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- •Contents
- •Contributors
- •Preface
- •1. A Focused History of Surgery
- •2. Preoperative and Postoperative Management
- •3. Endoscopy and Endoscopic Intervention
- •4. Fundamentals of Laparoscopic Surgery
- •5. Laparoscopic Staging and Approaches to Cancer
- •6. Incisions, Closures, and Management of the Abdominal Wound
- •7. Hernias
- •9. Intestinal Stomas
- •10. Abdominal Abscess and Enteric Fistulae
- •11. Gastrointestinal Bleeding
- •12. Management of Abdominal Trauma
- •13. Abdominal Vascular Emergencies
- •14. Benign Esophageal Disorders
- •15. Gastroesophageal Reflux Disease and Hiatal Hernia (Including Paraesophageal)
- •16. Perspective on Benign Esophageal Disease
- •17. Cancer of the Esophagus
- •18. Surgical Procedures to Resect and Replace the Esophagus
- •19. Video-Assisted Thoracic Surgery of the Esophagus
- •20. Perspective on Malignant Esophageal Disease
- •21. Benign Gastric Disorders
- •22. Gastric Adenocarcinoma and Other Gastric Neoplasms (Except Gastrointestinal Stromal Tumors)

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PERSPECTIVE ON MALIGNANT ESOPHAGEAL DISEASE
Thomas R. DeMeester
20A
It was a pleasure to receive a letter from Dr Michael Zinner
inviting me to write a perspective on the chapters of Dr
Simon Law’s group from Hong Kong on the diagnosis and
treatment of esophageal cancer, Dr David Sugarbaker’s group
from Boston on the techniques used to resect the esophagus
and reconstruct the foregut, and Dr James Luketich’s group
from Pittsburgh on minimally invasive esophagectomy. Of
truth, I have rarely read such well-written and thoroughly
thought-out reviews. While reading, I identi ed areas where
I was motivated to comment on the discussion from my
personal experience. ese usually took the form of helpful
thoughts or alternatives. Occasionally, they raised a note of
caution or took a controversial point of view.
e reason for the dramatic rise in adenocarcinoma of
the esophagus continues to remain a mystery even though it
represents the largest epidemiologic change ever recorded for
a solid cancer. e rise is largely con ned to the Caucasian
population and is widely attributed to gastroesophageal re ux
disease and its complication, Barrett’s esophagus. Some have
also evoked the rise in obesity as the cause. Based on sound
logic, I still support the hypothesis that potent acid suppression therapy played a role in the epidemiologic change. e
incidence of adenocarcinoma began to rise in 1975; the same
time acid suppression with H
able. Over time the H
ton pump inhibitors that had a greater capacity to suppress
acid. Although this hypothesis has been di cult to prove short
of a large and long prospective randomized study, an unbiased
review of the small nonrandomized studies published in the
surgical and medical literature to date will convince the practitioner of the truth of this hypothesis. A recent study
that medically treated patients who had relief or mildly persistent re ux symptoms while on proton pump inhibitors have
signi cantly higher odds of developing esophageal adenocarcinoma than medically treated patients who have persistent
severe re ux symptoms. My explanation for this observation
is that acid suppression therapy decreases re ux symptoms by
decreasing the acid content of gastric juice and causing the
2
blockers became widely avail-
2
blockers were largely replaced by pro-
1
showed
pH to rise from less than 2 to 4 or greater, that is, in the range
of a weak acid. On the stealth side, this increase in pH also
increases the solubility of bile acids in the re uxed neutralized
gastric juice. Bile acids at the pH of 4–6 have ready access
into the Barrett’s epithelial cell. When in the cell, bile acids are
known stimulants of CDX2, the most powerful genetic stimulus for the development of intestinal metaplasia. ey also
stimulate the expression of genes involved in the carcinogenesis of intestinalized Barrett’s epithelium to adenocarcinoma.
In contrast, the persistence of severe re ux symptoms while on
medication indicates incomplete acid suppression. e persistent acidic gastric juice causes bile acids to precipitate out of
solution. is nulli es their e ect, hence less or no intestinal
metaplasia or adenocarcinoma.
I take exception, as does Dr Law, with the current dogma
that there is no evidence proving that surveillance will result
in a better survival of patients with Barrett’s esophagus who
progress to adenocarcinoma. Rather, I believe that all individuals who are identi ed as having Barrett’s esophagus should
enter a surveillance program. In our experience surveillance
of patients with Barrett’s esophagus does detect tumors at an
earlier stage. Indeed, the percentage of patients presenting
with an early T1 N0 adenocarcinoma has increased over time
and, in the more recent years, account for nearly 50% of all
resected tumors. Looked at from a di erent perspective, 86%
of esophageal adenocarcinomas identi ed by Barrett’s surveillance have stage I disease.
In the new staging system cancers of the gastric cardia
that extend into the gastroesophageal junction are classi ed as adenocarcinomas of the esophagus rather than the
stomach. is is an improvement but still is imprecise due
to the inability to consistently de ne the location of the gastroesophageal junction. In 2000, the Association of Directors of Anatomic and Surgical Pathology de ned the gas-
troesophageal junction as a horizontal line drawn across the
end of the tubular esophagus at the point where it begins
to are into the stomach. Using this de nition, there is evidence that adenocarcinomas of the gastric cardia commonly
433

434 Part III Esophagus
arise in areas of intestinal metaplasia within the gastric cardia that have strong similarities to adenocarcinomas of the
distal esophagus. We have suggested that the location of
thegastroesophageal junction is dened more accurately by
histology as the proximal limit of gastric oxyntic mucosa.
e area cephalad to this limit is histologically the esophagus and in normal people is lined by squamous epithelium
and in patients with reux is lined, to a variable extent, with
dierent types of metaplastic columnar epithelium (cardiac,
oxyntocardiac, and intestinal). Important to understanding
disease at this location is to obtain an accurate estimate of
the incidence of Barrett’s adenocarcinoma. With greater precision it is likely that the number of Barrett’s adenocarcinomas would be more than double. is would give us a greater
appreciation for the exponential rise of adenocarcinoma in
this area and could well make the screening of patients with
Barrett’s more cost-eective.
Endoscopic surveillance of patients with Barrett’s
esophagus has identied a rather large number with highgrade dysplasia in the Barrett’s segment. Most regard this
nding as a threshold for intervention. e new technique
of endoscopic mucosal ablation has allowed the treatment
of high-grade dysplasia with preservation of the esophagus
and a morbidity and mortality lower than an esophagectomy.
e survival following either treatment is similar. is has
reduced the use of surgical resection to treat these patients.
Many, however, have visible lesions within the at Barrett’s
segment such as a nodule or ulcer. Such lesions must be
removed by endoscopic mucosal resection to determine the
nature of the lesion and, if a cancer, its depth of penetration into the esophageal wall. If a cancerous lesion is limited
to the lamina propria, ablation of the Barrett’s segment can
proceed. If a cancerous lesion extends beyond the muscularis
mucosa, there is a signicant increase in the probability of
lymph node metastasis and an esophagectomy is required.
Despite awed statements to the contrary, there is no “safe”
level of invasion into the submucosa that would extend the
use of endoscopic resection. To manage these patients correctly requires that surgeons become adept at endoscopy and
endoscopic mucosal resection. e opportunity for this training is limited and is an issue that must get the attention of the
Residency Review Committee for Surgery and the American
Board of Surgery. e new therapy is extremely work intensive and is associated with the risk of developing cancer during the treatment. Consequently a vigilant support sta is
necessary to handle the patients. In our experience patients
who have high-grade dysplasia in a long segment of Barrett’s
esophagus, or in an anatomically short esophagus with a
large hiatal hernia, or in an esophagus with a severe motility
problem, or have multifocal high-grade dysplasia or multiple
failures of ablation therapy are not candidates for esophageal
preservation therapy and are better o having a vagal sparing esophagectomy. is form of esophagectomy is associated
with less perioperative morbidity and a shorter hospital stay
than a standard transthoracic or transhiatal esophagectomy.
Further, its late morbidity, including weight loss, dumping,
and diarrhea, is signicantly less.
2
Surgical resection remains the mainstay of treatment for t
patients with localized esophageal carcinoma that has invaded
into the submucosa or beyond. In my mind, the only exception to this rule is a cervical esophageal cancer that is located
suciently close to the cricopharyngeal muscle to prevent a
clear resection margin. ese patients are better o receiving
denitive radiochemotherapy. If a recurrence occurs, a pharyngolaryngoesophagectomy is performed as a salvage procedure. It is critical that these patients understand this approach
prior to treatment and are willing to submit to yearly surveillance after the denitive radiochemotherapy. Fit patients
with tumors in the lower cervical or upper thoracic esophagus
are treated with cytoreduction of the tumor by radiochemotherapy followed by resection and reconstruction with a free
jejuno-interposition. Fit patients with tumors in the mid or
lower thoracic esophagus, gastroesophageal junction, or gastric cardia are treated with an en bloc esophagectomy and
complete lymphadenectomy. e superiority of this approach
has become gradually apparent over the years with the greatest benet seen in patients with fewer than eight lymph nodes
involved in specimens that contain more than 30 resected
nodes. e historical development of this position is nicely
documented in the 10 publications.
3–13
Critical in performing an en bloc esophagectomy is that
the proximal, distal, and radial margins are free of tumor. I
agree with Dr Law’s comment that the proximal esophageal
margin is most critical and a good guide is to obtain 10 cm
of grossly normal esophagus above the superior margin of the
tumor. After removal, the fresh specimen contracts to approximately 50% of its length or down to 5 cm of grossly normal
appearing esophagus. With this length of margin, there is less
than a 5% chance of an anastomotic recurrence. Similarly, it
is important to have a greater than l-mm free circumferential
radial margin on the specimen after a curative resection. is
has been shown to be an important independent prognos-
13
tic variable.
Simply put, patients with less than a 1-cm free
circumferential radial margin in what would otherwise have
been a curative resection doubles their risk of dying from cancer. As would be expected, the eect of a clear circumferential
radial margin is most important in patients who have limited
or no lymph node involvement.
An en bloc resection includes a complete lymphadenectomy.
e number of lymph nodes removed is an independent
predictor of survival. To maximize this survival benet, a
minimum of 23–29 nodes need to be removed. Taking additional nodes is of benet, but the eect begins to drop o.
When analyzed by Cox regression, the number of lymph
nodes removed modeled as a continuous variable was the
third most important prognostic factor behind the number of
involved nodes and the depth of tumor invasion. Of the three
factors, the number of nodes removed is the only predictor of
survival that can be inuenced by the surgeon. e operation
most likely to maximize the number of nodes removed is the
two-eld en bloc esophagectomy.
I am not convinced that adding a third eld, that is a
cervical node dissection, improves the survival suciently
to overcome the increased morbidity. Rather, we have taken

Chapter 20A Perspective on Malignant Esophageal Disease 435
the approach of obtaining a positron emission tomography
(PET) scan and ultrasound examination 1 year after the initial
resection and performing a modied radical neck dissection
if involved neck nodes are detected or suspected. An exception to this policy is when unsuspected involved recurrent
laryngeal nodes are discovered while performing the neck
dissection during the initial operation in preparation for a
neck anastomosis. In this situation a cervical node dissection
is added to the initial operation to remove recurrent laryngeal
and deep cervical nodes on the left.
In a unique study, the en bloc and transhiatal resections
were compared using a retrospective case-control study of
nonrandomized patients with similar-size transmural tumors
(T3) and lymph node metastasis selected at random from
our registry. e result showed that the survival benet of
an en bloc resection was limited to patients with eight or
fewer involved nodes. ere was no dierence in outcome
when nine or more lymph nodes were involved. When this
information was applied to the 5-year outcome of the only
randomized studies done to compare the two resections, only
those patients with one to eight involved lymph nodes signicantly beneted from an en bloc resection. is nding ts
with the results of a multi-institutional international study
showing that the probability of systemic disease is 50% when
three nodes are involved and approaches 100% when more
than eight nodes are involved. Based on these studies, the en
bloc resection is most likely to benet patients with eight or
fewer lymph nodes involved. Beyond this number the likelihood of systemic disease approaches 100%, and neither an en
bloc nor a transhiatal resection provides a long-term benet.
e most dreaded complication of esophagectomy is ischemic injury to the conduit used for reconstruction. is is
often the cause for an anastomotic leak and a cascade of sepsis, multiorgan failure, and death. Factors known to contribute to this complication are diabetes, hypertension, cardiac
arrhythmia, chronic obstructive pulmonary disease, and neoadjuvant therapy. Indeed, I believe that conduit ischemia is
the “Achilles heel” of a successful esophageal resection and
reconstruction. When faced with a worrisome ischemic conduit, we pull the conduit up and anchor it in the neck without performing the anastomosis. A Prolene stitch is placed
into the conduit and brought out to the subcutaneous tissue
for a guide to nd the conduit at the time of delayed reconstruction. e proximal esophageal remnant is brought out
to the neck as an esophagostomy and a feeding jejunostomy
constructed in the abdomen. Ninety days after the esophagectomy, a cervical esophagogastrostomy is performed through
the original neck incision. Over the years we have used this
strategy in 35patients. At the time of reconstruction, all had
well-perfused gastric conduits and the delayed anastomosis
healed without a leak, wound infection, or sepsis.
14
As Dr Law pointed out, the past two decades have witnessed
a proliferation in chemotherapy and chemoradiotherapy
trials in esophageal cancer. e basis for this explosion is the
suboptimal surgical cure rate for advanced cancer. True, distant failure remains a major problem in patients with advanced
cancer, and a search for more eective systemic drugs as wellas
a method to select the right drugs for the right patient needs
to be supported and encouraged. I agree with Dr Law that
currently the results of neoadjuvant chemoradiation therapy
are conicting, and that published meta-analysis show minimal to no benet. Despite this, neoadjuvant chemoradiation
is widely practiced in the United States. A limitation of the
current randomized trials is the lack of accurate staging prior
to randomization. If randomization is done correctly, major
known factors that aect survival, such as stage of disease,
need to be evenly distributed in the study groups prior to
randomization as the concept of randomization is used only
to manage unknown factors that aect survival. I have concluded that the studies done to date have shown neoadjuvant
therapy to be only eective in causing cytoreduction of the
primary tumor. e lack of a similar response in the secondary lesions is an indication that their sensitivity to chemotherapy is dierent than the primary tumor, perhaps through
tumor cell interaction with host tissues cells and their cellular
immune response. I would recommend that future neoadjuvant studies be done only on patients of similar stage based
on carefully done pretreatment minimally invasive surgical
staging. I would also suggest an adjuvant chemotherapy trial
where the chemotherapy given is based on chemosensitivity
studies done on the involved lymph nodes removed at the
time of surgery or on biopsies of solid-organ metastasis done
at the time they are discovered after surgery. Clearly, a new
approach is needed. e movement toward denitive chemotherapy is based on its known cytoreduction eect on the
primary tumor. e concept is designed to eliminate surgical
therapy because surgery as currently performed has failed to
control local disease. is is largely due to the resistance and
inability of surgeons to perform an en bloc resection. After
an appropriately done en bloc resection the local recurrence
rate is less than 2% whereas after transhiatal resection it is
25% or greater. My concern is that our failure to centralize
esophageal surgery in the United States, as is currently being
done in England, will relegate surgical therapy from a primary position in esophageal cancer to an adjuvant role.
Dr Wee and Dr Sugarbaker provide an excellent descrip-
tion of the en bloc esophagogastrectomy done through what
is known as the tri-incision or McKeown technique. We perform the operation similar to their description with a few
exceptions. We begin in the right chest by dividing the intercostal veins as they join the azygos vein from the arch down to
the diaphragmatic hiatus. We then dissect out the intercostal
arteries and follow them to where they join the aorta. e
aorta is then easily skeletonized from the right and over into
the left chest as the left intercostal arteries pass directly posterior to the costospinous junctions and have never interfered
with this dissection. e mobilized azygos vein is divided at
its junction with the superior vena cava. Both the azygos vein
and the thoracic duct are taken with the specimen. e distal
azygos vein and thoracic duct are ligated adjacent to the spine
deep within the esophageal diaphragmatic hiatus, using a laparoscopic endo-loop. e proximal thoracic duct is divided
later in the dissection and does not leak because of proximal
valves. Both the right and left sides of the chest are drained

436 Part III Esophagus
using ½-in Jackson-Pratt (J-P) drains positioned adjacent to
the spine on the right and aorta on the left and both resting
on the posterior chest wall. e drains are placed through the
esophageal diaphragmatic hiatus during the abdominal portion of the procedure after the specimen has been removed
and before the gastric conduit has been pulled up. e drains
are brought out through stab wounds in the right and left
upper quadrant. is allows the right and only chest tube
to be removed on the rst or second postoperative day. We
also skeletonize the superior and anterior wall of the common
and right hepatic artery, the superior and inferior wall of the
portal vein, and the superior and anterior wall of the splenic
artery out to the splenic hilum. Skeletonizing the inferior wall
of the portal vein is done by using a vein retractor to displace
the vein caudally and using the cautery along the superior
border of the pancreatic head. e width of our gastric conduit is 3–4 cm, and a pyloroplasty is performed using an endto-end stapler (EEA, US Surgical, Norwalk, CT) inserted
through the conduit staple line near the antrum and taking
a cookie bite out of the anterior portion of the pyloric ring.
Dr Luketich’s group deserves the credit for being on the
frontier of adapting esophagectomy into a laparoscopic and
thoracoscopic procedure. eir work is commendable and has
shown that there is some reduction in procedural morbidity,
postoperative discomfort, and length of hospital stay, but not
as much as one would suspect. To their credit they appear not
to have limited the extent of the resection to accommodate
the new approach but rather creatively altered their approach
to maintain the extent of the dissection. ere is a point
when the benets of minimally invasive surgery are overcome
by the extensiveness of the internal surgical dissection and
manipulation. When that point is reached, the advantages of
a minimally invasive procedure will diminish and the world
of surgery will continue to do such a procedure openly until
further technological developments occur that will allow us
to go further in our quest for “user-friendly” surgery. I believe
minimally invasive esophagectomy is near that point.
REFERENCES
1. Nason KS, Wichienkuer PP, Awais O, et al. Gastroesophageal reux disease
symptom severity, proton pump inhibitor use, and esophageal carcinogenesis. Arch Surg. 2011;146:851–858.
2. Peyre CG, DeMeester SR, Rizzetto C, et al. Vagal-sparing esophagectomy:
the ideal operation for intramucosal adenocarcinoma and Barrett with
high-grade dysplasia. Ann Surg. 2007;246:665–674.
3. DeMeester T, Zaninotto G, Johansson KE, et al. Selective therapeutic approach to cancer of the lower esophagus and cardia. J orac Cardiovasc Surg.
1988;95:42–52.
4. Letters to the editor; J Kirklin J, Blackstone E. e DeMeester paper on
carcinoma of the esophagus. J orac Cardiovasc Surg. 1990;100:456–458.
5. Hagen J, Peters JH, DeMeester TR, et al. Superiority of extended en
bloc esophagogastrectomy for carcinoma of the lower esophagus and
cardia. J orac Cardiovasc Surg. 1993;106:850–859.
6. Hagen J, DeMeester SR, Peters JH, Chandrasoma P, DeMeester TR.
Curative resection for esophageal adenocarcinoma, analysis of 100 en bloc
esophagectomies. Ann Surg. 2001;234:520–531.
7. Hulscher JBF, van Sandick JW, de Boer AG, et al. Extended transthoracic
resection compared with limited transhiatal resection for adenocarcinoma
of the esophagus. N Eng J Med. 2002;347:1662–1709.
8. Johansson J, DeMeester TR, Hagen JA, et al. En bloc vs. Transhiatal
esophagectomy for stage T3 N1 adenocarcinoma of the distal esophagus.
Arch Surg. 2004;139:627–633.
9. Portale G, Hagen JA, Peters JH, et al. Modern 5-year survival of resectable esophageal adenocarcinoma: single institution experience with 263
patients. J Am Coll Surg. 2006;202:588–598.
10. Omloo JMT, Lagarde SM, Hulscher JBF, et al. Extended transthoracic
resection compared with limited transhiatal resection for adenocarcinoma
of the mid/distal esophagus: ve-year survival of a randomized clinical
trial. Ann Surg. 2007;246:922–1001.
11. Peyre CG, Hagen JA, DeMeester SR, et al. e number of lymph nodes
removed predicts survival in esophageal cancer: an international study on
the impact of extent of surgical resection. Ann Surg. 2008;248:549–556.
12. Peyre CG, Hagen JA, DeMeester SR, et al. Predicting systemic disease
in patients with esophageal cancer after esophagectomy: a multinational
study on the signicance of the number of involved lymph nodes. Ann
Surg. 2008;248:979–985.
13. Dexter SP, Sue-Ling H, McMahon MJ, Quirke P, Mapstone N, Martin
IG. Circumferential resection margin involvement: an independent predictor of survival following surgery for oesophageal cancer. Gut. 2001;48:
667–670.
14. Oezcelik A, Banki F, DeMeester SR, et al. Delayed esophagogastrostomy:
a safe strategy for management of patients with ischemic gastric conduit at
time of esophagectomy. J Am Coll Surg. 2009;208:1030–1034.

PERSPECTIVE ON
MALIGNANT ESOPHAGEAL
DISEASE
Lee L. Swanstrom
20B
Descriptions of the techniques and reasons for esophageal
resections are presented by three leaders in esophageal surgery, working at major, high-volume esophageal centers. A
thorough review of the epidemiology (such as is known) and
international di erences in approaches and outcomes for
esophageal cancer treatments is made by Dr Law who points
out the ever-increasing di erences between the Western and
Eastern hemispheres. In the East and Middle East, mid and
proximal squamous cell cancers are by far the most prevalent,
related to the persistence of carcinogenic environmental exposures. e rapid growth of adenocarcinoma in the West is a
more complex issue; at our center, Barrett’s esophagus–related
cancers now represent 92% of esophageal cancers presenting
for treatment. Unfortunately this is not totally related to the
decrease in squamous cancers secondary to the decreasing
incidence of smoking and other environmental factors. It is
more related to the incredibly rapid growth in the incidence
adenocarcinoma—now the most rapidly increasing cancer
in North America. As Dr Law points out, this is probably
related to the increasing incidence of both morbid obesity
and gastroesophageal re ux (GER). An additional factor in
either the development or, more likely, the progression to
cancer may be the widespread use of proton pump inhibitors (PPIs) as a symptomatic treatment of GER. Avissar et al
have shown that, at the biologic level, genetic damage that is
related to dysplasia progression is facilitated by the pH environment created by usual doses of PPIs.
that many patients with Barrett’s esophagus have no or minimal GER symptoms complicates the possibility of screening
to turn the tide of this cancer. Dr Law presents the arguments against screening very well—basically, too rare a cancer
in too large an “at-risk” population. ere remains a movement, however, that argues strongly for screening of high-risk
individuals.
the high percentage of Barrett’s esophagus in the gastroesophageal re ux disease (GERD) population (8–17%), and
the 0.5–1% per annum dysplasia progression, which screening advocates describe as the equivalent risk pro le of colon
2
eir argument includes the ease of screening,
1
Certainly the fact
polyps. Colon polyps occur in 15% of colonoscopies, have a
cancer progression risk of 0.5–1% per year, and yet claim a
high priority for endoscopic screening. Finally, the argument
that Barrett’s screening is irrelevant because nothing would be
done for anything but high-grade dysplasia (HGD) Barrett’s
esophagus is falling by the way as technologies like radiofrequency ablation (RFA) or cryotherapy show good e cacy at
eradicating Barrett’s esophagus
surgery induces regression in 30–40% of cases.
we may still see a future where routine screening for Barrett’s
esophagus makes sense, particularly as cancer rates continue
to increase and better risk factor strati cation is developed.
All three chapters cover the never-ending controversy over
the transhiatal/transthoracic approaches. Save the obvious
holdout,
node-removing approach with a very gradual shift in outcomes
data to support better cancer outcomes with en bloc resection
at the cost of markedly increased operative morbidity.
introduction of laparoscopic/thoracoscopic surgical approaches
has further muddied these waters. is confusion arises from
the con ict between the aspects of minimally invasive esophagectomy (MIE) that emphasizes less patient morbidity (with
perhaps the implication of poorer oncologic outcomes) versus
the absolute push for curative resection (for those that survive the surgery). is movement toward “less invasiveness” is
not unexpectedly resisted by many established programs who
have worked hard to optimize surgical outcomes for esophageal cancers and who are sought out by patients familiar with
their well-publicized expertise. e majority of institutions,
however, are faced with the referral dilemma engendered by
the perception of esophagectomy being a highly morbid procedure, with poor long-term quality of life and having no survival advantage over chemoradiation. An actual quote from a
leading medical periodical states “Recent trials fail to identify
any signi cant advantage associated with the routine use of
surgery for most patients.”
endoscopic techniques is inevitable—not only because it o ers
a new paradigm of a better (or equivalent) oncologic outcomes
7
there seems to be a gradual move to a more aggressive
3,
4 and laparoscopic antire ux
9
In my opinion, the migration to
5
erefore,
8
e
6
437
437

438 Part III Esophagus
due to better imaging, better access, and less patient morbidity,
but also because most surgeons will never see patients with
esophageal cancer in referral if all they oer is “traditional”
esophagectomy. Arguments for minimally invasive approaches
to GI cancers have intrinsic appeal: applying the “minimally
invasive philosophy” to evidenced-based colorectal cancer
treatments has resulted in recommendations that all colorectal
cancers be approached laparoscopically whenever possible. In
2009, the National Health Service (NHS) in the United Kingdom, recognizing the preponderance of data in support of an
10
MIS approach, mandated its use to all HMS participants.
I
would propose that esophageal cancer treatments will eventually follow the same path.
As both Dr Sugarbaker and Dr Luketich have emphasized, esophagectomy is all about the details. is is true
both for intraoperative technique and for postoperative care.
Increasingly, it is obvious that to achieve a lower mortality
and morbidity rate, the institutional system may be more
important than a particular surgical approach or even to the
11
experience of the surgeon.
Ideally though, esophagectomy
is done both by a skilled experienced surgeon and in a highvolume system-oriented institution. Nonetheless, it is eternally interesting for surgeons to discuss the operative details
of a surgical procedure and esophagectomy is a fertile eld for
controversy and diering opinions.
To date, most MI esophagectomy techniques have
sought to replicate their open equivalents, but the focus
is on the minimally invasive approach; this has led to an
implication that minimally invasive approaches would be a
patient-pleasing compromise to oncologic outcomes. Perhaps a better mindset would be to address the question:
Can the potential advantages of an MI approach (magnication, precision, shorter hospital stay, fewer wound
complications, quicker return to presurgical activity levels,
less immunosuppression) be hybridized onto current established techniques? Our group has explored the possibility
of using laparoscopy or thoracoscopy to replicate en bloc
esophagectomy in a less morbid way—either by transhiatal laparoscopic en bloc esophagectomy for distal tumors
12
or thoracoscopic formal en bloc resections.
Replicating
the “gold standard” open procedure with no compromise
and with expected patient benet has been demonstrated
feasible by the aggressive program at the University of Pitts-
13
burgh.
Unfortunately it remains a consistent concern that
MI approaches take more time and demand extraordinary
(unobtainable?) skills. While the latter is perhaps irrefutably
true, but not insurmountable, the time element may require
innovative thinking to overcome.
STAGED ESOPHAGECTOMY
14
workload of an endoscopic approach.
No randomized comparisons have yet been published that would document any
advantages with this approach, but it has appeal for MIE as
it can be conceived as an initial staging laparoscopy followed
by the denitive resection 7 days later. Our current protocol
calls for laparoscopic staging, celiac/hepatic node dissection,
left gastric division, and placement of a feeding jejunostomy.
Changes in the thoracic portion of the procedure are an
interesting change from a standard approach. Cadier has
popularized the performance of the thoracic mobilization in
the prone position. is has the advantage of having gravity
as a retractor for the lung, which permits the surgeon to have
15
fewer ports and superb visualization.
We have also adopted
the use of positive-pressure capnothorax to perform thoracic
mobilization. is involves the use of standard laparoscopic
trocars rather than thoracoports without valves. e ports
are connected to a standard laparoscopic insuator set to a
low pressure (10 mm Hg) that eectively collapses the lung
without the need for a double-lumen endotracheal tube. is
has the additional advantage of displacing the mediastinum,
creating more operative space. Having used this technique
for the past 20 years, we have found that the vast majority of
patients will tolerate it and that the exposure and simplicity
of the approach are superior to standard VATS techniques.
A nal comment is made regarding the width of the gastric
conduit or “neoesophagus.” Narrow tubes versus wide tubes
versus full gastric pull-up remain a controversial topic. We
have favored a narrow conduit as per Akiyama, all be it at a
cost of a higher leak rate due to elevated intraluminal pres-
16
sures during the period of mucosal edema.
We feel that the
benets of long-term esophageal clearance and better swallowing outweigh the troublesome but self-limited risk of
anastomotic leaks. Once again, however, there is no prospective comparative data that conrm this personal bias.
CONCLUSION
Esophageal cancer and cancer surgery are rapidly changing—
epidemiologically and from the “consumer’s” (ie, patient’s
and referring physician’s) viewpoint. Surgery has been slow to
react to this change and is in danger of becoming increasingly
irrelevant in the face of improvements in noninvasive early
cancer treatments (mainly endoscopic), denitive chemoradiation, and, in the future, highly targeted novel therapies. It
is good that leaders in the eld are exploring improvements
in standard surgery outcomes as well as novel minimally invasive approaches—providing patient-friendly alternatives will
help ensure the continued relevancy of surgeons in esophageal cancer treatments.
ere has been some interest in performing MIE in a two-stage
manner—primarily to provide an ischemic preconditioning of
the gastric conduit in order to minimize the chance of ischemic
complications at the anastomosis but also to compensate for
the increased operative times of MIE and the increased mental
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STOMACH AND
DUODENUM
IV
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