F. M. Riegler

Solving the Problem of Difficult Stent Removal Due to Tissue Ingrowth in Partially Uncovered Esophageal Self-Expanding Metal Stents

Partially uncovered stents provide a better fixation to the esophageal wall than fully covered stents, but indication is limited to palliation because stent removal is compromised by mucosal ingrowth. After an unsuccessful attempt to remove a partially uncovered Evolution stent (Cook Medical Inc, Bloomington, IN) we placed a Polyflex stent (Boston Scientific, Natick, MA) inside the first stent, overlapping at the lower part to press the tissue out of the stent mesh. Both stents were easily removed 3 days later. By adopting this procedure to scheduled stent removals, partially uncovered SEMS may be used to prevent the frequently observed migrations of fully-covered stents in the treatment of esophageal perforation or anastomotic leakage.

Gastrointestinal reconstructions in 1200 patients with cancer at the pharyngesophageal junction

ZusammenfassungGRUNDLAGEN: Karzinome am pharyngoösophagealen Übergang haben eine schlechte Prognose aufgrund der späten Symptommanifestation und Diagnose. Therapie der Wahl die Ösophagusresektion mit gastrointestinaler Rekonstruktion bei resektablen Tumoren. Ziel dieser retrospektiven Studie war die Evaluation der Rekonstruktionsmethoden und deren Einfluss auf die postoperative Letalität, postoperative Komplikationen und funktionelle Ergebnisse. METHODIK: Von 114 evaluierten Publikationen zwischen 1956 und 2008, wurden 33 Arbeiten in den Review inkludiert. Die postoperative Spitalsletalität, nichtchirurgische und chirurgische Komplikationen wurden ausgewertet. Weiters wurde der funktionelle Erfolg beurteilt. ERGEBNISSE: Von 1200 evaluierten Patienten erhielten 60,8 % einen Magenhochzug, 24,5 % erhielten ein Dünndarminterponat und 14,7 % ein Dickdarminterponat. Die gesamte Spitalsletalität betrug 10,7 %. Patienten mit Dünndarminterponat hatten die niedrigste Spitalsletalität und die wenigsten nichtchirurgischen Komplikationen. Die geringsten chirurgischen Komplikationen und die besten funktionellen Resultate erzielten Patienten mit Magenhochzug. SCHLUSSFOLGERUNGEN: Die segmentale Ösophagusresektion mit Dünndarminterponat kann empfohlen werden, wobei diese Operation erfahrenen Spezialisten vorbehalten bleiben soll, da erhöhte chirurgische Komplikationen ein Risiko darstellen.SummaryBACKGROUND: Carcinomas at the pharyngesophageal junction have a poor prognosis due to late symptom manifestation and diagnosis. Treatment of choice includes gastrointestinal replacement after esophagectomy. The aim of this retrospective study was to evaluate whether the type of reconstruction influences postoperative mortality, complications and functional outcome. METHODS: Out of 114 reviewed papers between 1956 and 2008, 33 papers were included in the review. Postoperative hospital mortality, non-surgical and surgical complications were assessed. Furthermore, functional success rates were compared. RESULTS: A total of 1200 patients were evaluated, out of whom 60.8% were reconstructed with gastric pull-up, 24.5% with jejunal autograft and 14.7% with colon interposition. The overall hospital mortality was 10.7%. In particular, patients with jejunal autograft presented reduced hospital mortality and fewest non-surgical complications. Lowest surgical complications and best functional success rates were reported in the gastric pull-up group. CONCLUSIONS: Cervical segmental esophagectomy with jejunal autograft can be recommended but it has to be performed by highly experienced professionals due to risky surgical complications.

Barrett's esophagus: filling the gap

Dear Readers, We care about Barrett’s esophagus (BE), because it is a premalignant condition [1]. BE develops as a consequence of gastroesophageal reflux: the squamous lined mucosa of the normal esophagus is replaced by a columnar epithelium. Via a sequence involving lowand high-grade dysplasia, BE may progress toward the adenocarcinoma of the esophagus, the frequency of which dramatically increased in North America, Europe, and Asian countries within the last 20 years [1]. By definition BE is a columnar lined esophagus with intestinal metaplasia, this is columnar epithelium containing goblet cells. In keeping with the recent works by Paull et al. [2] from Boston and Chandrasoma [3] from Los Angeles non-dysplastic columnar-lined esophagus includes cardiac mucosa (mucus cell only epithelium), oxyntocardiac mucosa (mixture of mucus and acid producing parietal cells), and intestinal metaplasia (cardiac mucosa with goblet cells, this is Barrett’s esophagus) (Fig. 1A–C). The group around the Bostonian pathologist Robert Odze included the fourth type of non-dysplastic columnar-lined esophagus: multilayered epithelium, which represents a multi-layered mixture of squamous and columnar epithelium [4]. Conceptually, repeated gastric over-distentions (over eating) extend into the distal esophagus [5]. Over time the dilation of the esophagus becomes permanent and shortens the high-pressure zone at the esophagogastric junction (i.e., anti-reflux barrier) [3]. Due to impaired function of the esophagogastric junction high-pressure zone and reflux-induced formation of CLE the distal esophagus resembles the proximal stomach during endoscopy: this is the dilated distal esophagus, which is frequently attributed to the stomach and mistaken as hiatal hernia [3]. Recent studies show that the dilated distal esophagus is exposed to a pH less than 4.0 for 80–95% of the time [6]. Therefore, in patients with gastroesophageal reflux, CLE is interposed between the squamous-lined esophagus and the oxyntic mucosa of the proximal stomach (with straight tubular glands containing parietal, chief cells; CLE contains lobulated glands) [7]. This is the squamo-oxyntic gap, a term coined by the pathologist Para Chandrasoma. The proximal portion of the squamo-oxyntic gap may be visible during endosopy, this endoscopically visible CLE, the length of the CLE covering the dilated distal esophagus (i.e., the cardia) can be assessed by multi-level biopsies obtained from the proximal portion of the endoscopically visible ‘‘gastric type folds’’ [3, 7]. The proximal to distal distribution of the mucosal types within the squamo-oxyntic gap follows a specific zonation with intestinal metaplasia at the squamocolumnar junction followed by cardiac and oxyntocardiac mucosa more distally [2, 3, 7]. According to the surgeon Steven DeMeester, Los Angeles, this zonation is paralleled by the pH gradient and the genetic profile gradient across the squamo-oxyntic gap [8] (Fig. 2). CDx2 and Sonic Hedge hog pathway mediate the formation of goblet cells and parietal cells, respectively. Alkaline and acidic pH activate the CDx2 and Sonic hedge hog pathway, respectively. During reflux the lumen of the proximal segment of the squamo-oxyntic gap is increasingly exposed to an alkaline pH, whereas the distal segment of the gap is exposed to acidic pH. As a consequence, goblet cell containing intestinal metaplasia develops at the squamo-columnar junction and parietal cell containing oxyntocardiac mucosa develops within the distal portion of the squamo-oxyntic gap [8]. Increased length of columnar lined esophagus (CLE) is associated with an increased risk for BE, dysplasia, and carcinoma [9]. However, recent evidence indicates the presence of BE within shorter segments of CLE, an observation which may be related to the life style (eating habits, obesity), the use of proton pump inhibitors, unknown genetic factors, and increased diagnosis of BE due to meticulous biopsy sampling during routine endoscopy of the esophagus. Remains the possibility that the milieu responsible for the development of BE, dysplasia, and cancer does not only depend on the luminal content. Using an in vivo animal model of gastroesophageal reflux, the group around Stuart Spechler and Rhonda Souza indicated the participation of complex immune responses in the development of esophagitis including bone marrowderived stem cells [9]. CLE seems to result from a complex reflux-induced neurohumoral orchestration including immune-, nerve-, muscle-, and connective tissue cells (fibroblasts and myofibroblasts) and mediators released from these cells. This ‘‘cocktail of mediators’’ forms the micromilieu, which mediates the symptoms and formats the genetic program of the stem cells within the esophageal epithelium [8, 9]. Thus the micro-milieu contributes to define the cellular composition of the columnar lined Correspondence: Franz Martin Riegler, M.D., Associate Professor of Surgery, Manometry Lab & Department of Surgery, Medical University of Vienna, Währinger Guertel 18–20, 1090 Vienna, Austria. Fax: þþ43-1-40400 3478 E-mail: Franz.Riegler@meduniwien.ac.at

Selected Commentary to "The position of the acid pocket as a major risk factor for acidic reflux in healthy subjects and GERD patients"

Here we summarize an excellent study with major clinical relevance for the management of gastroesophageal reflux disease (GERD). Gastroesophageal reflux disease (GERD) affects 20–30% of the population in Europe and North America [1]. Due to the symptoms GERD causes an impairment of the life quality. In addition, GERD is associated with morphologic changes within the esophagus ranging from esophagitis to adenocarcinoma, the frequency of which significantly increased over the last 15 years [2–6]. Thus GERD became a significant health problem and causes respective costs for the health care systems. A typical feature of GERD includes the occurrence of symptoms 30–60min after the intake of a meal [1]. These postprandial symptoms are associated with nonswallow-induced relaxations of the anti-reflux highpressure zone at the esophagogastric junction (i.e., the lower esophageal sphincter; LES): transient relaxations of the lower esophageal sphincter (TLESRs) [7]. Furthermore, TLESRs are linked to abnormal reflux activity, as assessed by reflux monitoring (classical pH monitoring or combined impedance pH monitoring) [7]. During the postprandial period the pH within the stomach increases. However, recent studies revealed the development of an acidic environment at the level of the esophagogastric junction during the postprandial period: this is the so-called ‘‘acid pocket’’, which has been suggested to be responsible for the postprandial pH gradient across the esophagogastric junction and represents the source for the postprandial acid refluxes [8–11]. Thus the TLESRs and the acid pocket could be the cause for postprandial symptoms and explain the relieve of these GERD symptoms, following proton pump inhibitor (PPI) administration 30min prior to a meal. The study by Beaumont et al. [12] included a highly sophisticated armamentarium of methods to elucidate the impact of the postprandial acid pocket for TLESRsassociated reflux episodes.

Selected Commentary to "Radiofrequency ablation in Barrett's esophagus with dysplasia"

Barrett’s esophagus (BE) results from gastroesophageal reflux, is defined by the presence of intestinal metaplasia within columnar lined esophagus (CLE) and harbors a 0.5% annual risk for the development of esophageal adenocarcinoma [1]. Via low grade and high grade dysplasia BE may progress towards the adenocarcinoma of the esophagus, the frequency of which significantly increased over the past 15–20 years in Europe and North America. However, it is not known who of those with BE will definitely develop cancer. Thus those with BE were enrolled into surveillance programs to be able to act when dysplasia and cancer were detected [2]. The patients with BE resorted to mucosal resection, argon laser ablation or esophagectomy [2]. Therefore a new technology termed radiofrequency ablation (RFA) came as a bliss upon those managing patients with BE and dysplasia [3, 4]. Via a catheter mounted balloon, radiofrequency energy (12 J, 40W) is delivered to the columnar lined esophagus, which in turn is destroyed and detached. Using these technologies recent studies demonstrated that RFA was capable of eliminating intestinal metaplasia and dysplasia [3, 4].

Selected commentary to "Incidence of adenocarcinoma among patients with Barrett's esophagus"

Barrett’s esophagus – this is columnar lined esophagus (CLE) with intestinal metaplasia (IM)-results from gastroesophageal reflux disease (GERD) [1–4]. Presence of CLE with goblet cells within biopsies obtained from the esophagus defines Barrett’s esophagus (Fig. 1) [5, 6]. Barrett’s esophagus deserves our attention, because it is a premalignant condition [7]. Via low and high grade dysplasia nondysplastic Barrett’s esophagus may progress toward esophageal adenocarcinoma. The reported annual cancer risk ranges from 0.16 to 0.5% [8–11]. Individuals with Barrett’s esophagus without dysplasia, lowand high grade dysplasia have a 200x, 560x, and 2.200x increased cancer risk, respectively, when compared to the normal population [12]. These numbers are the basis for current surveillance and treatment strategies, i.e. radiofrequency ablation (Fig. 2) [13], endoscopic resection [13, 14], limited or radical esophagectomy [15]. Frederik Hvid-Jensen from the Aarhus University in Denmark addressed this important issue [16]. His study assessed the annual cancer risk among persons with Barrett’s esophagus in Denmark (5.4 million inhabitants) [16].

Selected Commentary to "Laparoscopic sphincter augmentation device eliminates reflux symptoms and normalizes esophageal acid exposure. One- and 2-year results of a feasibility trial"

Gastroesophageal reflux disease (GERD) affects approximately 30% of the Western population [1]. Due to the symptoms, GERD affects the life quality and productivity [2]. In addition GERD may be associated with cancer development [3]. Consequently, GERD represents a significant health problem resulting in considerable expenses for the health care and social security system (sick leave, diagnosis, and treatment costs) [1]. Proton pump inhibitor (PPI) administration represents the mainstay of GERD treatment [4]. Those with advanced disease, where PPI treatment is insufficient or fails, are recommended to undergo anti-reflux surgery (laparoscopic fundoplication). Remains to be questioned how to manage those with so-called “early GERD” [5]. This increasing group of patients comprises those with partially PPI responsive GERD with frequently normal endoscopic findings, somewhat altered function of the esophagus, assessed during esophageal manometry and abnormal reflux monitoring. It seems that these patients are too good for laparoscopic fundoplication but lack adequate response to PPI treatment, i.e. thosewithin the so-called “therapeutic gap”. Bonavina et al. recently presented a novel and fascinating approach for the minimally invasive surgical treatment of GERD patients within the therapeutic gap [6]. The authors elegantly target their treatment to restore the function of the anti-reflux mechanism within the infra-diaphragmatic portion of the distal esophagus. The present paper summarizes the amazing 2 years data after laparoscopic implantation of a magnetic sphincter augmentation device (magnetic ring). Now let us see how the “Lord of Rings” works.

Trapped in the net

Dear Readers, Today it is really hard to keep up with the continuous flow of novel information leaving us in a state of frustration and the feeling not being able to do a good and adequate job. Remains to be questioned if the present time requires a novel definition of our scopes and aims as modern physicians and surgeons? Novel technologies are great and profoundly contribute to let us be better at our jobs. Surgery became hyper-minimal invasive,major procedures are conducted viamini single incisions. Optical devices allow fascinating magnified visualization of body cavities. The diagnostic tools became rapid and highly effective computer-based “play stations” allowing amazing visions into the complex texture of tissues, organs and pathophysiological processes. Medical science accelerates the conduct of knowledge acquisition. What is the price? In addition to do our job as physicians and surgeons, we are forced to keep up with this race of knowledge and science. Otherwise it seems that we are thrown out of the game. It seems there is no quiet place out there for rest and stop. Going in line with this trend we are continuously pushed to assess and acquire new information. Thus computers, cell phones, laptops and iPads (þelectronic radiations generated by the novel communication processes) place us within a continuous wave of global conduct. We became trapped in the net, so what? Running and hunting is good, but not always. Consequently one will get exhausted and name a “six feet at last”-stone. Therefore, we have to redefine ourselves in this global competition and see if WE really want to be part of it ALL the TIME. “Chill out” is important for the recreation and redefinition of our wants and needs. Otherwise we will directly drive into the burn out scenario and loss of life quality, happiness, well being. Man will cease like a fire in the wind, unfocused energy echoes along as part of the background noise. The highly motivating scope is to combine efficient acquisition of knowledge, sound performance of patient care and relaxed recreation of our body, soul and mind. This is the basis for a balanced orchestration of modern life: take your time to keep up with the world and with yourself. Let your life be a mix, as it is with music. Play the blues if you want blues, rock if youwant to rock, jam if you want to jam, but do never forget to be YOU. Expose yourself to good energies, communicate with persons with good vibrations. Distribute good energies and you will find yourself in a well-tuned groove. For surgeons it is important not to overestimate your performance, do not jump into the water, if you cannot swim, take your time to balance, step by step. Going in line with the technological developments regarding the diagnosis and management of benign and malignant diseases we became highly effective in the treatment of pathologies limited to specific organs (i.e. liver, kidney, heart, lungs, gut, thyroids, and brain). However, this technology-driven specialization evolves at the