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Chapter 14 Esophagus

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HISTORY
The anatomic and surgical history of the esophagus is shown in Table 14-1.
Table 14-1. Anatomic and Surgical History of the Esophagus
Smith Surgical Papyrus
(3000-2500 B.C.)

Description of a "gaping wound in the throat penetrating the gullet"

Chinese (ca. 1000 B.C.)

Description of dysphagia secondary to esophageal cancer

Aristotle (384-322 B.C.)

Theorized that the esophagus got its name from "its length and narrowness"

Galen (130-200 A.D.)

Mentioned growth as cause of esophageal obstruction

Lanfranc (d. 1315)

Placed a silver tube in the windpipe of a patient with false passage between the esophagus and trachea to assist
breathing

Vesalius

1543 Used endotracheal tube to maintain ventilation in animals

Durston

1670 May have seen a case of esophageal atresia

Willis

1679 First description of achalasia; treatment by dilatation

Gibson

1696 Described a "monstrous birth" with tracheoesophageal fistula

Monroe (1670-1740)

Repaired the trachea and esophagus of a patient with severed trachea and punctured esophagus

Goursald & Roland

1750 Mentioned esophagotomy and removal of foreign bodies

Ludlow

1769 Described pharyngoesophageal diverticulum

Tarenget

1786 Mentioned stricture of the cervical esophagus

Bell

1816 Performed external drainage of the diverticulum

Campbell

1848 Tried to convince a professional sword swallower to participate in experimental endoscopy; the latter replied, "I know I can
swallow a sword, but I'll be damned if I can swallow a trumpet"

Cheever

1867 Performed successful esophagotomies

Bevan

1868 Described an esophagoscope which used light reflected from a mirror. Used device for foreign body extraction and
examination of strictures and tumors.

Kussmaul

1868 Designed an esophagoscope illuminated by a gas lamp

Trendelenburg

1871 Performed tracheostomy and inserted an endotracheal tube with an inflatable tampon while administering anesthesia

Billroth

1871 Studied stricture of the esophagus

Lamb

1873 Published first report of an esophageal fistula without atresia

Zenker

1877 Discussed etiology, pathology, and symptomatology of the pharyngoesophageal diverticulum (Zenker's diverticulum)

Czerny

1877 Performed esophageal resection and sutured the lower end of the esophagus into the neck. The patient survived.

Nicoladoni

1877 Performed first operation on a pharyngeal diverticulum

Niehans

?

Macewen

1880 Inserted endotracheal tubes by mouth without performing laryngotomy or tracheostomy

Mikulicz-Radecki

1881 Developed esophagoscope and gastroscope

Gross

1884 Treated stricture of the esophagus

O'Dwyer

1885 Developed endotracheal intubation for diphtheria, etc.

Mikulicz-Radecki

1886 Treated carcinoma of the esophagus by resection and plastic reconstruction

Wheeler

1886 Performed first known successful resection of Zenker's diverticulum

Fell

1887 Used a foot bellows attached to a tracheostomy cannula for artificial ventilation

Nassilov

1888 Suggested, but did not employ, an extrapleural route through the posterior mediastinum to the esophagus

Biondi

1895 Proposed resection by pulling the stomach upward into the chest, followed by esophageal anastomosis

Milton

1897 Recommended midline sternotomy for anterior approach to the mediastinum

von Hacker

1899 Diagnosed esophageal carcinoma by esophagoscopy and biopsy

Gottstein

1901 Suggested esophagomyotomy for treatment of cardiospasm

Gosset

1903 Described transdiaphragmatic esophagogastrostomy through thoracotomy

Sauerbruch

1904 Developed and used a negative-pressure system chamber

Roux

1907 Performed a successful esophagojejunostomy

Voelcker

1908 Performed the first successful resection of the lower thoracic esophagus by transabdominal esophagogastrectomy

Schmid

1912 Performed diverticulopexy on cadavers

Excised an esophageal diverticulum; patient died of hemorrhage secondary to fistula

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Schmid

1912 Performed diverticulopexy on cadavers

Torek

1913 Successfully removed the esophagus for cancer. The patient was left with cervical esophagostomy and gastrostomy.

Heller

1913 Performed esophagomyotomy for dysphagia

Von Ach

1913 Used blunt dissection from neck and abdomen for esophagectomy

Denk

1913 Used blunt dissection for esophageal removal, with later restoration of esophageal continuity. The operation was not
successful.

Zaaijer

1913 Performed first successful transthoracic resection for carcinoma of the cardia

Mosher

1917 Using an endoscope, incised the septum between the esophagus and a Zenker's diverticulum

Hill

1918 Performed first diverticulopexy on a living patient

König

1922 Fixed a diverticular sac to the hyoid bone

Torek

1927 Described pharyngeal superpressure for surgery

Gray Turner

1931 Explored the distal esophagus from the abdomen

Ohsawa

1933 Performed first intrathoracic gastroesophageal anastomosis to restore gut continuity

Adams & Phemister

1938 Reported successful esophageal resections with esophagogastric anastomosis

Leven & Ladd

1939 Independently performed successful multiple-stage surgery to treat esophageal fistulas and atresia

Haight & Towsley

1941 Performed a single-stage anastomosis of the esophagus within the mediastinum

Churchill & Sweet

1942 Performed esophagectomy with end-to-side anastomosis

Garlock

1943 Developed technique for esophageal surgery

Kaplan

1951 Reported the first use of elective cricopharyngeal myotomy

Sweet

1954 Developed surgical technique for resection

Skandalakis et al.

1962 Collective review of cases of smooth muscle tumors of the esophagus as reported in the world literature

Belsey

1966 Developed surgery for achalasia

Ellis et al.

1969 Studied physiology of achalasia and Zenker's diverticulum

Gavriliu

1975 Revived use of the gastric tube for esophageal replacement

Orringer

1978 Recommended esophagectomy without thoracotomy

Liebermann-Meffert

1996 Studied surgery, anatomy, and embryology of the esophagus

History table compiled by David A. McClusky III and John E. Skandalakis.
References
Elmslie RG. Perspectives in the development of oesophageal surgery. In: Jamieson GG (ed). Surgery of the Oesophagus. New York: Churchill Livingstone, 1988,
pp. 3-8.
Haeger K. The Illustrated History of Surgery. London: Harold Starke, 1988.
Kittle CF. The history of esophageal surgery. In: Wastell C, Nyhus LM, Donahue PE (eds). Surgery of the Esophagus, Stomach, and Small Intestine (5th ed).
Boston: Little, Brown, 1995, pp. 4-29.
Naef AP. The Story of Thoracic Surgery. Lewiston NY: Hans Huber, 1990.
Skandalakis JE, Gray SW, Shepard D, Bourne GH. Smooth Muscle Tumors of the Alimentary Canal: Leiomyomas and Leiomyosarcomas, a Review of 2525 Cases.
Springfield, IL: Charles C. Thomas, 1962.
Skandalakis JE, Gray SW. Embryology for Surgeons (2nd ed). Baltimore: Williams & Wilkins, 1994.
Warren R. Surgery. Philadelphia: WB Saunders, 1963.

EMBRYOGENESIS

Normal Development
In the human, the primitive foregut forms during the fourth week of gestation by a longitudinal folding and incorporation of the dorsal part of the yolk
sac into the embryo.2,3,4 The trachea develops from the foregut about 22-23 days after fertilization as a median ventral diverticulum4 (Fig. 14-1).
Immediately after this diverticulum forms, the stomach develops further distally by an asymmetrical extension3-6 (Fig. 14-2).
Fig. 14-1.

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Division of the primitive foregut, with stippled area showing the future esophageal portion. Arrows indicate the local morphogenetic movements. Inset:
Transverse section through primitive foregut. Left, Trachea (ventral); Right, Esophagus (dorsal). (Modified from Skandalakis JE, Gray SW. Embryology for
Surgeons (2nd ed). Baltimore: Williams & Wilkins, 1994; with permission.)

Fig. 14-2.

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The embryonic gut, showing the primitive esophagus and the changes in the position of the stomach. A, Presumptive stomach area of the undifferentiated
foregut at 2.5 mm (fourth week). B, At 4.2 mm (fifth week). C, Shape of the stomach at 6.3 mm (6th week). D, At 10 mm (end of sixth week). E, Shape and
descent of stomach essentially completed at 17.5 mm (end of second month). C7, Seventh cervical segment; T1, First thoracic segment; T12, Twelfth thoracic
segment; L1, First lumbar segment. (Modified from Skandalakis JE, Gray SW. Embryology for Surgeons (2nd ed). Baltimore: Williams & Wilkins, 1994) Adapted
from Blechschmidt E. The stages of human development before birth. Philadelphia: WB Saunders, 1961; with permission.)

Foregut
Several phenomena take place at approximately the 34th day. The genesis of the submucosal and muscular layers of both trachea and esophagus
begins. The distal esophagus elongates first, followed by the proximal. Characteristically, the elongated esophageal segment carries the gastric-dilated
primordium below the forming diaphragm. Most likely, however, elongation results from pharyngeal ascent rather than gastric descent (Fig. 14-2).
Separate growth processes of the trachea and esophagus occur before the fifth week of intrauterine life. The esophagus attains its final dimensions in
the seventh week. At birth its length is 8-10 cm, which doubles in the first few years of life.
Early in the sixth week, the mesenchymal circular muscle coat develops. Three to nine weeks later, longitudinal musculature appears.4 During the 4th
month, the muscularis mucosa appears. Blood vessels enter the esophageal wall during the seventh month, and lymph capillaries enter the wall
between the third and fourth months of life after birth.7
At the seventh to eighth week the esophageal lumen (Fig. 14-3) is almost filled with cells from the proliferated esophageal epithelium. Because the
filling is never complete and small vacuoles are present, the so-called solid stage does not exist as such. Around the 10th week the lumen is restored
since the vacuoles coalesce.
Fig. 14-3.

Changes in the shape of the esophageal lumen. A, At 19 mm (eighth week). B, At 37 mm (ninth week). C, At 42 mm (late ninth week). D, At 120 mm (about
the fifteenth week). (Adapted from Lewis FT. The development of the digestive tract and of the organs of respiration: the development of the oesophagus. In:
Keibel F, Mall FP. Human Embryology, Vol II. Philadelphia: JB Lippincott, 1912; with permission.)

Changes are also taking place in the esophageal ciliated epithelium, which becomes stratified squamous in the proximal and middle esophagus. Columnar
epithelium remains unchanged in the distal esophagus.

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The esophageal wall receives both sympathetic (thoracic trunk and celiac plexus) and parasympathetic (vagus nerve) innervation.

Remember
Both endoderm and mesoderm participate in the formation of the esophageal wall. The endoderm produces the esophageal epithelium and glands, and the
mesoderm produces the connective tissue, muscular coat, and angioblasts.

Branchial Arch Formation and the Esophagus
The embryonic mesodermal branchial arches play a role by participating in the arrangement of vessels and nerves. Some of the embryonic mesodermal
branchial arches have a direct relation with the esophagus by their production of vessels and their association to specific nerves.
The third branchial arch is associated with the glossopharyngeal (IX) nerve. It participates in a very small way in the possible formation of pharyngeal
muscles and the pharyngeal lining. The third aortic arch lies within the third branchial arch. The external carotid artery arises de novo from the third
aortic arch. The common carotid and the proximal internal carotid arteries are derived from the third aortic arch. The superior thyroid artery perhaps
participates in the blood supply around the pharyngoesophageal junction.
The fourth branchial arch is associated with the vagus (X) nerve. The right fourth aortic arch contributes to the formation of the proximal portion of
the right subclavian artery. The left subclavian artery may be derived from the sixth intersegmental artery. The thyrocervical trunk arises from the
subclavian arteries. The inferior thyroid artery springs directly from the subclavian artery in 15% of individuals,8 and from the thyrocervical trunk in
85%. The inferior thyroid artery is responsible for the blood supply of the upper esophagus. The arch of the aorta and the right dorsal aorta are also
products of the fourth arch. Minute vessels from the aorta may participate in the blood supply of the esophagus.
The sixth aortic arch, the so-called pulmonary arch, most likely does not participate in the blood supply of the esophagus.

Congenital Anomalies and Surgical Repair
Abnormal growth processes of the trachea and esophagus produce a great number of anomalies. Problems in the gastroesophageal junction produce
other less dramatic effects (Fig. 14-4A & B).
Fig. 14-4.

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A, Pulsion diverticula are located most commonly in the distal esophagus. Heterotopic gastric mucosa most commonly is located at the proximal esophagus. B,
Usual locations of malformations of the esophagus. (Modified from Skandalakis JE, Gray SW. Embryology for Surgeons (2nd ed). Baltimore: Williams & Wilkins,
1994; with permission.)

It is not within the scope of this chapter to present a detailed discussion of embryology and embryologic anomalies of the esophagus. Kluth9 was able
to classify 10 types of tracheoesophageal defects and 88 subtypes of this anomaly alone. The interested student of embryogenesis is encouraged to
read Embryology for Surgeons.10 The main types of congenital esophageal anomalies are presented in Table 14-2.
Table 14-2. Anomalies of the Esophagus
Anomaly

Prenatal Age
at Onset

First
Sex Chiefly
Appearance Affected

Relative Frequency

Comments

Esophageal atresia, stenosis, and
tracheoesophageal fistula

21 to 34 days

At birth

Equal

Common



Laryngotracheoesophageal cleft

3rd to 5th
week

At birth

Equal

Rare

Type I to IV (larynx to bronchi)

VACTERL associations

Variable; 3 to 5 At birth
wk

Equal

10 to 23% of
esophageal atresia a



Esophageal webs and rings

7th wk(?) (if
congenital)

Any age

Male

Rare

May never produce symptoms

True duplication

7th wk

Any age

?

Very rare

May never produce symptoms

Enterogenous cysts

End of 3rd wk

Brith to any Female(?)
age

Rare

Diverticula (excluding traction diverticula) 5th mo to
birth(?)

Any age

Male

Uncommon

Muscular weakness may exist indefinitely
without herniation occurring

Heterotopic mucosa

5th mo to birth

Any age (if
at all)

Equal(?)

Common

May never produce symptoms

Congenital short esophagus

7th wk

Birth to any Male
age

Rare

May never produce symptoms

Achalasia

Late 6th wk(?)

Infancy

Uncommon

Cases appearing in later life are not of
embryonic origin

Chalasia

Late 6th wk(?)

Shortly after Equal
birth

Very common

Resolves spontaneously in most cases as LES
matures

a

Equal

From Chittmittrapap S, Spitz L, Kiely EM, Brereton RJ. Oesophageal atresia and associated anomalies. Arch Dis Child 1989;64:364-368.

VACTERL, vertebral (abnormalities), anal (atresia), cardiac (abnormalities), tracheoesophageal (fistula) and/or esophageal (atresia), renal (agenesis and
dysplasia) limb (defects); LES, lower esophageal sphincter.
Source: Modified from Skandalakis JE, Gray SW (Eds). Embryology for Surgeons, 2nd Ed. Baltimore: Williams & Wilkins, 1994; with permission.

Jobe et al.11 reported that Collis' gastroplasty permits a tension-free fundoplication for the treatment of shortened esophagus, but maintenance of
acid-suppression therapy is advised. As to surgical repair, Holder12 and Holder and Ashcraft 13 advise that ligation of the fistular and primary
anastomosis, if possible, should be done very early, preferably within 24 hours after birth, to avoid pneumonitis. Filson et al.14 reported on delayed
primary esophageal anastomosis. Healey et al.15 stated that delayed repair of both esophageal atresia and tracheoesophageal fistula, regardless of gap
length, can preserve the esophagus.

SURGICAL ANATOMY
NOTE TO THE READER: The organization of this chapter differs somewhat from that of other chapters in that the physiology, histology, and most surgical

applications of the esophagus have been incorporated into the presentation of surgical anatomy.
The esophagus, a soft muscular tube, allows food to pass between the pharynx and the stomach.
Aristotle (384-322 BC), Greek philosopher and physician, suggested that the source of the word esophagus related to "its length and its
narrowness."16 The term's origin is more likely related to the Greek term oisopagos, created from oisein ("to carry") and phagos ("to eat") or from
phagema ("food"). The term, adopted by Medieval Latin and Late Middle English, became isophagus or ysophagus.16-18 Current spelling in German and
in British English is oesophagus, in French esophage, and in Italian esòfago.
In Old Roman Latin, the popular noun for the esophagus was gula.18,19 Gula was defined as a narrow passage, the mouth, or the throat. From this
Latin term arose the English vernacular term gully, signifying a narrow course for water, an outlet, or the neck of a bottle. The related Old Latin

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Latin term arose the English vernacular term gully, signifying a narrow course for water, an outlet, or the neck of a bottle. The related Old Latin
adjective, gulosus or goulu, meant greedy, voracious, or gluttonous. The French word gula is kept alive as goulée or gueule, meaning snout or
mouth.19 More recently, the term gullet has reemerged in English as a synonym for esophagus. In American English, esophagus refers exclusively to
"the tube or channel from the mouth to the stomach, by which food and drink pass."18,19

Position of the Esophagus
The esophagus is a midline structure anterior to the spine and posterior to the trachea. From its origin at the cricoid cartilage in the neck opposite the
fifth to sixth cervical vertebra, it passes into the thorax at the level of the sternal notch and travels caudally within the chest in the posterior
mediastinum. It terminates in the abdomen at the esophagogastric junction opposite the twelfth thoracic vertebra (Fig. 14-5). The esophageal hiatus
of the diaphragm is at the level of the tenth thoracic vertebra.
Fig. 14-5.

Divisions, terminology, and relationships of the esophagus. UES, upper esophageal sphincter; LES, lower esophageal sphincter. (Courtesy Dr. Dorothea
Liebermann-Meffert; modified.)

Designations of the Esophagus
The esophagus, which progressively descends through the neck, chest, and abdomen, has been classified from three different medical perspectives:
classical anatomy, function, and surgical understanding (Fig. 14-5). These viewpoints are discussed in the following paragraphs.
Classical anatomy divides the esophagus into three parts:
Cervical
Thoracic
Abdominal

For the clinician, this view is unserviceable and has led to other perspectives.
Function divides the esophagus according to its differing forms of motility into the following three zones (Fig. 14-5)20 :
Upper esophageal sphincter (UES)

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Esophageal body
Lower esophageal sphincter (LES)

However, this classification also embraces the coordinated actions of the upper intestinal system, including the oropharynx, esophageal sphincters and
body, and stomach. In this context, Diamant 20 emphasizes that "control mechanisms within the central nervous system as well as peripherally within
the intramural neural and muscle properties, serve to integrate these functional zones in a region of the gut where voluntary and involuntary control
mechanisms act together, and where the activity of two different types of muscle is intimately coordinated."
Surgeons can benefit from viewing the esophagus as a two-part structure divided into proximal and distal segments bordering at the tracheal
bifurcation (Fig. 14-5). This approach best matches surgical needs and therapeutic strategies.21 There are three reasons for this approach:
(1) Antipodal lymphatic flow proceeds from the area of the tracheal bifurcation cranially and caudally.4,22,23 This affects the direction of early
lymphatic tumor spread and the procedures of lymphadenectomy.24
(2) The surgical viewpoint incorporates the expected locations of tumors and their respective prognoses. Carcinomas occur with greatest frequency in
the mucosa of the distal half of the esophagus.25,26 The prognosis for distal tumors is far better than that for the rarer tumors located in the proximal
half of the esophagus.26 Proximal tumors also rapidly perforate the esophageal wall to invade adjacent structures such as the trachea, bronchi, and
adjacent spaces such as the mediastinum.26
(3) This classification conforms with the embryologic development from two different tissue sources and the specific arrangement of vessels, muscle
types, and innervation.4,22,23,27,28 Further subdivision of these segments into cervical and proximal thoracic and distal thoracic and abdominal sections
may be justified.26

Configuration of the Esophagus
The esophagus is the narrowest tube of the gastrointestinal tract. It originates at the distal end of the laryngopharynx (hypopharynx), at the level of
the sixth cervical vertebra. It terminates by widening to form the stomach, the most voluminous part of the gastrointestinal tract. The esophagus is
flat in its upper and middle parts (Fig. 14-6A) and rounded in its lower part (Fig. 14-6B). When distended, these parts present diameters of 2.5 cm by
1.6 cm and 2.5 cm by 2.4 cm, respectively. The esophageal tube collapses when at rest and ranges in size from 0.6 cm to 1.5 cm in diameter.29
Fig. 14-6.

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Transverse section through the neck and upper chest of a human autopsy specimen. A, The histological section shows the esophagus still in midline posterior
position. B, In the more distal level of the macroscopic cut surface, the esophagus has shifted toward the left (right in photograph). Note the intimate local
relationship between esophagus and trachea. 1, Esophagus; 2, Trachea; 3, Thyroid gland; 4, Vessels; 5, Pleura. (Courtesy Dr. Dorothea Liebermann-Meffert;
modified.)

In general, the axis of the esophagus is straight with only three minor deviations along its trajectory. The first deviation is toward the left at the base
of the neck (see Fig. 14-5, arrow 1). The second is at the level of the seventh thoracic vertebra, where the esophagus turns slightly to the right of
the spine (see Fig. 14-5, arrow 2). The third and most prominent deviation is located just above the esophagogastric (gastroesophageal) junction,
where the esophagus shifts dorsally and to the left (see Fig. 14-5, arrow 3). Any distortion of this axis revealed by radiological evaluation strongly
suggests mediastinal invasion and retraction. The cause is most often a malignant process.25,30

Dimensions of the Esophagus
In 52 adult cadavers the length of the esophagus between the cricoid cartilage and cardiac notch ranged from 21 cm to 34 cm (27 cm average). In
female cadavers the average distance was 23 cm (standard deviation of 2), and in the male cadavers it was 28 cm (standard deviation of 3). The
length related directly to the height of the body (153 cm to 187 cm). The cervical portion was 3 cm to 5 cm, the thoracic 18 cm to 22 cm, and the
abdominal 3 cm to 6 cm in length (Fig. 14-5). In practice, clinicians measure the esophagus by using the nostrils or the incisors as the landmark for
manometric and endoscopic procedures. The distances are from 13 cm to 16 cm to the cricoid cartilage, 23 cm to 26 cm to the tracheal bifurcation,
and 39 cm to 48 cm to the gastric opening.4,23

Tissue Composition of the Esophagus
The construction of the esophagus parallels the basic plan of the tissue organization of the digestive tube, except for the lack of a serosal coating.
The four layers (Fig. 14-7) are the tunica mucosa, tela submucosa, tunica muscularis, and tunica adventitia.
Fig. 14-7.

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Schematic illustration of the tissue organization of the esophagus (E), the esophagogastric junction (EGJ), and the stomach (S). The oblique narrowness at
the entry into the stomach is shown in the left upper corner. LC, lesser curvature; GC, greater curvature. 1, Tunica adventitia; 2, Tunica muscularis with (a)
longitudinal and (b) circular layers including the myenteric (Auerbach) nerve plexus; 3, Tela submucosa including the submucous (Meissner) nerve plexus and
blood and lymphatic vessels; 4, Tunica mucosa with (a) muscularis mucosa, (b) lamina propria mucosa, and (c) epithelium including glands. Arrow indicates the
transition (Z-line) between esophageal and gastric epithelium. (Modified from Liebermann-Meffert D, Duranceau A. Anatomy and embryology. In: Orringer MB,
Zuidema GD (eds). Shackelford's Surgery of the Alimentary Tract (4th ed). Vol I The Esophagus. Philadelphia: WB Saunders, 1996, pp. 3-38; reprinted by
permission.)

Tunica Mucosa
EPITHELIUM INCLUDING GLANDS
The mucosal layer confines the esophageal lumen. It consists of the following three parts.
Squamous epithelium is of the stratified, nonkeratinizing type. It normally covers the inner surface of the laryngopharynx and the tubular esophagus
Esophageal mucosa contains exclusively alveolar serous glands. Esophageal cardiac glands, closely resembling the cardiac glands of the stomach, are
present between the cricoid cartilage and the fifth tracheal ring.
Esophageal glands are small, tubular, mucous type glands lodged outside the muscularis mucosa (Fig. 14-7).31

POINTS OF CLINICAL AND SURGICAL RELEVANCE
The transition between the mucosa of the laryngopharynx and esophagus is inconspicuous.31 Macroscopically, the endoscopist sees the esophageal
mucosa as a reddish color in its cranial portion. It turns paler toward the lower third of the esophagus. The smooth surface of the esophageal mucosa
can be readily distinguished from the dark, mamillated gastric mucosa.
The transition between the squamous esophageal and columnar gastric epithelium is an objectively recognizable reference point. This abrupt, serrated
line, known as the Z-line (Fig. 14-8), has "four to six small, long or short tongues."32 It is normally located near the gastric orifice33,34 or just above it.
Endoscopists thus base their determination on differences in color, the degree of transparency of the epithelium, mucosal structure, and epithelial
thickness.32
Fig. 14-8.

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Schematic diagram of the tissue structures at the esophagogastric junction as seen from the luminal aspect. Esophagus and stomach have been opened
alongside the greater gastric curvature. The sidewalls are everted and show the intersecting line (i). The lesser curvature is in the center. The subperitoneal
connective tissue space extends from the insertion of the (a) upper to the (b) lower leaflet of the phrenoesophageal membrane. (Modified from LiebermannMeffert D, Duranceau A. Anatomy and embryology. In: Orringer MB, Zuidema GD (eds). Shackelford's Surgery of the Alimentary Tract (4th ed). Vol I The
Esophagus. Philadelphia: WB Saunders, 1996, pp. 3-38, reprinted by permission.)

Any proximal shift of gastric- or intestinal-type columnar epithelium into the esophagus is considered pathological. The change results from long-lasting
gastroesophageal reflux that causes chronic damage to the esophageal mucosa.35,36 The ultimate result may be that "the distal esophagus to a
greater or lesser extent is circumferentially lined by columnar epithelium"32 transformed to the gastric or intestinal type. This pathology, called Barrett's
esophagus, is regarded as a precancerous condition.26,32,34,36
Katada et al.37 and Wetscher et al.38 reported that increased apoptosis in the esophageal epithelium when Barrett's esophagus is present may be a
protective mechanism counteracting increased proliferation. Inhibition of apoptosis in Barrett's esophagus is interpreted by these investigators as
possibly promoting neoplastic progressive diseases. What is apoptosis? In brief, it is programmed cell death, the intricacies of which are reviewed in a
paper by Kuan and Passaro.39 According to Carlson (personal communication to Wood and Skandalakis, Feb. 19, 1998) the fibroblasts "commit suicide"
at the end of healing. The phenomenon of apoptosis needs more study.
The authors of this chapter recommend biopsy in all Barrett's patients. Collard et al.40 believe that early detection of high-grade dysplasia in Barrett's
esophagus and radical esophageal resection with radical lymph node resection gives the best chance of cure. Farrell et al.41 reported that
fundoplication will provide equivalent relief of symptoms for GERD (gastroesophageal reflux disease) patients with and without Barrett's esophagus.
LAMINA PROPRIA MUCOSA
Similar to the lamina propria of the stomach, the lamina propria mucosa of the esophagus consists of connective tissue built up of areolar, elastic, and
collagenous fiber networks (see also Fig. 14-24). In the pharynx, this layer is thin. In the esophagus, the layer is more voluminous and contains small
blood vessels, presumably terminal lymphatics, follicles, esophageal glands of mucous type, and, in the terminal esophagus, glands that resemble
cardiac glands. Projecting into the epithelium, the layer forms the papillae.
LAMINA MUSCULARIS MUCOSA
The lamina muscularis mucosa is a thin layer of short smooth muscle bundles. It begins 6 mm to 8 mm caudal to the pharyngoesophageal junction.
These muscle bundles are arranged transversely throughout the esophageal wall.
In the laryngopharynx, the mucosal folds are rather obliquely oriented. A change occurs just caudal to the pharyngoesophageal junction where the
lamina muscularis mucosa draws the lumen into three or four large longitudinal esophageal folds (Fig. 14-8).
Structural changes occur at the lower end of the esophagus. Here the lamina muscularis mucosa attains its greatest size in the esophagus,42 exhibits
a greater number of small transverse folds (Fig. 14-8), and takes a rippled shape when contracted.33,42,43 The cause of these ripples may be the local
increase of muscular mass and the fan-shaped insertion of its fibers into the lamina propria mucosa.44 When the endoscopist inflates the esophageal

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increase of muscular mass and the fan-shaped insertion of its fibers into the lamina propria mucosa.44 When the endoscopist inflates the esophageal
lumen, the wall extends widely and the folds disappear.
At the point of entry into the stomach the orientation of the mucosal folds abruptly changes from longitudinal esophageal folds to transverse gastric
folds (Fig. 14-8).

Tela Submucosa
The tela submucosa layer lies between the mucosa and the muscular coat. The tela submucosa of the pharynx is a firm sheath that functions as an
aponeurosis (pharyngeal aponeurosis)45,46 and differs from the loosely separating layer present in the wall of the esophagus and stomach (Fig. 14-7).
At this location the tela submucosa consists of:
Loose areolar connective tissue containing elastic and collagen fibers
Numerous fine blood vessels (Fig. 14-7)
A network of lymphatic channels (Fig. 14-7; see also Figs. 14-24 and 14-27)
Nerves, including the submucous nerve plexus (Meissner's plexus)
The deep mucous glands (Fig. 14-7)

Esophageal glands are small branching glands of mixed type with ducts penetrating the lamina muscularis mucosa. The submucosa increases in
thickness across the esophagogastric junction.

Tunica Muscularis
Similar to Figures 14-9 and 14-10, the pharyngeal musculature is mainly obliquely arranged. The transition from the oblique muscular fibers to the
transverse cricopharyngeal muscle produces a triangular area of sparse muscle cover (Figs. 14-9, 14-10) cranial to the upper esophageal sphincter, as
has been described and depicted by Killian.47 A single muscular layer coats the lumen of the pharynx, whereas two different muscular layers coat that
of the esophagus (Fig. 14-10). The muscle of the esophagus consists of a longitudinally arranged outer layer and a transverse inner layer (Fig. 14-11).
Fig. 14-9.

Disposition of the muscle bundles at the pharynx (P), pharyngoesophageal junction (PEJ), and esophagus (E) viewed from posterior. Human unopened dry
fiber specimen from autopsy with connective tissues removed. 1, Middle pharyngeal constrictor muscle; 2, Pars thyropharyngeal; 3, Pars cricopharyngeal of

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fiber specimen from autopsy with connective tissues removed. 1, Middle pharyngeal constrictor muscle; 2, Pars thyropharyngeal; 3, Pars cricopharyngeal of
the inferior pharyngeal constrictor muscle that corresponds with the upper esophageal sphincter (UES). Killian's triangle lies cranial to the UES. 4, Circular
muscle layer of the esophagus. Longitudinal muscle layer removed with only residual bundles preserved at the lateral aspect. 5, Residuals of the thyroid
glands; 6, Trachea. (Courtesy Dr. Dorothea Liebermann-Meffert.)

Fig. 14-10.

The disposition of the muscle fascicles at the pharyngoesophageal junction from the posterior aspect. There is one single layer in the pharynx with the upper
part of the constrictor muscle obliquely arranged (m. thyreopharyngeus) and the lower part transverse (m. cricopharyngeus). This direction change produces
triangle cranial to cricopharyngeal muscle. The cricopharyngeus is continued by the esophageal musculature, with its two layers in opposite orientation:
longitudinal and transverse. (From Liebermann-Meffert D. The pharyngoesophageal segment: anatomy and innervation. Dis Esoph 1995;8:242-251; reprinted
by permission.)

Fig. 14-11.

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The arrangement and disposition of the musculature of the pharynx, esophagus, and stomach viewed from the left lateral aspect. UES, Upper esophageal
sphincter; LES, Lower esophageal sphincter. (Modified from Liebermann-Meffert D, Duranceau A. Anatomy and embryology. In: Orringer MB, Zuidema GD (eds).
Shackelford's Surgery of the Alimentary Tract (4th ed). Vol I The Esophagus. Philadelphia: WB Saunders, 1996, pp. 3-38, reprinted by permission.)

Functionally, the pharynx and esophagus present a continuum of sequential contractions. In contrast, histologically the muscle types in these two
areas are completely different. The muscle of the pharynx is striated, while the lower tubular esophagus is smooth. Directly below the
pharyngoesophageal junction, isolated smooth muscle bundles28,48 appear intermingled with the striated muscles. The number of smooth muscle
bundles increases within the first centimeter of the esophageal tunica muscularis. This occurs somewhat higher in the inner, anterior muscle layer than
in the outer, longitudinal layer.4,23,28 No sharp transition lines occur. Instead both muscle types remain interwoven without any apparent anatomic
boundary. As they descend, the smooth muscle components simply become more numerous and replace – in the same proportion – the striated muscle
(Fig. 14-12). Finally, only isolated fibers or strands of the striated type lodge within the smooth muscles.4,23,28 Caudal to the tracheal bifurcation, the
fibers of both layers are exclusively of smooth muscle type.28,48 Measurements showed no essential individual variation.28
Fig. 14-12.

Distribution and transition of striated and smooth musculature in the human adult esophagus. No striated muscle exists caudal to the tracheal bifurcation.
(Modified from Liebermann-Meffert D. Anatomy, embryology, and histology. In: Pearson FG, Deslauriers J, Ginsberg RJ, Hiebert CA, McKneally MF, Urschel HC
(eds). Esophageal Surgery. New York: Churchill Livingstone, 1996, pp. 1-25, reprinted by permission.)

Tunica Adventitia
Tunica adventitia is presented later in the chapter.

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Peculiarities of the Tubular Esophagus
The primary orientations of the esophagus muscle layers are longitudinal and circular (Fig. 14-9 and Fig. 14-10) and the thickness of both layers of the
esophageal tube is similar, only 1 mm to 1.5 mm for each layer. There is no difference attributable to age.33,42

Longitudinal Muscle Layer
The longitudinal layer originates at the cranial margin of the cricoid cartilage and at the firm submucosal tissue covering the arytenoid muscles through
the cricoesophageal tendon (Fig. 14-13). The longitudinal musculature represents one sheath of multiple, flat, delicate muscle bundles that wrap the
esophageal wall in a complete layer. Adjacent bundles rarely converge, but connect with each other and with the circular muscle bundles by septa of
loose connective tissue (perimysium). Fine vessels and nerves irregularly perforate the muscle layers and create local oval or longitudinal slits. The
muscle bundles travel directly longitudinally down the esophagus for a considerable distance (Fig. 14-11) before they cross the gastric orifice. Here
they become organized partly transversely alongside the anterior and posterior gastric wall (Fig. 14-11). Beyond the esophagogastric junction, the
longitudinal muscles continue into those covering the stomach.
Fig. 14-13.

This human autopsy specimen, fixed with alcohol, shows view into the laryngopharynx, pharyngoesophageal junction, and cervical esophagus (1) from the
posterior aspect. The soft pharyngeal wall (2) is shown, with the constrictor musculature divided and the line of intersection (3) reflected laterally (arrows).
The tunica mucosa covering the constrictor muscles and the cricoesophageal tendon (4) has been preserved, but removed above both piriform fossae, lateral
to the cricoesophageal tendon (4) and the posterior cricoarytenoid muscle (5) to expose the laryngeal part of the inferior laryngeal nerve (recurrent laryngeal
nerve [RLN]) and superior laryngeal nerve (6, 7). Cervical branch of the RLN (8) and its entry into the larynx is shown between two arrows. Subclavian artery
is indicated by (9). Longitudinal muscle of the esophagus (1) inserts at the cranial margin of the cricoid cartilage and in the firm connective tissue caudal to the
cuneiform and corniculate tubercles (10) opposite the epiglottis (11) using the cricoesophageal tendon. (Courtesy Dr. Dorothea Liebermann-Meffert;
modified.)

Circular Muscle Layer
The circular layer is a continuation of the cricopharyngeus muscle, the most caudal part of the musculature of the pharynx (Fig. 14-11) and the lowest
point of voluntary control of swallowing. It begins at the level of the cricoid cartilage and descends along the esophagus by wrapping it completely. At
no place do the muscles form closed rings, but present imperfect circles with superimposed ends.33
Additional distinctive threadlike muscle strands face the inner surface of the circular layer toward the end of the esophagus and can be seen beneath
the mucosa and submucosa after they are removed. They are short, thin, sparse, irregularly distributed, and straight with X- or Y-shaped endings.

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the mucosa and submucosa after they are removed. They are short, thin, sparse, irregularly distributed, and straight with X- or Y-shaped endings.
They correspond to Laimer's49 description and illustration of "bracket fibers." However, they never form a continuous layer or a fascicular network.

Sphincters
Sphincters divide the alimentary canal into functional segments. They are characterized by a resting tone that is higher than in the two adjacent
segments. Sphincters are anatomically ill-defined.
The word sphincter is derived from the Greek term for string, cord, or lace and has long been used to designate a circular muscle.50 Galen employed
the name for muscular arrangements that were able to tie up, to strangle or throttle, but he also termed some of them constrictores or adstrictores
according to their property to constrict, draw together or contract. Because of their circular shape, such muscles were also termed musculi
orbiculares.
More recently, in the anatomic definition, sphincter designates a circular or anular muscle surrounding an opening,51 or a ringlike band of muscle fibers
that constrict a passage.17
The term cardia, alternatively used for the area of the esophagogastric junction, has two meanings: one is the heart; the other, the gastric
orifice.52,53,54 The noun was first recorded in the Hippocratic writings and referred to as the cardiac end of the stomach.52

Upper Esophageal Sphincter (UES)
The complex mechanisms of the pharyngoesophageal functions20,55,56 that involve swallowing, breathing, and speech are possible because of various
tissue materials such as bony and cartilaginous structures, and soft structures such as the palate, pharynx, and esophageal muscles including the
supplying vessels and nerves.
The pharynx includes the nasopharynx, oropharynx, and laryngopharynx (hypopharynx). The laryngopharynx divides into two tubes, the larynx with the
trachea, and the esophagus (Fig. 14-14). The larynx is formed by a framework of cartilages connected by membranes and ligaments; they are moved
by the laryngeal muscles. These structures are responsible for the mechanisms of air passage, epiglottic movement, phonation, and, together with the
inferior laryngeal constrictor muscles, sphincter action at the pharyngoesophageal junction.
Fig. 14-14.

Positional relationships of anatomic structures involved in swallowing, breathing, and speech. Shown in sagittal section. (Courtesy Dr. Dorothea LiebermannMeffert; modified.)

The upper esophageal sphincter (UES) lies at the end of the pharynx and controls the entry into the esophagus and larynx. It is constructed of two
anatomic elements. The anterior wall is rigid, corresponding to the posterior surface of the cricoid cartilage that also forms the posterior wall of the
larynx (Fig. 14-13). The posterior wall of the UES is soft and formed by one continuous muscle sling, the transverse, horseshoelike loop of the lower
part of the inferior pharyngeal constrictor muscle (Figs. 14-9 and 14-10). This cricopharyngeus muscle inserts at the lateral process of the cricoid
cartilage. Measurements of the muscular thickness across the pharynx and upper esophagus showed that the cricopharyngeus (sphincter) muscle is
smaller by far than the more proximal parts of the bilateral, obliquely arranged inferior and middle pharyngeal constrictor muscle.57
The sphincter serves primarily to prevent distension of the esophagus during respiration and to protect the trachea and lungs against the uptake of
reflux material or reflux aspiration. Normally the sphincter remains in a state of strong, nerve-controlled tonic contraction between episodes of
swallowing.
On manometry, the UES has a length of 2 cm to 4.5 cm and can be identified radiologically by a posterior indentation. The upper esophageal

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On manometry, the UES has a length of 2 cm to 4.5 cm and can be identified radiologically by a posterior indentation. The upper esophageal
sphincter's asymmetrical pressure measurements58 clearly equate with its anatomic construction.

Lower Esophageal Sphincter (LES)
The lower esophageal sphincter (LES) begins approximately 3 cm cranial to the junction with the stomach. Here the number of muscle fibers of the
circular layer of the tubular esophagus increase and superimpose on each other, producing a progressive muscular thickening (Fig. 14-15). This is
consistent with the rearrangement of the muscle bundles across the junction to the stomach (Fig. 14-16 left). The muscle bundles at the side of the
greater gastric curvature change direction to form the oblique gastric sling fibers. Those at the side of the lesser curvature retain their previous
horizontal orientation to become the short muscle clasps33 shown in Figures 14-11, 14-16 left, and 14-17.
Fig. 14-15.

Measurements of thickness of tunica muscularis between esophagus and stomach. Average thickness measured in 32 formaldehyde-fixed human specimens
at 4 points of circumference and at 5 mm steps, using the maximum thickness as landmark. Numbers clearly demonstrate asymmetry of LES (lower
esophageal sphincter). EGJ, Esophagogastric junction. (Modified from Stein HJ, Liebermann-Meffert D, DeMeester TR, Siewert JR. Three dimensional pressure
image and muscular structure of the human lower esophageal sphincter. Surgery 1995;117:692-698, reprinted by permission.)

Fig. 14-16.

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Correlation between radial and axial muscle thickness (in mm) and muscular arrangement (left), and three dimensional manometric pressure image (right)
across the human esophagogastric junction (EGJ), i.e. lower esophageal sphincter. Radial pressures at the EGJ (in mm of mercury) were plotted around axis
representing atmospheric pressure. PW, Posterior wall; GC, Greater curvature; AW, Anterior wall; LC, Lesser curvature; SM-M, Submucosa-Mucosa; MP,
Muscularis propria (smooth muscle). (Modified from Stein HJ, Liebermann-Meffert D, DeMeester TR, Siewert JR. Three dimensional pressure image and muscular
structure of the human lower esophageal sphincter. Surgery 1995;117:692-698, reprinted by permission.)

Fig. 14-17.

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Muscle structures at esophagogastric junction (at lower esophageal sphincter) (view from luminal aspect). Esophagus and stomach opened alongside greater
gastric curvature, the sidewalls everted, and mucosa and submucosa stripped off. Muscle fascicles of the gastric sling (1) and clasps (2) exposed and showing
the fascicular relationship. Human autopsy specimen. (Courtesy of Dr. Nakamura and Prof. Minori Oi, Tokyo.)

The gastric sling fibers begin at the terminal esophagus (Fig. 14-11), hook around the esophagogastric junction, and form the angle of His. They then
run down at the anterior and posterior aspect of the stomach and fan outward in the direction of the greater gastric curvature. There they form slings
(Fig. 14-11) and end between the fibers of the inner muscle layer of the gastric antrum.33
The short bundles on the lesser curve side that Liebermann-Meffert calls clasps33 anchor firmly in the connective tissue along the inner margin of the
sheath of the gastric sling fibers (Fig. 14-11). To some extent, these clasps are suspended from or partly supported by fibers of the gastric sling (Fig.
14-17). DiDio and Anderson51 show Curti's59 original photograph of the clasps in their publication on sphincters, but they do not mention them.
The maximum muscular thickness occurs at the junction between the esophagus and stomach and tapers off within the stomach (Fig. 14-15).
Macroscopic examination of the fresh specimen or of the living individual does not reveal marked thickening. This soft, often stretched muscle tissue
readily escapes palpation due to its concealed position near the spine, covered by the filmy connective tissue and fat under the phrenoesophageal
membrane. The anatomic specimen, however, shows the musculature in the contracted stage. The maximum muscular thickness of 4 mm at the
esophagogastric junction is twice that of the esophagus and the stomach.
It must be stressed in this context that the normal pressures of the LES are much lower than those of other sphincters. They range only from 14.5 mm
Hg to 34 mm Hg58,60 while, for example, the pressure of the upper esophageal sphincter ranges from 30 mm Hg to 142 mm Hg.58
POINTS OF CLINICAL AND SURGICAL RELEVANCE
The rearrangement of the pharyngeal muscle into the UES musculature leaves an area of potential tissue weakness (Killian's triangle). It may be
predisposed to the formation of a protrusion of the pharyngeal wall cranial to the UES.47 Such a diverticulum may contain the full thickness of the wall
or only mucosa and submucosa,54 but because it originates in the pharynx, it never contains muscularis mucosa. Zenker's diverticulum is, by definition,
the midline protrusion.47 Lateral laryngopharyngeal diverticula develop at the entry of vessels, as described at length by others.45,46 They seem to be
rare in humans. The mechanisms leading to the formation of a diverticulum are not yet clear, and anatomic and pathophysiologic causes are still
debated. For surgical treatment of Zenker's diverticulum Peracchia et al.61 advised minimally invasive surgery using a linear endostapler introduced
through a Weerda endoscope.
The literature includes abundant claims that the diaphragmatic crura represent the mechanical equivalent of the LES. However, dissection of the
diaphragm and/or disruption of the phrenoesophageal membrane altered neither the LES pressure nor the pressure characteristics.62 Regarding the
normal anatomic location of the LES, muscular rearrangement and maximum thickness are most prominent precisely at the esophagogastric junction, at
the transition of esophageal into gastric folds.33
The following points support the argument that the unique muscular structures at the end of the esophagus constitute the physiologic LES:
Simultaneous radiomorphological motility studies using wall markers identified the location of maximum muscular thickening at the site of the LES high
pressure zone.62
When muscle strips of the esophagogastric junction are placed in vitro into a bath of low dose pentagastrin, they maintain, or even increase, tonic
contractions. Muscle strips taken from levels above or below do not.63
The extent of the specialized muscle structure is identical with the length of the functional sphincter.58,60 The asymmetric muscle bundle arrangement of the
inner layer matches the asymmetric thickening of the esophagogastric junctional musculature (Fig. 14-11b and Fig. 14-16). The established axial and radial
asymmetry of the functional sphincter reflects the asymmetry of the muscular structures. This is shown by different manometry techniques 58,64 including the
new technique 65-67 of three-dimensional imaging (Fig. 14-16 right). In addition, the irregular distribution of forces within the LES clearly demonstrates the
absence of a muscular "ring."
The special musculature, muscular arrangement, and corresponding thickening extend upward for 3 cm to 4 cm through the diaphragm and pass beyond the
distal end of the esophagus into the stomach wall for another 1 cm to 2 cm. The area of the greatest fiber concentration and muscle thickness is at the angle
of His.33 Therefore, one may suggest that the gastric sling fibers exert the antireflux effect of the sphincter.53,68,69
Surgical disruption of the junctional musculature by partial or total myotomy or myectomy significantly reduces or even abolishes LES pressure values.68,69
For surgical management of patients with achalasia, the main principle is division of the LES musculature. Recently, a modified Heller's operation with myotomy
of the anterior wall of the esophagogastric junction has been performed. However, the proper length of the myotomy is still debated.68,70,71 The incision has
been commonly recommended to begin at least 10 cm proximally on the esophagus and to extend the myotomy at least 3 cm into the body of the stomach.
This is considerably longer than the anatomic sphincter. Bombeck and associates 68 and Ellis and others 72 limited the length of the gastric myotomy to 0.5 cm
and 1 cm, respectively, in order to preserve the function of the sphincter, to avoid reflux by its disruption, and to avoid disruption of the muscular sling of the
oblique gastric fibers. Gozzetti and coworkers 70 question the benefit of this function-preserving procedure. However, although still extending the myotomy far
into the stomach, they take great care not to damage the sphincteric function of the gastric fiber sling and divide only the "muscular clasps" at the lesser
curvature.
Cosentini et al.73 reported excellent to fair results with myotomy and antireflux surgery in 23 patients in whom previous dilatations had not yielded
satisfactory results. Holzman et al.74 reported that laparoscopic myotomy is a simple and effective treatment for achalasia. Spiess and Kahrilas 75 reported that
laparoscopic Heller's myotomy is emerging as the optimal surgical therapy for achalasia. Since laparoscopic Heller myotomy is superior in relieving dysphagia
and preventing heartburn for some patients, Stewart et al.76 prefer it to thorascopic Heller myotomy.

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77

Koshy and Nostrant
reported good results using botulinum toxin in patients with esophageal motor disorders. Endoscopic and balloon treatment for
various dysmotility disorders are also advised.
Gowen et al.78 identified five risk factors for gastroesophageal intussusception in patients with noncardiac chest pain:
– Eating disorders or alchohol abuse
– Sudden sustained exertion
– Small bowel obstruction
– Acid bile peptic disease
– Pregnancy

Adventitia and Stabilizing Structures
Tunica Adventitia
In contrast to the buccopharyngeal fascia in the neck, the periesophageal tissue, or adventitia, is composed of loose connective tissue that envelops
the esophagus and connects it with the mediastinum and the neighboring structures. It contains small vessels, lymphatic channels, and nerve fibers.

Tissue Mantle
The esophagus lies loosely tied through the adventitia in its bed of areolar connective tissue. No mesentery or serosa coats it within the mediastinum.
This property allows the esophagus great mobility both in transverse and longitudinal directions. As a consequence, respiration induces an esophageal
movement over some millimeters, and swallowing results in displacement over a few centimeters.79
The unique location of the esophagus subjects it to blunt stripping from the mediastinum when performed by the surgeon in pull-through
esophagectomy.25,27,80,81 Blunt dissection may occasionally be hazardous, however, and is strongly contraindicated in the presence of periesophageal
tumor invasion, particularly if it occurs close to the azygos vein or if inflammatory adhesions are present.
The intimate proximity of esophagus, trachea, and pleura (see Fig. 14-6) all the way down to the tracheal bifurcation, in conjunction with the lack of
any intervening partitions or connective tissue sheaths, paves the way for ready and rapid local spread of malignancy and fistula formation.

Tissues Anchoring and Stabilizing the Esophagus
A framework of bony, cartilaginous, and membranous structures stabilize the pharynx and esophagus (Fig. 14-18). The buccopharyngeal membrane
attaches the nasopharynx and laryngopharynx to their cartilages and to the cranium and, by way of the prevertebral fascia, to the vertebral column.
The attachments of the esophagus are far more flexible than those of the pharynx.
Fig. 14-18.

Anchoring and stabilizing structures of esophagus and stomach. Gastroretroperitoneal attachments and reflections include gastrophrenic, gastrosplenic, and
splenorenal ligaments, lesser omentum. UES, Upper esophageal sphincter; LES, Lower esophageal sphincter. (Modified from Liebermann-Meffert D, Duranceau
A. Anatomy and embryology. In: Orringer MB, Zuidema GD (eds). Shackelford's Surgery of the Alimentary Tract (4th ed). Vol I The Esophagus. Philadelphia: WB

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A. Anatomy and embryology. In: Orringer MB, Zuidema GD (eds). Shackelford's Surgery of the Alimentary Tract (4th ed). Vol I The Esophagus. Philadelphia: WB
Saunders, 1996, pp. 3-38, reprinted by permission).

ATTACHMENT OF THE CRANIAL END OF THE ESOPHAGUS
At the cranial end of the esophagus the cricoesophageal tendon, which is a strong tendon 2 cm to 3 cm long and 1 cm wide, attaches the longitudinal
esophageal muscle onto the posterior plane of the lamina of the cricoid cartilage (Fig. 14-13, Fig. 14-18).
ATTACHMENT OF THE TUBULAR ESOPHAGUS
Between the origin of the esophagus and the bifurcation of the trachea, several delicate fiber strands – or, more precisely, membranes – anchor the
esophageal wall elastically to the trachea, the pleura, and dorsally toward the prevertebral fascia (Fig. 14-18).4,23,82

Research Results
Large field histological transverse sections in two studies by Liebermann-Meffert et al.4,82 showed that the fiber strands, or membranes, that anchor
the esophageal wall vary in number, size, and extension but were present in all their specimens. They are composed mainly of elastic and collagen
fibers (Fig. 14-19). Occasionally they contain striated or smooth muscle bundles.
Fig. 14-19.

One of tiny fiber membranes (single arrow) connecting esophagus (1) with trachea (2); 5 thick transverse histological section. Membrane mimics slightly
coiled band in transverse section, 250 m thick and 14 mm long, and 90% elastic fiber elements. Typical fan-shaped insertion of band into perimysium of
longitudinal, outer layer of esophageal musculature (double arrow). Human autopsy specimen, 4 cm caudal to the lower margin of the cricoid cartilage.
(Modified from Liebermann-Meffert D, Huber W, Häberle B, Wurzinger LJ, Siewert JR. Relationship between esophagus, trachea and pleura. In: Nabeya K,
Hanaoka T, Nogami H (eds). Recent Advances in Diseases of the Esophagus. New York: Springer, 1993, pp. 1045-1049, reprinted by permission).

At the trachea, the fiber strands insert most often mediolaterally into the dense connective tissue that forms the tracheal membrane or in the
perichondrium of the cartilages. They then turn toward the lateral aspect of the esophageal wall, expand near the esophageal muscle, and become
continuous with the perimysium (Fig. 14-19).
In histological cross sections by Liebermann-Meffert et al.,4,82 the coiled strands presented definitive lengths from 1 mm to 17 mm and thicknesses of
30 to 300 microns (1000 microns in one singular case). When analyzed in consecutive serial sections, the strands actually formed laminated membranes
of 1.5 mm to 3 cm in craniocaudal extent. The same studies found a larger number of similar fiber strands originating in all specimens dorsal to, and
lateral from the esophagus, and radiating into the meshes of the periesophageal connective tissue space or inserting into the tissue of the pleura.
The tiny, delicate, laminated membranes, individually varying in number and size, are far smaller and shorter than the long, coarse fibroelastic cords
that Laimer49 depicted in 1883 and Netter83 later adopted into his illustrations. Nor was their orientation found to be longitudinal to the

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that Laimer49 depicted in 1883 and Netter83 later adopted into his illustrations. Nor was their orientation found to be longitudinal to the
esophagotracheal axis,82 but instead was regularly transverse. One other factor useful for the stabilization of the esophagus not yet discussed is
provided by the numerous fine membranes that anchor it laterally in the connective tissue network of the mediastinum and to the pleura, and also
membranes that extend dorsally, presumably to the prevertebral fascia.
Clinical Considerations and Relevance. One may agree that the short anchoring membranes restrict the mobility of the esophagus. Yet, the capacity of
the collagen membranes to extend and of the elastic components to recoil yields adequate mobility when they are stretched under normal tension.
When the tiny membranes are torn, they may break easily without damage to either the tracheal or pleural wall.
The unpredictable presence of individually developed coarser membranes may cause damage when the esophagus is stripped during esophagectomy.
Therefore, transdiaphragmatic esophagectomy may benefit from mediastinoscopic dissection to reduce the incidence of tears in case unusually strong
membranes are present. The distal half of the esophagus within the mediastinum is more loosely adherent.
ATTACHMENT AT THE DISTAL END
In its passage through the esophageal hiatus, the esophagus is bounded by the two diaphragmatic crura and the phrenoesophageal membrane (Fig.
14-18).
The subdiaphragmatic and the endothoracic connective tissues of the diaphragm blend to create the phrenoesophageal membrane (Fig. 14-18). This
tissue sheath has also been called Laimer's fascia or Allison's membrane. Because it originates from a fascia, the phrenoesophageal membrane is
relatively strong. The membrane splits into parts, described in the following paragraphs.
The upper sheath of the membrane extends upward for 2 cm to 4 cm through the hiatus (see Fig. 14-8). Here its fibers traverse the esophageal
muscle and insert into the tunica muscularis and the submucosa.84 This resembles the insertion of the tiny membranes that attach the esophageal
muscle to the membranous part of the trachea (Fig. 14-19).
The lower sheath passes down alongside the cardia to the level of the top of the gastric fundus. Here it blends into the gastric serosa (see Fig. 14-8),
the hepatogastric ligament, and the dorsal gastric mesentery (Fig. 14-18).
The lower sheath of the phrenoesophageal membrane can be recognized during surgery and laparoscopy by its well-defined lower edge and slightly
yellow tissue color, even if severe periesophagitis is present. The membrane is composed of equal portions of elastic and collagenous fiber elements,
guaranteeing sufficient plasticity. It wraps the esophagogastric junction like a wide collar (Fig. 14-18). Despite a somewhat loose fibrous connection
with the wall of the esophagogastric junction through the underlying areolar connective tissue, the entire phrenoesophageal membrane clearly
separates from the esophageal muscle across the junction.4,23

Clinical Considerations and Relevance
The structural arrangement of the phrenoesophageal membrane allows free vertical movement of the terminal esophagus and of the junction of the
stomach in relation to the diaphragm. It is able to "slip through the hiatus as in a tendon sheath."85
With advancing age, the tissue proportions of the phrenoesophageal membrane change. Collagenous fibers progressively replace the elastic fibers,84
loosening the attachments. The membrane becomes slack and inelastic, and fat tissue usually gathers within the areolar connective tissue between
the membrane and the muscular wall. The result is a loss of pliability. These events, when combined with a wide hiatus, may contribute to the
development of the diaphragmatic hernia.84 Abnormally loose anchorage of the phrenoesophageal membrane in youth, together with an extraordinarily
large accumulation of adipose tissue in the connective tissue space between the phrenoesophageal membrane and the cardia muscle may cause similar
problems.84
In normal individuals, various firm ligaments and membranes attach the cardia and gastric fundus posteriorly to the fascial retroperitoneal planes,
providing adequate stability to the esophagogastric junction.
In sliding hiatal hernia, both the terminal esophagus and gastric fundus protrude into the thorax. In the less common paraesophageal hernia, the
terminal esophagus is positioned normally, but the gastric fundus and body advance beside the esophagus into the mediastinum through the
diaphragmatic hiatus.86
In the discussion of the different etiological factors leading to hiatal hernia, one potentially important anatomic aspect has been consistently ignored.
This is the close proximity of the gastric fundus to the hiatus. In conjunction with weakening and slackening of the gastric attachments by aging, this
may produce the precondition for herniation.4,23 This condition would be consistent with what Eliska84 has suggested for sliding hernias and with the
observation of Ellis,86 who found that the "symptoms usually develop only in adults or in the elderly."

Compartments and Spaces
The loose connective tissue in which both the esophagus and trachea are embedded is bounded by fascial planes anteriorly and posteriorly, forming
two potential spaces between neck and chest. The anterior or pretracheal (previsceral) space is limited distally by the fibrous tissue of the
pericardium. The posterior or prevertebral space may, however, extend from the base of the skull down to the diaphragm.
The posterior space is of clinical importance because most instrumental perforations occur in the laryngopharynx above the cricopharyngeal sphincter.
Subsequent outflow of the heavily contaminated esophageal content spreads rapidly down the fascial space. Ruptures of the esophagus (Boerhaave's
syndrome) and leakage of an esophageal anastomosis occurring within the chest usually cause a similar effect by spreading up or down through these
planes. Early diagnosis is vital for the patient, because the prognosis for esophageal perforation is still poor and depends entirely upon swift surgical
treatment.

Constrictions
Some structures compress the lumen of the tube and cause clinically identifiable narrowings. The first constriction is caused by the tonus of the
cricopharyngeus muscles and is identified about 15 cm caudal to the incisors. The second, the aortic compression, is caused by the crossing of the

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cricopharyngeus muscles and is identified about 15 cm caudal to the incisors. The second, the aortic compression, is caused by the crossing of the
aortic arch and the left main bronchus at 22 cm from the incisors. The third narrowing is inconstant. If prominent, it is located about 44 cm from the
incisors and may be caused by the tonic effect of the lower esophageal sphincter. The two muscular constrictions correspond with the upper and the
lower esophageal sphincters and can be identified manometrically at either end of the esophagus.

Vessels and Nerves: Structures of Support
Vessels and nerves are supporting structures of the esophagus.4,22 They do not properly belong to the esophageal tissue, but the channellike vascular
or solid nerve cords feed, drain, and provide motility and sensory impulses to the tissue components of the esophageal wall. In short, these structures
maintain esophageal function.
For the purpose of differentiating the parts of the system located external to the esophagus from those within the wall, the structures have been
classified as extrinsic or intrinsic. Both are discussed below.

Arterial Supply
One might be concerned about fatal mediastinal bleeding from esophageal vessels; however, "blunt stripping" of the esophagus without thoracotomy
for carcinoma has been shown to be relatively safe.25,27,80,81 The remarkably low blood loss during the procedure and the low susceptibility to
postoperative anastomotic leaks suggest a primarily poor esophageal vascular supply. Nevertheless, the surgically mobilized esophagus retains viability
"over a long distance," in the words of Williams and Spencer Payne, when handled carefully.87
EXTRAMURAL, EXTRINSIC ARTERIES
The pharynx and the UES are supplied by small arteries originating from the superior thyroid arteries.

Inferior Thyroid Arteries: Cervical Esophagus
The cervical esophagus is supplied by the paired inferior thyroid arteries (Fig. 14-20). They arise from the thyrocervical trunk of the subclavian artery.
The inferior thyroid arteries give off branches 2 cm to 3 cm long called tracheoesophageal arteries. These travel caudal and medial on each side
toward the tracheoesophageal groove. The vessels of both sides are "joined by anastomotic twigs along the trachea"88 and divide into three to four
tracheal branches with two to three branches to the esophagus. These, in turn, subdivide within the periesophageal tissue into vessels of less than
500 m luminal diameter before they enter the esophageal wall. Variants, such as direct esophageal branches from the subclavian artery, the superior
thyroid artery, the thyroidea ima artery, and the common carotid artery are infrequent and rather insignificant.27,89
Fig. 14-20.

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Most common pattern of arterial supply of esophagus. Dotted lines show larger intramural anastomoses. Dashed lines behind stomach show splenic artery and
its esophageal branches. Dimensions not proportional. (Modified from Liebermann-Meffert D, Duranceau A. Anatomy and embryology. In: Orringer MB,
Zuidema GD (eds). Shackelford's Surgery of the Alimentary Tract (4th ed). Vol I The Esophagus. Philadelphia: WB Saunders, 1996, pp. 3-38; reprinted by
permission.)

Tracheobronchial and Bronchoesophageal Arteries: Intrathoracic Esophagus
The intrathoracic esophagus receives blood from two sources (Fig. 14-20): the unpaired tracheobronchial arteries,27,89 which arise as a group from
the concavity of the aortic arch27 and can number between one and four; and the bronchoesophageal artery. The tracheobronchial arteries give off
several small branches to the esophagus which subdivide within the periesophageal tissue into vessels of 350 m to 500 m in diameter. Frequently,
one bronchoesophageal artery originates 1 cm to 3 cm caudal to the vascular bundle from the anterolateral aspect of the descending aorta.27 In this
area, which relates to the tracheal bifurcation, all the vessels are straight and short (less than 1.5 cm) and form a firm connection between the aorta,
trachea, and esophagus. Variants, if any, such as branches from intercostal arteries,89 seem to be insignificant for the blood supply of the human
esophagus.

Aortic Proper Esophageal Artery: Intrathoracic Esophagus
One (or rarely, two) unpaired proper esophageal artery with a luminal diameter of 1 mm to 2 mm may arise more caudally from the anterior aspect of
the descending aorta as an exclusive source for the esophagus.27,89 If present, this vessel travels obliquely down toward the esophagus within the
mediastinum to divide into recurrent ascending and descending branches. Both subdivide into several periesophageal vessels of less than 500 m in
diameter.

Left Gastric and Splenic Arteries: Abdominal Esophagus and Gastric Cardia
The abdominal esophagus and gastric cardia are supplied by the unpaired left gastric 27,89 and splenic arteries.27 These derive from the celiac axis (Fig.
14-20). With as many as 11 arterial branches, the left gastric artery mainly supplies the anterior and right lateral aspects of the esophageal wall. The
splenic artery primarily supports the posterior and left lateral aspects (cardiac notch) by either one or two direct branches or by vessels of the gastric
fundus, including connections with the short gastrics. The branches from both stem vessels that supply the esophagus extend straight upward 4 cm to
6 cm within the periesophageal tissue across the diaphragmatic hiatus. At variable distances small tributaries of less than 500 m internal diameter
emerge before the main vessels pierce the esophageal wall.27 The left inferior phrenic artery affords additional arterial supply.
INTRAMURAL, INTRINSIC ARTERIES
Having penetrated both layers of the muscular wall, the small vessels form the submucosal plexus. Many of the fine vessels in the submucosa parallel
each other in longitudinal orientation. Less frequently, others form circumferential vessels.90 Numerous arterioles and venules are present beneath the
epithelium.
POINTS OF CLINICAL AND SURGICAL RELEVANCE
One important point is that after entering the esophagus the periesophageal branches extend to form a dense and complete intrinsic submucosal
network that can compensate in the event that an artery is severed. The continuity of the intramural vascularity retains viability and a good
circulation over a long distance within the surgically mobilized esophagus.27,87 This also explains why carefully handled ligation of extramural vessels
does not compromise the underlying tissue and why the line of dissection maintains adequate circulation.
With the exception of one vessel of direct aortic origin, the vascular pattern derives from the larger stem vessels needed for the supply of different
organs (Table 14-3). This demonstrates that the esophagus depends on "a shared vasculature."89
Table 14-3. Common Extrinsic Blood Sources of the Esophagus

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Section*

Sources

Sharing Organs

Cervical

Two paired stem vessels

+ Thyroid gland
+ Trachea

Thoracic

Several unpaired stem vessels

+ Trachea
+ Bronchi

Abdominal

Proper unpaired vessel

— None

Two paired stem vessels

+ Stomach
+ Spleen

*In neck, chest, and abdomen, the esophagus shares blood supply with other organs by using same vascular sources.
Source: Courtesy of Dr. Dorothea Liebermann-Meffert.

Repetitive branching of the already small esophageal vessels results in the formation of very small vessels in the periesophageal tissue before their
entry into the wall of the esophagus. These vessels, therefore, may undergo contractile hemostasis when torn.
A continuous regular network located in the submucosa connects all the extramural vessels. There is no poorly supplied or avascular zone. Further,
surgical experience clearly shows that problems due to circulatory disturbances are greatly overestimated. Anastomotic failures almost always arise
from the visceral substitute.91
It is crucial that the esophagus receives an excellent blood supply through longitudinally oriented intramural vessels that permit the placement of
anastomoses at any level. The intramural network thus provides a luxurious, albeit fine, vascularity for the esophagus by a system of small arteries,
arterioles, and capillaries. Nevertheless, this area needs careful surgical handling.

Venous Drainage
The intramural, intrinsic veins commence as fine venules to form the subepithelial plexus within the lamina propria of the tunica mucosa (Fig. 14-21).
They receive blood from the adjacent capillaries and drain into the submucosal plexus.92,93
Fig. 14-21.

Diagram of venous drainage of esophagus in normal human. (Modified from Kitano S, Terblanche J, Kahn D, Bornman PC. Venous anatomy of the lower
esophagus in portal hypertension: practical implications. Br J Surg 1986;73:525-531, reprinted by permission.)

Aharinejad et al.90 recently studied the human microvasculature system in detail. They observed that two small veins usually accompany the
circumferential arteries in the lamina submucosa. Perforating veins originating from the small communicating veins of the submucous plexus pierce the
muscular wall of the esophagus together with the perforating arteries. They receive tributaries from the muscle coats and form the extramural,
extrinsic veins at the surface of the esophagus.90-93 No valves were found in the esophageal venous circulatory system.
The extrinsic veins drain into the locally corresponding large vessels. The superior vessels drain to the jugular veins or the azygos and hemiazygos
veins. The inferior veins terminate in the left gastric and splenic veins.
As well described in 1918 by Elze and Beck,94 there are two clearly delineated venous plexuses in the laryngopharynx within the extremely thin
submucosa beneath the mucosa (Fig. 14-22). These are exactly at the level of the pharyngoesophageal junction. One plexus lies on the dorsal aspect
of the inferior constrictor muscle; the other in the midline posterior to the cricoid cartilage.
Fig. 14-22.

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Laryngopharyngeal venous plexuses viewed from posterior aspect as depicted by Elze and Beck.94 The first deep plexus (depicted on the left side of the
drawing) lies medial on the anterior side of the pharynx covering the posterior, transverse, and oblique aryepiglottic muscles and the hard posterior surface
of the cricoid cartilage (seen from the luminal aspect of the pharynx). A second deep plexus (shifted after cutting of the wall to the right side of the drawing)
lies exactly on the opposite side of the lumen of the pharynx, posteriorly underneath the inferior constrictor muscles and the cricopharyngeal muscles (UES).
(Modified from Elze C, Beck K. Die venösen Wundernetze des Hypopharynx. Z Ohrenhk 1918;77:185-194.)

Ten specimens (unpublished data by Liebermann-Meffert, publication in preparation) showed both plexuses to be similar in size, approximately 2 cm to
3 cm wide, and consisting of several thick veins with a maximum width of 4 mm. These were primarily longitudinal in orientation and were joined by
several transverse anastomoses. These veins receive blood from the mucosa of the laryngopharynx, larynx, and esophagus and drain into the thyroid
and jugular veins.94 These venous plexuses may cause a recognizable postcricoid impression on the esophagus95,96 and may be involved in the "globus
sensation" in patients with venous stasis and tissue swelling.47,94 These plexuses may also contribute to the competence and action of the upper
esophageal sphincter.
Vianna et al.97 clearly documented a specialized venous arrangement at the terminal esophagus (Fig. 14-23). These venous anastomoses have been
suggested to possibly supply communication between the azygos and the portal system. The intermediate "palisade zone" (Fig. 14-23) may act as a
high-resistance watershed between both systems, providing bidirectional flow.97
Fig. 14-23.

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Radiographic illustration of venous circulation in middle and lower esophagus, esophagogastric junction, and stomach after injection with barium gelatin.
Various zones present different venous architecture. A few longitudinally arranged veins in truncal zone (TZ), additional transverse veins in perforating zone
(PfZ), unique arrangement of veins in palisade zone (PZ) that seems to correspond to area of ampulla of radiologists, and gastric zone (GZ) with netlike
rearrangement of veins. (From Vianna A, Hayes PC, Moscoso G, Driver M, Portmann B, Westaby D, Williams R. Normal venous circulation of the
gastroesophageal junction. A route of understanding varices. Gastroenterology 1987;93:876-889, reprinted by permission.)

In a paper about progress and changes in surgery, Idezuki98 stated that over the last five decades, the accepted treatment of esophageal varices
with portal hypertension has moved from decompression shunts to selective shunts and direct operation, and now to endoscopic sclerotherapy,
sometimes combined with variceal ligation, or to transjugular intrahepatic portosystemic shunt. Hashizume et al.99 reported that laparoscopic gastric
devascularization and splenectomy for sclerotherapy-resistant esophagogastric varices in patients with hypersplenism is a feasible and relatively safe
procedure.
Jenkins et al.100 stated that distal splenorenal shunt is a safe, durable, and effective procedure for the treatment of recurrent bleeding secondary to

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Jenkins et al.100 stated that distal splenorenal shunt is a safe, durable, and effective procedure for the treatment of recurrent bleeding secondary to
gastroesophageal varices and portal hypertension in patients with acceptable operative risk and good liver function.

Lymphatic Drainage
Presumably due to the considerable technical difficulty of identifying the minute channels both in vivo and post mortem, anatomic knowledge of the
lymphatic system of the esophagus is extremely limited. Accounts of previous investigations have so far not been substantiated.4,23 Nevertheless one
may accept that the lymphatic system of the esophagus includes the lymph ducts and lymph nodes as described for other parts of the gut.
Lymph capillaries may commence in the tissue spaces as a network of endothelial channels (Fig. 14-24) or as blind endothelial sacculations (Fig. 1425) similar to those found in mesenteric tissues.101,102
Fig. 14-24.

Initial lymphatics (arrows) between lower border of tunica mucosa and tela submucosa in the histological (A) and electronmicroscopic (B) display. Taken from
gastric wall, but is relevant also for esophagus. MM, muscularis mucosae. (A, from Lehnert T, Erlandson A, Decosse JJ. Lymph and blood capillaries of the

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gastric wall, but is relevant also for esophagus. MM, muscularis mucosae. (A, from Lehnert T, Erlandson A, Decosse JJ. Lymph and blood capillaries of the
human gastric mucosa. A morphologic basis for metastasis in early gastric carcinoma. Gastroenterology 1985;89:939-950, reprinted by permission. B,
Courtesy Dr. Dorothea Liebermann-Meffert.)

Fig. 14-25.

Initial lymphatic network in mesentery originates in blind endothelial sacculations and small channels. Measurements refer to the diameter of the lymphatic
vessels. (Reconstruction from a preparation after direct in vivo injection of dye into lymphatic channels of greater omentum.) (Modified after Zweifach BW,
Prather JW. Manipulation of pressure in terminal lymphatics in the mesentery. Amer J Physiol 1975;228:1326-1335; with permission.)

The submucosa of the human stomach has recently been shown to contain a network of numerous lymph vessels. These show parallel orientation
along the longitudinal axis of the organ (Fig. 14-26). They send occasional branches to the collecting subadventitial and surface trunks.97 All these
channels possess valves (Fig. 14-25). Studies by Mayr and Liebermann-Meffert 103 using autopsy specimens and electron microscopic techniques imply
that a similar pattern is present in the esophagus. Initial lymphatics seem to originate exclusively in the region between the mucosa and submucosa
and to form longitudinally arranged collecting channels in the submucosa.

Fig. 14-26.

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Local lymphatic drainage within esophageal wall. A, Lymphatic flow as expected under normal healthy conditions and in early malignancy. Valves, present
even in small channels, determine the flow direction (see Fig. 14-27). B, Flow may reverse when tumor masses block lymphatic pathways; resulting elevated,
reversed pressure may interfere with function of lymphatic valves. (A, Modified from Liebermann-Meffert D, Duranceau A. Anatomy and embryology. In:
Orringer MB, Zuidema GD (eds). Shackelford's Surgery of the Alimentary Tract (4th ed). Vol I The Esophagus. Philadelphia: WB Saunders, 1996, pp. 3-38;
reprinted by permission. B, Courtesy Dr. Dorothea Liebermann-Meffert, modified.)

Fig. 14-27.

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Lymphatic pathways of esophagus. Also shows how, under normal conditions, lymph from areas above tracheal bifurcation empties cranially, and lymph from
below that point preferentially empties caudally to pass through celiac lymph nodes. Flow at tracheal bifurcation seems to be oriented bidirectionally. This
feature is essential to understanding of potential spread of malignancies. (Modified from Liebermann-Meffert D. Anatomy, embryology, and histology. In:
Pearson FG, Deslauriers J, Ginsberg RJ, Hiebert CA, McKneally MF, Urschel HC (eds). Esophageal Surgery. New York: Churchill Livingstone, 1996, pp 1-25,
reprinted by permission.)

The lymphatic trunks at the surface of the esophagus may drain into the regional lymph nodes. Lymph from the esophagus most likely drains into the
following lymph nodes104,105,106:
Paratracheal
Tracheobronchial bifurcation
Juxtaesophageal
Intraaorticoesophageal

The lymph of the abdominal esophagus empties into the following lymph nodes:
Superior gastric
Pericardiac
Inferior diaphragmatic

In noncancerous autopsy specimens, Liebermann-Meffert et al. and Mayr and Liebermann-Meffert 4,103,107 found only a few small lymph nodes in the
mediastinum. The lymph nodes were larger and more numerous around the tracheal bifurcation. Most of these contained black coal-like particles. The
authors could not determine whether these nodes drained the esophagus and/or the lungs or if they transported proximally or distally. This observation
coincides with the report of Wirth and Frommhold108 who found mediastinal lymph nodes in only 5 per cent of 500 normal lymphograms. The classical
chain of lymph nodes surrounding the esophagus as described in textbooks and illustrated by Netter83 could not be substantiated at this time.
POINTS OF CLINICAL AND SURGICAL RELEVANCE
The clinical observation that initial tumor spread follows the longitudinal axis of the esophagus within the submucosa rather than extending in a circular
manner supports the following concepts:
Lymph flows more readily longitudinally in the submucosal channels than through the few transverse connections in the muscle (Fig. 14-26)
Lymph flows only finally through the subadventitial lymphatics and small trunks into the mediastinal lymph nodes 4,23
As a consequence, esophageal tumors may spread far cranially or caudally within the esophageal submucosal channels before obstructing the lumen

The paucity of lymphatics within the lamina mucosa and the abundance of submucosal lymphatic channels101,109 (Fig. 14-26) may explain why
intramural cancer spreads predominantly within this layer. Undetected malignant mucosal lesions may be accompanied by extensive tumor spread
underneath an intact mucosa. Tumor cells may follow the lymphatic channels for a considerable distance before they pass the muscular coat to empty
into the regional lymph nodes.
Tumor-free margin at the resection line, as confirmed by the anatomic point of view (histologic), does not guarantee radical tumor removal. This
feature may be consistent with the relatively high postoperative recurrence rate at the resection line, including satellite tumors and metastasis in the
submucosa far distant from the primary tumor,25 even if the margins at the resection line had been previously tumor-free.
Law et al.110 reported that histologic tumor infiltration at the esophageal resection margins on patients with esophageal carcinoma most likely is not
responsible for leakage. The anastomotic recurrence was related to the length of esophageal resection margin.
From clinical observations in cancer patients,23,25,26 the following patterns may be deduced (Fig. 14-27):
Lymph from above the carina flows cranially toward the thoracic duct or the subclavian lymph trunks 31
Lymph from below the carina flows mainly toward the cisterna chyli via the lower mediastinal, left gastric, and celiac lymph nodes 31
Flow may change under pathological conditions.111 When lymph vessels become blocked and dilated due to tumor invasion, the valves become ineffectual
and the flow reverses (Fig. 14-26). This phenomenon explains the retrograde, unexpected spread of some of the malignant tumors, but limits the value of
establishing pathways of normal flow.

Nakagawa et al.112 reported that tumor angiogenesis expressed as microvessel density correlates with clinicopathologic parameters for tumor
progression. They consider this an independent prognostic indicator for patients undergoing extended radical esophagectomy for invasive [squamous
cell] esophageal cancer.

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Cooper et al.113 reported that combined chemoradiotherapy increases the survival rate of patients with squamous cell carcinoma or adenocarcinoma of
the esophagus over radiotherapy alone.

Innervation
The pharynx, larynx, and esophagus are innervated by both visceral components of the autonomic nervous system, the sympathetic and the
parasympathetic systems, which exert mutually antagonistic influences on the viscera.20,31,114,115 The sympathetic efferent pathways, common in
the gut, are concerned with vasoconstriction, contraction of sphincters, and relaxation of the muscular wall. The parasympathetic efferent fibers
increase the glandular and peristaltic activity of the gut.20
SYMPATHETIC NERVES
The sympathetic nerves supply the pharynx, larynx, and proximal esophagus through the cervical and thoracic sympathetic chains (Fig. 14-28). These
chains travel downward lateral to the spine and from the cardiobronchial and the periesophageal splanchnic nerves that arise from the celiac plexus.
Interlaced with fibers of the parasympathetic cervical and thoracic plexuses, the sympathetic nervous system uses the vagus nerve as a carrier for
some of its fibers.31
Fig. 14-28.

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Innervation of esophagus. (Modified from Liebermann-Meffert D, Duranceau A. Anatomy and embryology. In: Orringer MB, Zuidema GD (eds). Shackelford's
Surgery of the Alimentary Tract (4th ed). Vol I The Esophagus. Philadelphia: WB Saunders, 1996, pp. 3-38, reprinted by permission.)

PARASYMPATHETIC NERVES
The parasympathetic nerve supply is through the vagus, the tenth cranial nerve. The vagus carries general somatic and visceral sensory, skeletal
motor, and parasympathetic fibers to the esophagus. The laryngopharynx receives general somatic sensory and skeletal motor innervation via the
vagus nerve. The sensory neuron cell bodies contribute to forming the ganglion nodosum (Fig. 14-28).
The right and left vagi pass as thick trunks through the respective jugular foramina. The innervation of the musculature and mucosa of the pharynx,
larynx, UES, and upper half of the esophagus is by the bilateral superior laryngeal nerves (SLN) and/or inferior laryngeal (recurrent) nerves (RLN). The
SLN is said to be mainly sensory and secretory, although its external laryngeal branch is motor to the larynx and the cricopharyngeus. The RLN is
largely motor and supplies most of the laryngeal muscles and the UES.
The superior laryngeal nerve originates from the vagal trunk near the nodose ganglion, travels down alongside the carotid arteries, and divides into the
internal laryngeal branch and the external laryngeal nerve. This latter nerve supplies the cricothyroid muscle and the cricopharyngeus portion of the
inferior pharyngeal constrictor, which serves as the upper esophageal sphincter. The internal laryngeal nerve, containing parasympathetic and sensory
fibers, supplies the laryngeal mucosa above the vocal folds and the region of the piriform fossae.31,116-118
The RLN arises on the right side from the vagus nerve in front of the subclavian artery, turns backward around the artery (Fig. 14-28), and ascends
obliquely to the right lateral aspect of the trachea and posterior to the common carotid artery.31,116,117
On the left side the RLN arises from the vagus nerve in front of the aortic arch, turns backward around the aorta behind the ligamentum arteriosum,
and ascends obliquely to the left of the trachea.
As both RLNs travel cranially, they approach the esophagus and trachea, often positioning in the tracheoesophageal groove,117 and they distribute an
equal number of nerve fibers to both structures (Fig. 14-29). Reaching the pharyngoesophageal junction, both RLNs gain close proximity to the
esophagus, the left side usually closer than the right. Near the lower pole of the thyroid gland, both nerves are always intimately related to the gland
and often pass between branches of the inferior thyroid vessels (Fig. 14-29). Some of the nerve branches dip into the parenchyma of the gland.
Fig. 14-29.

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Example of innervation of laryngopharynx (1), cervical esophagus (2), and thyroid gland (3) in human autopsy specimen viewed from right lateral posterior
aspect. Right recurrent laryngeal nerve (4), sends branches alternatively to esophagus (2) and trachea (6) before its terminal branch enters larynx caudal and
lateral to cricopharyngeal muscle (7). Thyroid gland is pulled aside to display inferior thyroid artery (5) that entangles the recurrent laryngeal nerve. Note also
small nerve branches entering gland (8, arrow). (Courtesy Dr. Dorothea Liebermann-Meffert.)

On both sides, a single thick terminal branch of the RLN enters the larynx just below the cricopharyngeal muscle band (Fig. 14-29). Here both divide
into several branches to supply all the intrinsic laryngeal muscles (except the cricothyroid), including the arytenoid (vocal) and epiglottic muscles.
Occasionally the major terminal branch communicates with the superior laryngeal nerve107 (see Fig. 14-13).
Posterior to the lung hilum at the level of the tracheal bifurcation, the vagal nerves form a network of fascicles, the pulmonary and esophageal plexus.
The left vagus contributes primarily to the anterior, and the right vagus to the posterior esophageal plexus.
At the lower end of the esophagus, the fibers reorganize into two trunks that pass down on the anterior and posterior esophageal wall.118 Together
with the esophagus the vagi pierce the diaphragm, grossly recognizable under the phrenoesophageal membrane. The posterior vagus nerve divides into
smaller branches, 2 cm to 4 cm distant from the tube and to its right. The anterior vagus nerve is positioned to the left of the cardia and toward the
anterior gastric wall.

Points of Clinical and Surgical Relevance
In a study of management of patients with esophagectomies, Ferguson et al.119 calculated operative risks. Their results pointed to the importance of
preoperative evaluation of cardiopulmonary function, meticulous operative technique, and aggressive respiratory care. They noted that a preoperative
statistical predictive model must never be the sole criterion for selecting patients; surgical judgment must also play an important role.
Matsubara et al.120 reported that despite the risk known to accompany pulmonary surgery on patients also being surgically treated for cancer of the
thoracic esophagus, this combination of surgeries is not contraindicated for patients whose general condition is both adequate and accompanied by
acceptable risk factors.
During esophageal resection and thyroidectomies the recurrent laryngeal nerves are at high risk.107,115,116,121-123 Injuries involving both inferior and
superior laryngeal nerves cause clinical pictures of a variety of transient or even lasting motor and sensory disorders of the pharyngolaryngoesophageal
junction area. These can include hoarseness by vocal cord palsy and respiration and swallowing failures connected with problems of aspiration.
Dia et al.124 emphasized the risks of injury of the recurrent laryngeal nerve during transhiatal esophagectomy. In the adult they noted the constancy
of the low origin of the nerve under the aortic arch, its course in the tracheal angle, its close relation to the anatomic entities of the posterior
mediastinum, and its minimal anastomosis between the esophageal and tracheal nervous network. Dia and colleagues stated that perhaps nerve lesions
can explain the postoperative respiratory complications of this surgical approach. In patients with carcinoma of the thoracic esophagus, Matsubara et
al.125 recommended the cervicothoracic approach for total mesoesophageal dissection including the lymph nodes in the area of the recurrent nerve.

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Baba et al.126 reported that of 141 patients with esophagectomy for carcinoma, 51 experienced hoarseness from vocal cord paralysis (VCP) on release
from the hospital. For twenty-one of these patients (41%), VCP healed spontaneously within one year, and four patients healed within two years.
Many of those who experienced persistent VCP showed debilitation in climbing stairs, swallowing, etc.
Because of their positions, the vagus nerves, also, may be damaged during esophageal surgery. Injury to the vagal trunks is considered to produce
neurogenic dysphagia or gastric atony. Complete truncal vagotomy has been shown to abolish LES function. Selective denervation of the terminal
esophagus up to 5 cm to 7 cm cranial to the junction of the stomach, however, does not affect the resting tone of the LES or its competency. This
procedure is used for parietal cell vagotomy of the stomach in gastroduodenal ulcer patients.34
Differences of opinion abound in regards to several procedures for the surgical treatment of gastroesophageal reflux. Examples of recent studies are
listed here to emphasize the controversy:
Wetscher et al.128 reported that in patients with gastroesophageal reflux disease surgery is the treatment of choice, since medical treatment does not
control reflux or inhibit regurgitation, and has little effect on dysphagia.
Mason et al.129 reported that Nissen fundoplication prevents sphincter shortening and thereby makes the lower esophageal sphincter more competent
when challenged by progressive gastric distention.
Jordan and Thornby130 found that parietal cell vagotomy with Nissen fundoplication is a safe procedure that protects the vagal trunks, but that it
should be done only in patients with peptic ulcer disease.

Read an Editorial Comment
Farrell et al.131 compared the Nissen fundoplication (a 360° anterior wrap fundoplication) with the Toupet fundoplication (a 270° posterior wrap
fundoplication). They found that following the Nissen procedure, stomachs never refluxed until rupture; with the Toupet procedure, reflux occurred at
very low intragastric pressure (<2 mm Hg), above which no reflux occurred until rupture.
Gadenstätter et al.132 found partial posterior fundoplication an effective antireflux barrier for patients with impaired esophageal body motility;
postoperative dysphagia diminished with improved esophageal body function.
Pélissier et al.133 stated that a combination of posterior hemifundoplication and a short circular fundoplication with their fixation to crura is effective
and improves motor activity and prevents the occurrence of the Nissen procedure complications. It does not, however, alleviate side effects.
Horgan et al.134 concluded that the main reasons for failure of antireflux procedures is failure of the crural closure and malformation of the wrap. They
stressed the importance of proper surgical technique, meticulous closure, and appropriate construction and fixation of the wrap.
Spechler and colleagues135 caution that antireflux surgery for patients with gastroesophageal reflux disease (GERD) should not be undertaken with the
expectation that antisecretory medication can be abandoned. In patients with GERD and Barrett esophagus, surgical therapy alone will not prevent
esophageal cancer.
We quote Kahrilas136 :
Herein lies the good news for patients with GERD. Despite the heavy and long-term symptom burden it imparts on the population, GERD has a
remarkably low mortality rate. In fact, it can be argued that GERD mortality is too low to be significantly affected by any intervention in a
controlled trial.
Another implication of the low GERD mortality rate is that the yield of any preventive strategy for esophageal adenocarcinoma will be low at
best. Even among patients with Barrett esophagus, generally accepted to be at greatest risk, the annual incidence of esophageal
adenocarcinoma was only 0.4%.
Spivak et al.137 stated that laparoscopy provides optimal access to the gastroesophageal junction.
Richardson and Hunter138 reported that good results and low incidence of dysphagia are obtained when laparoscopic floppy Nissen fundoplication
includes fundus mobilization. Mobilization is performed by ligating the short gastric vessels and the posterior gastric vessels to reveal the base of the
left crus, removing all posterior gastropancreatic adhesions, and mobilizing the peritoneal fold.
Rantanen et al.139 reported complications between laparoscopic and open Nissen fundoplication.
With laparoscopic fundoplication:
a. 67% temporary dysphagia
b. 20% persistent dysphagia
c. 97% mild or no reflux
d. 50% bloating

With open fundoplication:
a. 41%

temporary dysphagia

b. 18%

persistent dysphagia

c. 100% mild or no reflux

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bloating

The authors of the above study concluded that, except for temporary dysphagia and belching ability, laparoscopic and open fundoplication produce
similar outcomes.
Karim et al.140 found no significant difference in postoperative complications (i.e., bloating, dysphagia) between the Nissen (total) and Toupet (partial)
procedures in patients with gastroesophageal reflux disease who had laparoscopic repair.
Coelho et al.141 stated, "Conversion and complications of laparoscopic fundoplication are low and decrease significantly with the surgeon's experience,
but severe and lethal complications may occur." These complications included pneumothorax, bleeding, acute pancreatitis, intraabdominal abscess,
esophageal perforation, sepsis, shock, and gastric obstruction secondary to fundoplication herniation.
Eshraghi et al.,142 after reviewing Nissen fundoplications performed in a single practice from January 1989 to March 1997, concluded that the
laparoscopic Nissen fundoplication is preferred over the open method for the treatment of gastroesophageal reflux.
Velanovich143 found equivalent symptom relief and quality of life improvement for laparoscopic and open surgery.
Frantzides and Richards144 stated that with strict criteria, experience, and standardization of technique the laparoscopic Nissen fundoplication is safe
and the results are effective for treating chronic symptoms of gastroesophageal reflux disease.
Wetscher et al.145 reported that laparoscopic Toupet fundoplication (partial posterior fundoplication) is a more effective antireflux procedure for
patients with poor esophageal peristalsis than the floppy Nissen fundoplication as it causes less esophageal outflow resistance and results in a low
incidence of postoperative dysphagia. Commenting on this paper, Jamieson146 stated that there is no better operation than loose total fundoplication
for all patients with uncomplicated gastroesophageal reflux disease.
Weber147 recommended Toupet fundoplication for the treatment of gastroesophageal reflux in children.
Dunn et al.148 recommended fundoplication and concomitant antroplasty in symptomatic children with documented gastroesophageal reflux and delayed
gastric emptying.
Floch et al.149 advised that failures of antireflux surgery may be corrected by laparoscopic antireflux procedures.
Ritter and colleagues150 reported an excellent outcome using the Collis-Belsey procedure in patients with advanced gastroesophageal reflux disease
without dysphagia. This procedure, which consists of gastroplasty for esophageal lengthening followed by partial fundoplication, was less effective for
patients with dysphagia as a preoperative symptom. They recommended esophagectomy for patients with dysphagia when there was a combination of
stricture and a profound loss of esophageal motility.
Patti et al.151 stated that laparoscopic antireflux procedures control the symptomatology of gastroesophageal reflux disease by (1) repairing the
hernia, (2) reducing the hiatus to a normal size, (3) dividing and ligating the short gastric vessels, and (4) using a partial or total wrap that is anchored
to the right or left crus.
Richardson and Bowen152 advocated minimally invasive esophageal surgery for antireflux procedures (fundoplication), achalasia (Heller myotomy), and
paraesophageal hernia. The authors stated that laparoscopic procedures achieved results equivalent to open surgery.
Aye et al.153 advised laparoscopic Hill repair in patients with reflux-associated abnormal motility.
Rydberg et al.154 hypothesized that adjusting antireflux surgery – either a total or partial wrap based upon the motor function of the esophagus – can
help avoid dysphagia and other obstructive complaints. With their randomized clinical trial, however, the authors demonstrated that esophageal motor
dysfunction could not be used to tailor antireflux surgery for patients with gastroesophageal reflux disease.
Szwerc et al.155 and Curet et al.156 reported that, although technically challenging, laparoscopic reoperation is safe and effective for patients with
recurrent esophageal reflux disease who have had a previous laparoscopic antireflux procedure.
Disagreement about the surgical treatment of esophageal neoplasia of epithelial and non-epithelial types also continues. Even the stomach has distinct
forms of epithelial malignancy. According to Driman and Riddell,157 adenocarcinoma of the gastric cardia differs distinctly from adenocarcinoma of the
body and antrum. Controversy also exists about the "ideal" or optimal mode of esophageal resection (transhiatal or transthoracic) and how much of the
esophagus should be removed when esophageal cancer is present.
Chu et al.158 stated that the transthoracic approach is preferred over the transhiatal approach for esophageal resection of lower-third esophageal
carcinoma. Pommier et al.159 reported that Ivor Lewis and transhiatal esophagectomies for esophageal cancer produce equivalent survival rates. Anikin
et al.160 advised total thoracic esophagectomy through the left chest with a separate left cervical incision for carcinoma of the esophagus. Swanstrom
and Hansen161 reported that despite the unknown role of laparoscopic total esophagectomy as a curative procedure in esophageal malignant process,
technically such a procedure is feasible, but also difficult.
However, Orringer et al.162 stated that transhiatal esophagectomy can be performed with greater safety and less morbidity than traditional
transthoracic approaches for most patients requiring esophageal resection for benign and malignant conditions.
Bumm et al.163 compared short- and long-term results of radical transhiatal esophagectomy (RTE) combined with two-field lymphadenectomy and
mediastinoscopic dissection of the upper thoracic esophagus (endodissection) with conventional transhiatal esophagectomy (THE) for adenocarcinoma

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of the distal esophagus. They reported that distal adenocarcinoma of the esophagus can be safely resected by RTE with two-field lymphadenectomy
and endodissection, and this technique permits radical "en bloc" resection of the tumor-bearing distal third of the esophagus (including the lower
mediastinum and paracardial region). RTE incurred fewer cardiac complications and a better overall survival in N1-positive patients when compared
retrospectively to THE.
Gluch et al.164 compared the transhiatal esophagectomy with the Ivor Lewis procedure and reported that neither procedure is preferable when patients
were matched for tumor type and stage. The authors concluded, therefore, that the transhiatal esophagectomy is a valid alternative to the Ivor Lewis
procedure.
Parshad et al.165 reported that adenocarcinoma of the distal esophagus and gastroesophageal junction may be treated by transhiatal esophagectomy
with good palliation and also with possible cure for stage I and II disease. We quote Law and Wong166 :
Whether the application of neoadjuvant therapies can replace more radical surgical approaches to local control and eliminate systemic
metastases remains to be proven. For locally advanced or metastatic tumors, primary chemoradiation seems a reasonable alternative.
There is still much debate over the use of extensive lymphadenectomy and partial or total esophagectomy in patients with carcinoma of the thoracic
esophagus. Nishihira and colleagues167 stated that extended lymphadenectomy of the cervical and superior mediastinal nodes may prevent recurrence
and prolong survival after resection of thoracic esophageal carcinoma.
In a study comparing total esophagectomy with proximal esophagectomy, Fujita et al.168 reported that "proximal esophagectomy with or without
laryngectomy and with cervical or upper mediastinal lymphadenectomy (or both) is better indicated for patients with an esophageal cancer localized at
the cervicothoracic junction unless the tumor involves the esophagus distal to the tip of the aortic arch and metastasis is found in the lymph nodes
caudal to the aortic arch preoperatively."
Baisi et al.169 reported that a radical esophagectomy is possible in 91% of patients with squamous cell carcinoma of the thoracic esophagus if
compression is slight and the tracheobronchial tree is not fixed. Bolton et al.170 presented the following anatomic complications of esophageal
resection for cancer:
Recurrent laryngeal nerve injury 3-16%
Anastomotic leak

3-39%

Anastomotic stricture

20-40%

Chylothorax

2%

Occasionally a patient with esophageal cancer at the cervicothoracic junction has no involvement of the larynx, trachea, pharynx, or distal esophagus.
For carefully selected patients in this situation Fujita et al.171 advised considering proximal esophagectomy without laryngectomy associated with
cervical and upper mediastinal lymphadenectomy through an upper median sternotomy followed by free jejunal transfer.
Healing of the cervical esophagogastrostomy is frequently impaired; leakage and stricture formation are common. Pierie et al.172 offer the following
guidelines for the procedure:
1. A handmade anastomosis is preferred over use of a circular stapler device.
2. Construction of a wide gastric tube, including preservation of the right gastric artery, is recommended.
3. The relatively safe cervical position of the anastomosis is preferred over an intrathoracic position.

In comparing stapled and hand-sewn esophagogastric anastomotic leaks, Beitler and Urschel173 reported equivalent leak rates. However, strictures
were more common with stapled anastomoses. They agreed with several other reports that technical errors and occult ischemia of the mobilized
gastric fundus are the two major causes of leakage.

ANATOMIC ENTITIES RECOMMENDED FOR ESOPHAGEAL REPLACEMENT AFTER ESOPHAGECTOMY OR
ESOPHAGOGASTRECTOMY

Stomach
To treat cancer of the esophagus, most surgeons use the stomach or the gastric tube26,80,174,175 to replace the partially or totally resected
esophagus (Fig. 14-30).
Fig. 14-30.

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Elongation of the stomach can be obtained by a longitudinal cut to lengthen it. A, Isoperistaltic cut. B, Retroperistaltic cut. (Modified from Earlam R. Surgical
treatment of carcinoma of the esophagus. In: Wastell C, Nyhus LM, Donahue PE (eds). Surgery of the Esophagus, Stomach, and Small Intestine (5th ed).
Boston: Little, Brown, 1995, pp. 254-269; with permission.)

The secret of good gastric mobilization is:
extensive Kocher maneuver
ligation of the right gastric and short gastric arteries
preservation of the gastroepiploic arteries (Fig. 14-31)

Fig. 14-31.

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Mobilization of the greater curve of the stomach, preserving the gastroepiploic artery (2a) and tying the short gastric vessels (2b). The line of resection is
near the gastroesophageal junction in high esophageal tumors or includes the lesser curve and the perigastric glands (14) extending to the origin of the left
gastric artery (5). (Modified from Earlam R. Surgical treatment of carcinoma of the esophagus. In: Wastell C, Nyhus LM, Donahue PE (eds). Surgery of the
Esophagus, Stomach, and Small Intestine (5th ed). Boston: Little, Brown, 1995, pp. 254-269; with permission.)

Liebermann-Meffert et al.27,175 reported that the right gastroepiploic (gastroomental) artery is the exclusive blood supply of the gastric tube. Other
arteries participating in very minor ways are:
Superior mesenteric
Left gastroepiploic
Submucosal capillaries and arterioles (especially in the cranial 20% of the greater curvature, which is used as a tube)

The same authors recommended gentle handling of the stomach.27,174
The following is the observation of Murakami et al.176 regarding anastomosing vessels of the gastric tube and vessels of the neck when the stomach is
used in esophageal reconstruction:
A significant increase in tissue blood flow was observed after venous anastomosis alone (mean, 19%, P <0.05) and after arterial and venous
anastomoses (mean, 43%, P <0.05). There was no anastomotic leakage or hospital death. . . This procedure may reduce the risk of anastomotic
leakage especially in the case of pharyngogastrostomy following total esophagectomy.

Colon
The right, transverse, or left colon may be used for esophageal replacement employing an isoperistaltic or retroperistaltic technique (Fig. 14-32).
Fig. 14-32.

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Colon replacement can be done by using the right colon (isoperistaltic, A) or the left and transverse colon (isoperistaltic, B) or retroperistaltic (C). (Modified
from Earlam R. Surgical treatment of carcinoma of the esophagus. In: Wastell C, Nyhus LM, Donahue PE (eds). Surgery of the Esophagus, Stomach, and Small
Intestine (5th ed). Boston: Little, Brown, 1995, pp. 254-269; with permission.)

Cheng et al.177 employed colonic replacement after esophagectomy in 240 cases. They recommended utilization of the left colic artery if possible, the
isoperistaltic position for replacement, and single-layer anastomosis. The same authors reported mortality to be 2.8%; morbidity, 17.5%; and incidence
of anastomotic leaks, 10.4%.

Small Bowel
Procedures for the use of small bowel for esophageal replacement are demonstrated in Figure 14-33.
Fig. 14-33.

Procedures to use after a total gastrectomy. A, The original Roux-en-Y procedure followed a partial gastrectomy with a gastrojejunostomy (1897). B, The
Roux-en-Y anastomosis can be done after a total gastrectomy with the esophagojejunal anastomosis above or below the diaphragm (see inset). C, The Roux
loop (1907) is different from a Roux-en-Y anastomosis and consists of a loop of jejunum completing normal continuity after a total gastrectomy. D, The Braun
anastomosis (1893) is another method used to divert bile from the lower esophagus. It is less efficient than a Roux-en-Y anastomosis, taking bile 25 cm away
from the esophagus. (Modified from Earlam R. Surgical treatment of carcinoma of the esophagus. In: Wastell C, Nyhus LM, Donahue PE (eds). Surgery of the
Esophagus, Stomach, and Small Intestine (5th ed). Boston: Little, Brown, 1995, pp. 254-269; with permission.)

The jejunum is used retrosternally or subcutaneously for palliation. Tachimori et al.178 reported reconstruction with jejunal interposition in cancer of
the cardia. DeMeester179 stated that the reconstruction reported by Tachimori limits the esophageal resection to the level of the inferior pulmonary
vein. DeMeester argued that this is inadequate because an esophageal margin of 10 cm or more should be removed above the tumor to avoid
recurrence.

Skin
Tubes formed by human skin are no longer used for esophageal replacement because of severe complications.

ANATOMIC COMPLICATIONS OF ESOPHAGEAL SURGERY
Anatomic complications of esophageal surgery are presented in Table 14-4.
Table 14-4. Anatomic Complications of Esophageal Surgery
Procedure

Vascular

Esophagoscopy (rigid
or flexible)

Hemorrhage Esophageal perforation, mediastinal
pleura tear and pneumothorax and
subcutaneous emphysema and
aspiration pneumonitis

Organ Injury

Sclerotherapy of
esophageal varices

Hemorrhage Esophageal perforation, esophageal
stricture

Hiatal herniorraphy

Hemorrhage, Esophageal perforation, vagal nerve Dysphagia, disruption of the posterior crural sutures with migration of the
chylothorax injury
fundoplication into the chest

Esophagomyotomy for Hemorrhage Reflux esophagitis, esophageal
achalasia
perforation, fistula formation,
iatrogenic hiatal hernia, dysphagia

Inadequate Procedure
No early diagnosis of complications

Myotomy too short or too long

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Diverticulectomy
a. Zenker

Hemorrhage Recurrent laryngeal nerve injury

Inadequate cricopharyngeal myotomy

b.
Supradiaphragmatic

Hemorrhage Injury of the vagal trunk or to
esophageal plexus, leak, fistula
formation, supradiaphragmatic
stricture, inadequate myotomy,
perforation, fistula

and upper esophageal myotomy, leak, fistula formation, supradiaphragmatic
stricture

Esophagectomy

Hemorrhage Puncture of aorta, perforation of
trachea, perforation of bronchus

Anastomotic leak, mediastinitis or peritonitis, anastomotic stenosis, partial
necrosis of greater curvature of stomach

Esophagogastrectomy Hemorrhage As above and spleen-bleeding,
As above and inadequate cancer procedures by not removing 2/3 of the proximal
pancreas-pancreatitis, diaphragmatic stomach and 10 cm of the lower esophagus up to the carina
paralysis sec. to disruption of
phrenic nerve, partial or total
necrosis of the gastric remnant
Interposition jejunum, Hemorrhage Infarction of jejunum or colon
As above and inadvertent jejunal twist with production of adhesions and
colon, stomach
secondary to venous ligation, pleura obstruction
injury and pneumothorax, recurrent
laryngeal nerve injury
Transhiatal
esophagectomy

Hemorrhage, Injury of the left thoracic duct
chylorrhea,
chylothorax

As above

Nissen,
transabdominal
fundoplication

Hemorrhage Pleural injury and pneumothorax,
esophageal perforation, gastric
perforation, spleen-bleeding, vagus
nerve injury, injury to left hepatic
vein, injury to inferior vena cava

As above and inadequate mobilization of abdominal esophagus, gastroesophageal junction and gastric fundus, wrap too tight: gas bloat, dysphagia,
wrap too loose, hiatal closure too tight, hiatal closure too loose, inadequate
suturing of fundoplication (unsecured), continuation of gastroesophageal reflux or
obstruction, herniation of fundoplication into the mediastinum

Gastropexy

Hemorrhage Spleen-bleeding, injury to left
hepatic vein-bleeding

As above and hiatus too tight, median arcuate ligament not present

Transthoracic Collis &
Nissen

Hemorrhage As above with esophageal
As above and unsecured fundoplication, disruption of fundoplication
perforation, vagus nerve injury,
injury of recurrent left hepatic artery,
inferior phrenic, left gastric, short
gastrics, inferior pulmonary vein

Source: Based on data from Orringer MB. Complications of esophageal surgery and trauma. In: Greenfield LJ (ed). Complications in Surgery and Trauma, 2nd Ed.
Philadelphia: JB Lippincott, 1990; with permission.

Pohl et al.180 classified complications of laparoscopic antireflux surgery as minor (not expected to result in permanent disability and/or not requiring
invasive treatment) and major (resulting in permanent disability and/or requiring invasive treatment). Their findings are summarized in Tables 14-5 and
14-6.
Table 14-5. Frequency of Minor Complications Stratified by Primary Operations and Reoperations
Primary Operations (n = 500)

Reoperations (n = 38)

Total (N = 538)

Ileus

30 (6.0)*

7 (18.4)

37 (6.9)

Pneumothorax

11 (2.2)

2 (5.3)

13 (2.4)

Urinary retention

10 (2.0)

0

10 (1.9)

Other

8 (1.6)

0

8 (1.5)

Total

59 (11.8)

9 (23.7)

68 (12.6)

*P = .002.
Source: Pohl D, Eubanks TR, Omelanczuk PE, Pellegrini CA. Management and outcome of complications after laparoscopic antireflux operations. Arch Surg
2001;136:399-404; with permission.
Table 14-6. Frequency of Major Complications Stratified by Primary Operations and Reoperations
Primary Operations (n = 500)

Reoperations (n = 38)

Total (N = 538)

Dysphagia

9 (1.8)

2 (5.3)

11 (2.0)

Liver trauma

2 (0.4)

0

2 (0.4)

Acute herniation

1 (0.2)

0

1 (0.2)

Perforated viscus

1 (0.2)*

3 (7.9)*

4 (0.7)

Reoperation

3 (0.6)

1 (2.6)

4 (0.7)

Death

2 (0.4)

0

2 (0.4)

Total

18 (3.6)*

6 (15.8)*

24 (4.5)

*P <.05.
Source: Pohl D, Eubanks TR, Omelanczuk PE, Pellegrini CA. Management and outcome of complications after laparoscopic antireflux operations. Arch Surg
2001;136:399-404; with permission.

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REFERENCES
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2. Moore KL. The Developing Human: Clinically Oriented Embryology, 4th Ed. Philadelphia: Saunders, 1988, pp. 217-222.
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York: Springer, 1990, pp. 516-570.
4. Liebermann-Meffert D, Duranceau A. Anatomy and embryology. In: Orringer MB, Zuidema GD (eds). Shackelford's Surgery of the Alimentary Tract
(4th ed). The Esophagus, Vol I. Philadelphia: WB Saunders, 1996, pp. 3-38.
5. Liebermann-Meffert D. Form und Lageentwicklung des menschlichen Magens und seiner Mesenterien. Acta Anat (Basel) 72:376-410, 1969. [PubMed:
5812064]
6. Liebermann-Meffert D. Die Entwicklung der Mesenterien des menschlichen Oberbauches unter neuen Gesichtspunkten. Acta Anat (Basel) 75:373395, 1970. [PubMed: 5471624]
7. Hillemeier C. Development of the esophagus. In: Lebenthal E (ed). Human Gastrointestinal Development. New York: Raven Press, 1989, pp. 241-250.
8. Daseler EH, Anson BJ. Surgical anatomy of the subclavian artery and its branches. Surg Gynecol Obstet 1959;108:149-174. [PubMed: 13625063]
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