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correlate episodes of acid reflux with the patient’s symptoms (Figure 1.18). This test records the percentage of time
within a 24-h period when esophageal pH registers below
4 and correlates it with the extent of both reflux episodes
and the presence of complications of esophagitis. In
normal subjects, esophageal pH is below 4 about 2% of the
time. This incidence increases to 8% in patients with
uncomplicated GERD, to 12% in those with GERD and
esophagitis, to 15% in those with GERD and stricture, and
to almost 30% in those with GERD and Barrett’s mucosa.
SCINTIGRAPHIC ASSESSMENT Scintigraphic assessment
of gastroesophageal reflux has the added value of assessing
not only gastroesophageal reflux but also gastric emptying.
It is useful only in selected patients.
Tr e at m e n t
5
FIGURE 1.17. Paraesophageal hernia is best demonstrated by
barium study of the upper GI tract, which shows herniation of
all or part of the stomach into the chest through a defect in the
hiatus. As in this patient, the herniation (H) is usually to the left
of the gastroesophageal junction, which maintains its normal
position below the diaphragm (arrow). (Courtesy of Henry I.
Goldberg, MD.)
UPPER GI ENDOSCOPY Upper GI endoscopy is the best
way to determine the presence of esophagitis and Barrett’s
mucosa and to evaluate the severity of the esophagitis. Multiple biopsy samples are required for adequate assessment.
SOPHAGEAL MANOMETRY
E
Manometry is a useful
technique to detect hypotensive LES (i.e., <15 mm Hg);
abnormal motility in the body of the esophagus; and
abnormal UES function, which has been described in
patients with respiratory complications of gastroesophageal reflux. Manometry is a vital preoperative
investigation because it may identify coexisting motility
disorders that rule out the use of unmodified Nissen
fundoplication.
WENTY-FOUR-HOUR PH MONITORING
T
Twenty-fourhour pH monitoring is of paramount importance to determine the extent of acid reflux, to measure the ability of the
esophagus to clear acid reflux, and most importantly, to
N
ONSURGICAL THERAPY
Most patients with early
symptoms of esophagitis can be managed effectively with
medical therapy and other measures designed to minimize
reflux, reduce production of gastric acid, neutralize acid in
the esophagus, provide a mucosal barrier, or improve
gastric emptying. Medical therapy must be well planned
and is most effective if administered under the supervision
of a gastroenterologist.
Minimizing Reflux Key strategies to minimize reflux
include reduction of abdominal pressure by weight loss and
avoidance of abdominal compression by articles of clothing. Other methods include elevating the head of the bed
6in on blocks; avoiding large meals; taking evening meals
at least 4h before bedtime; avoiding fatty foods, which are
potent releasers of CCK; and avoiding smoking because
nicotine reduces LESP.
Reducing Acid Acid secretion can be effectively
suppressed with histamine H
proton-pump inhibitors. Proton-pump inhibitors have
TABLE 1.5. Essentials: Consequences of Severe
Gastrointestinal Reflux Disease (GERD)
Injurious refluxate
䊏
Acid and pepsin
䊏
Bile and pancreatic juice
䊏
Succus entericus
Pathophysiologic responses
䊏
Pain without inflammation
䊏
Inflammation
Low-grade esophagitis
High-grade esophagitis
Stricture formation
䊏
Metaplastic/dysplastic response
Columnar metaplasia (e.g., Barrett’s mucosa)
Dysplasia
Adenocarcinoma in situ
Adenocarcinoma
-receptor antagonists or
2
C linical D isorders.............................................................................................................................. 19
FIGURE 1.18. Monitoring esophageal pH measures the percentage of time during a 24-h period when
the pH is outside the normal range and can be used to evaluate acid reflux incidents and correlate
them with the patient’s symptoms. (Courtesy of Marco G. Patti, MD.)
two advantages over H2-receptor antagonists. First, they
more effectively suppress acid secretion, often causing
achlorhydria after several days of treatment. Second,
theoretically, achlorhydria improves LES function by
preventing gastric acidification, which reduces LESP; and
by leading to hypergastrinemia, which enhances LESP.
Omeprazole (20–40mg/day) has become the drug of
choice and can be administered for 6 to 8 weeks at a time.
Neutralizing Acid Neutralizing acid within the esophagus and stomach may be accomplished with antacids,
which provide effective and cheap symptomatic therapy in
most patients early in the disease. After an initial rigorous
antacid therapy for some 12 weeks, patients can safely carry
out self-medication with these drugs. Antacids containing
calcium have the theoretical advantage of being potent
releasers of gastrin, which increases LESP.
Providing Barrier Protection Sucralfate and alginic
acid in combination with antacids are said to provide a
barrier to the esophageal mucosa against the action of acid
and other irritants in the refluxate.
Improving Gastric Emptying Metoclopramide, cisapride, and domperidone have been used because of their
action to improve gastric emptying and LESP. The value of
this therapy in severe disease is questionable.
NDICATIONS FOR SURGICAL THERAPY The essentials of
I
surgical treatment of gastroesophageal reflux disease are
given in Table 1.6.
Nonresponsiveness to Medical Therapy If a wellplanned and administered program of medical therapy
fails, usually after several months or years of therapy, both
patient and physician may agree that more needs to be
done. DeMeester et al. believe that a defective LES is
the most important factor predicting failure of medical
therapy.
6
They argue that antireflux surgery should be considered in the presence of a defective LES—irrespective of
the presence or degree of esophagitis—providing that
24-hpH monitoring studies have proven that the symptoms are due to reflux. This recommendation is increasingly being put into practice as minimally invasive surgery
has become the preferred surgical approach.
Severe Endoscopic Esophagitis A patient with severe
endoscopic esophagitis, poorly controlled symptoms, and
a structurally defective LES is a candidate for surgery.
Esophageal Stricture Esophageal strictures must be
dilated by bougies. Malignancy in strictures must be
excluded by endoscopy and biopsy. Although this condition can be successfully managed nonsurgically following
stricture dilatation, the development of strictures often
indicates severe disease that is best managed surgically.
Strictures must be dilated adequately before antireflux
surgery is done. Because of to the excellence of medical
therapy,nondilatable strictures are now rare. When they do
occur, strictures must be resected and an antireflux procedure or jejunal interposition performed.
Barrett’s Esophagus The presence of Barrett’s metaplasia, or Barrett’s esophagus, indicates severe disease and
20 .......................................................................................................................................... Esophagus
TABLE 1.6. Essentials: Surgical Treatment of Gastroesophageal
B
Reflux Disease (GERD)
Indications
䊏
Symptomatic failure of medical therapy
䊏
Severe endoscopic esophagitis
䊏
Esophageal stricture (following dilatation)
䊏
Barrett’s esophagus to arrest progression to cancer
Preoperative work-up
䊏
Endoscopy and biopsy
䊏
Motility studies to assess LESP and rule out associated
motor disorder
䊏
24-h pH monitoring to ensure symptoms are caused by reflux
Principles of surgical treatment
䊏
Reduce hernia into abdomen
䊏
Restore LESP by fundoplication
䊏
Narrow hiatus by crural approximation
䊏
Anchor wrap to preaortic fascia (optional)
Surgical procedures
䊏
Most now performed laparoscopically
䊏
Nissen fundoplication most popular (complete wrap,
2–5 cm long)
䊏
Toupet fundoplication (270° posterior wrap)
䊏
Short esophagus: Collis-Nissen repair
Outcome
䊏
Operative mortality 0.2%–0.3%
䊏
Complication rate 3%–10%
䊏
Long-term symptom relief in 90%–95%
Abbreviation: LESP, lower esophageal sphincter pressure.
TABLE 1.7. Objectives of Surgical Therapy for Hiatal Hernia
and Gastroesophageal Reflux Disease (GERD)
䊏
Restore gastroesophageal continence.
䊏
Reduce the hiatal hernia and create a 5- to 6-cm length of
abdominal esophagus.
䊏
Improve LESP by wrapping the gastric fundus around the
distal 2–3 cm of the esophagus, either totally or partially.
䊏
Narrow the hiatus by approximating the crura.
䊏
Anchor the wrap within the abdomen by suturing it to the
preaortic fascia or crura, if this can be done expeditiously.
䊏
Avoid damage to the vagus nerves, which not only regulate
LES function but are critical for preservation of normal gastric
emptying.
often tips the balance in favor of surgery.Antireflux surgery
has not been shown to reverse Barrett’s metaplasia, but it
might arrest progression of the disease. Evidence is accumulating that the risk of progression to cancer may be
reduced. Of course, if severe dysplasia or carcinoma in situ
is present, esophageal resection is necessary.
URGICAL PROCEDURES Some form of simple antire-
S
flux procedure is applicable to the patients just described,
except the few with short esophagus and those with undilatable fixed stricture. The goals of surgery for patients with
hiatal hernia and gastroesophageal reflux disease, also just
described, are summarized in Table 1.7.
Nissen Fundoplication Nissen fundoplication (Figure
1.19), the most common antireflux procedure, can be
A
FIGURE 1.19. Nissen fundoplication is commonly performed to treat gastroesophageal reflux. (A) The
esophagus is mobilized, the hiatal hernia reduced, and the crura approximated. (B) The gastric fundus
is then mobilized and wrapped around the distal esophagus to augment the sphincteric function. The
procedure is most commonly performed laparoscopically. The dotted line represents the bougie that
has been introduced by mouth and passed into the stomach. It serves to prevent the wrap from being
too tight.
C linical D isorders.............................................................................................................................. 21
performed laparoscopically or open by the abdominal or
thoracic route. After esophageal mobilization with careful
identification and preservation of the vagi, the hiatus is dissected and the crura identified. The surgeon then reduces
the hiatal hernia and places, but leaves untied two to four
large sutures to approximate the crura. The surgeon then
mobilizes the gastric fundus by dividing several short
gastric vessels between ligatures taking care not to injure
the spleen. The surgeon next takes the fundus behind the
esophagus to the right side and then wraps it around the
distal 2 to 3cm of the esophagus with sutures that incorporate the anterior fundus, part of the anterior esophageal
wall, and the posterior fundus. Usually,two or three sutures
are needed, placed 1cm apart, with the distal-most suture
at the gastroesophageal junction. Before any sutures are
tied, an assistant passes a 60F bougie from the mouth into
the stomach. The crural sutures are tied first, then the
fundoplication sutures. The wrap should be loose and the
hiatus not too tight.
The identical procedure can be done either open or
laparoscopically. It has been previously thought that the
wrap should be 3 to 5 cm. A current tendency is to limit
the wrap to 1 to 2 cm, especially with laparoscopic fundoplication. Long-term outcome studies are needed to determine the optimal length of the wrap.
Nissen fundoplication can also be performed thoracically in special circumstances in which the abdominal
approach is difficult or unsuitable.
A
B
FIGURE 1.20. The Belsey Mark IV procedure, performed thoraci-
cally, accomplishes a 270° fundic wrap of the distal esophagus,
(A) using “ink-welling” sutures, (B) reduction of the wrap below
the diaphragm, and (C) narrowing of the hiatus. (Adapted from
Jamieson GG, Debas HT, eds. Rob & Smith’s Operative Surgery:
Surgery of the Upper Gastrointestinal Tract. London: Chapman &
C
Hall Medical; 1994.)
22 .......................................................................................................................................... Esophagus
Belsey Mark IV The Belsey Mark IV procedure is done
thoracically (Figure 1.20) and involves a 270° wrap of the
esophagus by the gastric fundus.
Hill Repair An abdominal operation, the Hill repair
(Figure 1.21) accomplishes a 90° anterior wrap of the
esophagus by the stomach and anchors the wrap to the
preaortic fascia.
Toupet Fundoplication Also a partial fundoplication,
Toupet fundoplication is usually performed laparoscopically, involving a 270° posterior wrap of the esophagus.
HOICE OF
C
SURGICAL PROCEDURE
The most popular
operation and the one for which outcome data are most
complete, the Nissen fundoplication, which accomplishes
a 360° wrap of the esophagus, is contraindicated in
patients in whom propulsive motility in the body of the
esophagus is diminished or absent. Such patients may have
an associated motility disorder such as achalasia or
scleroderma. When the “pump action” of the body of the
esophagus is lacking, Nissen fundoplication may result
in obstruction that cannot be overcome by esophageal
peristalsis. Significant postoperative dysphagia ensues.
The major argument for performing preoperative
esophageal manometry is to identify these patients. When
identified, they are best treated by one of the procedures
that accomplish a partial wrap (e.g., Belsey Mark IV, or
Toupet).
A
B
FIGURE 1.21. The Hill repair is performed abdominally and
involves (A) approximation of the crura, (B) a 90° wrap of the
esophagus at the anteromedial cardia, and (C) suturing the wrap
C
to the preaortic fascia.
C linical D isorders.............................................................................................................................. 23
LONG-TERM O
UTCOME OF
SURGICAL THERAPY
In
most reported series, Nissen fundoplication results in
a doubling of the resting LESP from about 10 mm Hg
to more than 20mm Hg. Similarly, symptomatic relief is
accomplished in about 90% of patients. Persistent postoperative dysphagia occurs in 5% to 10% of patients. The
incidence of postoperative dysphagia can be reduced by
performing preoperative manometry and avoiding the
Nissen procedure in patients with abnormal esophageal
motility. The incidence of dysphagia is also reduced when
the length of total wrap is less than 3 cm.
In patients with Barrett’s esophagus, good-to-excellent
symptomatic response is 80% to 90% following surgery,
but postoperative regression of metaplasia is uncommon.
Increasing evidence, however, supports that progression to
dysplasia and malignant degeneration is reduced after surgical correction of reflux. Nevertheless, all patients with
Barrett’s esophagus should undergo annual endoscopic
surveillance.
Sliding Hiatal Hernia with Short Esophagus
Despite arguments to the contrary, the number of patients
who have short esophagus because of GERD is low. In
these patients, the surgical procedure of choice is the
Collis-Nissen procedure (Figure 1.22). Performed thoracically, this operation lengthens the esophagus; a
“neoesophagus” length of stomach is created by stapling
A
B
FIGURE 1.22. (A) In the Collis-Nissen procedure, the esophagus is
lengthened by stapling along a 60F bougie in the esophagus for
a length of 4–5 cm. (B and C) The fundus is then wrapped 360°
around the stapled stomach to form a “neoesophagus.”
(Adapted from Jamieson GG, Debas HT, eds. Rob & Smith’s
C
Operative Surgery: Surgery of the Upper Gastrointestinal Tract.
London: Chapman & Hall Medical; 1994.)
24 .......................................................................................................................................... Esophagus
down (with or without cutting) 4 to 5 cm from the gastroesophageal junction distally, along a 60 F bougie within
the lumen. The gastric fundus is then wrapped 360°
around the “neoesophagus.” Although the number of
patients in individual reports is understandably small, the
operation is reported to have an 80% success rate in relieving symptoms.
PERFORATED ESOPHAGUS
Early recognition and immediate operation are keys to the
successful outcome in patients with esophageal perforation. Primary repair and drainage as well as provision of a
route for early nutrition are important in early perforation. The nonoperative approach has a limited place in
the management of this problem. Esophageal perforations
seen late may be managed in a variety of ways from
drainage alone, to closure with muscle flaps, to esophageal
exclusion. In the few patients with underlying severe
motility disorder or benign stricture, total esophagectomy
with immediate esophagogastrostomy in the neck or
delayed reconstruction may be necessary.
FIGURE 1.23. Esophageal perforation is best diagnosed radiologically. Chest x-ray often demonstrates a left pleural effusion;
mediastinal widening (arrows); or free mediastinal air, which is
manifest as dark vertical streaks overlying the left side of the
heart. (Courtesy of Henry I. Goldberg, MD.)
Clinical Presentation
Esophageal perforation can be caused iatrogenically, traumatically, and/or spontaneously by ingestion of a foreign
body or by tumor (Table 1.8). It is associated with intense
periesophageal inflammatory response and cytokine
release.
The site of perforation determines the evolution of the
clinical picture. For example, cervical perforation is associated with local pain, and the systemic response is slow
to develop. Subcutaneous emphysema may be detectable
clinically and/or radiologically. On the other hand, perforation of the thoracic esophagus is likely to present with
TABLE 1.8. Causes, Incidence, and Sites of Esophageal
Perforation
Iatrogenic (54%)
䊏
Instrumentation (44%)
䊏
Intraoperative (8%)
䊏
Radiation, sclerotherapy, and other therapies (2%)
Traumatic (19%)
䊏
Penetrating
䊏
Blunt
䊏
Ingestion of caustic substance
Spontaneous, also known as Boerhaave syndrome (16%)
Ingestion of foreign body (7%)
Tumor (4%)
Site of perforation
䊏
Thoracic (54%)
䊏
Cervical (40%)
䊏
Abdominal (6%)
more florid symptoms and signs. Chest pain, dysphagia,
and fever develop early, and a most characteristic finding
is tachycardia out of proportion to other systemic signs.
Auscultation of the chest may reveal a crunching precordial sound (Hamman’s sign), pathognomonic of free air
in the mediastinum. The inflammatory response spreads
rapidly from the site of perforation to cause spreading
mediastinitis. Untreated, mediastinitis can lead to septic
shock and associated multiorgan failure. By contrast,
intraabdominal esophageal perforation causes generalized
peritonitis akin to that following perforated peptic ulcer.
Although presentation of esophageal perforation is sometimes obvious, diagnosis often necessitates a high index of
suspicion.
Diagnosis
The diagnosis of perforated esophagus is best confirmed
radiologically. Endoscopy plays only a secondary role
when perforation is suspected but cannot be documented
radiologically.
ADIOLOGICAL TESTING Chest radiography frequently
R
shows a left pleural effusion, mediastinal widening, or free
mediastinal air (Figure 1.23). The presence of perforation
can be established by oral administration of Gastrografin.
If a leak is not detected, the barium swallow test or
endoscopy may be required.When perforation is suspected
but no leak has been demonstrated radiologically, a
follow-up computerized tomography (CT) scan may be
helpful.
C linical D isorders.............................................................................................................................. 25
E
NDOSCOPY
Endoscopic examination is used only
when perforation is suspected and radiologic studies have
failed to demonstrate it. Endoscopy must be performed
carefully to avoid exacerbation of the perforation.
Management
PRINCIPLES OF MANAGEMENT The essential management principles of esophageal perforation are summarized
in Table 1.9. Successful treatment depends on prompt diagnosis and immediate operation. Delays in diagnosis only
increase the mortality. In all cases, broad-spectrum antibiotics should be administered immediately. The site of
perforation can be identified by Gastrografin swallow,
which facilitates selection of the proper incision: either thoracotomy (left or right), cervical incision, or laparotomy.
Early perforations are closed in two layers after excising any
devitalized tissue, and the closure is reinforced with adjacent tissue (i.e., pleural flap, omentum, or stomach). Adequate suction drainage is instituted. A decision must be
made about the route for providing nutrition (i.e., either
parenterally or enterally). Enteral nutrition is best provided
via a feeding jejunostomy. When the jejunostomy is constructed, a gastrostomy tube should also be provided to
obviate the need for nasogastric suction. The gastrostomy
tube should be used for gastric decompression and not for
feeding.
N
ONSURGICAL MANAGEMENT
Most esophageal perforations should be treated operatively; therefore, nonoperative management is only rarely employed. The conditions that must be present to undertake the nonoperative
form of treatment include: (1) a perforation well contained
within the mediastinum; (2) the cavity drains well back
into the esophagus; (3) minimal symptomatology; and, (4)
presence of no or minimal sepsis. Nonoperative treatment
is appropriate only in tears caused by endoscopy or foreign
bodies.
L
AT E
ESOPHAGEAL PERFORATION
There is little controversy about the approach to treatment of early perforation.
Surgical management of late perforations, however, is
complex and subject to considerable variation. Several
options exist, including drainage only, transesophageal
drainage by interventional radiology and irrigation, closure
with muscle flap, and esophageal exclusion. Selecting the
appropriate technique depends on the location of the perforation, the age and condition of the patient, the age of
the perforation, and the degree of mediastinal sepsis and
necrosis.
Drainage Only In patients who present several days
after the perforation has occurred, closure is no longer
an option. An immediate strategy is to perform pleural
drainage through a chest tube, with adequate decompression of the stomach and nasoesophageal suction proximal
to the perforation. This allows the patient to be transferred
to a tertiary care center for further management. An
early strategy for enteral or parenteral nutrition must be
developed.
Transesophageal Drainage by Interventional Radiology
On occasion, the periesophageal abscess may be drained by
a tube placed into the abscess cavity through the mouth
and esophagus. A chest tube may also be placed into the
cavity. With time, an irrigation system can be established.
A gastrostomy tube and a feeding jejunostomy can also be
placed percutaneously.
Closure with Muscle Flap In patients with late perforation and established mediastinitis with or without tissue
necrosis, extensive drainage and closure of the perforation
may be accomplished with vascularized muscle flap. A
rhomboid flap is used to close perforations in the upper
third of the esophagus, while a serratus or latissimus dorsi
flap is used in the mid- or lower third. Perforations in the
distal esophagus may be closed by gastric fundus wrap,
much as is done in the Nissen procedure.
Esophageal Exclusion In patients whose diagnosis was
delayed or who are too sick for thoracotomy, esophageal
exclusion is the treatment of choice. This procedure is also
used for patients in whom a previous attempt at closure has
failed or in whom sepsis is not controlled by drainage. The
esophagus is divided in the neck, the proximal end is exte-
26 .......................................................................................................................................... Esophagus
TABLE 1.9. Essentials: Management of Esophageal Perforation
Diagnosis
䊏
Clinical: Chest pain, fever, tachycardia
䊏
“Hamman’s sign”: Air in mediastinum
Radiologic
䊏
Chest x-ray: (L) Pleural effusion, free mediastinal air,
mediastinal widening
䊏
Gastrografin swallow: Identifies leak
䊏
Endoscopy: Only if suspected but not shown by Gastrografin
or barium swallow
Principles of management
Early perforation
䊏
Prompt diagnosis
䊏
Institution of IV antibiotic therapy
䊏
Early operation to close perforation with reinforcement
(pleura, omentum, stomach) and establish adequate drainage
䊏
Establish enteral or parenteral nutrition
Late perforation
䊏
Individualized treatment
䊏
Options: Simple drainage, transesophageal drainage, closure
with muscle flap, esophageal exclusion
Nonsurgical management (rare)
䊏
Small, contained perforation; drains well into esophagus;
minimal symptoms; no sepsis
Role of esophageal resection
䊏
Perforation in presence of severe, underlying motility
disorder (e.g., achalasia)
䊏
Proximity of perforation to severe benign stricture, or
malignancy
A
FIGURE 1.24. Esophageal exclusion is performed to isolate
the perforated esophagus in selected patients. (A) Cervical
esophagostomy and stapled division of the gastroesophageal junction are performed and a gastrostomy
tube is inserted. (B) The perforation is approximated over a
T-tube and the chest drained. (Adapted from Sabiston DC,
ed. Textbook of Surgery: The Biological Basis of Modern
Surgical Practice. Philadelphia: WB Saunders; 1997.)
B
riorized to create an esophagostomy, and the distal end is
closed (Figure 1.24). A laparotomy or laparoscopy is then
performed, and the gastroesophageal junction is stapled
closed. A gastrostomy and feeding jejunostomy is also provided. Adequate tube drainage of the chest is accomplished.
If the patient survives the procedure, esophageal reconstruction will be necessary many months later. This may
require esophageal resection and esophagogastric reconstruction in the neck or colon interposition.
C linical D isorders.............................................................................................................................. 27
OLE OF RESECTION Certain circumstances dictate
R
that it is best to resect the perforated esophagus. Indications for resection include the presence of a severe underlying motility disorder such as achalasia or scleroderma, or
proximity of the perforation to a severe benign stricture
of the esophagus. Under these conditions, the preferred
management strategy is to perform a total esophagectomy
with either immediate esophagogastrostomy in the neck
or delayed reconstruction.
Early perforation in the distal esophagus due to pneumatic dilatation can be safely managed by surgical closure
and concomitant Heller’s myotomy without resection.
CARCINOMA OF THE ESOPHAGUS
Incidence
The incidence of squamous cell carcinoma in the United
States and Western Europe is about 20 per 100,000.
7
The
incidence is higher among smokers, persons addicted to
alcohol, and black men. The disease occurs with eight
times this frequency in the Henan province of China
and in the Transkei province of South Africa and is 20 to
30 times as high in some districts of Kazakhstan.
7
Nitrosamine compounds, fungal contamination of food,
and deficiencies of zinc and molybdenum have been cited
as possible explanations for the high frequency.
The incidence of adenocarcinoma of the esophagus in
the West has increased steeply in recent years (Figure 1.25).
In some areas, adenocarcinoma approaches or exceeds the
incidence of squamous cell carcinoma. While the steep rise
in the incidence of adenocarcinoma in the West has not
been explained, GERD and its consequences and therapy
may provide partial explanation.
Pathology
Premalignant conditions for squamous cell carcinoma
(Figure 1.26) include achalasia, chronic iron deficiency,
and congenital tylosis of the esophagus. The most
important premalignant condition for adenocarcinoma
is Barrett’s epithelium, which is metaplastic columnar
epithelium that results from chronic gastroesophageal
reflux. About 10% of patients with GERD have Barrett’s
esophagus. Patients with Barrett’s esophagus are 40 times
more at risk to develop adenocarcinoma than those
without Barrett’s.
Preoperative staging of esophageal cancer has been
made possible by endoscopic ultrasound, which can detect
with 80% accuracy the presence of transmural invasion
and periesophageal lymphadenopathy. Ultrasonographic
evidence of wall penetration has been used to develop
the WNM classification, which some prefer to the TNM
classification. Five-year survival is well correlated to the
stage of the disease (Table 1.10).
8
Clinical Presentation
The level at which food seems to stick in the patient’s
esophagus usually indicates the location of the lesion.
Weakness, weight loss, and iron deficiency anemia are frequently present. Late symptoms include regurgitation and
aspiration, which indicate obstruction; chest pain, which
indicates invasion of structures outside the esophagus; and
coughing during swallowing, which might indicate the
presence of a tracheoesophageal fistula.
Diagnosis
ENDOSCOPY AND BIOPSY Flexible endoscopy visualizes
the lesion and facilitates evaluation of its luminal and circumferential extension as well as the degree of obstruction
the lesion causes. The extent of transmural invasion,
however, is poorly evaluated. The presence or absence of
Barrett’s esophagus should be assessed carefully. Multiple
biopsies must be obtained from the lesion and adjacent or
suspicious mucosa.
E
NDOSCOPIC ULTRASOUND Endoscopic ultrasound is
a useful guide to staging the lesion, as discussed earlier. It
assesses the degree of extension of the tumor within the
wall of the esophagus and to adjacent tissue outside. The
presence or absence of lymphadenopathy is also indicated.
B
ARIUM SWALLOW Useful in indicating the extent of
the lesion, the barium swallow test (Figure 1.27) can also
provide the extent of any luminal narrowing and any angulation of the axis of the esophagus.
C
OMPUTERIZED TOMOGRAPHIC SCAN OF CHEST AND
ABDOMEN CT scan of the chest and abdomen can be used
to assess pulmonary metastases, extension of the tumor
into adjacent structures, and presence or absence of any
liver metastases. CT scan cannot accurately diagnose mediastinal and celiac lymphadenopathy.
28 .......................................................................................................................................... Esophagus
FIGURE 1.25. The increasing incidence of adenocarcinoma of the
esophagus as determined by several studies of United States and
European populations. The increase in the West is unexplained,
but may be due to GERD, its consequences and its therapy.
(Reprinted with permission from Pera M, Cameron AJ, Trastek
VF, et al. Gastroenterology 1993;104:510–513.)
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