C 1+ 2 Surgicl Pathology of Oesophagus

SURGICAL PATHOLOGY
OF ESOPHAGUS
4 hours
SURGICAL PATHOLOGY OF THE ESOPHAGUS - 4

hours
C 1 2 hours
Esophageal trauma: corrosive esophagitis: etiology, clinical
aspects, evaluation, diagnosis, treatment.
Motility disorders: diffuse esophageal spasm, achalasia of
cardia(definition,etiology,
clinical
aspects,
evaluation,
diagnosis, differential-diagnosis,complications, treatment)
Esophageal diverticula: definition, etiology, clinical aspects,
evaluation, diagnosis, differential diagnosis, complications,
treatment
C 2 2 hours
Tumors of esophagus: Benign tumors of the esophagus:
pathology, evaluation diagnosis treatment. Malignant tumors
of the esophagus: classification, clinical aspects, pathology,
evaluation, diagnosis, differential diagnosis, treatment.
SURGICAL PATHOLOGY OF ESOPHAGUS

I. MECHANICAL AND CHEMICHAL TRAUMA
MECHANICAL TRAUMA OF ESOPHAGUS
ESOPHAGEAL PERFORATION
CAUSES OF ESOPHAGEAL PERFORATION
INSTRUMENTAL
Endoscopy
Dilation
Intubation
Sclerotherapy
Laser therapy
NON INSTRUMENTAL
Barogenic trauma
Postemetic (Boerhaave syndrome)
Blunt chest or abdominal trauma
Other (eg, labor, convulsions, defecation)
Penetrating neck, chest, or abdominal trauma
Operative trauma
Esophageal reconstruction (anastomotic disruption)
Vagotomy, pulmonary resection, hiatal hernia repair,
esophagomyotomy
Corrosive injuries (acid or alkali ingestion)
Erosion by adjacent infection
Swallowed foreign body

Pathophysiology
Regardless of the specific cause, the resulting mediastinitis and his severe consequences
demand prompt recognition and treatment of the esophageal disruption.
disruption
Esophageal and gastric contents are sucked into the mediastinum by respiratory movements
and negative intrathoracic pressure.
Salivary enzymes, gastric acid, bile, and food enter the mediastinum, the presence of oral
bacteria in these fluids initiates a fulminant infection and an inflammatory response
progresses.
This mediastinal burn produces massive fluid accumulation, which can displace the
trachea, heart, or lungs
The entire process is aggravated if there is preexisting esophageal disease causing
obstruction distal to the perforation.
Clinical Features
Patients with esophageal perforation characteristically present with:
cervical or thoracic pain,
difficulty swallowing,
respiratory distress,
fever.
Pain features depends with esophageal perforation location
Cervical or upper thoracic esophagus generally cause cervical or high retrosternal pain
Middle or distal esophagus produce anterior thoracic, posterior thoracic, interscapular, or
epigastric pain.
Upper thoracic esophageal perforations may produce signs of right pleural effusion,
effusion while
Distal esophageal perforation is associated with left pleural effusion.
effusion
4

Diagnosis
Barium esophagogram demonstrates

a perforation (arrow) in the middle
third of the thoracic esophagus.
Pain or fever after esophageal instrumentation

or operation is indicative of an esophageal
perforation and is an indication for an
immediate contrast esophagogram with
hidro - soluble contrast substance.
A chest roentgenogram may help to confirm
the diagnosis by demonstrating air in the soft
tissues of the neck or
mediastinum(pneumomediastinum)
pneumomediastinum or a
hydrothorax or pneumothorax.
A contrast-enhanced CT scan may lead to
the diagnosis
The morbidity and mortality rates associated
with esophageal perforation are directly
related to the time interval between diagnosis
of the injury and its repair or drainage

Management(Principles of Surgical Treatment)

The initial treatment of an acute esophageal perforation focuses on:
decreasing bacterial and chemical contamination of the mediastinum
restoring intravascular volume losses.
Oral intake is withheld, the patient is instructed not to swallow saliva. A disposable oral
dental suction is often helpful for evacuating oral secretions.
Broad-spectrum intravenous antibiotics with activity against oral flora are administered
using a combination of a cephalosporin (cefazolin or cefamandole), 1 g/4 h, and an
aminoglycoside (gentamicin or tobramycin), 1 to 1.5 mg/kg/8 h, and metronidasole
2g/24h.
Nasogastric tube decompression of the stomach is instituted to minimize possible
gastroesophageal reflux and further soiling of the mediastinum.
Therapy of esophageal perforation is influenced by:
The location of the tear
The size of the tear
The cause of the tear,
The length of delay in diagnosis,
The extent of mediastinal and pleural contamination
The presence of intrinsic esophageal disease.
The treatment of an acute esophageal perforation must be individualized.
6

Nonoperative Therapy
Although most esophageal perforations require operative intervention; only selected
patients may be managed nonoperatively with:
Cessation of oral intake,
Administration of antibiotics,
Intravenous hydration until the disruption heals or the small contained cavity begins
to decrease in size.
Criteria for nonoperative therapy of an esophageal perforation include the following:
A local, contained disruption without evidence of pleural contamination (hydrothorax
or pneumothorax),
A walled-off extravasation in which contrast material drains back into the esophagus,
Minimal or no symptoms,
Minimal or no evidence of systemic infection (fever or leukocytosis).
The usual clinical settings in which such perforations are encountered are:
cervical esophageal tears caused by esophagoscopy;
intramural dissections that have occurred during dilation of a stricture or pneumatic
dilation for achalasia;
asymptomatic esophageal anastomotic disruption discovered on a routine
postoperative contrast study.

When treating such perforations conservatively,

oral hygiene should be optimized to minimize further contamination by oral bacteria
A nasogastric tube is seldom helpful.
Nutrition may be maintained by a nasogastric feeding tube, gastrostomy, or jejunostomy
or by intravenous hyperalimentation until oral intake can be resumed, usually 1 to 3
weeks after the injury.
nonoperative therapy is best suited for patients presenting no more than 24 hours after
the injury with no systemic evidence of sepsis and clearly demonstrable, contained,
internally drained leaks on barium esophagogram.
Infants with iatrogenic perforation can often be successfully managed without operation.
Perforations complicating pneumatic dilation for achalasia occur in 4% to 6% of patients, and
most are small and well-managed medically with antibiotics and intravenous
hyperalimentation.
For the remainder of patients with perforations, operative therapy is generally
indicated.
OPERATIVE THERAPY OF ESOPHAGEAL PERFORATIONS
Cervical and Upper Thoracic Esophageal Perforations lead to:
Progressive contamination of the mediastinum as infection descends dependently along the
fascial planes from the neck.
Unless adequate drainage is accomplished, death from mediastinitis follows.
Most cervical and upper thoracic perforations may be adequately drained through a cervical
approach, placing drains in the retroesophageal space.
An incision is made parallel to the anterior border of the sternocleidomastoid muscle, which is retracted laterally along with the
carotid sheath and its contents. The trachea, thyroid gland, and strap muscles are retracted medially. It may be necessary to divide
the omohyoid muscle, middle thyroid vein, and occasionally the inferior thyroid artery to reach the prevertebral fascia. Once this is
identified, blunt finger dissection into the prevertebral space gives access to the abscess cavity, and appropriate drains are placed
and brought out through the skin incision.
When a cervical esophageal perforation extends into either pleural cavity or the lower mediastinum, the cervical approach is
inadequate, and transthoracic drainage is required.

Operative Therapy Of Esophageal Perforations(suite)
Approach for drainage of a cervical

esophageal perforation.


Thoracoesophageal Perforations
Normal esophagus
The earlier an esophageal perforation is recognized and treated, the better is the chance for
successful primary repair.
Most agree that such perforations that are not associated with intrinsic esophageal disease
are best treated with primary repair of the tear combined with wide mediastinal drainage.
A change in philosophy has occurred regarding the application of primary repair to
perforations occurring in an normal esophagus regardless of the duration of the injury.
Perforations of the lower third of the esophagus are approached through a left thoracotomy
in the sixth or seventh interspace, while more proximal thoracic esophageal tears are
approached through a right thoracotomy.
Mediastinal drainage is achieved by opening the mediastinal pleura from the level of the
tear to the thoracic inlet superiorly and the diaphragm inferiorly, irrigating the
mediastinum, and placing a large-bore chest tube that allows transpleural drainage.
Perforations of the intraabdominal esophagus unassociated with pleural contamination are
approached through the abdomen.
Esophagus With Intrinsic Disease
Perforations associated with distal obstruction from intrinsic esophageal disease constitute
a problem because breakdown of an attempted repair is common in the presence of distal
obstruction.
The associated obstruction must be relieved at the same time of repair and drainage.
10


Patients with intrinsic esophageal disease that cannot be treated effectively by more
conservative means are best treated by esophageal resection.
Immediate esophageal substitution with colon(retrosternal) or stomach (in the posterior
mediastinum) in the native esophageal bed.
Final position of the mobilized stomach in the posterior mediastinum

after transhiatal esophagectomy and cervical esophagogastric
anastomosis.
11


In situations in which immediate esophageal reconstruction is not possible, the stomach
is divided from the esophagus, the cardia is oversewn, The intrathoracic esophagus is
then mobilized through the diaphragmatic hiatus and a cervical incision, delivering the
entire thoracic esophagus through the neck wound and placing it on the anterior chest
wall.
The mediastinum can be copiously irrigated through the cervical incision and the
diaphragmatic hiatus at the time of esophagectomy
A feeding jejunostomy is used for enteral alimentation until reconstruction is performed
several weeks later.
Irrigation of the posterior mediastinum

after transhiatal esophagectomy for
irreparable esophageal disruption.
12

Late Esophageal Perforation
The longer the time interval between the occurrence of the perforation and operative
treatment, the more inflamed are the tissues adjacent to the tear and, at least
theoretically, the greater is the risk of failure of primary suture repair.
Patients with late-recognized esophageal perforations have been treated in a variety of

ways, with wide drainage alone, drainage and closure, drainage over a T-tube,
esophageal resection, exclusion and diversion, and even nonoperative management.
13

CAUSTIC INJURY OF ESOPHAGUS
Caustic ingestion occurs in two categories of patients:

Children younger than 5 years of age who accidentally swallow these agents
Adults who are attempting suicide.
The most common agents responsible for caustic esophageal injuries are alkalis(sodiun
hydroxide), acids, bleach, and detergents containing sodium tripolyphosphate.
tripolyphosphate
Ingestion of detergents and bleach causes only mild esophageal irritation, which heals
without adverse sequelae.
Acids and alkalis, may have devastating effects that range from acute multiorgan
necrosis and perforation to chronic esophageal and gastric strictures.
Alkalis are more destructive, producing liquefaction necrosis, which almost ensures deep
penetration
Acids usually cause coagulation necrosis that in part limits the depth of the injury.
In response to either ingested acid or alkali, reflex pyloric spasm occurs, with resultant
pooling of these agents in the gastric antrum.
Laboratory studies using the canine model have shown that both cricopharyngeal and
pyloric sphincter spasm occur when concentrated lye enters the esophagus and stomach.
The esophagus contracts vigorously, propelling the caustic into the stomach. Pyloric and
gastric contraction follows and propels the caustic agent back up into the esophagus.
This seesaw movement of the caustic agent between the esophagus and stomach occurs
for several minutes until both gastric and esophageal atony occur as the result of
extensive damage to both organs.
14

CAUSTIC INJURY OF ESOPHAGUS AND STOMACH
Caustic stricture of the

esophagus and stomach.
Detail of stomach showing

the typical hourglass
deformity due to severe
antral stenosis
15

Clinical Features
The clinical manifestations of caustic ingestion are directly related to the amount and
character of the agent ingested.
Solid alkali typically causes burns of the mouth, pharynx, and upper esophagus. The
resulting severe pain usually causes immediate expectoration so that relatively little of
the caustic agent is swallowed. On examination, the mucosa of the mouth and
oropharynx shows patchy areas of white to gray-black pseudomembranes.
Patients may present with
Excessive salivation
Hoarseness,
Stridor,
Aphonia, and
Dyspnea from laryngotracheal edema or destruction.
Liquid alkali ingestion. This form of alkali is usually swallowed quickly, producing less
injury to the mouth and pharynx but more damage to the esophagus, stomach, or both.
Patients may present with
Dysphagia,
Odynophagia, and
Aspiration,
Severe retrosternal, back, or abdominal pain and
signs of peritoneal irritation suggest that mediastinitis or peritonitis resulting from
esophageal or gastric perforation has occurred.
16

Acid ingestion, gastric injury is more common; therefore, signs and symptoms are
frequently localized to the abdomen.
When esophageal or gastric perforation results from caustic ingestion,
progressively severe sepsis and
hypovolemic shock until appropriate resuscitative measures are instituted.
In the absence of gastric or esophageal perforation, the acute clinical manifestations
typically resolve within several days, with clinical improvement lasting for several weeks.
After this, symptoms due either to esophageal or gastric stricture formation begin. Although
only 10% to 25% of adult patients who ingest solid alkali develop strictures, most patients
who ingest liquid alkali have severe esophageal and usually gastric injury that often results
in stricture formation. Children with limited exposure from accidental ingestions are less
likely to have severe injuries. Acid ingestion most often results in stricture or contracture of
the antrum or pylorus.
Immediate Diagnosis And Treatment
Acute caustic ingestion is an indication for hospitalization.
Initial management centers on stabilizing the patient and assessing the severity of the
injury.
Vomiting should not be induced.
Because caustic injuries produce almost instantaneous tissue damage,
Attempts to dilute the agent by having the patient drink water are futile and dangerous. In
fact, this may only aggravate the problem by producing increased gastric distention and
vomiting.
Oral intake should be withheld and hypovolemia corrected with intravenous fluids.
17

Immediate Diagnosis And Treatment (suite)

Careful observation for evidence of airway obstruction is mandatory. Endotracheal intubation
or tracheostomy may be required if there is significant laryngeal edema or actual laryngeal
destruction.
Broad-spectrum antibiotics are indicated once the diagnosis of substantial esophageal injury
has been established to diminish the risk of pulmonary infection from aspiration as well as
bacterial invasion through the damaged esophageal wall.
Although corticosteroids have been advocated in the acute phase of caustic ingestion to
minimize subsequent stricture formation, their efficacy has not been established.
Because corticosteroids may mask signs of sepsis and visceral perforation and impair healing,
their use in caustic esophageal injury is potentially deleterious and is therefore not
recommended.
A relatively urgent contrast examination of the esophagus may provide important information
in the patient with a caustic injury.
Radiographically, acute mucosal esophageal injuries are seen as blurred irregular margins
with linear streaking of contrast in deeper ulcers. Submucosal edema may be manifest by
scalloped or straightened esophagogastric junction margins.
Dilation of the esophagus and stomach, gastric ulcerations, air in the gastric wall, and frank
extravasation of contrast material from the esophagus or stomach are common.
A contrast esophagogram is the best way to make the diagnosis of esophageal perforation
and should be performed if the diagnosis is suspected either at the time of admission or in
subsequent follow-up.
Identification of the site of perforation is vitally important in the planning of subsequent
intervention. The initial esophagogram in these patients can be performed with a watersoluble agent (eg, Gastrografin), but dilute barium provides much better mucosal detail and
should be used if the diagnosis of perforation is suspected.
18

Management
Esophagogastroscopy should be performed soon after admission to establish whether
significant esophageal injury has occurred and to permit grading of the severity of the
injury
ENDOSCOPIC GRADING OF CAUSTIC ESOPHAGEAL INJURY

Severity of Injury
Endoscopic Findings
First-degree
Mucosal hyperemia and edema
Second-degree
Mucosal ulceration with vesicles and

exudes; pseudomembrane formation
Third-degree
Deep ulceration with charring and eschar

formation; severe edema obliterating
the lumen
19

Management (suite)
After the initial resuscitative and diagnostic measures are performed, patients with caustic
injuries must be observed carefully.
Those with first-degree burns require no other specific therapy for 24 to 48 hours. The
incidence of subsequent esophageal stricture is low in patients with such injuries.
Those who have second- or third-degree burns require careful and more prolonged
observation for evidence of esophageal or gastric necrosis during the acute phase of the injury.
Full-thickness necrosis of the esophagus, stomach, or other organs requires emergent resection.
Patients with free intraperitoneal air, mediastinal air, extravasation of contrast material from the
stomach or esophagus, peritonitis, or abdominal or mediastinal sepsis require immediate
surgical exploration. Similarly, exploration is indicated in patients with severe persistent back or
retrosternal pain suggesting mediastinitis and in those with metabolic acidosis suggesting
visceral necrosis.
When esophageal or gastric resection for acute caustic injury is required, restoration of
alimentary continuity should be deferred until the patient has recovered from the acute insult
and the development of chronic stricture formation in retained organs can be evaluated.
Esophageal stricture formation after second- and third-degree burns is the rule, and dilation
therapy has been the traditional therapy for chronic caustic esophageal strictures.
Dilation therapy should not be instituted until at least 6 to 8 weeks after the injury, when
reepithelialization is complete, to minimize the risk of esophageal perforation
If a caustic esophageal stricture is perforated during dilation, esophagectomy and visceral
esophageal substitution is the best approach because repair of a perforation proximal to a
stricture is rarely successful.
20

Management (suite)
Strictures that cannot be adequately dilated (to a 46F dilator or larger for adults) and those that
remain refractory to dilation after 6 to 12 months require esophageal substitution, usually with
colon or stomach which is the preferred esophageal substitute, but its use in these patients may
be precluded by gastric scarring and contracture secondary to the original injury.
Severe esophageal strictures resulting from caustic ingestion have been managed in the past by
retrosternal colonic interposition, leaving the native, destroyed esophagus in situ in the
posterior mediastinum.
Recent data, favor resection of the damaged esophagus in virtually every case, for several
reasons:
First, the obstructed esophagus can develop into a posterior mediastinal retention cyst or
abscess.
Second, caustic injuries may result in destruction of the lower esophageal sphincter, resulting
reflux esophagitis in the retained esophagus
Finally, the risk of esophageal carcinoma developing after a caustic injury is about 1000 times
the usual risk, with an incidence of 0.8% to 4%, typically after a latent period of 20 to 40 years.
Therefore, a young patient whose caustic esophageal stricture is simply bypassed must be
followed indefinitely for the development of carcinoma in the native esophagus,
Resection of the strictured esophagus also permits placement of the esophageal substitute in
the posterior mediastinum in the original bed. This is the shortest and most direct route
between the neck and abdominal cavity and does not require resection of the clavicle and
adjacent sternum to enlarge the superior opening into the anterior mediastinum, as is required
when carrying out a retrosternal esophageal substitution.
21

II. DIVERTICULA OF ESOPHAGUS
22

An esophageal diverticulum is an epithelial-lined mucosal pouch that protrudes from the

esophageal lumen.
Most esophageal diverticula are acquired, and they occur predominantly in adults.
Esophageal diverticula may be classified according to their location:
Pharyngoesophageal (Zenker) diverticula occur at the junction of the pharynx and
esophagus;
Parabronchial (mid-esophageal) diverticula occur in proximity to the tracheal
bifurcation; and
Epiphrenic (supradiaphragmatic) diverticula occur in the distal 10 cm of the esophagus .
Diverticula containing all layers of the normal esophageal wall (mucosa, submucosa, and
muscle) are termed true diverticula, while those consisting of only mucosa and
submucosa are false diverticula.
Most esophageal diverticula arise because elevated intraluminal pressure forces
the mucosa and submucosa to herniate through the esophageal musculature;
these are false diverticula.
Traction diverticula result from external inflammatory reaction in adjacent mediastinal
lymph nodes that adhere to the esophagus and pull the wall toward them as healing and
contraction occurs, and these are true diverticula.
Pharyngoesophageal and epiphrenic diverticula are pulsion diverticula that are generally
associated with abnormal esophageal motility.
Parabronchial diverticula are usually but not always of the traction variety and include all
layers of the esophageal wall.
23

Pharyngoesophageal Pulsion Diverticulum

The pharyngoesophageal (Zenker) diverticulum is the most common esophageal
diverticulum and typically occurs in patients between 30 and 50 years of age.
The diverticulum consistently arises within the inferior pharyngeal constrictor muscle,
muscle
between the oblique fibers of the thyropharyngeus muscle and the more horizontal
fibers of the cricopharyngeus muscle - the upper esophageal sphincter. The point of
transition in the direction of these muscles ( Killian triangle)
triangle represents an area of
potential weakness in the posterior pharynx and is the site of formation of the
diverticulum.
Formation of pharyngoesophageal
(Zenker) diverticulum. (A) Herniation
of the pharyngeal mucosa and
submucosa occurs at the point of
potential weakness (Killian triangle;
arrow) between the oblique fibers of
the thyropharyngeus muscle and the
more horizontal fibers of the
cricopharyngeus muscle
24

Pharyngoesophageal Pulsion Diverticulum(suite)

Manometric measurement of upper esophageal sphincter function is difficult with existing
standard recording equipment.
Some degree of incoordination in the swallowing mechanism, is thought to be the basis for
formation of the Zenker diverticulum.
Pharyngeal contraction that occurs inappropriately after cricopharyngeal closure
has been demonstrated in these patients.
Regardless of the precise motor dysfunction, a pulsion diverticulum would not occur in
these patients unless there were some reason for unusually elevated esophageal
pressures.
As the swallowed bolus exerts pressure within the pharynx, mucosa and submucosa
herniate through the anatomically weak area above the cricopharyngeus muscle. The
diverticulum gradually enlarges with time, extending over the cricopharyngeus muscle, and
dissects downward in the prevertebral space posterior to the esophagus and occasionally
into the superior mediastinum.
Clinical Features
Patients with pharyngoesophageal diverticula characteristically present with complaints of :
Cervical dysphagia,
Effortless regurgitation of undigested food or pills,
A gurgling sensation in the neck on swallowing,
Periodic choking, and
Aspiration
Marked weight loss and dysphagia in an elderly patient may be misdiagnosed as an
esophageal malignancy
25


Diagnosis
The diagnosis of a Zenker diverticulum is established with a barium esophagogram.
In evaluating the patient with a Zenker diverticulum, it must be realized that it is the
degree of upper esophageal sphincter muscle dysfunction, not the absolute size of the
pouch, that determines the severity of symptoms experienced by these patients.
Small Zenker diverticulum. (A) The 2.5-cm

pouch and the esophageal narrowing distal
to it representing the tight cricopharyngeus
sphincter. (B) Detail of pouch showing
retained barium.
Posteroanterior (A) and oblique (B)

views from barium esophagogram in an
15-cm pharyngoesophageal diverticulum
26


The first surgical approaches to Zenker diverticula involved simply excising the pouch
and suturing the pharyngeal defect.
The underlying upper esophageal sphincter dysfunction was not appreciated, and there
was a high incidence of suture line disruption with resulting cervical and mediastinal
infection.
Cricopharyngeal myotomy, which relieves the relative obstruction distal to the pouch, is
regarded as the most important aspect of surgical treatment in these patients.
Cervical esophagomyotomy and

concomitant pharyngoesophageal
diverticulum resection.
27


The results of treatment(diverticulectomy) are excellent, and recurrence is rare if the relative
obstruction distal to the pouch has been relieved by complete division of the upper esophageal
sphincter.
An alternative approach is diverticulopexy, which involves mobilizing the pouch, inverting it, and
suspending it from adjacent tissues so that the mouth is dependent. This operation is successful
only if combined with a cervical esophagomyotomy.
Endoscopic division of the common wall between the diverticulum (internal pharyngoesophagomyotomy, or the Dohlman procedure) has been used with success by a small number of
surgeons for treatment of Zenker diverticulum.
Mid-esophageal Traction Diverticulum
Mediastinal granulomatous disease (eg, tuberculosis or histoplasmosis) is the common cause
This type of diverticulum is much smaller than the pulsion diverticulum and has a characteristic
blunt tapered tip that points toward the adjacent subcarina and parabronchial lymph nodes to
which it adheres
It is typically diagnosed as an incidental finding on a barium esophagogram and almost always is
asymptomatic.
No specific treatment is indicated.
At times, however, inflammatory necrosis of the granulomatous reaction may produce a fistula
between the esophagus and the tracheobronchial tree, requiring division of the fistula and
interposition of normal tissues.
Mid-esophageal traction diverticula must be differentiated from pulsion diverticula, which may also
occur in this location and are associated with neuromotor esophageal dysfunction, as is the case
with epiphrenic diverticula.
28

Epiphrenic diverticulum
An epiphrenic or supradiaphragmatic diverticulum occurs within the distal 10 cm of the
thoracic esophagus.
It is a pulsion diverticulum that arises because of abnormally elevated intraluminal
esophageal pressure
Barium esophagogram showing an epiphrenic diverticulum as well

as a small traction diverticulum (arrow) of the middle esophagus.
29

Epiphrenic diverticulum(suite)
Although many patients do not have symptoms at the time of diagnosis on barium
esophagogram, others have symptoms from the frequently associated esophageal conditions:
hiatal hernia, diffuse esophageal spasm, achalasia, reflux esophagitis, and carcinoma.
Dysphagia and regurgitation are the common symptoms of an epiphrenic diverticulum, and
retrosternal pain may occur from associated diffuse esophageal spasm.
Esophageal manometry and acid reflux testing in these patients should be performed to define
the associated motor abnormality and to assess competence of the lower esophageal sphincter
mechanism
Pouches smaller than 3 cm and causing little or no symptoms require no treatment.
Severe dysphagia, chest pain, or an anatomically dependent or enlarging pouch are indications
for repair. Unless there is an associated distal esophageal stricture or tumor, it must be inferred
that the patient with an epiphrenic diverticulum has abnormally elevated intraesophageal
pressure that has produced the pouch and is the result of neuromotor dysfunction. This can be
documented manometrically.
The surgical approach to epiphrenic diverticula is through a left sixth or seventh interspace
posterolateral thoracotomy. This is the case even for diverticula that present to the right of the
esophagus.
A long extramucosal thoracic esophagomyotomy is performed from the level of the aortic arch
to the esophagogastric junction.
If there is an associated hiatal hernia or incompetent lower esophageal sphincter, an antireflux
operation should be carried out at the same operation. If an adequate esophagomyotomy is
performed, and the abnormally elevated intraesophageal pressure is thus relieved, suture line
disruption and recurrence of the diverticulum are rare.
30

III. FUNCTIONAL MOTOR DISORDERS OF ESOPHAGUS
Classification: Primary and Secondary

Primary motor disorder implies that the cause of the muscular defect is not known,
Secondary motor disorders are the result of some systemic disease affecting the
esophagus.
The most common secondary motor disorder is the hypoperistalsis associated with
complicated GERD, but the term usually refers to a systemic connective tissue or
neuromuscular disease, such as scleroderma or polymyositis.
There are four identifiable categories of primary motor disorders:
Achalasia,
DES,
Nutcracker esophagus, and
Hypertensive LES.
Nonspecific motor disorder
Includes those patients whose motor function is clearly
abnormal but who do not fall into one of the four major categories.
These five categories are derived from the manometric features on stationary motility.
In clinical activity these categories may not be as distinct as the classification implies. For
example, intermediate forms exist.
Pharyngoesophageal Disorders
Disorders of the pharyngoesophageal phase of swallowing result from a discoordination
of the neuromuscular events involved in :
chewing,
initiation of swallowing,
propulsion of the material from the oropharynx to the cervical esophagus.
31

The causes of pharyngoesophageal dysphagia are:

Neuromuscular diseases. The most important are
cerebrovascular disease,
myasthenia gravis,
Parkinson disease,
motor neuron disease,
multiple sclerosis, and
Muscular diseases such as
myotonic dystrophy and
polymyositis.
Structural lesions of pharynx, including
tumors,
Zenker diverticula, and
scarring of the tongue or pharynx from caustic injury, Sequence of events during the
previous surgery, or
oropharyngeal phase of swallowing.
radiotherapy.
Extrinsic compression (rarely) from goiter or cervical spine osteophytes.
Pathophysiology
All the diseases mentioned earlier produce their effects by disrupting one or more of the
components of the pharyngeal function.
Weakness or immobility of the tongue produces difficulty in oropharyngeal transfer.
Paralysis of the soft palate this accounts for the frequent occurrence of nasal regurgitation
and the nasal quality to the voice in these patients.
If the larynx cannot be elevated, there is loss of airway protection, and patients are prone to
aspiration.
32

In neuromuscular diseases, dysphagia is often worse for liquids than for solids.
Clinical features
Choking,
Repetitive pneumonia,
Nasal regurgitation, and hoarseness are also prominent features.
A prominent cough on assuming the recumbent position suggests the presence of
Zenker diverticulum because retained food then flows back into the pharynx.
In neuromuscular disorders examination may reveal a characteristic pattern of signs
depending on the underlying cause easily recognizable.
The voice may sound weak from vocal cord paralysis, or wet because of uncleared
laryngeal secretions, or it may exhibit a nasal quality from palatal paresis. It is worthwhile
watching the patient swallow during the examination.
33

Investigation
Until recently, objective assessment of these conditions has been difficult, because of the
rapidity of the events during the oropharyngeal phase of swallowing. Careful analysis of
videoroentgenographic studies,
esophagoscopy,
manometry with specially designed catheters, and
24-hour esophageal pH monitoring can identify the cause of a pharyngoesophageal
dysfunction in most of the conditions described.
Videoroentgenography is the most objective test to evaluate oropharyngeal bolus
transport, pharyngeal contraction, relaxation of the pharyngoesophageal segment, and the
dynamics of airway protection during swallowing.
Carefully performed motility studies may demonstrate insufficient relaxation or premature
contraction of the cricopharyngeus, high sphincter pressure, inadequate pharyngeal
pressurization, or an elevated intrabolus pressure suggesting decreased compliance of the
pharyngoesophageal segment.
Treatment
Therapeutic options in all these diseases are limited by the nature of the pathology.
Medical treatment is confined to:
Drug treatment for a specific neurologic condition (eg, myasthenia gravis or Parkinson
disease), and
Therapy from a speech pathologist designed to train the patient to maximize residual
function.
34

The surgeons role is to reduce outflow resistance by performing cricomyotomy. Initially,

this was recommended only for patients with demonstrable failure of UES relaxation. More
recently, a number of reports indicate that a wide variety of neuromuscular diseases may
be improved by cricomyotomy.This is because a weak or uncoordinated pharyngeal
contraction may be sufficient to permit improved swallowing if outflow resistance
is reduced.
The outcome of cricomyotomy is also affected by the presence of more distal esophageal
disease; when gross GERD and an associated motility defect of the esophageal body
coexist, the risk of aspiration of gastric juice is increased.
Thus, all surgical procedures for this condition should include a myotomy of the
cricopharyngeus and proximal esophagus.
Completed cricomyotomy
35

All operations on the cervical esophagus carry the risk of hematoma formation and recurrent
nerve paralysis. If the diverticulum is opened during operation, there is a significantly
increased risk of salivary fistula and wound infection.
Finally, in patients who fail to benefit from reduction of outflow resistance and swallowing
therapy, the only option is tube feeding. (A percutaneous endoscopic gastrostomy but a
jejunostomy is the most trouble-free solution but requires a general anesthetic .
Primary Motor Disorder Of The Esophagus
Achalasia
Achalasia is the best known primary motility disorder of the esophagus.
It is characterized by failure of esophageal body peristalsis and incomplete relaxation
of the LES.
It is generally thought to be caused by:
neuronal degeneration in the myenteric plexus of the esophageal wall, causing
aperistalsis, and by
loss of activity of inhibitory neurons in the LES, leading to incomplete relaxation.
The cause of the neuronal degeneration is obscure; there is some evidence that previous
infection with varicella-zoster virus may be responsible.
There is also some experimental evidence, however, that obstruction at the gastroesophageal
junction may produce a condition with the radiologic and manometric features of achalasia.
This evidence suggests that outflow resistance is a primary phenomenon and that
degeneration of the esophageal body is secondary.
36

Clinical Features And Diagnosis

Patients with achalasia all have dysphagia, and regurgitation.
Careful questioning is needed to distinguish the regurgitation from vomiting.
Generally, regurgitation occurs during or at the end of a meal, and the material regurgitated
tastes bland rather than sour or bitter.
Patients often have to leave the table to regurgitate, and are usually slow eaters.
Nighttime regurgitation causes staining of the pillow.
Late in the disease, patients often lose weight and may become socially isolated.
Respiratory symptoms are common and are due to aspiration.
One further characteristic is the length of time (frequently several years), that the symptoms
persist before the diagnosis is made.
Chest pain is common in patients with achalasia and may not be related to eating. In some
patients, was demonstrated simultaneous occurrence of chest pain and manometric
contractions in the esophagus.
The roentgenographic appearance of the esophagus with achalasia depends on the stage of
the disease.
In early stages, it may be normal, and these patients may be falsely reassured.
Later, esophageal dilation develops, and an airfluid level may be noted. Both of these
findings indicate outflow obstruction. Barium is rarely seen to enter the stomach, and when
a good view of the cardia is obtained, it has a narrow, tapering, birds beak appearance.
Late achalasia is characterized by a tortuous, sigmoid esophagus, and an epiphrenic
diverticulum may be present.
Absence of the gastric air bubble may be noted and is due to the inability to propel
swallowed air into the stomach.
37

Barium esophagogram demonstrating a

dilated esophagus and the characteristic
birds beak deformity in a patient with
achalasia.
Barium esophagogram in a patient with

advanced achalasia showing a dilated
sigmoid esophagus and an epiphrenic
diverticulum (arrow).
38

Endoscopy frequently reveals:

Residual liquid or food in the esophagus.
The narrowing at the lower end which permits the passage of the endoscope, usually with a
characteristic popping sensation
Mild esophagitis may be observed, sometimes attributable to fermentation or stagnation of
esophageal contents, in untreated cases.
When the patient has had previous treatment for achalasia(pneumatic dilation), such
inflammation is likely to be caused by gastroesophageal reflux.,
In every patient with presumed achalasia it is important to view the cardia from below with
the endoscope retroflexed because a small infiltrating gastroesophageal tumor may
otherwise be missed.
Manometry is required to establish the diagnosis of achalasia.
The following are classic features of achalasia seen at stationary manometry:
Elevated LES pressure
Incomplete LES relaxation
Absence of esophageal body peristalsis
Positive intraesophageal body pressure
Not every patient has all four features.
Data are limited with regard to 24-hour pH and motility studies in patients with achalasia.
Generally, excessive acid exposure is rare before dilation or operation.
A characteristic pattern is the gradual fall in pH over a period of hours, and this may
represent fermentation of residual food material because it clears after swallowing water.
When true reflux episodes occur, they are prolonged because of the absence of peristalsis.
39

Treatment
Although some patients show a short-lived symptomatic and manometric response to calciumchannel blocking agents,
The mainstay of treatment for achalasia is either balloon dilation or surgery.
The description of botulinum toxin injection has created much interest, but the reduction in LES
pressure obtained by the investigators is small and the follow-up short. Its role is therefore unproven.
Balloon dilation has the advantages that it can be done on an outpatient basis and has minimal
recovery time. It is less likely to be effective than surgical treatment and frequently needs to be
repeated.
The risk of gastroesophageal reflux after dilation is not known because large studies of 24-hour pH
monitoring after dilation are lacking, but the risk of clinically significant symptoms appears to be low.
All surgical procedures employ a variant of Heller myotomy, in which the circular muscle of the lower
esophagus is divided. In the United States, most myotomies are carried out through the chest, but
the abdominal route is favored in Europe.
Regardless of the route chosen, the four important principles are
(1) adequate myotomy,
(2) minimal hiatal disturbance,
(3) antireflux protection without the creation of obstruction, and
(4) prevention of closure of the myotomy with healing.
The advent of minimally invasive surgery has led to the development of thoracoscopic and
laparoscopic myotomies, and these are widely performed with comparable results to open surgery.
There is broad agreement that if the myotomy is performed through the abdomen, an antireflux
procedure should be added, Either a posterior (Toupet) or anterior (Dor) hemifundoplication should be
used.
40

When approached through the chest, there is controversy about the need for an antireflux
procedure; it has been suggested that less hiatal disturbance and a more limited myotomy
are possible by this route
Myotomy of the LES, extending from below

the aortic arch proximally and 1 to 2 cm
beyond the gastroesophageal junction on
to the stomach.
Laparoscopic approach
41

Diffuse Esophageal Spasm

Diffuse esophageal spasm is an esophageal motor disorder characterized clinically by:
substernal chest pain or
dysphagia.
DES differs from classic achalasia in that it represents a primary disease of the esophageal body
and produces:
Less dysphagia,
Causes more chest pain, and has
Less effect on the patients general condition.
True symptomatic DES is more rare than achalasia.
Roentgenographic abnormalities, such as segmental spasm with compartmentalization of the
esophagus or formation of a diverticulum, are the anatomic correlates of the disordered motility
function.
Manometric abnormalities in DES can be present over the total length of the smooth muscle
portion of the esophageal body. In segmental esophageal spasm, the manometric abnormalities
are confined to a short segment of the esophagus. The classic manometric finding in these
patients is the frequent occurrence of simultaneous and repetitive esophageal contractions, which
may be of abnormally high amplitude or long duration.
Key to the diagnosis of DES is that the esophagus retains a degree of peristaltic ability, in contrast
to that of achalasia. A criterion of 20% or more simultaneous contractions in 10 wet swallows has
been used to define DES.
The LES in patients with DES usually shows normal resting pressure and relaxation on deglutition.
A hypertensive sphincter with poor relaxation may also be present and may represent early
achalasia.
In patients with advanced disease, the radiographic appearance of tertiary contractions appears
helical and has been termed corkscrew esophagus or pseudodiverticulosis.
DES is a benign disease that rarely causes nutritional problems and does not lead to lifethreatening complications. For this reason, symptom control is the only significant goal of
treatment.
42

Medical treatment for DES is designed to abolish strong simultaneous contractions and
generally employs calcium-channel blockers or long-acting nitrates.
The surgical option is to perform myotomy of the esophageal body.
Surgery for DES is not as successful as for achalasia and is considered only when medical
treatment is ineffective.
Esophageal body myotomy should always be accompanied by myotomy of the LES (with
partial fundoplication if performed by open surgery) because even a normal LES can
impose an outflow resistance too great for the myotomized body to overcome.
Barium esophagograms of two patients with diffuse esophageal spasm,

showing corkscrew esophagi with multiple contractions
43

Nutcracker Esophagus
This term nutcracker esophagus is used to describe a manometric abnormality in which the
amplitude of esophageal body peristalsis is greater than 2 standard deviations above
normal.
It was first recognized when increasing numbers of patients with noncardiac chest pain
were investigated by esophageal manometry, and is the most common primary motility
disorder of the esophagus.
The dominant symptom of this condition is central crushing chest pain.
It may have no relation to food ingestion but differs from angina in that it more frequently
comes on at rest.
Dysphagia or classic heartburn may be present, but this tends to be overshadowed by the
chest pain.
Patients with nutcracker esophagus are usually referred from cardiologists with normal
coronary angiograms and a request for esophageal motility testing.
Barium radiography and endoscopy are not usually helpful.
The pathognomonic feature on manometry is the presence of prolonged high-amplitude
waves, with a peak of more than 180 mmHg.
The waves are normally peristaltic. Many patients with noncardiac chest pain are found to
have increased esophageal acid exposure, and this subgroup is important to identify
because they respond well to fundoplication.
Myotomy for isolated nutcracker esophagus with symptoms of chest pain has a low success
rate, and the mainstay of treatment for these patients is muscle relaxants, such as nitrates
and calcium-channel blockers.
If features of DES are discovered on ambulatory manometry, myotomy is more likely to be
successful.
44

Secondary motor disorders of esophagus

Many connective tissue and neuromuscular diseases affect the esophageal body, but the
most significant is scleroderma. Most patients with this condition develop dysphagia.
The loss of esophageal function is caused by replacement of the muscle of the lower
esophagus and LES by fibrous tissue.
The manometric hallmark of the condition is absence of LES pressure and severely
impaired contraction amplitude in the smooth muscle portion of the esophagus.
The grossly defective LES allows superimposed reflux-induced injury to occur, accelerating
the loss of body function.
Many patients experience esophageal strictures. Antireflux surgery in this situation must
involve a partial fundoplication, but some patients eventually require esophageal
replacement. Sometimes, the situation is compounded by a severe delay in gastric
emptying, and patients are greatly improved by performing total gastrectomy and
reconstruction with a Hunt-Lawrence jejunal pouch in a Roux-en-Y fashion.
Surgical treatment of motor disorders by myotomy cannot normally reverse the disease
process; rather, it creates a defect to overcome an existing defect. In advanced disease
when residual esophageal function has been destroyed, myotomy is ineffective. Further, the
superimposition of an esophageal stricture on top of a primary motor disorder makes any
procedure aimed at preserving the esophagus unlikely to succeed. If more than one
myotomy has been attempted in the past, it is highly unlikely that any procedure short of
esophagectomy will provide symptomatic relief. The indications and choice of esophageal
substitute are considered in the section on esophageal replacement in benign disease.
45

IV. Gastroesophageal Reflux Disease
Gastroesophageal reflux is a normal phenomenon.

This can be measured only by 24-hour pH monitoring.
Most normal people experience short episodes of reflux, usually after meals.
Gastroesophageal reflux disease occurs when esophageal acid exposure exceeds that of a
normal population.
Other definitions used in the past were either nonspecific (eg, symptoms of heartburn or regurgitation) or indirect (eg,
the presence of a hiatal hernia), or they detected the disease only when complications such as esophagitis were
present.
The ready availability of 24-hour esophageal pH monitoring allows the physician to quantitate
the abnormality, to assess objectively the response to treatment, and to formulate a logical
approach to therapy.
It is estimated that 7% of Americans suffer from daily heartburn, and up to 30% use antacids at
least once a month.
Most people whose symptoms are controlled by such means do not consult a physician, and of
those who do, few are referred to surgeons.
Pathophisiology
Pathologic gastroesophageal reflux may result from the following causes:
a mechanical defect in the LES. This accounts for about 50% to 60% of patients with
increased esophageal acid exposure. It is important to identify these patients because they
generally have a good outcome after antireflux surgery but a poor response to medical
treatment.
inefficient esophageal clearance of refluxed gastric juice and
abnormalities of the gastric reservoir that augment physiologic reflux.
Clinical features
Symptoms of GERD can be classified as either:
Typical (ie, heartburn and regurgitation) or
Atypical (ie, noncardiac chest pain, pulmonary problems such as asthma, recurrent
pneumonia or progressive fibrosis, laryngeal symptoms such as hoarseness and aspiration,
and loss of dental enamel).
46

Heartburn is the most common symptom associated with GERD, usually occurring 30 to 60
minutes after meals. Heartburn exacerbated by lying flat or bending over suggests a profound
weakness of the LES. It may be associated with
Belching and regurgitation of acid into the throat. If the regurgitated material comes from the
esophagus, it tastes bland and suggests a motor disorder, and if it regurgitates from the stomach
and tastes bitter, it suggests GRD.
Variable respiratory symptoms may result if the regurgitation is associated with aspiration:
Sometimes, the picture resembles asthma, and GERD should always be considered in
managing this condition.
A history of isolated episodes of pneumonia or
Frequent bouts of wheezing and coughing at night is also suggestive of GERD.
Hoarseness may be present from laryngeal irritation.
Dysphagia resulting from GERD is usually insidious and results from a motility disorder
secondary to esophagitis, loss of esophageal compliance, or stricture formation. Patients usually
localize dysphagia to the level of the lower sternum, but we have found that cervical dysphagia is
common in GERD. Patients localization of the site of obstruction is not always reliable; generally, an
obstructing lesion does not cause symptoms to be perceived distal to the lesion. It is common to find that heartburn ceases to be a
prominent symptom when a stricture has developed. By contrast, the sudden development or rapid progression of dysphagia suggests a
tumor. In the absence of a history of heartburn, a squamous cancer of the esophagus is likely, but if heartburn was prominent, the most
common cause is adenocarcinoma arising in Barretts esophagus.
Angina-like chest pain, sometimes called noncardiac chest pain, is frequently caused by GERD.
These patients often describe other classic symptoms of GERD, which tend to be mild and
overshadowed by the chest pain. Of patients with angiographically negative chest pain, 20% to
50% have an esophageal cause, and of these, 50% have increased esophageal acid exposure.
Epigastric pain and nausea may be associated with other symptoms of GERD and usually result
from pathologic DGR or delayed gastric emptying. It is important to recognize these symptoms
before offering a patient antireflux surgery because they may persist after operation, and the
patient should be warned of their presence and the possibility of future medical or surgical
therapy.
47

Bloating is mainly a gastric symptom suggesting gastric dilation secondary to aerophagia or

delayed gastric emptying. It may be accompanied by adaptive relaxation of the abdominal
muscles causing visible distention.
Investigations
the initial investigations include a barium esophagogram and upper gastrointestinal endoscopy.
In patients with GERD, these only uncover a pathologic lesion if a complication of the disease,
such as esophagitis, stricture, or Barretts esophagus, or a potentially related condition, such as
hiatus hernia, is present.
The next step in investigation is physiologic testing of the esophagus and stomach using
esophageal manometry and pH monitoring. Additional tests depend on the abnormalities
revealed by these basic assessments.
Combined pH monitoring and :
chest roentgenography is helpful if there are respiratory symptoms;
gastric emptying tests,
gastric acid analysis for hypersecretion, and
esophageal and gastric bile probe monitoring may be required to elucidate gastric
symptoms.
Ambulatory esophageal motility may help define an esophageal motility disorder if stationary
manometry is equivocal.
As a result of this process of investigation, a comprehensive understanding of
esophageal function will be reached, enabling the physician to identify the etiologic
factor responsible and predict the outcome of alternative treatments.
Complications of the GERD
Complications of GERD are defined by the presence of tissue injury and include:
Esophagitis,
Stricture, and
Barretts esophagus.
48

1.
Why some patients experience complications and others do not is not known,
Several factors appear to be associated:
The status of the LES has emerged as a significant factor in several long-term studies,
and LES dysfunction predicts a poor response to medical treatment. The table below shows
the relation of a defective sphincter to complications in 150 consecutive adult patients
with proven gastroesophageal reflux.
Note that Barretts esophagus is almost always associated with a mechanically
defective sphincter.
COMPLICATIONS OF GASTROESOPHAGEAL REFLUX DISEASE IN 150 CONSECUTIVE

ADULT PATIENTS
Complication
None
Esophagitis
Stricture
Barretts esophagus
LES, lower esophageal sphincter.

* Grade of esophagitis more severe with defective LES.
Patients
59
47
19
25
Normal LES (%)

58
23*
11
0
Defective LES (%)

42
77
89
100
LES failure is an early event in the pathogenesis of GERD and that patients with tissue
injury have more profound impairment of LES function.
49

2. A defect of esophageal clearance that prolongs the contact time between the refluxate and
the mucosa is likely to lead to increased esophageal injury. This may be due to failure of
esophageal propulsion, as in primary motor disorders. More commonly, the defect in
clearance is secondary to reflux-induced damage, creating a vicious cycle of increasing
esophageal injury.
Patients with strictures and Barretts esophagus may thus have a profound defect in esophageal
contractility.
When the injury extends beyond the mucosa, the consequent interference with esophageal
function may not revert to normal when the mucosa has healed : the mucosa may heal by
intensive acid-suppression therapy, the abnormalities in the LES and esophageal body
generally do not. This is because the mucosa is repeatedly being renewed, whereas muscle
cells once damaged are unlikely to recover.
3. The presence of a hiatal hernia is also associated with more complications of GERD.
The cause-and-effect relation between hiatal herniation and GERD is controversial :
Early workers used the terms hiatal hernia and reflux esophagitis as near synonyms,
whereas
Later studies showed that the feature that distinguished pathologic from physiologic
reflux was not the presence of a hiatal hernia but rather the LES pressure.
As the diagnosis of hiatal herniation has become more standardized, it has become clear that
the presence of a hiatal hernia interferes with the emptying of the distal esophagus and
causes a defect in acid clearance. Thus, patients with GERD associated with a hiatal hernia
have more complications of the disease than those without. Conversely, the prevalence of
hiatal herniation in patients with GERD increases as the complications become more severe.
Most patients with Barretts esophagus or stricture have a hiatal hernia.
4. The composition of the refluxed material also has an effect on the development of
complications. The injurious effect of refluxed gastric juice depends on a number of factors:
50

Pepsin-induced mucosal damage is likely only at a pH of 1.0 to 2.5, but in the presence of bile
salts and a higher pH, trypsin may be more important.
Not only is trypsin activated at a pH higher than 5.0, but the solubility of potentially injurious
bile
salts is greatest at neutral pH. In the clinical situation, complications of GERD are more
common when there is an alkaline component to the refluxate.
In Barretts esophagus, the development of complications such as stricture and ulceration is
strongly associated with increased alkaline exposure.
The presence of acid or alkaline reflux and the presence of a mechanically defective
sphincter are independent determinants of mucosal damage, and when combined, the
effects are additive. A patient with both features has a 95% incidence of complications.
Esophagitis
Esophagitis is usually diagnosed by the presence of macroscopic mucosal erosions at
endoscopy.
Mere erythema of the mucosa is subjective, especially on a video screen, and is consequently
of little significance.
Erosions first appear on the apex of distal mucosal folds and progress to affect multiple folds,
eventually becoming confluent.
Histologically, erosions are characterized by loss of surface epithelium and neutrophil
infiltration. Histologic abnormalities of esophagitis when the epithelium is visually normal are of
uncertain relevance. Esophageal Ulceration
Historically, esophageal ulcers were the first clinical manifestation of GERD to be described.
They resemble peptic ulcers in the stomach or duodenum in that they have a tendency to
penetrate deeply and lead to bleeding or perforation.
They are found most commonly in association with Barretts esophagus, often near the
squamocolumnar junction and, when healed, may lead to the high mid-esophageal stricture
characteristic of that condition.
51

Esophageal Ulceration
Historically, esophageal ulcers were the first clinical manifestation of GERD to be described.
They resemble peptic ulcers in the stomach or duodenum in that they have a tendency
to penetrate deeply and lead to bleeding or perforation.
They are found most commonly in association with Barretts esophagus, often near the
squamocolumnar junction and,
When healed, may lead to the high mid-esophageal stricture characteristic of that
condition.
Esophageal Stricture
More severe esophagitis causes circumferential changes that can cause fibrosis in the
deeper layers, leading to stricture and esophageal shortening.
Strictures have an inflammatory component as well as fibrous replacement of muscle.
Improvement in the former is partly responsible for diminished dysphagia after corrective
antireflux surgery or intensive medical treatment. Most reflux strictures occur in the distal
esophagus unless Barretts esophagus is present, in which case the stricture is often more
proximal. The development of a reflux stricture causes slowly progressive dysphagia for
solids, usually after a long history of heartburn and regurgitation. Rapidly progressive
dysphagia or severe weight loss are uncommon and suggest malignancy.
52

Barretts Esophagus
The condition in which the esophagus is lined with columnar epithelium was first described by
Norman Barrett in 1950, although he incorrectly believed it to be congenital in origin.
It is now realized that Barretts esophagus represents advanced GERD and is found in 7% to 10% of
patients with GERD.
It is characterized :
endoscopically by the presence of velvety orange-red mucosa that lines the esophagus, and
histologically by the presence of columnar epithelium.
The visual appearance at endoscopy can be confused with herniation of normal gastric mucosa
above the crura, and in the past, Barretts esophagus was only diagnosed if the columnar mucosa
extended 2 cm or more above the esophagogastric junction.
The histologic hallmark of Barretts esophagus is the presence of specialized columnar
epithelium, which shows features of intestinal metaplasia, easily recognized by the presence of
goblet cells.
cells These features may be seen in biopsies of segments less than 2 cm above the
esophagogastric junction, sometimes called short-segment Barretts esophagus. Short-segment
Barretts esophagus often appears as a small tongue of columnar epithelium extending above the Zline into the lower esophagus. The presence of specialized epithelium is now regarded as the
pathognomonic feature of Barretts esophagus regardless of how far it extends into the esophagus.
Barretts esophagus can exist alone or can be complicated by ulceration, stricture, and malignant
change.
Once Barretts epithelium is present, medical therapy or antireflux surgery rarely causes it to
regress.
Unless it (Barretts epithelium) is actually ablated (eg, with laser therapy), it persists.
The most significant feature of Barretts esophagus is its malignant potential.
The metaplastic epithelium usually undergoes dysplastic change before becoming frankly
neoplastic, but the changes may be focal and thus missed on biopsy.
Most pathologists distinguish only two grades of dysplasia:
Low grade dysplasia and
High-grade dysplasia which is synonymous with carcinoma in situ, and up to half of esophagi
removed for such a condition demonstrate foci of invasive carcinoma.
53

The exact magnitude of the risk of malignancy is debated and ranges from 1 per 50 to 1 per 150
patient-years. Even the most conservative estimates indicate a risk 40 times that seen in the
general population.
Adenocarcinoma of the esophagus is rapidly increasing in most Western countries, and Barretts
esophagus is the only known risk factor. In the United States, adenocarcinoma accounted for
about 3% of esophageal cancers between about 1930 and 1970; since the mid-1970s, its incidence
has risen by 10% per year. It now accounts for almost 50% of all esophageal cancers .
The male/female ratio is 5:1.
Physiologic dysfunction in Barretts esophagus is characteristic of advanced reflux disease; a
defective LES, poor distal esophageal body peristalsis, and fixed hiatal herniation are all common.
Mucosal insensitivity to acid-induced pain is present and may explain why many patients present
late.
late
Abnormal composition of gastric juice may be found, specifically the presence of duodenal juice. In
the past, this was inferred by the presence of so-called alkaline reflux (increased percentage of time at a pH of more
than 7.0) on esophageal pH monitoring, but reports monitoring bilirubin confirm that Barretts esophagus is
frequently associated with excessive bile in the esophagus.
Repetitive injury from noxious gastric juice can lead to mutations during the repair process in the
p53 gene, a gene that controls programmed cell death. Patients with adenocarcinoma arising in
Barretts esophagus have a high incidence of p53 mutations.
Short Esophagus
The term short esophagus is used by surgeons to describe the situation in the operating room when
the gastroesophageal junction cannot be brought down into the abdominal cavity without tension.
tension
Esophageal shortening begins to occur early in the development of GERD
Manometric studies demonstrate that shortening of the esophageal body increases as complications
become more severe.
Shortening of the longitudinal muscle, is associated with hiatal herniation, and periesophageal
inflammation. Radiologically, it is associated with fixation of the hiatal hernia; that is, the hernia
does not reduce in the upright position after a swallow. Any hernia greater than 5 cm in length is
likely to be associated with esophageal shortening.
54

Manometric length of the esophagus in

patients with gastroesophageal reflux
disease compared with normal subjects.
Esophageal length progressively shortens
as the complications of the disease become
more severe. *P < .001 versus normal
subjects.
Manometrically, the peristaltic amplitude in the distal esophagus is often subnormal. If this
condition is detected only at the time of an abdominal fundoplication, the surgeons options
are severely limited. It is much better to detect it ahead of time and plan the operative
strategy accordingly
55

Surgical Treatment
The aim of surgery is to restore the patient to a life free of symptoms, without the need to take
regular medications, and without undue social, dietary, or other lifestyle restrictions.
The status of a patient whose reflux symptoms must be controlled by
taking regular acid suppression therapy,

taking prokinetic agents,
avoiding late meals and
rich or spicy food,
eschewing tea,
coffee,
alcohol,
tobacco,
chocolate, and peppermint,
wearing only loose clothes, and
sleeping with the head of the bed elevated cannot be considered ideal.
Only two randomized trials have compared the relative merits of medical versus surgical
treatment.
Both showed a clear advantage for surgical treatment, but some are reluctant to accept this
conclusion, arguing that the medical treatment in both did not include omeprazole.
An ongoing trial comparing laparoscopic Nissen fundoplication with proton pump inhibitors may
provide a conclusion more relevant to current practice.
There is no doubt that proton pump inhibitors represent a great advance in the medical
treatment of GERD, but until recently, long-term use was discouraged by the US Food and Drug
Administration.
56

Serum gastrin levels are usually raised in patients on long-term omeprazole, and there are
theoretic and experimental reasons to believe that the trophic effect of long-term gastrin
elevations may predispose to neoplasia. In rats, gastric carcinoid tumors have been
reported.
reported
Long-term omeprazole use in patients with severe esophagitis generally heals the
esophagitis if a high dose is given but is associated with atrophic gastritis.
No reports of cancer in humans attributable to omeprazole have been made.
A limiting factor in the medical treatment of GERD is that treatment addresses only acid
suppression,
suppression ignoring the other potentially injurious components of the refluxate, which
continue to cause damage despite symptomatic relief.
The traditional reasons for an internist to refer a patient with GERD for surgery are:
an unsatisfactory response to medical treatment and
the development of uncontrollable complications.
Operative Indications
The first requirement in the consideration of antireflux surgery are:
Objective demonstration of the presence of GERD by 24-hour pH monitoring. Second,
The patient must have either symptoms or complications of the disease.
The disease should be caused by a defect remediable by surgical therapy,
therapy such as a
mechanically defective LES. Studies have indicated that a Nissen fundoplication has
beneficial effects in addition to restoring the characteristics of the LES. It may accelerate
gastric emptying and reduce the frequency of transient LES relaxations. Consequently, even in patients
without defective sphincters, there are situations in which a Nissen fundoplication can correct the
underlying abnormality.
57

Algorithm for selecting patients with symptoms suggestive of

gastroesophageal reflux disease (GERD) for further study.
58

CONCEPTUAL SCHEME OF THE APPROPRIATE TREATMENT AT EACH
STAGE OF THE SPECTRUM OF GASTROESOPHAGEAL REFLUX DISEASE
(GERD).
59

Nissen Fundoplication
Dissection of the left crus and the angle of His.
Creation of the fundoplication.
A.
Exposure for crural closure.
Fixation of the fundoplication.
B.
The completed closure.
60

Partial Fundoplications
The most widely used is the transabdominal Toupet procedure,
procedure in which the anterior
and posterior lips of the fundoplication are sutured, not to each other, but to the right and
left crura and to the esophageal wall, to produce a 270-degree fundoplication.
fundoplication It can be
performed without having to divide the short gastric arteries.
61

V. Esophageal Tumours
General considerations
Most esophageal tumors are malignant; less than 1% are benign.
A knowledge of the anatomic relations between the esophagus and adjacent structures is
important both in understanding the presentation of esophageal tumors at various levels
and in planning therapy.
For example, tumors involving the cervicothoracic esophagus (the segment from the
cricopharyngeal sphincter to the thoracic inlet at the level of the suprasternal notch) often
involve the larynx and therefore require a laryngopharyngectomy for complete resection.
The upper thoracic esophagus is contiguous with the posterior membranous trachea
anteriorly and the aortic arch and great vessels. Thus, patients with cancer involving the
upper thoracic esophagus should routinely undergo preoperative bronchoscopy to rule out
invasion of the posterior membranous trachea, which would preclude resection. When
resecting an upper thoracic esophageal tumor through a thoracotomy, the approach is a
right fourth or fifth interspace incision because the aortic arch interferes with mobilization
of the upper thoracic esophagus through the left chest.
Mid-thoracic esophageal tumors can involve the carina or proximal main-stem bronchus,
particularly where the esophagus passes behind the left main-stem bronchus, the common
site for presentation of a malignant tracheoesophageal fistula. Once again, because of its
anatomic proximity to the tracheobronchial tree, a mid-thoracic esophageal tumor may
require a right thoracotomy, which provides optimal exposure to the carina and proximal
bronchi.
Distal esophagus Distal esophageal tumors are approached transthoracically through a leftsided approach because the most distal esophagus and esophagogastric junction cannot be
adequately visualized through the right chest.
62

Another important anatomic consideration when performing esophageal resection is

the tunique submucosa of the esophagus, the unusual fat content of which allows a
great deal of mobility of the overlying mucosa.
Unless great care is taken to ensure that every anastomotic stitch transfixes the
submucosa, an anastomotic leak may occur as a result of the mucosa retracting
proximally and accurate apposition of the mucosa not being achieved.
The esophagus is a mucosa-lined muscular tube that lacks a serosa. It is surrounded
by adventitia, or mediastinal connective tissue, which is a loose fibroareolar layer.
Transmural invasion by esophageal carcinomas is exceedingly common, the tumor
not being limited by overlying pleura, in contrast to intestinal cancers, which often
extend to, but not through, the adjacent peritoneum.
Benign tumors and Cysts of the esophagus
Benign tumors of the esophagus are rare, constituting only 0.5% to 0.8% of
esophageal neoplasms.
They are classified into two major groups:
epithelial (mucosal) and
intramural (extramucosal) .
Even more rare are
heterotopic collections of tissue within the esophageal wall.
63

Leiomyomas
Leiomyomas are the most common benign intramural esophageal tumor which occur in
patients between 20 and 50 years.
The tumors are multiple in 3% to 10% of patients, they have no established gender
preponderance, and can occur at any level within the esophagus but rarely occur in the
cervical segment.
More than 80% of esophageal leiomyomas occur in the middle and lower thirds of the
esophagus.
esophagus
Because calcification can occur within a leiomyoma, this must be considered in the
differential diagnosis of a calcified mediastinal mass.
Histologically, leiomyomas are composed of interlacing bundles of smooth muscle cells.
cells
Tumors less than 5 cm in diameter rarely cause symptoms.
When larger than this, dysphagia, retrosternal pressure, and pain are the common
complaints.
When a leiomyoma virtually encircles the esophageal lumen, obstruction and regurgitation
can occur.
Bleeding more often occurs with the malignant form of the tumor, leiomyosarcoma.
Malignant degeneration of leiomyomas is exceedingly rare,
rare with fewer than 10 reported
cases.
Most leiomyomas, however, are solitary and vary from 2 to 5 cm in diameter.
Another interesting variation of this tumor is diffuse leiomyomatosis of the esophagus, in
which there is extensive infiltration of the entire esophagus.
64

Benign tumors and Cysts of the esophagus(suite)

Esophageal leiomyomas produce a characteristic smooth, concave
submucosal defect with sharp borders and abrupt sharp angles
where the tumor meets the normal esophageal wall on barium
swallow examination.
The tumor often appears to lie half within and half outside the
esophagus
Esophagoscopy is indicated to exclude the presence of carcinoma.
If the radiologic impression of a leiomyoma is confirmed
endoscopically, a biopsy of the mass should not be performed so
that subsequent extramural resection is not complicated by scarring
at the biopsy site. At esophagoscopy, these tumors are
characteristically mobile, have an intact overlying mucosa, and can
be displaced by the advancing esophagoscope.
Endoscopic ultrasonography has provided a new means for
evaluating the esophageal leiomyoma, which is seen as a distinct
intramural mass of characteristic low echodensity.
An asymptomatic leiomyoma or one discovered incidentally on a
barium swallow examination can be safely observed and followed
with periodic barium esophagograms and endoscopic
ultrasonography.
Esophagogram showing a leiomyoma with

the typical acute angle at its junction with the
esophageal wall.
Tumors that are symptomatic or larger than 5 cm in diameter

should be excised.
65

Once the esophagus is encircled and the tumor located, the overlying longitudinal muscle is split
in the direction of its fibers. The tumor is then gently dissected away from the contiguous
underlying submucosa and adjacent muscle. When enucleation of the tumor is complete, the
longitudinal esophageal muscle is reapproximated, although a large extramucosal defect may be
left without complication.
When resection is complete, leiomyomas virtually never recur.
recur
Polyps
Benign polyps of the esophagus are rare and typically arise in the cervical esophagus.
Traction on these polyps caused by repeated peristaltic contractions results in progressive
lengthening of their pedicles.
This may be responsible for their dramatic presentations, extruding into and even out of the
mouth or producing asphyxia as the upper airway becomes obstructed.
obstructed
Most benign polyps occur in older men, and these frequently are attached to the cricoid cartilage.
The tumors typically produce dysphagia, but hematemesis or melena may occur if the overlying
mucosa becomes ulcerated.
These polyps tend to be solitary with a long, cylindric configuration that may produce marked
esophageal dilation. Histologically, they are composed of fibrovascular tissue with varying
amounts of associated fat.
Barium swallow findings may be nondiagnostic or inaccurately interpreted in these patients. The
polyp may be overlooked as an air bubble or may be misdiagnosed as a carcinoma, or even as a
foreign body or achalasia if it has caused marked esophageal dilation .
Similarly, esophagoscopy may fail to define the polyp,
polyp particularly if the pedicle is not
demonstrated and the mucosa overlying the polyp is normal. The endoscopist simply passes the
lesion, which is soft and easily displaced with the esophagus.
Although esophageal polyps have been removed endoscopically by electrocoagulation of the
pedicle, the recommended approach is resection through a lateral cervical esophagotomy,
delivering the polyp from the esophagus, resecting its mucosal base of origin, and repairing the
defect under direct vision
66

Barium esophagogram of a patient with a

giant benign fibroepithelial polyp,
showing a large intraluminal mass
distending the cervical and upper
thoracic esophagus.
The giant polyp has been delivered

out of the cervical esophagus
through a left-sided neck incision.
The patients head is toward the
right, and the retractors are
67

Hemangiomas
Esophageal hemangiomas are rare, constituting 2% to 3% of benign tumors.
They are generally asymptomatic, they can be responsible for periodic gastrointestinal
bleeding or even massive and fatal hematemesis.
Asymptomatic lesions discovered incidentally during performance of an esophagoscopy

should be followed with periodic endoscopy.
Those that have bled require treatment, and although resection has been the standard
approach, laser endoscopy provides an effective alternative for control of the small bleeding
sites visualized through the esophagoscope.
Miscellaneous Benign Tumors
Benign esophageal tumors other than leiomyomas and polyps are extremely rare.
Granular cell myoblastomas actually arise from Schwann cells, not muscle as their name
implies. They produce dysphagia, retrosternal pain, nausea, and vomiting.
vomiting They are
difficult to diagnose endoscopically because of their submucosal location and have a
characteristic grayish yellow appearance. The overlying mucosa typically shows
pseudoepitheliomatous hyperplasia, which may be misdiagnosed histologically as
squamous cell carcinoma. Local excision is sufficient treatment of symptomatic tumors.
Papillomas,
Papillomas sessile lobulated tumors that have a fibrous core and are covered by
squamous mucosa, have been reported. Most occur in association with some degree of
esophageal obstruction, most often in the distal esophagus. Papillomas have been
postulated to represent localized epithelial hyperplasia or even to be premalignant
lesions,
lesions but their true significance is unknown. On the basis of their size and radiographic
configuration, papillomas at times warrant esophageal exploration to exclude
malignancy, but a major resection should be avoided because local excision is adequate
therapy.
Esophageal adenomas,
Carcinoid tumors,
tumors and
Inflammatory pseudotumors also have been reported but are so rare that they are
mentioned only for the sake of completeness.
68

Cysts
Esophageal cysts arise as outpouchings of the embryonic foregut.
foregut
The esophageal duplication cyst is a variation of the foregut cyst; it extends along the length of
the thoracic esophagus and is lined by squamous epithelium. It has submucosal and muscle
layers, the latter of which interdigitate with the outer longitudinal muscle layer of the normal
esophagus.
Three quarters of esophageal duplication cysts present in childhood, and more than 60% are
located along the right side of the esophagus.
Esophageal duplication cysts are frequently associated with vertebral anomalies (Klippel-Feil
deformity or spina bifida) and spinal cord abnormalities.
More than 60% of esophageal cysts cause either respiratory or esophageal symptoms in the first
year of life.
life Those located in the upper third of the esophagus tend to present in infancy, while
lower-third cysts may be asymptomatic initially and present later in childhood.
Adults present with: dysphagia, choking, or retrosternal pain when previously asymptomatic cysts
enlarge as a result of bleeding or infection. In the rare cyst that contains ectopic gastric mucosa,
a perforation of the cyst may occur.
The diagnosis of an esophageal cyst can usually be made on the basis of its typical radiographic
appearance. On the standard posteroanterior chest roentgenogram, the cyst may cause:
displacement of the trachea; on
lateral chest roentgenogram, it may appear as a retrocardiac posterior mediastinal mass.
The barium esophagogram demonstrates a smooth extramucosal esophageal mass that rarely
communicates with the esophageal lumen.
With computed tomography (CT), may be identified The cystic nature of the lesion and its relation
with adjacent mediastinal structures
When a duplication cyst is suspected, spinal radiographs should be obtained preoperatively to
identify an origin of the cyst in the notochord.
Because esophageal cysts have a predilection for bleeding, ulceration, perforation, and infection,
excision is generally recommended. This can generally be achieved with low morbidity by an
extramucosal resection.
69

Esophageal duplication cyst presenting as a high posterior mediastinal mass.

(A) Barium esophagogram showing the intramural, extramucosal esophageal
mass. (B) CT scan showing the cystic nature of the lesion (arrow).
70

Heterotopic Tumors
Islets of columnar mucosa may be found lining the pharynx and esophagus. Given the
embryologic replacement of the initial columnar ciliated epithelium by stratified squamous
epithelium, the occurrence of preserved inlet patches of columnar epithelium is readily
explained
These islets are much more common near the upper end than the lower end of the
esophagus.
Endoscopically, they are described as an inlet patch of columnar mucosa.
This tissue is not to be confused with Barretts mucosa and has little, if any, premalignant
disposition.
There have also been isolated reports of
sebaceous gland tumors as well as
ectopic pancreatic and thyroid tissue within the esophagus. These are primarily
autopsy reports that have little clinical significance.
71

Malignant Esophageal Tumors
Squamous Cell Carcinoma

World-wide, 95% of all esophageal cancers are squamous cell carcinomas.
In the United States and Europe, however, the incidence of adenocarcinoma arising in Barretts
mucosa is increasing at an alarming rate and in many areas surpasses that of squamous cell
tumors.
The incidence of squamous cell carcinoma of the esophagus throughout the world is relatively
low 3 or 4 per 100,000 population.
This disease occurs most commonly in the seventh decade of life and generally is 1.5 to 3 times
more common in men than in women.
The cause of esophageal carcinoma is unknown. It is thought to occur most often as a result
of prolonged exposure of the esophageal mucosa to noxious stimuli in patients who
have a genetic predisposition to the disease:
Carcinogenic nitrosamines in the soil,
soil
Contamination of foods by mutagenic fungi, Geotrichum candidum,
candidum
The ingestion of very hot tea
Chewing tobacco with or without betel nut, betel leaf ,
Alcohol consumption and cigarette smoking
malnutrition,
vitamin deficiencies,
anemia,
poor oral hygiene, dental caries,
previous gastric surgery
certain premalignant esophageal conditions
72

Pathologically, esophageal carcinoma occurs over a spectrum that ranges from the early
lesion, which is limited to the mucosa, to the more advanced form, in which the tumor
penetrates the muscle layers of the esophagus or beyond.
Carcinoma in situ typically is found in patients between 40 and 50 years of age and
gradually progresses to invasive squamous cell carcinoma over 2 to 4 years. Microscopically,
early esophageal carcinoma is defined in terms of the depth of tumor involvement,
involvement
either intraepithelial (carcinoma in situ),
intramucosal (limited to the lamina propria), or
submucosal.
The histologic features of esophageal dysplasia as dysplasia becomes severe, histologic
differentiation from carcinoma in situ becomes difficult. Once dysplastic cells are seen
traversing the basement membrane and extending into the underlying connective tissue,
the diagnosis of early invasion is made.
made
Carcinoma in situ of the esophagus tends to be multifocal.
multifocal
Macroscopic growth patterns :
a coarsely granular, reddish, slightly raised, plaque-like type;
an erosive type;
the occult form, which is not apparent on gross inspection of the esophagus; and
the papillary type, in which a slightly polypoid lesion of less than 3 cm is seen.
Advanced squamous cell carcinoma of the esophagus is defined as a tumor that involves the
muscle layers of the esophagus or beyond.
The TNM classification for staging esophageal cancer, divide esophagus into four main
sections:
the cervical esophagus (from the lower border of the cricoid cartilage to the thoracic
inlet, or 15 to 18 cm from the upper incisor teeth);
the upper thoracic esophagus (from the thoracic inlet to the level of the carina at about
24 cm at endoscopy);
the middle third esophagus (from the carina to half the distance to the esophagogastric
junction, or about 32 cm);
the lower esophagus (to the esophagogastric junction at 40 cm).
73

Using this arbitrary division of the esophagus,

8% of squamous cell carcinomas occur in the cervical esophagus,
55% in the upper and mid-thoracic segments, and
37% in the lower thoracic segment.
Macroscopically, 60% of these lesions are fungating intraluminal growths,
25% are ulcerative lesions associated with extensive infiltration of the adjacent esophageal
wall,
15% are infiltrating.
infiltrating
Microscopically, most squamous cell carcinomas of the esophagus are moderately differentiated
and contain islands of atypical squamous cells that infiltrate the underlying adjacent normal
tissues and contain keratin pearl formation and intercellular bridges between the tumor cells.
Esophageal carcinoma tends to be multifocal, and a patient who survives treatment of one
carcinoma has at least twice the risk of developing a second primary esophageal neoplasm.
Esophageal carcinoma is notorious for its aggressive biologic behavior.
behavior
It tends to infiltrate locally, involving adjacent lymph nodes and spreading along the extensive
submucosal esophageal lymphatic channels.
Lack of an esophageal serosa favors tumor extension into adjacent structures such as the
pericardium, aorta, tracheobronchial tree, diaphragm, stomach, and left recurrent laryngeal
nerve.
nerve
Mediastinal, supraclavicular, or celiac lymph node metastases are present in at least 75% of
patients with esophageal cancer at the time of initial diagnosis.
Cervical esophageal cancers tend to drain to the deep cervical, paraesophageal, posterior
mediastinal, and tracheobronchial lymph nodes, while the lower esophageal tumors spread to
paraesophageal, celiac, and splenic hilar lymph nodes.
Distant spread to the liver and lungs is seen in 90% of cases at autopsy.
The prognosis of invasive SCC is dismal, with 5% to 12% of patients surviving 5 years.
Unfortunately, extraesophageal tumor extension is present in 70% of cases at the time of
diagnosis,
diagnosis and when lymph node metastases are present, 5-year survival is only 3%, compared
with 42% when there is no lymph node spread.
74

Adenocarcinoma
Adenocarcinomas account for 2.5% to 8% of primary esophageal cancers, but the frequency of this
tumor is increasing at a rate surpassing that of any other cancer.
This increase is the result of the growing prevalence of adenocarcinoma arising in Barretts mucosa.
mucosa
Adenocarcinomas most often involve the distal third of the esophagus,
esophagus have a peak incidence in the
sixth decade of life, and are three times more common in men than in woman.
Esophageal adenocarcinoma has three potential origins:
origins
The malignant degeneration of metaplastic columnar epithelium (Barretts mucosa),
Heterotopic islands of columnar epithelium,
epithelium or
The esophageal submucosal glands.
glands
!!! In addition, the esophagus may be involved secondarily by a gastric carcinoma growing
upward.
upward
Severe gastroesophageal reflux is a major factor in the development of a columnar epitheliumlined
(Barretts) esophagus.
Refluxed gastric acid, proteases, and bile erode the normal squamous epithelium,
epithelium and the residual
pluripotential basal cells may differentiate along multiple cell lines, producing a variety of columnar
epithelial cell types.
types
The diagnosis of Barretts esophagus is established at endoscopy by histologic documentation of
columnar mucosa extending into the tubular esophagus at least 2 cm above the anatomic
esophagogastric junction. This metaplasia may extend up to the thoracic inlet
It has been estimated that patients with Barretts esophagus are 40 times more likely to develop
adenocarcinoma than the general population.
Barretts mucosa occurs in three characteristic histologic patterns:
patterns
Gastric fundus-type epithelium, which has a foveolar surface pattern (no villi), but contains
glands with parietal cells, chief cells, and mucous cells
Junctional-type epithelium,
epithelium in which there are no villi present and in which cardiac-type mucous
glands without parietal or chief cells are seen. The mucosa has a foveolar pattern that is flat
and typically is seen in normal colon, gastric cardia, and villous atrophy of the small bowel.
75

Specialized columnar epithelium,

epithelium which is typically characterized by villiform folds lined
by a single layer of glycoprotein-secreting columnar cells and mucus-secreting goblet
cells. Cryptlike glands between the villi are also lined by columnar and goblet cells and
contain few if any parietal or chief cells. This epithelium has also been termed
incomplete intestinal metaplasia because only the goblet cell component of intestinal
epithelium is present.
Dysplasia occurs to varying degrees in Barretts mucosa, and dysplasia clearly is a
premalignant esophageal lesion.
lesion
The histologic features of dysplasia are:
an increased nuclear/cytoplasmic ratio,
loss of the basilar orientation of the epithelial cells along the basement membrane,
irregular chromatin clumping, hyperchromatic nuclei, and prominence of the nucleoli
Severe dysplasia is almost always associated with carcinoma in situ and mandates
aggressive therapy.
Barretts mucosa with intestinal metaplasia and no dysplasia.
Barretts mucosa with intestinal metaplasia and high-grade dysplasia.
76

Esophageal adenocarcinoma has an aggressive biologic behavior that is characterized by

frequent transmural invasion and lymphatic spread.
Because these tumors arise in the lower third of the esophagus, paraesophageal, celiac axis, and
splenic hilum lymph node metastases are common .
The lung and liver are the visceral organs most frequently involved by metastases.
Esophageal adenocarcinoma is associated with a 5-year survival rate of 0% to 7%.
Without lymph node involvement, survival of 5 years is possible, compared with an average
survival of only 9 months in patients with lymph node involvement.
Other Malignancies
Anaplastic small cell (oat cell) carcinoma arises in the esophagus from the same argyrophilic cells
that give rise to this tumor in the lung. As is the case with their pulmonary counterparts, these
tumors contain neurosecretory granules on electron microscopy. They are extremely aggressive
tumors, they are commonly associated with distant spread at the time of diagnosis, and survival
beyond 1 year is rare.
Adenoid cystic esophageal carcinoma is another rare lesion, and fewer than 50 cases have been
reported. These tumors typically occur in the middle third of the esophagus, are discovered late
in their course, metastasize widely, and are associated with a median survival of only 9 months.
About 100 cases of malignant melanoma of the esophagus have been reported, and these rare
lesions constitute less than 0.1% of esophageal malignancies. Malignant melanoma may involve
the esophagus either as a primary tumor or as a secondary metastasis. In the former situation, it
is thought to arise from melanocytes that occur in the esophagus. These tumors typically present
as large (7 cm or more) polypoid masses, which may or may not be pigmented. The average
survival is only 13.4 months, and less than 5% survive 5 years. Metastasis to liver, lymph nodes,
lung, and brain is common.
Carcinosarcoma describes a lesion of the esophagus that has histologic features of both
squamous cell carcinoma and malignant spindle cell sarcoma. These typically polypoid tumors
generally occur in the distal two thirds of the esophagus, grow to large size (10 to 15 cm), and
have a poor prognosis, with 2% to 6% of patients surviving 5 years.
77

Local Effects
Symptoms from esophageal carcinoma may be insidious in onset:
nonspecific retrosternal discomfort,
indigestion, or
transient dysphagia.
Early esophageal carcinoma that is limited to the mucosa or submucosa may be completely
asymptomatic or may produce localized spasm that is manifested as periodic esophageal
obstruction.
obstruction
Because the esophagus is a distensible tube, a major portion of the circumference must be
involved before obstructive symptoms develop.
develop
Many patients subconsciously alter their eating habits by eliminating some foods, chewing their
food more thoroughly, and using more liquids to wash down food.
By the time of presentation to a physician with a complaint of dysphagia, symptoms have often
been present for 6 to 8 months.
Dysphagia is the most common presenting symptom of esophageal carcinoma. It develops in
90% of patients and is the primary manifestation of the disease in more than 80%. It may be:
a subtle retrosternal discomfort as a bolus of food is swallowed,
a transient feeling of retrosternal discomfort with swallowing that may not recur for several
weeks or months,
painful swallowing (odynophagia),
complete esophageal obstruction.
obstruction
Weight loss is the next most common symptom and is present in about 40% of patients with
esophageal carcinoma.
Pain is the initial symptom in 10% of patients. It may be:
precordial, retrosternal, epigastric, or intrascapular.
Transient retrosternal pain radiating to the back or neck as the solid bolus of food passes
through the tumor and causes local distention or muscle contraction has a much different
implication than constant, boring retrosternal or epigastric pain, which more often
represents local invasion by the tumor.
78

Regurgitation of undigested food that has not passed through the esophagus should not be
confused with the vomiting of gastric contents.
Respiratory symptoms may be due either to aspiration or to direct invasion of the
tracheobronchial tree by the tumor. These symptoms include cough, dyspnea, pleuritic pain,
or hemoptysis.
hemoptysis
Hematemesis is a rare, early symptom of esophageal carcinoma, but bleeding from an
esophageal malignancy is seldom of sufficient quantity to cause melena.
Hoarseness from recurrent laryngeal nerve involvement is an ominous sign of unresectability.
The course of the left main-stem bronchus anterior to the esophagus at the level of the
carina is significant in the patient with a mid-esophageal tumor because the common wall
between the esophagus and left main-stem bronchus may become involved with tumor and
lead to the development of a malignant tracheoesophageal fistula.
fistula
Systemic Effects
Although the systemic effects of esophageal carcinoma are less well recognized than the
local effects, they may have important clinical significance.
Weight loss and

Negative nitrogen balance due to starvation have direct implications on the morbidity and mortality of
esophageal resection in these patients. Virtually every patient with advanced esophageal obstruction is
Dehydrated and total body volume depleted from impaired oral intake. The patient with esophageal
obstruction is prone to the development of
Severe hypokalemia with secondary muscle weakness. One to 2 L of saliva is produced each day, and
the concentration of potassium within saliva (20 mEq/mL) is higher than that in any other
gastrointestinal secretions. Patients who are unable to swallow their saliva, therefore, may present with
marked hypokalemia.
Fever and systemic toxicity may be due to aspiration from the obstructed esophagus.
The production of parathormone by some squamous cell esophageal carcinomas has been
documented and may result in hypercalcemia, even in the absence of bone metastases.
metastases
Preoperative hypercalcemia in the patient with esophageal carcinoma and no demonstrable
bone metastases has been suggested to be a poor prognostic sign.
Apparently a vagal nervemediated response, the occurrence of swallow syncope
syncope has been
reported in a few patients with esophageal obstruction due to carcinoma.
79

Diagnostic Investigations
History and Physical Examination

90% of patients with esophageal carcinoma experience dysphagia as their primary presenting
symptom, thus a complaint of dysphagia in any adult 50 years of age or older cannot be taken
lightly.
A complaint of dysphagia warrants both a barium swallow examination and an endoscopic
evaluation to rule out the presence of carcinoma. The combination of esophageal biopsy and
brushings for cytologic evaluation establishes a diagnosis of carcinoma in 95% of patients with
malignant strictures.
Patients with long-standing reflux symptoms that have been well controlled with medical therapy
who then develop an increase in retrosternal discomfort should not be presumed to have
esophagitis.
esophagitis Rather, they should undergo appropriate radiographic and endoscopic evaluation.
evaluation
Aside from evidence of weight loss, most patients with esophageal carcinoma have few objective
findings on physical examination to aid in the diagnosis.
Nonetheless, careful examination for cervical or supraclavicular lymph node metastases, abdominal
masses, and liver nodularity is warranted. The finding of a hard, supraclavicular lymph node in the
patient with an intrathoracic esophageal carcinoma warrants fine-needle aspiration biopsy. If
metastatic disease is documented, the presence of a stage IV tumor has been established.
Resectional therapy of the esophageal tumor in this situation is seldom justified because the
patients expected survival is so poor.
Laboratory studies should include a complete blood count,
count blood urea nitrogen,
nitrogen and serum
creatinine to assess the state of hydration, as well as liver function tests,
tests including total protein and
albumin levels to assess nutrition. Serum electrolytes, particularly potassium and calcium levels,
should also be obtained.
obtained
In obtaining a history from the patient who complains of dysphagia, the physician should ask the
patient to localize with one finger on the anterior chest or neck the point at which food lodges when
swallowing.
swallowing The patient with a mechanical esophageal obstruction such as a carcinoma is able to
localize the consistent point of obstruction without difficulty.
difficulty This is in contrast to the patient with
neuromotor obstruction, who may only sense slow esophageal emptying diffusely in the retrosternal
area.
80

Radiographic Studies
A barium swallow examination is the first study that should be obtained in a patient who
complains of dysphagia. Tumors of the cervical esophagus are most difficult to identify by
barium swallow examination, and carcinoma of the cardia may be confused with achalasia,
a benign stricture, or esophageal spasm.
The typical esophageal carcinoma presents radiographically as an irregular, rigid narrowing
of the esophageal wall.
The normal mucosal pattern is frequently destroyed. Polypoid fungating tumors present as
irregular filling defects with ulcerated borders within the esophagus.
An old dictum relates that an esophagus that is dilated proximal to a stenosis is most
indicative of a benign chronic obstruction, whereas an esophagus proximal to a carcinoma
has not had enough time to dilate. (This observation has proved to be incorrect on
numerous occasions).
Similarly, although a smooth, tapered radiographic esophageal stricture supposedly reflects
benign disease, any stenosis merits esophageal biopsy and brushings for cytologic
evaluation to rule out carcinoma.
carcinoma
The barium swallow examination may also show a soft tissue mass adjacent to the
esophageal tumor indicative of extraesophageal local invasion.
invasion
In half of patients with esophageal carcinoma is the plain chest radiograph abnormal,
abnormal the
most common findings being:
an airfluid level in the obstructed esophagus,
a dilated esophagus,
abnormal mediastinal soft tissue representing adenopathy,
pleural effusions, or
pulmonary metastases.
81

(A) Barium esophagogram showing an upper esophageal squamous cell carcinoma at the level of the
aortic arch. Note the mucosal irregularity and shelf of tumor, which is characteristic of carcinoma. (B)
Esophagogram showing a distal esophageal adenocarcinoma presenting as a characteristic applecore constriction above the esophagogastric junction.
82

The chest and upper abdominal CT scan is the standard radiographic technique for staging
esophageal carcinoma.
carcinoma
esophageal wall thickness should not exceed 5 mm on CT scanning,
regional adenopathy or
pulmonary, liver, adrenal, or distant nodal metastasis.
CT scan, guided tissue diagnosis with fine-needle aspiration biopsy is warranted. A positive
histologic diagnosis of stage IV carcinoma translates to an average survival of only 6 to 12
months, and therefore an operation of the magnitude of esophagectomy is contraindicated.
Several investigators have reported the value of CT in evaluating resectability of esophageal
carcinoma.
carcinoma
Bronchoscopy
Bronchoscopy should be performed in patients with carcinoma of the upper and middle thirds of
the esophagus to exclude invasion of the posterior membranous trachea or main-stem bronchi,
which precludes a safe esophagectomy.
Other Studies.
Magnetic resonance imaging to evaluate mediastinal invasion has not gained widespread
popularity.
Bone scan is not warranted unless the patient has specific complaints suggesting that bone
metastases exist.
routine brain scans are not indicated because brain metastases from carcinoma of the
esophagus are uncommon (less than 4% in patients being evaluated for esophagectomy).20
83

Esophagoscopy
Esophagoscopy is one of the most important diagnostic tools in the assessment of the patient
with esophageal symptoms from any cause. The flexible fiberoptic esophagoscope permits
endoscopic assessment with greater ease gf obstructing lesions of esophagus
Endoscopic Vital Staining, Endoscopic Ultrasound and Endoscopic Abrasive cytology
Vital staining of the esophageal mucosa is a technique that is useful in detecting dysplastic
esophageal lesions that are not obvious on direct endoscopic assessment. Carcinoma in situ
(intraepithelial carcinoma) or microinvasive carcinoma may appear endoscopically as flat,
nondescript lesions (leukoplakia or erythroplakia) and therefore can be difficult to diagnose. Lugol
(3% iodide) solution or 2% toluidine blue may be applied through the esophagoscope to the
esophageal mucosa.
Lugol solution stains normal glycogenic esophageal mucosa brown, while abnormal mucosa
(early carcinoma, esophagitis, Barretts mucosa) remains unstained.
Toluidine blue is a metachromatic stain with affinity for cell nuclei. Therefore, tissues with a
high cellular density and high nucleus/cytoplasm ratio take up the stain quickly and retain it
for about 1 hour.
Endoscopic ultrasound is being used with increasing frequency as an adjunct to the standard
radiologic and endoscopic assessment of esophageal disease. It offers the potential for more
sensitive staging of esophageal carcinoma by detecting the depth of invasion and the presence of
abnormal mediastinal adenopathy.
adenopathy Ultrasound permits the endoscopic delineation of the mucosa,
submucosa, and muscular layers of the esophagus as well as adjacent tissues. Lymph nodes as
small as 5 mm can be recognized with this instrument.
Endoscopic Abrasive cytology using a swallowed balloon catheter (balloon cytology) has been
extremely effective in screening for carcinoma
Combining abrasive cytology with vital staining of the esophageal mucosa may prove to yield the
best sensitivity and specificity for screening populations.
84

Premalignant Lesions
Premalignant Esophageal Lesions Chronic irritation of esophageal mucosa by a variety

of noxious stimuli (alcohol, tobacco, hot foods and liquids) eventually may lead to the
development of esophageal carcinoma. A variety of esophageal lesions have a recognized
premalignant nature:
The premalignant nature of Barretts esophagitis was discussed earlier.
Reflux Esophagitis constitutes a chronic chemical injury of the esophageal mucosa, it is
regarded as a potentially premalignant abnormality of the esophagus that requires
aggressive medical therapy or surgical control.
About 10% to 12% of patients with achalasia of cardia who are observed for 15 years or
longer develop esophageal carcinoma. The cause is thought to be related to the irritating
effects of the fermenting intraesophageal contents on the adjacent esophageal mucosa.
Plummer-Vinson syndrome (Paterson-Kelly syndrome or sideropenic dysphagia)
dysphagia is a
premalignant esophageal condition. The term sideropenic dysphagia refers to the
development of cervical dysphagia in patients who have iron-deficiency anemia.
Familial keratosis palmaris et plantaris (tylosis) is associated with an increased incidence of
esophageal carcinoma
Radiation Esophagitis during the course of treatment for lymphoma, lung, breast, or other
mediastinal malignancies are at increased risk for developing esophageal carcinoma years
later.
Within Esophageal Diverticula several isolated reports have been made of esophageal
carcinomas that have been found incidentally presumably as a result of the irritating effects
on the mucosa of stagnant, putrefying food within the pouch. Esophageal diverticula are
therefore also regarded as premalignant esophageal lesions, although this occurrence is
extremely rare.
85

Principles of Treatment
Treatment of Esophageal Cancer

Therapy of esophageal carcinoma is influenced by the knowledge that in most of these
patients, local tumor invasion or distant metastatic disease precludes cure. Neither
chemotherapy, radiotherapy, nor surgery alone has achieved significant and consistent longterm survival in patients with esophageal carcinoma.
Radiation
Although squamous cell carcinoma is generally regarded as a radiosensitive and therefore
potentially curable tumor,
tumor radiotherapy alone has not achieved cure in most of these patients.
Radiotherapy is used in the treatment of esophageal carcinoma to provide either palliation or
cure as an adjunct to esophagectomy.
Palliative radiotherapy in the range of 4000 to 5000 cGy over 3 to 4 weeks relieves dysphagia
sufficiently in nearly half of patients with advanced metastatic carcinoma and severe
dysphagia to allow them to swallow liquids and diet supplements.
Curative supervoltage radiotherapy is delivered in doses of 5000 to 7000 cGy over 5 to 7
weeks, using rotational and oblique ports to avoid spinal cord injury.
injury Unfortunately, the
average 5-year survival after such treatment is between 6% and 10% in most series because
radiation alone fails to control either the primary tumor or distant metastatic disease.
Thus, reported 5-year survival rates after esophageal resection for carcinoma usually average
between 10% and 15%, with more than 80% of patients dying within 1 year of diagnosis.
Several Japanese reports indicate 5-year survival rates of 25% to 38%, with combined
preoperative radiotherapy followed by resection.
Intubation
A variety of endoesophageal tubes (Celestin, Fell, Mackler, Mousseau-Barbin, Souttar, WilsonCook) have been used to provide palliation in patients with esophageal carcinoma.
A variety of expandable intraesophageal metallic stents have been used to achieve palliation
in patients with unresectable esophageal carcinoma.26,27 These stents are easier to insert
than the older plastic tubes, have a larger lumen, and theoretically, carry less risk of
perforation. They are inserted under fluoroscopy using a flexible esophagoscope.
86

Laser
Endoscopic laser fulgurating of esophageal carcinoma, particularly with the Nd:YAG laser, has
been used to achieve temporary relief of the esophageal obstruction in patients with
unresectable tumors. Generally, multiple sessions are required to resect sufficient tumor to
achieve an adequate lumen, and functional success with restoration of comfortable swallowing
is achieved in 75% to 80% of patients.
patients
Bypass
A variety of surgical procedures, such as substernal gastric or colon bypass, have been
developed as palliative internal bypasses of unresectable esophageal carcinomas. This is simply
too large an operation for a patient with so advanced a malignancy.
Surgical Resection
Transthoracic Resection. For most patients with localized esophageal carcinoma, resection
provides the most effective and reliable palliation of dysphagia.
The traditional surgical approach to distal esophageal carcinoma is a left thoracoabdominal
incision (Fig. 19-11). After resecting the distal esophagus, proximal stomach, and adjacent
lymph nodes, an intrathoracic esophagogastric anastomosis is performed.
Tumors involving the mid-esophagus are resected through either a thoracoabdominal or
separate thoracic and abdominal incisions, and a high intrathoracic esophagogastric
anastomosis is performed (Fig. 19-12).
Transhiatal Resection.
Resection During the past two decades, the technique of transhiatal
esophagectomy without thoracotomy has been popularized as an operation that minimizes the
factors responsible for most poor results from traditional transthoracic esophageal resection
and reconstruction. In this operation, irrespective of the level of the tumor, the entire
intrathoracic esophagus is resected, the stomach is repositioned in the posterior mediastinum
in the original esophageal bed, and the gastric fundus is anastomosed to the cervical
esophagus above the level of the clavicles.
87

Standard thoracoabdominal esophagogastrectomy for

carcinomas of the distal esophagus and cardia. (A)
Thoracoabdominal incision. (B) Tissue to be resected
(colored area). (C) Completed reconstruction after
intrathoracic esophagogastric anastomosis
Standard thoracoabdominal esophagogastrectomy for tumors

of the upper and middle thirds of the thoracic esophagus. (A)
Either the continuous thoracoabdominal incision or separate
thoracic and abdominal incisions are used. (B) Portion of
esophagus to be resected (colored area). (C) Completed
reconstruction with high intrathoracic esophagogastric
anastomosis and gastric drainage procedure.
88

Transhiatal Esophagectomy
Mobilization of the thoracic esophagus from
the posterior mediastinum
89

This operation has been criticized because of its limited exposure of the intrathoracic
esophagus through the diaphragmatic hiatus and, therefore, the risk of intraoperative
bleeding from the divided aortic esophageal branches. In addition, one cannot carry out a
complete mediastinal lymph node dissection through the diaphragmatic hiatus for purposes
of staging or potential cure.
Radical Resection.
The radical transthoracic esophagectomy with en bloc dissection of contiguous lymph
nodebearing tissues for esophageal carcinoma. This is a much more formidable operation,
the results of which, when compared with those of transhiatal esophagectomy without
thoracotomy and no formal lymph node dissection. As a general rule, the stomach is the
preferred visceral esophageal substitute, being far more resilient than intestine and readily
reaching to the neck for replacement of the entire esophagus. Colonic interposition is a
major operative undertaking in patients with esophageal carcinoma and should be used
only in selected cases in which the stomach is not available for esophageal replacement.
Multimodality Therapy
Efforts have been made to improve survival in patients with esophageal carcinoma by using
multimodality therapy in combination with surgery.
Combined preoperative chemotherapy and radiotherapy before transhiatal esophagectomy
for carcinoma, for example, has provided encouraging survival statistics. They received 3
weeks of chemotherapy with cisplatin, vinblastine, and 5-fluorouracil, concurrent with 3750
to 4500 cGy of radiotherapy. After a 3-week recovery period, transhiatal esophagectomy
was accomplished.
90

91

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SURGICAL PATHOLOGY

SURGICAL PATHOLOGY OF THE ESOPHAGUS - 4

SURGICAL PATHOLOGY OF ESOPHAGUS

SURGICAL PATHOLOGY OF ESOPHAGUS

SURGICAL PATHOLOGY OF ESOPHAGUS

Barium esophagogram demonstrates

Pain or fever after esophageal instrumentation

SURGICAL PATHOLOGY OF ESOPHAGUS

Management(Principles of Surgical Treatment)

SURGICAL PATHOLOGY OF ESOPHAGUS

SURGICAL PATHOLOGY OF ESOPHAGUS

When treating such perforations conservatively,

SURGICAL PATHOLOGY OF ESOPHAGUS

Operative Therapy Of Esophageal Perforations(suite)

Approach for drainage of a cervical

SURGICAL PATHOLOGY OF ESOPHAGUS

Operative Therapy Of Esophageal Perforations(suite)

SURGICAL PATHOLOGY OF ESOPHAGUS

Operative Therapy Of Esophageal Perforations(suite)

Final position of the mobilized stomach in the posterior mediastinum

SURGICAL PATHOLOGY OF ESOPHAGUS

Operative Therapy Of Esophageal Perforations(suite)

Irrigation of the posterior mediastinum

SURGICAL PATHOLOGY OF ESOPHAGUS

Late Esophageal Perforation

Patients with late-recognized esophageal perforations have been treated in a variety of

SURGICAL PATHOLOGY OF ESOPHAGUS

Caustic ingestion occurs in two categories of patients:

SURGICAL PATHOLOGY OF ESOPHAGUS

CAUSTIC INJURY OF ESOPHAGUS

CAUSTIC INJURY OF ESOPHAGUS AND STOMACH

Caustic stricture of the

Detail of stomach showing

SURGICAL PATHOLOGY OF ESOPHAGUS

CAUSTIC INJURY OF ESOPHAGUS

SURGICAL PATHOLOGY OF ESOPHAGUS

CAUSTIC INJURY OF ESOPHAGUS

SURGICAL PATHOLOGY OF ESOPHAGUS

CAUSTIC INJURY OF ESOPHAGUS

Immediate Diagnosis And Treatment (suite)

SURGICAL PATHOLOGY OF ESOPHAGUS

CAUSTIC INJURY OF ESOPHAGUS

ENDOSCOPIC GRADING OF CAUSTIC ESOPHAGEAL INJURY

Mucosal hyperemia and edema

Mucosal ulceration with vesicles and

Deep ulceration with charring and eschar

SURGICAL PATHOLOGY OF ESOPHAGUS

CAUSTIC INJURY OF ESOPHAGUS

SURGICAL PATHOLOGY OF ESOPHAGUS

CAUSTIC INJURY OF ESOPHAGUS

SURGICAL PATHOLOGY OF ESOPHAGUS

SURGICAL PATHOLOGY OF ESOPHAGUS

An esophageal diverticulum is an epithelial-lined mucosal pouch that protrudes from the

SURGICAL PATHOLOGY OF ESOPHAGUS

Pharyngoesophageal Pulsion Diverticulum

SURGICAL PATHOLOGY OF ESOPHAGUS

Pharyngoesophageal Pulsion Diverticulum(suite)

SURGICAL PATHOLOGY OF ESOPHAGUS

Pharyngoesophageal Pulsion Diverticulum(suite)

Small Zenker diverticulum. (A) The 2.5-cm

Posteroanterior (A) and oblique (B)

SURGICAL PATHOLOGY OF ESOPHAGUS

Pharyngoesophageal Pulsion Diverticulum(suite)