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........................................................................................................................................................... xiii
Preface
The previous discussion applies to clinical conditions
in which surgical strategies exist to correct the abnormal
physiology. Unfortunately, in many surgical diseases, extirpation of the diseased organ is possible while correction
of the pathophysiology is not. But, even here, the physio-
logic approach to surgical therapy has relevance. It enables
the reader to better understand not only the cause of clinical symptoms and signs but also the physiologic insult
that invariably results when organs or portions of them are
removed. I have also attempted, therefore, to discuss the
altered pathophysiology imposed by certain surgical procedures and the adaptive physiologic processes that are
brought into play postoperatively.
I have not intended that this book provide the comprehensive information that multiauthored texts can
provide. Rather, I attempt to offer a clinical and therapeutic approach to surgical diseases of the gastrointestinal
tract based on how diseases and surgical procedures alter
normal physiology. In this way, again, I hope that understanding will replace rote memorization of details. While
the book should primarily serve the needs of medical students and surgical residents and fellows, I hope that surgeons in practice and academic environments will also
find it useful.
Haile T. D ebas, MD, FRCS (C), FACS
San Francisco, California
Many excellent textbooks of surgery exist. Most of these
are large, multiauthored, and have the distinct advantage
of drawing on the experience of many surgeons with
expertise in specific areas. The advantage, however, is often
obtained at the expense of a unified approach and style
that a book written by a single author can provide.
In writing this book about gastrointestinal surgery,
I use an integrated approach to discuss fundamental
anatomy and physiology; then examine how normal function is altered by disease, i.e., pathophysiology; and finally,
provide the clinical correlates. Based on these three pillars
of understanding particular disease processes, I then
discuss surgical treatment as a means of correcting the
abnormal physiology to restore health. I hope this
approach will provide the reader a coordinated understanding that minimizes the need for rote memorization.
I believe that, when the student understands normal
physiology, how disease disturbs that physiology, and how
surgical treatment might restore normalcy, one need not
remember too many extraneous facts. Instead, a foundation of understanding is established that stays with the
student even after the details are forgotten. The Jesuits
have an attractive definition of culture as “that which
remains after you have forgotten all you have learnt.”
While I hope that the readers of this book will not totally
forget all the facts they have learnt, the concept of a culture
of understanding is, nevertheless, valid.
........................................................................................................................................................... xv
I wish to express my deepest gratitude and appreciation to
Ms. Patricia Meagher, without whose commitment to the
project, hard work, perseverance, organization, and sense
of editorial perfection, this book would not have been possible. To her, the book has been a labor of love. I just hope
that the final product is worthy of her Herculean effort to
see this ambitious book to the finish.
Ms. Christine Gralapp provided the illustrations. Her
beautifully simple drawings have enlivened the pages of
the book and will, undoubtedly, simplify the reader’s task
in understanding concepts of pathophysiology and treatment of surgical diseases.
Dr. Henry I. Goldberg, Clinical Professor of Radiology
at the University of California, San Francisco (UCSF),provided the radiological images for the book. I am most
appreciative of his indispensable contribution to the book
and grateful for the privilege of tapping into his enormous
experience and expertise in gastrointestinal radiology.I am
also grateful to Dr.Vincent McCormick, Clinical Professor
of Radiology at UCSF,for providing the radiological images
for abdominal trauma.
Dr. Linda Ferrell, Professor of Pathology at UCSF, con-
tributed most of the figures depicting gross and microscopic surgical pathology. Dr. Ferrell’s vast case collection
and enormous experience and expertise in gastrointestinal
pathology adds an important dimension to the book. I am
very indebted to her.
I am also grateful to three other colleagues at UCSF:
Dr. James Ostroff, Professor of Medicine, and Dr. John
Cello, Professor of Medicine and Surgery, who contributed
the endoscopic images; and Dr. Theodore Schrock, Professor of Surgery, who contributed several photographs of
surgical specimens.
Finally, I wish to thank Ms. Daisy Leo, my Senior
Executive Assistant, who somehow juggled my busy schedule to enable me to spend the time necessary to write the
book.
Finally, I would like to acknowledge the contributions
of generations of surgical residents with whom I have had
the privilege to associate and from whom I have learnt so
much in an enjoyable 30-year career in academic surgery.
Haile T. D ebas, MD, FRCS (C), FACS
San Francisco, California
Acknowledgments
The esophagus is a simple muscular tube closed at each
end with a sphincter. It begins where the pharynx ends at
the level of the C-6 vertebra and ends at the cardia of
the stomach, some 3 to 5cm below the diaphragm, after
passing through the diaphragmatic hiatus. The esophagus
is approximately 40cm in length and, for the sake of convenience and clarity in discussion, it is distinguished
by three sections: cervical, thoracic, and abdominal.
Anatomic relationships of the esophagus are detailed in
Figure 1.1 and Table 1.1.
The major function of the esophagus is to transport
food from the pharynx into the stomach in a coordinated
fashion. Although its mucosal lining secretes mucus, secretion is not considered an important part of esophageal
function.
UPPER ESOPHAGEAL SPHINCTER
Located at the upper end of the esophagus, the upper
esophageal sphincter (UES) is composed of striated
muscle condensation covering 2 to 3 cm, reinforced by the
transverse fibers of the cricopharyngeus muscle (Figure
1.2). The UES remains closed except during swallowing,
when it relaxes in response to pharyngeal contraction. In
the resting state, the UES maintains a pressure of approximately 40mm Hg. This pressure is essential to prevent
aspiration of esophageal contents during gastroesophageal
reflux or when swallowed food empties poorly. Failure of
the UES to relax in response to swallowing may result in
upper esophageal dysphagia and aspiration.
BODY OF THE ESOPHAGUS
The muscular coat of the upper third of the body of the
esophagus (i.e., the cervical esophagus) is composed of
striated muscle, while that of the lower two thirds is
smooth muscle. The smooth-muscle coat consists of an
........................................................................................................................................................... 1
1
Esophagus
ANATOMY AND PHYSIOLOGY
inner circular and an outer longitudinal layer. The esophagus has no serosal layer.
The mean resting pressure in the body of the esopha-
gus varies from -8 to +5mm Hg, depending on the
respiratory cycle. In response to swallowing, however, a
coordinated peristalsis sweeps from the upper to the lower
end of the esophagus. The mean amplitude of contractions
during esophageal peristalsis is 60 ± 5mmHg.When the
lumen of the esophagus is acidified, strong peristaltic
waves are initiated that serve to rid the esophagus of acid.
This “esophageal pump” mechanism is important in the
overall health of the gastrointestinal system.
LOWER ESOPHAGEAL SPHINCTER
The lower esophageal sphincter (LES) is located at the terminal end of the esophagus and represents the distal 3 to
5 cm of the organ (see Figure 1.2). Most of the LES lies
within the abdominal cavity, but a short segment often
extends above the diaphragm. A small condensation of circular smooth-muscle fibers resides in this region, too
indefinite to constitute an anatomical sphincter. The specialized nature and unique innervation of the smooth
muscle of the terminal esophagus provide the basis for a
physiological sphincter. These specialized smoothmuscled fibers contain receptors for a number of peptide
(e.g., vasoactive intestinal peptide, substance P) and nonpeptide neurotransmitters that are released locally from
peptidergic and nonpeptidergic neurons.
The LES is a high-pressure zone interposed between
the body of the esophagus and the cardia of the stomach
(Figure 1.3). Normally, a mean pressure of 20 ± 5mmHg
is maintained at all times except during swallowing,
when the pressure falls to 0mm Hg, allowing esophageal
peristalsis to empty the swallowed food into the stomach.
In its resting state, therefore, the high pressure of the
LES prevents reflux of gastric contents into the
esophagus.
TABLE 1.1. Essentials: Esophageal Anatomy
Muscular tube, 40-cm long
䊏
Closed at proximal end by UES
䊏
Closed at distal end by LES
䊏
Inner circular muscle coat
䊏
Outer longitudinal muscle coat
䊏
Striated muscle at upper one third
䊏
Smooth muscle at distal two thirds
No serosa
Nerve supply
䊏
Vagus nerve
Blood supply
䊏
Cervical: Inferior thyroid
䊏
Thoracic: Aortic branches
䊏
Abdominal: Left gastric, inferior phrenic
Abbreviations: LES, lower esophageal sphincter; UES, upper esophageal
sphincter.
coordinated contraction of the body of the esophagus and
carrying the food past the LES—which remains in a state
of relaxation—and into the stomach. The LES then contracts in sequence with esophageal peristalsis. By the time
the bolus reaches it, the stomach is in a state of receptive
relaxation brought about by esophagogastric vagal reflexes
and activated by increases in luminal pressure due
to esophageal contraction. This process of stomach
relaxation is mediated by release of VIP and NO from
nerve terminals within the fundus and body of the
stomach. This normal swallowing mechanism is depicted
in Figure 1.4.
FIGURE 1.1. The cervical, thoracic, and abdominal esophagus, its
blood supply and anatomic relationships.
The LES contracts and increases its pressure in
response to sudden increases in abdominal pressure and
to alkalinization of the gastric lumen. As mentioned above,
the LES relaxes in response to swallowing, a function
mediated by local release from neurons in the LES musculature of vasoactive intestinal peptide (VIP) and nitric
oxide (NO). Other factors contributing to the lowering of
LES pressure are nicotine, gastric acidification, ingestion
of fats, and release of cholecystokinin (CCK). Essential
features of LES anatomy are summarized in Table 1.2.
SWALLOWING MECHANISM
When food or fluid enter the pharynx, pharyngeal contractions are initiated. At the very beginning of swallowing, both the UES and LES relax. Pharyngeal contractions
deliver the food into the upper esophagus, initiating a
ESOPHAGEAL MUCOSA
The innermost lining of the esophagus is composed of
nonkeratinized squamous cell epithelium, except for the
distal 3 to 5cm, where the lining progresses from squamous epithelium to columnar mucosa, similar to that in
the upper cardia of the stomach.
BLOOD AND NERVE SUPPLY
AND LYMPHATICS
The cervical esophagus receives its blood supply from the
inferior thyroid arteries; the thoracic esophagus from the
bronchial arteries, from direct branches of the thoracic
aorta, and from the intercostal arteries; and the abdominal esophagus from ascending branches of the left
gastric artery and the inferior phrenic arteries (see
Figure 1.1). Venous drainage accumulates in the
periesophageal venous plexus, which empties into the inferior thyroid veins in the neck, into bronchial azygous and
hemiazygous veins in the thorax, and into the coronary
vein in the abdomen. The coronary vein drains into the
portal vein, and hence, in portal hypertension, the venous
plexus at the distal esophagus dilates to form esophageal
varices.
2 ......................................................................................................................................... Esophagus
FIGURE 1.2. The upper esophageal sphincter (UES) and lower esophageal sphincter (LES) govern the
swallowing mechanism to prevent aspiration and reflux of food. The UES is at the level of the cricoid,
of which the cricopharyngeus muscle is an important component. The LES straddles the diaphragmatic
hiatus and is more a physiological than an anatomical sphincter. The squamo-columnar junction
between esophageal and gastric mucosa lies within the LES. (Adapted from Rothberg M, DeMeester
TR. Surgical anatomy of the esophagus. In: Shields TW, editor. General Thoracic Surgery, 3rd ed.
Philadephia: Lea & Febiger; 1989:78; and Feldman M, Sleisenger MH, Scharschmidt BF, eds. Sleisenger
& Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, Management. Philadelphia: WB Saunders; 1998.)
The nerve supply of the esophagus (Figure 1.5) derives
from the vagus and the cervical sympathetic trunk. The
vagus provides the essential innervation of the body
and sphincters of the esophagus. The cervical esophagus
is innervated by branches of the recurrent laryngeal
nerves, while the thoracic and abdominal portions are
innervated directly from the vagal neural plexus surrounding the organ. At the hiatus, considerable variation
exists from individual to individual. In about 60% of
human subjects, the anterior vagus is a single strand
at the hiatus, while the posterior vagus is single in more
A natomy and P hysiology ..................................................................................................................... 3
than 90% (Figure 1.6). Sensory innervation is provided
by C-fibers that contain substance P and calcitonin generelated peptide (CGRP), two neuropeptides that mediate
sensation.
Lymphatic drainage of the cervical esophagus goes to
deep cervical and paratracheal nodes (Figure 1.7). The
thoracic esophagus drains into the pulmonary hilar and
subcarinal nodes. The lower thoracic esophagus drains
into inferior paraesophageal and parahiatal nodes, while
the abdominal esophagus drains primarily into nodes
along the left gastric artery.
FIGURE 1.3. The lower esophageal sphincter (LES) can be identified by measuring the resting pressure
of the distal esophagus at various points. It is 3.0–5.0 cm in length, with a mean resting pressure of
20 ± 5 mm Hg. When the sensing device is below the diaphragm, inspiration causes a positive pressure
inflection. The opposite is true above the diaphragm. The pressure inversion point (PIP) indicates the
level of the diaphragm.
TABLE 1.2. Essentials: Lower Esophageal Sphincter (LES)
Length: 3–5 cm
Mean resting pressure (LESP): 20 ± 5mmHg
Factors that increase LES pressure
䊏
Increased abdominal pressure
䊏
Alkalinization of stomach
䊏
Hypergastrinemia
Neurotransmitters
䊏
Relaxation: Vasoactive intestinal peptide, nitric oxide
䊏
Contraction: Acetylcholine
Factors that lower LES pressure
䊏
Gastric acidification
䊏
Ingestion of fat
䊏
Cholecystokinin
䊏
Nicotine
FIGURE 1.4. Normal swallowing mechanism: At the initiation of
䉴
swallowing, the pharynx contracts and the upper esophageal
sphincter (UES) relaxes. At the same time, the lower esophageal
sphincter (LES) relaxes and stays relaxed until the peristaltic
wave of contraction sweeps down the esophagus and arrives at
the LES. The LES then contracts in sequence with the peristalsis,
by which time the swallowed bolus has entered the stomach.
4 .......................................................................................................................................... Esophagus
A
B
FIGURE 1.5. Nerve supply of the esophagus: The nerve supply, shown (A) anteriorly and (B) posteriorly,
derives from the vagus and the cervical sympathetic trunk.
PATHOPHYSIOLOGY
Normal function of the esophagus and its sphincters is
impaired in a number of clinical conditions. Motility
impairments are summarized in Table 1.3.
may drool saliva or suffer from intermittent aspiration.
Failure of UES relaxation is considered a primary defect
in the etiology of pharyngoesophageal, or Zenker’s,
diverticulum.
ABNORMALITIES OF THE UPPER
ESOPHAGEAL SPHINCTER
Increased UES and/or Failure of Relaxation
Sometimes seen in elderly patients who have sustained a
cerebrovascular accident, failure of normal relaxation of
the UES causes an inability to swallow. These patients
P athophysiology ................................................................................................................................. 5
Hypotensive UES
Occasionally seen in patients with severe gastroesophageal
reflux, hypotensive UES causes a susceptibility to pulmonary aspiration. Whether hypotensive UES occurs as an
isolated phenomenon unrelated to gastroesophageal reflux
is unknown.
FIGURE 1.6. Configurations of the anterior and posterior vagus at the level of the diaphragm can vary
from individual to individual and may be important in performing surgical procedures.
ABNORMALITIES OF THE BODY OF
THE ESOPHAGUS
Diffuse Esophageal Spasm
In diffuse esophageal spasm (DES), coordinated
esophageal peristalsis is lost. Instead, a large segment of the
esophagus contracts at once, generating very high luminal
pressures. The distal half of the esophagus is often affected.
The patient experiences squeezing retrosternal pain
accompanied by difficulty in swallowing. In DES, both
upper and lower sphincters function normally and relax
appropriately in response to swallowing. The motility
abnormalities of DES are depicted in Figure 1.8. A significant association exists between DES and epiphrenic diverticulum, suggesting that high intraluminal pressures may
contribute to the development of this pulsion-type
diverticulum.
Achalasia
In classic achalasia, esophageal peristalsis is lost (Figure
1.9). Instead, in response to swallowing, the body of the
esophagus exhibits feeble, uncoordinated contractions. In
advanced cases, the esophagus may show little, if any, contractile function. Because failure of the LES to relax is a
dominant feature of achalasia, the condition is described
again later under Abnormalities of the Lower Esophageal
Sphincter.
Scleroderma
When scleroderma affects the esophagus, it spares the
sphincters. The abnormality is in the body of the esophagus, where peristalsis is lost and contractions in
response to swallowing are uncoordinated. While DES
causes high-amplitude contractions, in scleroderma the
contractions are often feeble. The condition is distinguishable from achalasia because LES function is normal,
both in its pressure profile and in its normal relaxation
response to swallowing. The patient might also exhibit
other manifestations of scleroderma, such as Raynaud’s
phenomenon.
When esophageal scleroderma coexists with abnormal
gastroesophageal reflux, severe esophagitis and esophageal
shortening are apt to occur due to loss of the protective
“esophageal pump,” favoring stasis of acid refluxate in the
distal esophagus.
6 .......................................................................................................................................... Esophagus
TABLE 1.3. Essentials: Motility Disorders of the Esophagus
Upper esophageal sphincter
䊏
Failure of UES relaxation (e.g., stroke)
䊏
Zenker’s diverticulum
Body of the esophagus
䊏
Diffuse esophageal spasm
High-amplitude aperistaltic contractions
Loss of peristalsis
Normal LES
䊏
Scleroderma
Loss of peristalsis
Low-amplitude contractions
Normal LES
Lower esophageal sphincter
䊏
Achalasia
Failure of LES relaxation
Increased LESP (not always)
Feeble aperistaltic contractions of esophageal body
䊏
Hypertensive LES
High resting body pressure
Normal LES relaxation
䊏
Hypotensive LES
LESP < 15 mm Hg
Normal LES relaxation
Abbreviations: LES, lower esophageal sphincter; LESP, lower esophageal
sphincter pressure; UES, upper esophageal sphincter.
FIGURE 1.7. Lymphatic drainage of the esophagus: The three
major groups of nodes that drain the esophagus are the tracheobronchial, posterior mediastinal, and celiac axis nodes.
Other Conditions
Loss of normal esophageal peristalsis that cannot be categorized under any diagnosis may be seen. Patients with
severe gastroesophageal reflux disease sometimes demonstrate abnormal motility in the body of the esophagus.
This abnormality typically reverses when reflux is corrected and the esophagitis disappears.
ABNORMALITIES OF THE LOWER
ESOPHAGEAL SPHINCTER
with reflux esophagitis have LES pressures far lower than
15 mm Hg.
Chronic Gastroesophageal Reflux
Chronic reflux of acid peptic contents of the stomach into
the lower esophagus may manifest in different ways: heartburn, chest pain, esophagitis, Barrett’s esophagus, and
Barrett’s ulcer.
Heartburn
Heartburn is the classic substernal burning pain of reflux
described earlier.
Chest Pain
The chest pain characteristic of gastroesophageal reflux is
substernal or left chest pain that might mimic myocardial
infarction. This symptom can occur even in the absence of
gross esophagitis. Once cardiac causes are eliminated, the
esophagus as the source of the pain must be investigated,
either by the Bernstein test or, better still, through 24-hpH
monitoring of the esophagus in the ambulatory setting.
This procedure is described below.
Hypotensive LES
Hypotensive LES is often seen in patients with sliding
hiatal hernia and reflux esophagitis. Typically, patients
P athophysiology ................................................................................................................................. 7
Esophagitis
Chronic reflux of acid induces inflammatory injury of the
esophageal mucosa, particularly if the esophageal pump
A
FIGURE 1.8. In diffuse esophageal spasm (DES), a large segment of the esophagus contracts at once,
generating high luminal pressure and resulting in a corkscrew-shaped esophagus. (A) The distal half of
the esophagus is often affected by multiple indentations, indicating local contractions, as demonstrated in the x-ray. (B) As shown in motility studies, the lower esophageal sphincter (LES) is usually
normal and relaxes normally. Contractions are uncoordinated and esophageal peristalsis is lost.
(Courtesy of Henry I. Goldberg, MD.)
B
mechanism is defective. The result is development of a
Barrett’s Esophagus
low-grade esophagitis, seen histologically as expansion of
the basal zone to more than 15% of the epithelium and
lengthening of the papillae toward the surface (Figure
1.10). Vascular lakes and balloon cells may be present, but
polymorphonuclear (PMN) and eosinophilic cell infiltration is absent. When destruction of the epithelium is
severe, high-grade esophagitis may be present and is often
associated with ulcerated lesions and PMN infiltration
(Figure 1.11). Ulcerative esophagitis can cause upper
gastrointestinal bleeding. The continuous process of inflammation, ulceration, and repair eventually causes
stricture of the distal esophagus and may lead to
esophageal shortening.
The metaplasia from squamous to columnar epithelium
represents the development of Barrett’s esophagus. Typically, Barrett’s mucosa appears as a circumferential sheet
or discontinuous islands of pinkish mucosa. The epithelium resembles intestinal mucosa. The clinical concern
with Barrett’s esophagus is its propensity to progress to
dysplasia and then form adenocarcinoma (Figure 1.12).
The incidence of adenocarcinoma is estimated to be one
case per 441 patient years. However, in patients who show
aneuploidy on flow cytometry, the 5-year cumulative incidence of cancer is 43%, compared to 5% in those with no
aneuploidy.
1
8 .......................................................................................................................................... Esophagus
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