Dysphagia

and
Esophageal
Cancer
GROUP – 3
BONKE MOSES
PAVITHRA MURUGNATHAN
GNANA JACOB SEBASTIAN
Surgical anatomy

 The oesophagus is a muscular tube, approximately

25 cm long, mainly occupying the posterior
mediastinum and
 Extending from the upper oesophageal sphincter
(the cricopharyngeus muscle) in the neck to the
junction with the cardia of the Stomach
 The musculature of the upper oesophagus, including
the upper sphincter, is striated.
 This is followed by a transitional zone of both striated
and smooth muscle with the proportion of the latter
progressively increasing so that, in the lower half of
the oesophagus, there is only smooth muscle. It is
lined throughout with squamous epithelium.
Anatomy

Esophageal wall
Physiology

 The main function of the oesophagus is to transfer

food from the mouth to the stomach in a
coordinated fashion.
 The initial movement from the mouth is voluntary.
 The pharyngeal phase of swallowing involves
sequential contraction of the oropharyngeal
musculature, closure of the nasal and
respiratorypassages, cessation of breathing and
opening of the upper oesophageal sphincter.
 The body of the oesophagus propels the bolus
through a relaxed lower oesophageal sphincter
(LOS) into the stomach, taking air with it
 Coordinated oesophageal wave which follows a conscious
swallow is called primary peristalsis
 The upper oesophageal sphincter is normally closed at rest and
serves as a protective mechanism against regurgitation of
oesophageal contents into the respiratory passages.
 The LOS is a zone of relatively high pressure that prevents gastric
contents from refluxing into the lower oesophagus
 The normal LOS is 3–4 cm in length and has a pressure of 10–25
mmHg.
 Secondary peristalsis is the normal reflex preceded by a
conscious swallow
Symptoms of oesophageal
disease
 Difficulty in swallowing described as food or fluid
sticking (oesophageal dysphagia): must rule out
malignancy
 Pain on swallowing (odynophagia): suggests
inflammation and ulceration
 Regurgitation or reflux (heartburn): common in
gastrooesophageal reflux disease
 Chest pain: difficult to distinguish from cardiac
pain
Dysphagia
 difficulty with swallowing.
 When there is a problem with swallowing in the voluntary (oral
or pharyngeal) phases, patients will usually say that they
cannot swallow properly,
 but they do not characteristically describe ‘food sticking’.
 Instead, when they try to initiate a conscious swallow, food
fails to enter the oesophagus, stays in the mouth or enters the
airway, causing coughing or spluttering.
 Mostly all causes of this type of dysphagia are chronic
neurological or muscular diseases.
CONTD,

 Oesophageal dysphagia occurs in the involuntary

phase and is characterised by a sensation of food
sticking. The nature of this type of dysphagia is
often informative for a possible diagnosis.
 Dysphagia may occur acutely or chronic ,
 Can affect solids and/or fluids,
 and it can be intermittent or progressive.

 Causes of esophageal dysphagia – zenker’s

diverticulum , barrett esophagus, Gastric
esophageal reflux disease, carcinoma etc..,
Investigations

 Radiography
 Plain CXR, contrast oesophagography (barium)
and CT scan of chest
 Endoscopy: rigid and flexible oesophagoscopy
 Endosonography: endoscopic ultrasonography
 Oesophageal manometry: to diagnose
oesophageal motility disorders
 Twenty-four-hour pH and combined
pHimpedance recording: most accurate method
for diagnosis of GORD
Barium Swallow
Endosonography
Oesophageal Diverticulum
 Most oesophageal diverticula are pulsion diverticula that
develop at a site of weakness as a result of chronic pressure
against an obstruction.
 diverticulum - sac or pouch arising from a tubular organ, such
as the esophagus.
 Symptoms are mostly caused by the underlying disorder unless
the diverticulum is particularly large.

 Esophageal diverticula are more common in people who

have motility disorders of the esophagus, such as achalasia.
 Diverticula are indicators of a motor disorder and not
necessarily the cause of symptoms
Classifications

Esophageal diverticula are classified by their location

within the esophagus:
 Zenker’s diverticula (pharyngoesophageal) is the most
common type of diverticula of the esophagus.
Zenker’s diverticula are usually located in the back of the
throat, just above the esophagus
 Mid-oesophageal diverticula, in the mid-chest
 Epiphrenic diverticula, above the diaphragm
Diverticula also may be classified on the basis of
histopathology.
 True diverticula contain all layers of the intestinal tract wall.
 False diverticula also known as pseudodiverticula, occur
when herniation of mucosa and submucosa through a
defect in the muscular wall occurs

Acquired diverticula of the esophagus and hypopharynx also

may be classified according to their pathogenesis
 Pulsion diverticula - form as a result of high intraluminal
pressures against weaknesses in the GI tract wall
 Traction diverticula - occur as a consequence of pulling
forces on the outside of the esophagus from an adjacent
inflammatory process
Zenker’s diverticulum (pharyngeal pouch)
 False and pulsion diverticulum
 It is not really an oesophageal diverticulum as it protrudes
posteriorly above the cricopharyngeal sphincter through the
natural weak point (the dehiscence of Killian) between the
oblique and horizontal (cricopharyngeus) fibres of the inferior
pharyngeal constrictor
 The exact mechanism that leads to its formation is unknown,
but it involves loss of the coordination between pharyngeal
contraction and opening of the upper sphincter.
 due to increased pressure in the oropharynx during swallowing
against a closed upper esophageal sphincter.
Clinical features
 When the diverticulum is small, symptoms largely reflect this
incoordination with pharyngeal dysphagia.
 As the pouch enlarges, it tends to fill with food on eating, and the
fundus descends into the mediastinum. This leads to halitosis and
oesophageal dysphagia.

Treatment can be done

 endoscopically with a linear cutting stapler to divide the
septum between the diverticulum and the upper
oesophagus, producing a diverticulo-oesophagostomy,
 or can be done by open surgery involving pouch
excision, pouch suspension (diverticulopexy)
 and/or myotomy of the cricopharyngeus.
All techniques have good prognosis.
Mid-oesophageal diverticula
 are usually small pulsion diverticula of no particular consequence.
 The underlying motility disorder does not usually require treatment.
 Some pulsion diverticula may fistulate into the trachea, but this is more
common with traction diverticula in granulomatous disease.

Epiphrenic diverticula
 are pulsion diverticula
 situated in the lower oesophagus above the diaphragm
 may be quite large, but presents with few symptoms.
 They again probably reflect some loss of coordination between an
incoming pressure wave and appropriate relaxation of the LOS.
 This needs to be acknowledged in the surgical management of the
patient.
 Large diverticula may be excised, and this should be combined with a
myotomy from the site of the diverticulum down to the cardia to relieve
functional obstruction
GASTROESOPHA-
GEAL REFLEX DISEASE
 It is a pathological reflux from the stomach into
the lower oesophagus.
 Gastro-oesophageal reflux disease (GORD) is the
most common upper gastrointestinal disorder in
western countries.
Causes

Anatomic factors
 Obesity.
 Altered length of intra-abdominal oesophagus
 Altered obliquity of O-G junction (alteration in
angle of ‘His’).
 Reduced pinching action (Pinch-Cock effect) of
right crus of diaphragm
Physiological factors
 Reduced LOS pressure
 Altered transient relaxation period in LOS..
 Delayed gastric emptying
 Increased gastric distension and gastric acid
hypersecretion.
Other factors like Alcohol, smoking, stress, lifestyle.
Pathophysiology

 GERD begins from distended fundus due to variety of

causes and other anatomical and physiological factors,
repetitively unfolding the sphincter to the gastric juice
leading to all problems.
 There is reduced and low LES resistance causing loss of
barrier to reflux.
Fundic distension → stretching of fundus → LOS squamous
epithelium exposed to acid gastric juice → oesophagitis →
increased stimulus to swallow saliva to neutralise oesophagitis
→ further fundal distension → cycle repeats → sphincter is
taken into stretched fundus → effects like erosion, ulceration,
fi brosis, mucosal metaplasia.
Clinical features

 The classical triad of symptoms is retrosternal

burning pain(heartburn), epigastric pain
(sometimes radiating through to the back) and
regurgitation.
 Symptoms are often provoked by food,
particularly those that delay gastric emptying
 Heartburn and regurgitation can be brought on
by stoopingor exercise.
 A proportion of patients have odynophagia with
hot beverages, citrus drinks or alcohol
 Some patients present with less typical symptoms
such as angina-like chest pain, pulmonary or
laryngeal symptoms.
Complications

 Reflux oesophagitis.
 Sliding hiatus hernia.
 Stricture lower end oesophagus.
 Oesophageal shortening.
 Barrett‘s oesophagus.
 Carcinoma (adeno) oesophagus (10% of GERD).
Diagnosis

 Barium study in head down position.

 Endoscopy
 Mucosal biopsy to confirm metaplastic trans
formation.
 24 hours oesophageal pH monitoring
 DeMeester scoring system is used to assess the
severity of the GORD.
DeMeester scoring system
Treatment

LIFE STYLE MODIFICATIONS

 Control of obesity.
 Stop smoking and alcohol.
 Avoid tea, coffee and chocolate.
 Propped up position.
 Small frequent meals.
Drugs
H2 antagonists; antacids.
Proton pump inhibitors (PPIs)—very effective
– Omeprazole 20 mg—BD for 3-6 months.
– Lansoprazole 30 mg.
– Pantoprazole 40 mg.
– Esomeprazole 20 mg.
– Rabeprazole 20 mg.
Prokinetic drugs
– Metoclopramide,
Indications for surgical treatment
– Failure of drug treatment
– Sliding hernia
– Barrett’s ulcer
– Severe pain
– Presence of complications like bleeding/stricture/
shortening, respiratory problems
Antireflux surgery is the only effective long-term
beneficial therapy ideally available and considered
now.
Laparoscopic fundoplication (most popular), Collis-
Nissen vertical gastroplasty and fundoplication,
resection of OG junction when metaplasia is present,
Belsey Mark 4 operation (technically difficult) are the
procedures used now
Fundoplications
 Nissen’s—total 360° posterior
fundoplication
 Toupet’s—partial 180° posterior
fundal/posterolateral
 Rosetti Hell—total anterior fundal
 Dor—anterior partial
 Watson’s—anterolateral 120° partial
 Lind—posterior and anterior
Complication of surgery

 Oesophageal/gastric perforation.
 Haemorrhage.
 Pneumothorax/pyothorax.
 Vagus nerve injury.
 Cardiac arrhythmias.
 Sepsis – mediastinitis or septicaemia.
 Disruption/failure of fundoplication.
BARRETT’S OESOPHAGUS

 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).
 The hallmark of ‘specialised’ Barrett’s epithelium is
the presence of mucus-secreting goblet cells
(intestinal metaplasia)
 It affects lower oesophagus commonly often
middle oesophagus also.
Types (Based on Length)

 If the length of metaplasia is more than 3 cm, it is

called as long segment Barrett’s oesophagus—
classic Barrett type.
 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.
 Cardia metaplasia is metaplasia at OG junction
without any macroscopic change in gastroscopy.
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)
Management
 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.
 Anti reflux treatment by surgery.
 Resection—Always better choice—for high grade dysplasia.
 Transhiatal oesophagectomy is preferred.
Foreign Bodies

 The esophagus is the most common site of foreign

body impaction.
 Infants and toddlers do not have fully mature
oropharyngeal coordination and often
inadvertently swallow small, round foods (eg,
grapes, peanuts, candies), which may become
impacted.
 Impacted disc batteries are particularly worrisome
because they may cause esophageal burns,
perforation, or tracheoesophageal fistula.
 Complications also depend on the nature of the
object involved. Despite their small size, impacted
disk or button batteries are objects of particular
concern because liquefaction necrosis and
perforation can occur rapidly.
 The main complications of esophageal foreign
bodies are
Obstruction
Perforation
Patients with Esophageal
foreign bodies:
 Pediatric patients
 Psychiatric patients
 Patients with underlying esophageal disorders like
malignancy, strictures, aclasia.
 Edentulous patients (elderly)
 Clinical presentation
 This depends on whether the patient is a child or adult. Adults usually describe the event
clearly and acknowledge the possibility of the presence of foreign body in the food passage
 In children symptoms include:
 Irritability
 Poor feeding
 Drooling
 Chest pain
 Coughing
 Respiratory symptoms due to esophageal foreign body is common in children because of
their small and compressible tracheal lumen. These symptoms include stridor, coughing, and
labored breathing.
 Physical examination: This does not play an important role in establishing the diagnosis.
Children with oesophageal foreign body tends to drool. Clinical examination is usually
unremarkable in most of these patients
SYMPTOMS

 The main presenting symptom is acute dysphagia.

 Patients with complete obstruction of the esophagus
hypersalivate and are unable to swallow oral secretions.
 Other symptoms include retrosternal fullness, regurgitation,
odynophagia, blood-stained saliva, and gagging and
choking.

 Hyperventilation resulting from anxiety and discomfort

often gives the appearance of respiratory distress, but
actual dyspnea or auscultatory findings of stridor or
wheezing strongly suggest the foreign body is in the airway
rather than the esophagus.

DIAGNOSIS

 Clinical evaluation
 Imaging studies
 Often endoscopic
evaluation
Treatment

 Sometimes trial of observation and/or

IV glucagon
 Often endoscopic removal
CARCINOMAS
INTRODUCTION:

 The disease usually presents between the ages of 50-

70 years.
 Esophageal cancer is the sixth most common cause
of cancer deaths worldwide. 4 - 6% of total GI
tumors.
 asymptomatic.
 Dysphagia.
 Unintentional weight loss is also common.
 Manifestations of back or chest pain, hoarseness of
voice, unexplained coughing, protracted hiccups,
and severe reflux may be presenting or associated
symptoms. More rarely, neck swelling from
adenopathies may be the initial manifestation.
 Esophageal cancer is classified according to the
type of cells that are involved.
 Adenocarcinoma. Adenocarcinoma begins in the
cells of mucus-secreting glands in the esophagus.
 Squamous cell carcinoma. The squamous cells
are flat, thin cells that line the surface of the
esophagus.
 Other rare types. Some rare forms of esophageal
cancer include small cell carcinoma, sarcoma,
lymphoma, melanoma and choriocarcinoma.
ETIOLOGY:

 The etiology is unknown, but many risk factors for

esophageal cancer have been identified.
 Alcohol abuse, smoking, lye ingestion, radiation
therapy and achalasia are associated with ESCC.
 EAC is associated with Barrett's esophagus , which
is intestinal metaplasia, associated with chronic
gastroesophageal reflux disease.
 EAC has also been associated with obesity, in
particular visceral obesity and metabolic
syndromes which are more common in men than
in women.
Risk factors
 Having gastroesophageal reflux disease (GERD)
 Smoking
 Having precancerous changes in the cells of the
esophagus (Barrett's esophagus)
 Being obese
 Drinking alcohol
 Having bile reflux
 Having difficulty swallowing because of an esophageal
sphincter that won't relax (achalasia)
 Having a steady habit of drinking very hot liquids
 Not eating enough fruits and vegetables
 Undergoing radiation treatment to the chest or upper
abdomen
Spread

Cancer can spread through tissue, the lymph system,

and the blood:
 Tissue: The cancer spreads from where it began by
growing into nearby areas.
 Lymphatic system: The cancer spreads from where
it began by getting into the lymph system. The
cancer travels through the lymph vessels to other
parts of the body.
 Blood: The cancer spreads from where it began by
getting into the blood. The cancer travels through
the blood vessels to other parts of the body.
SQUAMOUS CELL
CARCINOMA:
 90% cases of esophageal carcinomas are
squamous cell carcinoma.
 Esophageal disorders
 Esophageal disorders: • Long standing esophagitis
• Achalasia • Plummer-Vinson Syndrome
 Age. Over 45. M:F 4:1. Race- more common in
BLACKS (6 times). Previous radiation therapy to
the mediastinum.
 Frequent consumption of very hot beverages.
 Most studies have shown that alcohol is the
primary risk factor but smoking in combination
with alcohol consumption can have a synergistic
effect.
 The pathogenesis appears to be linked to
inflammation of the squamous epithelium that
leads to dysplasia and in situ malignant
transformation.
 SCC arise about (locations): 20% in the cervical&
upper thoracic esophagus, 50% in the middle third
& 30% in the lower third.
Genetic predisposition

 Tylosis Howel-Evans syndrome -A genetic disorder

characterized by thickening (hyperkeratosis) of
the palms and soles, white patches in the mouth
(oral leukoplakia), and a very high risk of
esophageal cancer.
 Autosomal dominant - Abnormalities affecting the
p16/INK4 tumor suppressor gene and the
epidermal growth factor receptors are frequently
present in SCC of the esophagus. Mutation in of
these tumors. p53 in 50%
Clinical Features

 Dysphagia
 Odynophagia
 Obstruction
 Weight loss
 Hemorrhage
 Sepsis
 In months to years these lesions become
tumorous, taking one of three forms:
 1. Polypoid fungating type (60%): The most
common type. Cauliflower-like friable mass
protruding into the lumen.
 2. Ulcerating type (25%): A necrotic ulcer with
everted edges that extend deeply and
sometimes erode into the respiratory tree
(Pneumonia), aorta or elsewhere.
(exsanguination)
 3. Diffuse infiltrative type (15%): appears as
annular, stenosing narrowing of the lumen due to
infiltration into the wall of esophagus.
ADENOCARCINOMA

 Adenocarcinoma of the esophagus most

commonly occurs in the distal esophagus and has
a distinct relationship to GERD.
Morphology

 Esophageal adenocarcinoma usually occurs in

the distal third of the esophagus and may invade
the adjacent gastric cardia.
 Initially appearing as flat or raised patches in
otherwise intact mucosa, large nodular masses of
5 cm or more in diameter may develop.
Alternatively, tumors may infiltrate diffusely or
ulcerate and invade deeply.
 Barrett esophagus is frequently present adjacent
to the tumor. Tumors most commonly produce
mucin and form glands, often with intestinal-type
morphology.
 Clinical Features: Dysphagia, Odynophagia (
severe pain on swallowing) Obstruction
progressive weight loss, Anorexia, Fatigue,
Weakness, hematemesis, chest pain, Cough
vomiting.
STAGING
5-year relative survival rates for esophageal cancer
(Based on people diagnosed with esophageal cancer between 2008 and 2014.)
These survival rates do not separate squamous cell carcinomas from adenocarcinomas, although people
with adenocarcinomas are generally thought to have a slightly better prognosis (outlook) overall.

Stage 5-Year Relative Survival Rate

Localized 45%

Regional 24%

Distant 5%

All SEER stages combined 19%

Investigation

 Endoscopy
 Blood test
 Transcutaneous ultrasonography
 Bronchoscopy
 Laproscopy
 CT
 MRI
 Endoscopic ultrasonography
Treatment of carcinoma of
the oesophagus
 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 treatments