A 66 year-old male with chronic gastroesophageal reflux disease. Barrett's esophagus is a condition in which an abnormal columnar epithelium replaces the stratified squamous epithelium that normally lines the distal esophagus. It is the most severe histologic consequence of chronic gastroesophageal reflux and predisposes to the development of adenocarcinoma of the esophagus. Endoscopically obvious Barrett's esophagus can be seen in 3 to 12 percent of patients who have endoscopic examinations for symptoms of GERD.
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Barrett's Esophagus with residual islands of squamous epithelium.
Squamous islands are frequently visualized at the time of upper endoscopy in patients with Barrett's esophagus, especially those on proton pump inhibitor therapy (PPI). Barrett's esophagus is usually discovered during endoscopic examinations of middle-aged and older adults whose mean age at the time of diagnosis is approximately 55 years old. Although Barrett's esophagus can affect children, it rarely occurs before the age of five. The definition of Barrett esophagus has evolved considerably over the past 100 years. In 1906, Tileston, a pathologist, described several patients with "peptic ulcer of the esophagus" in which the epithelium around the ulcer closely resembled that normally found in the stomach. The debate for the next 4 decades centered on the anatomical origin of this mucosal anomaly. Many investigators, including Barrett in his treatise published in 1950, supported the view that this ulcerated columnar-lined organ was, in fact, the stomach tethered within the chest by a congenitally short esophagus.
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Barrett's Esophagus retroflexed view.
The columnar metaplasia in Barrett's esophagus causes no symptoms. Thus, most patients are seen initially for symptoms of the associated GERD such as heartburn, regurgitation, and dysphagia.
Norman Barrett, a British surgeon, is widely believed to be the first to describe the transformation of the esophageal lining that bears his name. In a landmark paper in 1950. Barrett noted ulcers in a tubular, intrathoracic organ that appeared to be the esophagus but was lined by gastric-type columnar epithelium. Barrett argued (in retrospect, incorrectly) that this was a segment of stomach that had become tethered in the chest because of a congenitally short squamous-lined esophagus.
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More images and video clips of Barrettīs Esophagus. Several tongues of gastric-appearing mucosa extend above the esophagogastric junction into the distal esophagus. Squamous islands may be remnants of squamous mucosa or originate from esophageal gland duct epithelium following injury.
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Residual islands of squamous epithelium.
Definition of Barrett's Esophagus -- Barrett's esophagus is a change in the esophageal epithelium of any length that can be recognized at endoscopy and is confirmed to have intestinal metaplasia by biopsy.
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The video clip shows the reflux evidence due to the fact that gastric juice emerging to the esophagus.
Falk GW. Gastroenterology. 2002 May;122(6):1569-91. Barrett's esophagus is an acquired condition resulting from severe esophageal mucosal injury. It still remains unclear why some patients with gastroesophageal reflux disease develop Barrett's esophagus whereas others do not. The diagnosis of Barrett's esophagus is established if the squamocolumnar junction is displaced proximal to the gastroesophageal junction and if intestinal metaplasia is detected by biopsy. Despite this seemingly simple definition, diagnostic inconsistencies remain a problem, especially in distinguishing short segment Barrett's esophagus from intestinal metaplasia of the gastric cardia. Barrett's esophagus would be of little importance were it not for its well-recognized association with adenocarcinoma of the esophagus. The incidence of esophageal adenocarcinoma continues to increase and the 5-year survival rate for this cancer remains dismal.
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Zoom endoscopy of a tongue of Barretts mucosa showing cerebriform villous architecture.
Enhanced magnification endoscopy.
The endoscopic classification of Barretts esophagus is based on the similarities between the intestinal metaplasia found in the esophagus of patients with Barretts and the intestinal mucosa seen in the duodenum of patients with celiac sprue using dissecting microscopy. Zoom endoscopy has the potential to enhance diagnostic yield by improving targeting of biopsies.
Enhanced magnification endoscopy involves the combined use of magnification endoscopy and acetic acid. Barrett's mucosa is frequently translucent when observed with magnification endoscopy. To improve the visualization of the mucosal surface, a variety of different enhancement techniques, including both stains and acetic acid, have been used in conjunction with magnification. The use of 1.5% to 3% acetic acid in the distal esophagus has been shown to enhance the ability to visualize the small details of the mucosal surface. This method is safe, rapid, clean, and inexpensive.
Tongue of Barretts mucosa showing cerebriform villous architecture. The salmon-colored mucosa in the distal esophagus is columnar and consists of a mosaic of fundic mucosa, cardiac mucosa, and intestinal metaplasia. The yield of intestinal metaplasia from biopsies of columnar-type mucosa in the distal esophagus varies from 25% to 50% in short-segment Barretts esophagus to 80% in longsegment Barretts esophagus. Ideally, a method that improves the visualization of the mucosal surface would aid in the detection ofBarretts esophagus and assist in more accurate surveillance. Magnification endoscopy with chromoendoscopy provides a unique approach with a more specific evaluation of the fine details of the mucosal surface and high-yield targeted biopsies for a more accurate diagnosis.
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Chromoendoscopy using methylene blue.
Chromoendoscopy involves the topical application of stains or dyes to improve mucosal visualization during endoscopy.
The image and the video clip display, the violet light of the APC. Studies have demonstrated reversal of Barrett's mucosa after endoscopic coagulation with different techniques associated with acid inhibition. However, most of these studies have shown that residual Barrett's glands are found underneath the new squamous epithelium in up to 40% of patients. but using high power setting argon plasma coagulation is most promising.
Appearance post using the argon plasma coagulator.
Optical methods either alone or in combination with chromoendoscopy are likely to hold the key to better targeting, to increase biopsy yield in Barrett’s esophagus and in some other disorders of the GI tract.
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Appearance post using the argon plasma coagulator.
For methylene blue staining, the patient should be told that the urine and stool might adopt a blue color.
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The image and the video clip shows magnification of the tissue that have coagulated.
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One month after the therapy with argon plasma coagulator APC. An endoscopic follow up. Note that the long segments of the Barrett have been diminished.
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A hiatus hernia with complete incompetence of the sphincter is observed.
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One month after the therapy with argon plasma coagulator APC.
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Chromoendoscopy using Lugol's solution.
Chromoendoscopy involves the application of vital dyes that enhance the visibility of dysplastic mucosa. Vital dyes that have been studied include those that preferentially stain normal squamous mucosa (such as Lugol's iodine), Diagnosis of squamous cell carcinoma of the esophagus is usually late. Staining of the mucosa with Lugol's solution during endoscopy has been suggested to identify early cancer and dysplasia that may improve prognosis.
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Endoscopic techniques to detect dysplasia. Several endoscopic techniques that could augment the ability to detect dysplasia have been evaluated. These include chromoendoscopy, magnification endoscopy, endoscopic ultrasound, optical coherence tomography, and fluorescence detection techniques. Lugol's staining have suggested that it may be helpful for detection of high grade dysplasia and early squamous cell cancers of the esophagus.
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High power setting argon plasma coagulation.
One month of the previous therapy another endoscopic session with APC. In this endoscopy we used adouble-channelendoscope and APC catheter of 3.2 mm.
The management of patients with Barrett's esophagus involves three major components. Treatment of the associated gastroesophageal reflux Endoscopic surveillance to detect dysplasia Treatment of dysplasia.
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APC treatment of Barrett's esophagus is simple, efficacious and safe. Reversal of Barrett's mucosa can be achieved by a few endoscopic sessions. But long term follow-up studies on many patients are necessary to establish the frequency of endoscopic surveillance on the basis of recurrence or dysplasia evolution risk, in spite of APC treatment.
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The image and the video clip display the APC ablation.
Most patients with BE will not develop esophageal cancer and will die of other causes, as in the general population. The risk of progression to adenocarcinoma of the esophagus is estimated at approximately 0.5% per year in patients without dysplasia on initial surveillance biopsies.
Why only some people with GERD develop BE also is not clear.
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Alcian Blue Stains.
There is ectopic gastric mucosa with incomplete intestinal metaplasia , with goblet cells (alcian blue). The diagnosis of Barrett’s esophagus requires both endoscopic and histologic evidence of metaplastic columnar epithelium. Endoscopically, there must be columnar epithelium within the esophagus. Histologically, the epithelium must be metaplastic, as defined by the presence of goblet cells. An Alcian blue stain at pH 2.5 stains the acidic mucin present in the goblet cells. The most common errors in the identification of goblet cells are: 1) "pseudogoblet" cells; and 2) Alcian blue positive cells that are not goblet cells. Pseudogoblet cells are barrel-shaped gastric surface or foveolar cells that do not stain with Alcian blue. These cells commonly have a blush of eosinophilia, due to neutral mucin, on H&E stained sections, in contrast to the blush of basophilia, imparted by the acidic mucin in goblet cells.
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Alcian Blue Stains.
Alcian blue goblet cells are seen at the ectopic gastric mucosa. Specialized columnar epithelium characterized by alcian blue-positive and mucin-containing goblet cells. This type of epithelium is diagnostic of Barretts esophagus.
Pseudogoblet cells are barrel-shaped gastric surface or foveolar cells that do not stain with Alcian blue. These cells commonly have a blush of eosinophilia, due to neutral mucin, on H&E stained sections, in contrast to the blush of basophilia, imparted by the acidic mucin in goblet cells.
Alcian blue positivity in a columnar cell does not necessarily indicate a metaplastic goblet cell; it should have a barrel shape. Other types of cells that can be alcian blue positive but which lack the barrel shape include: reactive gastric foveolar cells, which may be present in the pits and on the mucosal surface, mucous neck cells of the gastric glands, esophageal cardiac glands, and submucosal glands in the esophagus.
High Magnification Video Endoscopy.
This picture shows the differences between both mucosas of the gastroesophagic junction.
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Gastric Heterotopia (inlet pach).
Mucosal defect that has to disclosed Barrett Esophagus. A 50 year-old female with long-standing GERD. A hiatus hernia is seen.
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Magnification Endoscopy combined with Enhanced magnification.
The image and the video clip display magnification endoscopy following instillation of acetid acid. The magnified image displays a retilcular mucosa pattern sugestive of cardiac epithelium (rather than intestinal metaplasia) which was confirmed on biopsy.
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Magnification Endoscopy combined with enhanced magnification.
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Chromoendoscopy using methylene blue.
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Barrett's Esophagus of long segment.
This 41 year-old male presented with long-standing GERD. Endoscopy shows tongues of Barrett esophagus.
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People with "long-segment" Barrett's esophagus, in which the red lining is 3 cm or more in length, are about 40 times more likely than those in the general population to develop esophageal cancer. As a result, they typically undergo regular endoscopic screening and biopsies to ensure their condition has not progressed to cancer. Substantially more common, however, is "short -segment" Barrett's, in which the patch of affected tissue is no more than 3 cm long. Until recently, esophageal-cancer risk in people with shorter segments was largely unknown because such patients often were excluded from studies because their condition was more difficult to diagnose through endoscopy, and because researchers initially were uncertain whether short-segment Barrett's indeed was a cancer risk factor at all.
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Among patients who have endoscopic examinations because of chronic GERD symptoms, long segment Barrett's esophagus can be found in 3 to 5 percent, whereas 10 to 15 percent have short-segment Barrett's esophagus.
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Esophagectomy has been the treatment of choice for patients with Barrett's esophagus and high-grade dysplasia (HGD). or adenocarcinoma. However, the reported morbidity and mortality rates for this indication are in the range of 18% to 48% and 3% to 5%, respectively. In view of these risks, a considerable proportion of patients are unable or unwilling to undergo surgery because of comorbidity or age. A recent large prospective trial showed that HGD in Barrett's esophagus follows a relatively benign course in the majority of patients.
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Ablative Therapy with APC.
90 W. argon plasma coagulation (APC) for the ablation of Barrett's esophagus.
Preliminary studies have demonstrated reversal of Barrett's mucosa after endoscopic coagulation with different techniques associated with acid inhibition. However, most of these studies have shown that residual Barrett's glands are found underneath the new squamous epithelium in up to 40% of patients.
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The goal of ablative therapy is to destroy the Barrett epithelium to a sufficient depth to eliminate the intestinal metaplasia and allow regrowth of squamous epithelium. A number of modalities have been tried, usually in combination with medical or surgical therapy because successful ablation appears to require an anacid environment.
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Human studies have been performed with photodynamic therapy (PDT), argon plasma coagulation (APC), multipolar electrocoagulation (MPEC), heater probes, and various forms of lasers, endoscopic mucosal resection (EMR), cryotherapy, and radiofrequency ablation. Ablative therapy remains largely investigational with the exception of PDT, which is approved by the Food and Drug Administration (FDA) for high-grade dysplasia only.
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The long-term relapse rate of non-neoplastic BE following complete ablation with high-power APC is low.
APC is a method of contact-free high-frequency current coagulation in which the burning of tissue stops as soon as the area is ablated. One recent study using high-power APC was reported to result in complete restoration of squamous mucosa in 33 out of 33 patients after a mean of 1.96 sessions. The major complication was chest pain and odynophagia, which occurred in 57.5% of patients and lasted 3-10 days. Only 3 patients experienced stricture, which was treated easily with dilation. Other studies have been less encouraging, with persistence of residual foci of Barrett epithelium under the neosquamous lining in 22-29%, and deep esophageal ulceration with massive bleeding.
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Final status, after the Argon plasma coagulation therapy.
Another area of intense research in the setting of BE is the study of biomarkers that may predict an increased risk of progression to cancer. 17p (p53) LOH (loss of heterozygosity) predicts progression of BE to cancer. Fluorescence in situ hybridization (FISH) is able to detect simple deletion of DNA, but in a subset of patients with BE, 17p (p53) LOH may arise by mitotic recombination or other mechanisms that cannot be detected by FISH. LOH analysis is more complex and labor-intensive, whereas FISH technology is more readily available and can be performed by various clinical laboratories.
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Six months after, a follow up endoscopy was performed.
The tongues of Barrett epithelium have been shortened.
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A new session of ablative therapy will be needed.
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Tongue-like columnar mucosal protrusions in the distal esophagus.
A 68 year-old, female with long standing GERD.
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More images and video clips of this endoscopic sequence.
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The gastroesophagic junction is observed.
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Vital staining with Lugol's solution is performed at the time of upper endoscopy to aid in cancer detection. Lugol's staining involves the application of a solution that contains potassium iodide and iodine through a spraycatheter. The dye stains the glycogen in normal squamous epithelium a dark brown color. Areas that are unstained, particularly those that are larger than 5 mm in size, are likely to be dysplasic or malignant and can be readily targeted for endoscopic biopsy. Smaller unstained areas (less than 5 mm) may result from inflammatory change.
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Magnifying Endoscopy of gastroesophagic junction.
For the surveillance of malignant lesions from Barrett's esophagus, periodic endoscopic examination is necessary with chromoendoscopy or magnifying endoscopy. Treatment strategies are EMR and other endoscopic treatment for mucosal cancer, and surgical treatment for submucosal and advanced cancer. Several surgical modalities are employed depending on the stage of cancerous progression, the location of the cancer in Barrett's esophagus, and the length of Barrett's esophagus.
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Chromoendoscopy using methylene blue.
It is believed that adenocarcinoma develops only in epithelium containing specialized intestinal metaplasia. Therefore, investigators have focused on the utility of chromoendoscopy in identifying these areas of intestinal metaplasia for biopsy. Within this setting, showed that methylene blue, selectively stained specialized intestinal metaplasia in Barrett's esophagus, with excellent specificity and sensitivity.