Gastrointestinal Endoscopy
Volume 67, Issue 1 , Pages 26-27, January 2008

Removable endoprosthetics in the management of esophageal pathology: all strictures and fistulae are not created equal…

GI Division, University of Pennsylvania Health System, Philadelphia, Pennsylvania, USA

Article Outline

 

Little is known about the pathophysiology of the various potential etiologies of strictures in humans, or the force and dilating diameter required to effectively remediate a given stricture.

The forefront of endoscopic management of complex GI pathology has been increasingly intertwined with the intricate interface of endoscopic will and the margins of device and endoscopic technology. From time immemorial, physicians have struggled to remediate dysphagia, early on relying on whale bones, wax candles, and other devices that we may (in retrospect) term “crude.” Thankfully, we have progressed somewhat and now have an armamentarium for the treatment of esophageal strictures and fistulae that includes a variety of techniques, including the use of various dilation devices, endoprosthetics, and pharmacologic manipulation.1, 2 Unfortunately, often our desire to treat these strictures and fistulous processes is not met with a level of success commensurate with the effort, time, and resources expended. In the future (which is now), it is likely that practitioners will consider these devices and techniques crude and ineffective. In this issue of Gastrointestinal Endoscopy, Holm et al3 have published an extraordinarily honest and disconcerting article recounting their retrospective experience with the use of self-expanding plastic endoprosthetics for a variety of esophageal pathologies.3

Holm et al3 placed 84 plastic endoprosthetics in 30 patients for the purpose of remediating strictures and fistulae, leaks, and perforations. They found that the use of the endoprosthetics was not met with the same level of success for the remediation of strictures that other investigators had in early experiences, but did find that the endoprosthetics appeared to remediate a variety of esophageal leaks and fistulae with efficacy. In their article, the authors provide an excellent review of the literature, and I will not recapitulate that in this editorial. They also provide us with data concerning the exact indications for their procedures, but do not provide a uniform dysphagia scoring system to better allow us to compare these patients to those we see in our daily practices. The use of a dysphagia score, albeit an imperfect measure, is critical to best understand the true impact of one's endoscopic intervention in the setting of a stricture and other dysphagia-inducing pathologies; nonetheless, in their article it is clear that the failure of remediation is obvious and easily categorized. A number of the patients in this study had leaks and fistulae despite the persistence of luminal patency; the exact size of the leaks and their locations and symptomatology are not reported. Pertinently, the authors do not report the length or starting diameter of the strictured segments, although it may eventually be clear that the starting diameter is irrelevant to the recovery of adequate oral intake in the setting of certain subsets of pathology, and that the etiology is more pertinent.1 Importantly, the authors do not provide any information concerning the management of these patients before the time at which a decision was made to place an endoprosthetic. It would be beneficial to know the duration of the stricture, the presence or absence of ongoing inflammation, the time from surgery, and details concerning any attempts at prior endoscopic therapy, including prior dilation and pharmacologic therapy such as acid-suppression and steroid injection.

A recently published definition of refractory and recurrent strictures was proposed so that entry criteria and treatment groups could be compared across studies and centers.4 In the instance of anastomotic strictures, various additional modalities (including serial dilation, needle-knife techniques, and removal of migrating staples and sutures) may be beneficial, as the current authors acknowledge.5 With the large variety of techniques and technologies available, it is difficult to compare across studies that have varying entry criteria and etiologies. Nonetheless, the data the authors present in the current article are compelling and match the clinical experience of other seasoned groups, which until now, has only been hinted at in the literature and not directly studied or reported in a full article.

There is currently only one commercially available plastic self-expanding endoprosthetic, and some may make a take-home point that the Mayo experience finds fault with the device, although in the final analysis, I believe that the device itself is only a piece of the puzzle. I believe that the issue surrounding our difficulty with the endoscopic management of these patients is really the result of the potpourri of various pathologic processes we encounter, which ultimately result in the clinical scenarios of dysphagia and leaks; not all strictures are created equal.1, 6 Photodynamic therapy strictures and those with an ongoing inflammatory component are more difficult to remediate in the short run but will usually ultimately have a satisfactory outcome. On the other hand, transmural insults to the esophagus—such as those that occur postoperatively and with radiation, causing strictures—may not have a satisfactory response in some cases. There is scant evidence that luminal dilation or endoprosthetic placement alters the basic mechanisms resulting in refractory strictures. Rather, it appears that the endoprosthetic may provide for a temporizing maneuver, such that the inflammatory insult resulting in the stricture may be given adequate time to resolve. In the case of leaks, the clinical scenarios are significantly different.

Clearly, the migration rate of endoprosthetics is of concern; to this point, major complications from distal migration have been few, and the authors in this series did not have any migration beyond the stomach. Others have noted elimination of these endoprosthetics per rectum.7 Alterations to the design of endoprosthetics may decrease the migration rate, but careful selection of patients and a better understanding of the pathophysiology and expected clinical response of the stricture to the endoprosthetics are needed. Most bothersome in the current study is the low overall response rate to endoprosthetic placement, suggesting that the real issue is the pathophysiologic process and not the endoprosthetic itself. It may be best to use indwelling removable endoprosthetics in patients with predictably difficult-to-remediate strictures and in those with complex leaks and fistulae. For patients with nonremitting strictures, we may eventually find that clinical treatment paradigms may necessitate the placement of near lifelong indwelling endoprosthetics. Our group and others have accumulated experience with a number of patients who achieve palliation of dysphagia only with an indwelling endoprosthetic and are not willing or able to undergo any effective surgical therapy.8

Ultimately, the issue is that our understanding of the disease processes we are treating is woefully inadequate. Little is known about the actual pathophysiology of the various potential etiologies of strictures in humans.9 Likewise, little is known concerning the force and dilating diameter required to effectively remediate a given stricture.10 In regard to the endoprosthetic device used in this study, it is difficult to draw firm conclusions that either technique or devices are individually responsible, although some generalities may be made. It makes sense to try to carefully select those who will respond to dilation therapy and adjunctive techniques early on and to treat those patients aggressively. For those patients who are believed to be good candidates, an endoprosthetic should be placed and the patient and other treating physicians should be informed as to what the goals of the therapy and the expected outcome will be. For some patients that will be the temporary use of an endoprosthetic in a bridging role; for others that may be recurrent and long-term placement of the endoprosthetic.

The next generation of temporary endoprosthetics, be they removable or biodegradable, need to be designed with an increased attention to the migration issue. Further investigation into the forces in play within a stricture is needed to determine for which strictures endoprosthetic placement alone (continuous dilation) is adequate for stricture remediation. The work of Holm et al3 is good evidence that at least for some strictures, endoprosthetics are ineffective at remediating the basic pathology. As we learn more about the basic pathologic processes that contribute to the various esophageal strictures we encounter, we will hopefully be better able to select the treatment options that will accomplish the best long-term outcomes for our patients.

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Disclosure 

The author reports that there are no disclosures relevant to this publication.

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References 

  1. Lew R, Kochman ML. A review of endoscopic methods for esophageal dilation. J Clin Gastroenterology. 2002;35:117–126
  2. Gillespie MB, Day TA, Sharma AK, et al. Role of mitomycin in upper digestive tract stricture. Head Neck. 2007;29:12–17
  3. Holm AN, De La Mora-Levy JG, Gostout CJ, et al. Self-expanding plastic stents in treatment of benign esophageal conditions. Gastrointest Endosc. 2008;67:20–25
  4. Kochman ML, McClave SA, Boyce HW. The refractory and the recurrent esophageal stricture: a definition. Gastrointest Endosc. 2005;62:474–475
  5. Hordijk ML, Siersema PD, Tilanus HW, et al. Electrocautery therapy for refractory anastomotic strictures of the esophagus. Gastrointest Endosc. 2006;63:157–163
  6. Said A, Brust DJ, Gaumnitz EA, et al. Predictors of early recurrence of benign esophageal strictures. Am J Gastroenterol. 2003;98:1252–1256
  7. Oh YS, Kochman ML. Polyflex esophageal stent migration with elimination per rectum. Gastrointest Endosc. 2007;66:633
  8. Oh YS, Kochman ML, Ahmad NA, et al. Clinical outcomes after PolyflexTM stent placement for refractory benign esophageal stricture (RBES). [abstract] Gastrointest Endosc. 2007;65:AB132
  9. Tugay M, Utkan T, Utkan Z. Effects of caustic lye injury to the esophageal smooth muscle reactivity: in vitro study. J Surg Res. 2003;113:128–132
  10. McLean GK, LeVeen RF. Shear stress in the performance of esophageal dilation: comparison of balloon dilation and bougienage. Radiology. 1989;172(3 Pt 2):983–986

PII: S0016-5107(07)02596-5

doi:10.1016/j.gie.2007.08.033

Gastrointestinal Endoscopy
Volume 67, Issue 1 , Pages 26-27, January 2008

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