OF ESOPHAGUS
4 hours
ESOPHAGEAL PERFORATION
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
ESOPHAGEAL PERFORATION
Diagnosis
ESOPHAGEAL PERFORATION
ESOPHAGEAL PERFORATION
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.
ESOPHAGEAL PERFORATION
ESOPHAGEAL PERFORATION
ESOPHAGEAL PERFORATION
ESOPHAGEAL PERFORATION
11
ESOPHAGEAL PERFORATION
12
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.
13
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
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
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 Findings
First-degree
Second-degree
Third-degree
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
22
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
26
27
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
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
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
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 .
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
38
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
Laparoscopic approach
41
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.
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
45
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
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.
Complication
None
Esophagitis
Stricture
Barretts esophagus
Patients
59
47
19
25
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
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
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
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
59
A.
B.
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.
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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.
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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
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
Hemangiomas
They are generally asymptomatic, they can be responsible for periodic gastrointestinal
bleeding or even massive and fatal hematemesis.
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.
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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.
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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
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).
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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.
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76
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.
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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.
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.
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Diagnostic Investigations
Diagnostic Investigations
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.
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Diagnostic Investigations
(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.
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Diagnostic Investigations
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
Diagnostic Investigations
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.
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Premalignant Lesions
Principles of Treatment
Principles of Treatment
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
Principles of Treatment
88
Principles of Treatment
Transhiatal Esophagectomy
Mobilization of the thoracic esophagus from
the posterior mediastinum
89
Principles of Treatment
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
Principles of Treatment
91