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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 thegastroesophageal junction is dened 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 reux is lined, to a variable extent, with dierent 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-eective.
Endoscopic surveillance of patients with Barrett’s esophagus has identied 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 signicant 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 signicantly 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 suciently close to the cricopharyngeal muscle to prevent a clear resection margin. ese patients are better o receiving denitive 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 denitive 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 benet 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 eect 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 benet, a minimum of 23–29 nodes need to be removed. Taking addi­tional nodes is of benet, but the eect 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 inuenced 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 suciently 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 modied 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 benet of an en bloc resection was limited to patients with eight or fewer involved nodes. ere was no dierence 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 signi­cantly beneted 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 benet 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 benet.
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 35patients. 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 eective systemic drugs as wellas
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 conicting, and that published meta-analysis show mini­mal to no benet. 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 aect 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 aect survival. I have con­cluded that the studies done to date have shown neoadjuvant therapy to be only eective 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 dierent 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 denitive che­motherapy is based on its known cytoreduction eect 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 benets 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 reux 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 signicance 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 oer 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 diering 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 (mag­nication, 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 benet 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 denitive 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 insuator set to a low pressure (10 mm Hg) that eectively 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 benets 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 conrm 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), denitive 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
REFERENCES
1. Avissar NE, Toia L, Hu Y, et al. Bile acid alone, or in combination with
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STOMACH AND
DUODENUM
IV