
• Not good because of early spread, longitudinal lymph atics,
aggressiveness, difficult approach, late presentation.
• Nodal involvement carries bad prognosis.
• 5-year survival rate is only 10%.

Esophagus : Benign and Malignant diseases

Esophagus : Benign and Malignant diseases

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