Esophagus

Surgical anatomy
• Esophagus is a narrow muscular tube extending from pharynx to the stomach.
• descends in front of the vertebral column goes through superior and posterior
mediastinum.
• It begins with lower part of the neck at the inferior border of the cricoid
cartilage(C6), extending to the cardiac orifice of the stomach(T11).
• It gives passage for chewed food (bolus) and liquids during the third stage of
deglutition.
PARTS OF THE ESOPHAGUS

The esophagus is split into the following 3 parts:

Cervical part (4 cm in length).
◦ The cervical part extends from the lower border of cricoid cartilage to the superior border of manubrium
sterni.

Thoracic part (20 cm in length).

◦ The thoracic part extends from superior border of manubrium sterni to the esophageal opening in the
diaphragm.

• Abdominal part (1-2 cm in length).

◦ • The abdominal part extends create esophageal opening in the diaphragm to the cardiac end of the
stomach.

– The narrowest part of esophagus is its commencement at the cricopharyngeal sphincter.

Constrictions:

The distance of each constriction is measured from the upper incisor teeth.
First constriction (cervical) at the pharyngo- esophageal junction (at C6) 9 cm (6 inches) from
the incisor teeth.
Second constriction (thoracic) where it’s crossed by the arch of aorta (at T4) 22.5 cm (9 inches)
from the incisor teeth.
Third constriction (thoracic) where it’s crossed by the left principal bronchus(at T5-T6) 27.5 cm
(11 inches) from the incisor teeth
Fourth constriction (diaphragmatic) where it pierces the diaphragm (at T10) 40 cm (15 inches)
from the incisor teeth.
These constrictions are important as they are the likely sites of obstruction in the event of
oesophageal scarring due to the swallowing of caustic or acidic material.
CLINICAL IMPORTANCE OF ESOPHAGEAL CONSTRICTIONS

• The anatomical constrictions of esophagus are of considerable clinical importance because

of the following reasons:
 • These are the sites where swallowed foreign bodies may stuck in the esophagus.
 • These are the sites where strictures develop after ingestion of caustic substances.
• These sites have predilection for the carcinoma of the esophagus.
 • These are sites via which it might be difficult to pass esophagoscope/gastric tube.
The esophagus musculature

• The esophagus consists of

– Striated (voluntary) muscle in its upper third,
– Smooth (involuntary) muscle in its lower third,
– Mixture of striated and smooth muscle in between.
• Externally, the pharyngoesophageal junction appears as a constriction produced by the
cricopharyngeal part of the inferior constrictor muscle (the superior esophageal sphincter)
and is the narrowest part of the esophagus.
Oesophageal Sphincters
• There are two sphincters present in the oesophagus, known as –The upper and –The lower
oesophageal sphincters.
• They act to prevent the entry of air and the reflux of gastric contents respectively.
Upper Oesophageal Sphincter
◦ • The upper sphincter is an anatomical, striated muscle sphincter at the junction between the
pharynx and oesophagus.
◦ • It is produced by the cricopharyngeus muscle.  
◦ • Normally, it is constricted to prevent the entrance of air into the oesophagus.
 Lower Oesophageal Sphincter

• The lower oesophageal sphincter is a physiological sphincter located in the gastro-

oesophageal junction (junction between the stomach and oesophagus).
The gastro-oesophageal junction is situated to the left of the T11 vertebra, and is marked by
the change from oesophageal to gastric mucosa.
• The sphincter is classified as a physiological (or functional) sphincter, as it does not have any
specific sphincteric muscle. Instead,
the sphincter is formed from four phenomena:
◦ 1. The oesophagus enters the stomach at an acute angle.
◦ 2. The walls of the intra-abdominal section of the oesophagus are compressed when there is a
positive intra-abdominal pressure.
◦ 3. The folds of mucosa present aid in occluding the lumen at the gastro- oesophageal junction.
◦ 4. The right crus of the diaphragm has a “pinch-cock” effect.
LES
ARTERIAL SUPPLY
• A.The cervical part is by – Inferior thyroid arteries.
• B.The thoracic part is by – Esophageal branches of – Descending thoracic aorta, and –
Bronchial arteries.
• C.The abdominal part is by – Esophageal branches of • Left gastric artery, and • Left inferior
phrenic artery.
VENOUS DRAINAGE •
A. Cervical part is drained by inferior thyroid veins.
• B. Thoracic part is drained by azygos and hemiazygos veins.
• C. Abdominal part is drained by 2 venous channels, viz, – Hemiazygos vein, a tributary of
inferior vena cava, and – left gastric vein, a tributary of portal vein.
• Thus abdominal part of esophagus is the site of portocaval( porto-systemic ) anastomosis.
 Lymphatics
• The lymphatic drainage of the oesophagus is divided into thirds:
• Superior third : – Deep cervical lymph nodes.
• Middle third: – Superior and posterior mediastinal nodes.
• Lower third: – Left gastric and celiac nodes.
NERVE SUPPLY
• The esophagus is supplied by both parasympathetic and sympathetic fibres.
• The parasympathetic fibres are originated from recurrent laryngeal nerves and esophageal
plexuses created by vagus nerves.
They supply sensory, motor, and secretomotor supply to the esophagus.
• The sympathetic fibres are originated from T5-T9 spinal segments are sensory and
vasomotor.
Symptoms
Dysphagia.
This term means a sensation of obstruction during the passage of liquid or solid through the
pharynx or oesophagus, i.e. within 15 seconds of food leaving the mouth.
The characteristics of the progression of dysphagia to solids can be helpful, e.g. intermittent
slow progression with a history of heartburn suggests a benign peptic stricture;.
Relentless progression over a few weeks suggests a malignant stricture.
The slow onset of dysphagia for solids and liquids at the same time suggests a motility
disorde
Symptoms
Odynophagia
is pain during the act of swallowing and is suggestive of oesophagitis.
 Causes include reflux, infection, chemical oesophagitis
Substernal discomfort, heartburn.
This is a common symptom of reflux of gastric contents into the oesophagus usually a
retrosternal burning pain that can spread to the neck, across the chest, and when severe can be
difficult to distinguish from the pain of ischaemic heart disease.

Chest pain-GERD;motility disorders.

Symptoms
Regurgitation
is the effortless reflux of oesophageal contents into the mouth and pharynx.
 it occurs frequently in patients with gastro-oesophageal reflux disease or organic stenosis.
Reflux
:Passive return of gastro duodenal contents to mouth :
 OtherSymptoms- 1. loss of weight 2. Change of voice-irritation of vocal cord 3. Cough
Investigations
Investigation of oesophageal disorders
1. Barium swallow and meal.
2. endoscopy 1. Oesophagoscopy. 2. Video endoscopy
3. Manometry Is particularly necessary to confirm the diagnosis of specific primary esophageal motility
disorders (i.e., achalasia, diffuse esophageal spasm, nutcracker esophagus, and hypertensive LES).
4.PH recording: Prolonged monitoring of esophageal pH is performed by placing the pH probe or telemetry
capsule 5 cm above the manometrically measured upper border of the distal sphincter for 24 h.
It measures the actual time the esophageal mucosa is exposed to gastric juice, measures the ability of the
esophagus to clear refluxed acid, and correlates esophageal acid exposure with the patient’s symptoms.
. Radiographic Evaluation :The first diagnostic test in patients with suspected esophageal disease should
be a barium swallow including a full assessment of the stomach and duodenum
ESOPHAGEAL PERFORATON
Perforation of the esophagus is a surgical emergency.
 Early detection and surgical repair within the first 24 hours results in 80% to 90% survival; after 24
hours, survival decreases to less than 50%.
 Upon presentation, patients suspected of having a perforation based on initial history and
physical exam are evaluated quickly so that surgical intervention may be initiated promptly.
 Perforation from forceful vomiting (Boerhaave's syndrome), foreign body ingestion, or trauma
accounts for 15%, 14%, and 10% of cases, respectively.
 Most esophageal perforations occur after endoscopic instrumentation for a diagnostic or
therapeutic procedure, including dilation, stent placement, and laser fulguration.
 Other iatrogenic causes that have been noted include difficult endotracheal intubation, blind
insertion of a mini-tracheostomy, and inadvertent injury during dissections in the neck, chest and
abdomen
Boerhaave's Syndrome-”baro trauma”
recurrent emesis disrupts the normal vomiting reflex that enables sphincter relaxation, resulting in an
increase in intrathoracic esophageal pressure and perforation.
Postemetic rupture of the esophagus, now known as Boerhaave's syndrome, is only one of many causes
of esophageal rupture.
Clinical picture :
Severe pain in chest following meal ,
Upper abdomen rigid Mistaken as MI or perforated peptic ulcer
*Pathological perforation :
Perforation of ulcers(barret ulcer or tumours)  Causes erosion in to aorta or ventricle-fatal
*Penetrating injury by knifes & bullet-un common
*During removal of foreign body
*Instumental perforation
Diagnosis :
Mediastinal emphysema, a strong indicator of perforation –
The diagnosis is confirmed with a contrast esophagogram, which will demonstrate
extravasation in 90 percent of patients.
Treatment
The management of patients with esophageal perforation takes place in both the ICU and in the
operating room.
 Patients with an esophageal perforation can progress rapidly to hemodynamic instability and
shock.
 If perforation is suspected, appropriate resuscitation measures with the placement of large-bore
peripheral IV catheters, a urinary catheter, and a secured airway are undertaken before the patient
is sent for diagnostic testing.
 IV fluids and broad-spectrum antibiotics are started immediately, and the patient is monitored in
an ICU
.  Surgery is not indicated for every patient with a perforation of the esophagus, and management
is dependent on several variables: stability of the patient, extent of contamination, degree of
inflammation, underlying esophageal disease, and location of perforation
Principles of non-operative management :
 Analgesia
 Nil by mouth
 Abx
 IV fluids
Op management :
Thoracotomy & repair of perforation done with in few hours of perforation .
Insertion of stents for treatment of perforated cancer.
MALLORY–WEISS SYNDROME
Forceful vomiting may produce a mucosal tear at the cardia rather than a full perforation.
The mechanism of injury is different.
In Boerhaave’s syndrome, vomiting occurs against a closed glottis and pressure builds up in the
oesophagus.
In Mallory–Weiss syndrome, vigorous vomiting produces a vertical split in the gastric mucosa,
immediately below the squamocolumnar junction at the cardia in 90% of cases
The condition presents with haematemesis.
Usually, the bleeding is not severe, but endoscopic injection therapy may be required for the
occasional, severe case.
Surgery is rarely required.
 GASTRO-OESOPHAGEAL REFLUX
DISEASE
Backflow of gastric and/or duodenal contents into the esophagus and past the lower esophageal sphincter
(LES), without associated belching or vomiting
* Reflux may cause symptoms or pathologic changes
Pathophysiology :
LES – a physiological entity not a distinct anatomical structure .
Located just cephalad to the GEJ : Identifiable as a zone of high pressure during manometric evaluation
Factors contributing to high pressure zone
 Intrinsic musculature of distal esophagus
 Sling fibres of cardia
 Diaphragm
 Transmitted pressure of abdominal cavity
GASTRO ESOPHAGEAL REFLUX OCCURS WHEN
 Pressure of high pressure zone is too low to prevent gastric contents from entering the
esophagus
 Sphincter of normal pressure undergoes spontaneous relaxation, not associated with
peristaltic wave in the body of esophagus
 Shortening of High pressure zone
 Cephalad displacement
 Gastric distension
GERD is often associated with HIATAL HERNIA.
Symptoms
• Esophageal •
◦ Heartburn and Regurgitation •
◦ Dysphagia and Odynophagia (stricture and severe esophagitis) •
◦ Barrett’s esophagus •
◦ Esophageal adenocarcinoma •
◦ Noncardiac chest pain

•Pulmonary complications •
◦ Asthma •
◦ Chronic dry cough • .
◦ Aspiration Pneumonia •
◦ Bronchiectasis •
◦ Pulmonary Fibrosis
• Miscellaneous •
◦ Dyspepsia (nausea, vomiting, abdominal Pain) •
◦ Anorexia, Wt. Loss •
◦ Anemia, Fatigue •
◦ Hiccups •
◦ Burning Mouth •
◦ Sleep disturbances
• E.N.T Complications •
◦ Sore Throat •
◦ Hoarseness/Laryngitis •
◦ Globus sensation •
◦ Throat Clearing •
◦ Chronic Otitis media and Sinusitis •
◦ Dental erosions •
◦ Laryngeal cancer
 Evaluation

 Endoscopy :Exclude other diseases esp. tumour . Document presence of peptic esophageal
injury and To assess the degree of injury and Biopsy
 Manometry : To rule out primary motility disorders
 pH monitoring :24 hr pH test- gold standard for diagnosing and quantifying acid
reflux .Assess : 1-total number of reflux episodes ( pH <4) 2- Number of episodes >5 min 3-
Extent of reflux in upright position 4-Extent of reflux in supine position
 Esophagography :True value of the study is to determine the external anatomy of esophagus
and stomach ** To rule out peptic esophageal strictures, diverticula, tumors, hernias
 Imaging??
Treatment
 Medical:
Medical and Lifestyle modifications :
◦ Weight loss
◦ Head end elevation of bedAvoidance of meal 2-3 hrs before bed time
◦ Avoidance of chocolate, caffeine, alcohol, spicy/acidic foods
◦ 8 week course of PPI ‘s

 Surgical : Surgery is cost effective after 8 -10 years of medical therapy

◦ NISSEN FUNDOPLICATION
◦ PARTIAL FUNDOPLICATION

 Endoscopic :
◦ Plicating gastric mucosa just below cardia to accentuate Angle of His
◦ Radiofrequency ablation of sphincter
◦ Injection of submucosal polymers to lower esophagus
Barrett’s oesophagus (columnarlined
lower oesophagus)
Barrett's oesophagus, sometimes called Barrett syndrome or Columnar epithelium lined lower
oesophagus (CELLO).
Barrett esophagus is a complication of chronic GERD ( 5-15%) that is characterized by intestinal
metaplasia within the esophageal squamous mucosa.
• Barrett esophagus is defined as the replacement of the normal distal stratified squamous
mucosa by metaplastic columnar epithelium containing goblet cells.
 Epidemiology
• The incidence of Barrett esophagus is rising, and it is estimated to occur in as many as 10% of
individuals with symptomatic GERD.
• Barrett esophagus is most common in white (Caucasian) males and it typically presents
between 40 and 60 years of age.
• The greatest concern in Barrett esophagus is that it confers an increased risk of esophageal
adenocarcinoma. *30-40
Barrett’s oesophagus
A pre-malignant condition Molecular studies suggest that Barrett epithelium may be more
similar to adenocarcinoma than to normal esophageal epithelium, consistent with the view
that Barrett esophagus is a pre- malignant condition.
Epithelial dysplasia Epithelial dysplasia, considered to be a pre-invasive lesion, is detected in
0.2% to 2.0% of persons with Barrett esophagus each year and is associated with prolonged
symptoms and increased patient age
 Although the vast majority of esophageal adenocarcinomas are associated with Barrett
esophagus, it is important to remember that most (90%) individuals with Barrett esophagus do
not develop esophageal tumors.
Diagnosis•
◦ Diagnosis of Barrett esophagus requires both endoscopic evidence of abnormal mucosa
above the gastroesophageal junction and histologically documented intestinal metaplasia.

 Clinical Features.
◦ • Barrett esophagus can only be identified thorough endoscopy and biopsy, which are
usually prompted by GERD symptoms (dysphagia, heartburn, regurgitation of sour-tasting
gastric contents & attacks of severe chest pain)
Treatment
Surgical resection, or esophagectomy, Photodynamic therapy, Laser ablation, and
Endoscopic mucosectomy.
MOTILITY DISORDERS AND
DIVERTICULA
Introduction
◦ Disruption of coordinated, sequential motility pattern limiting motion of delivery of food and fluid
◦ Common symptoms dysphagia and chest pain •
◦ Not very common •
◦ May be part of a more diffuse gastrointestinal motility problem •
◦ May be associated with GERD
 Achalasia

• Greek – ‘failure to relax’ •

Primary esophageal motility disorder characterized by :
A hypertonic LES which fails to relax in response to swallowing wave.
 Failure of propagated esophageal contraction, leading to progressive dilatation .
Incidence –1 per 100,000 people •
Trypanosoma cruzi (Chagas disease) causes similar syndrome.
 Pathogenesis •
It is due to loss of ganglionic cells in Myentric (Auerbach’s) plexus, cause of which is unknown •
May be due to neurotropic viruses ( varicella zoster)
Different from Hirschsprung’s disease of colon as dilated colon contains normal ganglionic cells •
Pseudoachalasia produced by adenocarcinoma of cardia
Pathophysiology
 Hypertensive non-relaxed esophageal sphincter Imbalance in excitatory and inhibitory
neurotransmission Lack of non-adrenergic, non-cholinergic inhibitory ganglion cells
Achalasia
Clinical features •
History •
 Weight loss (predominant)
Dysphagia (both to solid and liquid foods) more to liquid first
 Regurgitation (especially at night)
Chest pain
Heart burn
Predisposes to SCC of esophagus
Investigations

Manometry :Gold standard for diagnosis (raised resting pressure) •

Barium Studies •  “Bird’s Beak”

Endoscopy: Rule out other diseases (esophagitis or cancer) and GERD

 Management •
Respond well to treatment among motility disorders •
Medical:
To relieve symptoms :
◦ Calcium channel blockers and nitrates used to decrease LES pressure •

Botulinum toxin •
◦ Acts by interfering with cholinergic excitatory neuronal activities at LES •
◦ Not permanent and has to be injected every few months endoscopically •
◦ For elderly patient if surgery contraindicated
 Pneumatic dilatation •
• Involves stretching the cardia with a balloon to disrupt the muscle and render it less
competent •
• Perforation is the major complication •
• The risk of perforation increases with bigger balloons •
• should be used cautiously for progressive dilatation over a period of weeks •
• Forceful dilatation is curative in 75–85% of cases •
• The results are best in patients aged more than 45 years
Heller’s myotomy •
• This involves cutting the muscle of the lower esophagus and cardia •
• The major complication is gastro-esophageal reflux •
• most surgeons therefore add a partial anterior fundoplication (Heller–Dor’s operation)
• It is successful in more than 90% of cases and may be used after failed dilatation
Zenker’s diverticulum (pharyngeal
pouch)
Posterior protrusion of esophageal wall above cricopharyngeal sphincter through the natural
weak point (the dehiscence of Killian) between the oblique and horizontal (cricopharyngeus)
fibres of the inferior pharyngeal constrictor
exact mechanism to its formation is unknown, but it involves loss of the coordination between
pharyngeal contraction and opening of the upper sphincter
As the pouch enlarges, it tends to fill with food on eating, and the fundus descends into the
mediastinum
This leads to halitosis and esophageal dysphagia •
Coughing out of same food several hours after ingestion
Treatment
• Endoscopically with a linear cutting stapler to divide septum between the diverticulum and
the upper esophagus, producing a diverticulo-esophagostomy,
or
.Open surgery involving pouch excision, pouch suspension (diverticulopexy) and/or myotomy
of the cricopharyngeus •
All techniques have good results
 Disorders of body of esophagus
Diffuse Esophageal Spasm: •
f>m
Motor abnormality of lower 2/3rd of esophagus •
Muscular hypertrophy and degeneration of vagus branches •
Repetitive simultaneous and high amplitude esophageal contractions •
C/f: Chest pain (mimics angina), dysphagia • Aggravated by acid reflux, dinking cold liquids,
heightened emotional stress •
10% LES relaxation on wet swallow
Diffuse Esophageal Spasm:
Diagnosis:
◦ Radiograph- Corkscrew esophagus or pseudo- diverticulosis on esophagogram, distal bird beak sign
or normal peristalsis can also be present
◦ Manometry- Simultaneous multipeaked contractions and intermittent normal peristalsis of high
amplitude (>120mmHg) or long duration (>2.5 secs)
Diffuse Esophageal Spasm
Treatment: •
◦ Psychiatric evaluation is done along with elimination of trigger factor •
◦ Acid suppression, nitrates, calcium channel blockers, sedatives or
anticholinergics is used •
◦ Bougie dilatation of esophagus (50-60 fr) •
◦ Botulinum toxin injection
◦ Surgery:
◦ Indication- severe chestpain, dysphagia or pulsion diverticula of thoracic esophagus Procedure-
long Esophagomyotomy through left thoracotomy or video assisted technique (proximally, from
thoracic inlet to distal extent to LES)
Nutcracker Esophagus (hypercontractile esophagus):

•M/c esophageal hypermotility disorder

•m=f
• most painful, dysphagia, chest pain
• Hypertrophic musculature with high amplitude contractions(DCP > 8000 or >180mmHg), long
duration (>6 secs)
• The LES pressure is normal
• LES relaxation occurs with each wet swallow.
• Ambulatory monitoring can help distinguish this disorder from DES
• Treatment- mainly medical with Nitrates, Antispasmodics to avoid caffeine, cold & hot drinks
Leiomyoma –

Benign smooth muscle tumor –

Most common (70% of Benign eso tumor) –
Age – Younger patient –
M= F - Most arise from the inner circular muscle layer of the distal and midthoracic esophagus
Symptoms :
1. Asymptomatic
2.• -/S  dysphagia, pain , bleeding •
3.-/S  distal tumor .asso GERD
 Leiomyoma –
Diagnosis and workup
 Barium esophago: smooth-contoured filling defects
 Esophagoscopy and EUS: a normal overlying mucosa is seen over a hypoechoic tumor arising from the
fourth ultrasound layer
 Atypical EUS findings -tumor 4 cm or larger, -irregular margins -mixed internal echo characteristics, -
associated regional lymphadenopathy
 Bx: can’t diff b/t leiomyoma & leiomyosarcoma

treatment :
• asymptomatic tumors with typical EUS features: expectant therapy and EUS observation •
Symptomatic : removal :ENUCULATION
• DDx • Leiomyosarcoma • GISTs :(originate from GI pacemaker cells of Cajal, stain positively for
tyrosine kinase and should be excised by esophagectomy.
Esophageal lio-myoma
OTHER NON-NEOPLASTIC
CONDITIONS
Schatzki’s ring
Schatzki’s ring is a circular ring in the distal oesophagus , usually at the squamocolumnar
junction.
cause is obscure, but there is a strong association with reflux disease.
The core of the ring consists of variable amounts of fibrous tissue and cellular infiltrate.
 Most rings are incidental findings.
Some are associated with dysphagia and respond to dilatation in conjunction with medical
antireflux therapy.
Chagas’ disease

This condition is confined to South American countries, but is of interest because oesophageal
symptoms occur that are similar to severe achalasia.
It is caused by a protozoan, Trypanosoma cruzi, transmitted by an insect vector.
Parasites reach the bloodstream and, after a long latent period, there is damage particularly to
cardiac and smooth muscle.
Destruction of both Auerbach’s and Meissner’s plexus leads to acquired megaoesophagus.
Plummer–Vinson syndrome
This is also called the Paterson–Kelly (or Paterson–Brown Kelly) syndrome or sideropenic dysphagia
Dysphagia is said to occur because of the presence of a postcricoid web that is associated with iron
deficiency anaemia, glossitis and koilonychia.
The classic syndrome is rarely complete.
Some patients may have oropharyngeal leukoplakia, and this may account for an alleged increased risk
of developing hypopharyngeal cancer.
Webs certainly occur in the upper and middle oesophagus, usually without any kind of associated
syndrome.
They are nearly always thin diaphanous membranes identified coincidentally by contrast radiology.
Even symptomatic webs that cause a degree of obstruction may be inadvertently ruptured at endoscopy.
Few require formal endoscopic dilatation
Cancer of the Esophagus
Ca esophagus is the 6th most common cancer in the world. 
Worldwide, squamous cell cancer is most common, but adenocarcinoma predominates in the
west and is increasing in incidence
Esophageal cancer most commonly presents in the sixth to seventh decades of life.
 It is a male predominant disease with M:F ratio of 3:1 for Sq. ca and 15:1 for Adeno Ca.
Types of Ca Esophagus:

Squamous cell carcinoma

Adenocarcinoma
Less common types:
Mucoepidermoid cancer
Adenosquamous cancer
Small cell cancer
Basaloid squamous cancer
Sarcomatoid
Lymphoma, melanoma, and various subtypes of Stromal tumor
Etiology
Squamous Carcinoma
◦ Smoking
◦ Alcohol consumption
◦ Hot beverages
◦ N- nitroso compounds – Pickled / smoked food
◦ Caustic ingestion
◦ Acalasia
◦ Bulimia tylosis
◦ Plummer Vinson Syndrome
◦ External beam radiation
 Etiology 
Adenocarcinoma
Smoking
 Alcohol consumption
Esophageal diverticula
 GERD
 Acid suppression medication
 Barretts esophagus
Malignancy of aerodigestive tract.
Squmaous Cell carcinoma
Squamous cell carcinomas arise from the squamous mucosa that is native to the esophagus
Found in the upper and middle thirds of the esophagus 70% of the time.
Male to female ratio is 3:1.
 It occurs in the 5th decade of life.
Infrequent before 30 years of age.
 It has highest mortality in 60-70 years of age in men.
The 5-year survival rate varies but can be as high as 70% with polypoid lesions and as low as
15% with advanced tumors.
. Adenocarcinoma
Adenocarcinoma now accounts for almost 70% of all esophageal carcinomas diagnosed in the
United States and Western countries.
There are a number of factors responsible for this shift in cell type:
 Increasing incidence of GERD
Western diet
Increased use of acid-suppression medications
As an adaptive measure, the squamous-lined distal esophagus changes to become lined with
metaplastic columnar epithelium (Barrett’s esophagus).
 Progressive changes from metaplastic (Barrett’s esophagus) to dysplastic cells may lead to
the development of esophageal adenocarcinoma.
Adenocarcinoma
Histologically, esophageal adenocarcinoma arises from one of three sites:
◦ Submucosal glands of the esophagus
◦ Heterotopic islands of columnar epithelium
◦ Malignant degeneration of metaplastic columnar epithelium (Barrett’s esophagus)

Male to female ratio – 15:1

Infrequent before the age of 40 years.
Symptoms
Asymptomatic
 Mimic symptoms fo GERD
 Heartburn,
regurgitation,
 Indigestion
Dysphagia
 Weight loss A
dvanced Disease ,Choking ,Coughing ,Aspiration Suggests tracheoesophageal fistula
Hoarseness .Vocal cord paralysis Suggests invation of Recurrent Layngeal nerve.
Jaundice – Liver metastasis
Chronic pain - Bone metastasis
Respiratory symptoms – lung metastasis
 Diagnosis
Hx and examination
Esophagram:
◦ A barium esophagram is recommended for any patient presenting with dysphagia.
◦ The esophagram provides an overview of anatomy and function.
◦ It can differentiate intraluminal from intramural lesions and discriminate between intrinsic (from a
mass protruding into the lumen) and extrinsic (from compression of a structures outside the
esophagus) compression.
◦ The classic finding of an apple core lesion in patients with esophageal cancer is recognized easily.
Diagnosis
 Endoscopy:
The diagnosis of esophageal cancer is best made from an endoscopic biopsy.
During endoscopy, it is critical to document the following:
◦ Location of the lesion (with respect to distance from the incisors)
◦ Nature of the lesion (e.g., friable, firm, polypoid)
◦ Proximal and distal extent of the lesion
◦ Relationship of the lesion to the cricopharyngeus muscle, GEJ, and gastric cardia Distensibility of
the stomach.
Diagnosis
 A CT scan of the chest and abdomen is important to assess the :
◦ length of the tumor,
◦ thickness of the esophagus and stomach,
◦ regional lymph node status (including cervical, mediastinal, and celiac lymph nodes),
◦ distant disease to the liver and lungs.
◦ It is also helpful for determining T4 lesions, in which the lesion is invading surrounding structures.
◦ It may identify a fistula or other anatomic variations, such as a deviated trachea.

Although a CT scan is helpful, its accuracy is only 57% for T staging, 74% for N staging, and
83% for M staging.
Diagnosis
 PET: An 18 F-fluorodeoxyglucose (FDG)– positron emission tomography (PET) scan evaluates
the primary mass, regional lymph nodes, and distant disease.
 MRI
. It can accurately detect T4 lesions and metastatic lesions in the liver but overstages T and N
status, with only a 74% accuracY
 Diagnosis
 Endoscopic ultrasound:
EUS is the most critical component of esophageal cancer staging
The information obtained from EUS will help guide medical and surgical therapy
The experienced endoscopic ultrasonographer can identify
◦ the depth and length of the tumor,
◦ degree of luminal compromise,
◦ status of regional lymph nodes,
◦ involvement of adjacent structures.
◦ biopsy samples can be obtained of the mass and lymph nodes in the paratracheal, subcarinal,
paraesophageal, celiac, lesser curvature, and gastrohepatic regions.
Diagnosis
 Bronchoscopy, mediastinoscopy, thoracoscopy, and laparoscopy are all useful staging tools
Tis High-grade dysplasia
T1 Tumour invading lamina propria or submucosa
T2 Tumour invading muscularis propria
T3 Tumour invading beyond muscularis propria
T4a Tumour invading adjacent structures (pleura, pericardium,
diaphragm)
T4b Tumour invading adjacent structures (trachea, bone, aorta)
N0 No lymph node metastases
N1 Lymph node metastases in 1–2 nodes
N2 Lymph nodes metastases in 3–6 nodes
N3 Lymph node metastases in 7 or more lymph nodes
M0 No distant metastases
M1 All other distant metastases
Stage 1A: T1N0M0; 1B: T2N0M0; 2A: T3N0M0; 2B: T1/2N0M0;
3A: T4aN0M0, T3N1M0, T1/2N2M0
Stage 3B: T3N2M0; 3C: T4aN1/2M0, T4bN0–3M0, T1–4N3M0;
4T:1–4N1–3M
Treatment of malignant tumours
PRINCIPLES:
At the time of diagnosis, around two-thirds of all patients with oesophageal cancer will already
have incurable disease.
The aim of palliative treatment is to overcome debilitating or distressing symptoms while
maintaining the best quality of life possible for the patient.
As dysphagia is the predominant symptom in advanced oesophageal cancer, the principal aim of
palliation is to restore adequate swallowing.
A variety of methods is available and, given the short life expectancy of most patients, it is
important that the choice of treatment should be tailored to each individual.
Once oesophageal neoplasms reach the submucosal layer of the oesophagus, the tumour has
access to the lymphatic system, meaning that, even at this early local stage, there is an incidence
of nodal positivity for both squamous cell carcinoma and adenocarcinomas of about 20%.
.Radical oesophagectomy is the most important aspect of curative treatment
 Neoadjuvant treatments before surgery may improve survival in a proportion of patients
 Chemoradiotherapy alone may cure selected patients, particularly those with squamous cell
cancers
 Useful palliation may be achieved by chemo-/radiotherapy or endoscopic treatment
Treatments with curative intent
SURGERY
Histological tumour type, location and the extent of the proposed lymphadenectomy.
TWO-PHASE OESOPHAGECTOMY (ABDOMEN AND RIGHT CHEST, IVOR LEWIS)
TRANSHIATAL OESOPHAGECTOMY (WITHOUT THORACOTOMY).
NEOADJUVANT TREATMENTS WITH SURGERY .
Postoesophagectomy
● Reflux may be a problem after resection
● Symptoms may be atypical
● Reflux may be limited or avoided by subtotal oesophagectomy and gastric transposition high in the
chest
Non-surgical treatments
Radiotherapy alone.
Chemoradiotherapy. : may be a useful alternative to surgery, especially in unfit patients .
Palliative treatment:
Surgical resection and external beam radiotherapy may be used for palliation, but are not suitable
when the expected survival is short, because most of the remainder of life will be spent recovering
from the ‘treatment’.
Intubation: metallic stent
Endoscopic laser treatment may be used to core a channel through the tumour. It is based on
thermal tumour destruction.
Brachytherapy is a method of delivering intraluminal radiation with a short penetration distance
(hence the prefix ‘brachy’) to a tumour.
Malignant tracheo-oesophageal fistula.
Some have advocated surgical bypass and oesophageal exclusion, but this is a major procedure.
An expanding metal stent is probably the best treatment.