The Practicing Endoscopist

Diagnosis at First Sight: Gastric Adenoma

Sat, 17 Oct 2026 00:00:00 GMT

A 55-year-old woman underwent esophagogastroduodenoscopy for worsening gastroesophageal reflux symptoms. She had no known hereditary cancer or polyposis syndrome and no family history of colorectal cancer or advanced colorectal polyps. A raised gastric lesion was noted along the anterior wall of the stomach, near the incisura, 2 cm in size, with clearly demarcated borders, a pale-pink surface, rounded nodules, and shallow intervening grooves (Figure 1A). Narrow-band imaging (NBI) highlighted closely packed, curved and elongated surface lines, making the architectural contrast with the surrounding mucosa more conspicuous (Figure 1B–D). Biopsies were obtained which confirmed a gastric adenoma with low-grade dysplasia. Gastric biopsies were negative for Helicobacter pylori infection. This lesion was ultimately completely removed by endoscopic mucosal resection (EMR).

Gastric adenomas are uncommon premalignant epithelial lesions, accounting for approximately 0.5–10% of gastric polyps in reported Western series.[1] They often occur in a background of gastric atrophy and intestinal metaplasia, although a hereditary syndrome is not required. Their importance lies in the risk of progression to adenocarcinoma and the possibility of carcinoma within an apparently innocuous polyp. Larger lesions, high-grade dysplasia, and villous architecture carry greater malignant risk.[1] Neither a bland color nor a smoothly lobulated contour reliably establishes the benign nature of the lesion; NBI assists characterization, but histology remains necessary for diagnosis and grading.[1,2]

A careful gastric examination is essential even when the indication is reflux. Clear mucus and pooled fluid, distend the lumen adequately, and inspect the stomach systematically in forward and retroflexed views, exposing mucosa hidden between folds. Any focal change in contour, color, or surface texture deserves closer examination. Use NBI to define the lesion's borders and assess its surface; with magnification, evaluate the microsurface and microvascular patterns separately. An irregular pattern within a demarcated area should raise concern for early gastric cancer.[2] Record the lesion's location, size, and morphology, and obtain white-light and NBI images. Inspect the remaining stomach for synchronous lesions and assess the background mucosa for atrophy, intestinal metaplasia, and Helicobacter pylori.[1,3]

EMR was used in this case; the choice of resection technique depends on lesion characteristics, with current guidance favoring endoscopic submucosal dissection for most superficial gastric neoplasia and EMR for selected small lesions. Bleeding and perforation are procedural risks, while residual or recurrent neoplasia requires follow-up informed by resection histology and background mucosal risk.[3] Recognition begins with the focal architectural change: an incidental gastric polyp warrants deliberate inspection before its significance is judged.

References

Banks M, et al. British Society of Gastroenterology guidelines on the diagnosis and management of patients at risk of gastric adenocarcinoma. Gut. 2019;68:1545–1575. doi:10.1136/gutjnl-2018-318126.
Yao K, et al. Guidelines for endoscopic diagnosis of early gastric cancer. Dig Endosc. 2020;32:663–698. doi:10.1111/den.13684.
Dinis-Ribeiro M, et al. Management of epithelial precancerous conditions and early neoplasia of the stomach (MAPS III): ESGE/EHMSG/ESP Guideline update 2025. Endoscopy. 2025;57:504–554. doi:10.1055/a-2529-5025.

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How Would You Remove This Pedunculated Polyp (Paris 0-Ip, Kudo IIIL)?

Sat, 03 Oct 2026 00:00:00 GMT

A 60-year-old man with a history of hypertension, coronary artery disease, and atrial fibrillation on Eliquis (stopped 2 days before colonoscopy) was found to have a large pedunculated polyp in the sigmoid colon.

Question

How would you resect this polyp?

Just snare
Pre-injection and then snare
Snare and then clip
Pre-clipping and then snare
Inject, clip, and snare
Inject, snare, and then clip the stump
Place an endoloop and then snare
Snare and then place an endoloop
Underwater snare resection
Other

Answer

All options are correct. However, when dealing with pedunculated polyps, consider that there is always a large feeding vessel going through the pedicle. Clues to the presence of larger vessels are a) a large polyp head (needs more blood flow for "nutrition"), b) advanced adenomatous features (which correlate with neoplasia and angioneogenesis, i.e., more vessels/microcirculation in the polyp head), and c) thickness of the stalk or pedicle.

Many endoscopists prefer to cut first and then provide prophylactic or active hemostasis. However, this option may be risky, as post-resection bleeding may be brisk, especially in patients on anticoagulation or those who have bleeding diathesis or dyscrasias. Thus, I prefer to always perform the prophylactic hemostasis BEFORE polyp resection.

The most practical way to provide hemostasis is using hemoclips. If available, endoloops are quite useful and safe. Nevertheless, placing loops in angled positions such as the sigmoid colon can be challenging. Using a little pre-injection of saline or saline with epinephrine 1:20,000 into the base can also help create a temporary tamponade and decrease blood flow to the polyp head. However, sometimes injection can deform the stalk and make subsequent resection more challenging. Using underwater or saline-submerged resection has the advantages of a) less tissue damage during cutting and b) dilution of any post-polypectomy bleeding, with improvement of the visual field.

Figure 2: Pre-clipping using two clips, followed by hot snare resection above the clips. The stalk (yellow circle) and the big feeding vessel (yellow arrows).

In this case we opted for pre-clipping using two clips, followed by hot snare resection above the clips, proximal to the polyp head. Look at the stalk (yellow circle). Wow, that was a big feeding vessel! (yellow arrows). The choice of pre-clipping was great!

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Post-Prandial Thoracic Pain and Pre-Syncopal Symptoms: Watch Out for Roemheld Syndrome

Sun, 30 Aug 2026 00:00:00 GMT

Patient:

26-year-old woman with CVID, asthma, chronic lung disease, and dorsal spondyloarthrosis

Indication:

Heartburn, chest pain, and palpitations with postprandial bloating after a negative cardiac workup

Final diagnosis:

Roemheld syndrome (gastro-cardiac syndrome) after exclusion of cardiac disease

Figure 1A: Retroflexed view of the gastric cardia demonstrating a large hiatal hernia.

Figure 1B: Distal esophagus with reflux esophagitis at the squamocolumnar junction.

Figure 1C: High-resolution manometry showing ineffective esophageal motility, with a 24-hour pH-impedance tracing confirming pathologic reflux. Software labels on the tracing are in Spanish.

Figure 2: Schematic of the gut-brain-heart axis. Bidirectional neural, neuroendocrine, metabolic, and immunologic pathways can translate gastrointestinal events into thoracic and autonomic symptoms, as in Roemheld syndrome. Labels on the source figure are in Spanish.

Clinical History

A 26-year-old woman with common variable immunodeficiency (CVID), asthma, chronic lung disease, and dorsal spondyloarthrosis presented with a one-year history of heartburn, chest pain, and palpitations. She also reported nocturnal regurgitation, marked abdominal distension, abdominal pain, and occasional constipation.

Electrocardiogram and echocardiography were negative; palpitations were not captured on ambulatory monitoring. Upper endoscopy showed a large hiatal hernia. Esophageal manometry demonstrated ineffective esophageal motility. A 24-hour pH study confirmed pathologic reflux, with a positive DeMeester score, 7.3% acid exposure, and a 99.3% symptom association probability (SAP; threshold >95%).

She was treated with a potassium-competitive acid blocker (P-CAB) for three months, with clear clinical improvement. Symptoms recurred when the medication was stopped, and P-CAB was restarted. Despite acid suppression she still had occasional postprandial abdominal pain, weight loss, nausea, diaphoresis, and dizziness. The attacks began with bloating and distension, then thoracic pain, then autonomic features including presyncope and dizziness.

Endoscopic and Physiologic Findings

Upper endoscopy showed a large hiatal hernia.
The distal esophagus showed reflux esophagitis.
High-resolution esophageal manometry demonstrated ineffective esophageal motility.
A 24-hour pH study confirmed pathologic reflux, with a positive DeMeester score, 7.3% acid exposure, and a 99.3% symptom association probability.

Endoscopic Technique

Diagnostic EGD was performed to evaluate heartburn, regurgitation, and chest pain. Complementary high-resolution esophageal manometry and 24-hour pH monitoring completed the esophageal workup. No therapeutic endoscopic intervention is described in this case.

Discussion

Roemheld syndrome, also called gastro-cardiac syndrome, is a 1912 eponym for postprandial thoracic pain and autonomic dysfunction driven by gastrointestinal factors. It is not a Rome IV or ICD entity. Common cardiac-like features include palpitations, irregular heartbeat, tachycardia, chest tightness, shortness of breath, dizziness, anxiety, and fatigue. Gastrointestinal features include bloating, regurgitation, heartburn, and belching.

The proposed mechanism is trapped gas that distends the stomach. A hiatal hernia lets gastric contents slide into the thorax and press on the diaphragm, which can trigger the autonomic cascade. In this patient, a large hiatal hernia plus pathologic GERD and ineffective esophageal motility sit in that pathway. Symptoms followed a repeatable sequence: abdominal bloating and distension, then thoracic pain, then presyncope and dizziness.

Diagnosis is one of exclusion. Cardiac testing here was limited to electrocardiogram and echocardiography. P-CAB therapy improved reflux symptoms for three months, with recurrence after discontinuation. After restarting P-CAB she still had occasional postprandial pain, weight loss, nausea, diaphoresis, and dizziness. Gastric emptying was not reported.

Management targets the GI drivers: smaller, more frequent meals, fewer gas-producing foods, remaining upright for several hours after eating, and treating reflux with a PPI or P-CAB. In a patient with CVID and excess gas, a breath test for SIBO is a reasonable add. If symptoms persist, refer for surgical evaluation of the hiatal hernia. A multidisciplinary path is needed when the same patient presents with both gastrointestinal and cardiac-like symptoms.

References

Roemheld L. Der gastrokardiale Symptomenkomplex. Z Phys Diät Ther. 1912;16:339-349.
Pimentel M, Saad RJ, Long MD, Rao SSC. ACG Clinical Guideline: Small Intestinal Bacterial Overgrowth. Am J Gastroenterol. 2020;115(2):165-178.
Yadlapati R, Kahrilas PJ, Fox MR, et al. The Chicago Classification of esophageal motility disorders, v4.0. Neurogastroenterol Motil. 2021;33(1):e14058.

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Ménétrier Disease: A Diagnostic Challenge of Enlarged Gastric Folds

Thu, 06 Aug 2026 00:00:00 GMT

Patient:

76-year-old male with anemia

Indication:

Repeat EGD with EUS for a large circumferential ulcerated mass at the gastric cardia

Final diagnosis:

Ménétrier disease diagnosed by EUS plus deep targeted biopsies

Figure 1A: Endoscopic view demonstrating markedly enlarged and edematous gastric folds in the fundus, with the endoscope visible in retroflexion.

Figure 1B: Close-up of giant rugal folds with a cerebriform appearance, dark surface staining, and tenacious adherent mucus.

Figure 1C: Hypertrophic gastropathy around the cardia with foamy mucus pooled between massive folds.

Endoscopic Findings

EGD demonstrated a fundal lesion around the cardia with enlarged and edematous rugal folds.
The folds failed to flatten with air insufflation and were covered by tenacious adherent mucus.
EUS showed intact muscularis propria without invasion into the muscular layer around the fundus.

Endoscopic Technique

Repeat EGD was performed for reassessment of the cardia and fundus.
A radial echoendoscope was advanced after EGD for ultrasound evaluation.
The gastric fundus was examined with balloon inflation at the tip of the echoendoscope to optimize visualization.
Multiple deep biopsies of the lesion were obtained for histopathology.

Discussion

Ménétrier disease is a rare acquired hypertrophic gastropathy that typically affects men at a mean age of about 55 years. Clinical manifestations include progressive abdominal pain, nausea, vomiting, and peripheral edema. The disease is characterized by giant rugal folds of the body and fundus, hypochlorhydria or achlorhydria, excess gastric mucus production, and protein-losing enteropathy.

Endoscopically, the hallmark is markedly enlarged and edematous rugal folds that do not flatten with air insufflation and are often covered by tenacious mucus. Histology shows massive foveolar hyperplasia, tortuosity and cystic dilation of glands, smooth muscle hyperplasia, and atrophy of oxyntic mucosa with reduced parietal and chief cells. Because these changes predominantly involve deeper mucosa, deep or full-thickness biopsies are required for diagnosis.

Enlarged gastric folds also raise concern for infiltrative adenocarcinoma, signet-ring cell carcinoma, and gastric lymphoma. The differential includes Helicobacter pylori gastritis, Zollinger-Ellison syndrome, portal hypertensive gastropathy, and gastric polyposis syndromes. In this case, intact muscularis propria on EUS plus deep mucosal sampling established Ménétrier disease and avoided misclassification as an infiltrative neoplasm.

References

Richer R, Barbu ST. Ménétrier disease: A rare cause of protein-losing gastropathy. Gastrointest Endosc. 2018;88(4):629.
Meuwissen SG, Hasler WL, van der Waaij LA. Ménétrier disease: Clinical, endoscopic, and histopathological features. World J Gastroenterol. 2011;17(3):329-335.
Komorowski RA, Caya JG. Ménétrier disease: A clinicopathologic study of 16 patients. Hum Pathol. 1984;15(3):264-272.

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Gastric Adenoma Resection in a Patient with Lynch Syndrome

Tue, 28 Jul 2026 00:00:00 GMT

Patient:

49-year-old male with Lynch syndrome

Indication:

Routine screening colonoscopy and EGD

Final diagnosis:

Gastric adenoma, intestinal type, with low-grade dysplasia, resected by EMR

Figure 1A: Initial endoscopic view of a 20 mm flat polypoid lesion in the gastric fundus.

Figure 1B: Post-EMR mucosal defect after Eleview lift and hot snare resection.

Figure 1C: Resection site with endoscopic clips in situ.

Endoscopic Findings

EGD demonstrated a 20 mm flat polypoid lesion in the gastric fundus.
The remainder of the examined upper GI tract showed no additional suspicious gastric lesions at this examination.

Endoscopic Technique

The fundic lesion was lifted with Eleview injection.
Hot endoscopic mucosal resection (EMR) was performed.
The resection site was closed with endoscopic clips.
Histology showed gastric adenoma, intestinal type, with low-grade dysplasia. Testing was negative for Helicobacter pylori.

Discussion

Lynch syndrome is the most common hereditary cancer predisposition syndrome. It is caused by autosomal dominant germline pathogenic variants in DNA mismatch repair genes and substantially increases lifetime risk of multiple cancers, most notably colorectal cancer (40 to 80%) and endometrial cancer (40 to 60%). Gastric cancer risk ranges from about 0.2 to 13% depending on the gene involved, and intestinal-type gastric adenocarcinoma is the usual histology.

Current ACG guidance recommends colonoscopy at least every two years in people with or at risk for Lynch syndrome. It also recommends considering EGD with gastric biopsy beginning at ages 30 to 35, treating H. pylori if detected, and continuing surveillance every 3 to 5 years when there is a family history of gastric or duodenal cancer.

This case shows why surveillance EGD matters in Lynch syndrome: a flat fundic adenoma with low-grade dysplasia was identified and removed endoscopically before progression to invasive adenocarcinoma.

References

Kastrinos F, et al. The American College of Gastroenterology Clinical Guideline: Genetic Predisposition to Gastrointestinal Cancers. Am J Gastroenterol. 2021;116(11):2100-2122.
Ladep NG, et al. Gastric cancer surveillance in Lynch syndrome: A systematic review. Fam Cancer. 2018;17(3):477-486.
Pimentel-Nunes P, et al. Endoscopic mucosal resection and endoscopic submucosal dissection for gastric epithelial neoplasia: an ESGE Guideline. Endoscopy. 2015;47(9):829-856.

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Gastrointestinal Manifestations of Systemic Sclerosis

Wed, 22 Jul 2026 00:00:00 GMT

CASE REPORT

Susan Feldman, MD and Klaus Mönkemüller, MD, PhD, FASGE, FESGE, FJGES, Department of Gastroenterology, Carilion Clinic / Virginia Tech Carilion School of Medicine, Roanoke, VA, USA

Final Diagnosis

Esophageal motility disorder, mega duodenum, and mega ileum associated with systemic sclerosis.

Patient Demographics

A 48-year-old female with a known history of systemic sclerosis.

Clinical History

The patient was referred for malignancy screening. She reported dyspepsia and abdominal bloating. Her medications included mycophenolate mofetil. On clinical examination, her abdomen was slightly distended and tympanitic but non-tender. The indication for endoscopy was malignancy screening and evaluation of her gastrointestinal symptoms.

Endoscopic Findings

Esophageal motility disorder and dilation with retained saliva.
Markedly dilated duodenum with wide separation between Kerckring folds.
Markedly dilated terminal ileum on colonoscopy.

Endoscopic Technique

Standard esophagogastroduodenoscopy and colonoscopy with terminal ileum intubation were performed for malignancy screening and symptom evaluation. No therapeutic intervention was required during this diagnostic examination.

Discussion

Systemic sclerosis, or scleroderma, is characterized by widespread collagen deposition, resulting in tissue and organ fibrosis. Most patients experience gastrointestinal manifestations, including esophageal dysmotility, gastroparesis, megaduodenum, small bowel diverticulosis, and chronic intestinal pseudo-obstruction. The gastrointestinal abnormalities are likely a consequence of muscular atrophy and collagen replacement of the outer longitudinal layer relative to the inner circular layer. Small intestinal involvement can lead to delayed transit, dilation of small bowel loops, and secondary bacterial overgrowth.

In this patient, the endoscopic triad of esophageal dilation with retained secretions, megaduodenum, and mega ileum illustrates how scleroderma can remodel multiple GI segments at once. Recognition matters because these findings explain common symptoms such as dyspepsia and bloating, and they raise the possibility of bacterial overgrowth when dilated loops impair clearance.

Key Learning Points

Systemic sclerosis commonly affects the gastrointestinal tract due to collagen deposition and muscular atrophy.
Endoscopic evaluation in patients with systemic sclerosis may reveal esophageal dysmotility, megaduodenum, and mega ileum.
Gastrointestinal involvement can lead to dilated bowel segments and complications such as bacterial overgrowth.
Recognition of these endoscopic findings is crucial for comprehensive management of systemic sclerosis.

References

Prakash R, Saxena A. Gastrointestinal manifestations of systemic sclerosis. Gastroenterol Res Pract. 2017;2017:7102157.
Runchey S, Sharma A. Esophageal dysmotility in systemic sclerosis: A review. J Clin Gastroenterol. 2021;55(8):666-673.
Abu-Amara M, et al. Small bowel involvement in systemic sclerosis: Clinical and endoscopic features. World J Gastroenterol. 2011;17(30):3594-3599.
Hokama A. Megaduodenum in systemic sclerosis. Rheumatology. 2022;61:e194.

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Acetic Acid Chromoendoscopy in Barrett Esophagus for Dysplasia Detection

Tue, 02 Jun 2026 00:00:00 GMT

Patient 1:

54-year-old male with a 10-year history of Barrett esophagus

Patient 2:

75-year-old male with a 20-year history of Barrett esophagus

Indication:

Routine surveillance endoscopy with dysplasia screening using acetic acid chromoendoscopy

Figure 2: Endoscopic view after acetic acid application showing diffuse whitening of the Barrett mucosa in the 75-year-old patient.

Endoscopic Findings

In Patient 1, no suspicious areas were identified. The Barrett segment extended 15 mm proximal to the gastric folds.
In Patient 2, after acetic acid application, areas showing loss of aceto-whitening were observed. These specific red areas were targeted for biopsy.

Endoscopic Technique

Standard upper endoscopy was performed.
Acetic acid chromoendoscopy was executed using a 2.5% solution. High concentrations (such as 5%) were avoided due to the risk of cellular damage and reduced diagnostic accuracy from excessive whitening.
Acetic acid breaks disulfide bonds in the mucin glycoproteins of the cylindrical epithelial cells. The acid penetrates the cytoplasm, causing reversible denaturation and coagulation of cytoplasmic proteins. This scatters light, making the tissue appear white and masking the vascular pattern.
In dysplastic or cancerous cells, the cytoplasmic proteins have a reduced capacity to retain the acid due to abnormal, overcrowded nuclei. The whitening effect dissipates rapidly, resulting in a visible redness (loss of aceto-whitening).
Targeted biopsies were obtained from the areas showing rapid loss of aceto-whitening.

Discussion

Acetic acid chromoendoscopy is a low-cost, valuable technique for detecting dysplasia in Barrett esophagus. The method relies on the differential cellular response. Normal Barrett epithelium whitens and retains the effect for several minutes. In contrast, dysplastic cells show transient whitening followed by rapid clearance, appearing red.

This biological response allows the endoscopist to transition from random biopsy protocols to targeted biopsies, which significantly improves diagnostic yield. In Patient 2, biopsies from the red zones showing loss of aceto-whitening confirmed high-grade dysplasia.

References

Pohl H, Rösch T, Wallace MB. Acetic acid chromoendoscopy for Barrett's esophagus. Endoscopy. 2008;40(7):594-599.
Curvers WL, Alvarez Herrero L, Fockens P, et al. Mucosal morphology in Barrett's esophagus: correlation between magnification endoscopy and histology. Clin Gastroenterol Hepatol. 2008;6(2):167-173.
Singh R, Sharma S, Rastogi A, et al. Acetic Acid Chromoendoscopy for Early Detection of Dysplasia in Barrett's Esophagus: A Meta-Analysis. Dig Dis Sci. 2018;63(1):1-10.

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Endoscopic Balloon Dilation of a Benign Duodenal Stenosis

Tue, 02 Jun 2026 00:00:00 GMT

Patient:

75-year-old male

Presentation:

Nausea, vomiting, and abdominal distension

Indication:

Gastric outlet obstruction confirmed by CT scan

Endoscopic Findings

A ring-like fibroinflammatory stenosis was identified between the first and second portions of the duodenum (Panel A).
The stenosis was approximately 5 mm thick and 8 mm in diameter.
The gastroscope could not pass through the stenosis.

Endoscopic Technique

A guidewire was advanced through the stenosis.
A through-the-scope, controlled radial expansion balloon dilation catheter was advanced over the guidewire (Panel B).
A 13-14-15 mm balloon catheter was positioned such that the first marker was visible. It was then pulled back to ensure approximately half the length of the balloon was across the stenosis (Panels C, D) for homogeneous dilation.
The balloon was inflated with water (Panel E) under direct endoscopic visualization, observing mucosal rips (Panel F).
Post-dilation inspection (Panel G) was performed by advancing the deflated balloon deep into the dilated area.
Mucosal breaks were even and not deep (Panel H).
The endoscope could easily pass through the post-dilation stenosis.

Discussion

Endoscopic balloon dilation is a safe and effective technique for benign duodenal stenoses, particularly when a guidewire is utilized to prevent distal perforation.

Visualizing mucosal rips during dilation provides real-time feedback on the adequacy of dilation. This feedback helps prevent over-dilation.

The use of water for balloon inflation in cases without fluoroscopic guidance offers smoother and easier inflation compared to contrast medium.

A final inspection with the balloon catheter after deflation confirms successful dilation and assesses for complications.

References

Adler DG, Baron TH, Mashimo R, et al. Endoscopic balloon dilation of gastrointestinal stenoses: methodology and future directions. Gastrointest Endosc. 2004;60(1):151-155.
Standards of Practice Committee, ASGE. The role of endoscopy in the management of benign adult esophageal strictures. Gastrointest Endosc. 2021;93(3):525-538.
Kim M, Kim SJ, Lee TH, et al. Endoscopic balloon dilation for benign anastomotic stricture after gastric cancer surgery. BMC Gastroenterol. 2018;18(1):157.

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Endoscopic Placement of a Self-Expanding Metal Stent for Obstructing Sigmoid Diverticulitis

Tue, 02 Jun 2026 00:00:00 GMT

Patient:

72-year-old female

Presentation:

Abdominal pain, distention, nausea, and vomiting

Indication:

Acute sigmoid diverticulitis with partial bowel obstruction and significant retained stool confirmed by CT scan

Endoscopic Findings

A stenotic sigmoid colon due to severe diverticulitis was identified.
The stenosis prevented passage of the therapeutic scope.

Endoscopic Technique

The stricture site was determined under direct visualization (Panel B).
A therapeutic gastroscope with a 3.7 mm working channel was utilized. A transparent distal cap was fitted on the scope to stabilize the tip and retract mucosal folds.
A 0.035-inch guidewire was advanced through the stenosis using a balloon catheter (Panel C), guided by combined endoscopy and fluoroscopy (Panel D).
Once the guidewire position proximal to the stricture was confirmed, contrast was injected to verify the luminal position. The catheter was then removed.
A non-covered Evolution self-expanding metal stent (Cook Medical, USA) was advanced over the guidewire, through the scope, and across the stricture (Panel E).
Deployment was performed under fluoroscopic and endoscopic visualization (Panels F, G). The yellow marker on the delivery catheter was monitored continuously to ensure proper deployment of the distal flange distal to the stricture (Panels F, H). Constant traction was maintained to counter proximal migration.
Successful decompression was achieved, allowing the patient to undergo elective surgery after adequate bowel prep.

Discussion

This case highlights the utility of uncovered self-expanding metal stents for the decompression of benign colonic obstructions. In the setting of acute diverticulitis, partial bowel obstruction increases the risks of emergency surgery. Bridge-to-surgery stenting allows for bowel decompression and elective prep, reducing the need for an emergent colostomy.

The technique requires precise guidewire placement under dual guidance. Stabilizing the scope tip with a transparent cap is highly beneficial. Close attention to delivery device markers is essential because colonic stents tend to migrate proximally during deployment.

While self-expanding metal stents are more commonly applied in malignant obstructions, this approach demonstrates they are effective in benign stenoses under careful monitoring.

References

van Hooft JE, van Halsema EE, Baron TH, et al. Self-expanding metal stents for obstructing benign colonic strictures: a systematic review. Endoscopy. 2012;44(6):581-591.
Lamazza A, et al. Self expandable metal stents for left-sided colon obstruction from diverticulitis. A single center experience. Medicina (Kaunas). 2021;57:299.

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Hyperplastic Duodenal Polyp in Portal Hypertensive Gastrointestinal Disease

Mon, 18 May 2026 00:00:00 GMT

Final Diagnosis

Duodenal inflammatory polyp with surface erosion and gastric foveolar surface metaplasia, resected via hot snare polypectomy.

Patient Demographics

A 71-year-old female patient with a history of metabolic-associated hepatic steatosis and cirrhosis.

Clinical History

The patient presented for Esophagogastroduodenoscopy due to chronic anemia and guaiac-positive stools.

Endoscopic Findings

Upon upper endoscopy, the esophagus demonstrated normal mucosa. Diffuse portal hypertensive gastropathy was noted. Small gastric fundic gland polyps were observed. In the duodenum, a large, pedunculated polypoid lesion was identified. The lesion exhibited areas of erosion on its surface. The mucosal surface pattern of the polyp showed an irregular pit pattern consistent with Kudo classification IIIL and IV. Final histological analysis of the resected lesion revealed an inflammatory-type polyp with multifocal surface erosion and ulceration, associated with active inflammation and scattered foci of gastric foveolar surface metaplasia.

Endoscopic Technique

The base of the duodenal lesion was injected with 1.5 mL of normal saline. The lesion was then resected using a hot snare technique. The resulting defect was closed with an endoscopic clip.

Discussion

This case illustrates an unusual gastrointestinal presentation of cirrhosis with portal hypertension. Patients with cirrhosis and portal hypertension may present with various upper gastrointestinal abnormalities, including esophageal varices, portal hypertensive gastropathy, portal hypertensive enteropathy, colonopathy, and rectal varices (1-3). We have also described the presence of gastric antral vascular ectasia (GAVE)-like lesions in the cardia in patients with portal hypertension and cirrhosis (4). While GAVE, also known as watermelon stomach, is a recognized manifestation of portal hypertension, other lesions are less known and less frequently recognized. This case is notable because it demonstrates that inflammatory polyps can present in patients with cirrhosis and portal hypertension.

Key Learning Points

Inflammatory polyps can occur in the setting of portal hypertension and cirrhosis.
Chronic anemia and positive stool occult blood tests in cirrhotic patients warrant thorough endoscopic evaluation for unusual lesions beyond typical varices or gastropathy.
Endoscopic resection using a hot snare with saline injection and clip closure is an effective treatment for such lesions.
Histopathological analysis is crucial for definitive diagnosis of unusual polypoid lesions in portal hypertensive patients.

References

Hashiba Y, Okai K, Tokuhira R, et al. Histological characteristics of gastric hyperplastic polyps in patients with portal hypertension. Dig Endosc. 2011;23(4):307-313.
Koulaouzidis A, Bhatnagar S, Rondonotti E, et al. Duodenal pathology in patients with portal hypertension: A systematic review. World J Gastrointest Endosc. 2013;5(11):532-539.
Tripathi D, Makharia GK. Portal hypertensive gastropathy and enteropathy: Current concepts. J Clin Exp Hepatol. 2014;4(2):167-176.
Monkemuller K, Dwivedi A. CAVE - Cardia Antral Vascular Ectasias - A New Entity? The Practicing Endoscopist. https://thepracticingendoscopist/p/cave

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Pseudo-Mirizzi on ERCP: A Warning Sign for Vanishing Calot Syndrome

Wed, 06 May 2026 00:00:00 GMT

CASE REPORT

Juan De Dios Diaz Rosales, MD, MSc, Gastrointestinal Endoscopy Surgeon at Instituto Mexicano del Seguro Social and Universidad Autonoma de Ciudad Juarez. His clinical and academic interests include digestive diseases, biliary tract disorders, and therapeutic endoscopy.

Daniel A. Portillo-Rodriguez, MD, PGY-2 Resident, Hospital General de Zona No. 35. Dr. Portillo-Rodriguez is an early-career researcher and earned his medical degree from the Universidad Autonoma de Ciudad Juarez.

Clinical History

A 61-year-old woman presented with two weeks of postprandial upper abdominal pain, mild scleral icterus, dark urine, and a palpable right upper quadrant mass. Laboratory tests showed a mixed hepatocellular-cholestatic pattern: total bilirubin 2.31 mg/dL, direct bilirubin 1.77 mg/dL, AST 259 U/L, ALT 290 U/L, alkaline phosphatase 231 U/L, and GGT 852 U/L. Abdominal ultrasound demonstrated a markedly distended gallbladder measuring 138 x 63 x 55 mm, with sludge and multiple stones, the largest measuring 25 mm, without intrahepatic bile duct dilation. Non-contrast CT confirmed gallbladder hydrops and cholelithiasis, with a gallbladder measuring approximately 120 x 66 x 69 mm and heterogeneous intraluminal content.

Endoscopic Findings

ERCP was performed because the biochemical profile and mild jaundice suggested functional biliary obstruction despite the absence of significant bile duct dilation on initial CT imaging. The initial cholangiogram demonstrated opacification of the extrahepatic bile duct with a smooth extrinsic indentation and focal narrowing of the proximal-to-mid common bile duct, without an obvious intraductal filling defect. The was proximal dilation of the bile ducts. This configuration was considered compatible with pseudo-Mirizzi syndrome in the setting of a markedly distended gallbladder filled with stones (Figure 1).

Figure 1. ERCP cholangiogram. Extrinsic narrowing and deformation of the main bile duct, compatible with pseudo-Mirizzi syndrome.

Endoscopic Technique

After biliary sphincterotomy, balloon sweeping was performed. The post-sweep cholangiogram showed improved ductal clearance, preserved distal bile duct patency, and no definite residual filling defects, supporting the absence of retained choledocholithiasis after endoscopic extraction maneuvers (Figure 2).

Figure 2. ERCP after balloon sweeping. Balloon sweep of the bile duct. The distal radiopaque structure corresponds to the extraction balloon, not a retained common bile duct stone.

Given the extrinsic inflammatory deformation of the bile duct and the anticipated high-risk surgical anatomy, a plastic transpapillary biliary stent was placed to secure internal drainage and maintain ductal decompression (Figure 3).

Figure 3. Final ERCP image. Transpapillary biliary stent in adequate position, securing internal biliary drainage.

Discussion

Subsequent surgery confirmed an obliterated hepatocystic triangle, consistent with vanishing Calot anatomy. The key teaching point is that pseudo-Mirizzi on ERCP should alert both the endoscopist and the surgeon that the problem is not merely intraductal. Extrinsic biliary compression from a hostile gallbladder neck or infundibular inflammatory process may be the fluoroscopic signature of a dangerous Calot dissection. In this setting, endoscopic biliary drainage can serve as a bridge to safer surgical management, and the operative strategy should prioritize avoidance of major bile duct injury over completion of a conventional cholecystectomy.

References

Mercado MA, Rueda De Leon A, Cisneros-Correa J. Vanishing Calot Syndrome: Pseudo-Mirizzi Syndrome. J Am Coll Surg. 2020;230(5):841-842. doi: 10.1016/j.jamcollsurg.2020.01.036.
Mergener K, Enns R, Eubanks WS, Baillie J, Branch MS. Pseudo-Mirizzi syndrome in acute cholecystitis. Am J Gastroenterol. 1998;93(12):2605-2606. doi: 10.1111/j.1572-0241.1998.00559.x.
Brunt LM, Deziel DJ, Telem DA, et al. Safe Cholecystectomy Multi-society Practice Guideline and State-of-the-Art Consensus Conference on Prevention of Bile Duct Injury During Cholecystectomy. Ann Surg. 2020;272(1):3-23. doi: 10.1097/SLA.0000000000003791.

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Endoscopic Findings of Eosinophilic Esophagitis: A Case Report

Wed, 29 Apr 2026 00:00:00 GMT

CASE REPORT

Klaus Mönkemüller, MD, PhD, FASGE, FESGE, FJGES

Professor of Medicine, Department of Gastroenterology, Carilion Memorial Hospital, Virginia Tech Carilion School of Medicine, Roanoke, USA

Correspondence: Klaus Mönkemüller, MD, PhD — Department of Gastroenterology, Carilion Memorial Hospital, Virginia Tech Carilion School of Medicine, Roanoke, VA, USA

Abstract

Background: Eosinophilic esophagitis (EoE) is a chronic, immune-mediated inflammatory disorder of the esophagus increasingly recognized as a leading cause of dysphagia and food impaction in young adults. Diagnosis relies on recognition of characteristic endoscopic features and histopathological confirmation demonstrating eosinophilic infiltration of the esophageal mucosa.

Case: A 32-year-old man with a history of atopic dermatitis presented with intermittent dysphagia to solids. Upper endoscopy revealed classic findings of eosinophilic esophagitis including mucosal edema, concentric rings (trachealization), small white exudates and plaques, and longitudinal furrows. Biopsies were obtained for histological confirmation.

Conclusion: This case illustrates the characteristic endoscopic appearance of eosinophilic esophagitis. Recognition of these hallmark findings — rings, furrows, exudates, and edema — is essential for timely diagnosis and initiation of appropriate therapy. The association with atopic conditions should further raise clinical suspicion in patients presenting with dysphagia.

Keywords: eosinophilic esophagitis; EoE; concentric rings; longitudinal furrows; white exudates; trachealization; dysphagia; atopic dermatitis; crepe paper esophagus; esophageal biopsy

★ Key Clinical Takeaways

Eosinophilic esophagitis is characterized by four cardinal endoscopic signs: concentric rings (trachealization), longitudinal furrows, white exudates/plaques, and mucosal edema — memorized using the mnemonic EREFS (Edema, Rings, Exudates, Furrows, Stricture).
A history of atopic conditions (atopic dermatitis, asthma, allergic rhinitis, food allergy) in a young patient with dysphagia should raise immediate suspicion for EoE.
The "crepe paper esophagus" (mucosal fragility with tears during endoscope passage) and "tug sign" (resistance during scope advancement through a narrow-caliber esophagus) are additional endoscopic clues.
Endoscopic suspicion must be confirmed with esophageal biopsies — a minimum of 6 biopsies from at least 2 different esophageal levels is recommended, targeting areas with visible endoscopic abnormalities.
Early recognition and treatment with proton pump inhibitors, topical corticosteroids (swallowed fluticasone or budesonide), or dietary elimination therapy can prevent progression to fibrotic stricture formation.

Clinical History

A 32-year-old man presented with intermittent dysphagia to solids. He reported a diagnosis of atopic dermatitis five years prior. Endoscopy was performed to investigate the cause of his dysphagia.

Endoscopic Findings

Classic endoscopic findings of eosinophilic esophagitis were observed, including mucosal edema, concentric rings (trachealization), small white exudates and plaques on the mucosal surface, and longitudinal furrows running parallel to the length of the esophagus.

Additional potential findings in eosinophilic esophagitis that may be encountered include crepe paper esophagus, where the esophageal lining is fragile and tears easily during endoscope passage, and narrow-caliber esophagus, which produces a subjective feeling of resistance or stiffness during scope navigation — referred to as the "tug" sign.

Discussion

The endoscopic findings are highly suggestive of eosinophilic esophagitis (EoE), a chronic inflammatory disorder of the esophagus. The presence of concentric rings, longitudinal furrows, and white exudates are characteristic features. The patient's history of atopic dermatitis further supports the diagnosis, as EoE is often associated with other atopic conditions.

While not all classic features were explicitly mentioned as being present, the described findings are sufficient for a strong endoscopic suspicion of EoE. Confirmation typically requires histopathological analysis of esophageal biopsies demonstrating eosinophilic infiltration. Differentiation from other causes of esophagitis is crucial for appropriate management.

References

Abe Y, et al. Endoscopic diagnosis of eosinophilic esophagitis. Diagnostics (Basel). 2022;12:3202.
Pech O. Endoscopic appearance of eosinophilic esophagitis. Video Journal and Encyclopedia of GI Endoscopy. 2013;1:21–22.
Neumann H, Mönkemüller K. Endoscopic characterization of Esophageal Imaging and Swallowing (EGIS). Video Journal and Encyclopedia of Endoscopy. 2013;1:23–24.

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When to Perform Endoscopy or Radiological Tests in Patients with Unresponsive Celiac Disease?

Wed, 29 Apr 2026 00:00:00 GMT

In general, celiac disease patients with unresponsive or worsening GI symptoms are the ones at higher risk of complicated disease or complications such as EATL (lymphoma), adenocarcinoma, or ulcerative enteritis (1).

In patients with persistent symptoms, one should perform capsule endoscopy, deep enteroscopy, or radiological imaging (small bowel follow-through/enteroclysis) or MR enterography (2).

Alerting findings on endoscopy

Ulcerations
Polypoid or tumor lesions
Raised discoid (round) type lesions

Figure 2: Small bowel adenocarcinoma: 5% of all GI tumors and the second most common after NET (neuroendocrine tumor, carcinoid). It also occurs in celiac disease. Poor prognosis: 30% 5-year survival. Fry LC, Gutierrez JP, Mönkemüller K. Gastrointest Tumors 2014;1:9-17.

Figure 3: "Small" EATL (enteropathy-associated T-cell lymphoma) in a patient with celiac disease: fever, night sweats, weight loss, anorexia, abdominal pain. Terminal ileum: Kerckring folds ++. Courtesy of Prof. Chris Mulder, Holland.

Signs on x-ray

Reversed fold pattern (more Kerckring folds in the ileum than in the jejunum)
Small bowel dilation
Small bowel wall thickening
Cavitating mesenteric lymphadenopathy
Mesenteric hypervascularization
Splenic atrophy

Figure 4: A 69-year-old woman with longstanding CT stenosis near the ligament of Treitz and pre-stenotic dilatation. Courtesy of van Weyenberg, Holland.

Indeed, splenic atrophy is more common in RCD II (refractory celiac disease), but not in celiac disease and lymphoma (likely because the lymphoma brought the spleen size back to "normal") (3).

Because of both functional hyposplenism and spleen atrophy, patients with celiac disease are prone to infections with encapsulated organisms such as Klebsiella, Staphylococcus aureus, and Streptococcus pneumoniae (pneumococcus). Vaccination against Streptococcus pneumoniae is indicated.

References

Al-Toma A, Branchi F, Zingone F, et al. European Society for the Study of Coeliac Disease (ESsCD) 2025 updated guidelines on the diagnosis and management of coeliac disease in adults. Part 2: Management, follow-up, and complex disease courses. United European Gastroenterol J. 2026;14(2):e70195.
Al-Toma A, Zingone F, Branchi F, et al. European Society for the Study of Coeliac Disease 2025 updated guidelines on the diagnosis and management of coeliac disease in adults. Part 1: Diagnostic approach. United European Gastroenterol J. 2025;13(10):1855-1886.
van Gils T, Nijeboer P, van Waesberghe JHT, et al. Splenic volume differentiates complicated and non-complicated celiac disease. United European Gastroenterol J. 2017;5(3):374-379.

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Upper Esophageal Stenosis, Microcytic Anemia, and Plummer-Vinson Syndrome

Mon, 16 Mar 2026 00:00:00 GMT

CASE REPORT

Álvaro Martínez-Alcalá, MD, Klaus Mönkemüller, MD, PhD, FASGE, FESGE, FJGES, Professor of Medicine, Department of Gastroenterology, Virginia Tech Carilion School of Medicine

Final Diagnosis

Upper esophageal stenosis due to Plummer-Vinson syndrome with concomitant lymphocytic esophagitis, treated with endoscopic balloon dilation.

Patient Demographics

A 78-year-old White female with a history of chronic iron deficiency anemia and hypertension.

Clinical History

The patient presented with chronic dysphagia. The indication for upper endoscopy was evaluation of chronic dysphagia.

Endoscopic Findings

Upper endoscopy revealed a proximal esophageal stenosis. The mucosa of the stenosis appeared shiny, and multiple rings were visible. Biopsies were obtained coincidentally with dilation.

Endoscopic Technique

An endoscopic procedure was performed to address the esophageal stenosis.
Through-the-scope balloon dilation was utilized.
A controlled radial expansion balloon was advanced over a guidewire.
The balloon was inflated incrementally from 13 mm to 15 mm.
Biopsies of the esophageal mucosa were obtained. Histopathology of the biopsies revealed lymphocytic esophagitis. No complications occurred during the procedure.

Discussion

Plummer-Vinson syndrome, also known as Paterson-Brown-Kelly syndrome, is an exceedingly rare condition characterized by the triad of chronic iron deficiency anemia, dysphagia, and the presence of esophageal webs or rings. Patients may also present with glossitis, angular cheilitis, and koilonychia; these accessory findings are attributable to iron deficiency anemia. The diagnosis of Plummer-Vinson syndrome is typically established via barium swallow or upper endoscopy. The primary therapeutic interventions include esophageal dilation to alleviate dysphagia and iron supplementation to correct the underlying iron deficiency. Plummer-Vinson syndrome is recognized as a premalignant condition with an increased risk of esophageal squamous cell carcinoma; therefore, these patients require regular endoscopic surveillance to facilitate early detection and treatment of potential malignancies. The association of lymphocytic esophagitis with microcytic anemia in the context of Plummer-Vinson syndrome has not been previously described in the literature.

Key Learning Points

Plummer-Vinson syndrome is a rare condition presenting with iron deficiency anemia and dysphagia due to esophageal webs or rings.
Endoscopic dilation is effective for symptomatic relief of dysphagia in Plummer-Vinson syndrome.
Patients with Plummer-Vinson syndrome require lifelong endoscopic surveillance due to the increased risk of esophageal cancer.
Lymphocytic esophagitis may be an incidental finding in patients with Plummer-Vinson syndrome and requires further investigation regarding its clinical significance in this context.

References

Goel R, Maydonovitch CL, Arora M, et al. Plummer-Vinson syndrome: A rare and forgotten cause of dysphagia. Am J Case Rep. 2017;18:1052-1056.
Hoffman RM, Jaffe PE. Plummer-Vinson syndrome. A case report and review of the literature. Arch Intern Med. 1995;155(18):2008-2011.
Drossman DA. Esophageal dilation. Endoscopy. 2017;49(12):1201-1202.

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Massive Hemorrhage After Biliary Sphincterotomy Treated with Self-Expanding Metal Stent

Sat, 07 Mar 2026 00:00:00 GMT

CASE REPORT

Final Diagnosis

Massive hemorrhage after biliary sphincterotomy, successfully treated with fully covered self-expanding metal stent placement.

Patient Demographics

A 71-year-old female patient with a history of hypertension and stage 3 chronic renal disease presented with jaundice.

Clinical History

On CT and MRCP a biliary stricture at the bifurcation was found (Fig. A-C). Following endoscopic retrograde cholangiopancreatography (ERCP) and subsequent brushing, the stricture was diagnosed as adenocarcinoma. Panel D shows the stenosis. Two-seven French double pigtail plastic stents were placed across the stricture into the left intrahepatic system (Panel E). A billiary sphincterotomy was performed prior to stent placement. Three days post-discharge, the patient presented to an emergency room with melena, hypotension, and a drop in hemoglobin from 12 g/dL to 5 g/dL. She was resuscitated, transfused with two units of packed red blood cells, and transported with an helicopter to our facility for urgent ERCP.

Endoscopic Findings

During the urgent ERCP for bleeding, active hemorrhage was noted at the papilla, emanating around the two previously placed pigtail plastic stents.

Endoscopic Technique

Urgent ERCP for bleeding: After successful cannulation of the biliary tree with a balloon catheter and a 0,035 inch biliary guidewire, a fully covered self-expanding metal stent (Viabil) was advanced and deployed. The stent expanded well, achieving tamponade of the bleeding area, with no further hemorrhage observed.

Discussion

Massive post-sphincterotomy bleeding represents a catastrophic complication that is particularly challenging to manage due to the constraints of side-viewing endoscopy and potentially difficult papillary positioning (1-3). Various methods exist to achieve hemostasis, including local injection, endoscopic clips, balloon tamponade over a guidewire, thermal coagulation, topical hemostatic agents such as Purastat, and placement of a fully covered self-expanding metal stent. In this case, the rapid deployment and expansion of a fully covered self-expanding metal stent over a guidewire effectively controlled the hemorrhage through tamponade. This approach is considered among the most efficient and safest methods for immediate hemostasis in such critical situations.

Key Learning Points

Post-ERCP bleeding, particularly after sphincterotomy, can be life-threatening and requires prompt intervention.
Management of post-sphincterotomy bleeding can be challenging due to endoscopic limitations and papillary anatomy.
Fully covered self-expanding metal stents offer a fast, safe, and effective method for achieving hemostasis via tamponade in cases of massive post-sphincterotomy hemorrhage.
Recognition of predisposing factors and preparedness for potential complications are crucial in advanced endoscopic procedures.

References

Sethi S, Trieu H, Chen B, et al. Fully covered self-expandable metal stents for refractory postsphincterotomy bleeding. Endoscopy. 2012;44(S 02):E333-E334.
Barkun AN, Cotton PB, Shah RJ, et al. ERCP-related complications: The new ASGE guideline on endoscopy and complications in gastrointestinal endoscopy. Gastrointest Endosc. 2022;95(3):395-400.
Kim HJ, Kim MH, Lee SK, et al. Fully covered self-expandable metallic stents for bleeding from biliary sphincterotomy: Initial experience in four patients. Dig Dis Sci. 2013;58(5):1414-1418.

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Top Tips for Endoscopic Banding of Hemorrhoids

Fri, 06 Mar 2026 00:00:00 GMT

Final Diagnosis

Final diagnosis: Endoscopic rubber band ligation for symptomatic internal hemorrhoids.

Clinical History

A 75-year-old woman with intermittent, painless rectal bleeding. During colonoscopy, internal hemorrhoids were found. This patient was referred for colonoscopy and therapy of internal hemorrhoids using rubber band ligation. Endoscopic rubber band ligation is a safe, effective, non-operative, and well-tolerated endoscopic procedure for treating symptomatic internal hemorrhoids.

Endoscopic Findings

Visualization of targeted hemorrhoids in retroflex position (Figure 1A, B).
Inflation is useful to confirm the hemorrhoids to be treated, as those remain bulging, whereas the small hemorrhoids flatten out (Figure 1B).
Water instillation through the endoscope's water channel, with the patient in the left lateral decubitus position, indicates the location of hemorrhoids based on water accumulation (Figure 1C, D). The yellow arrow shows the water accumulation on the left side of the rectum. Thus, the bulging hemorrhoid is located on the right side.

Endoscopic Technique

The endoscope is advanced to the rectal canal and positioned in retroflex. The targeted hemorrhoids are visualized (Figure 1A, B).
Inflation is performed to identify bulging hemorrhoids; those that disappear with inflation may not require treatment (Figure 1C, D).
To precisely localize hemorrhoids, water is instilled through the endoscope's water channel. With the patient in the left lateral decubitus position, water accumulation identifies the corresponding hemorrhoid on the right side. The yellow arrow highlights the area of water accumulation (Figure 1E).
Before banding, the location of the hemorrhoid in relation to the dentate line is determined. The dentate line is avoided during ligation to prevent pain.
The endoscope, loaded with the banding device, is advanced to the rectal canal. Hemorrhoids are banded in either an antegrade or retroflex position. The retroflex position is preferred for internal targeting and reduced risk of engaging the dentate line, providing excellent visualization of the anorectal area (Figure 1F, G, H).
During suctioning of the hemorrhoid into the cap, excessive suctioning or filling more than two-thirds of the cap is avoided to prevent subsequent large ulcer formation. Also, if too much tissue is suctioned into the cap, the chances of including the dentate line are increased. Therefore, controlled and careful suctioning should be applied.
After deployment of the rubber band, the area is inspected to confirm appropriate distance from the dentate line (Figure 1H).

Discussion

Endoscopic rubber band ligation remains a cornerstone in the management of symptomatic internal hemorrhoids (1-3). This technique, when performed with careful attention to procedural details, offers a safe and effective treatment option (1-3). Key considerations include precise localization of hemorrhoids, particularly in relation to the dentate line, to minimize patient discomfort and complications. The use of water instillation and retroflex viewing enhances accurate identification and targeting.

Optimal suctioning during band placement is critical to prevent over-ligation and potential ulceration. The described preference for retroflex banding highlights an approach aimed at maximizing precision and safety by allowing for direct visualization and internal targeting of the hemorrhoidal tissue, thereby reducing the risk of complications associated with inadvertent banding of the dentate line.

References

MacRae HM, McLeod RS. Comparison of hemorrhoidal treatment modalities: a meta-analysis. Dis Colon Rectum. 1995;38(8):687-694.
Lohsiriwat V. Hemorrhoids: from a single symptom to a medical condition. World J Gastroenterol. 2012;18(17):2021-2023.
Gaj FF, Brattoli S, Di Leo M, et al. Rubber band ligation for hemorrhoids: new insights into a traditional technique. World J Gastrointest Endosc. 2021;13(5):170-179.

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Endoscopic Placement of Colonic Self-Expanding Metal Stent for Malignant Obstruction

Mon, 02 Mar 2026 00:00:00 GMT

Patient:

70-year-old woman with metastatic colon cancer

Indication:

Acute colonic obstruction; decompressing self-expanding metal stent

Final diagnosis:

Malignant colonic obstruction treated with endoscopic SEMS placement

Clinical History

A 70-year-old woman presented with acute colonic obstruction in the setting of metastatic colon cancer. CT showed a large metastasis with distended large and small bowel loops. The indication for endoscopy was decompressing self-expanding metal stent placement.

Endoscopic Findings

Tight stenosis in the distal sigmoid colon on endoscopy.
CT confirmation of obstruction with dilated proximal bowel loops and a large metastasis.

Endoscopic Technique

Therapeutic gastroscope with a 3.7 mm working channel.
Biliary balloon catheter and 0.035-inch J-tip guidewire advanced across the stenosis under combined endoscopic and fluoroscopic guidance.
Contrast through the catheter confirmed position in the dilated proximal colon, then deep wire advancement for safe stent delivery length.
Balloon inflated distal to the stricture and pulled back until resistance to estimate length and choose stent size.
SEMS advanced over the wire. Proximal flange released under endoscopic view while gently pulling back both the endoscope and delivery catheter to prevent proximal stent shoot-up.
Delivery catheter marking monitored for proximal positioning. Immediate endoscopic and fluoroscopic confirmation of expansion and decompression.

Discussion

Why SEMS here. Malignant colonic obstruction often needs urgent decompression. In advanced disease or high surgical risk, SEMS provides palliation or a bridge to surgery without an emergent resection or colostomy.

Equipment and imaging. Channel size is not a detail. Pediatric or thin channels under about 3.2 mm commonly fail to accept the delivery system. Dual guidance keeps the wire honest and shows deployment in real time.

Length and deployment control. Contrast plus balloon pullback improves stent sizing and coverage. The synchronized scope-and-catheter pull-back is the maneuver that keeps a distally expanding stent from migrating proximally. Full expansion can continue over hours to days; immediate balloon dilation is often unnecessary unless the lumen stays critically narrow.

References

Small AJ, Coelho-Prabhu N, Lieberman DA, et al. American Society for Gastrointestinal Endoscopy guideline on the role of endoscopy in the management of colorectal cancer. Gastrointest Endosc. 2017;85(4):689-701.
Van Hooft JE, van Halsema EE, Vanbiervliet G, et al. Self-expandable metal stents for the palliation of malignant colonic obstruction: updated recommendations from the European Society of Gastrointestinal Endoscopy. Endoscopy. 2014;46(12):1070-1081.
Spinelli A, Galasso E, Contino G, et al. Endoscopic stenting for malignant colorectal obstruction: A systematic review and meta-analysis of outcomes in 2200 patients. Dig Liver Dis. 2018;50(1):11-18.

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Acute Pancreatitis Following Laparoscopic Intraoperative Cholangiogram and Exploration

Sun, 01 Mar 2026 00:00:00 GMT

CASE REPORT

Klaus Mönkemüller, MD, PhD, Professor of Medicine, Department of Gastroenterology, Virginia Tech Carilion School of Medicine

Final Diagnosis

Acute pancreatitis following laparoscopic intraoperative cholangiogram with common bile duct exploration and balloon dilation of the papilla.

Patient Demographics

A 45-year-old male patient.

Clinical History

The patient presented with acute cholecystitis. He underwent laparoscopic cholecystectomy with Intraoperative cholangiogram (IOC) and common bile duct exploration after the identification of multiple filling defects within the CBD. Twenty-four hours post-OP, the patient developed epigastric abdominal pain radiating to the back with an elevated lipase of 750 IU/l, consistent with acute pancreatitis.

Endoscopic Findings

Multiple stones were visualized during exploration of the common bile duct.

Endoscopic Technique

A laparoscopic cholecystectomy was performed.
Multiple filling defects were identified, prompting the decision for common bile duct exploration.
A SpyGlass cholangioscope was utilized for exploration of the common bile duct, revealing multiple stones.
Stone removal was performed.
A guidewire was advanced across the papilla into the duodenum.
Balloon dilation of the papilla was performed using an 8 mm balloon.

Discussion

Acute pancreatitis occurring after an intraoperative cholangiogram with common bile duct exploration is generally considered to have a very low incidence. Many institutions perform intraoperative cholangiography and common bile duct exploration with the belief that this approach carries a lower risk of pancreatitis compared to endoscopic retrograde cholangiopancreatography (ERCP). Furthermore, many gastroenterology textbooks do not list intraoperative cholangiogram or balloon dilation of the papilla as causes of pancreatitis. However, there is evidence to suggest that this complication can occur.

A retrospective study by Matias Czerwonko, et al., published in the World Journal of Surgery in 2018, analyzed 447 patients who underwent laparoscopic transcystic common bile duct exploration between 2007 and 2017. Of these, 70 patients developed post-procedure hyperamylasemia, and 20 patients (4.5%) developed acute pancreatitis, confirmed clinically, radiologically, and by laboratory work. One patient developed severe necrotizing pancreatitis. This study highlights that the risk of acute pancreatitis after intraoperative cholangiogram and common bile duct exploration is not insignificant, and clinicians should be aware of this potential complication.

Key Learning Points

Acute pancreatitis is a rare but recognized complication of laparoscopic intraoperative cholangiogram and common bile duct exploration.
The incidence of pancreatitis following this procedure may be higher than traditionally perceived.
Clinicians should maintain awareness of acute pancreatitis as a potential adverse event after intraoperative bile duct interventions.
Elevated lipase and characteristic abdominal pain post-procedure warrant investigation for pancreatitis, even after laparoscopic common bile duct exploration.
While often considered safer than ERCP in terms of pancreatitis risk, laparoscopic approaches involving papillary manipulation are not entirely without risk.

References

Morgan S, Traverso LW. Intraoperative cholangiography and post operative pancreatitis. Surf Endosc 2000;14:264-6.
Czerwenko M, et al. Postoperative pancreatitis after laparoscopic transcystic common bile duct exploration. World J Surg. 2018;42(8):2527-2533.

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Bile Duct Injury After Laparoscopic Intraoperative Cholangioscopy

Sun, 01 Mar 2026 00:00:00 GMT

CASE REPORT

Klaus Mönkemüller, MD, PhD, FASGE, FESGE, FJGES, Professor of Medicine, Department of Gastroenterology, Virginia Tech Carilion School of Medicine

Final Diagnosis

Bile duct injury with associated bile leak and choledocholithiasis, managed with endoscopic retrograde cholangiopancreatography and self-expanding metal stent placement.

Patient Demographics

A 45-year-old patient.

Clinical History

The patient was admitted with acute cholecystitis and underwent emergent laparoscopic cholecystectomy. During intraoperative cholangiogram, multiple stones were visualized within the bile duct. A direct laparoscopic intraoperative cholangioscopy was performed (panel B) revealing multiple stones, some of which were impacted within the bile duct. Spy Glas cholangioscopy-lithotripsy was performed. The bile duct subsequently appeared damaged and swollen. An intraoperative cholangiogram revealed a large bile leak (panel D).

Endoscopic Findings

Endoscopic retrograde cholangiopancreatography (ERCP) demonstrated a significant bile leak (E, yellow arrow).
A rounded filling defect, consistent with a bile stone, was observed within the bile duct near the area of the injury (F, yellow arrow).
The wire was seen exiting through the bile duct injury (panel E, green arrow).

Endoscopic Technique

ERCP was performed following the discovery of a bile duct injury.
A wire was manipulated past the stone and the bile leak into the proximal common bile duct and left hepatic system (panel F)
An 8 mm diameter, 60 mm long self-expanding metal stent (Viabil) was inserted into the common bile duct, bridging the bile duct injury (G, F, yellow oval).
An occlusion cholangiogram through the stent confirmed resolution of the bile leak (H).
A plastic stent was placed through the metal stent to maintain patency and prevent occlusion from proximal stones. This also aimed to prevent a stone-induced valve mechanism effect.
The patient is scheduled for stent removal in approximately six months. If bile leak persists, a new stent will be inserted.

Discussion

This case highlights a rare but significant complication of laparoscopic intraoperative cholangioscopy for choledocholithiasis: bile duct injury and subsequent bile leak. The immediate recognition and endoscopic management of this complication are crucial for patient outcomes. The use of a self-expanding metal stent provided immediate sealing of the bile leak, while the placement of an additional plastic stent addressed the concern of continued obstruction from residual stones. The decision to prioritize bile leak sealing over complete stone extraction during the initial ERCP was appropriate given the acuity of the injury and the technical challenges posed by the inflamed duct. Subsequent follow-up for stent removal and potential further stone management is essential.

Key Learning Points

Bile duct injury is a potential complication of advanced endoscopic procedures such as intraoperative cholangioscopy and lithotripsy.
Endoscopic retrograde cholangiopancreatography is an effective method for the diagnosis and management of bile duct injuries and bile leaks.
Self-expanding metal stents can effectively seal bile duct injuries and leaks.
Consideration should be given to placing a plastic stent within a metal stent to maintain patency and prevent occlusion from residual stones or debris.
Long-term follow-up is essential to ensure resolution of the injury and to manage any remaining biliary pathology.

References

Cotton PB, et al. Endoscopic management of bile duct injuries. Gastrointest Endosc. 2007;65(6):830-836.
Singhal D, et al. Endoscopic treatment of bile leaks. Curr Opin Gastroenterol. 2013;29(5):540-545.
Davids PH, et al. Bile duct strictures after laparoscopic cholecystectomy: a new challenge for the endoscopist. Gut. 1993;34(9):1260-1262.

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Interventional Chromoendoscopy for Colorectal Lesion Resection

Sat, 28 Feb 2026 00:00:00 GMT

Final Diagnosis

Final diagnosis: Laterally spreading tumor of the colon, resected via endoscopic mucosal resection with interventional chromoendoscopy.

Clinical History

A 54-year-old woman underwent surveillance colonoscopy for colorectal cancer screening.

Endoscopic Findings

A flat lesion was identified in the colon (A, yellow arrow). Close-up examination revealed a small laterally spreading tumor measuring approximately 15 mm, classified as Paris 2a, with a Kudo pattern IIIS (B, yellow circle).

Endoscopic Technique

The lesion was injected with Everlift, a submucosal lifting agent that includes a pre-mixed colored substance (C). This created a visible interface, with the neoplastic flat lesion appearing white against the blue submucosal layer (C and D).
The presence of the blue color allowed for clear differentiation of the superficial lesion from deeper layers, such as the submucosa and muscularis propria (C, yellow stars).
After resection, a white color corresponding to the muscularis propria was observed, indicating the depth of resection (E, blue arrow). The submucosa has a bluish color.
Prophylactic clips were applied to close the post-resection defect (F).

Discussion

Interventional chromoendoscopy offers several advantages during endoscopic resection (EMR or ESD). First, it provides a color interface that delineates lesions that may be challenging to visualize under white light endoscopy, ensuring complete lesion characterization.

Second, the submucosal cushion created by the lifting agent provides a safety base for resection, minimizing the risk of perforation.

Third, it allows for clear visualization of the third space, including submucosal layers, providing a visual element to prevent complications. If the resection is carried out too deeply, the absence of blue color in the submucosa signals excessive depth, prompting prophylactic closure with clips to prevent immediate or delayed colon perforation.

References

Parra-Blanco A, Gimeno-García AZ, Quintero E. Chromoendoscopy and new endoscopic imaging techniques. World J Gastroenterol. 2011;17(41):4541-4552.
Kudo S, Hirota S, Nakajima T, et al. Colorectal tumors and pit pattern analysis. J Clin Gastroenterol. 1994;18(3):218-222.
Tanaka S, Kashida H, Saito Y, et al. JGES guidelines for colorectal endoscopic submucosal dissection/endoscopic mucosal resection. Dig Endosc. 2020;32(1):154-180.
Mönkemüller K, Wilcox CM. Interventional chromoendoscopy. Gastrointest Endosc. 2013;78:346-350.

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Severe Esophageal Necrosis Following Caustic Ingestion

Fri, 27 Feb 2026 00:00:00 GMT

CASE REPORT

Dr Jhordy Garcia, Department of Gastroenterology, Hospital Francisco Moscoso Puello, Dominican Republic

Final Diagnosis

Extensive esophageal necrosis from sodium hydroxide ingestion.

Patient Demographics

A 58-year-old male.

Clinical History

The patient presented after intentional ingestion of a caustic substance (sodium hydroxide, a cleaning material) in a suicide attempt. Endoscopy was performed 6 hours post-ingestion. He is currently receiving ventilatory support in the intensive care unit.

Endoscopic Findings

Extensive necrosis of the esophageal mucosa was observed throughout the visible esophagus.
Significant damage to the vocal cords was noted.
The scope was not advanced beyond the esophagogastric junction due to concern for perforation.

Endoscopic Technique

Endoscopy was performed approximately 6 hours after caustic ingestion. A standard endoscope was used. The procedure was limited to the esophagus and did not proceed beyond the esophagogastric junction to mitigate the risk of iatrogenic perforation given the severe mucosal damage observed.

Discussion

Caustic ingestion poses a significant medical emergency with high morbidity and mortality. Sodium hydroxide, an alkaline substance, typically causes liquefactive necrosis, leading to deep tissue injury and potential perforation, as well as stricture formation in survivors. The extensive esophageal necrosis observed within hours of ingestion indicates severe injury. The involvement of the vocal cords suggests aspiration or direct contact during ingestion, further complicating the patient's respiratory status and prognosis. The decision to limit the endoscopic examination due to perforation risk was appropriate and highlights a critical aspect of managing caustic injuries. Early endoscopy is crucial for assessing the extent of injury and guiding management, but it must be performed cautiously. The patient's presentation with extensive necrosis and respiratory compromise strongly suggests a grave prognosis.

Key Learning Points

Caustic ingestion is an urgent medical emergency requiring prompt evaluation.
Sodium hydroxide causes liquefactive necrosis, often leading to extensive and deep tissue damage.
Early endoscopy is essential for assessing injury extent but should be performed carefully, stopping if perforation risk is high.
Vocal cord involvement signifies severe upper airway injury and worsens prognosis.
Extensive esophageal necrosis observed within hours of ingestion is indicative of a very poor prognosis.

References

Hall AH, et al. Caustic injury to the upper gastrointestinal tract. J Emerg Med. 1999;17(4):713-718.
Contini S, et al. Caustic injury of the esophagus and stomach: An analysis of 170 patients. Dig Dis Sci. 2005;50(12):2273-2278.
Poley JW, et al. The management of caustic injuries to the upper gastrointestinal tract. Endoscopy. 2002;34(7):559-563.

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Severe Gastric Ulcers due to Radiation with Yttrium-90 Microspheres

Thu, 26 Feb 2026 00:00:00 GMT

CASE REPORT

Final Diagnosis

Gastric ulceration due to Yttrium-90 microsphere embolization.

Patient Demographics

A 75-year-old female.
History of stage IIIC hepatocellular carcinoma.
History of Yttrium-90 selective tumor embolizatio for two years.

Clinical History

The patient also received monoclonal antibody therapy for hepatocellular carcinoma.
She underwent Yttrium-90 transarterial radioembolization for hepatocellular carcinoma.
She presented with severe abdominal pain, nausea, vomiting, and weight loss several weeks after her last embolization, prompting esophagogastroduodenoscopy.

Endoscopic Findings

Esophagogastroduodenoscopy revealed multiple, very large gastric ulcers located in the fundus and proximal body of the stomach.
The ulcers were covered by fibrin.
Two areas of visible vessels were noted within the ulcers.
No active bleeding was observed during the procedure.

Endoscopic Technique

A standard upper endoscope was used to visualize the stomach.
The ulcers were documented and characterized.
Biopsies were obtained.

Discussion

Yttrium-90 (Y-90) transarterial radioembolization is an interventional radiology technique used to treat hepatocellular carcinoma and metastatic colon cancer (1-3).
This therapy is generally considered safe and effective, with increasing utilization over time.
Complications such as duodenal and gastric ulcers have been reported, with an incidence ranging from 2% to 4% (4).
These ulcers result from inadvertent delivery of Y-90 microspheres to the microvasculature of the stomach or duodenum, leading to direct radiation toxicity (4).
Symptoms, including abdominal pain, weight loss, vomiting, anorexia, and bleeding, typically arise hours to months after therapy (1-4).
Severe cases of sepsis due to perforation have been reported (3).
Diagnosis is made endoscopically and histologically.
These radiation-induced gastric ulcers are often recalcitrant to standard proton pump inhibitor therapy due to a distinct pathophysiology, as the damage is radiogenic and extends transmurally across the entire thickness of the gastrointestinal tract wall.

Key Learning Points

Yttrium-90 radioembolization can cause severe gastric and duodenal ulcers due to inadvertent microsphere delivery.
Endoscopic diagnosis is crucial for characterizing these radiation-induced ulcers.
Radiation-induced gastrointestinal ulcers typically present with abdominal pain, nausea, vomiting, and weight loss, and may not respond to conventional acid suppression therapy.
These ulcers can have significant morbidity, including perforation and sepsis.
Awareness of this complication is essential for appropriate patient management following Y-90 radioembolization.

References

Riaz A, Lewandowski RJ, Kulik LM, et al. Practical management of complications following yttrium-90 radioembolization. Semin Intervent Radiol. 2011;28(4):450-459.
Hasteh F, Dasyam AK, Kothary N, et al. Gastric and Duodenal Ulceration after Yttrium-90 Radioembolization: Etiology, Clinical Presentation, and Management. J Vasc Interv Radiol. 2017;28(10):1442-1448.
Kallini JR, Gabr A, Wade T, et al. Complications of Yttrium-90 Radioembolization. Tech Vasc Interv Radiol. 2017;20(2):121-127.
Mushtaq M et al. Gastric ulcers located with Ytrrium-90 microsphere selective internal radiation therapy. Cureus 2024;16:e58702.

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Ileal Carcinoid Tumor

Tue, 24 Feb 2026 00:00:00 GMT

CASE REPORT

Jay Bapaye, MD, Kerry Whitt, MD. Department of Gastroenterology, Virginia Tech Carilion School of Medicine

Final Diagnosis

Ileal neuroendocrine tumor with G1 differentiation, diagnosed via colonoscopic biopsy.

Patient Demographics

A 54-year-old woman.

Clinical History

The patient presented with two weeks of abdominal pain. She had a history of chronic constipation but was
otherwise healthy.
Given her new symptoms, a CT scan of the abdomen and pelvis was obtained.
The CT scan identified a 2.6 cm hyperenhancing, pedunculated-appearing lesion within the terminal ileum
with adjacent right lower quadrant soft tissue thickening and no lymph node enlargement, concerning for a neoplasm.

Endoscopic Findings

During ileocolonoscopy, a large and partially lumen-obstructing mass was observed, measuring
approximately 3 cm and located 4 to 5 cm from the ileocecal valve.
The lesion appeared rounded and polypoid, with a yellowish color, a smooth surface with multiple
superficial vessels, and was firm to the touch with the biopsy forceps.

Endoscopic Technique

A colonoscopy was performed.
Eight biopsies were obtained from the ileal lesion using biopsy forceps.
Histology confirmed a neuroendocrine tumor with G1 differentiation.
No complications occurred during the procedure.

Discussion

Carcinoid or neuroendocrine tumors are slow-growing neoplasms arising from enterochromaffin cells in the
small intestine. They account for approximately 28% of terminal ileal carcinoids.
These tumors are frequently diagnosed late due to non-specific symptoms such as abdominal pain or
diarrhea, at which point metastasis to the liver and lymph nodes may have already occurred. Most early carcinoids are asymptomatic, though patients may experience intermittent abdominal pain, nausea, and some weight loss.
In the presented case, the incidental discovery on CT imaging led to the early recognition of this lesion.
Advanced carcinoid syndrome occurs in about 10% of cases, commonly after metastasis, and is
characterized by flushing, chronic watery diarrhea, and sweating.
Common complications of ileal carcinoids include small bowel obstruction and intestinal bleeding. Rarely,
tricuspid cardiac valve damage (carcinoid heart disease) occurs, but only in the setting of metastatic disease.
Diagnostic tests for ileal carcinoid include CT or MRI scans of the abdomen and pelvis, serum blood tests
such as chromogranin A, 24-hour urine for 5-hydroxyindoleacetic acid, and somatostatin receptor imaging (Octreoscan or PET/CT).
Obtaining direct tissue visualization via capsule endoscopy or deep endoscopy, such as single or
double-balloon enteroscopy with biopsies, is crucial for histological confirmation of the disease.

Key Learning Points

Ileal neuroendocrine tumors can present with non-specific abdominal pain, making early diagnosis
challenging.
Cross-sectional imaging such as CT scans can be instrumental in the incidental discovery of these lesions.
Endoscopic visualization reveals characteristic features such as a yellowish, firm, polypoid lesion with
superficial vessels.
Biopsy and histological confirmation are essential for definitive diagnosis and grading of neuroendocrine
tumors.
While often slow-growing, these tumors can metastasize and lead to carcinoid syndrome, necessitating
prompt identification and management.

References

Gaujoux S, Itzkowitz SH. Ileal carcinoid tumors. Gastroenterology. 2009;137(3):805-809.
Kulke MH. Carcinoid tumors. Curr Opin Oncol. 2006;18(1):52-57.
Ramage JK, Ahmed A, Ardill J, et al. Guidelines for the management of gastroenteropancreatic
neuroendocrine (including carcinoid) tumours (NETs). Gut. 2012;61(1):6-32.

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Esophageal Inlet Patch Causing Acute Dysphagia and Food Impaction

Mon, 23 Feb 2026 00:00:00 GMT

CASE REPORT

Department of Gastroenterology, Virginia Tech Carilion School of Medicine

Final Diagnosis

Esophageal inlet patch causing stricture and food impaction, managed with endoscopic foreign body removal and subsequent dilation.

Patient Demographics

A 52-year-old female patient.

Clinical History

The patient presented with acute dysphagia. Upper endoscopy was indicated to evaluate the cause of acute dysphagia.

Endoscopic Findings

A 20 x 30 mm esophageal inlet patch was identified.
A distal fibrotic stricture was noted in the esophagus.
Distal to the fibrotic stricture, a piece of chicken was impacted in the midesophagus.
Another esophageal stricture was observed distal to the food impaction.

Endoscopic Technique

The impacted chicken meat was removed using a distal transparent cap attached to the endoscope.
Following the initial procedure, the patient was initiated on proton pump inhibitors.
A subsequent upper endoscopy was performed where esophageal dilation was carried out up to 16 mm.

Discussion

An inlet patch, also known as esophageal heterotopic gastric mucosal patch or cervical inlet patch, is a common but often overlooked area of ectopic gastric mucosa found in the upper esophagus. It is present in approximately 3 to 5% of patients undergoing upper endoscopy. While most patients are asymptomatic, some may experience symptoms such as dysphagia, cough, globus sensation, or hoarseness. Treatment for symptomatic inlet patch involves ablating the tissue, typically using techniques like argon plasma coagulation or radiofrequency ablation. Proton pump inhibitors are beneficial in reducing acid secretion from the ectopic gastric mucosa. Moreover, patients with associated esophageal strictures, as in this case, benefit from endoscopic dilation. This case highlights an uncommon presentation of an inlet patch causing esophageal stricture and acute food impaction.

Key Learning Points

Esophageal inlet patches, while often asymptomatic, can cause significant symptoms including dysphagia and stricture formation.
Food impaction can occur in the setting of an underlying esophageal stricture caused by an inlet patch.
Endoscopic removal of foreign bodies and subsequent esophageal dilation are effective treatments for managing symptomatic inlet patch-associated strictures.
Proton pump inhibitor therapy can help mitigate acid-related complications from ectopic gastric mucosa.

References

Behrens C, Yen NPP. Esophageal patch. Radiology Research and Practice. 2011;2011:2460890.
Bindlish S, Murali R. Inlet patch stricture: a case report. American Journal of Gastroenterology. 2010;105:23.
Bajbpuj, M et aI. Argon plasma coagulation of cervical heterotopic gastric mucosa as an alternative treatment for globus sensation. Gastroenterology. 2009;137:440–4.

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Gastric Neuroendocrine Tumors (NET) (Carcinoids): A Quick Mini-Review

Tue, 17 Feb 2026 00:00:00 GMT

Gastric Neuroendocrine Tumors (NET) (Carcinoids) – A Quick Mini-Review

Klaus Mönkemüller, MD, PhD, FASGE, FESGE, FJGES

Professor of Medicine, Department of Gastroenterology, Carilion Memorial Hospital, Virginia Tech Carilion School of Medicine, Roanoke, USA

Figure 1. Spectrum of gastric neuroendocrine tumors (NET, carcinoids). A. NET located in stomach body, type II. Note the “squared” sessile shape with depressed top. NET also have spotty areas of increased vascularity. B. Note the areas of neo-angiogenesis. C. NET are often found in the stomach body, on stomach folds. Note this “broadened” fold with reddish, depressed center. D. This NET located on the pyloric channel was found due to its spontaneous bleeding and protruding aspect. E. NET type I located on stomach fold. F. Close up view revealed an irregular mucosal surface with fatty villous structures. G. These pit pattern can be better appreciated using narrow band imaging (NBI). H. “Typical” type I NET in patient with chronic atrophic gastritis. Notice the hypervascular, sessile lesion in the setting of gastric mucosal atrophy. I. NBI is ideal to show the vascularity of these lesions and demarcate from the surrounding tissue. J. Many NET have a characteristic yellowish color and many superficial vessels. K, L and M. Histology of NET. K. Notice the well-differentiated, organoid arrangement of tumor cells, often appearing as small, uniform, round-to-oval cells with characteristic "salt and pepper" chromatin. These tumors typically arise in the submucosa and can grow in various patterns, including nests, ribbons, trabeculae, or glandular (rosette-like) structures. umor cells are positive for neuroendocrine markers, specifically: chromogranin (M), synaptophysin and INSM1.

Classification and Workup of Gastric Neuroendocrine Tumors

▸ Gastric NETs are classified into three types:

Type 1 (80% of cases, associated with autoimmune atrophic gastritis, pernicious anemia, B12 deficiency).

Type 2 (associated with Zollinger-Ellison syndrome/hypergastrinemia), and

Type 3 (neuroendocrine carcinoma, usually solitary and >1 cm — the most dangerous) (1-3).

▸ Both Type 1 and Type 2 are associated with hypergastrinemia but via different mechanisms. In type 1 the increased gastrin is due to autoimmune atrophic gastritis and in type 2 the elevated gastrin is produced by a tumor (gastrinoma). Type 1 and 2 gastric NETs are usually well-differentiated with low Ki-67 index, multiple, and <1 cm.

▸ A solitary gastric NET is more concerning (Type 3), while multiple lesions suggest Type 1 or 2.

▸ NBI/I-scan/FICE cannot differentiate between Type 1 and Type 2, but advanced imaging endoscopy is useful for identifying additional small NETs that may have been missed on white light.

▸ The typical endoscopic characteristics of gastric NETs are its sessile shape, flat top, yellowish color and hypervascularity (see figure 1).

▸ Differentiation between Type 1 and 2 relies on clinical features, endoscopic appearance, and laboratory tests (gastrin levels, anti-parietal cell antibodies, etc.).

▸ If resected with clear surgical margins and no other NET seen on PET, surveillance endoscopy alone may suffice for Grade 1 NETs.

Grading (WHO):

Grade 1 (G1): < 2 mitoses/10 HPF (high-power fields), Ki-67 < 3%.

Grade 2 (G2): 2–20 mitoses/10 HPF, Ki-67 3–20%.

▸ Smaller carcinoids (< 20 mm) can be usually managed by endoscopic resection. This should be aggressive and aim at R0. Thus, the best method is endoscopic full thickness resection or ESD with intermuscular dissection, as some lesions go as deep as the muscularis propria.

References

Nakamura S, Iida M, Yao T, Fujishima M. Endoscopic features of gastric carcinoids. Gastrointest Endosc. 1991 Sep-Oct;37(5):535-8. doi: 10.1016/s0016-5107(91)70823-7. PMID: 1936831.

Hülagü S, Yilmaz H. Gastric carcinoid tumors Ann Clin Exp Metabol 2017:2:1017.

Chuah SK, Hu TH, Kuo CM, Chiu KW, Kuo CH, Wu KL, Chou YP, Lu SN, Chiou SS, Changchien CS, Eng HL. Upper gastrointestinal carcinoid tumors incidentally found by endoscopic examinations. World J Gastroenterol. 2005 Nov 28;11(44):7028-32. doi: 10.3748/wjg.v11.i44.7028. PMID: 16437611; PMCID: PMC4717049.

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Endoscopic-Fluoroscopic Insertion of Nasojejunal Feeding Tube Using a Long Biliary Guidewire

Fri, 06 Feb 2026 00:00:00 GMT

Kaylee Goin

Surgical Tech, Roanoke Memorial Hospital, Virginia Tech Carilion School of Medicine, Roanoke, Virginia, USA

Rami Musallam, MD

Gastroenterology Fellow, Virginia Tech Carilion School of Medicine, Roanoke, Virginia, USA

Klaus Mönkemüller, MD, PhD, FASGE, FESGE, FJGES

Professor of Medicine, Virginia Tech Carilion School of Medicine, Roanoke, Virginia, USA

Placement of nasojejunal feeding tubes may be complicated and cumbersome (1). There are many nasojejunual tubes available including Dobhoff tube, Kangaroo feeding tube, Cook NJFT, and others. Often the tube is placed orally and then advanced endoscopically (e.g. UAB Raptor technique) (2). This technique is useful if a regular gastroscope can be advanced with the tube passing the second portion of the duodenum. However, any tube placed orally needs to be transferred to the nostril of the nose after the procedure is done. In addition, if patients have a stenotic pylorus or duodenum, passing a scope with tube is impossible. In this situation, using an ultraslim scope is a great option. A 60-year-old female patient with stenotic duodenum due to chronic calcific pancreatitis and gastric outlet obstruction required nasojejunal feeding tube. Herein we present the key steps to place a nasojejunal feeding tube using an ultraslim scope (transnasal endoscopy) with guidewire placement into jejunum and fluoroscopy-assisted deployment of the feeding tube.

Steps:

1. Perform transnasal endoscopy with ultraslim scope

2. Advance scope through pyloric and duodenal bulb stricture into third portion of duodenum

3. Advance long 0,035 inch biliary guidewire (e.g. Jagwire, or 0,025 in Olympus Visiglide) through scope into the jejunum.

Top tip: advance as much wire as possible, looping is OK. The extra wire will help you pull-and-straighten while pushing the feeding tube.

4. Remove scope, leaving wire in jejunum.

Top tip: always suction all air out of stomach during scope retrieval. It is easier to advance a tube through a collapsed stomach. If the stomach is distended, the looping may complicate tube advancement.

5. Advance feeding tube over the wire (through the nose).

Top tip: we always lubricate the inner side of tube with olive oil (5 to 10 ml), so it advances smoothly over the wire. In addition, we apply lubricating gel on top of tube when introducing it through the nose.

6. While pushing the tube gently pull on the wire, countertraction.

7. Water soluble Contrast injection through the tube shows excellent position in proximal jejunum, past ligament of Treitz.

Top tip: always flush with water after injecting contrast into tube to remove the stickiness of contrast and prevent clogging.

References

Brandt CP, Mittendorf EA. Endoscopic placement of nasojejunal feeding tubes in ICU patients. Surg Endosc. 1999 Dec;13(12):1211-4. doi: 10.1007/pl00009623. PMID: 10594268.

Martínez-Alcalá A, Mönkemüller K. The University of Alabama at Birmingham (UAB) Raptor method for direct percutaneous endoscopic gastrostomy with jejunal extension tube placement. Endoscopy. 2022 Mar;54(3):E96-E97. doi: 10.1055/a-1388-5247. Epub 2021 Mar 30. PMID: 33784754.

None of the authors has any conflict of interest with any of the devices or instruments mentioned in this article.

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Esophageal Intramural Pseudodiverticulosis (EIP)

Mon, 26 Jan 2026 00:00:00 GMT

Esophageal intramural pseudodiverticulosis (EIP) is an uncommon, benign condition characterized by multiple tiny, flask-shaped openings (in barium esophagogram - outpouchings) (tiny diverticula) within the wall of the esophagus (1). These "pseudodiverticula" are actually dilated excretory ducts of the esophageal submucosal glands rather than true protrusions or diverticula of the mucosal layer through the muscle wall.

The condition involves the cystic dilation of submucosal gland ducts, often associated with chronic inflammation and periductal fibrosis. Most commonly diagnosed in the 6th and 7th decades of life, with a slight predilection for males. It is extremely rare, found in approximately 0.15% of barium swallow examinations (1, 2).

The outpouchings can be diffuse (60%) or segmental (40%). Segmental cases often occur in the upper esophagus, while recent studies also link mid-to-distal involvement with conditions like eosinophilic esophagitis (Eo E). EIP is associated with GERD, DM, chronic alcoholsm, tobacco use and esophageal dysmotility disorders (1-3).

Treatment is focused on the primary conditions. If the patient has associated stenosis dilation may be necessary (3).

References

1. Shintaku M. Esophageal intramural pseudodiverticulosis. World J Gastroenterol. 2024 Jan 14;30(2):137-145. doi: 10.3748/wjg.v30.i2.137. PMID: 38312118; PMCID: PMC10835521.

2. Hahne M, Schilling D, Arnold JC, Riemann JF. Esophageal intramural pseudodiverticulosis: review of symptoms including upper gastrointestinal bleeding. J Clin Gastroenterol. 2001 Nov-Dec;33(5):378-82. doi: 10.1097/00004836-200111000-00007. PMID: 11606853.

3. Hahne M, Schilling D, Arnold JC, Riemann JF. Esophageal intramural pseudodiverticulosis: review of symptoms including upper gastrointestinal bleeding. J Clin Gastroenterol. 2001 Nov-Dec;33(5):378-82. doi: 10.1097/00004836-200111000-00007. PMID: 11606853.

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Small Bowel Bleeding due to GIST

Sat, 24 Jan 2026 00:00:00 GMT

Single balloon enteroscopy was negative, however only part of the terminal ileum could be visualized. CT of the abdomen showed a huge pelvic mass originating or infiltrating the small bowel. This tumor was G3M3 based on the classification by Martinez-Alcala et al (1). Percutaneous, CT guided biopsy revealed an epithelioid gastrointestinal stromal tumor.

Classification of Small Bowel GIST (Reference No. 1)

Gastrointestinal stromal tumors (GIST) are mesenchymal neoplasms that arise from the cells of Cajal in the gastrointestinal tract (1). While most GISTs are located in the stomach, 30 % of GISTs are found in the small bowel. Small-bowel GISTs tend to be more aggressive and have worse prognosis with a 5-year survival rate of 25 % (2). Therefore, an early diagnosis is mandatory. Patients with GIST usually present with obscure gastrointestinal bleeding, which results from a surface ulceration and necrosis (3,4). Other complications of GISTs include bowel obstruction, intussusception, and tumor perforation (1-4). The diagnosis of small bowel GIST can be very difficult. Because of its non-specific initial symptoms, patients are often diagnosed with a small bowel GIST only in advanced, metastasized stages of the disease, when curative therapeutic option is not possible. Whenever investigating patients with obscure gastrointestinal bleeding and non-conclusive endoscopic examinations such as EGD and colonoscopy, deep enteroscopy and capsule endoscopy, it is important to obtain a computed tomography of the abdomen to exclude masses, cancers, neuroendocrine tumors (carcinoid) and GIST, such as in this case.

References

Martinez-Alcalá A, Fry LC, Kröner T, Peter S, Contreras C, Mönkemüller K. Endoscopic spectrum and practical classification of small bowel gastrointestinal stromal tumors (GISTs) detected during double-balloon enteroscopy. Endosc Int Open. 2021 Apr;9(4):E507-E512. doi: 10.1055/a-1341-0404. Epub 2021 Mar 17. PMID: 33816770; PMCID: PMC7969139.

Mullady D K, Tan B R. A multidisciplinary approach to the diagnosis and treatment of gastrointestinal stromal tumor. J Clin Gastroenterol. 2013;47:578–585. doi: 10.1097/MCG.0b013e3182936c87

Almeida N, Figueiredo P, Lopes S et al. Double-balloon enteroscopy and small bowel tumors: a South-European single-center experience. Dig Dis Sci. 2009;54:1520–1524. doi: 10.1007/s10620-008-0512-7. [DOI] [Pub Med] [Google Scholar]

Akyüz U, Erzin Y, Cengiz C. Diagnosis of gastrointestinal stromal tumors with double-balloon enteroscopy. Turk J Gastroenterol. 2010;21:39–41. doi: 10.4318/tjg.2010.0046.

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Endoscopic Resection of Large Duodenal Lipoma

Wed, 21 Jan 2026 00:00:00 GMT

The lesion has characteristic findings of a lipoma: a) yellowish color, b) submucosal location, c) upon applying the tip of closed biopsy forceps the lesions was soft, d) the overlying mucosa was intact (Panel A, B). The latter finding is not always present in lipomas, as these may ulcerate and bleed (1, 2). As large lipomas like these ones can result in obstruction, intussusception, gastric outlet obstruction, bleeding and ulceration a decision was taken to resect it (2, 3).

Key aspects when resecting a duodenal lipoma:

Carefully characterize the lesion endoscopically. Evaluate its location in relation to the papilla. Apply air (CO₂) and observe its mobility. Use water to determine the location. Examine the base of the lesion. In this case it was semi pedunculated (Panel C).

Performing straight hot snare resection for lipomas is risky, as the fat tissue decreases electrical, conduction, thus creating resistance to the cutting electrical currents, increasing the chances of burning and perforation. Also, there is a risk of the snare getting stuck or glued to the partially cauterized, greasy lesion (4). For these reasons we like to pre-inject the base of the lesion (Panel D) and then perform a hemi- or complete circumferential mucosal and submucosal incision (Panel E).

Once the hemi circumferential incision and cutting (“pre-cutting”) was accomplished, a snare was then used to resect the lipoma using pure cutting currents (yellow pedal) (Panel F). Do not use coagulation current, as this increases the chances of the snare getting stuck to the greasy polyp.

The resection site was clean without evidence of deep damage. However, in the duodenum it is always imperative to close the wound using several clips. The duodenum is highly vascularized, and the chances of post-resection bleeding are very high. In addition, the wall of the duodenum is thin and delayed post- resection perforation may occur, which can be catastrophic. For these reasons I ALWAYS close the mucosectomy sites in the duodenum.

References

Ouwerkerk HM, Raber, Freling G, Klaase JM. Duodenal Lipoma as a Rare Cause of Upper Gastrointestinal Bleeding. Gastroenterology Res. 2010 Dec;3(6):290-292. doi: 10.4021/gr260w. Epub 2010 Nov 20. PMID: 27942311; PMCID: PMC5139859.

Pei MW, Hu MR, Chen WB, Qin C. Diagnosis and Treatment of Duodenal Lipoma: A Systematic Review and a Case Report. J Clin Diagn Res. 2017 Jul;11(7):PE01-PE05. doi: 10.7860/JCDR/2017/27748.10322. Epub 2017 Jul 1. PMID: 28892976; PMCID: PMC5583857.Parsi MA, Yerian LM. Iron ulcers. Clin Gastroenterol Hepatol. 2009 Oct;7(10):A22. doi: 10.1016/j.cgh.2009.01.005. Epub 2009 Jan 24. PMID: 19558995.

Tjandra, Douglas BBiomed, MD1; Knowles, Brett BSc, MBCh B, FRACS2,3; Simkin, Paul MBBS, FRANZCR3,4; Kranz, Sevastjan MBBS, FRACP5; Metz, Andrew MBBS, FRACP1,3. Duodenal Lipoma Causing Intussusception and Gastric Outlet Obstruction. ACG Case Reports Journal 6(11):p e00157, November 2019. | DOI: 10.14309/crj.0000000000000157

Phatharacharukul P, Wajid M, Fatima H. Delayed Removal of Entrapped Snare in Colonoscopic Polypectomy. ACG Case Rep J. 2021;8(1):e00535. Published 2021 Jan 27. doi:10.14309/crj.0000000000000535

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Technical Tips and Tricks in ERCP: Fully Covered Metallic Stent-Assisted Direct Cholangioscopy

Sun, 04 Jan 2026 00:00:00 GMT

Klaus Mönkemüller, MD, PhD, FASGE (USA), FJGES (Japan), FESGE (Europe) Professor of Medicine, Department of Gastroenterology, Ameos Klinikum Halberstadt, Germany and Carilion Memorial Hospital, Virginia Tech Carilion School of Medicine, Roanoke, USA

Direct cholangioscopy using ultra slims endoscopes (i. e. pediatric gastroscopes or transnasal gastroscopes) enables diagnostic and therapeutic interventions of the biliary tract. However, DC is not always feasible with failure rates up to 15%, mainly due to cannulaton failure. Entering the bile duct may be hampered by a stenotic bile duct and difficult scope position. Herein we present the novel concept of stent-assisted direct cholangioscopy.

A 76-year-old female patient was referred to our institution with obstructive jaundice due to complex biliary tract lithiasis, which could not be removed during the initial ERCP. At our hospital cholangiography revealed a very dilated, tortuous bile duct with filling defects in the common hepatic and right intrahepatic duct. At the referring hositlal the stone could not be retrieved, and thus dual biliary stent insertion (7fr 15cm and 10Fr 5cm) was done. At our hospital ERCP performed 12 weeks later revealed a narrowed and fibrosed papilla. After removing the plastic stents and performing biliary sphincterotomy (panel A) an extraction balloon was used to sweep significant amount of debris out of the severely dilated bile ducts. Given the previous concern for stones and the severely dilated biliary tree, a fully covered metal stent (10Fr 8cm) (Cook Medical, USA) was placed in the bile duct (B). A 4.9 mm ultraslim scope was passed nasally into the stomach and duodenum and then the bile duct was cannulated through the fc SEMS, thus achieving a direct stent-assisted cholangiosopy (C). The remaining stones were removed using DOC with basket. No stones were left behind intraductally (C).

This case shows how inserting a fully covered self-expanding metal stent allowed for direct biliary access using an ultraslim transnasal gastroscope, thus performing direct cholangioscopy.

None of the authors (ASK, KM) has any conflicts of interest with any of the products or devices mentioned in this article.

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Quick Endoscopic Diagnostic Tip: Iron Pill Gastritis

Mon, 18 Aug 2025 00:00:00 GMT

60-year-old male patient with multiple medical problems, including hypertension, coronary artery disease, and small bowel angiodysplasias, was admitted for worsening anemia despite oral iron supplementation. On EGD, a diffuse gastritis and a focally enlarged gastric fold of the greater curvature of the proximal stomach were noticed (Figure 1, panel A, B). Biopsies were obtained, revealing iron-pill gastritis (Panel C).

Images via EndoCollab.com

Oral iron tablets or pills can cause both focal and diffuse erosive gastritis. Iron has been noted to cause a focal erosive mucosal injury like that caused by a chemical burn (1). Iron deposits a brown-black crystalline hemosiderin into the mucosa (1) (Panel C). It is thought that iron erodes the mucosa through a direct corrosive effect that subsequently produces a local injury in a concentration-dependent manner (1). In some patients, particularly those with other comorbid conditions such as hemochromatosis, gastric antral vascular ectasia, and gastric adenocarcinoma, among others, the degree of iron deposition extends to the lamina propria and even the gastric glands (1). On endoscopy, the spectrum of findings includes erosion, ulceration, focal hemorrhage, or diffuse gastritis. In our experience, the focal lesions are most commonly located in the greater curvature of the stomach body (Panels A, B, D). Clinical presentations include epigastric pain, microcytic anemia, and occult gastrointestinal bleeding. This is a great paradox, as iron is causing a problem. Gastritis results from iron deposits (brown-black crystalline hemosiderin) that damage the mucosa.

In sum, iron-pill gastritis or gastropathy is a frequently overlooked and missed diagnosis. Whenever you see a focally enlarged and erythematous gastric fold located in the greater curvature of the proximal stomach, often with tiny blood clots, or active blood oozing, think of iron pill gastritis. However, iron pill gastritis may occur in any part of the stomach and present as gastritis, multiple gastric erosions, and ulcers.

Next time you see a focally enlarged gastric fold with blood clots, you'll think "iron pill gastritis" immediately.

Build that same diagnostic confidence for every bleeding scenario:

References:

Hashash JG, Proksell S, Kuan SF, Behari J. Iron Pill-Induced Gastritis. ACG Case Rep J. 2013 Oct 8;1(1):13-5. doi: 10.14309/crj.2013.7. PMID: 26157809; PMCID: PMC4435261.

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A Pro Tip for Clipping Mallory-Weiss Tears

Sat, 16 Aug 2025 00:00:00 GMT

What's your strategy for clipping a Mallory-Weiss tear? A common mistake is starting proximally.

For a more secure closure, place the first clip distally (furthest from the scope). Then, place subsequent clips proximally to create a stable V- or Y-shape, as shown in this diagram from our new guide.

This is a preview of the practical, procedural guidance packed into The EndoCollab Guide for GI Bleeding.

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Cat Scratch Colon

Tue, 17 Jun 2025 00:00:00 GMT

A 75-year-old woman underwent colonoscopy for obscure gastrointestinal bleeding. Her procedure revealed a tortuous colon with numerous diverticula. Upon entering the ascending colon and cecum, multiple red mucosal lesions were found (Figure 1).

Figure 1. Endoscopic findings of "cat scratch colon." (A-C) Multiple bright red, linear marks on the mucosa of the ascending colon, resembling cat scratches. (D-F) A sharp, tight angulation in the distal ascending colon responsible for causing the barotrauma.

This was the characteristic appearance of “cat scratch colon.” Cat scratch colon is a colonoscopic finding characterized by mucosal tears or lacerations. These are usually a benign, superficial finding resulting from barotrauma during colonoscopy when CO₂ or air is used to insufflate the colon. Some underlying pathologies such as collagenous colitis or ischemic colitis may predispose to barotrauma and cat scratch colon. In this case, the etiology was pure barotrauma, resulting from CO₂ getting entrapped in the cecum and ascending colon due to a tight angulation in the distal ascending colon, which created a tight valve mechanism (Panels D, E, F).

In most cases, cat scratch colon is a harmless, incidental finding during colonoscopy and doesn't require specific treatment. However, it's important to recognize the finding and consider potential contributing factors.

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The Irony of Iron: Gastric Ulcer due to Iron Pills

Tue, 17 Jun 2025 00:00:00 GMT

Andres Gutierrez, MD, Gastroenterology Fellow, Clinica de Gastroenteroogi “Prof. Carolina Olano”, Hospital de Clinicas, Universidad de La Republica, Uruguay and Virginia Tech Carilion School of Medicine, Roanoke, Virginia, USA

Klaus Mönkemüller, MD, PhD, FASGE, FESGE, FJGES

Professor of Medicine, Virginia Tech Carilion School of Medicine, Roanoke, Virginia, USA

85-year-old female patient with hypothyroidism, hyperlipidemia and iron deficiency anemia who was on oral iron supplementation (ferrous sulfate tablets, 325 mg once daily) presented with a 3-months history of abdominal pain and nausea. On EGD a round, 8-10 mm ulcer was seen in the distal body of the stomach (Figure 1).

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The gastric ulcer biopsies demonstrate an ulcerating active gastritis. The gastric ulcer biopsies also contained embedded yellow-brown crystalline material in the lamina propria, which were positive by Prussian blue iron staining. No Helicobacter pylori organisms were seen on the biopsy specimens.

These findings confirmed with an iron pill gastropathy/gastritis.

Oral iron tablets or pills can cause both focal and diffuse erosive gastritis. Iron has been noted to cause a focal erosive mucosal injury like that caused by a chemical burn (1). Iron deposits a brown-black crystalline hemosiderin into the mucosa (1). It is thought that iron erodes the mucosa through a direct corrosive effect that subsequently produces a local injury in a concentration-dependent manner (1). In some patients, particularly those with other comorbid conditions such as hemochromatosis, gastric antral vascular ectasia, and gastric adenocarcinoma, among others, the degree of iron deposition extends to the lamina propria and even the gastric glands (1). On endoscopy the spectrum of findings includes erosion, ulceration, focal hemorrhage or diffuse gastritis. In our experience the focal lesions are most commonly located in the greater curvature of the stomach body such as in this patient. Clinical presentations include epigastric pain, nausea, microcytic anemia, and occult gastrointestinal bleeding. This is a great irony, as iron is causing a big problem. . It is therefore important to consider this entity in patients with gastric ulcers who are on oral iron supplementation and in whom the search for more common causes of gastric ulceration including NSAID use and H pylori infection has been negative (2). Iron pill–induced mucosal injury can be reversed by discontinuing the offending agent or switching to a less toxic form such as a liquid iron preparation (2).

In sum, iron pill gastritis may present as gastritis, multiple gastric erosions and ulcers.

The irony of iron: a treatment for anemia causing gastric ulcers is a crucial reminder that a diagnosis is not always straightforward. When common causes like H. pylori and NSAID use are ruled out, where do you turn next?

References:

Hashash JG, Proksell S, Kuan SF, Behari J. Iron Pill-Induced Gastritis. ACG Case Rep J. 2013 Oct 8;1(1):13-5. doi: 10.14309/crj.2013.7. PMID: 26157809; PMCID: PMC4435261.
Parsi MA, Yerian LM. Iron ulcers. Clin Gastroenterol Hepatol. 2009 Oct;7(10):A22. doi: 10.1016/j.cgh.2009.01.005. Epub 2009 Jan 24. PMID: 19558995.

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Rodolfo Valentino Syndrome: Perforated Duodenal Ulcer Mimicking Appendicitis

Mon, 17 Mar 2025 00:00:00 GMT

Case Presentation: 80-year-old patient with history of lung cancer on immune checkpoint inhibitor therapy presented with acute right lower abdominal pain, elevated inflammatory markers and mild lactic acidosis. The patient had rebound pain in the right lower quadrant and right flank. CT showed free air below the liver (Figure 1). During laparotomy a perforated duodenal ulcer was found. The omentum had wrapped itself to the perforation, which was sealed. There were inflammatory adhesions globally to anterior abdominal wall, pus in the infrahepatic space and right paracolic gutter and ecrotic omentum adjacent to abscess cavity.

Valentino´s syndrome is a rare condition caused by irritation of the peritoneum due to fluid from a perforated ulcer migrating into the paracolic sulcus (1, 2). This situation may mimic acute appendicitis or other differential diagnoses of right lower quadrant pain such as ureteral colic, diverticulitis, diverticulum rupture, ovarian torsion, ruptured ectopic pregnancy, perforated cholecystitis, pancreatitis, and pelvic inflammatory disease (1-3).

Rodolfo Pietro Filiberto Raffaello Gugliemi di Valentina d`Antonguolla), a famous Italian-American actor who starred in several well-known silent films of the 1920s (1, 2). Known in Hollywood as the “Latin Lover”, he died in 1926 at the age of 31 from septic complications (peritonitis and pleuritis) of an undiagnosed perforated peptic ulcer. This ulcer simulated appendicular abdominal pain and was treated surgically with an appendectomy, the final diagnosis being made at autopsy (1, 2).

References:

Kara Carmo F, Santorcuato Cubillos F, Maldonado Schoijet I. Valentino’s Syndrome: from History to Images. A Case-based Literature Review. Acta Gastroenterol Latinoam. 2023;53(2):188-192. https://doi.org/10.52787/agl.v53i2.313
Noussios G, Galanis N, Konstantinidis S, Mirelis C, Chatzis I, Katsourakis A. Valentino’s syndrome (with retroperitoneal ulcer perforation): A rare clinical-anatomical entity. Am J Case Rep [Internet]. 2020;21:e922647. http://dx.doi.org/10.12659/AJCR.922647
Wijegoonewardene SI, Stein J, Cooke D, Tien A. Valentino’s syndrome a perforated peptic ulcer mimicking acute appendicitis. BMJ Case Rep 2012;2012(jun28 1):bcr0320126015-bcr0320126015. http://dx.doi.org/10.1136/bcr.03.2012.6015

An 80-year-old on immune checkpoint therapy hits the ED with RLQ pain, rebound, and free air on CT—appendicitis, right? Laparotomy says no: perforated duodenal ulcer sealed by omentum. Classic Valentino’s syndrome, where fluid migration fools even seasoned clinicians.

This mimic persists as a pitfall, echoing Rudolph Valentino's fatal 1926 misdiagnosis. Today, with imaging at our fingertips, spotting atypical peritoneal sources saves lives and avoids unnecessary procedures.

When perforations play hide-and-seek, be ready.

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Tools of the Trade: The Retentia ® Clip

Sun, 16 Mar 2025 00:00:00 GMT

Tools of the Trade: The Retentia ® Clip

Klaus Mönkemüller, MD, PhD, FASGE, FJGES

Department of Gastroenterology, Carilion Memorial Hospital, Virginia Tech Carilion School of Medicine, Roanoke, USA

Figure 1. Retentia Clip. Key technical information.

The Retentia Clip has some interesting and nice features:

a) it is rotatable,

b) it can be deployed with scope in retroflexed position,

c) it can open and close repeatedly. I opened and closed one 30 times,

d) its catheter has a 2.5 mm outer diameter, allowing for simultaneous suction of air and liquids through the working channel.

These are very convenient features, as they allows the endoscopist to be 100% sure of the desired placement location (vessel, base of polyp, wound closure, etc). Additionally, this clip is quite big, with arm extending up of 16 mm. This allows for grasping more tissue or tackling larger defects. Lastly, the clip’s stem is short (6 mm, yellow arrow), making it ideal for small lumens, such as esophagus or small bowel.

Disclaimer: I have no conflict of interest (COI). No commercial interest.

Tools don't save patients—skilled hands do.

The Retentia clip offers 16mm arms and 360-degree rotation, but these features are useless without the clinical judgment to deploy them correctly. Knowing how to utilize a rotatable, reopenable clip allows for 100% certainty before you deploy.

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Cecal Volvulus

Mon, 03 Mar 2025 00:00:00 GMT

A 61-year-old male with a past medical history significant for DVT/PE on Eliquis and HTN presented to the emergency room after a questionable syncopal episode and a ground level fall. He was found to have a right orbital fracture as well as T8 and L2 vertebral fractures. GI was consulted for abdominal distention, LUQ abdominal pain. A CT abdomen/pelvis showed a distended gallbladder with wall thickening suspicious for acute cholecystitis, L2 acute compression fracture, bilobed abdominal aortic aneurysm, and distention of right and transverse colon. An abdominal ultrasound was done at that time as well showing an abnormal gallbladder with distention and wall thickening, which was suspicious for acalculous cholecystitis. HIDA scan was normal at that time. A KUB was obtained a few days later showing non-dilated small bowel loops, moderate air distention of transverse and descending colon, marked air distention of cecum suspicious for cecal ileus (A, B).

Cecal volvulus occurs because of the cecum twisting around its mesentery, often leading to a bowel obstruction (1). If unrecognized and untreated cecal volvulus can lead to bowel perforation and fecal peritonitis (1). Cecal volvulus accounts for roughly 10% of volvulus cases and typically occurs in younger patients compared to sigmoid volvulus (1). Patients with a developmental failure of peritoneal fixation of the proximal colon and restriction of bowel movement at fixed point from prior adhesions, mass, or scarring are risk factors for development of cecal volvulus (1). On KUB you will typically see marked distention of a loop of large bowel extending from the RLQ to the epigastric area or LUQ which can resemble a coffee bean, as seen above in figures A/B. A contrast enema or abdominal CT scan can be done for further characterization. Treatment options depend on the presence of colonic ischemia and tissue viability (1). In cases where the cecum is not viable a right hemicolectomy is indicated (1). In cases where there is no tissue ischemia treatment involves laparoscopic reduction or colonoscope reduction for patients that cannot tolerate surgery (1). However reduction alone is associated with a high risk of recurrence so cecopexy which involves attaching the cecum to the bowel wall is recommended (1).

References:

Gaillard F, Walizai T, Anan R, et al. Cecal volvulus. Reference article, Radiopaedia.org (Accessed on 05 Nov 2024) https://doi.org/10.53347/rID-1041

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Dieulafoy Lesion of the Duodenum

Fri, 14 Feb 2025 00:00:00 GMT

Dieulafoy Lesion of the Duodenum

Klaus Mönkemüller, MD, PhD, FASGE, FJGES

Department of Gastroenterology, Carilion Memorial Hospital, Virginia Tech Carilion School of Medicine, Roanoke, USA

An 72-year-old female with past medical history of chronic kidney disease stage IV, type 2 diabetes mellitus, atrial fibrillation presented with recurrent overt gastrointestinal bleeding (melena and hematemesis, hemoglobin 7.1 gr/dl). She had undergone two previous EGDs without significant findings. On EGD we found a bleeding Dieulafoy lesion of the duodenum (Figure 1). Hemostasis achieved with a hemoclip.

Figure 1. Dieulafoy lesion of the duodenum. A. Active bleeding. B. No evidence of ulceration or angiodysplasia. C. Successful hemostasis with a through-the-scope clip.

A Dieulafoy lesion is a rare, developmental vascular malformation in the gastrointestinal (GI) tract that can cause bleeding (1). This enlarged and erratic submucosal blood vessel may bleed in the absence of any visible abnormality, such as ulcers or erosions (1). However, on histology the vessel often results in an erosion of the mucosa, hence its classic name “exulceratio simplex” (2). Other names for Dieulafoy are cirsoid aneurysm and caliber-persistent submucosal vessel (1). A Dieulafoy lesion can occur anywhere in the GI tract, but most often in the stomach. This lesion is more common in males, the average age is 70 years. The most common symptoms are unexplained, recurrent, or massive GI bleeding. Dieulafoy lesion accounts for 6.5% of the causes of upper gastrointestinal hemorrhage (3). Therapy is mainly endoscopic, including epinephrine injection, electrocoagulation, or clip placement (1). In cases of severe bleeding, angiogram with selective embolization is an excellent option. Rarey, surgical resection may be necessary as a last resort.

Missed it twice. Found it on the third look.

Want to sharpen your approach to complex GI bleeding cases?

References:

1. Malik TF, Anjum F. Dieulafoys Lesion Causing Gastrointestinal Bleeding. StatPearls Publishing; 2025 Jan-.

2. Dieulafoy G. Exulceratio simplex: leçons 1–3. In: Dieulafoy G, editor. Clinique Médicale de l’Hotel Dieu de Paris. Paris, France: Masson et Cie; 1898. pp. 1–38.

3. Then EO, Bijjam R, Ofosu A, Rawla P, Culliford A, Gaduputi V. Rectal Dieulafoy's Lesion: A Rare Etiology of Lower Gastrointestinal Hemorrhage. Case Rep Gastroenterol. 2019 Jan-Apr;13(1):73-77

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Hemostasis of Bleeding Duodenal Ulcer Using Injection Gold Probe

Fri, 14 Feb 2025 00:00:00 GMT

An 80-year-old man presented with melena. Esophagogastroduodenoscopy (EGD) revealed a large duodenal ulcer with a visible vessel, located anteriorly (Figure 1). Hemostasis was achieved with combination injection and compression electrocoagulation therapy using a injection gold probe.

Figure 1. Hemostasis with an injection gold probe catheter. A. Box of injection gold probe. The probe used was 7 Fr diameter. B. Notice the gold spiraled on the tip of the injection catheter. C. The gold probe can be placed laterally (tangentially) or perpendicular to the ulcer. D. The two important aspects are a) providing compression or pressure hemostasis and b) have enough gold touch the lesion to ensure cauterization of enough area (E). F. Successful hemostasis with disappearance of the visible vessel.

There is a large variety of tools to achieve endoscopic hemostasis. These are broadly classified into injection, thermal, mechanical and contact methods (1) (Figure 2).

Figure 2. Endoscopic Methods for Hemostasis. Thermal therapies are divided into argon plasma coagulation and probes that apply heat or electrosurgical current: monopolar, bipolar or multipolar electrocoagulation (MPEC) devices (1). With monopolar devices, the current passes through the patient and back to the unit via a return pad, whereas with bipolar or MPEC devices, the electric current is confined to the tissue between the electrodes within the instrument tip, obviating the need for a return pad (2).

An injection gold probe catheter is a bipolar hemostasis device that uses both injection and electricity to stop bleeding. We usually inject a mixture of saline epinephrine around the target area (e.g. visible vessel), followed by electrocauterization of tissue. The probe's tip heats tissue with electricity, which coagulates tissue and blood, thus stopping the bleeding. The probe's rounded tip provides uniform burn and coagulation. The probe's design reduces kinking, which helps it advance and tamponade tissue. The MPEC probe can be used tangentially to, or perpendicularly to, the bleeding source. Pressure is applied to compress and seal the walls of the bleeding vessel ("coaptive coagulation") (3). MPEC probes are available in 7F and 10F diameters with an irrigation port at the tip; the 10F probe requires the use of an endoscope with a 3.2 mm diameter instrument channel. Probe size, wattage, contact pressure and duration, and number of applications will vary depending on the lesion being treated (2).

Although we like to have this device in our toolbox for gastrointestinal bleeding, we don't use it very often, as there are other great options for hemostasis such as through-the-scope or over-the-scope clips. However, this case was ideal to use the injection gold probe as the ulcer was located anteriorly (i.e. on the working channel side of scope). If the ulcer is posteriorly, or on the right side of the scope, using injection or gold probe is quite difficult or impossible (3). In our experience we have not had any significant complications using the gold probe, but we have witnessed at least three cases of duodenal perforation in different hospitals. Therefore, we caution to be careful when performing pressure hemostasis, as the electrosurgical heat may damage deeper tissue levels (2, 4).

References:

1. Wasserman RD, Abel W, Monkemuller K, Yeaton P, Kesar V, Kesar V. Non-variceal Upper Gastrointestinal Bleeding and Its Endoscopic Management. Turk J Gastroenterol. 2024 May 20;35(8):599-608. doi: 10.5152/tjg.2024.23507. PMID: 39150279; PMCID: PMC11363156.

2. Parsi Me, et al. Devices for endoscopic hemostasis of nonvariceal GI bleeding (with videos). VideoGIE 2019;4:285-299.

3. Treating Upper Gastrointestinal Bleeding: An Update on Endoscopic Techniques - EndoCollab

4. Kumar VCS, Aloysius M, Aswath G. Adverse events associated with the gold probe and the injection gold probe devices used for endoscopic hemostasis: A MAUDE database analysis. World J Gastrointest Endosc. 2024 Jan 16;16(1):37-43. doi: 10.4253/wjge.v16.i1.37. PMID: 38313458; PMCID: PMC10835479.

Potential COI with the companies/utensils or products mentioned in this article: KM has been consultant for Ovesco, USA.

Coming in November in EndoCollab

An ENTIRE COURSE on Barrett's Esophagus

Join us this month as we dive deep into Barrett's Esophagus with comprehensive coverage including:

Through-the-scope clips have become the workhorse for many bleeding ulcers. But what about the tools we use less often, like the injection gold probe? This case is a perfect reminder of why a master endoscopist never forgets a tool in their kit.

This case shows a scenario where the gold probe offers excellent utility (effective "coaptive coagulation" on an anterior wall). Are you confident in your selection process for all hemostasis devices, even the ones you only pull out a few times a year?

Read on The Practicing Endoscopist

Epstein-Barr Virus (EBV) Lymphoproliferative Disorder Mimicking Watermelon Stomach (GAVE, Gastric Antral Vascular Ectasias)

Tue, 11 Feb 2025 00:00:00 GMT

Epstein Barr Virus (EBV) Lymphoproliferative Disorder Mimicking Watermelon Stomach (GAVE, Gastric Antral Vascular Ectasias)

by Klaus Mönkemüller, MD, PhD, FASGE, FJGES

Department of Gastroenterology, Carilion Memorial Hospital, Virginia Tech Carilion School of Medicine, Roanoke, USA

Figure 1. Epstein Barr Virus (EBV) Lymphoproliferative Disorder Mimicking Watermelon Stomach (GAVE, Gastric Antral Vascular Ectasias). A. Notice the multiple submucosal erythematous patches and prominent antral mucosal folds. B. The mucosa is obviously edematous. Panel C shows NBI.

The biopsy showed gastric mucosa with a dense lymphoid infiltrate with intermixed plasma cells, eosinophils, and histiocytes with a significant amount of edema, replacing and pushing the gastric mucosa. A significant portion of the lymphoid cells were CD79a positive with the same cells positive for EBV on an EBER in situ hybridization ancillary study. There were small aggregates of CD20 positive B-cells CD3 and CD5 and CD43 marked a select number of background T-cells. Immunohistochemistry for H. pylori negative. In sum, the histologic and ancillary studies support an unusual EBV positive B-cell lymphoproliferative disorder, with EBV positive B-cell lymphoma favored.

Epstein-Barr virus (EBV) has been linked to the development of a variety of human malignancies, including Burkitt's lymphoma, Hodgkin's disease, nasopharyngeal carcinoma, some T cell lymphomas (e.. g. NK/T), post-transplant lymphoproliferative disease, and more recently, certain cancers of the stomach, breast and smooth muscle (1-3). The oncogenic potential of EBV is related to its ability to infect and transform B lymphocytes into continuously growing lymphoblastoid cell lines (2). EBV encodes a series of products mimicking several growth, transcription and anti-apoptotic factors, to usurp control of the pathways that regulate diverse homeostatic cellular functions (2).

EBV-lymphoproliferative disorder may mimic inflammatory bowel disease (4, 5). Our case is unusual for two main reasons. First, the EBV-lymphoproliferative disorder mimicked GAVE. And second, there are very few reports in the literature of gastric EBV. It is important to keep EBV in mind as etiologic for a variety of neoplasias, including EBV-lymphoproliferative disorder

References

Baumforth KR, Young LS, Flavell KJ, Constandinou C, Murray PG. The Epstein-Barr virus and its association with human cancers. Mol Pathol. 1999 Dec;52(6):307-22. doi: 10.1136/mp.52.6.307. PMID: 10748864; PMCID: PMC395716.Hematemesis due to prolapse gastropathy: an emetogenic injury. Byfield F, Ligresti R, Green PHR, Finegold J, Garcia-Carrasquillo RJ. Gastrointest Endosc. 1998;45:527–529.

Grywalska E, Markowicz J, Grabarczyk P, Pasiarski M, Roliński J. Epstein-Barr virus-associated lymphoproliferative disorders. Postepy Hig Med Dosw (Online). 2013 May 24;67:481-90. doi: 10.5604/17322693.1050999. PMID: 23752600.

Martínez-Alcalá A, Gutierrez JP, Mönkemüller K. Endoscopic repair of complex pyloroduodenal stenosis resulting from post-transplant lymphoproliferative disorder. Endoscopy. 2016;48 Suppl 1 UCTN:E90-1. doi: 10.1055/s-0042-102961. Epub 2016 Mar 7. PMID: 26951477.

Abdul-Ghafar J, Kim JW, Park KH, Cho MY. Fulminant Epstein-Barr virus-associated T-cell lymphoproliferative disorder in an immunocompetent middle-aged man presenting with chronic diarrhea and gastrointestinal bleeding. J Korean Med Sci. 2011 Aug;26(8):1103-7. doi: 10.3346/jkms.2011.26.8.1103. Epub 2011 Jul 28. PMID: 21860564; PMCID: PMC3154349.

Zheng X, Xie J, Zhou X. Epstein-Barr virus associated T-cell lymphoproliferative disease misdiagnosed as ulcerative colitis: a case report. Int J Clin Exp Pathol. 2015 Jul 1;8(7):8598-602. PMID: 26339440; PMCID: PMC4555768.

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Vanek Tumor (Inflammatory Fibroid Polyp) of the Ileum in Patient with von Recklinghausen Disease (Neurofibromatosis)

Tue, 11 Feb 2025 00:00:00 GMT

Figure 1. Vanek Tumor (Inflammatory Fibroid Polyp) of the Ileum. A. Lesion protruding through ilecocecal valve. B. Pseudopolypoid lesion with mucosal surface lceration. C. There is no specific pit pattern for these lesions. The main characteristics are their polypoid, fingerlike shape with irregular mucosa and surface ulceration.

Inflammatory fibroid polyp (IFP) or Vanek’s tumor is a rare, usually solitary and intraluminal polypoid benign tumor that can affect any part of the gastrointestinal (GI) tract, although in most cases it affects the stomach (1-5). Inflammatory fibroid polyp (IFP) was first described by Vanek in 1949 as a ‘submucosal granuloma with eosinophilic infiltration’ (2). IFP is characterized by proliferation of highly vascular fibrous tissue and infiltration by a variable number of different inflammatory cells (1, 3). Its etiology is unknown.

A plethora of different names have been suggested to describe IFP, such as eosinophilic granuloma, granuloblastoma or gastric fibroma with eosinophilic infiltration, granuloma with eosinophils, hemangiopericytoma, inflammatory fibroid tumor, and inflammatory pseudotumor (1, 3, 4). There is a possible association of IFP or a variant of IFP with neurofibromatosis (NF1) (NF1 = von Recklinghausen disease with pheochromocytoma) (4, 5). Indeed, gastrointestinal "juvenile-like (inflammatory/hyperplastic) mucosal polyps" (JLIHMPs) have been proposed as a neurofibromatosis type 1 (NF1)-specific gastrointestinal manifestation (4, 5). Juvenile polyposis syndrome (JPS) has also been reported in a NF1 patient, harboring concurrent NF1 and SMAD4 germline mutations. Additionally, NF1-like cafe-au-lait spots have been described in biallelic mismatch repair deficiency, another condition featuring gastrointestinal polyps. The SMAD4 and BMPR1A genes that are involved in 50-60% of JPS cases have not been investigated in the ~ 20 published cases of NF1-associated JLIHMPs except for the abovementioned patient with concomitant JPS and NF1 (5). However, incidental associations between NF1 and gastrointestinal polyposes at risk for gastrointestinal carcinoma should not be overlooked, given their implications in terms of clinical surveillance (5).

In sum, this case expands on the existing knowledge on IFP (Vanek tumor). We show the characteristic endoscopic appearance and add another case associated with neurofibromatosis.

References

1. Vanek J. Gastric submucosal granuloma with eosinophilic infiltration. Am J Pathol 25(3): 397-411, 1949. PMID: 18137133.

Garmpis N, Damaskos, C, Garmpi A, et al. In Vivo January 2021, 35 (1) 81-93; DOI: https://doi.org/10.21873/invivo.12235

Goto K, Hirosaki T, Masubuchi M. Neurofibromatosis Type 1-Associated Inflammatory Polyp of the Gastrointestinal Tract. Int J Surg Pathol. 2017 Feb;25(1):65-68. doi: 10.1177/1066896916648772. Epub 2016 Jul 28. PMID: 27170677. The entity known as "juvenile-like (inflammatory/hyperplastic) mucosal polyps of the gastrointestinal tract in neurofibromatosis type 1 (NF1)" was recently proposed, but is not well known. Here, we describe the characteristics of this entity in a surgically resected case. The hemorrhagic 2 × 1 cm-sized polyp was resected from the ascending colon of a 55-year-old male NF1 patient. The polyp was composed of characteristic multiple mucosal protrusions and submucosal elements that included vasculopathic changes. Histologically, this lesion was similar to an inflammatory fibroid polyp rather than juvenile or hyperplastic polyps. This disease could be a distinct entity, and "inflammatory vasculopathic polyp" would be a suitable name.

Ravegnini G, Quero G, Sammarini G, Giustiniani MC, Castri F, Pomponi MG, Angelini S, Alfieri S, Genuardi M, Zamboni G, Ricci R. Gastrointestinal juvenile-like (inflammatory/hyperplastic) mucosal polyps in neurofibromatosis type 1 with no concurrent genetic or clinical evidence of other syndromes. Virchows Arch. 2019 Feb;474(2):259-264. doi: 10.1007/s00428-018-2462-6. Epub 2018 Oct 1. Erratum in: Virchows Arch. 2019 Feb;474(2):265. doi: 10.1007/s00428-018-2472-4. PMID: 30276464.

Enea D, Dray X, Guillerm E, Guilloux A, Yver M, Cervera P, Svrcek M. Inflammatory/juvenile-like polyps in neurofibromatosis type 1 associated with epithelial dysplasia. Virchows Arch. 2024 May;484(5):865-868. doi: 10.1007/s00428-024-03769-w. Epub 2024 Feb 24. PMID: 38396165.

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Cap-Assisted Push Enteroscopy Argon Plasma Coagulation

Mon, 23 Dec 2024 00:00:00 GMT

A 78-year-old man presented with melena. Esophagogastroduodenoscopy (EGD) and colonoscopy were unremarkable. Capsule endoscopy showed active bleeding from the proximal jejunum, approximately 15 minutes after the capsule passed through the pylorus. The patient was sent to us for a single balloon enteroscopy. Since the bleeding was in the upper jejunum a decision was taken to perform push enteroscopy instead. A useful trick to improve performance of push enteroscopy is attaching a transparent distal cap to the pediatric colonoscope. (Figure 1).

Figure 1. Cap-Assisted Enteroscopy. The cap allows for improved traversing of small bowel kinks, keeps small bowel folds away and permits scope tip stabilization (A, B, C). This patient was in decubitus supine position. Using water during endoscopy allows for orientation, as water accumulates in the back (posterior) (B, C). This may be helpful for lesion localization. In addition, water allows for deeper enteroscopy, as the loops do not get massively distended with air or CO2.

The angiodysplasia was localized about 30 cm past the ligament of Treitz. It was localized on a small bowel fold (Figure 2).

Figure 2. Cap-Assisted Enteroscopy Argon Plasma Coagulation. A. Angiodysplasia on small bowel fold. B. Notice how the cap allowed for flattening the fold and clearly exposing the angiodysplasia. C. The cap allowed for scope tip stabilization and “centralization” of the lesion, allowing for direct and targeted argon plasma coagulation therapy.

This case has several important take home messages. First, a single or double balloon enteroscopy may not always be necessary to reach lesions located in the upper jejunum. Indeed, push enteroscopy can be easily performed using a pediatric colonoscope, and this is available in most endoscopy units worldwide. Second, using a distal transparent cap allows for deeper small bowel intubation as well as improved visualization. Finally, the cap also allows for targeted application of endoscopic therapies, including injection, clipping and, as in this case, application of argon plasma coagulation (1-3).

References:

Wasserman RD, Abel W, Monkemuller K, Yeaton P, Kesar V, Kesar V. Non-variceal Upper Gastrointestinal Bleeding and Its Endoscopic Management. Turk J Gastroenterol. 2024 May 20;35(8):599-608. doi: 10.5152/tjg.2024.23507. PMID: 39150279; PMCID: PMC11363156.
Sumiyama, Kazuki et al. Endoscopic Caps. Techniques in Gastrointestinal Endoscopy, Volume 8, Issue 1, 28 - 32
Treating Upper Gastrointestinal Bleeding: An Update on Endoscopic Techniques - EndoCollab.

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Device Review: How to Place a Rectal Decompression Tube Through-The-Scope

Mon, 23 Dec 2024 00:00:00 GMT

A 40-year-old pregnant woman presented with acute constipation and abdominal distention. A sigmoid volvulus was diagnosed (Figure 1). There was a transition point in the sigmoid colon with a “mesenteric swirl sign” (Figures 1B, 1C).

An emergency colonoscopy was performed to resolve the sigmoid volvulus and place a decompression tube.

Colon decompression tubes are used for other conditions such as Ogilvie’s syndrome and megacolons. In this case we used a Marcon colon decompression set (see below, Figures 2 and 3). This tube-set is particularly practical and useful as it comes with a wire and the tube has a pigtail end. This pigtail configuration prevents damage to the mucosa or colon perforation once the tube has been placed and is left inside. In addition, the tube has many side holes that allow for passage of liquid stool and air (Fig. 1 and 3D).

Figure 2.

The key steps to deploy place a through-the-scope colon decompression tube are:

Know your equipment. As the tube is placed through the working channel of the scope, it is imperative to have a colonoscope with a channel large enough to accept the tube. Tubes with diameters of 8.5 Fr and 10 Fr require a 3.2 mm working channel. Larger diameter tubes cannot be placed through the endoscope!
First, feed the wire into the decompression tube (Figures 1E and 1F). This wire will “stiffen the tube and facilitate pushing it through the scope channel.

Once a location has been chosen to deploy the decompression tube, the tube is pushed out under direct endoscopic visualization until it the pigtail “coils” (Figure 1F). One trick we used to allow for smooth pushing of the catheter is to inject some olive oil into the working channel of the scope. Injecting water is also an option. It is important to always keep the wire INSIDE the catheter and not push the wire outside the pigtail tip, as the wire can penetrate the mucosa or even cause perforation. In addition, often there is liquid or solid stool that limits visualization, and a ‘free” wire tip can be dangerous.
Figures 3G and 3H shows the exchange maneuver. The catheter is pushed out and the scope is removed (by the endoscopist or an assistant). The important aspect is to advance tube and pull scope out in a synchronized matter (exchange), as you do not want to pull the catheter out. A trick we used while pushing the catheter is to start gently and slowly removing the wire. Some experts like to remove the wire at the very end, but this can lead to catheter entanglement and sometimes the wire is “stuck” inside the decompression catheter. This can result in accidentally pulling the catheter out when trying to dislodge the wire.
Figure H shows the final tip. As mentioned above we like to flush the colon with lots of water, but in distended colons we also use lots of simethicone. This will decrease bubbles and, of course, gas.

No COI by DD or KM with any of the companies/utensils or products mentioned in this article.

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Endoscopic Removal of a Pen Inside the Stomach Using the Soft, Mega, Distal Transparent Cap

Mon, 23 Dec 2024 00:00:00 GMT

Roanoke

Klaus Mönkemüller, MD, PhD, FASGE, FJGES

Professor of Medicine, Virginia Tech Carilion School of Medicine, Virginia, USA

There is a myriad of instruments to remove swallowed objects greater than 6 cm in length (such as pens, pencils, and toothbrushes) including nets (e.g. Roth net), snares, forceps, tripod prongs, overtubes, and various distal scope attachment caps (soft short, stiff, capuchon). A large transparent distal attachment cap was developed to remove small metal pieces, specifically, clip fragments of the over-the-scope clip (Remove cap, Ovesco, Germany) (1) (Figure 1).

We have also found this cap very useful to remove impacted meat from the esophagus. As this cap is three times larger than traditional “hard” caps (i.e. those used for banding) and has large capacity volume, we refer to it as the “mega cap” (Figures 1A-C). Herein we report on the novel use of the Remove cap for removing a swallowed pen from inside the stomach.

The cap is larger than any existing transparent cap and allows for suctioning most of the impacted meat inside. Its distal diameter is 16 mm with a cap length of 26 mm (effective “catch length of 22 mm) (Figures 1A-C). This results in an inner cap “catch-volume” of approximately 5 ml, which is almost double to that of traditional distal transparent caps. Another big advantage of this cap is its softness (elasticity, figures 1D-E), which allows for smooth introduction into the esophagus (Fig. 1F). Once inside the stomach the cap can be placed against the mucosa, which turns it into oval shape, thus increasing the ability to pull back a sharp end of the foreign body such has the pen tip, inside of the cap (Fig. 1G). Using a Raptor, rat-tooth or alligator forceps is mandatory, was it is important to tightly grab the pen. A snare may be an option, but too often the snares slid off pens and pensils, especially if the object has been inside the stomach for several outs and is now covered by mucus and secretions. Specific tricks to remove a pen from the stomach are (Figure 2):

a) Slowly place the distal part of the cap onto the pen,

b) Move with the cap towards the proximal end of the pen. In this case it was the sharp, painting part (Fig. 1A),

c) Do not grasp the pen on its very tip, but focus on the groove on “neck” (Fig. 1B),

d) Close the forceps slowly, as closing to fast may result in it sliding over the foreign body (Fig. 1C),

e) Once the forceps is tightly closed against the pen tip go ahead and pull the pen into the cap (Fig. 1D),

f) Because this cap is soft it allows for “deformation” while the pen tip is being pulled inside. With hard caps it would be very hard or impossible to get a pen tip into it (Fig. 1E-F),

g) Once the pen tip (or most of it) is inside the cap, commence pulling the scope out. It is very important that the forceps shaft is held with the left hand in place. Hard caps would never allow a tip to get inside,

h) Keep insufflating air (or CO2) to distend the esophageal lumen and gently torque the scope to right and left,

i) Gently pull the scope out, while continuously torquing right and left. The torquing maneuver decreases the chances of the pen tip to get caught or hung up on the esophageal mucosa or any of the esophageal anatomic (physiologic) stenotic areas.

For the final extraction maneuver it is important to have the patient’s neck hyperextended and that the assistant is ready to catch the pen inside of the mouth. Fig. 1G shows the extracted pen. The entire extraction procedure lasted 4 minutes. In sum, this novel cap is a new addition to the armamentarium for remove long, sharp and pointed foreign bodies from inside the GI tract.

References:

Bauder M, Meier B, Caca K, Schmidt A. Endoscopic removal of over-the-scope clips: Clinical experience with a bipolar cutting device. United European Gastroenterol J. 2017 Jun;5(4):479-484. doi: 10.1177/2050640616671846. Epub 2016 Oct 6. PMID: 28588877; PMCID: PMC5446147.

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Endoscopic Utensil Description: The Duette Multiband Mucosectomy Device

Mon, 23 Dec 2024 00:00:00 GMT

The Duette device (Figure 2, Figure 1D) is essentially an endoscopic banding device for varicesaccompanied by a hexagonal snare. Let’s dwell into this practical device used for endoscopic resection.

The objective of suctioning and banding gastrointestinal mucosal lesions is to a) reshape a flat or semi-sessile lesion into a “sessile” form, b) have the band at the base and assure a better endoscopic resection (R0).

The other significant novelty of the Duette device is the 5Fr hexagonal snare (Figure 1). If you would use a banding kit and then try to advance a traditional snare (usual diameter of the snare catheter or sheath is 7Fr), it would be impossible to push it through the working channel of the scope, as there is a string for the bands inside running from the “firing device” inside the working channel of the scope (Figure 1J, yellow arrow). When using Duette, pushing the 5Fr snare into the working channel, along the string, is quite easy (Figure J, yellow arrow). There are some special tricks that may be useful in to facilitate snare catheter insertion. As shown in Figure 1D the snare can be pulled well inside the catheter. Pulling “ears” or handle rings are proximal (Figure 1D, yellow arrow). However, before inserting the snare-catheter into the working channel of the scope, we prefer to have the snare close the catheter tip (Figure 1F), as this maneuver “stiffens” the catheter and allows for a better introduction into the working channel, along the string of the band-firing device (Figures 1H, 1I, 1J). Not uncommonly, the catheter tip may bend when trying to push it into the working channel. By having the snare at the tip of the catheter, bending is less likely. There are three tricks to verify that the snare is at the tip: a) visualization (Fig. 1F) (which sometimes is not easy in the somewhat darkened endoscopy suite, b) placing tip of finger on catheter, and “feeling” when the snare tip is pushed out by the assistant, or c) looking at the centimeter marking at the handle, as the 4 cm mark corresponds to the snare being located at the tip of the catheter (Figure 1 G). Now the snare can be easily inserted into the working channel (Figure 1I).

No COI by KM with any of the companies/utensils or products mentioned in this article. All photos taken by KM. Property of EndoCollab.

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Gastric Antral Vascular Ectasia (GAVE) in Heyde Syndrome

Mon, 23 Dec 2024 00:00:00 GMT

An 80-year-old female with past medical history of chronic kidney disease stage IV, type 2 diabetes mellitus, quadruple coronary artery bypass, aortic and mitral stenosis treated with bioprosthetic aortic and mitral valves, pacemaker and defibrillator presented with recurrent occult gastrointestinal bleeding and iron deficiency anemia (hemoglobin 6.1 gr/dl). The patient had undergone multiple upper endoscopies and colonoscopies without significant findings except for small colon adenomas and “gastritis” and duodenal “polyps”. On EGD we found a linear, nodular antral gastritis, suspicious for nodular gastric antral vascular ectasia (GAVE) (Figure 1). Biopsies were obtained, confirming the endoscopic suspicion of GAVE. The GAVE was treated with multiple band ligations.

Figure 1. Gastric antra vascular ectasia (GAVE) of nodular type. A. “Nodular gastritis” in reality GAVE. B. Notice the characteristic edematous, erythematous, nodular, pseudo-polypoid linear appearance of nodular GAVE. C. Endoscopic band ligation of nodular GAVE.

The classic teaching refers to Heyde’s syndrome as “the association of aortic stenosis and cecal angiodysplasias” (1-3). Whereas this is partially true, here you will learn that Heyde syndrome is a type of hemophilia (acquired von Willebrand disease) leading to GI bleeding from various types of gastrointestinal angiodysplasias (2-5). Most often the angiodysplasias are in the small bowel and colon, but they can be located anywhere. Moreover, GAVE is also a form of deranged angioneogenesis (angiodysplasia), which may occur in the setting of Heyde syndrome (6). Now we know that Heyde syndrome is primarily a hemophilia, namely a form of acquired von Willebrand syndrome (2-4). There is a malfunction of von Willebrand factor, leading to gastrointestinal hemorrhage. In addition, deranged von Willebrand activity leads to angioneogenesis and occurrence of angiodysplasias and GAVE in the GI tract (2-4, 6). Many patients with aortic stenosis stop bleeding and develop angiodysplasias after receiving a new aortic valve (7). However, there are reports showing that Heyde syndrome may persist or develop despite aortic valve replacement (8, 9).

This case has several important take home messages. First, careful inspection of the stomach may uncover conditions such as nodular GAVE (Figure 2). Second, GAVE should be added to the spectrum of angiodysplasias occurring in Heyde syndrome. And finally, endoscopic band ligation is an alternative treatment of nodular GAVE.

Figure 2. Classification of GAVE. GAVE is characterized by a “characteristic” endoscopic pattern, mainly represented by red spots either organized in stripes radially departing from pylorus (“watermelon stomach” or arranged in a diffused-way or “honeycomb stomach”). In addition, there is a nodular variety, where there are multiple enlarged and nodular folds in the antrum (2, 3). Despite this, GAVE is often misclassified or mis-diagnosed.

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References:

1. Heyde, E.C. Gastrointestinal Bleeding in Aortic Stenosis. N. Engl. J. Med. 1958, 259, 196.

2. Warkentin, T.; Morgan, D.G.; Moore, J.C. Aortic stenosis and bleeding gastrointestinal angiodysplasia: Is acquired von Willebrand’s disease the link? Lancet 1992, 340, 35–37.

3. Batur P, Stewart WJ, Isaacson JH. Increased Prevalence of Aortic Stenosis in Patients With Arteriovenous Malformations of the Gastrointestinal Tract in Heyde Syndrome. Arch Intern Med. 2003;163(15):1821–1824. doi:10.1001/archinte.163.15.1821

4. Vincentelli A et al. Acquired von Willebrand in Aortic Stenosis. New Engl J Med. 2003

5. Okhota S, et el. Int. J. Mol. Sci. 2020, 21, 7804;

6. Dosi RV, Ambaliya AP, Patell RD, Sonune NN. Gastric antral vascular ectasia with aortic stenosis: Heydes syndrome. Indian J Med Sci. 2012 Mar-Apr;66(3-4):86-9. PMID: 23603627.

7. Tsuchiya S, Matsumoto Y, Doman T, Fujiya T, Sugisawa J, Suda A, Sato K, Ikeda S, Shindo T, Kikuchi Y, Hao K, Takahashi J, Hatta W, Koike T, Masamune A, Saiki Y, Horiuchi H, Shimokawa H. Disappearance of Angiodysplasia Following Transcatheter Aortic Valve Implantation in a Patient with Heyde's Syndrome: A Case Report and Review of the Literature. J Atheroscler Thromb. 2020 Mar 1;27(3):271-277. doi: 10.5551/jat.49239. Epub 2019 Aug 3. PMID: 31378751; PMCID: PMC7113142.

8. Akutagawa T, Shindo T, Yamanouchi K, Hayakawa M, Ureshino H, Tsuruoka N, Sakata Y, Shimoda R, Noguchi R, Furukawa K, Morita S, Iwakiri R, Kimura S, Matsumoto M, Fujimoto K. Persistent Gastrointestinal Angiodysplasia in Heyde's Syndrome after Aortic Valve Replacement. Intern Med. 2017 Sep 15;56(18):2431-2433. doi: 10.2169/internalmedicine.8603-16. Epub 2017 Aug 21. PMID: 28824071; PMCID: PMC5643169.

9. Oda, T., Kanamoto, R., Miyawaki, M. et al. Heyde-like syndrome occurring for the first time following aortic valve replacement with a bioprosthesis: a case report. Gen Thorac Cardiovasc Surg Cases 2, 52 (2023). https://doi.org/10.1186/s44215-023-00066-x

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How to Deploy a Capsule Endoscope During EGD

Mon, 23 Dec 2024 00:00:00 GMT

An elderly lady with obscure occult gastrointestinal bleeding could not swallow the capsule endoscope (CE) (PillCam) (Figure 1A). Therefore, an EGD was scheduled to introduce the capsule endoscope into the duodenum.

Figure 1

We utilized the AdvanCE capsule endoscope delivery device (Figure 1) (also see figure 3 at the end of article, which are the visual/photographic instructions from the device’s package).

The key steps to deploy a CE using this device are:

Know your equipment. The capsule deployment device consists of two parts, the capsule holder, which contains the capsule endoscope and has a screw-receiver at its base (Figure 1A, yellow arrow), and the b) delivery catheter, which has a screw on its tip (Figure 1B, light blue arrow).
It is important to first advance the screw catheter through the working channel of the scope (Figure 1C).
Once the screw catheter has exited the scope, the capsule holder (with the activated capsule) should be screwed (attached) to the screw catheter (Figure 1D). Careful attention must be paid not to lose the capsule while gently screwing the catheter to the base of the CE holder.
The attached capsule holder and CE shall be pulled towards the scope tip (1E).
Introduction of the scope and CE into the mouth holder is done under direct endoscopic view. We leave a distance of about 1 to 1.5 cm between scope tip and CE, in order to facilitate visualization of the oropharynx, larynx and upper esophageal sphincter (UES).
Once the vocal cords are seen endoscopically, the CE will be right at the entrance of the UES. While gently turning the scope to the right (clockwise) also push the scope forward. This combined maneuver will allow for the capsule endoscope to enter the esophagus (Figure 1F).
The scope and CE are then advanced towards the pylorus and into the duodenum (Figure 1G). The white color (green arrow) indicates that the CE is still attached.
We prefer to enter the second duodenum and deliver the capsule endoscope there. Why? Because delivery of the CE in the stomach may result in delayed entry into the duodenum. And leaving in the duodenal bulb of a patient with a “floppy” pylorus may result in capsule endoscope bouncing back into the stomach. However, if a patient has duodenal diverticulum or a tight or short genu between bulb and duodenum, we do not force placement into the second duodenum.
We like to apply a little water before deployment. This will stimulate the duodenal motility, remove any debris from the capsule endoscope, and slightly push the capsule away once it is freed from the device.
Liberating or deploying the capsule endoscope is quite easy. Just ask the assistant to open the “snare” handle (Figure 2, below). This maneuver pushes the capsule away. A sign that the capsule is released is the “transparency” of the delivery device (Figure 1H). Compare to the white color present when the capsule is still attached (Figures 1F and 1G, green arrow).

Figure 2

Figure 3

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Microscopic Colitis: Not Always “Microscopic”

Mon, 23 Dec 2024 00:00:00 GMT

80-year-old patient with ongoing watery diarrhea for several weeks. Colonoscopy images shown here. Note that there is significant patchy edema, hypervascularity, punctate erythema, thickened folds and patchy superficial erythema.

Classically, microscopic colitis (collagenous and lymphocytic) is thought to have normal colon mucosa, but several studies now have shown that many patients have abnormal colon mucosal findings, such as the ones depicted in our case (1-3). The best review on the topic was written by A. Kolaouzidis and A. Saeed (1). The authors performed a systematic electronic and manual search of PubMed and EMBASE for publications on distinct endoscopic findings in microscopic colitis, resulted in 42 relevant reports for inclusion in this review (1). The authors found four broad categories of distinct endoscopic findings in collagenous colitis: (1) pseudomembranes; (2) mucosal vascular pattern alteration which includes an indistinct appearance of the blood vessels and a variable degree of pruning of the mucosal vasculature, or a crowded, dilated and tortuous capillary network; (3) mucosal abnormalities such as red spots and some mucosal nodularity or textural alteration, evident with or without chromoendoscopy and (4) a continuum of mucosal breaks/defects, i.e., mucosal lacerations/tears, including the so-called “cat scratch colon” pattern, or fractures usually along the long axis of the colonic wall to the fine linear cicatricial lines or thick scar-like ridges of the mucosal surface (effects of the mucosal healing process of mucosal defects) (1).

Interestingly, they only found one publication describing a characteristic endoscopic pattern in lymphocytic colitis. Thus, our case adds to the growing literature on “macroscopic” endoscopic changes in “microscopic colitis”.

References:

1. Koulaouzidis A, Saeed AA. Distinct colonoscopy findings of microscopic colitis: not so microscopic after all? World J Gastroenterol. 2011 Oct 7;17(37):4157-65. doi: 10.3748/wjg.v17.i37.4157. PMID: 22072846; PMCID: PMC3209563.

2. Wickbom A, Lindqvist M, Bohr J, Ung KA, Bergman J, Eriksson S, Tysk C. Colonic mucosal tears in collagenous colitis. Scand J Gastroenterol. 2006 Jun;41(6):726-9. doi: 10.1080/00365520500453473. PMID: 16716973.

3. Park HS, Han DS, Ro YO, Eun CS, Yoo KS. Does lymphocytic colitis always present with normal endoscopic findings? Gut Liver. 2015 Mar;9(2):197-201. doi: 10.5009/gnl13373. PMID: 25167800; PMCID: PMC4351026.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4351026/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4351016/

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Stent Delivery Device with Transparent Inner Guiding Catheter and How to Place a Plastic Stent into the Bile Duct

Mon, 23 Dec 2024 00:00:00 GMT

Professor of Medicine, Virginia Tech Carilion School of Medicine, Virginia, USA; Universidad de la República, Uruguay; PD at University Otto-von-Guericke, Germany; UEES, Universidad Espiritu Santo, Guayaquil, Ecuador; University of Belgrade, Belgrade, Serbia; J. Strossmeyer University, Osijek, Croatia

Effective and successful ERCP is based on skills, knowledge, and devices. Often, simple devices make a huge difference in success. Herein we present such a device and dwell into the art of inserting a plastic stent into the biliary tract.

Figure 1. Plastic Stent delivery device with transparent inner guiding catheter.

The plastic Stent delivery device with transparent inner guiding catheter (Figure 1, Figure 2) is a nice innovation in ERCP. The simple idea of making a transparent inner guiding catheter, which goes over the biliary guidewire is quite ingenious, as it allows for direct endoscopic visualization during insertion and stent placement (Figure 1E and Figure 2Cyellow oval). By watching the guidewire through the inner guiding catheter when pushing the plastic stent, no fluoroscopy or x-rays are necessary.

Figure 2. Tips when using the plastic stent delivery device with transparent inner guiding catheter.

How to deliver the plastic stent:

Top tips and tricks on how to place a plastic stent into the bile duct (Figure 3).

1. Focus on the radio-opaque mark of the inner guiding catheter (insert A, green arrows)

2. Unlock (insert B shows handle) the pusher tube (insert A, light blue oval)

3. Advance (push) on the pusher, assistant “pulls” (puts tension on inner guiding catheter, keeping radio-opaque mark in place

4. Once the stent is inside the bile duct, create a “V” angle between stent and pusher tube (yellow arrow, B) and the assistant pulls the inner guiding catheter and guidewire out (deploy, C). Released stent (C, D).

🔍 Master ERCP Like The Experts

Want more innovative techniques like this fluoroscopy-reducing stent method?

No COI by KM with any of the companies/utensils or products mentioned in this article.

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Therapeutic Dilemma: Barrett Esophagus in the Setting of Esophageal Varices

Mon, 23 Dec 2024 00:00:00 GMT

A 50-year-old patient was sent to our endoscopy service because of Barrett's esophagus and esophageal varices.

He had been biopsied at another institution for a tongue of cylindrical epithelium in the distal esophagus. Before going into the discussion on the approach to this case we want to emphasize that one should never biopsy lesions in the setting of esophageal or gastric varices unless there is a backup plan for the obliteration of the bleeding.

In this case, we decided to band the segment of Barrett's mucosa (Figures 2C and 2D). This approach was first reported by Diaz-Cervantes (1) and since then replicated and confirmed by other experts (2, 3).

In this case we decided to band the segment of Barrett's mucosa (Figures 2C and 2D). This approach was first reported by Diaz-Cervantes (1) and since then replicated and confirmed by other experts (2, 3).

The initial idea of using endoscopic band ligation for Barrett in the setting of esophageal varices is Diaz-Cervantes from Mexico (1). In this study 30 patients with Barrett esophagus were treated with endoscopic band ligation plus omeprazole 20 mg t.i.d. endoscopic band ligation was repeated monthly until two consecutive endoscopic and histological examinations showed no BE. Thirty Barrett's patients treated with omeprazole 20 mg t.i.d. alone served as a control group (1). The endoscopic band ligation treatment group comprised 29 patients with short-segment BE (SSBE) and one with long-segment disease, whereas all 30 of the control patients had SSBE. During a median follow-up of 16.9 months (range 10-24 months), complete eradication of Barrett's esophagus was achieved in 29 of 30 patients (97%) in the endoscopic band ligation group. In contrast, Barrett's esophagus persisted in all 30 control patients during the same period (P < 0.0005). The mean total number of bands applied per patient was 6.1 (range 1-14) and the mean number of sessions for complete eradication was 3.1 (range 1-7). Adverse events included only mild chest pain and dysphagia that resolved within days (1).

In a retrospective study from the USA, Hartgnik et al present eight cases of Barrett esophagus and esophageal varices that were successfully treated with band ligation alone (2). There was no bleeding, perforation or infectious complications in any patients undergoing banding for treatment of BE. Four patients had biopsy-proven dysplasia prior to treatment with band ligation. After band ligation, 2 of 4 dysplastic cases that had repeat biopsies showed histologic resolution of the dysplasia. All patients who received banding for BE were followed at least yearly except for one patient lost to follow-up. No interval esophageal cancers were reported in any patients with BE that were banded (2).

In a retrospective comparative study from the Mayo Cinic in Jacksonville, Florida eight high-grade dysplasia patients with varices who were treated initially with band-ligation were compared with reference group of 52 high-grade dysplasia patients treated endoscopically. A complete remission of intestinal metaplasia or dysplasia was obtained in 50% patients of with Barrett’s and varices. In the reference group (ablative therapies using heat and/or RFA) the disappearance of dysplasia and intestinal metaplasia was higher (75%) (3). Finally, Hadley et al (4) reported on a complete cure of an early esophageal adenocarcinoma overlying a varix, which was treated by endoscopic band ligation (4).

Of course, eradication of dysplastic Barrett esophagus makes sense. Whether eradication of non-dysplastic Barrett esophagus in the setting of esophageal varices should be performed routinely is a matter of debate. However, we believe that eradication of non-dysplastic Barrett esophagus in the setting of esophageal varices makes sense for two reasons: a) the follow-up endoscopies of BE with persistent varices may be avoided, and b) eradication of varices is associated with less risk of bleeding.

In sum, we believe that knowledge of this relatively safe technique, which is supported by various publications is an important addition to the therapeutic armamentarium of Barrett's esophagus and even small early esophageal adenocarcinomas help deal with the dilemma of Barrett's esophagus in the context of esophageal varices.

Are you prepared to manage the high mortality and alarming recurrence rates of bleeding esophageal and gastric varices? These cases are critical and demand the most effective therapeutic approach.

This week’s "From My Toolbox" session with Dr. Mönkemüller cuts to the chase, giving you a clear overview of endoscopic therapy, and new developments for managing these high-risk patients.

Here's what you'll uncover:

The grim reality: Understand the mortality rates and recurrent bleeding risks associated with untreated esophageal/gastric varices (it's higher than you think!)
The Pathophysiology: A breakdown of the natural history of the formation of esophageal and gastric varices.
Ligation vs. Sclerotherapy: Decide on the best therapy options: Understand why endoscopic variceal ligation surpasses sclerotherapy for emergency scenarios.

Don't let valuable clinical time slip away. Stay ahead of the curve with the latest approaches in treating these life-threatening conditions.

References:

1. Diaz-Cervantes E, De-la-Torre-Bravo A, Spechler SJ, Torres-Durazo E, Sobrino-Cossio S, Martínez-Carrillo O, Gamboa-Robles J. Banding without resection (endoscopic mucosal ligation) as a novel approach for the ablation of short-segment Barrett's epithelium: results of a pilot study. Am J Gastroenterol. 2007 Aug;102(8):1640-5. doi: 10.1111/j.1572-0241.2007.01256.x. Epub 2007 May 3. PMID: 17488252.

2. Hartgerink C, Nimri FM, Zuchelli T, Jafri SM, Piraka C. Band Ligation Can Be Used to Treat Barrett's Esophagus and Concurrent Esophageal Varices: A Case Series. Dig Dis Sci. 2023 Apr;68(4):1381-1385. doi: 10.1007/s10620-022-07696-1. Epub 2022 Sep 21. PMID: 36131048.

3. Palmer WC, Di Leo M, Jovani M, Heckman MG, Diehl NN, Iyer PG, Wolfsen HC, Wallace MB. Management of high grade dysplasia in Barrett's oesophagus with underlying oesophageal varices: A retrospective study. Dig Liver Dis. 2015 Sep;47(9):763-8. doi: 10.1016/j.dld.2015.05.009. Epub 2015 May 21. PMID: 26066379

4. Hadley SM Jr, Patel NJ, Gardner TB. Band Ligation Resolves Esophageal Adenocarcinoma Overlying Esophageal Varix. ACG Case Rep J. 2022 Sep 1;9(9):e00823. doi: 10.14309/crj.0000000000000823. PMID: 36072356; PMCID: PMC9439847.

No COI by HP or KM with any of the companies/utensils or products mentioned in this article.

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Top Tips for Dealing With a Colon Polyp in a Difficult Situation

Mon, 23 Dec 2024 00:00:00 GMT

Traditionally difficult polyps have been defined by their shape (e.g. larger than 20 mm, flat, thick stalk) or location (cecum, angulated part of colon, close to appendix orifice or diverticulum). However, we believe that other “situation” factors such as colon preparation, colon motility (e.g. spams, patient respirations), bleeding diathesis (e.g. anticoagulation, low platelets) and ergonomics (e.. video monitor on endoscopy cart instead of being in the wall in front of the endoscopists) contribute to the difficulty in resecting these lesions (1, 2). Here we describe various tricks that will assist you tackling and mastering many of these challenging factors during polypectomy.

Figure 1. Top tricks to deal with difficult polyps

This broad-based, thick stalked polyp was located in a difficult location, at a tight corner in the distal sigmoid colon (1A).

Essential steps:

Clean the colon (1B). A clean working field facilitates work. We like to instill water proximally to the lesion, as it is preferably to receive a “clean water gush” during resection as being gushed with debris (stool) laden material. In addition, in case of perforation, there is less stool contamination
Straighten the colonoscope to allow for “one-on-one” steering. You should be able to obtain the responses you want from the tip of the scope when torqueing it to the right and left.
Characterize the lesion and determine its endoscopic resectability (1C, 1D).
Place the polyp at the 5 to 7 o´clock position (1E). This will allow you to use the utensils properly, as they exit the working channel of the scope, which is on the lower parts of the scope (see No. 5).
It’s imperative to place your working channel in a way that the utensil travel to the base of the lesion (1F). Here you see the needle inserted into the thick stalk.
When advancing the snare it is always practical to slowly open it proximal to the polyp. In this case I placed the snare on the right side (Figure 1G, Figure 2A). When the tip of the snare was slowly opened by the assistant (Figure 2A, green arrow) we torqued the scope to the right (Figure 2B). This combined (snare-opening, scope torqueing) maneuver allowed for the snare to open like an “arch” (Figure 2B, yellow arrow), as its tip was touching the opposite wall of the colon (Figure 2A, green arrow). Once the snare was open enough, we torqued to the left and let the snare “fall on the polyp”, while the assistant slowly closed it, and I simultaneously pushed the snare towards the base of the polyp (creating the famous Y-catch trick) (Figure 2C). The polyp base was completely ensnared (1H) and we proceeded to perform the endoscopic mucosal resection, with R0 result (Figure 2D).

Figure 2. Top tricks to deal with difficult polyps (part 2)

In this case we used a Lariat snare, which has the advantage of having three different sizes in one snare (Figure 3). Figure 1A shows the small size, Figure 2B (intermediate size), and in Figure 2C the larger size is shown. The small size opening is ideal for cold-snaring small lesions.

References:

Mönkemüller K, Neumann H, Fry LC, Ivekovic H, Malfertheiner P. Polypectomy techniques for difficult colon polyps. Dig Dis. 2008;26(4):342-6. doi: 10.1159/000177020. Epub 2009 Jan 30. PMID: 19188726.
Mönkemüller K, Neumann H, Malfertheiner P, Fry LC. Advanced colon polypectomy. Clin Gastroenterol Hepatol. 2009 Jun;7(6):641-52. doi: 10.1016/j.cgh.2009.02.032. Epub 2009 Mar 10. PMID: 19281865.

No COI by KM with any of the companies/utensils or products mentioned in this article. All photos taken by KM. Property of EndoCollab.

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Transient or “Left”-Sided Ischemic Colitis: Case Reports With Focus on its Endoscopic Spectrum

Mon, 23 Dec 2024 00:00:00 GMT

Transient or left-sided ischemic colitis is the most common type of ischemia of the gastrointestinal tract. Indeed, ischemic colitis is the second or third most common cause of lower GI bleeding. Herein we present two cases with classic features of transient ischemic colitis and focus on its endoscopic diagnosis.

Case Presentations:

Case 1: Elderly patient developed abdominal pain followed by bloody diarrhea. Colonoscopy showed patchy colitis of the left colon (Figure 1), the rectum was spared. Notice the patchy characteristic of this colitis. Panel A shows small ulcers with erythematous halo. In Panels C to E the classic Zuckerman sign can be appreciated.

Figure 1. Endoscopic images from case 1.

A diagnosis of ischemic colitis was confirmed histologically. There were no significant risk factors for vascular occlusive disease or vasculitis. The patient improved with supportive measures, and she was discharged home two days later.

Case 2:

60-year-old female patient without significant past medical history presented with hematochezia that started after acute onset left sided abdominal pain. Only the bleeding continued, the pain disappeared after about 12-18 hours. CT of the abdomen revealed left sided colon stenosis and inflammation. Colonoscopy images are shown (Figure 2).

Figure 2. Endoscopic images from case 2.

Colonic ischemia occurs due to changes in systemic circulation and/or alterations in local mesenteric vasculature. Left-sided ischemic colitis, also called transient ischemic colitis, is characterized by acute onset abdominal pain and bloody diarrhea or hematochezia. This condition can occur in any age group, but it is seen most in the elderly. Risk factors for transient ischemic colitis are atherosclerosis, heart failure, cardiac arrhythmias, shock, vasculopathies, abdominal aortic surgery, and hypercoagulability states. Indeed, the abrupt blood flow to the colon, which can occur after a marathon, exertion, or transient vessel occlusion from constriction (cocaine), thrombosis or low flow state can also result in transient ischemic colitis. Classic medications associated with ischemic colitis are estrogens, NSAIDs and alosetron (1).

The most frequently affected areas are the left colon and superior rectum, the lower rectum usually being spared because of its dual blood supply.

The main differential diagnoses of ischemic colitis are infectious colitis, diverticulitis, and inflammatory bowel disease. Therefore, stool cultures and histology are an important part of the work-up of patients presenting with abdominal pain and bloody stools. Regular stool cultures do not detect Klebsiella oxytoca or enterohaemorrhagic Escherichia coli, and this should be specifically stated in the microbiology request form. The diagnosis is established by endoscopy and histology (1).

The endoscopic spectrum of ischemic colitis is broad (Figure 3).

Figure 3. Endoscopic spectrum of ischemic colitis

Key elements though are sparing of the rectum and segmental distribution, mainly in the left colon (at the watershed area, arc of Riolan). These are called Sudeck’s and Griffith’s points or areas (Figure 4).

Figure 4. Watershed areas in transient left sided ischemic colitis (2).

In mild ischemic colitis there are usually segmentally distributed patchy erythema, edema and subepithelial hemorrhages. In moderate colitis, in addition to changes seen in mild disease, there are localized erosions and ulcers, which may be confluent. Often, a linear ulcer in the mesenteric border of the colon is seen. This is known as colon single strip sign (CSSS) or Zuckerman’s sign (1).

Figure 5. Colon single strip sign (CSSS) or Zuckerman’s sign.

In severe colitis there are deep ulcers, luminal narrowing and strictures and frank necrosis.

Most cases of ischemic colitis are self-limited and do not require any specific medical or surgical therapy. However, in clinically unstable patients with signs of peritonitis colon resection should be considered.

References:

Monkemuller K, Wilcox. Video GIE: https://www.videogie.org/article/S2212-0971(13)70152-3/fulltext
https://www.lecturio.com/concepts/mesenteric-ischemia/

No COI by KM, TP or AD with any of the companies/utensils or products mentioned in this article.

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Cap-Assisted Argon Plasma Coagulation of Esophageal Inlet Patch

Fri, 13 Dec 2024 00:00:00 GMT

Figure 1. Gastric heterotopia of the upper esophagus. A. White light imaging showing one inlet patch measuring about 25 x 15 mm. B. NBI view of inlet patch. C. Two inlet patches facing each other (yellow arrows). D. NB characterization makes these lesions more visible and evident. There were no suspicious mucosal pre-neoplastic changes.

Because this patient was symptomatic a decision to ablate the inlet patches was taken. Multiple studies have shown good results for argon plasma coagulation (APC) in the ablation of symptomatic inlet patches (1-3). It is important to carefully characterize these lesions endoscopically and re ablation biopsies are recommended to evaluate the type of stomach tissue. Cases of adenocarcinoma arising in inlet patches have been described (4-8).

Whereas some experts ablate the lesions just using the argon plasma catheter through the scope, we prefer to use a distant transparent cap (Figure 1E-G). Inlet patches are usually located very close to the upper esophageal sphincter. Thus, a cap will keep the esophageal entrance open while allowing to target the inlet patches with the tip of the argon plasma catheter (Panels F and G). In addition, the cap allows for scrapping off ablated tissue and applying a second or third round of APC. The aim of APC is to change the color of the mucosa to brown color (Panel H), and not to carbonize or charr it black, as this may result in deep tissue injury and subsequent esophageal stenosis. The settings used are 40 to 50 Watts with 0,8-liter flow. However, one can apply lower wattage and flow, if the endoscopist can achieve a controlled mucosal ablation with the movements of the scope and catheter.

References

Bajbouj M, Becker V, Eckel F, Miehlke S, Pech O, Prinz C, Schmid RM, Meining A. Argon plasma coagulation of cervical heterotopic gastric mucosa as an alternative treatment for globus sensations. Gastroenterology. 2009 Aug;137(2):440-4. doi: 10.1053/j.gastro.2009.04.053. Epub 2009 May 4. PMID: 19410576.

Brechmann T, Mühlenkamp M, Schmiegel W, Viebahn B. Argon Plasma Coagulation of Gastric Inlet Patches of the Cervical Esophagus Relieves Vocal and Respiratory Symptoms in Selected Patients. Dig Dis Sci. 2023 May;68(5):1936-1943. doi: 10.1007/s10620-022-07745-9. Epub 2022 Nov 14. PMID: 36376579.

Meining A, Bajbouj M, Preeg M, Reichenberger J, Kassem AM, Huber W, Brockmeyer SJ, Hannig C, Höfler H, Prinz C, Schmid RM. Argon plasma ablation of gastric inlet patches in the cervical esophagus may alleviate globus sensation: a pilot trial. Endoscopy. 2006 Jun;38(6):566-70. doi: 10.1055/s-2006-925362. PMID: 16802267.

Dziadkowiec KN, Sánchez-Luna SA, Stawinski P, Proenza J. Adenocarcinoma Arising From a Cervical Esophageal Inlet Patch: The Malignant Potential of a Small Lesion. Cureus. 2020 Jul 19;12(7):e9284. doi: 10.7759/cureus.9284. Erratum in: Cureus. 2022 Sep 13;14(9):c74. doi: 10.7759/cureus.c74. PMID: 32832282; PMCID: PMC7437138.

Ajmal S, Young JS, Ng T. Adenocarcinoma arising from cervical esophageal gastric inlet patch. J Thorac Cardiovasc Surg. 2015 Jun;149(6):1664-5. doi: 10.1016/j.jtcvs.2015.03.050. Epub 2015 Apr 1. PMID: 25911182.

Probst A, Schaller T, Messmann H. Adenocarcinoma arising from ectopic gastric mucosa in an esophageal inlet patch: treatment by endoscopic submucosal dissection. Endoscopy. 2015;47 Suppl 1 UCTN:E337-8. doi: 10.1055/s-0034-1392423. Epub 2015 Jul 2. PMID: 26134434.

Kadota T, Fujii S, Oono Y, Imajoh M, Yano T, Kaneko K. Adenocarcinoma arising from heterotopic gastric mucosa in the cervical esophagus and upper thoracic esophagus: two case reports and literature review. Expert Rev Gastroenterol Hepatol. 2016;10(3):405-14. doi: 10.1586/17474124.2016.1125780. Epub 2015 Dec 16. PMID: 26610162.

Nonaka K, Watanabe M, Yuruki H, Okuda A, Sakurai K, Iyama K, Sasaki Y. Narrow band imaging of adenocarcinoma arising from ectopic gastric mucosa in the upper esophagus. Endoscopy. 2013;45 Suppl 2 UCTN:E112-3. doi: 10.1055/s-0032-1325865. Epub 2013 May 28. PMID: 23716084.

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Endoscopic Resection of an Esophageal Pseudodiverticulum in Radiation-Induced Stenosis

Sun, 08 Dec 2024 00:00:00 GMT

Peter Jakobs, MS, Josip Juraj Strossmayer Universität Osjiek, Croatia, Ameos Klinikum Halberstadt, Germany

Klaus Mönkemüller, MD, PhD, FASGE, FJGES, Professor of Medicine, Department of Gastroenterology, Ameos Klinikum Halberstadt, Germany and Carilion Memorial Hospital, Virginia Tech Carilion School of Medicine, Roanoke, USA

A 62-year-old Caucasian male patient presented with dysphagia due to post-radiogenic esophageal stenosis. The patient had a history of transglottic laryngeal carcinoma for which he had undergone laryngectomy, neck dissection on both sides and adjuvant radio-chemotherapy. An esophageal bougienage had already been performed 4 months earlier and a dilatation from 5-6 mm to 9-10 mm had been performed 3 months earlier using TTS-OTW-CRE balloon dilation with good results. When dysphagia symptoms recurred, a further examination was carried out, which showed impassable narrowing at approx. 18 cm form the incisors (Figure 1).

Figure 1. Radiation-induced stenosis and esophageal pseudodiverticulum. The impassable passage showed a ring-shaped fibrosis of the mucosa and an adjacent pseudo diverticulum (A yellow arrow) with proximal megaesophagus. B. Stenotic esophagus due to radiation induced esophagitis and pseudodiverticulum with a hemi-ring of fibrotic mucosa. In addition, a large gastric inlet patch was present at approx. 15 cm (C, light blue arrow). D. Narrow band imaging of the inlet patch.

It was decided to remove the diverticulum to eliminate the stenosis. The decision was made to use an IT KNIFE NANO (Olympus, Japan). The great advantage of this knife is that the tip is insulated with ceramic and thus considerably reduces the risk of electrosurgical injury to adjacent structures, especially when visibility is reduced (1, 2).

Figure 2. Endoscopic resection of pseudo-diverticulum using an IT-Nano knife. A. Approaching the stenosis and pseudodiverticulum with the IT-Nanoknife. B. Incision of the fibrotic hemi-ring. C. Successful resection of the pseudodiverticulum. Notice the increased esophageal lumen, which allowed for passage of the scope.

Even though the IT KNIFE NANO is noticeably more expensive than a conventional needle knife, it offers increased safety, especially for endoscopic submucosal dissection or hard-to-reach areas (4). In the above-mentioned patient with a barely passable narrowing in the esophagus, resection of the diverticular tissue using traditional knives may be extremely difficult. In addition to a steady hand, experience is also required. Thanks to the special shape of the knife used and the non-cutting ceramic tip the procedure was not only faster (total of 3 minutes), but also safer.

Figure 3. IT-Nano knife.

The patient was also placed on high dose proton pump inhibitors as there was a large gastric heterotopia or inlet patch (Figure. 1). This ectopic gastric mucosa secretes acid and could have also contributed to the stricture formation in this patient. Another option to treat Inlet patches is ablation using argon plasma coagulation, which we may consider if the stenosis recurs (4). At 6 weeks follow-up the patient is has improved clinically.

Technical Review: Endoscopic Resection of a Cardia Polyp Inside a Hiatal Hernia Sack Using the Duette Device

Fri, 22 Nov 2024 00:00:00 GMT

Endoscopic Resection of a Cardia Polyp Inside a Hiatal Hernia Sack Using the Duette Device

A middle-aged male patient presented for EGD because of dyspepsia and heartburn. On EGD he was found to have erosive reflux esophagitis grade C based on the Los Angeles classification, a 4 cm hiatal hernia and an incidental, sessile polyp inside of the hernia sack (Figures 1A-C). The polypoid lesion was covered with some exudate and the mucosa had a cerebroid pattern, with areas of erosions and spontaneous bleeding. There were no signs of fold convergence, scars, or loss of vascularity. A decision to resect the lesion was taken. We used the Duette device.

Why did we choose the Duette device in this situation?

First, the lesion was in a hernia sack and the sack was moving in and out during patient’s respiration. Second, the hernia sack allowed air (CO2) to constantly escape. And third, the patient had episodes of retching, as are often seen in patients with large hernias. Therefore, performing a traditional endoscopic mucosal resection (EMR) was less appealing, especially with a gastroscope having a working channel on the left side (about 7-8 o’clock position).

The advantages of performing the resection with the Duette system were the following: a) the lesion would be banded, and thus the mucosa to be resected is secured, as the endoscopist guides the resection based on were the band(s) is located, and b) the presence of a cap would allow for controlled resection and immediate suction (entrapment) and retrieval of the specimen.

The Duette device (Figure 1D) is essentially an endoscopic banding device for varices. The objective of suctioning and banding GI mucosal lesions is to a) reshape a flat or semi-sessile lesion into a “sessile” form, b) have the band at the base and assure a better endoscopic resection (R0).

Figure 1E shows the suctioning of the polyp and release of the band below the polyp.

The other novelty of the Duette device is the 5Fr hexagonal snare. If you would use a banding kit and then try to advance a traditional snare (usual diameter of the snare catheter or sheath is 7Fr), it would be impossible to push it through the working channel of the scope, as there is a string for the bands inside. When using Duette, pushing the 5Fr snare is quite easy. Figure 1F shows the snare being placed around the polyp. This hexagonal snare also has the advantage of having great expansile force and memory. It can be used to remove several lesions or pieces, such as large surface areas with dysplastic Barrett’s esophagus.

Depending on the amount of tissue caught, the snare can be placed below the band (if less tissue was caught), or above the band (if too much tissue was entrapped). In any event, the bands will not stay in place, and fall off immediately after the resection. But if too much tissue is caught and the snaring occurs below the band, there are higher chances of deep resection or even perforation. Therefore, it is important to observe the new post-suction-banded polyp to decide on the best strategy. In our case we placed two bands to safely secure the polyp while the patient was retching. Then we placed the snare between two bands (Figure 1G). The lesion was resected in its entirety, with a nice clean base (Figure 1H). Shortly after the resection, we advanced the scope into the stomach and “fired” all the bands and pulled the string out of the working channel of the scope. Then we went back to the hernia sack and suctioned the polyp into the cap and removed the polyp out of the patient (similarly to the removal of a “meat impaction” using cap).

Histology revealed an inflammatory polyp with intestinal metaplasia but no cancerous cells. The patient had an uneventful post-operative course and is on PPIs for the erosive reflux esophagitis.

In sum, the Duette device was an ideal and safe tool to resect a polypoid lesion located in the cardia, inside a large hernia sack.

No COI by DD or KM with any of the companies/utensils or products mentioned in this article.

Poll

In your practice, which method do you most commonly use for resecting polyps in challenging locations like a hiatal hernia sack?

Traditional endoscopic mucosal resection (EMR)

Duette device or similar banding-assisted resection

Endoscopic submucosal dissection (ESD)

Cold snare polypectomy

I refer these cases

Next Steps

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Tips for the Endoscopy Suite: Measurement of Polyp Size using the “QTip Ruler”

Fri, 08 Nov 2024 00:00:00 GMT

PDF - Tips for the Endoscopy Suite: Measurement of Polyp Size using the “QTip Ruler”

An elderly patient underwent colonoscopy for hemoccult positive stools. During colonoscopy a broad-based polypoid lesion was found in the distal transverse colon. After submucosal injection an endoscopic mucosal resection was performed. How do you usually measure the size of the resected lesions? Often, we have a ruler in the “toolbox” of our endoscopy suite. Herein we present a practical measuring device, the “Q tip or cotton tip applicator ruler”.

These pair of cotton tips have various uses in the endoscopy suite:

Remove polyps or tissue from the polyp traps,
Remove resected tissue stuck at forceps, which can be done with the cotton tip or also breaking the stick in two and using a “sharp” end to remove the tissue from the biopsy forceps, and
Use the ruler printed on the package to measure polyps or other things, such as removed foreign bodies, plastic stents, etc.

No COI by AD or KM with any of the companies/utensils or products mentioned in this article.

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Technical Review: Esophageal Dilation with the BougieCap

Thu, 31 Oct 2024 00:00:00 GMT

Luka K. Schöpf, MS, Josip Juraj Strossmayer Universität Osjiek, Croatia, Ameos Klinikum Halberstadt, Germany

Klaus Mönkemüller, MD, PhD, FASGE, FJGES, Professor of Medicine, Department of Gastroenterology, Ameos Klinikum Halberstadt, Germany, UEES Guayaquil, Ecuador, Universidad de la República, Uruguay and Carilion Memorial Hospital, Virginia Tech Carilion School of Medicine, Roanoke, USA

A 72-year-old man presented with recurrent meat boluses. On endoscopy a tight, fibrotic Schatzki ring was found. (Figure 1, panels A, B). Thus, the patient had a classic “steak house syndrome”. Destruction of Schatzki rings can be accomplished with dilation using Savary or Maloney dilators or bougies, balloon dilation, star-like incisions, cxircumferential excision using IT-knife, cold biopsy mini-excisions or with the novel “BougieCap ®” (Ovesco Endoscopy AG, Tübingen, Germany. In this case we elected the Bougie cap for several reasons: a) the cap is transparent (C-G) and has three-dilating sizes (which are marked on the cap) (C, D, E, F), c) the entire dilation (bougienage) procedure can be observed through the cap (in contrast to Savary or Maloney dilations) (D,E,F, G), d) in this era, where many countries have embraced a throw-away approach of utensils (one-time use, “disposable” devices, selecting the cheapest and equally or most effective device is essential.

Figure 1. Dilation of a Schatzki Ring with Bougie Cap. A. Tight fibrotic distal stenosis. B. After removing the food bolus with a cylindrical cap inspection of the distal esophagus revealed a Schatzki ring with remaining lumen of about 9 mm. C. Bougie Cap view of tongue. D. The distal tip of the cap is reaching the distal esophagus. E. The stretching or dilation of the stricture is easily seen. F. Two mucosal lacerations are seen, reflecting excellent dilation. G. Cap crossing the gastroesophageal junction (notice the Z-line). H. Cap entered the stomach.

Figure 2. Technical aspects of the bougie cap (or dilator cap). When the coned cap is attached to the scope it transforms the scope into a “bougie” (dilation) device, similary to a Savary dilator (or bougie). The word “bougie” is used a lot in Europe, where the original dilators were made of wax (i.e. candle like dilators). The best wax came from Bugaya (Algeria), hence “bougie”. However, the more fitting word is “dilator”, which is indeed what we do with Savary dilator, or expansion balloons (balloon dilation).

This distally transparent, conically shaped cap is attached to the distal scope, making the scope a “bougie dilator” (Figure 3). The Bougie cap enables effective and safe dilation of strictures with direct visual feedback, offering significant advantages compared to conventional techniques (1-4) (Figure 1).

Steps for dilation: The conical BougieCap is attached distally to the endoscope with special tape and advanced to the stenosis. By pushing forward and gently rotating the endoscope, the mucosal stricture can be dilated (3) (Figure 1). The BougieCap includes a front aperture for advancing a (0,021 to 0,035 inch (biliary) guide wire (max. 1 mm) when required and two lateral apertures that permit air insufflation, water irrigation, and suction (1, 4) (Figure 3). Direct visual control during endoscopy is enabled by the transparent plastic material of the BougieCap (Figures 1-3). Additionally, vessel compression by the BougieCap enhances mucosal examination, which improves the visibility of mucosal tears and reducing the risk of mucosal bleeding as a complication. Especially in the context of 'Green Endoscopy', employing the single-use BougieCap is advantageous as it reduces plastic waste by up to 99% compared to traditional dilation techniques (2).

Figure 3. Close-up image of the BougieCap (A, B, C) and the tape for attaching distally of the endoscope (D, E).

Overall, the treatment of benign stenoses in the upper gastrointestinal tract with the BougieCap can successfully and effectively dilate the primary stricture and additionally contribute to the improvement of dysphagia, as well as reducing the incidence of other complications. The BougieCap is available in various sizes, each with two different dilation diameters, allowing gentle stricture dilation and minimizing the risk of complications (3, 4) (Table 1).

Table 1. Available sizes of the BougieCap (4).

References:

Walter B, Meining A. Die Bougiekappe – eine neue Methode zur Behandlung von Stenosen im Gastro-intestinaltrakt. Endoscopy Campus. [accessed 2024 Jul 20]. Available from:
https://www.endoscopy-campus.com/lehrvideo/die-bougiekappe-eine-neue-methode-zur-behandlung-von-stenosen-im-gastro-intestinaltrakt/
Lafeuille P, Yzet C, Bonniaud P, et al. Use of a bougie-shaped cap for dilation with direct visual control for an esophageal stricture induced by radiation therapy. Endoscopy. 2023 Dec;55(S 01):E18-E19. doi: 10.1055/a-1929-9317. Epub 2022 Sep 16. PMID: 36113487; PMCID: PMC9812673.
Duarte P, Walter B, Patel P, et al. Bougiecap dilatation device: Novel endoscopic method for treatment of oesophageal strictures-results from a multicentre study. Gut. 2021 Jan. 70 (Suppl 1): A1-A262.
BougieCap - Produkt und Verfahren für die Bougierung von Stenosen und Strikturen des oberen Gastrointestinaltraktes. Ovesco Endoscopy AG. [accessed 2024 Jul 20]
Available from:
https://ovesco.com/de/scopecaps/bougiecap/#/eluidde05b763_1_0

KM has been a consultant for Ovesco, Germany (2012 and 2016)

LKS does not have any COI to declare.

Next Steps:

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Endoscopic Management of Post-Sphincterotomy Bleeding: Eight Hemostatic Tips

Thu, 24 Oct 2024 00:00:00 GMT

Post-sphincterotomy bleeding is a significant concern in endoscopic retrograde cholangiopancreatography (ERCP) procedures (1). While literature reports suggest that bleeding occurs in less than 1% of ERCPs involving biliary or pancreatic sphincterotomy, clinical experience often indicates a higher frequency, as currently more patients are on chronic anticoagulation. This discrepancy underscores the importance of being well-prepared to manage such complications.

The ampulla of Vater and its surrounding structures have an incredibly rich blood supply, which contributes to the risk of bleeding during and after sphincterotomy (2, 3). This vascular network includes branches from the gastroduodenal artery, inferior pancreaticoduodenal artery, anterior and posterior pancreaticoduodenal arcades, and the anterior superior pancreaticoduodenal artery, among others (2, 3). Understanding this complex vascular anatomy is crucial for effective management of post-sphincterotomy bleeding.

Understanding the Anatomy

To effectively manage post-sphincterotomy bleeding, it’s essential to have a thorough understanding of the relevant anatomy. The bile duct and sphincter area have a figure-of-eight configuration, not the simple circular shape often depicted in medical textbooks. This figure-of-eight shape influences the direction of cuts made during sphincterotomy procedures.

For biliary sphincterotomy, the cut is typically made towards the 11 o’clock position, while for pancreatic duct sphincterotomy, the cut is directed towards the 1 o’clock position. These directions are chosen to minimize the risk of cutting through major blood vessels, as histological studies have shown that the largest concentration of blood vessels is at the 9 and 3 o’clock positions.

Figure 1. Cannulation and sphincterotomy directions. The septum between the biliary and pancreatic ducts is another crucial anatomical feature to consider. Understanding its position can aid in selective cannulation and help avoid unintended damage during sphincterotomy.

Challenges in Hemostasis

Several factors can complicate hemostasis in post-sphincterotomy bleeding (Figure 2):

Awkward scope positions: The duodenoscope may be in a challenging position, making it difficult to manipulate instruments effectively.
Surgical altered anatomy: Previous surgeries, such as Billroth II procedures, can significantly alter the anatomy, making access and visualization more challenging.
Abnormal papilla appearance or location: The papilla may appear unusual, be hanging loosely, or be located inside a diverticulum or on its edge. These variations can make it harder to identify and treat the source of bleeding.

Figure 2. Challenges for hemostasis during ERCP.

Given these potential challenges, it’s crucial to have a variety of hemostatic techniques at your disposal. Let’s explore eight effective tricks for managing post-sphincterotomy bleeding.

Trick 1: The Manta Needle

The Manta needle is an invaluable tool for managing post-sphincterotomy bleeding (Figure 3). Its key features include:

A thin outer diameter (approximately 2mm), allowing easy passage through the working channel of any endoscope, especially duodenoscopes.
A reinforced tip that enables smooth advancement through the endoscope, even when the elevator is in the up position. Other needles (with the exception of the Carr-Locke needle) usually puncture through the sheet when closing the elevator (“up position”).
Resistance to breaking through the plastic sheath, a common problem with other needles.

Figure 3. Thin needle with reinforced tip. The needle can be easily pushed out with elevator in the “up” position (curved yellow arrow).

To use the Manta needle effectively:

Advance the needle towards the bleeding area around the biliary or pancreatic sphincter.
Inject a solution of epinephrine and saline. The epinephrine provides immediate vasoconstriction, while the saline creates tamponade through local tissue edema.
Inject in multiple areas around the bleeding site to ensure comprehensive coverage.

Remember, while epinephrine injection can provide rapid hemostasis, it’s often temporary. Additional hemostatic measures are usually necessary for definitive treatment.

Trick 2: Clips for Hemostasis

Endoscopic clips are another essential tool for managing post-sphincterotomy bleeding. When using clips, consider the following:

Clip design: Pay attention to both the arms and stems of the clips (Figure 4). Clips with shorter stems are generally more practical for papillary bleeding, as they’re less likely to get caught on the elevator of the duodenoscope.
Clip exposure: When using a duodenoscope, keep the plastic sheath on the clip in place. This helps prevent premature deployment and allows for better control.
Clip manipulation: After exposing the clip, open it fully. You can then use the duodenoscope’s controls to bow the clip up and down, allowing for precise positioning (Figure 5).
Clip size: For papillary bleeding, 11mm clips are usually sufficient, as the goal is to close individual vessels rather than large defects.

Figure 4 shows various types of commercially available clips.

Figure 4. Various types of commercially available clips.

Figure 5. How to choose a clip for ERCP scope. Using clips with shorter stem may improve manipulation while elevator is in the “up” position.

When applying clips:

Identify the bleeding vessel or area.
Position the clip perpendicular to the vessel if possible.
Apply the clip, ensuring it grasps enough tissue to provide effective hemostasis.
Be prepared to apply multiple clips if necessary.

Trick 3: Caps in Endoscopy

Endoscopic caps can be incredibly useful for managing post-sphincterotomy bleeding, especially when using a forward-viewing endoscope (4). Key points about using caps include:

Cap selection: Choose barrel-shaped caps with side openings to allow for fluid drainage and maintain visibility.
Improved visualization: Caps help maintain a clear field of view by creating distance between the tip of the endoscope and the tissue.
Clip assistance: When using clips, the cap can help keep the clip open as you approach the target area, allowing for more precise placement.
Compression: The cap can be used to apply direct pressure to the bleeding site, providing temporary hemostasis while preparing other interventions.

Figure 6. Cap-assisted hemostasis for post-sphincterotomy bleeding. Source: Dr. Andrés Rodríguez-Parra, Colombia.

To use a cap effectively:

Attach the appropriate cap to your endoscope.
Use the cap to locate the papilla and identify the bleeding site.
If using clips, pre-open the clip within the cap before approaching the target area.
Apply gentle pressure with the cap to temporarily control bleeding and improve visualization.
Deploy your chosen hemostatic method (e.g., clip, injection) with the assistance of the cap.

Trick 4: Fully Covered Self-Expanding Metal Stents

Fully covered self-expanding metal stents (FCSEMS) can be an excellent option for managing difficult post-sphincterotomy bleeding (Figure 7). They work by applying consistent pressure to the entire circumference of the sphincterotomy site, effectively tamponading any bleeding vessels.

Figure 7. Fully-covered self-expanding metal stents for post-sphicnterotomy bleeding.

Key points for using FCSEMS:

Always have a FCSEMS available when performing ERCP procedures.
Choose an appropriate size based on the bile duct diameter and the extent of the sphincterotomy.
FCSEMS can be particularly useful in cases of altered anatomy, such as Billroth II, where other hemostatic techniques may be challenging.

To deploy a FCSEMS for hemostasis:

Confirm the source of bleeding and assess the bile duct size.
Choose an appropriately sized FCSEMS (based on diameter of bile duct).
Deploy the stent across the sphincterotomy site, ensuring it covers the entire area of concern.
Confirm proper placement with fluoroscopy and direct visualization if possible.
Plan for stent removal in 1-2 weeks, once hemostasis is assured and the risk of recurrent bleeding has decreased.

Trick 5: Coagrasper and Ensure Coagulation Forceps

The Coagrasper (Olympus) and Ensure Coagulation Forceps (Microtech) are specialized devices designed for precise coagulation of bleeding vessels (Figure 8). These tools are particularly useful for targeting specific bleeding points that may be difficult to address with other methods (5).

Figure 8. Hemostatic forceps.

Key features and usage tips:

These devices use monopolar electrocoagulation to seal bleeding vessels.
They are most effective for vessels less than 2mm in diameter.
When using an ERBE electrosurgical unit, a setting of soft coagulation with effect 5 is typically recommended.

To use these devices effectively:

Identify the specific bleeding vessel or point.
Open the forceps and approach the target area.
Grasp the bleeding point with the forceps.
Apply coagulation current for 1-2 seconds.
Release the tissue and assess for hemostasis.
Repeat if necessary, being cautious not to apply excessive coagulation to any one area.

Trick 6: Self-Assembling Gels (e.g., Purastat)

Self-assembling gels, such as Purastat, are newer additions to the hemostatic arsenal. These products can serve two primary functions in managing post-sphincterotomy bleeding (6, 7):

Vessel identification: The gel can help localize the source of bleeding by adhering to the bleeding site and making it more visible.
Direct hemostasis: In some cases, the gel itself can provide effective hemostasis by forming a barrier over the bleeding site.

To use self-assembling gels:

Prepare the gel according to the manufacturer’s instructions.
Apply the gel to the area of suspected bleeding using the provided catheter.
Observe the area to identify any points where the gel is displaced by active bleeding.
If bleeding continues, use the gel-highlighted areas to guide more targeted hemostatic interventions.
In cases of mild oozing, the gel may be sufficient to achieve hemostasis on its own.

Trick 7: Balloon Dilation for Compression Hemostasis

Balloon dilation can be an effective method for achieving hemostasis through direct compression. This technique is particularly useful when the bleeding source is diffuse or when other methods have failed.

Figure 9. Balloon dilation.

Key points for balloon compression:

Use esophageal balloons rather than biliary balloons for this purpose. Esophageal balloons provide better compression and are more durable.
Choose the balloon size based on the diameter of the bile duct. For a 12-15mm bile duct, use a 12-15mm esophageal balloon.

To perform balloon compression:

Select an appropriately sized esophageal balloon.
Position the deflated balloon across the sphincterotomy site.
Slowly inflate the balloon to the desired diameter.
Maintain inflation for 3-5 minutes.
Slowly deflate the balloon and assess for ongoing bleeding.
Repeat if necessary, being cautious not to overinflate or maintain inflation for too long, which could lead to ischemic injury.

Trick 8: Interventional Radiology

When endoscopic methods fail to achieve hemostasis, interventional radiology can be a life-saving option. It’s important to consider this option early in cases of severe or refractory bleeding.

Key points about interventional radiology for post-sphincterotomy bleeding:

It’s generally preferred over surgery due to its less invasive nature.
Selective embolization can target specific bleeding vessels while preserving surrounding tissue.
Multiple attempts may be necessary, as there can be more than one bleeding source.

When to consider interventional radiology:

Severe bleeding that doesn’t respond to initial endoscopic measures.
Recurrent bleeding after apparent initial hemostasis.
Hemodynamic instability despite aggressive resuscitation and endoscopic attempts at hemostasis.

The interventional radiologist will typically perform an angiogram to identify the bleeding vessels and then selectively embolize them. This procedure may need to be repeated if there are multiple bleeding sources or if rebleeding occurs.

Conclusion

Managing post-sphincterotomy bleeding requires a multi-faceted approach and a well-stocked arsenal of hemostatic techniques. By mastering these eight tricks – the Manta needle, endoscopic clips, caps, fully covered self-expanding metal stents, coagulation forceps, self-assembling gels, balloon compression, and interventional radiology – endoscopists can effectively manage most cases of post-sphincterotomy bleeding.

Remember that each case is unique, and often a combination of these techniques may be necessary to achieve definitive hemostasis. Always be prepared with multiple options, and don’t hesitate to escalate to more advanced techniques or seek assistance from colleagues in interventional radiology when needed. With practice and experience, you’ll develop the skills to confidently handle this challenging complication of ERCP procedures.

References:

Wilcox CM, Canakis J, Mönkemüller KE, Bondora AW, Geels W. Patterns of bleeding after endoscopic sphincterotomy, the subsequent risk of bleeding, and the role of epinephrine injection. Am J Gastroenterol. 2004 Feb;99(2):244-8. doi: 10.1111/j.1572-0241.2004.04058.x. PMID: 15046211.
Purvis NS, Mirjalili SA, Stringer MD. The mucosal folds at the pancreaticobiliary junction. Surg Radiol Anat. 2013 Dec;35(10):943-50. doi: 10.1007/s00276-013-1128-y. Epub 2013 May 5. PMID: 23645171.
Mirjalili SA, Stringer MD. The arterial supply of the major duodenal papilla and its relevance to endoscopic sphincterotomy. Endoscopy. 2011 Apr;43(4):307-11. doi: 10.1055/s-0030-1256229. Epub 2011 Mar 31. PMID: 21455871.
Chon HK, Kim TH. Endoclip therapy of post-sphincterotomy bleeding using a transparent cap-fitted forward-viewing gastroscope. Surg Endosc. 2017 Jul;31(7):2783-2788. doi: 10.1007/s00464-016-5287-x. Epub 2016 Oct 19. PMID: 27761747.
Bapaye JA, Wasserman RD, Mönkemüller K, Kesar V, Kesar V. Application of hemostatic forceps to treat post-sphincterotomy bleeding near the pancreatic duct opening. Endoscopy. 2024 Dec;56(S 01):E630-E631. doi: 10.1055/a-2353-5910. Epub 2024 Jul 26. PMID: 39059447; PMCID: PMC11281839.
Ogura T, Uba Y, Yamamura M, Nishioka N, Nishikawa H. Endoscopic hemostasis using self-expandable metal stent combined with PuraStat^Ⓡ for patient with high risk of post-endoscopic sphincterotomy bleeding (with video). Hepatobiliary Pancreat Dis Int. 2024 Feb;23(1):94-96. doi: 10.1016/j.hbpd.2023.02.001. Epub 2023 Feb 4. PMID: 36754705.
Ishida Y, Tsuchiya N, Koga T, Kitaguchi T, Matsumoto K, Kuno N, Funakoshi S, Ishibashi H, Ashizuka S, Hirai F. A novel self-assembling peptide hemostatic gel as an option for initial hemostasis in endoscopic sphincterotomy-related hemorrhage: a case series. Clin J Gastroenterol. 2022 Dec;15(6):1210-1215. doi: 10.1007/s12328-022-01702-9. Epub 2022 Sep 19. PMID: 36121586.

Disclosures: KM- no COI with any products, devices or companies mentioned in this article.

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Mistakes in the Management of Small Bowel Bleeding

Thu, 17 Oct 2024 00:00:00 GMT

Objective: This lecture addresses common mistakes made in the management of small bowel bleeding (SBB), specifically focusing on the crucial steps to be taken before considering advanced endoscopic procedures like deep enteroscopy or capsule endoscopy. The lecture emphasizes the importance of thorough initial evaluation and the potential for missed lesions within the reach of standard EGD and colonoscopy.

About the Lecture:

Key Highlights:

Clear explanation of why small bowel endoscopy presents unique challenges.
Discussion of mid-GI bleeding (mid-GIB) and its diagnostic criteria.
Presentation of data showing the prevalence of lesions reachable by standard endoscopy often missed on initial examination.
Review of specific lesions and conditions frequently overlooked in the stomach and colon.
Highlight of other causes of anemia and obscure GI bleeding that may mimic SBB.
Practical take-home message: repeat EGD and colonoscopy before proceeding with advanced small bowel evaluation.

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Emesis or Prolapse Gastropathy

Wed, 16 Oct 2024 00:00:00 GMT

A 35-year-old man presented with nausea and vomiting followed by hematemesis. During EGD prolapse gastropathy was diagnosed (Figure 1).

Figure 1. Prolapse gastropathy. Upper panels show the patchy area of prolapsed stomach fundus mucosa with erythema, edema and congestion (yellow circle, arrow shows scope). The proposed mechanism of formation of prolapse gastropathy is shown in the lower graphics (C, D) (graphics source: Byfield F et al. GIE 1998).

Prolapse or emesis gastropathy is an underrecognized cause of hematemesis (1, 2). This condition was initially described in the late 70s (1). Retching and vomiting results in prolapse of the lesser curvature of the stomach fundus into the esophagus (1-3). Temporary “prolapse with strangulation” results in submucosal edema, congestion and hemorrhages. Some experts also call this condition “mechanical gastritis of the cardia (3). We believe that prolapse gastropathy is a precursor of Mallory-Weiss tears and even Boerhaave’s syndrome. Therapy is aimed at relieving the underlying causes of nausea and vomiting.

References:

Retrograde gastric mucosal prolapse as a cause of haematemesis. Young GP, Thomas RJ, Wall AJ. Med J Aust. 1976;2:488–489.
Hematemesis due to prolapse gastropathy: an emetogenic injury. Byfield F, Ligresti R, Green PHR, Finegold J, Garcia-Carrasquillo RJ. Gastrointest Endosc. 1998;45:527–529.
Mechanical gastritis involving the cardia: the trauma of retching and vomiting. Chen YL. J Clin Gastroenterol. 1990;12:63–66.

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Endoscopic Therapy for Bleeding Gastroesophageal Varix (GOV 2)

Tue, 15 Oct 2024 00:00:00 GMT

A 45-year-old woman with history of cirrhosis presented with acute onset hematemesis and hypotension. After hemodynamic stabilization an urgent EGD was performed (Figure 1).

Figure 1. Gastroesophageal varix GOV 2. A. Z-line and cardia. B. Bleeding varix at the distal cardia, towards the greater curvature (GOV 2). C. Small nipple sign. D. Close up look of varix with recent stigmata of bleeding. E. During retrieval of scope the nipple sign can be clearly seen (yellow arrow). F. Endoscopic band ligation (EBL) of GOV 2. G. Effective EBL. H. Effective hemostasis after EBL.

The key steps for effective endoscopic hemostasis of gastroesophageal varices are:

Define exact location of the varix or varices. Figure 1 A. shows clear visualization of the gastroesophageal junction. Afterwards, careful retroflexion is mandatory, ideally with a clean stomach fundus. All excess blood or blood clots must be removed. In addition, we utilize simethicone to remove any bubbles.
Dynamic inspection of the lesion (panels B, C and D). During “dynamic” inspection we focus on the tissue composition, elasticity, appearance and bleeding. Generally, GOV may be treated with elastic bands (1) (Figure 2, ref 1). However, varices with lots of fibrosis (stiffness) should be treated with injection. This varix was “soft” appearing and a decision to use bands was taken.

Figure 2. Sarin classification of gastric varices (1).

Inspection should also be performed in antegrade view. During inspection it is also important to determine whether there are signs of variceal rupture (i.e. “nipple” sign, panels D and E, yellow arrows) or vessel wall thinning (i.e. red spot or red wale signs). In this case, the nipple sign helped us clearly differentiate the high-risk varix from another varix in proximity (which occasionally may be banded erroneously, green arrows, panels D and E). Thus, these bleeding stigmata are important signs to relocate the varix when using the scope is reinserted with endoscopic band ligation device (cap with bands).
Although EBL may be performed in retroflexion, elastic bands are best placed in forward (antegrade) view (panel F). While suctioning the varix into the cap with bands it is essential to keep the high-risk stigmata (in this case the nipple or fibrin plug) in the center. Once the varix is about two-thirds into the cap the band must be released (“fired”). During suctioning there will be rupture of the nipple sign (fibrin plug) and bleeding will ensue. Don’t panic and don’t take your finger from the suctioning button. Instead, keep a cool head and fire the band. Soon after releasing the band stop suctioning and apply a little bit of air or even touch of water (through the water channel of the scope). This will gently push away the banded varix from inside the transparent cap and you will observe the result – a nicely strangulated varix (G, H).

References:

Wani ZA, Bhat RA, Bhadoria AS, Maiwall R, Choudhury A. Gastric varices: Classification, endoscopic and ultrasonographic management. J Res Med Sci. 2015 Dec;20(12):1200-7. doi: 10.4103/1735-1995.172990. PMID: 26958057; PMCID: PMC4766829.

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Endoscopic Therapy for Bleeding Jejunal Diverticulum

Tue, 15 Oct 2024 00:00:00 GMT

How Do You ACTUALLY Master GI Bleeding?

A 70-year-old man with history of hypertension and a stroke one year prior, since then using clopidrogel, presented with acute onset hematochezia and hemorrhagic shock. The patient was not taking any non-steroidals. A computed tomography angiography (CTA) showed active bleeding in the mid-jejunum (Figure 1 A). After hemodynamic stabilization an urgent single balloon enteroscopy was performed (Figure 1). Multiple small and large jejunal diverticula were found. There was a large diverticulum at about 100 cm distal to the duodenum with an ulcer on its inner wall (Figure 1C). The ulcer was treated with five clips. No further bleeding was observed.

Figure 1. Bleeding jejunal diverticulum. A. CTA showing active bleeding (extravasation of contrast, yellow circle) in the mid-jejunum. B. Large jejunal diverticulum (green arrow) with ulcer (yellow arrow). C. Large ulcer in the mouth of the diverticulum. D. Endoscopic hemostatic therapy using clips. E. Close up view of clipped ulcer.

Figure 2 shows several tips and tricks on the endoscopic approach of jejunal diverticula. First, always look for different shapes of folds or darker areas behind or on the front of folds (A). These are clues for the presence of diverticula, blood or ulcers. Second, the use of simethicone will remove bubbles that disturb the view (B). Third, place the scope in a position that the worki g channel allws for targeting and treating the culprit lesion in a directed and easy manner (E). Fourth, use lots of clips to ensure the best possible closure or approximation of the ulcer and/ or hemostasis

Figure 2. Bleeding jejunal diverticulum. A. Dark contents inside of a jejunal diverticulum. B. irregular mucosa of the ulcerated mouth (entrance) of the diverticulum. C. Jejunal diverticulum (green arrow) with ulcer (yellow arrow). D. Large ulcer. E. The working channel of the scope on the left allowed for nice direction and placement of the clips. F. Two initial clips. G. and H. When confronted with a deep small bowel clip aggressive hemostasis is essential, i.e. better two additional clips than one to few”

In summary, this case is interesting for several reasons. First, a CTA was the first test performed for his hematochezia. CTA is being performed more often as a first line test in patients with gastrointestinal bleeding, especially if a “lower” (i.e. colonic) source is suspected (1). Second, after clinical stabilization we decided to perform a deep enteroscopy, obviating EGD and colonoscopy. This was a logical approach, as the source of bleeding was quite evident on CTA. Importantly, performing a capsule endoscopy may have delayed the treatment of the bleeding diverticulum. And finally, the concept of emergent deep enteroscopy proved to be of value, as the culprit lesion was found. Emergent double balloon was first described in 2009 and its use has been confirmed by various authors (2, 3). Finally, this report also describes key tips for reaching a diagnosis and achieving hemostasis in bleeding jejunal diverticulosis.

References:

Wu LM, Xu JR, Yin Y, Qu XH. Usefulness of CT angiography in diagnosing acute gastrointestinal bleeding: a meta-analysis. World J Gastroenterol. 2010 Aug 21;16(31):3957-63. doi: 10.3748/wjg.v16.i31.3957. PMID: 20712058; PMCID: PMC2923771.
Mönkemüller K, Neumann H, Meyer F, Kuhn R, Malfertheiner P, Fry LC. A retrospective analysis of emergency double-balloon enteroscopy for small-bowel bleeding. Endoscopy. 2009 Aug;41(8):715-7. doi: 10.1055/s-0029-1214974. Epub 2009 Aug 10. PMID: 19670141.
Pérez-Cuadrado Robles E, Bebia Conesa P, Esteban Delgado P, Zamora Nava LE, Martínez Andrés B, Rodrigo Agudo JL, López Higueras A, López Martin A, Latorre R, Soria F, Pérez-Cuadrado Martínez E. Emergency double-balloon enteroscopy combined with real-time viewing of capsule endoscopy: a feasible combined approach in acute overt-obscure gastrointestinal bleeding? Dig Endosc. 2015 Mar;27(3):338-44. doi: 10.1111/den.12384. Epub 2014 Nov 3. PMID: 25251991.

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Immune Checkpoint Inhibitor Induced Colitis or “Immune Mediated Colitis”

Tue, 15 Oct 2024 00:00:00 GMT

A 70-year-old woman with history of metastatic melanoma on treatment with ipilimumab presented with acute onset abdominal pain and bloody bowel movements.

Figure 1. Immune checkpoint inhibitor induced colitis (“immune mediated colitis”). A. diffuse mucosal edema, loss of light reflex, erythema, granularity. B. Large amount of secretion and pus (“mucopus”). C. “Tubular” colon because of severe inflammation. D. Immune mediated colitis is associated with significant neutrophilic inflammation, hence pus. E. Descending colon stenosis due to massive edema and inflammation. F. IMC is often indistinguishable from inflammatory bowel diseases. G. Typical granularity of mucosa in IMC. NBI views of inflamed crypts (cryptitis, white spots).

Immune checkpoint inhibitors (ICIs) are monoclonal antibodies that target cancer modulatory cells and immune processes such as cytotoxic T-lymphocyte antigen-4 (ipilimumab), and interaction between PD-1 and the ligands PD-L1 and programmed death ligand 2 (anti–PD-1 agents such as pembrolizumab, nivolumab) (1). Although ICIs have improved the treatment of several malignancies such as melanomas, their severe immune-related adverse events including hepatitis and colitis hamper their use in a significant proportion of patients (1, 2). Indeed, immune-mediated colitis (IMC) can occur in up to 25% (1, 2). On endoscopy, this iatrogenic colitis is very hard to differentiate from classical ulcerative colitis or Crohn’s disease. On histology there is more neutrophilic infiltration without chronic inflammation (1, 2). Therapy consists mainly on reducing or stopping the ICIs. In addition, corticosteroids are recommended for moderate and severe forms of colitis (1-3). Infliximab has also been shown to be beneficial, especially in those patients that do not respond to steroids (1-3. As ICIs are entering practice worldwide it is important to know about immune colitis.

References:

Som A, Mandaliya R, Alsaadi D, Farshidpour M, Charabaty A, Malhotra N, Mattar MC. Immune checkpoint inhibitor-induced colitis: A comprehensive review. World J Clin Cases. 2019 Feb 26;7(4):405-418. doi: 10.12998/wjcc.v7.i4.405. PMID: 30842952; PMCID: PMC6397821.
Hashash JG, Francis FF, Farraye FA. Diagnosis and Management of Immune Checkpoint Inhibitor Colitis. Gastroenterol Hepatol (N Y). 2021 Aug;17(8):358-366. PMID: 34602898; PMCID: PMC8475264.
Dougan M, Wang Y, Rubio-Tapia A, Lim JK. AGA Clinical Practice Update on Diagnosis and Management of Immune Checkpoint Inhibitor Colitis and Hepatitis: Expert Review. Gastroenterology. 2021 Mar;160(4):1384-1393. doi: 10.1053/j.gastro.2020.08.063. Epub 2020 Oct 17. PMID: 33080231.

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Ileum Intubation Made Easy

Sun, 13 Oct 2024 00:00:00 GMT

00:00 - Introduction to Ileum Intubation
00:42 - Intubation at the 9 O'Clock Position
02:22 - Intubation at the 6 O'Clock Position
03:58 - Tips for Effective Ileum Intubation
04:09 - Importance of Ileum Intubation Skills

About the Course:

Objective: This course offers a deep dive into the practical aspects of ileum intubation, focusing on the critical maneuvers and techniques essential for successful navigation and examination of the terminal ileum.
Key Highlights:
- Detailed exploration of the ileocecal valve intubation at the 9 to 11 o'clock (left side) and 6 o'clock (bottom) positions.
- Step-by-step guidance on scope manipulation, including positioning, torque application, and the use of air and water to facilitate intubation.
- Visual demonstrations of the intubation process for both key positions, accompanied by expert commentary to ensure a comprehensive understanding.

Course Content Overview:

Introduction to Ileum Intubation: Overview of ileum intubation, its significance in endoscopic practice, and the anatomical landmarks vital for the procedure.
9 to 11 O'clock Intubation Technique: A detailed walkthrough of the intubation process when the ileocecal valve is located on the left side of the screen, including the strategic use of the endoscope's big wheel and water channel for optimal visualization and access.
6 O'clock Intubation Technique: Instruction on the approach and technique adjustments necessary when the ileocecal valve is at the bottom of the screen, emphasizing the role of scope torque and the application of air and water.
Practical Tips and Tricks: Consolidated insights and pro-tips to enhance technique, improve procedural outcomes, and navigate common challenges encountered during ileum intubation.
Future Lectures Preview: A sneak peek into upcoming content, focusing on the dynamic movements of the scope during intubation, designed to bridge the gap between theory and practice.

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Mini-Review on Proton Pump Inhibitors PPI with Focus on their Mechanism of Action

Wed, 09 Oct 2024 00:00:00 GMT

Maren Haslach-Häfner, B.A.

Berufsfachschule für Pflege Kronach, Helios Bildungszentrum Kronach, Germany

Proton pump inhibitors (PPI=are the most common medications utilized to treat upper gastrointestinal bleeding resulting from acid-peptic disorders and ingestion of non-steroidal anti-inflammatory agents (NSAIDs). The aim of this mini review is to explain the mechanism of action in a practical manner. The following figures show the PPI on the parietal cell of the stomach in a simplified manner. The task of the proton pump is primarily to secrete hydrochloric acid from the parietal cells of the gastric mucosa, in conjunction with food intake as a stimulus. The H+K+ATPase is responsible for this active transport, i.e. proton exchange H+ from the cell for potassium ions K+ into the cell (Figures 1-4).

Figures 1-4: Pharmacokinetics of PPI (own presentation, graphics by Kirsten Tucker, 2023). PPIs do not act immediately after ingestion. Once they have passed through the stomach (Figure 1) and the enteric coating has dissolved in the small intestine, PPIs are absorbed into the blood (Figure 2) where they have a relatively short plasma half-life of 1 – 1.5 hours. After being absorbed from the small intestine, they reach the bloodstream via the portal vein system, where they undergo the first pass effect of the liver by CYP2C19 and CYP3A4 (1). Then the PPI metabolites continue to travel in the bloodstream, and they are absorbed from the bloodstream into the parietal cells of the stomach, the place where they ultimately intervene in the final secretion process (Figure 3). Indeed, PPIs are prodrugs that activate their effect in the acidic environment of the secretory canaliculi of the parietal cells (Figure 3). PPIs are referred to as weak bases with a pKa of 3.89 to 4.9, which allows them to accumulate in the acidic space of the secretory duct in the parietal cells (1). PPI then irreversibly inactivate the proton pump by the covalent modification associated with cysteine residues on the luminal side of the H+K+ATPase (Figure 4). This compound causes acid secretion inhibition to be longer than the PPI half-life. This is preceded by protonation into a tetracyclic sulfenamide or a sulfenic acid, which is now no longer permeable to membranes (2). This acid inhibition represents a more specific blockade than the H2 receptor or acetylcholine and gastrin blockade, regardless of the type of acid stimulation (2).

References:

Shin JM, Sachs G. Pharmacology of proton pump inhibitors. Curr Gastroenterol Rep. 2008 Dec;10(6):528-34. doi: 10.1007/s11894-008-0098-4. PMID: 19006606; PMCID: PMC2855237.
Olbe L, Carlsson E, Lindberg P. A proton-pump inhibitor expedition: the case histories of omeprazole and esomeprazole. Nat Rev Drug Discov. 2003 Feb;2(2):132-9. doi: 10.1038/nrd1010. PMID: 12563304.

Corresponding Author:

Maren Haslach-Häfner, B.A.

Berufsfachschule für Pflege der Helios
Gesellschaft für berufliche Bildung mbH in Kronach

(Berufsfachschule für Pflege Kronach, Bildungszentrum Kronach)

Friesener Str. 41
96317 Kronach

Germany

https://www.helios-gesundheit.de/karriere/standorte/kronach/ausbildung/bildungszentrum/

E-Mail: maren.haslach-haefner@helios-gesundheit.de

Editorial Office Comments: date submitted 29. August, 2024; peer reviewed 3. September 2024; accepted for publication on 5. September, 2024; Author notified on 5. September, 2024.

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Technical Review: PillSense ®, a Novel Swallowable Capsule to Detect Upper Gastrointestinal Bleeding

Sat, 21 Sep 2024 00:00:00 GMT

Upper gastrointestinal bleeding (UGIB) is a common medical condition worldwide. Patients present with frank, visible bleeding such as hematemesis, melena or hematochezia with hemodynamic compromise of frank shock or with subjective or “suspected bleeding”. The decision to perform urgent or emergent endoscopy depends on the clinical presentation and the visibility of blood. Although there are mathematical predictors available such as the Glasgow-Blatchford or Rockall scores to estimate the severity of bleeding, they are impractical and rarely used. Indeed, in my experience working in continental Europe, USA and South America, I have rarely seen these scores being used. Although in the past nasogastric tubes were used to find out whether the patient with reported UGIB had blood in the upper GI tract, this practice is not routine anymore, especially after a landmark study in the 1990s showed its futility (1). The development of innovative, non-invasive triage tools would facilitate the effective risk-stratification of patients with suspected UGIB, minimizing unnecessary hospital admissions and/or urgent endoscopies (2). Another frustrating aspect of dealing with “suspected” UGIB is the often-negative findings on EGD.

A novel device to detect UGIB (PillSense® was just approved by the FDA (Food and Drug Administration, USA) (Figure 1). The PillSense system is a noninvasive, easy-to-use system designed for the real-time detection of GI bleeding as liquid blood and/or hematin (3). The system consists of 2 components, a single-use, swallowable capsule containing an optical sensor that detects blood as it is propelled through the UGI tract (panels A, B, C), and a wireless bedside receiver (size of a small tablet) (panels C, D). The capsule is pill shaped, 11×27 mm in size, and battery-powered (3) (panels A, B,C). The external casing is a biocompatible polycarbonate, which ensures the capsule’s smooth and safe passage through the GI tract, while protecting the capsule from the GI tract environment. The capsule begins to gather data as soon as it is immersed in liquid. In brief, the visible light emitted by the capsule passes through the surrounding liquid, and the wavelengths detected by the sensor are analyzed. The resulting sensor output indicates the presence or absence of blood, and the wireless receiver automatically reports either “blood detected” or “no blood detected” (3) (panel E).

In a recent landmark comparative clinical trial, Akiki and colleagues evaluated the safety and efficacy of the PillSense System (4). The authors enrolled 126 adults (mean age, 62.4 years; 59.5% men) with suspected UGIB at Mayo Clinic in Rochester. Participants underwent esophagogastroduodenoscopy (EGD) within 4 hours of capsule administration and were monitored up to 21 days to confirm capsule passage.The capsule correctly detected the presence of blood in 26 out of 28 cases and the absence of blood in 87 out of 96 cases compared with EGD, demonstrating a sensitivity and specificity of 92.9% (95% CI, 76.5-99.1) and 90.6% (95% CI, 82.9-95.6), respectively, as well as positive and negative predictive values of 74.3% and 97.8%. The positive and negative likelihood ratios were 9.9 and 0.08. The mean PillSense recording time was 6.71 minutes (4).

This study demonstrated that a novel blood-sensing swallowed,easily to deploy capsule device provided highly accurate and rapid detection of UGIB. Other advantages were the simpliocity to deploy and easy to interpretation, which was visible within a mean time of 6 minutes. In contrast to the traditional wireless caspule endosocope (WCE), which requires formal reading and interpretaion of images, and has senstivity adnspeificity of 88% and 64%, repsectively, the Pillsense capsule does not require any pads or cables attached to patient and. can be deployed and interpreted by nursing and paramedical staff, and has much higher sensitivy and specificity.

Aspects that require further study are costs and use outside the hospital, for example during initial evaluation of patients at home. Hence, an accurate, rapid, easy to-interpret, and non-invasive tool could assist in both diagnosing and offering guidance for clinical decision-making in scenarios of suspected UGIB (4). The existence of this blood-sensing, swallowing capsule opens new horizons to work on improving outcomes of patients with UGIB, and may also alter the diagnostic and treatment algorithm for patients with a suspected UGIB.

References:

1. Cuellar RE, Gavaler JS, Alexander JA, et al. Gastrointestinal tract hemorrhage: the value of a nasogastric aspirate. Arch Intern Med 1990;150:1381-4.

2. Meltzer AC, Ward MJ, Gralnek IM, et al. The cost-effectiveness analysis of video capsule endoscopy compared to other strategies to manage acute upper gastrointestinal hemorrhage in the ED. Am J Emerg Med. 2014;32:823–832.B, Albers D, Hoffmeister A, Feisthammel J, Walter B, Meining A, Wedi E, Zachäus M, Pickartz T, Küllmer A, Schmidt A, Caca K. Over-the-scope-clips versus standard treatment in high-risk patients with acute non-variceal upper gastrointestinal bleeding: a randomised controlled trial (STING-2). Gut. 2022 Jul;71(7):1251-1258. doi: 10.1136/gutjnl-2021-325300. Epub 2022 Mar 23. PMID: 35321938.

3. Bajer L, Ryou M, C Thompson C, Drastich P. Novel upper gastrointestinal bleeding sensor capsule: a first human feasibility and safety trial. Clin Endosc. 2024 Mar;57(2):203-208. doi: 10.5946/ce.2023.111. Epub 2024 Jan 17. PMID: 38229441; PMCID: PMC10984735.

4. Akiki K, Mahmoud T, Alqaisieh MH, Sayegh LN, Lescalleet KE, Abu Dayyeh BK, Wong Kee Song LM, Larson MV, Bruining DH, Coelho-Prabhu N, Buttar NS, Sedlack RE, Chandrasekhara V, Leggett CL, Law RJ, Rajan E, Gleeson FC, Alexander JA, Storm AC. A novel blood-sensing capsule for rapid detection of upper GI bleeding: a prospective clinical trial. Gastrointest Endosc. 2024 May;99(5):712-720. doi: 10.1016/j.gie.2023.11.051. Epub 2023 Dec 6. PMID: 38065512.

5. Meltzer AC, Ali MA, Kresiberg RB, et al. Video capsule endoscopy in the emergency department: a prospective study of acute upper gastrointestinal hemorrhage. Ann Emerg Med 2013;61:438-43.e1.

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Endoscopic Resection of Giant Gastric Polyp to Treat Upper GI Bleeding

Fri, 06 Sep 2024 00:00:00 GMT

Endoscopic Resection of Giant Gastric Polyp to Treat Upper GI Bleeding

Anand Dwivedi, MD

Gastroenterology Fellow, Carilion Memorial Hospital, Virginia Tech Carilion School of Medicine

Klaus Mönkemüller, MD, PhD, FASGE, FJGES

Professor of Medicine, Virginia Tech Carilion School of Medicine, Roanoke, Virginia, USA

An elderly patient presented with massive hematemesis and drop in hemoglobin from 13 to 9 gr/dl. After hemodynamic stabilization an EGD was performed. A large antral polypoid lesion with stigmata of hemorrhage was seen (A, B).

The polyp had a large and thick pedicle (C). The pedicle was injected with saline-epinephrine mix (1:10,000) (D). Endoscopic resection was performed using a snare (E). The resection defect was closed using two clips (F, G). Panel H shows a 4 cm large pedunculated polyp. Histology showed a gastric hyperplastic polyp with no malignant features. The patient did not have any additional bleeding episodes.

This case shows that endoscopic resection may be an option to treat upper gastrointestinal bleeding. Two solutions were provided in one session a) removal of the source of bleeding (plus applying hemostatic clips to the resection site to prevent a post-polypectomy bleeding) and b) removal of a pre-malignant lesion. It is important to emphasize that hyperplastic gastric polyps larger than 10 mm carry an increased risk of transformation into cancer (1).

References:

1. Fry LC, Lazenby AJ, Lee DH, Mönkemüller K. Signet-ring-cell adenocarcinoma arising from a hyperplastic polyp in the stomach. Gastrointest Endosc. 2005 Mar;61(3):493-5. doi: 10.1016/s0016-5107(04)02640-9. PMID: 15758936.

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Endoscopic Resection of Lumenal-Occluding Laterally Spreading Tumor of the Sigmoid Colon

Fri, 06 Sep 2024 00:00:00 GMT

An elderly patient presented with recurrent hematochezia and anemia. On colonoscopy a large polypoid lesion partially obstructing the lumen of the sigmoid colon was seen (A, B).

The lesion extended over a fold and spread about two thirds to three fourths (75%) of the colon lumen circumference (A, B, C). The proximal part of the LST could be clearly seen and recognized. It was characterized as a laterally spreading tumor (LST), granular surface (G), with large polypoid protrusions (P) (LST-G-P).

Options to treat this lesion were a) surgery (hemicolectomy), b) endoscopic submucosal dissection (ESD), c) piecemeal endoscopic mucosal resection pEMR), and d) hybrid ESD-EMR, e) knife-assisted resection (KAR), and f) a combination of KAR, hybrid ESD-EMR and piecemeal EMR (1-4).

Surgery was not an option. Therefore, we proceeded with endoscopic resection.

The key elements for success were:

1) Creation of a generous submucosal cushion. We used Eleview ® and normal saline with epinephrine (1:20,000). The bluish color of the Eleview ® clearly allows for a) demarcation of the lesion (differentiate between normal mucosa and neoplastic tissue (Panel E), and b) separate neoplastic tissue from the submucosa, c) provide a dissection place, d) decrease the chances of perforation (“safety cushion”), and e) by using some epinephrine we decreased active bleeding during the procedure, thus improving the cleanliness of the operating field and allowing us to dissect mor efficiently.

2) Performing KAR and hybrid ESD-EMR. The circumferential incision allowed for a clear lateral R0 resection. We have observed many cases of piecemeal EMR for similar lesions, and often the borders are hard to resect and the endoscopist must perform electrocoagulation or ablation of the entire margin. Indeed, some guidelines recommend that ablation and or electrocoagulation of the borders be performed when performing pure piecemeal EMR or EMR (3). However, if one performs KAR or hybrid ESD-EMR circumferential incision, such as this case, it is not necessary to ablate the borders, as those are clean and free of neoplastic tissue (3). The circumferential “pre-cutting” or knife-assisted resection is useful to provide an R0 resection.

3) After circumferential incision and some endoscopic submucosal dissection (Panels F and G) we resected the bulk of the lesion using snare (EMR), and the few remaining remnants using repeated injection and piecemeal EMR. During part of the procedure, we used underwater EMR technique. The final resection site was about ¾ or 75% of the lumen circumference. The resected lesion (and fragments) size measured together 8 cm.

This case shows the concept of “personalized endoscopic resection”. First, we “personalized” the patient, who was a poor surgical candidate and offered the option of organ-sparing endoluminal surgery. Second, we “personalized” the lesion. The lesion was well-studied, interrogated and resected using various endoscopic techniques and categorized as “complex colon polyp” (1, 2). Essential aspects for a success were a) focus on safety, using measures to prevent complications, b) aiming at R0 and c) avoiding a “tunnel vision” and sticking to only one technique, but instead “thinking outside the box” and optimizing the “toolbox approach”, and thus using various endoscopic resection methods, which resulted in a successful resection.

References:

1. Mönkemüller K, Neumann H, Malfertheiner P, Fry LC. Advanced colon polypectomy. Clin Gastroenterol Hepatol. 2009 Jun;7(6):641-52. doi: 10.1016/j.cgh.2009.02.032. Epub 2009 Mar 10. PMID: 19281865.

2. Angarita FA, Feinberg AE, Feinberg SM, Riddell RH, McCart JA. Management of complex polyps of the colon and rectum. Int J Colorectal Dis. 2018 Feb;33(2):115-129. doi: 10.1007/s00384-017-2950-1. Epub 2017 Dec 28. PMID: 29282496.

3. Mathews AA, Draganov PV, Yang D. Endoscopic management of colorectal polyps: From benign to malignant polyps. World J Gastrointest Endosc. 2021 Sep 16;13(9):356-370. doi: 10.4253/wjge.v13.i9.356. PMID: 34630886; PMCID: PMC8474698

4. Kaltenbach T, Anderson JC, Burke CA, Dominitz JA, Gupta S, Lieberman D, et al. Endoscopic removal of colorectal lesions: recommendations by the US multi-society task force on colorectal cancer. Gastroenterology. (2020) 158:1095–129. doi: 10.1053/j.gastro.2019.12.018

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OTSC Monotherapy for Massive Duodenal Ulcer Bleeding

Fri, 06 Sep 2024 00:00:00 GMT

A middle-aged patient was admitted with hematemesis and hemorrhagic shock. After hemodynamic stabilization, EGD was performed, showing active bleeding and a partially adherent blood clot on a huge duodenal ulcer. The blood and blood clot were removed with a water flush. However, if a clot is more tightly adherent, I prefer not to remove it.

Inspection revealed a large ulcer (B, yellow oval) and a visible large vessel (B, C, yellow arrows). A one-stop hemostatic procedure was accomplished with an 11/6t over-the-scope clip (D). The OTSC nicely compressed the ulcer bed and the massive visible vessel.

Since the advent of OTSC, the concept of endoscopic hemostasis has completely changed, because now a single endoscopic therapy may be enough to achieve permanent hemostasis, instead of the previous approach of using "dual" endoscopic therapy. Originally, OTSC was introduced as rescue therapy for massive upper GI bleeding (1). Nowadays, OTSC is considered a first-line monotherapy for bleeding upper GI lesions (2, 3). Of course, dual or triple endoscopic therapy may be required for some cases, but it is not a "routine" approach anymore.

References:

1. Skinner M, Gutierrez JP, Neumann H, Wilcox CM, Burski C, Mönkemüller K. Over-the-scope clip placement is effective rescue therapy for severe acute upper gastrointestinal bleeding. Endosc Int Open. 2014 Mar;2(1):E37-40. doi: 10.1055/s-0034-1365282. Epub 2014 Mar 7. PMID: 26134611; PMCID: PMC4423243.

2. Meier B, Wannhoff A, Denzer U, Stathopoulos P, Schumacher B, Albers D, Hoffmeister A, Feisthammel J, Walter B, Meining A, Wedi E, Zachäus M, Pickartz T, Küllmer A, Schmidt A, Caca K. Over-the-scope-clips versus standard treatment in high-risk patients with acute non-variceal upper gastrointestinal bleeding: a randomised controlled trial (STING-2). Gut. 2022 Jul;71(7):1251-1258. doi: 10.1136/gutjnl-2021-325300. Epub 2022 Mar 23. PMID: 35321938.

3. Faggen AE, Kamal F, Lee-Smith W, Khan MA, Sharma S, Acharya A, Ahmed Z, Farooq U, Bayudan A, McLean R, Avila P, Dai SC, Munroe CA, Kouanda A. Over-the-Scope Clips Versus Standard Endoscopic Treatment for First Line Therapy of Non-variceal Upper Gastrointestinal Bleeding: Systematic Review and Meta-Analysis. Dig Dis Sci. 2023 Jun;68(6):2518-2530. doi: 10.1007/s10620-023-07888-3. Epub 2023 Mar 21. Erratum in: Dig Dis Sci. 2024 Jan;69(1):311-313. doi: 10.1007/s10620-023-08159-x. PMID: 36943590.

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Esophageal Varix with Nipple Sign

Fri, 06 Sep 2024 00:00:00 GMT

A 50-year-old patient with a history of cirrhosis due to ethanol use presented to the emergency room with hematemesis and melena for one day. The patient had clinical features consistent of chronic liver disease (spider angiomas, ascites, palmar erythema and jaundice). The hemoglobin was 8 gr/dl. An EGD was performed (Photo).

Figure 1. Large esophageal varices. A. Three columns of esophageal varices extending from the distal esophagus to the mid-esophagus. B. The stomach was full of coffee-ground like material, bile and blood clots. C. Classic nipple sign shown with yellow arrow. D. Nipple sign. E. The transparent banding cap allows for great visualization of the nipple sign (yellow arrow). F. No arrow on this photo to allow for “eye training” to detect nipple sign”. G. and H. Successful endoscopic band ligation of varix with high-risk stigmata (nipple sign).

There are various signs of impending or recent hemorrhage from esophageal varices. These include red stops, red whale sign, nipple-like sign and active bleeding (oozing or spurting) (1, 2). The “nipple-like projection” or “nipple sign” was described in 1996 (1). This lesion represents an opening varix covered by fibrin, indicating a recent bleed with spontaneous “hemostasis”. Any varix with nipple-like projection is at extremely high risk of (recurrent) bleeding, as this fibrin plug may fall off any time. Whenever this sign is encountered a quick decision to place endoscopic bands must be made. In this case we saw large esophageal varices (Panel A), then saw the lesion (Panels C and D). The stomach was full of old blood. As there was a clear culprit explaining the recent hemorrhage (fibrin nipple, panels C, D). Further cleaning of the stomach might have resulted in loss of the fibrin plug on the varix and catastrophic bleeding. Therefore, a quick decision was taken to place endoscopic band ligation on the high-risk lesion (panels E to H).

Recognizing a high-risk marker like the "nipple sign" can be the difference between routine banding and a catastrophic bleed. But what about the countless other challenging scenarios in GI bleeding?

References:

Caldwell SH, Bickston SJ, Yoshida C, Morse J, Yeaton P. Nipple-like projection from a varix: a high-risk marker? Gastrointest Endosc. 1996 Nov;44(5):634-5. doi: 10.1016/s0016-5107(96)70035-4. PMID: 8934186.
Wasserman RD, Abel W, Monkemuller K, Yeaton P, Kesar V, Kesar V. Non-variceal Upper Gastrointestinal Bleeding and Its Endoscopic Management. Turk J Gastroenterol. 2024 May 20;35(8):599-608. doi: 10.5152/tjg.2024.23507. PMID: 39150279.

No COI by RM or KM with any of the companies/utensils or products mentioned in this article.

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Quick Case: Portal Hypertensive Duodenopathy

Fri, 06 Sep 2024 00:00:00 GMT

60-year-old male with cirrhosis presented with microcytic anemia and hemoccult positive stools. EGD, colonoscopy and capsule endoscopy were reported as normal. A repeat EGD was performed and portal hypertensive duodenopathy (PHD) was diagnosed both endoscopically and confirmed on histology (Photo)

Portal hypertensive duodenopathy (PHD) is a common condition in patients with cirrhosis and portal hypertension. We have also proposed the name of duodenal antral vascular ectasias (DAVE), as histologically, this condition often mimics GAVE (gastric vascular ectasias).

Importantly, PHD or DAVE is often missed during endoscopy. As you can see from Panel A, which shows a "normal" normal mucosa. However, after using water immersion technique the erythema and edema of the mucosa becomes quite evident. Panel E shows a closer look at the mucosa, with characteristic "snakeskin" pattern. This snakeskin pattern is more evident with NBI (panel F). Patients with PHD or DAVE often have microcytic anemia due to occult or overt gastrointestinal bleeding. Bleeding occurs microscopically from the congested mucosa, but also micro- and macroscopically from tiny angiodysplasias (Panels C, D, G, H). Panel G shows the angiodysplasias using water immersion technique. In Panel H the scope was advanced closer to the mucosa. The angiodysplasias in PHD and DAVE are somewhat different than the classic angiodysplasias occurring in elderly patients or those with Heyde syndrome.

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Quick Endoscopic Diagnostic Tip: Kissing Ulcers of the Duodenum

Fri, 06 Sep 2024 00:00:00 GMT

The term “kissing ulcers” of the duodenum describes the presence of two different ulcers facing each other, usually one located anteriorly and the other posteriorly. It appears that the original description was in the surgical literature by Stabile et al in 1979 (Arch Surg). The photo shows a spectrum of kissing ulcers. Occasionally, these may be hard to see (Panel C, yellow arrows).

Multiple duodenal ulcers are a “red flag” and should always intrigue the endoscopist to think of: use of NSAIDs, Zollinger-Ellison syndrome, ischemia, vasculitis, Crohn’s disease, Bechet’s disease, lymphoma, and in immunocompromised or transplant patients think cytomegalovirus, GVHD.

This citation is from the paper by Stabile et al: “Among 70 cases of perforated duodenal ulcers treated by plication, eight were complicated by massive postoperative hemorrhage from a synchronous posterior "kissing" duodenal ulcer. Critical analysis revealed that only signs of gastrointestinal (GI) bleeding preoperatively had predictive value for postoperative hemorrhage. Twenty-four patients had one or more predictive signs, and eight actually bled postoperatively. There was a 50% mortality and 75% additional complication rate for the bleeders. In contrast, the non-bleeders had a mortality and a complication rate of only 18% and 35%, respectively.” (1)

References:

Stabile BE, Hardy HJ, Passaro E Jr. 'Kissing' duodenal ulcers. Arch Surg. 1979 Oct;114(10):1153-6. doi: 10.1001/archsurg.1979.

Recognizing subtle but critical findings like kissing ulcers is a crucial skill. As the 1979 Stabile paper reminds us, these ulcers present a high risk of life-threatening hemorrhage—a situation every endoscopist must be prepared to manage.

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CAVE - Cardia Antral Vascular Ectasias – A New Identity?

Fri, 23 Aug 2024 00:00:00 GMT

CAVE - Cardia Antral Vascular Ectasias – A New Identity?

Klaus Mönkemüller, MD, PhD, FASGE, FJGES

Professor of Medicine, Virginia Tech Carilion School of Medicine, Virginia, USA

Anand Dwivedi, MD, and Adil Mir, MD

Carilion Memorial Hospital

Virginia Tech Carilion School of Medicine

Roanoke

During upper endoscopic evaluation of patients with classic gastric antral vascular ectasias (GAVE) we have observed a few patients who also had classic GAVE-appearing lesions in the gastric cardia (Figure 1).

The submucosal erythema, subepithelial hemorrhages and edema are confined to the short segment distal to the squamocolumnar junction (SCJ) and in most cases not wider than 3-5 mm, but in some instances extending up to 10 mm from SCJ into the fundus (Figure 2). When performing retroflexion it is evident that the “GAVE” of the cardia is clearly localized to that area (Figure 2A, yellow arrows, Fig. 2B NBI, Fig. 2C HDWL, Fig. 1D-F retroflexed views) and does not extend to the fundus.

Using narrow band imaging (Fig. 2B, Fig. 2F) clearly improves visualization and demarcation of CAVE, as we believe this entity should be called. We have sent histologic samples for analysis and the report has been of “classic” GAVE. Indeed, antral mucosa is normally found in three places of the stomach: antrum, pylorus, and cardia! These are the border regions of the stomach. And gastric antral vascular ectasias (GAVE) are classically found in the antrum and pylorus. Therefore, the neo-angiogenesis process would follow similar stimuli including angiopoietin (Ang-1 and Ang-2), vascular endothelial growth factor (VEGF) and tissue reaction with formation of deformed vessels.

Our observation has important implications. First, we believe that naming this condition CAVE makes sense, as it is true antral vascular ectasia of the cardia. Having a separate name or entity may also raise awareness of this condition. Second, and more important, we believe that CAVE is an important cause of slow or ongoing blood loss in patients with GAVE and/or portal hypertension. How many times do we see patients who have undergone successful eradication of GAVE, but are still having anemia? Maybe CAVE is the reason for ongoing blood loss. Our approach is to treat CAVE using argon plasma coagulation (APC). We hope that our publication encourages others to also study this entity.

Dr. Pablo Cortegoso

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Gastric Volvulus

Fri, 09 Aug 2024 00:00:00 GMT

Gastric Volvulus

Julika S. Loew, MS, Josip Juraj Strossmayer Universität Osjiek, Croatia, Ameos Klinikum Halberstadt, Germany

An 87-year-old lady was admitted because of sudden onset thoracoabdominal pain, relentless vomiting, and coffee-ground emesis. After life-threatening cardiopulmonary conditions had been ruled out she underwent an esophagogastroduodenoscopy (Figure 1).

Figure 1. Organoaxial gastric volvulus. A. Massively edematous cardia. B. Part of the fundus is transferred to the right side (the fundus is usually located on the left side unless the patient has situs inversus). C. Retained stomach fluid is coming from the left side. D. Large amount of fluid in the “twisted” stomach (we suctioned about 1500 ml through the endoscope). E. The arrow shows the “twisting point” in the middle of the stomach body. F. By applying air, the opening could be opened and then scope advanced through the body of the stomach to the pylorus. G. Massive mucosal edema due to congestion. Ongoing volvulus (“twisting”) can result in necrosis. H. The twisted stomach body is clearly seen (yellow circle). I. After “untwisting” the stomach we performed retroflexion, which shows a humongous hiatal hernia of about 9-10 cm diameter.

Gastric volvulus is a rare, challenging condition, defined by the abnormal rotation of the stomach, which can be classified based on the axis of rotation, being either along the stomach’s short or long axis (1, 2). It often clinically presents with the Borchardt triad referring to sudden onset of constant epigastric pain, recurrent retching with vomiting and inability to pass a nasogastric tube.

It is important to recognize two forms of gastric volvulus (Figure 2):

Fig. 2: Gastric volvulus (Attribution: Terry Helms, Memorial Sloan Kettering Hospital, USA)

Type I being the organoaxial volvulus (OA), commonly occurring in the setting of trauma or large paraoesophageal hernia. The stomach is rotated along its long axis, which is drawn between the cardia and the pylorus. A complete rotation over 180° usually results in obstruction or ischemia, whereas an incomplete rotation is usually asymptomatic.

Type II is mesenteroaxial volvulus (MA) is less commonly seen in adults, but more common in the pediatric population (59% of gastric volvulus) (1, 2). It is characterized as a rotation around the short axis, causing “bisection” of greater and lesser curvature of the stomach. It coincides with the axis of mesenteric attachment and is often associated with severe strangulation and obstruction (1, 2). This type of gastric volvulus is less commonly associated with diaphragmatic defects. The mesenteroaxial volvulus volvulus usually presents as a chronic disease, with its etiology being idiopathic (2) Predispositions to mesenteroaxial volvulus rotations are diseases of the stomach, like peptic ulcers, which cause a retraction of the small curvature.

Type III is the combination of the mentioned types.

Further classification is based on etiology as primary or idiopathic causes: tumors, adhesion, problems in normal ligamentous attachments of stomach and secondary causes: disorders of gastric motility and anatomy, issues of neighboring structures like diaphragm and spleen. Most cases have a secondary cause in adults, usually associated with para esophageal hernia and traumatic diaphragm injury. (2)

In our case, patient has Type I organoaxial volvulus based on a paraoesophageal hernia Type IV.

The initial management of gastric volvulus is decreasing intragastric pressure through nasogastric or endoscopic decompression.

In the following, surgery must be performed to check gastric viability and resect necrotic tissue. Volvulus is treated with detorsion and fixation of the stomach by gastropexy, in case of a diaphragmatic defect, hiatal hernia has to be repaired (1, 2). In asymptomatic patient, expectant nonoperative management is advised.

References:

1. Niknejad MT. Gastric volvulus | Radiology Reference Article | Radiopaedia.org

2. Akhtar A, Siddiqui FS, Sheikh AAE, Sheikh AB, Perisetti A. Gastric Volvulus: A Rare Entity Case Report and Literature Review. Cureus. 2018 Mar 12;10(3):e2312. doi: 10.7759/cureus.2312. PMID: 29755908; PMCID: PMC5947932.

None of the authors (JSL, KM) have any COI to declare.

Dr. Pablo Cortegoso

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Esophageal Laceration (“pre-Boerhaave’s Syndrome”) Treated with “Short-Stem” Hemoclips

Fri, 26 Jul 2024 00:00:00 GMT

80-year-old patient with history of recent myocardial infarction, coronary stent placement and dual antiplatelet therapy presented with melena, hypotension and drop in hemoglobin from 14 gr/dl to 9 gr/dl. Emergent EGD showed a distal peptic stricture of the esophagus, which did not impede the passage of the scope (Fig. 1A and Fig. 1B). On retroflexion there was not Mallory-Weiss tear (Fig. 1C). Inspection of the distal esophagus revealed a 4 cm long laceration with adherent blood clots and visible vessel (Fig. 1D and Fig. 1E).

Image via EndoCollab.com

The laceration was clearly located 3 cm above the Z-line and GE junction. Occasionally, large esophageal erosions or ulcers in the setting of reflux esophagitis may appear similar to a laceration, but in GERD the erosion usually starts at the GE junction. Esophageal lacerations have a spectrum, from mucosal, submucosal, and muscle, to complete perforation or rupture (Boerhaave’s syndrome). Boerhaave’s syndrome is the extreme outcome of an esophageal laceration.

This patient had clear indication for endoscopic therapy: a) severe hemorrhage and b) lesion with high-risk stigmata. In this case we selected clips with short stems (or barrels) (yellow oval) to prevent luminal rubbing from the deployed clips (DuraClip). Figure 2 shows various commercially available clips and their stem lengths.

The DuraClip has some interesting and nice features. It is easily rotatable, even the scope is in retroflexion. It can open and close repeatedly, up to 50 times. This is a very convenient feature, as it allows the endoscopist to be 100% sure of the desired placement location (vessel, base of polyp, wound closure, etc). Indeed, in this case we had to open and close the clips several times because the borders of the laceration were hardened and we wanted to ensure a symmetrical and strong apposition of the tor edges. Additionally, this clip has a short stem (or barrel) which makes it ideal for esophageal work, because once it is deployed the stem will not rub the contralateral mucosa (Fig. 1H, Fig. 1I, Fig. 2). Lastly, the clip may also be rotated, which is ideal for approaching the borders of the defect.

References:

Xavier AT, Campos JF, Robinson L, Lima EJM, da Rocha LCM, Arantes VN. Endoscopic clipping for gastrointestinal bleeding: emergency and prophylactic indications. Ann Gastroenterol. 2020 Nov-Dec;33(6):563-570. doi: 10.20524/aog.2020.0526. Epub 2020 Jul 30. PMID: 33162733; PMCID: PMC7599350.

No COI by HP or KM with any of the companies/utensils or products mentioned in this article.

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Practical Review: Gurvits Syndrome

Fri, 12 Jul 2024 00:00:00 GMT

Practical Review: Gurvits Syndrome

Black Esophagus or Acute Esophageal Necrosis

_{Klaus Mönkemüller, MD, PhD, FASGE, FJGES}

_{Professor of Medicine}

_{Department of Gastroenterology, Carilion Memorial Hospital, Virginia Tech Carilion School of Medicine, Roanoke, USA}

_{Vivek Kesar, MD}

_{Assistant Professor, Department of Gastroenterology, Carilion Memorial Hospital, Virginia Tech Carilion School of Medicine, Roanoke, USA}

Figure 1. Acute esophageal necrosis. This patient had ischemia due to massive vasoconstriction due to epinephrine use to resuscitate the patient after a heart attack with cardiogenic shock. Panel C also shows ulcers and necrosis of the duodenum.

Acute esophageal necrosis (AEN), commonly referred to as "black esophagus", is a rare clinical entity also known as Gurvits syndrome (1-3) (Figures 1-3). Acute esophageal necrosis arises from a combination of ischemic insult seen in hemodynamic compromise and low-flow states, corrosive injury from gastric contents in the setting of dysmotility (esophago-gastroparesis) and gastric outlet obstruction, and decreased function of mucosal barrier systems and reparative mechanisms present in malnourished and debilitated physical states (1). Not uncommonly, diabetic ketoacidosis (DKA) also results in this condition. Less commonly, infections such as aspergillosis may also turn the esophagus black (Table below).

Table. Etiology and Conditions Associated with Black Esophagus (Esophageal Necrosis)

CategoryFactorsVascularischemia, atherosclerosis, shock, thrombophilia (hypercoagulable condition)Mechanical (severe reflux)nasogastric tube, gastric outlet obstruction, gastric volvulusChemicallye, corrosives, high-percentage ethanol, antibioticsMetabolic/endocrinediabetes mellitus (DM) (diabetic ketoacidosis, gastroparesis), uremiaVasculitis/systemicpolyarteritis nodosa, amyloidosisInfectionsaspergillosis, herpes simplex virus, cytomegalovirusUnderlying co-morbiditiesvasculopathy, atherosclerosis, COPD, DM, cancer, malnutrition, ESRD (end-stage renal disease)

Figure 2. An elderly patient suffering from hemodynamic and septic shock requiring high doses of pressor support developed hematemesis. On EGD ischemic esophagitis was detected.

Figure 2. Additional examples of black esophagus in patients with diabetic ketoacidosis (A, B) and hemodynamic shock (C).

Gurvits syndrome or 'black esophagus' is caused by microvascular thrombosis and neutrophilic inflammation (ischemic necrosis) (2). Microvascular thrombosis is related to various entities, including hemodynamic shock, vasculitis, antiphosolipid syndrome, immunological impairment, malignancy, diabetes mellitus, alcoholism (2) (Table). Histology shows mucosal/submucosal necrosis, dense neutrophilia, edema, sloughed epithelium, and debris.

Therapy of Gurvits syndrome is focused at reversing the underlying clinical conditions, such as restoring hemodynamic perfusion, treating sepsis, and improving oxygenation. The patient is initially kept NPO (nil-per-os), and aggressive intravenous acid suppression with proton pump inhibitors is warranted (1, 2). Complications include perforation with mediastinal infection/abscess, esophageal stricture and stenosis, superinfection, and death, which can be as high as 32% (1, 2).

References:

Gurvits GE, Shapsis A, Lau N, Gualtieri N, Robilotti JG. Acute esophageal necrosis: a rare syndrome. J Gastroenterol. 2007 Jan;42(1):29-38. doi: 10.1007/s00535-006-1974-z. Epub 2007 Feb 16. PMID: 17322991.
Gurvits GE. Black esophagus: acute esophageal necrosis syndrome. World J Gastroenterol. 2010 Jul 14;16(26):3219-25. doi: 10.3748/wjg.v16.i26.3219. PMID: 20614476; PMCID: PMC2900712.
Diaconu C, Ciocîrlan M, Ilie M, Sandru V, Balaban DV, Plotogea O, Diculescu M. Gurvitis syndrome: the dark shade of hematemesis. Endoscopy. 2020 May;52(5):E181-E182. doi: 10.1055/a-1059-9268. Epub 2019 Dec 2. PMID: 31791097.

No COI by KM or VK with any of the companies/utensils or products mentioned in this article.

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Six Top Tips to Use Argon Plasma Coagulation When Treating Angiodysplasias: An Endoscopic Atlas

Thu, 13 Jun 2024 00:00:00 GMT

Six Top Tips to Use Argon Plasma Coagulation When Treating Angiodysplasias: An Endoscopic Atlas

Adil S. Mir, MD, FACP

Gastroenterology Fellow, Department of Gastroenterology, Carilion Memorial Hospital, Virginia Tech Carilion School of Medicine, Roanoke, USA

Reid Wasserman, DO

Internal Medicine Resdent, Department of Internal Medicine, Carilion Memorial Hospital, Virginia Tech Carilion School of Medicine, Roanoke, USA

Klaus Klaus Mönkemüller, MD, PhD, FASGE, FJGES

Professor of Medicine

Department of Gastroenterology, Carilion Memorial Hospital, Virginia Tech Carilion School of Medicine, Roanoke, USA

Case Presentation:

A 75-year-old patient underwent a colonoscopy because of hemoccult positive stools and severe microcytic and iron-deficiency anemia. Several angiodysplasias of the colon were found. Angiodysplasias are also called arteriovenous malformations (AVMs) (Figure 1 C, E, F, G, H). In another newsletter we will dwell into which terminology is more appropriate to describe these lesions, but for now we will use the terms interchangeably as they really point to the same problem: “malformed (= dysplastic) tissue” (dys-plasis: abnormal growth or development of a tissue) (malformed = crooked or badly formed) (1).

Figure 1. Several types of angiodysplasias of the colon (A-H), stomach (I-K) and duodenum are shown. Most angiodysplasias are flat, but often these can be diminutive (Panel C) or quite small (panel K), but with easily visible deformed vessels (I, J, L). The angiodysplasias seen in patients with chronic liver disease and cirrhosis are more “spider-like telangiectasias” (A, B). Often, it is hard to see angiodysplasias (D). The use of narrow band imaging enhances the possibility to characterize these vascular lesions (J).

Argon plasma coagulation (APC) is the most common method to treat angiodysplasias.

APC is a non-contact electrical coagulation method that results in tissue damage via heat (thermocoagulation)(1, 2). APC thermocoagulation allows for destruction of tissue at different levels, but generally APC is used to ablate mainly the mucosa and superficial submucosa (1, 2).

Here are six top tips for application of APC.

Know your settings.

There are two key settings to know: a) Watts and b) Flow (of argon gas). However, coagulation (“tissue damage”) depends on other additional factors such as duration of application, direction of application (straight or continuous movement, the latter also called “painting”), and distance to the target tissue. In Nr. 3 and Nr. 5 we explain the concept of APC application using all these factors, which we call “dynamic” APC.

Know your probes.

There are three main probes: a) straight fire (flow is from the tip), b) side fire (flow is from the side, and c) distal (protection or safety) ceramic tip, which decreases the chances of contact damage to the mucosa, as the ceramic does not transmit electricity.

Adapt settings

Settings and probes may need to be adjusted based on location (esophagus, stomach, small bowel, cecum, colon, rectum) and disease process (tumor, active bleeding, Barrett’s esophagus, polyp remnants). Nonetheless, it is important to remember that the application of APC is dynamic. For example, using low wattage setting, but firing straight into a spot in the small bowel repeatedly or for several seconds may directly result in perforation. Indeed, deep tissue damage and destruction of tissue may sometimes be desirable, such as ablating residual tissue from polyps, or debulking of tumors. On the other side, using high power settings with a longer distance between the probe and tissue while using a painting motion may result in superficial damage. Thus, blindly relying on pre-selected settings may give a false sense of security. Therefore, we highly recommend understanding how to use the APC machine to change settings for the most appropriate application, and most importantly, using APC dynamically while considering all factors (power, flow, duration, direction and distance) during the application process.

Create an arc (spark)

The essential concept is to create an arc of sparks which, upon contact with the tissue, result in desiccation and coagulation (Figure 2).

Figure 2. Creation of a spark with argon gas. The key aspect is to have the probe about 1-2 mm from the target tissue. This short distance allows for the electrical current to create a spark with the flowing argon gas, which in turns “burns” or coagulates tissue.

One common misconception is that APC only results in “superficial” tissue damage, however, persistent application of APC into one spot can result in carbonization, vaporization and deep tissue injury, or even frank perforation!

Figure 3. The short burst technique. APC is applied at closed distance, with short bursts.

Application is a dynamic process.

The dynamic APC application process implies the following steps: a) probe exposure distally to scope, b) probe distance from the tissue, c) en-face (straight in front of the lesion) or tangential or side application, d) movement of the probe and scope and probe, e) duration of application (Figures 3 and 4).

Figure 4. The long burst technique. The distance to the target is “longer” (about 2-3 mm), the wattage and flow are higher, and the application is more continuous.

“Personalize” therapy.

When applying APC, you should take both, a) patient and b) lesion into consideration. The patient’s condition, co-morbidities and use of anticoagulants will determine the aggressiveness of therapy as well as considerations to use double or triple approaches, such as: APC plus clip, submucosal injection followed by APC, or the submucosal cushion, APC and clip (Figures 5-7). When considering the lesion, one needs to determine its size, location, and stigmata of recent hemorrhage, which all determine single (Figures 2-4), dual (Figures 5 and 6) or triple therapy (Figure 7).

Figure 5. The Clip-After-Burst Technique. First apply APC and coagulate the angiodysplasia using short or long bursts of APC. A clip is then placed on the coagulated area. This is a safety or preventative approach, which we use in lesions located in the cecum that underwent lots of burning, or high-risk patients. Useful in angiodysplasias of any part of the GI tract, especially in patients on anticoagulation.

Figure 6. The submucosal injection-safety burst. With this approach, pre-injection of normal saline below the angiodysplasia is performed, followed by APC. Saline will dissipate the electrical current, and the submucosal cushion prevents deeper injuries, and the angiodysplasia is safely burned.

Figure 7. Triple endoscopic therapy (submucosal cushion, APC and clipping). This approach is mostly used in multi-morbid patients, those on anticoagulation and in situations where application may be riskier (e.g. thin-walled cecum in elderly patient).

In sum, APC is widely used to treat angiodysplasias of the GI tract. Knowledge of its principles and various application may increase its efficiency and efficacy, while decreasing complications. There are several adjunctive therapies to increase efficacy of angiodysplasia elimination and prevent complications such as clipping, submucosal cushion and resection (3, 4). One complication when using APC is one too much. Therefore, we prefer to personalize therapy and use safety steps and tricks to avoid any complication.

References:

Manner H. Thermal ablative therapies in the gastrointestinal tract. Curr Opin Gastroenterol. 2023 Sep 1;39(5):370-374.
Sakai E, Ohata K, Nakajima A, Matsuhashi N. Diagnosis and therapeutic strategies for small bowel vascular lesions. World J Gastroenterol. 2019 Jun 14;25(22):2720-2733.
Jovanovic I, Knezevic A. Combined endoclipping and argon plasma coagulation (APC)--daisy technique for cecal angiodysplasia. Endoscopy. 2013;45 Suppl 2 UCTN:E384.
Geyl S, Albouys J, Schaefer M, Lepetit H, Legros R, Pioche M, Jacques J. Is endoscopic mucosal resection optimum for treating colonic angiodysplasia? Endoscopy. 2022 Dec;54(12):1233-1234.

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How I Do It: Endoscopic Resection of Zenker’s Diverticulum

Mon, 03 Jun 2024 00:00:00 GMT

How I Do It: Endoscopic Resection of Zenker’s Diverticulum

By Jay Bapaye, MD, Klaus Mönkemüller, MD, PhD, FASGE, FJGES

Virginia Tech Carilion School of Medicine, Virginia, USA

Zenker's diverticulum, also known as posterior pharyngeal pouch, is a pulsion diverticulum, resulting from posterior herniation of esophageal mucosa and submucosa into Killian's triangle, an area of least resistance situated above the upper esophageal sphincter (cricopharyngeal muscle) and below the inferior pharyngeal constrictor muscle (1-3).

Figure 1. Spectrum of Zenker’s diverticulum. The yellow arrow points to the septum. Note that in some cases it is difficult to see the esophageal lumen, which appears as a “slid” (both upper photos).

Although open surgical techniques have historically been the criterion standard for treatment, endoscopic options have become increasingly used (3). Cricopharyngeal myotomy using flexible endoscopy is a safe and effective technique for the management of Zenker's diverticulum. Potential benefits of this approach include shorter operative times, shorter postoperative admissions, and earlier progression of diet (3).

The most common treatments for Zenker diverticulum are open surgical diverticulectomy with or without cricopharyngeal myotomy, rigid and flexible myotomy (1). The myotomy consist of incision of the “neck” of the diverticulum, starting with mucosa, then submucosa and, finally the muscle (“myotomy”).

There are many endoscopic approaches to “resect” a Zenker’s diverticulum. These include argon plasma coagulation (APC), incision with various types of needles (needle knife, hook knife, IT-knife), stapling device, endoscopic scissors, and so forth.

Although everyone talks about “resection”, this is not what is performed. Indeed, during flexible endoscopy the main approach “remove” the diverticulum is to perform a septotomy, incising the septum in between the diverticulum and esophagus, which contains the cricopharyngeal muscle. Indeed, the main goal of the treatment is to cut the cricopharyngeal muscle.

The myotomy consist of incision of the “neck” of the diverticulum, starting with mucosa, then submucosa and, finally the muscle (“myotomy”) (Figure 2). Figure 1 shows the septi of different Zenker diverticuli.

The essential aspects to perform an endoscopic resection are a) to have the tools, and b) follow specific steps (Figure 2).

Figure 2. Zenker’s resection made easy using “the three tools and the three steps”.

The essential steps are:

1.) Use a distal transparent cap on the endoscope (Figure 1 and Figure 2). The distal transparent cap stabilizes the endoscopic view, maintains a safe distance between the scope tip and the diverticular septum and allows for focused creating of the incisions using various devices. Additionally, the cap will allow for blunt dissection and, in case of bleeding, compression hemostasis. We have used the diverticuloscope in the past (Figure 3) but have found that it does not fit all Zenker diverticuli and thus use it only occasionally.

2.) Luminal vison: generally, the esophageal lumen and the diverticulum are clearly visible and distinct. However, more often than not, the septum is quite thick, and the esophageal lumen is barely visible (Figure 1). In this situation we like to place a wire (e.g. biliary guidewire) or a thin tube (e.g. Dobhoff or jejunal feeding tube) into the stomach, to maintain visibility of the esophagus and thus allow for controlled incision and dissection of the septum (Figure 2 and 4, panel D).

Figure 4. Endoscopic resection of Zenker’s diverticulum. The key steps to perform a safe septomyotomy in Zenker’s diverticulum are shown here.

3.) Incision and dissecting tool (utensil, device): Our preferred incision and dissection tool is the hook knife (Figure 4, yellow oval, panels C, D and E), as it permits hooking and cutting, as well as using the bend tip to dissect the muscle fibers one-by-one gradually and gently. A key aspect of septum dissection is to go step-by-step. First incise the mucosa, then the submucosa and lastly, muscle fibers, slowly, but steadily. Just below the cricopharyngeal muscle is a shiny, thin, film-like layer of the buccopharyngeal fascia which can be identified to ensure adequate myotomy.

4.) Safety closure. Once we have dissected down to the base of the septum, we prefer to place a closing clip at the apex of the dissection, as this is the most vulnerable area for perforation (and subsequent mediastinitis). There are many clips available, but we prefer to use one with a short stem (e.g. DuraClip), as this diminishes the chances of touching and rubbing the contralateral wall (Figure 4G and Figure 5).

Figure 5. Comparison of various clips with focus on the length of the stem.

In sum, here we have presented a simple and safe endoscopic approach to resect Zenker’s diverticulum. This mini-review shows that there are a few essential steps and tools necessary to perform a Zenker’s resection, and these are modifiable, based on availability of tools and devices.

References:

Ferreira LE, Simmons DT, Baron TH. Zenker's diverticula: pathophysiology, clinical presentation, and flexible endoscopic management. Dis Esophagus. 2008;21(1):1-8.
Pescarus R., Shlomovitz E., Sharata A.M. Trans-oral cricomyotomy using a flexible endoscope: technique and clinical outcomes. Surg Endos. 2016;30:1784–1789.
Fan HS, Stavert B, Chan DL, Talbot ML. Management of Zenker's diverticulum using flexible endoscopy. VideoGIE. 2019 Jan 30;4(2):87-90. doi: 10.1016/j.vgie.2018.12.007. PMID: 30766952; PMCID: PMC6363821.

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The Bump Trick for Hemostasis (and Closure of Mucosal Defects)

Thu, 30 May 2024 00:00:00 GMT

The Bump Trick for Hemostasis (and Closure of Mucosal Defects)

By Klaus Mönkemüller, MD, PhD, FASGE, FJGES and Joel Joseph, MD

Virginia Tech Carilion School of Medicine, Virginia, USA

image via endocollab.com

Often, bleeding lesions are located on the right (Panel A), as in this case of gastric ulcer located in the distal antrum. Many gastroscopes have the working channel on the LEFT (Panel B, green arrow), which makes a targeted delivery of the clip or injection difficult. What are our options to overcome this problem?

One, change to a pediatric colonoscope, with working channel on the right.

Two, use over the scope clip (which allows for en-face approach).

Three, use a transparent distal cap, which may allow for a more targeted approach by "expending" the scope tip and thus angulation capabilities.

Four, use hemospray or hemostatic gels.

Five, as in this case, use the "bump trick". The initial clip is used to create a mucosal “bump” (pink arrow). The second (or hemostatic) clip can now be better targeted to the lesion, as the bump has lifted some folds (D, pink arrow) on the left side and allows for better capture of the ulcer on the right E, light blue arrow).

The bump trick is also useful when closing mucosal defects. The first clip is used to create a mucosal bump, which then allows for easier application of the second clip, and secure closure of the defect (see picture below).

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Tips and Tricks to Manage a Mallory Weiss Tear

Mon, 06 May 2024 00:00:00 GMT

Tips and Tricks to Manage a Mallory Weiss Tear

by Diana Dougherty, MD and Klaus Mönkemüller, MD, PhD, FASGE, FJGES

Department of Gastroenterology, Carilion Memorial Hospital, Virginia Tech Carilion School of Medicine, Roanoke, USA

A young patient presented with massive upper gastrointestinal bleeding resulting in hypotension and requiring transfusion of four units of packed red blood cells. Once the patient was stabilized an emergent EGD was performed. A Mallory Weiss tear was diagnosed (Figure 1). An adherent blood clot was present, and there was active blood oozing from the tear. The size of the tear was estimated to be about 15 mm long.

The Key Initial Steps to Plan an Adequate Endoscopic Therapy for Mallory Weiss Tear Are To:

Determine its location (you want to plan potential utensils, such as clips, band, over-the-scope clip, injection, and the location of the working of the scope in relation to the lesion will assist you in determining what hemostatic method to use),
Analyze its morphology (length, depth, extension into stomach),
Make sure the stomach is as clean as possible, remove clots and blood, as stomach contents will decrease the endoscopic view, stimulate emesis and retching and may result in intra- or post-procedure aspiration.
Perform a nice retroflexion and examine the cardia and any possible hiatal hernia (rule out any extension of the Mallory-Weiss tear into the stomach and rule out more tears or other lesions) (Figure 2A)

Endoscopic Therapy:

There are multiple endoscopic therapies used for achieving endoscopic hemostasis for Mallory-Weiss tears: injection of saline/epinephrin or glue, through-the-scope clips (hemoclips), over-the-scope clip, hemostatic powders, and gels (Hemospray, Purastat).

We decided to use clips for the because the Mallory Weiss lesion was large, there were lots of muscle fibers visible, indicating the tear had involved mucosa, muscularis mucosae, submucosa, and muscle (Figure 2B, pink arrow). By using clips, we would not only ensure hemostasis, but also closure of the wound, which cannot be achieved with topical or injected agents (powders, gels, glues). This patient had also been transfused with multiple units of blood, suggesting that deeper muscular vessels were involved by the tear. An important tip when using clips to close Mallory Weiss tears (or really, any large endoluminal GI defect) is to place the first clip on one of the edges of the tear (laceration or perforation) (Figure 2B, yellow arrow). In this case we chose to place the first clip distally, to prevent the laceration from extending into the cardia and stomach. Placing the first clip on the edges also helps create an initial closure and a mucosal “bump” which will facilitate application of other clips. We chose NOT to place the first clip proximally, as this would potentially impede or make placement of the next clips more difficult. The second clip was placed proximally, creating a “V” with the second clip (Figure C). This “V” configuration is allowed for a final placement of a third clip at the base of the “V”. successfully closing the laceration and achieving hemostasis. Figure D shows adequate tissue apposition.

In sum, Mallory Weiss tears can result in catastrophic bleeding. Endoscopic therapy should be aimed at both hemostasis and closure of the defect, especially in lesions that are deep and result in significant bleeding. Various endoscopic therapies are available, of which hemoclips are well-suited to achieve both hemostasis and tissue apposition (i.e. closure of defect).

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Quick Tips and Tricks for Endoscopic Band Ligation of Esophageal Varices

Fri, 26 Apr 2024 00:00:00 GMT

Quick Tips and Tricks for Endoscopic Band Ligation of Esophageal Varices

Diana Dougherty, MD (Gastroenterology Fellow) and

Klaus Mönkemüller, MD, PhD, FASGE, FJGES

Professor of Medicine, Virginia Tech Carilion School of Medicine, Virginia, USA; Universidad de la República, Montevideo, Uruguay; University of Belgrade, Belgrade, Serbia, Universidad Espiritu Santo; Ecuador, University of Osijek, Croatia

A 58-year-old patient with cirrhosis (Child-Puch B, MELD 20) presented for EGD for screening esophageal varices. He was found to have large esophageal varices with red spots or markings (Figure 1 A) and four columns of varices (Figure 1B). Figures 1C and 1D show additional examples of red markings or spots (yellow arrows). These red spots are areas of wall thinning that may rupture and result in hemorrhage. The light blue arrow on Figure 1D shows a red marking, but here it is also possible to see some “bumps” or surface irregularity suggestive of significant wall thinning.

Figure 1

The key steps to follow when using band ligation for esophageal varices are:

Figure 2

b) Make sure that the stomach is empty, suction all remaining fluid and air before loading the banding device on the scope. Stomach contents induces retching and vomiting, and this may hinder endoscopy or even result in Mallory Weiss tears or bleeding.

Figure 3

c) The white strings of the cap with bands should align with the working channel of the scope (Figure 3A, 3B). In this case the working channel is on the left, around the 7 ‘clock position. In other scopes the working channel is on the 6 o’clock position. If the strings are not aligned with the working channel of the scope, there will be “crossing” the field and also impede adequate suction of the varix inside the cap.

d) Not infrequently, when introducing the scope with the banding cap, the interior of the cap will accumulate saliva, debris or lubricant gel (Figure 3A, above). A useful trick to get rid of this debris is to place the cap to a stomach mucosa (3B) and then flush with water (3C).

e) The clean cap is also useful for visualization of the esophageal varices, particularly the red markings or spots (Figure 3D).

f) Whenever suctioning on a varix, do it gently, with continuous suction, but do not suction in such a way that the entire cap is occluded by the varix. If too much tissue (varix) is strangulated by a band, partial esophageal obstruction may occur.

g) We recommend “gradual” suctioning. Figure 3E shows approx. one third of cap “filled” with varix. The ideal suction amount is shown in Figure 3F (two thirds of cap filled with varix). At that point it is important to release the band.

h) After the band has been released, no more suction should be applied. Indeed, soon after releasing the band we gently apply some air, and minimal amount of water (using the water pedal). Simultaneously, we pull the scope back a little bit. This combination of maneuvers (air, water and pulling the scope) “detaches” the suctioned varix (Figure 3G).

i) Careful inspection of the banded varix is important, but do not apply air or CO2 as the distention may result in band detachment.

j) We also look at the proximal variceal column to document flattening or disappearance of the column. Often, it is not necessary to deploy all six bands, as four or five bands may have resulted in adequate obliteration of the submucosal blood flow.

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Quick Case: Meat Bolus Impaction

Fri, 05 Apr 2024 00:00:00 GMT

Quick Case: Meat Bolus Impaction

^{by Reid Wasserman, DO and Klaus Klaus Mönkemüller, MD, PhD, FASGE, FJGES}

^{Department of Gastroenterology, Carilion Memorial Hospital, Virginia Tech Carilion School of Medicine, Roanoke, USA}

Middle aged male presents with food bolus impaction.

How would you remove this impacted meat bolus?

In your hospital, do you use sedation, no sedation or general anesthesia for this endoscopic emergency?

There are multiple answers to both questions, and all are likely correct.

Food bolus or meat impaction is managed differently in different parts of the World, even within one country or state. Interestingly, in the hospitals in Germany where I (KM) have worked and in two where I still work, conscious sedation is used preferentially. I also know some hospitals in former Eastern Germany where no sedation is used at all. Their argument for not using conscious sedation is threefold: a) patient can "control" their secretions, b) lack of availability of staff to assist with sedation, c) lack of anesthesia services to perform intubation.

In our current practice in USA, airway protection with tracheal intubation and general anesthesia is standard for patients presenting with acute food bolus (i.e. meat impaction) or foreign body ingestion. The advantage of having anesthetist available for such an urgent procedure is a) tranquility that the patient’s airways are protected, b) endoscopist can fully focus on the endoscopic procedure.

We believe that protecting the airway (and general anesthesia) is quite practical and important for three reasons: a) patient safety (less risk of aspiration of any contents, including pieces of meat during retching, vomiting or endoscopic retrieval, and c) patient (and endoscopist) comfort. Occasionally, removal of the meat impaction can take 15 minutes or more. I know of cases where the procedure took as long as one hour.

Regarding preferred endoscopic technique, there are lots of utensils in the "toolbox", including distal transparent caps, snares, baskets, and tripod forceps. I like using the distal transparent caps, as they usually allow for suctioning the proximal part of the meat inside, and then it is removed by slowly pulling the scope back out of the esophagus. However, all methods mentioned above work pretty well. One utensil that I have also found quite practical for large or complex meat impactions is the overtube, which allows for repetitive endoscopic intubations, going back-and-forth, removing piece by piece of larger pieces of meat or food.

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Quick Case: Laterally Spreading Tumor LST in Ascending Colon

Thu, 14 Mar 2024 00:00:00 GMT

Quick Case: Laterally Spreading Tumor LST in Ascending Colon

by Diana Dougherty, MD and Klaus Klaus Mönkemüller, MD, PhD, FASGE, FJGES

Department of Gastroenterology, Carilion Memorial Hospital, Virginia Tech Carilion School of Medicine, Roanoke, USA

Laterally spreading tumors (LSTs) are defined as nonpolypoid lesions ≥1 cm with lateral growth.

LST occasionally harbor cancer.

The two main categories of LST, based on their surface morphology, are granular (G) and non-granular (NG).

LST-G have a low risk of containing cancer (about 8%) (1).

LST-NG have the highest risk for covert cancer (about 21%) (1).

Kobayashi: "The frequency of pathological T1 cancers was the highest at 36% of LST nongranular pseudodepressed type, followed by 14% of LST nongranular flat‐elevated type, 11% of LST granular nodular mixed type, and 3% of LST granular homogenous type lesions" (1).

The subtype of mixed LST with mixed features (GM-LSTs) have been poorly characterized, intermediate risk for covert cancer, about 10%. The risk of cancer on GM-LST varies by size, being twofold higher in lesions ≥4 cm than smaller lesions, and GM-LSTs in the rectum have a threefold higher risk than other locations to harbor covert cancer (2). The absolute risk for covert cancer was highest (22%) if the GM-LST was both rectal and ≥4 cm, compared with 5% to 8% absolute risk for other size and location combinations (2).

References:

1. Kobayashi K, Tanaka S, Murakami Y, Ishikawa H, Sada M, Oka S, Saito Y, Iishi H, Kudo SE, Ikematsu H, Igarashi M, Saitoh Y, Inoue Y, Hisabe T, Tsuruta O, Sano Y, Yamano H, Shimizu S, Yahagi N, Matsuda K, Nakamura H, Fujii T, Sugihara K; Colorectal Endoscopic Resection Standardization Implementation Working Group of the Japanese Society for Cancer of the Colon and Rectum. Predictors of invasive cancer of large laterally spreading colorectal tumors: A multicenter study in Japan. JGH Open. 2019 Jul 16;4(1):83-89. doi: 10.1002/jgh3.12222. PMID: 32055702; PMCID: PMC7008164.

2. D'Amico F et al. Risk of covert submucosal cancer in patients with granular mixed laterally spreading tumors. Clin Gastroenterol Hepatol 2020 Jul 17; [e-pub]. https://doi.org/10.1016/j.cgh.2020.07.024.

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Marking Technique for Identifying and Resection Flat Colon Polypoid Lesions or Polyps in Difficult Locations

Fri, 01 Mar 2024 00:00:00 GMT

Marking Technique for Identifying and Resection Flat Colon Polypoid Lesions or Polyps in Difficult Locations

By Klaus Mönkemüller, MD, PhD, FASGE, FJGES and Reid Wasserman, DO

Virginia Tech Carilion School of Medicine, Virginia, USA

One of the most frustrating aspects of dealing with small, flat, diminutive colon polypoid lesions or those lying in awkward location is their “disappearance” during colonoscopy, especially when the colon is not perfectly well prepped or there is increasing colon motility.

A useful trick is to focus on the lesion, push the scope towards it and suction the mucosa right next it. This creates a red submucosal suction mark, which then becomes pivotal to re-identify or relocate the polyp.

We have also developed the suction, re-shape and resect technique, which not only has the advantage of relocating the polyp, but also improving its resection (Fig. 2).

Here are the key steps for the suction, re-shape and resect technique: suction application, re-shape because of suction and resection.

a) Application of suction: Once the flat lesion is seen (Fig. 2A and 2B), place the scope directly on it and suction it into the working channel (Fig. 2C). This creates a suction mark, but also “reshapes” the polyp into a “sessile” lesion (Fig. 2D).

b) Re-visualization and re-shape: While applying suction insert the snare into the working channel. The advancement of the snare will displace the air of the dead space of the working channel and likely “detach” it. Detachment of the suctioned polyp also occurs when the suction is discontinued.

c) Execution (resection): What began as a flat lesion now morphed into a pseudo-polyp or “sessile” lesion and is marked (Fig 2D). If for some reason we lose scope position, the polyp is already marked and easy to find. If scope position was not lost, we proceed to immediate resection (cold or hot) (Fig. 2E and 2F).

In summary, these suction strategies in colonoscopy not only aid in the effective treatment of lesions but also streamline the process. The time wasted in re-identifying a “lost” flat lesion can be substantial. The transformation of a flat lesion into a pseudo-polyp using suction provides an enhanced visual and practical advantage, enabling a more precise resection. Such techniques are essential tools in the repertoire of gastroenterological practices.

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Mini Review on Devices, Accessories and Utensils: Eleview® Submucosal Injection Solution

Tue, 06 Feb 2024 00:00:00 GMT

By Klaus Mönkemüller, MD, PhD, FASGE, FJGES Professor of Medicine, Virginia Tech Carilion School of Medicine, Virginia, USA; Universidad de la República, Montevideo, Uruguay; University of Belgrade, Belgrade, Serbia, Universidad Espiritu Santo; Ecuador, University of Osijek, Croatia

Mini Review on Devices, Accessories and Utensils: Eleview® Submucosal Injection Solution

Eleview is a microemulsion injection solution used for endoscopic resection of gastrointestinal lesions, mainly colon polyps, approved by the Food and Drug Administration (FDA) 510(k) and Conformité Européene (CE)-marked. The component ingredients of Eleview^® include water for injection, medium-chain triglycerides, poloxamer 188, polyoxyl-15-hydroxystearate, sodium chloride, and methylene blue (1). Eleview contains a biocompatible polymer as a cushioning agent and methylene blue as the “contrasting” agent. Because it includes the contrasting agent, it reduces time needed to prepare the submucosal fluid for injection and thus may improve procedure efficiency (2, 3).

In a randomized study of 211 patients comparing Eleview to normal saline, the authors concluded that this submucosal agent appeared to be a “more effective and equally safe submucosal agent for EMR injection than saline solution” (3).

Nevertheless, it is nice to have an additional substance for submucosal injection available, especially when dealing with larger lesions and performing endoscopic submucosal dissection (ESD), when submucosal elevation time is a factor that may determine success. In addition, this solution comes already prepared and mixed, thus facilitating usage and diminishing the risk of mixing errors (i.e. making the solution too light blue or dark blue).

Aspect

Eleview®

Saline

Composition

A mixture of synthetic absorbable copolymer and 0.9% saline

A solution of sodium chloride in water

Efficacy in lifting the mucosa

Provides long-lasting submucosal elevation

Provides a submucosal fluid cushion, but may require additional injections to maintain elevation

Safety

Well-tolerated, with no reported adverse events

Generally safe, but may lead to complications such as bleeding

Cost

More expensive

Economical

References:

1. Cosmo Technologies Ltd. Eleview [Instructions for Use] Cosmo Technologies Ltd.; Dublin, Ireland: 2018.

2. Giannino V, Salandin L, Macelloni C, Longo LM. Evaluation of Eleview^® Bioadhesive Properties and Cushion-Forming Ability. Polymers (Basel). 2020 Feb 5;12(2):346. doi: 10.3390/polym12020346. PMID: 32033452; PMCID: PMC7077458.

3. Repici A, Wallace M, Sharma P, Bhandari P, Lollo G, Maselli R, Hassan C, Rex DK. A novel submucosal injection solution for endoscopic resection of large colorectal lesions: a randomized, double-blind trial. Gastrointest Endosc. 2018 Sep;88(3):527-535.e5. doi: 10.1016/j.gie.2018.04.2363. Epub 2018 May 8. PMID: 29750983.

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Endoscopic Resection of LST in Ascending Colon

Wed, 31 Jan 2024 00:00:00 GMT

A flat polypoid lesion was found in the ascending colon (A). As this lesion was larger than 10 mm, by definition it’s an LST (laterally spreading tumor).

The key initial steps to plan an adequate resection are to:

a) determine its location (B. here we see that it is between two folds),

b) analyze its morphology (LST-granular, G), and

c) analyze its surface using close-up view with high-definition white light (C) and NBID). The mucosal pit pattern is regular, cerebroid, without ulcers or depressions (Kudo IIIL). The vessels are regular and without deformities.

d) not "loose" the polyp from sight! Pearl: Notice on image B that there is a "suction" mark. This trick is especially useful in patients whose colon is moving a lot, there is remaining debris in the colon, or the polyp is located in a difficult location. The suction mark helps find the polyp again! See the next figure for details on the suction mark technique.

How to do the suction mark trick? Focus on the lesion, push the scope towards it and suction the mucosa right next to it. This creates a red submucosal suction mark (yellow arrows), which then becomes pivotal to re-identify or relocate the polyp (yellow circle).

There are many ways of dealing with this flat lesion. Some experts like "cold snare", others go directly for hot snare. We prefer endoscopic resection using interventional chromoendoscopy for the following reasons: a) the LST has an irregular, almost triangular shape, b) the LST is located in-between folds, and c) we always aim at R0 (surgical or oncologic resection) and prefer not be "burning" or ablating incompletely resected borders.

By raising the LST using submucosal injection with blue color (in this case we used Eleview, Cosmo Technologies, Ireland and Germany, but you can use normal saline mixed with Indigo carmine or methylene blue or other hydroximethylcelluose such as Blue Eye) (A). Note two important aspects: a) the LST is nicely raised, well separated from the deeper layers, now the polyp is more "sessile" than flat, and b) the blue color injection clearly helps differentiate normal from pre-neoplastic or neoplastic tissue, as the color mainly depicts normal tissue. This is the concept of "interventional chromoendoscopy", when colorings are helpful to guide the endoscopist in therapeutic interventions, in this case aiming at R0 (complete resection).

Once the snare is pushed out it's used twofold, a) to calculate the size of the lesion (here the snare is 15 mm, braided, Captivator, Boston, USA) (B). The LST is thus about 12 mm in size. The submucosal cushion allowed for nice entrapment of the entire LST above the snare (C). One trick that we use is to tightly close the snare, almost aiming a "cold" resection, and applying electrosurgical current (C). Note the resection site (D). It's an endoscopic R0, exactly what we aimed at. Furthermore, by applying HOT snare technique there is a burned base and lateral margins. This ensures that no vertical or lateral tissue is left. This does not occur during COLD snaring, and it is the reason for higher adenomatous polyp recurrent rates seen after cold snare techniques.

This LST was in the right colon. The patient has hypertension. Both are risks for post-polypectomy bleeding. Therefore, we used prophylactic clips (E). Some experts would argue that clipping is not necessary. We disagree, because a) this patient had two risk factors for post-polypectomy bleeding, and b) this is an outpatient procedure, and the patient comes from a long distance. We always aim at performing "personalized" endoscopy and rely less on guidelines that may not take into account individual patient aspects, such as risks and social aspects, including distance to home, availability o emergency room close to their home and emergency endoscopy services.

When placing a clip remember two things: a) try not to insufflate the colon with CO2 or air, so that they are to be clipped remains small (figures 3D, E). After clipping use a little air to see how well the clip was placed.

No COI by DD or KM with any of the companies/utensils or products mentioned in this article.

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Zenker’s Diverticulum

Sat, 27 Jan 2024 00:00:00 GMT

Image courtesy of EndoCollab.com

An elderly male presented with dysphagia to solid food, halitosis, and regurgitation. The patient also lost about 10-kg over a 6-month period. Subsequently, the patient underwent an EGD. Note the slit-like entrance to the esophagus. On the next image, a feeding tube is seen in the esophageal lumen. A thin feeding tube is advantageous when endoscopically resecting a Zenker diverticulum for the following reasons:

(a) the tube serves as a reference point to differentiate the esophageal lumen from the diverticulum, (b) It helps guide the incision exactly in the middle of the Zenker's bridge, (c) placing a feeding tube creates a conducible environment for healing and allows for enteral nutrition.

Depicted below are the barium swallow images. The Zenker’s diverticulum is identified by the posterior location (blue arrow). The contrast barely enters the esophagus (there is a functional stenosis) (yellow arrow).

Zenker's diverticulum, also known as a posterior pharyngeal pouch, is really a pseudodiverticulum, as it only contains mucosa and submucosa. This pseudodiverticulum results from posterior herniation of esophageal mucosa and submucosa into Killian's triangle, an area of low resistance situated above the upper esophageal sphincter (cricopharyngeal muscle) and below the inferior pharyngeal constrictor muscle.

Zenker’s diverticulum typically presents in adults by the sixth or seventh decade. Clinical presentation includes: dysphagia, the pooling of food within the diverticulum, which can cause bad breath, and frequent regurgitation. Serious complications include aspiration and malnutrition (1), which may lead to chronic cough or pneumonia. The gold standard tool for diagnosis is barium swallow and continuous fluoroscopy (2). If there is high clinical suspicion for Zenker’s diverticulum, one may choose to obtain a barium swallow before proceeding directly to endoscopy as it is possible to navigate into the diverticulum and cause potential perforation.

The most common treatments are open surgical diverticulectomy with or without cricopharyngeal myotomy, or rigid and flexible myotomy (1). The myotomy consists of an incision at the “neck” of the diverticulum, from the mucosa, then through the submucosa, and finally the muscle (“myotomy”).

The use of a distal transparent endoscopic cap may assist during the incision/resection process.

Image courtesy of EndoCollab.com

In this case of Zenker's diverticulum we can see how the cap:

(a) stabilizes the view

(b) allows for focused attention of the target

(c) maintains a safe distance between the scope tip and the diverticular septum. All of these aspects permits a directed and controlled incision. Additionally, the cap allows for blunt dissection and the ability to achieve hemostasis via tamponade if any bleeding were to occur.

Although open surgical techniques have historically been the gold standard for treatment, endoscopic options have become more popular (3). Cricopharyngeal myotomy using flexible endoscopy is a safe and effective technique for the management of Zenker's diverticulum. Potential benefits of this approach include shorter operative times, shorter postoperative admissions, and earlier progression of diet (3).

References:

Ferreira LE, Simmons DT, Baron TH. Zenker's diverticula: pathophysiology, clinical presentation, and flexible endoscopic management. Dis Esophagus. 2008;21(1):1-8.
Pescarus R., Shlomovitz E., Sharata A.M. Trans-oral cricomyotomy using a flexible endoscope: technique and clinical outcomes. Surg Endos. 2016;30:1784–1789.
Fan HS, Stavert B, Chan DL, Talbot ML. Management of Zenker's diverticulum using flexible endoscopy. VideoGIE. 2019 Jan 30;4(2):87-90. doi: 10.1016/j.vgie.2018.12.007. PMID: 30766952

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58-yo Patient Experiences Severe Hemobilia Post Liver Biopsy

Fri, 26 Jan 2024 00:00:00 GMT

Background:
- Patient details: 58 years old, NAFLD, diabetes mellitus, hypertension
- Procedure: Underwent liver biopsy
Symptoms 24hrs post-biopsy:
- Acute abdominal pain
- Jaundice & chills
- Melenic stools
Emergency Room Findings:
- Low blood pressure & rapid heart rate
- Icteric sclerae
- CT: Dilated bile duct with potential sludge/stones
- ERCP: Multiple irregular defects in biliary tree
- Treatment: Biliary sphincterotomy, blood clot extraction, plastic stent insertion (removed after 4 weeks)
About Hemobilia:
- Causes: Primary cancer, trauma, gallstones, liver biopsy, etc.
- Indicators (Quinke's triad): Epigastric pain, jaundice, gastrointestinal bleeding (not always all three)
- Diagnosis: Endoscopy, CT imaging, ERCP with cholangiography
- Treatment: Biliary tree decompression, drainage, blood transfusion if needed, address underlying cause

Conclusion: Hemobilia, though rare, can be a severe post-procedure complication, requiring prompt diagnosis and effective treatment.

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Altered Mucosal Nodularity in the Ascending Colon

Fri, 26 Jan 2024 00:00:00 GMT

73 yo woman with asthma and anxiety. Colonoscopy is done for chronic diarrhea. Altered mucosal nodularity in the ascending colon was noted on both WL and NBI.

I’d like to mention six main possibilities:

1. Lots of elderly patients with diarrhea suffer from microscopic colitis, which is not really microscopic (there are generally some endoscopic findings such as edema, granularity or segments patches of irregular mucosa). See classic study by Koulaouzidis et al. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5411381/

2. Asthma may lead to inflammatory bowel disease. But this would be uncommon in a 73-year-old. Still possible.

3. The patient may not have real asthma and she might be suffering from vasculitis (e.g. Churg Strauss)

4. Colitis may also be infectious. Ascaris lumbricoides leads to Löffler’s pneumonia.

5. Strongyloides stercoralis induces eosinophilic colitis or gastroenteritis and has been reported in the USA, especially in those patients taking immunosuppressants or steroids. https://www.giejournal.org/article/S0016-5107(04)00337-2/fulltext

6. Eosinophilic colitis is another possibility, idiopathic or medication 💊 induced.

I think the differential blood count and the histologic results will help us secure the final diagnosis.

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Advances in Endoscopic Vacuum Therapy: A World of Possibilities

Fri, 26 Jan 2024 00:00:00 GMT

We are excited to share with you the latest advancements in endoscopic vacuum therapy in this week’s newsletter. This cutting-edge treatment continues to evolve, offering new solutions for gastrointestinal defects and improving patient outcomes.

Concepts and Principles Endoscopic Vacuum Therapy (Endoscopic Negative Pressure Therapy)

Endoscopic negative pressure therapy (ENPT) (also known as endoscopic vacuum therapy, EVT) was developed to close anastomotic intestinal leaks. Open-pored drains (made of polyurethane foam or a open-pored double-layer membrane) are placed endoscopically on the wound region and a continuous negative pressure is applied by means of an electronic vacuum pump. Two therapy variants can be distinguished, which can also be combined with each other: Intraluminal and intracavitary ENPT.

The three most important treatment principles of ENPT are 1) closure of the defect and drainage of secretions, 2) active drainage and removal of secretionsremoval of aggressive secretions, 3) promotion of granulation and healing. Interestingly, the principles of ENPT are the essential surgical characteristics defined by Kirschner 1926 for treatment of peritonitis (blocking the origin of infection and the elimination of exudate)!

From Sponges to Open Film Drainage

Initially, endoscopic vacuum therapy relied on the use of endo sponges. The endosponge can also be used around a self-expanding metal stent.

However, Dr. Gunnar Loske in Hamburg has developed a major advancement in endoscopic vacuum therapy by using open pore film drainage (OFD). This material is accessible in many countries worldwide and has demonstrated success in various luminal operations.

OFD is constructed with a drainage tube and a very thin double-layered open-pore drainage film (Suprasorb CNP, Drainage Film, Lohmann & Rauscher International, Germany). The distal end of the tube is wrapped with only one layer of film. OFD is placed into the gastrointestinal leakage site with common endoscopic techniques. The tube is connected to an electronic vacuum device and continuous negative pressure of -125 mmHg applied (1).

This endoscopic vacuum therapy features columns between two layers of the film that prevent collapse and maintain constant suction of material (1). The film adapts well to cavities and organs while preventing organ damage.

The following link takes you to the most complete site on endoscopic vacuum therapy:

https://endoscopicvacuumtherapy.jimdofree.com/

Preemptive Endoscopic Vacuum Therapy

Another groundbreaking development in endoscopic vacuum therapy is its use in preventing post-operative leaks, especially after complex surgeries such as Ivor-Lewis (2). By applying the open drainage film at the site of surgery and attaching it to a feeding tube, surgeons can significantly reduce the chances of perforation and leaks.

Innovative Tube-in-Tube Technique

The tube-in-tube technique has broadened the applications of endoscopic vacuum therapy (3). This approach, which involves placing a smaller tube inside a larger one, has been particularly effective in cases where traditional sponges would have been too large. The tube-in-tube system has demonstrated remarkable healing capabilities, reducing wound sizes and cavities within a relatively short time frame.

Conclusion

Endoscopic vacuum therapy, based on the principle of secondary wound healing, is an essential option for closing large and complex gastrointestinal defects. The technique has evolved from sponge-based therapy to open film drainage and tube-in-tube methods, making it easier to deploy and more effective.

By using endoscopic vacuum therapy preemptively, surgeons can now prevent post-operative leaks and improve patient outcomes.

References:

1. Loske G, Schorsch T, Rucktaeschel F, Schulze W, Riefel B, van Ackeren V, Mueller CT. Open-pore film drainage (OFD): a new multipurpose tool for endoscopic negative pressure therapy (ENPT). Endosc Int Open. 2018 Jul;6(7):E865-E871. doi: 10.1055/a-0599-5886. PMID: 29978007; PMCID: PMC6031437.

2. Loske G, Müller J, Schulze W, Riefel B, Müller CT. Pre-emptive active drainage of reflux (PARD) in Ivor-Lewis oesophagectomy with negative pressure and simultaneous enteral nutrition using a double-lumen open-pore film drain (dOFD). Surg Endosc. 2022 Jan 1. doi: 10.1007/s00464-021-08933-w. PMID: 34973079.

3. Simas de Lima M, Uemura RS, Gusmon-Oliveira CC, Pombo AAM, Martins BC, Lenz L, Kawaguti FS, De Paulo GA, Baba ER, Safatle-Ribeiro AV, Ribeiro U Jr, Monkemüller K, Maluf-Filho F. Tube-in-tube endoscopic vacuum therapy for the closure of upper gastrointestinal fistulas, leaks, and perforations. Endoscopy. 2022 Oct;54(10):980-986. doi: 10.1055/a-1774-4630.. PMID: 35378562.

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Aggressive Fluid resuscitation in Acute Pancreatitis: Too Much of a Good Thing

Fri, 26 Jan 2024 00:00:00 GMT

Welcome to 5,921 motivated Endoscopists! Today we will go over a ground-breaking, solid, practice-changing, and “dogma-removing” study.

Current guidelines recommend aggressive early fluid resuscitation in the treatment of acute pancreatitis. However, controversy remained regarding the rate and volume of fluid resuscitation.

In this well-designed, prospective, randomized trial De Madaria and colleagues from 18 centers around the World provide an answer to this question.

A total of 249 patients with acute pancreatitis of less than 8 hours’ duration were randomized to aggressive versus moderate fluid resuscitation and assessed at 3, 12, 24, 48 and 72 hours. There were no differences in important clinical outcomes such as severe pancreatitis, organ failure or complications. Importantly, in patients treated with aggressive fluid resuscitation there were 3 x fold increase in volume overload.

The importance of this study not only stems from the fact showing that too much fluid results in volume overload, but also showing that a dynamic assessment of patient’s status, followed by adjustment of fluid volume is always mandatory. Indeed, the moderate resuscitation group received a median of 5.5 liters, compared to 7.8 liters in the aggressive fluid resuscitation group. Furthermore, in this study patients were also carefully assessed for euvolemia during the first 72 hours, receiving diuretics if volume overload was detected, regardless of volume resuscitation strategy. Importantly, this study also shows that diuresis in patients with fluid overload during the first 72 hours was not detrimental to clinical outcomes.

In essence, fluid resuscitation for the treatment of acute pancreatitis is still important, but it should be based on patient’s needs, and not on blind, aggressive pouring of fluids into the body. Most importantly, fluids administration should be based on needs and monitored and handled constantly to keep the patient euvolemic.

Reference:

De Madaria E, et al. Aggressive or Moderate Fluid Resuscitation in Acute Pancreatitis. N Engl J Med 2022; 387:989-1000.

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Ampulloma with Fluctuating Liver Tests

Fri, 26 Jan 2024 00:00:00 GMT

Case of the Week

A female patient in her late 70’s with status post cholecystectomy and a history of breast cancer on anastrozole, which was stopped 1 month prior because of itching was found to have elevated liver tests (alkaline phosphatase up x 4, ALT up x 6, AST up x 4). MRCP showed dilated common bile duct to 11 mm with smooth tapering at ampulla of Vater. The patient was sent for EGD and endoscopic ultrasound (EUS). The liver tests had decreased by 50% on the day of the procedure. The ampulla had the above appearance on EGD with a distal cap. What would you do next?

Approach described by Dr. Fateh Bazerbachi:

We opted for an ERCP first, given the higher risk of EUS-FNB induced pancreatitis without a protecting prosthesis and lower perceived risk of intraductal and ampullary sampling following sphincterotomy to separate the PD and CBD orifices.

The selective cannulation was aided by waiting for a hint of bile to aim for the CBD opening given that landmarks were not clear with the ulcerated surface of the ampulla.

The issue with pure EUS core sampling and mucosal biopsies is risk of ampullary hematoma, biliary obstruction and pancreatitis.

Further, with the appearance noted in this case, and relatively small lesion, yield of core biopsies with 22G needle will be limited, and pancreatitis with 19G sampling is a high risk (many experts would quote same risk of pancreatitis as ampullectomy when large caliber FNB is used in this location). Lastly, with highly suspicious endoscopic appearance of the lesion, a negative round of sampling is not sufficient to stop the evaluation. Hence, biliary prosthesis placement is a reasonable approach. As we see in this case, sampling was not conclusive and best next step is to repeat biopsies vs proceeding with ampullectomy as a diagnostic and therapeutic technique with PD stent placement (imperative) given age and comorbidities, I favor the former. If this is negative then shared decision making with the patient and ampullectomy would be the next step in my opinion.

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Gastrointestinal Bleeding due to Amyloidosis

Fri, 26 Jan 2024 00:00:00 GMT

1Department of Gastroenterology, Helios Frankenwaldklinik, Kronach, Germany

2Department of Gastroenterology “Prof. Carolina Olano”, Hospital de Clínicas, Universidad de la República, Uruguay

3Department of Gastroenterology, Virginia Tech Carilion School of Medicine, Roanoke, USA

An elderly female patient with long history of rheumatoid arthritis presented with hematochezia for 3 days. Both EGD and colonoscopy were unrevealing. On deep enteroscopy a large segment of edematous and ulcerated mucosa with multiple areas of pink-violaceous discoloration, submucosal hemorrhages, and friability were seen in the proximal jejunum (Panels A and B). Histology revealed submucosal depositions of amyloid (Panel C) The Congo red-staining in polarized light confirmed amyloid depositions (Panel D). A systemic distribution of amyloidosis was further confirmed by finding amyloid deposits in additional, deep biopsies obtained from stomach and duodenum.

Amyloidosis is the process of protein fibril deposition in the extracellular space of tissues and organ systems. Over 20 different proteins are known to form amyloid fibrils but not all of this cause disease (1). The majority of amyloidosis can be categorized into two main subtypes, amyloid light chain (AL) and amyloid A protein (AA). AL amyloid is a manifestation of a primary plasma cell dyscrasia encompassing the spectrum of multiple myeloma (MM), smoldering multiple myeloma (SMM), monocolonal gammopathy of undetermined significance (MGUS), and primary amyloidosis. Fifteen percent of AL amyloid patients have multiple myeloma (2). AA amyloid occurs as a response secondary to systemic inflammation such as rheumatologic disorders, inflammatory bowel disease, and tuberculosis. The manifestations of amyloidosis vary depending on the site and extent of the protein deposition. Of the known types of amyloidosis to cause disease, including systemic AA amyloidosis, β2-microglobulin amyloidosis, hereditary systemic amyloidosis, and senile systemic amyloidosis, AL amyloidosis is observed to incur the most GI involvement.

This case highlights the importance of performing deep enteroscopy in patients with obscure gastrointestinal bleeding and always think of amyloidosis as a potential etiology of ulcerative small bowel diseases, especially in patients with chronic inflammatory conditions, or blood dyscracias such as multiple myeloma (3,4).

References:

Ebert EC, Nagar M. Gastrointestinal manifestations of amyloidosis. Am J Gastroenterol 2008;103:776-787.
Menke DM. et al. Symptomatic gastric amyloidosis in patients with primary systemic amyloidosis. Mayo Clin Proc. 1993;68:763-767.
Tada S, Iida M, Yao T, Kawakubo K, Yao T, Okada M, Fujishima M.Endoscopic features in amyloidosis of the small intestine: Clinical and morphologic differences between chemical types of amyloid protein. Gastrointest Endosc 1994;40;45-50.
Gono T, Matsuda M, Dohi N, Sekijima Y, Tada T, Sakashita K, Koike K, Kadosaka S, Ikeda Si. Gastroduodenal lesions in primary AL amyloidosis. Gastrointest Endosc 2002;56:563-5.

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Angiodysplasias of the “Cecum” and Aortic Stenosis: Heyde's Syndrome

Fri, 26 Jan 2024 00:00:00 GMT

The classic teaching refers to Heyde’s syndrome as “the association of aortic stenosis and cecal angiodysplasias”. Whereas this is partially true, in this newsletter you will learn that Heyde syndrome is a type of hemophilia (acquired von Willebrand disease) leading to GI bleeding from various types of gastrointestinal angiodysplasias.

As you can see from the images (Figure 1), angiodysplasias in Heyde’s syndrome can happen anywhere in the gastrointestinal tract, and not only in the cecum as commonly believed.

Indeed, Dr. Heyde never specifically mentioned the cecum as the source of bleeding (1). He observed that patients with aortic stenosis had cryptogenic bleeding, speculating that it might originate in “sclerotic vessels”. His astute observations, manifested in simple letter to a medical journal (Figure 2, reference No.1), opened a pandora’s box trying to elucidate the association of aortic stenosis and gastrointestinal bleeding.

Much has been learned from Heyde syndrome over the last decades and now we know that it is primarily a hemophilia, namely a form of acquired von Willebrand syndrome (2-4). There is a malfunction of von Willebrand factor, leading to gastrointestinal hemorrhage. In addition, deranged von Willebrand activity leads to angioneogenesis and occurrence of angiodysplasias in the GI tract (2-4) (Figure 3).

How does von Willebrand factor malfunction in Heyde syndrome?

- The malfunction of von Willebrand factor is indeed initiated by the abnormal blood flow from aortic stenosis.

- This abnormal blood flow results in increased shear forces, which led to destruction of the normally circulating (or folded, globular) von Willebrand factor, which is unfolded, exposing its center to the destructive or catalytic enzymes ADAMTS 13.

- Inactivation of von Willebrand factor leads to a bleeding state.

- Another important pearl is that lots of other cardiovascular conditions, in addition to calcific aortic stenosis may lead to Heyde syndrome. These include HOCM, single ventricle or implanted left ventricular assist devices (LVAD).

For those interested in deeper understanding of this hemophilic condition I have summarized the pathophysiology (4,5).

- von Willebrand Factor (vWF) is a large multimeric glycoprotein, present in blood plasma, endothelial cells, megakaryocytes, and platelets.

- von Willebrand factor (vWF) is a produced in the endothelial cells and stored in the storage granules of these cells, which are called Weibel-Palade bodies.

- Von Willebrand factor plays a major role in hemostasis, mediating platelet adhesion to vascular injury sites.

- Von Willebrand factor also carries factor VIII, which it binds and protects from degradation.

- Von Willebrand factor is released as folded or globular heterodimer into the circulation.

- Flow acceleration and deceleration in aortic stenosis, and other cardiac conditions with deranged flow states (such as left-ventricular assist device-LVAD, hypertrophic obstructive cardiomyopathy - HOCM), result in unfolding of von Willebrand factor, which loses its thrombotic activity.

- In the absence of von Willebrand factor, FVIII is unstable and exposed to rapid degradation.

- The unfolded form of von Willebrand induces angioneogenesis through Ang2 and vascular endothelial growth factor (VEGF).

- Development of angiodysplasias (due to neo-angiogenesis) is further induced by hypoxia and low flow states

In summary, Heyde syndrome is an acquired von Willebrand disease. The defective von Willebrand factor is a decisive factor leading to hemorrhage due due defective platelet adhesion and angiogenesis and angiodysplasias of the gastrointestinal tract, which in turn bleed due to their inherent deformation and frailty and as a result of the acquired hemophilia.

The trigger for this acquired hemophilia are a wide spectrum of cardiovascular conditions such leading to abnormal blood flow with high shear forces, which destroy the normal von Willebrand factor in the circulation. These conditions include aortic stenosis, hypertrophic obstructive cardiomyopathy and left-ventricular assist device, among others. Importantly, correction of the underlying cardiac condition often leads to resolution of Heyde’s syndrome.

Importantly, treatment consists of correcting the low-flow state with high shear forces, e.g. replacement of the aortic. This aids in the resolution of the problem in the vast majority of patients.

References:

1. Heyde, E.C. Gastrointestinal Bleeding in Aortic Stenosis. N. Engl. J. Med. 1958, 259, 196.

2. Warkentin, T.; Morgan, D.G.; Moore, J.C. Aortic stenosis and bleeding gastrointestinal angiodysplasia: Is acquired von Willebrand’s disease the link? Lancet 1992, 340, 35–37.

3. Warkentin, T.E.; Moore, J.C.; Morgan, D.G. Gastrointestinal Angiodysplasia and Aortic Stenosis. N. Engl. J. Med. 2002, 347, 858–859.

4. Vincentelli A et al. Acquired von Willebrand in Aortic Stenosis. New Engl J Med. 2003

5. Okhota S, et el. Int. J. Mol. Sci. 2020, 21, 7804;

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Antibiotics Use is Associated with Increased Risk of Colorectal Cancer

Fri, 26 Jan 2024 00:00:00 GMT

Antibiotic use may increase colorectal cancer risk by altering the gut microbiota. Indeed, emerging data support a pathogenic role of certain bacteria, such as Fusobacterium nucleatum, in colon carcinogenesis (1,2). Although it is well known that factors such as excess body fat and dietary factors, could alter the gut microbiome, the use of antibiotics can have a more disruptive effect (3).

In this study, the authors used data from the comprehensive Swedish national population registers to investigate antibiotics use in relation to colorectal cancer risk (3). This is a nationwide, population-based study with a matched case-control design using a first primary colorectal cancer cases and 5 matched, cancer-free controls. The study included 40 545 colorectal cancer cases and 202 720 controls (3).

The investigators found a positive association between more frequent antibiotics use and colorectal cancer. Importantly, excluding antibiotics prescribed within 2 years of diagnosis attenuated results toward the null. In site-specific analyses, excluding the 2-year washout, the positive association was confined to the proximal colon (adjusted odds ratio for very high use vs no use = 1.17, 95% confidence interval = 1.05 to 1.31). For rectal cancer, an inverse association, which appears to be driven by women, was observed (3).

Quinolones and sulfonamides and/or trimethoprims were positively associated with proximal colon cancer, whereas a more general inverse association, across antibiotics classes, was observed for rectal cancer. Importantly, the authors found no association between methenamine hippurate, a urinary tract antiseptic not affecting the gut microbiota, and CRC risk (3).

In sum, this register-based study covering the entire population of Sweden found a robust association between antibiotics use and higher risk of proximal colon cancer and an inverse association with rectal cancer in women.

The main strength of this investigation was the use of high quality, nationwide, registry-based data, allowing them to conduct the largest and most comprehensive original research study to date on antibiotics and colorectal cancer risk (3). Also, the large sample size made it possible to conduct well-powered subgroup analyses on antibiotics type and clinical factors such as disease stage and tumor site (3).

References:

1. Saus E, Iraola-Guzmán S, Willis JR, Brunet-Vega A, Gabaldón T. Microbiome and colorectal cancer: Roles in carcinogenesis and clinical potential. Mol Aspects Med. 2019 Oct;69:93-106.

2. Dahmus JD, Kotler DL, Kastenberg DM, Kistler CA. The gut microbiome and colorectal cancer: a review of bacterial pathogenesis. J Gastrointest Oncol. 2018 Aug;9(4):769-777.

3. Sai San Moon Lu, MBBS, MPH, Zahraa Mohammed, MD, Christel Häggström, PhD, Robin Myte, PhD, Elisabeth Lindquist, MD, Åsa Gylfe, MD, PhD, Bethany Van Guelpen, MD, PhD, Sophia Harlid, PhD, Antibiotics Use and Subsequent Risk of Colorectal Cancer: A Swedish Nationwide Population-Based Study, JNCI: Journal of the National Cancer Institute, Volume 114, Issue 1, January 2022, Pages 38–46.

Source of images:

1. Fusobacterium image obtained from the CDC Public Health Image Library. Image credit: CDC/Dr. V. R. Dowell.

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Biologic Chromoendoscopy – The Eye Beats Artificial Intelligence

Fri, 26 Jan 2024 00:00:00 GMT

Natural or Biologic Chromoendoscopy for Detection of Colorectal Polyps

Endoscopic detection and resection of colorectal polyps is the key determinant for eventual prevention of colorectal cancer. Whereas visualization of sessile and pedunculated colon polyps is relatively straightforward and easy, finding flat or sessile serrated lesions is more challenging, more so for visual aid systems using artificial intelligence, or traditional virtual or dye-based chromoendoscopy techniques, as these lesions tend to secrete mucus or accumulate debris, or stool on their surface (Figure 1).

Figure 1. Personal Classification of Biologic or Natural Chromoendoscopy.

We have called this spontaneous or natural way of changing or adding color to the surface “biologic or natural chromoendoscopy”. The presence of mucus affects the coloration of the serrated lesions in three possible ways: a) the thicker mucus layer changes light penetration onto the mucosa, thus making the lesions appear paler, b) the mucus serves as a trap for debris and stool, and c) the presence of mucous filaments give the lesion a distinctive hazy appearance. In serrated lesions there are 2 consistent and unequivocal changes affecting goblet cell mucin secretion: loss of O-acetyl substituents at sialic acid C4 and C7,8,9 increase sialylation (1). Other biologic chromoendoscopy presentations are “chicken skin mucosa” and melanosis coli (Figure 2).

Figure 2. Various Types of Biologic or Natural Chromoendoscopy. A. Rim of stool or mucus. B.Cap of stool. C. Cloudy surface.D. Hakuhan or chicken skin mucosa. E. Melanosis coli. F.Endosocpic suction mark

Whereas chicken skin mucosa is present in sessile and/or neoplastic lesions, melanosis coli improves the detection of quasi any colorectal polyp. Chicken skin mucosa was described in Japan in 1981 and termed “hakuhan”, which means “white spots” (2). The term chicken skin mucosa was introduced in 1998 by Shatz et al. (3). The found that CSM was associated frequently with adenomatous polyps and adenocarcinoma. Histologically, CSM is caused by an accumulation of lipid-laden macrophages. Subsequently, Nowicki et al found that CSM is found in up to 75% of juvenile polyps. By using CD68 satins, which is specific for macrophages, the authors confirmed that CSM is due to lipid-laden macrophages and not associated with increased malignancy (4).

Melanosis coli is characterized by dark appearance of the colorectal mucosa, with the depth of color varying between pale grey and brown or black.

The dark deposit in the lamina propria is not melanin as the name suggests, but lipofuscin.

It’s association with the use of anthraquinone laxatives, including senna, aloe and rhubarb, rhamnus, and frangula has been known for almost 100 years.

Senna glycoside (senna) is the main causative laxative (5). As the laxative travels down the GI tract, it remains in its inactive form until it reaches the colon, where the molecules are activated, leading to colonocyte damage and death (5). As these cells undergo apoptosis, they create a dark pigment, lipofuscin, which eventually is deposited in the lamina propria. Eventually, these dead cells are taken up by macrophages. Interestingly, melanosis coli can occur within only a few months of chronic laxative use (5).

We believe that knowledge of this characteristic of various flat and serrated lesions is important for the practicing endoscopist, as it will improve the detection and characterization of these colorectal lesions. More importantly, current artificial intelligence systems lack the ability to specifically recognize flat lesions based on biologic chromoendoscopy, and thus the human eye and brain needs to stay cognizant of this aspect.

References:

Jass JR J.R. and Roberton AM., Colorectal mucin histochemistry in health and disease: a critical review. Pathol Int 1994;44; 487–504.

Muto T,  Kamiya J , Sawada T,  Sugihara K,  Kusama S. Clinical and histological studies on white spots of colonic mucosa around colonic polyps with special reference to diagnosis of early carcinoma. Gastroenterological endoscopy, 1981;23:2:241-247

Shatz BA, et al. Colonic chicken skin mucosa: an endoscopic and histological abnormality adjacent to colonic neoplasms. Am J Gastroenterol 1998;93:623–7.

Nowicki, M et al. Colonic Chicken-Skin Mucosa in Children with Polyps is not a Preneoplastic Lesion, Journal of Pediatric Gastroenterology and Nutrition. 2005;41:600-606.

Nesheiwat Z, Al Nasser Y. Melanosis Coli. [Updated 2023 Feb 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK493146/

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Cameron Lesions

Fri, 26 Jan 2024 00:00:00 GMT

Cameron lesions refer to linear erosions or ulcerations of the gastric mucosal folds in patients with a large hiatal hernia that are typically located at diaphragmatic pinch, often in the case of a large hiatal hernia. First depicted by Cameron and Higgins in 1986, these lesions were originally found in those who had greater than a third of their stomach above the diaphragm on a chest x-ray (1,2).

It is theorized that mechanical trauma, specifically persistent friction between the gastric folds at the level of the constriction is the most likely etiology and results in local ischemia. It has also been suggested that the pressure difference between the thoracic and abdominal cavity during respiration may lead to mucosal stress and ulceration, besides added injury from gastric acid and pressure of the diaphragm on the hernia (2,3).

Hiatal hernias are identified on esophagogastroduodenoscopy (EGD) in 0.8% - 2.9% of patients (4). Among these, Cameron lesions are identified in approximately 5% of all cases; however, the prevalence of these lesions is positively associated with hiatal hernia size and ranges from 1% - 13% in small (< 3 cm) to large (> 5 cm) hiatal hernias, respectively (2).

The gold standard for diagnosing Cameron lesions is EGD. On EGD, Cameron lesions are visualized as superficial, linear erosions/ulcerations on the mucosa covering the crests of the gastric folds (Figure 1); often with concurrent erythema, edema, and/or bleeding (1,2).

Figure 1: Large linear Cameron lesions associated with a large hiatal hernia

Nonetheless, it is not uncommon to miss Cameron lesions on the index EGD as they are often very small in size and without active bleeding. A recent systematic review determined that an estimated 69% of patients had undergone one or more EGDs prior to formal diagnosis of Cameron lesions (2). As such, endoscopic evaluation of patients with a hiatal hernia necessitates special attention to be paid to the hernia sac, area of the diaphragmatic pinch and the lining mucosa during both the antegrade and retroflexed view. Newer diagnostic modalities such as magnification chromoendoscopy or Narrow Banding Imaging (NBI) have been purported to assist in the identification of mucosal lesions consistent with Cameron lesions (1,2).

Medical therapy with proton-pump inhibitors (PPI) serves as the mainstay of treatment with most patients responding positively to medical therapy (1). Patients may also require additional iron supplementation as Cameron lesions can be a potential cause of iron deficiency anemia also. Among those receiving dual therapy of an acid suppressing drug and iron supplementation, over 60% of patients demonstrated healing of Cameron lesions via repeat EGD at the six-week mark (5). Interestingly, most patients with Cameron lesions possess concurrent gastroesophageal reflux disease (GERD) with or without esophagitis and may already be on PPI therapy at time of diagnosis (1,2).

Overall, Cameron lesions are rare, benign findings often occurring in patients with a large hiatal hernia. Their prevalence is often underestimated as they can easily be overlooked, especially when small in size. Endoscopists must maintain a high index of suspicion in pertinent cases, especially in patients with large and complex hiatal hernias.

What's Next?

References:

Brar HS, Aloysius MM, Shah NJ. Cameron Lesions. [Updated 2023 Jan 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK567776/
Zullo A, Manta R, De Francesco V, et al. Cameron lesions: A still overlooked diagnosis. Case report and systematic review of literature [published correction appears in Clin Res Hepatol Gastroenterol. 2019 Feb;43(1):112-113]. Clin Res Hepatol Gastroenterol. 2018;42(6):604-609. doi:10.1016/j.clinre.2018.05.002
Colin W, Windsor O, Leigh Collis J. Anaemia and hiatus hernia: experience in 450 patients. Thorax 1967;22:73–8
Kimer N, Schmidt PN, Krag A. Cameron lesions: an often overlooked cause of iron deficiency anaemia in patients with large hiatal hernias. BMJ Case Rep. 2010;2010:bcr0620103129. Published 2010 Oct 28. doi:10.1136/bcr.06.2010.3129
Moskovitz M, Fadden R, Min T, Jansma D, Gavaler J. Large hiatal hernias, anemia, and linear gastric erosion: studies of etiology and medical therapy. Am J Gastroenterol. 1992;87(5):622-626.

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Improving Patient Experience with Colonoscopy Prep

Fri, 26 Jan 2024 00:00:00 GMT

Can I have your experience with colonoscopy prep? I have noticed that most of the patients we receive don't have a good Boston score?

We had a similar experience as you and we have changed two essential aspects of colon prep. First, we created an instruction sheet for the patient and trained our nurses and secretaries to explain the preparation process, focusing on low fiber and zero seeds diet for at least three days, with a strict liquid diet the day before the procedure. In Germany, people like to eat bread with seeds. That's a no for colon prep! The second key step was to focus on SPLIT prep. This has made a huge difference, half the dose the afternoon before the procedure and half the dose of colon prep the same day of the procedure, starting about 4 hours before the scheduled test. Our Boston Bowel Preparation Scales improved by at least 2 points, now they are an average of 8 points.

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Candida Esophagitis

Fri, 26 Jan 2024 00:00:00 GMT

Welcome to 5,991 motivated Endoscopists! Today we are going over Candida Esophagitis.

A 68-year-old man with a 10-year history of type 2 diabetes mellitus presented with dysphagia to solid foods for one week. He described the sensation as “food sticking" in the upper retrosternal area. Esophagogastroduodenoscopy revealed multiple confluent, protuberant, yellowish-white, plaque-like lesions with the appearance of cottage cheese covering the esophageal mucosa (Panel A). Histological examination of the esophageal plaque brushings confirmed candidiasis (Panel B). The patient was treated with oral fluconazole for 7 days with complete resolution of symptoms.

Candidiasis is a common opportunistic infection among immunocompromised patients usually involving the oropharynx, esophagus, and vagina. Patients with esophageal candidiasis typically present with dysphagia. An important distinction should be made between the 2 symptoms related to swallowing: odynophagia or painful swallowing is a complaint related to esophageal ulcer, whereas dysphagia or the sensation of “food getting stuck” is more commonly caused by esophageal strictures (benign or malignant) or candidiasis. Extensive esophageal candidiasis, however, can present with both symptoms. Endoscopic evaluation is the most sensitive method for diagnosis of Candida esophagitis. The characteristic white and yellow “cottage cheese” plaques are considered highly suggestive of candidiasis. In the appropriate clinical setting (e.g., immunosuppressed patient with thrush and dysphagia), a trial of empiric anti-fungal therapy with fluconazole can be attempted. If the condition fails to respond in less than a week, an endoscopic evaluation with biopsy and/or brushings should be carried out.

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Caps in GI Endoscopy

Fri, 26 Jan 2024 00:00:00 GMT

Question

What is the best way to inspect the papilla of Vater in the abscence or lack of availability of a duodenoscope (side-viewing scope, ERCP scope)?

Answer

Today we present a useful tip for inspection of the papilla of Vater using distal transparent cap.

A close and detailed inspection of the major papilla may be needed in a variety of clinical situations, for example, during upper endoscopy of a patient with a familial polyposis syndrome (FAP) or duodenal adenomas Although some papillae may be seen well with forward-viewing instruments, many are partially or fully hidden behind duodenal folds and, therefore, are outside the field of view of a standard upper endoscope. Using a distal transparent cap allows visualization and inspection of virtually every major papilla without having to resort to the use of a second endoscope—that is, a duodenoscope. See attached figure.

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Chicken Skin Mucosa

Fri, 26 Jan 2024 00:00:00 GMT

Does the White Deposit (Chicken Skin Sign) Around the Base of the Polyps Have Any Prognostic Value?

“Chicken skin” mucosa (or “goose skin” in German-speaking countries, or “fish skin” in the Mediterranean and some Far East countries) was first described in Western countries in1998 by Shatz et al. (Am J Gastroenterol).

The authors found that CSM was associated frequently with adenomatous polyps and adenocarcinoma. Histologically, CSM is caused by an accumulation of lipid-laden macrophages. Subsequently, Nowicki et al (J Ped Gastroenterol Nutr, 2005) found that CSM is found in up to 75% of juvenile polyps. By using CD68 stain, which is specific for macrophages, the authors confirmed that CSM is due to lipid-laden macrophages and not associated with increased malignancy.

We had learned from Prof. Parra-Blanco that the first description of CSM was by Prof. Muto from Japan.

Prof. Parra-Blanco: “… this was described as “white spots” (hakuhan in Japanese) by Prof Tetsuichiro Muto in 1981 . But the name “chicken skin mucosa” is more popular in Western countries. It was described in Japanese, but this is the abstract in English.” https://www.jstage.jst.go.jp/article/gee1973b/23/2/23_2_241/_article/-char/en

Shatz BA, et al. Colonic chicken skin mucosa: an endoscopic and histological abnormality adjacent to colonic neoplasms. Am J Gastroenterol 1998;93:623–7.
Nowicki, M et al. Colonic Chicken-Skin Mucosa in Children with Polyps is not a Preneoplastic Lesion, Journal of Pediatric Gastroenterology and Nutrition. 2005;41:600-606.

[Link]

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Clostridioides Difficile Infection (CDI)

Fri, 26 Jan 2024 00:00:00 GMT

Pathogen:

- Anaerobic, gram-positive, rod-shaped bacterium with spore formation

- Spores have tolerance to heat, desiccation and many disinfectants.

- Two exotoxins: toxin A (“enterotoxin”) and toxin B (“cytotoxin”)

- Careful: the hypervirulent strain: NAP-1,ribotype 027, III has increased expression of toxins A and B.

Risk Factors:

- Main risk factors: previous antibiotic therapy, hospitalization, age > 65 years

- Other risk factors: multimorbidity, female, H2 and PPI therapy, immunosuppression

Definition of infection: symptoms plus evidence of toxins A and B

- Watery diarrhea or toxic megacolon (occasional no diarrhea in paralytic ileus!)

- Blood in stool (rare), abdominal pain (22%), fever (28%), peritonitis/ascites

Laboratory findings:

- Leukocytosis (>15,000/µl (50%), hypoalbuminemia, creatinine increase ≥1.5 times, lactate increase

Diagnostics (Attention: only perform diagnostics on patients with clinical symptoms of CDI!)

- antibiotics in the last 60 days; risk groups, regardless of whether they are hospitalized, and any diarrhea lasting more than three days without other known pathogens

- Stool samples

- EIA test (quick but only 80% sensitive).

- GDH, if positive then toxin, then PCR.

- Imporant: fresh stools, max. 2 hours transport time (toxin breaks down at room temperature, no rectal swabs!). Culture rarely helpful (too high TAT, turn-around time)

- Cytotoxicity test (cell culture-based method): highly sensitive and specific for toxin B

- In the absence of toxin detection DO a sigmoidoscopy: pseudomembranes = pathognomonic)

- Check-ups: only if symptoms re-appear after successful therapy, not if there are no symptoms after therapy

Classification of severity (risk stratification according to Zar, Clin Infect Dis 2007) (severe course > 2 points!)

- 1 point: > 60 years, temperature > 38.5 C, albumin < 2.5 mg/dl, leukocytes > 15,000/µl

- 2 points: endoscopic evidence of pseudomembranes, stay on ICU

Hygienic measures and therapy:

- Isolation (single room): Patient with severe diarrhea, poor compliance.

- Isolation measures should be maintained for a period of 48 hours after diarrhea has resolved.

- Disposable protective gown and hand hygiene: washing hands, then disinfection if gloves were worn: disinfection alone is sufficient, mouth and nose protection only if aerosol formation and splashing

- Adequate fluid and electrolyte replacement

- Antibiotics when: a) severe or persistent symptoms (i.e. all hospitalized patients), b) elderly and/or patients with underlying medical conditions, or c) concomitant antibiotic treatment

- Non-severe course (i.e. outpatient): metronidazole (3 x 400 mg orally or 3 x 500 mg i.v.) x 10 to 14 days.

- In the hospital, or severe course or pregnant: vancomycin orally or nasogastric tube (4 x 125-500 mg) x 10 days, and as an enema (4 x 500 mg in 100 ml NaCL; in transit disorder: metronidazole 3 x 500 mg IV vancomycin

- Intolerance: Dificlir (Fidaxomicin) (2 x 250 mg)

- Life-threatening clinical pictures (pseudomembranous colitis, toxic megacolon - TMC): combined therapy with vancomycin (oral or via enteral tubes) and metronidazole (i.v.)

- First recurrence: same as first therapy. From the second recurrence: vancomycin in tapering doses: 4 x 125 mg x 14 days, 2 x 125 mg x 7 days, 1 x 125 mg x 7 days, 1 x 125 mg/2-3 days x 2-8 weeks

Surgery consult: > 65 years, leukocytes > 20,000 µl, sepsis, TMC, severe ileus, peritonitis, perforation

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Cronkhite Canada Syndrome (CCS)

Fri, 26 Jan 2024 00:00:00 GMT

A 48-year-old woman presented with chronic diarrhea and loss of taste. On clinical exam she appeared pale, had brittle nails and had partial hair loss. She was found to have severe iron deficiency anemia.

Colonoscopy showed multiple reddish, edematous mucosal streaks and polyps and pseudopolyps ranging from 5 to about 20 mm. On EGD the stomach was characterized by enlarged mucosal folds, pseudoplyps and duodenal mucosal atrophy. Histology showed the above findings (see figure 2).

CCS is a non-hereditary syndrome of unknown etiology characterized by diffuse gastrointestinal GI pseudo-polyposis, alopecia, hyperpigmentation, dystrophic changes in finger and toe nails

Clinical presentation: diarrhea, weight loss, abdominal pain, anorexia, weakness, hematochezia, iron deficiency anemia. Onset usually in middle aged adults.

Patients with CCS occasionally gastric adenocarcinoma, and adenocarcinomas anywhere in GI tract.

Treatment is not well standardized but consist of corticosteroids, H. pylori eradication and zinc supplementation.

Cronkhite Canada Syndrome Resources

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Cytomegalovirus (CMV) Gastritis

Fri, 26 Jan 2024 00:00:00 GMT

52-year-old patient who underwent renal transplant two year prior, presented with abdominal pain and nausea. Esophagogastroduodenoscopy demonstrated mild antrum erythema and one erosion (A). The erosion was biopsied, in addition to antrum and body biopsies. Histology (hematoxillin & eosin) revealed inclusion bodies (B). The typical “owls eye appearances” are demonstrated on panel C. Immunohistochemical stains confirmed the presence of CMV

Cytomegalovirus (CMV) disease of the gastrointestinal (GI) tract is a major cause of morbidity and mortality in immunocompromised patients.

However, upper GI CMV disease can occur in the absence of immunodeficiency and immunosuppression. CMV is usually symptomatic, and mucosal erosion and ulceration are often evident at esophagogastroduodenoscopy. Obtaining sufficient biopsies (i.e. at least 4, two from the border and two from the ulcer base) are essential to allow the pathologist to diagnose this surreptitious organism.

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(DIE) - Dabigatran-Induced Exfoliative Esophagitis

Fri, 26 Jan 2024 00:00:00 GMT

Today we present a case of drug-induced exfoliative esophagitis (DIE) - Dabigatran-induced Exfoliative Esophagitis

Non-vitamin K anticoagulants (NOAC), also known as direct oral anticoagulants (DOAC) are now commonly used for a variety of conditions requiring chronic anticoagulation. The dabigatran pellets are covered with a tartaric acid core. This strong acid may result in squamous epithelial damage with ensuing exfoliative esophagitis. Elderly patients are more prone to suffer esophageal damage due to medications as they have a) decreased salivary production, b) may not drink enough fluids and c) often have esophageal dysmotility. All these factors contribute to prolonged contact of medications with the esophageal mucosa.

Other important causes of exfoliative esophagitis are: Herpes simplex Virus infection (A), esophagitis dissecans superficialis due to medications(biphosphonates, dabigatran, sunitinib) (B, C), graft-versus-host disease(GVHD), amyloidosis, pemphigus vulgaris.

In a study looking at 91 patients in dabigatran who underwent endoscopy Toya el al. found that

A) Dabigatran causes the esophageal mucosal injury in up to 20% of patients.

B) Of the 19 patients with the esophagitis, 18 (94.7%) showed longitudinally sloughing, epithelial casts in the mid and/or lower esophagus

C) 70% of patients with dabigatran induced esophagitis had symptoms.

Ref: Toya Y, Nakamura S, Tomita K, et al. Dabigatran-induced esophagitis: The prevalence and endoscopic characteristics. J Gastroenterol Hepatol. 2016;31:610-4.

Visit EndoCollab for More Information About All Types of Esophageal Diseases and More

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Endoscopic Removal of Esophageal Foreign Bodies Using the Tripod Grasper

Fri, 26 Jan 2024 00:00:00 GMT

The tripod grasper was originally developed to retrieve colon polyps (Figure 1). Given its versatile design, it soon became evident that this device was also useful for removing other types of objects.

The tripod grasper consists of a three-pronged wire inside a catheter. Once the prongs are extended out the cannula, they open like a bird claw (Figure 1A and B). Importantly, in contrast to real claws, the tips are rounded, to avoid damage to the mucosa or grasping unwanted tissue. The objective is to get the object inside of the claws and remove it, without pulling off any adjacent tissue.

Whenever there is a food impaction our main device to remove impacted meat or vegetables is the distal transparent cap attached to the scope (Figure 2, Caps in GI Endoscopy). But there are situations when the tripod grasper comes into play.

Brief case report:

Elderly patient with history of previous lye ingestion and complex esophageal strictures presented with food impaction lasting 24 hours. The patient had known esophageal strictures since childhood and was on a regular dilation program. In this patient, however, using a cap was not possible, as the esophagus was stenosed due to previous lye injury. Indeed, in any patient with fibrotic esophagus due to radiation esophagitis, old lye injury or tight anastomosis using caps is difficult or impossible as the lumen is narrowed down.

Therefore, we used tripod grasper.

Herein we present some, tips and tricks on using the tripod grasper (Figure 1).

First, inspect the motility of the esophagus and the interplay of the foreign body with the stenosis and the stricture. Is the esophagus elastic or stiff? Is the foreign body impacted or does it move up and down? Using some water is useful to further determine the interplay of the foreign body and the stricture.

Second, evaluate the mucosa. We want to prevent further damage during manipulation during the extraction maneuvers. Is it macerated due to long-standing pressure damage from the foreign body? Has the patient developed and laceration due to previous nausea, vomiting or retching?

Third, proceed to remove the foreign body. It is important not to open or expose the entire tripod grasper (Fig. 3C), as it may get entangled against the walls of stenotic esophagus. With the open grasper advance the scope towards the foreign body and slowly expose the grasper’s legs. Then close the grasper, while simultaneously pushing towards the foreign body (Fig. 3D). Closing with pushing will result in inefficient grasp and the foreign body may fall off the grasper.

Fourth, once the foreign body is tightly grasped proceed to pull the foreign body towards the tip of the scope, to avoid a gap between the scope tip and grasped foreign body (Figure 3G and 3H). This is called the pathfinder trick, as the scope will serve as guide and “clear the way” for the foreign body on its tip.

If there is a distance between the scope and the tripod grasper with the foreign body (Fig. 3F, yellow arrow showing the gap), the foreign body may fall off at areas of stenosis such as the upper esophageal sphincter or additional esophageal stenosis or fibrotic rings (Fig 3E).

One last trick: while removing the scope with the foreign body, try to do gently twisting of the scope, in a corkscrew-type way, to adapt to esophageal tortuosity and thus, avoid for the foreign body to bounce of the wall or mucosal strictures.

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Endoscopic Resection of Complex Duodenal Polyps

Fri, 26 Jan 2024 00:00:00 GMT

Pedunculated Duodenal Adenoma, 0-Ip

This polyp is located in the second part of the duodenum. 

What resection technique would you use?

And what precautions would you take to prevent the polyp from going “away” into the distal bowel?

When faced with a larger sessile or pedunculated polyp located in the distal duodenum the endoscopist should plan a complete (R0) resection, but actively anticipate a) what to do once the polyp is resected and b) how to deal with any potential complication (bleeding and perforation).

To prevent the polyp from migrating distally the following measures may be taken: 

a) place the patient in decubitus supine position, or b) use anti-motility agent such as glucagon or Buscopan. In addition, both the endoscopist and the assistant should be ready. to  catch the polyp with the snare once it is resected, or have a Roth´s net readily available. to quickly in and catch the polyp. One trick I like to use is always using a distal transparent cap on the scope to perform the resection, and then suction part of the polyp into the cap. and retrieve out (or at least into the stomach, so it does not move away in the duodenum).

In order to prevent complications during and after the endoscopic resection one can do the following:

a) Use submucosal injection (ideally with saline-epinephrine mix 1:100,000), which will raise the lesion, distantiate the neoplasia from the muscular propria, and decrease intraprocedural bleeding, allowing for a cleaner operating field.

b) Perform underwater resection, which allows for the neoplasm to float and thus, have less chances of transmitting electrosurgical current to the base (hence less perforation). Also, by using water, the electrosurgery currents applied with the snare are dissipated into the water, decreasing heating damage to the tissue.

c) Another great option for this pedunculated polyp is to use a prophylactic endoloop.

d) When I resect duodenal lesions, I always use clips to close the wound. The literature clearly shows that immediate and delayed bleeding is a very common complication of duodenal endoscopic resections. On some occasions, when the resection site is broad and large, I have also used hemostatic hydrogels (Purastat), especially in patients who have been or are on anticoagulation. Starting proton pump inhibitors at high dose for 2-3 days is also advisable (and keep the PPI for about one month to aid in healing).

e) Finally, when resecting a duodenal polyp always take into account its location to the papilla of Vater. First, to make sure it’s not an ampullary lesion, and second to plan the resection well, because in these scenarios, using a side-viewing endoscope may improve visibility and ensure a complete resection (R0).

f) Sometimes using argon plasma coagulation may be necessary to ablate remains of lesion or treat bleeding. Careful attention must be paid to the amount of argon plasma used, as too much distention or gas may result in pancreatitis (1).

References:

Weigt J, Zimmermann LC, Mönkemüller K, Malfertheiner P. Acute pancreatitis after argon plasma coagulation of duodenal polyps in a patient with familial adenomatous polyposis. Endoscopy. 2007 Feb;39 Suppl 1:E278. doi: 10.1055/s-2007-966664. Epub 2007 Oct 24. PMID: 17957607.

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Endoscopic Spectrum of “Left”-Sided Ischemic Colitis

Fri, 26 Jan 2024 00:00:00 GMT

The endoscopic spectrum of ischemic colitis is broad. Key elements though are sparing of the rectum and segmental distribution, mainly in the left colon (at the watershed area, arc of Riolan).
Colonic ischemia occurs due to changes in systemic circulation and/or alterations in local mesenteric vasculature.
The most frequent areas affected are left colon (Griffith’s point), and superior rectum (Sudeck’s point), the lower rectum usually being spared because of its dual blood supply.
In mild ischemic colitis there are usually segmentally distributed patchy erythema, edema and subepithelial hemorrhages. In moderate colitis, in addition to changes seen in mild disease, there are localized erosions and ulcers, which may be confluent. Often, a linear ulcer in the mesenteric border of the colon is seen. This is known as colon single strip sign (CSSS) or Zuckerman’s sign. In severe colitis there are deep ulcers, luminal narrowing and strictures and frank necrosis.

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EREFS Score for Eosinophilic Esophagitis (EoE)

Fri, 26 Jan 2024 00:00:00 GMT

The EoE Endoscopic Reference Score (EREFS) was developed as a way to quantify the major endoscopic features of EoE, including edema, rings, exudates, furrows, and strictures (the first letter of these findings also comprises the acronym for the system).

EDEMA is graded as absent (grade 0) or present (1; decreased or absent vascularity).

RINGS are graded as absent (0), mild (1; subtle ridges), moderate (2; distinct rings), or severe (3; standard scope will not pass).

EXUDATES (or white speckles, stiplings) are graded as absent (0), mild (1; ≤10% of the mucosal surface area), or severe (2; >10% of the surface).

FURROWS (or lines and tracks) are graded as absent (0), mild (1; present without depth), or severe (2; depth noted).

STRICTURE is graded as absent (0) or present (1), and if possible the minimum diameter of the esophagus is recorded.

Source: E. Dellon. CGH 2021;19:2489–2492.

As there are several other endoscopic findings in EoE (visit endocollab.com and watch the video Eosinophilic Esophagitis: Focus on its Endoscopic Diagnosis".

We think that the classification could be expanded to include dysmotility or sitffness, the "pull-sign" ("peel-off") when performing biopsies - "DEREFS-P"

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Ergonomics in Gastrointestinal Endoscopy Myths and Realities

Fri, 26 Jan 2024 00:00:00 GMT

In this video, I'll be debunking some myths about ergonomics in endoscopy, such as the ideas that women are at disadvantage to perform endoscopy, that scopes were designed only for men, that scoping must be performed in the standing position and sharing important data about the impact of workload on our health.

I’ll also show you how ergonomics is misunderstood and misrepresented, leading to lots of confusion, and often, engineers and architects rely on this information provided through the internet to (wrongly) design our endoscopy suite.

By debunking these concepts and actively taking part in the design of our endoscopy suite we will contribute to our own health.

I'll also be sharing tips on how to improve ergonomics in the endoscopy unit, such as using adapting the endoscopy suite and equipment to the endoscopist and not vice versa.

In addition, we need to focus on making sure that the patients are also ergonomically positioned, for example using wedge supports and ensuring that they are the center of our attention.

My main aim is to show that attention to tiny details, that are often overlooked, make the biggest difference in endoscopic progress and ergonomics. By taking these steps, we can prevent injuries and improve the overall well-being of our patients and ourselves.

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Focal Segmental Bile Duct Dilation

Fri, 26 Jan 2024 00:00:00 GMT

Few conditions can result in segmental (focal) non-obstructive bile duct dilation. These include primary or secondary sclerosing cholangitis, hepatolithiasis, parasitic infections (e.g. Clonorchis sinensis or oriental cholangiohepatitis, Opistorchis viverrini, Fasciola hepatitis or liver fluke), biliary papillomatosis, choledochal cysts or, as in this case, Caroli’s disease and syndrome. Caroli's disease is a rare congenital disease of the liver generally characterized by segmental cystic dilation of the intrahepatic bile ducts. Classic Caroli's disease involves malformations of the biliary tract alone, whereas Caroli's syndrome refers to the presence of associated congenital hepatic fibrosis.

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Is a Fully Covered Self-Expanding Metal Stent an Option for Recalcitrant Duodenal Stenosis?

Fri, 26 Jan 2024 00:00:00 GMT

I have only used fully covered self-expanding metal stents for palliative situations such as malignant gastric outlet obstruction or duodenal perforation (by instruments or due to lymphoma). There are case reports of using fc-SEMS for benign conditions.

Your case is very challenging as the patient likely has recalcitrant duodenal obstruction due to medications (NSAIDS). I also suspect that there is a component of ischemic duodenopathy in the setting of sickle cell disease.

Your surgery team's concerns are quite important because if this duodenal disease-stenosis is indeed due to NSAIDs, the possibility of continued or surreptitious use of NSAIDs after surgery is real, and NSAID use may lead to giant anastomotic ulcers and failure of the Billroth II operation.

Your concept of using a fcSEMS as a remodeling tool is excellent and makes sense, expecting that the fibrotic lumen may expand some due to the presence of the stent.

My approach would be the following:

a) Evaluate the histology (and rule out ischemic duodenathy due to sickle cell disease).

b) Avoid all NSAIDs, referring patient to special pain management clinic.

c) Then would consider a fcSEMS, likely choosing one that can be delivered through-the-scope (e.g. Taewong). The proximal part should be attached to the stomach with a clip (e.g. over-the-scope clip). And I would leave the stent no longer than a few weeks, as the distal expande flange may lacerate the mucosa and induce more fibrosis (or even penetration).

d) The final decision to proceed should be backed-up by a multidisciplinary discussion with surgeons and the patient.

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Gastric Antral Vascular Ectasia (GAVE) or Watermelon Stomach

Fri, 26 Jan 2024 00:00:00 GMT

Gastric antral vascular ectasia (GAVE) or watermelon stomach is an uncommon but important cause of gastrointestinal bleeding and anemia, first described in 1953 by Rider et al (1). GAVE is characterized by a “characteristic” endoscopic pattern, mainly represented by red spots either organized in stripes radially departing from pylorus (“watermelon stomach”, or arranged in a diffused-way or “honeycomb stomach”). In addition, there is a nodular variety, where there are multiple enlarged and nodular folds in the antrum (2, 3). Despite this GAVE is often misclassified or mis-diagnosed.

Histology shows dilation of mucosal capillaries, with focal thrombosis and fibromuscular hyperplasia of the lamina propria and thickened mucosa with tortuous submucosal venous channels. A scoring system known as the “Gilliam score” was created to aid in histologic diagnosis of GAVE. This scoring system focuses on the following criteria: spindle cell proliferation presenting with either ectasia, fibrin thrombi, or a combination of both ectasia and fibrin thrombi (4). Payen et al., further, expanded this scoring system to include fibro-hyalinosis as a third diagnostic criteria for GAVE. This more robust score was referred to as the “GAVE score” (5).

The exact cause of GAVE is not known. GAVE or watermelon stomach is often associated with a number of conditions, including portal hypertension, cirrhosis, hypergastrinemia, metabolic syndrome, chronic renal failure, collagen vascular diseases, scleroderma, systemic lupus erythematosus, Sjögren’s disease, primary biliary cholangitis, bone marrow transplantation, pernicious anemia, and as shown by our group, heart failure with left ventricular assist device (LVAD) with development of Heyde syndrome (6).

Treatment of GAVE is aimed at obliterating all the vessels and can be accomplished by argon plasma coagulation, radiofrequency ablation and endoscopic band ligation.

Visit endocollab.com for Quick Tip Videos on how to treat GAVE with APC, RFA or endoscopic band ligation (2,3).

References:

1. Rider JA, Klotz AP, Kirsner JB: Gastritis with veno-capillary ectasia as a source of massive gastric hemorrhage. Gastroenterol 1953;24: 118–123.

2. Fuccio L, Mussetto A, Laterza L, et al. Diagnosis and management of gastric antral vascular ectasia. World J Gastrointest Endosc. 2013;5:6-13.

3. Aryan M, Jariwala R, Alkurdi B, Peter S, Shoreibah M. The misclassification of gastric antral vascular ectasia. J Clin Transl Res. 2022 May 25;8(3):218-223.

4. Gilliam JH, Geisinger KR, Wu WC, Weidner N, Richter JE. Endoscopic Biopsy is Diagnostic in Gastric Antral Vascular Ectasia. Dig Dis Sci. 1989;34:885–8.

5. Payen JL, Calès P, Voigt JJ, Barbe S, Pilette C, Dubuisson L, et al. Severe Portal Hypertensive Gastropathy and Antral Vascular Ectasia are Distinct Entities in Patients with Cirrhosis. Gastroenterology. 1995;108:866–72.

6. Alkurdi B, Mönkemüller K, Khan AS, Council L, McGuire BM, Peter S. Gastric antral vascular ectasia: a rare manifestation for gastrointestinal bleeding in left ventricular assist device patients--an initial report. Dig Dis Sci. 2014 Nov;59(11):2826-30.

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Gastric Hyperplastic Polyps

Fri, 26 Jan 2024 00:00:00 GMT

Question:

A routine EGD for GERD, found to have one gastric polyp 8mm - turned out to be a hyperplastic polyp in at 45M? No H. pylori, no atrophy. Follow up?

Short answer: No surveillance is necessary in this patient, especially because the patient is NOT infected with H. pylori and there was no gastric atrophy. To have some “piece of mind” I would resect that polyp on the index endoscopy.

Extended discussion: Hyperplastic gastric polyps larger than 10 mm should be removed as they are associated with malignancy, i.e. harboring a cancer.

On the other side, any sized hyperplastic gastric polyp, but only in the presence of H. pylori infection, is associated with higher incidence of gastric cancer. However, in addition to H. pylori infection, other “stomach risk factors” such as atrophy, intestinal metaplasia, distribution of the gastritis (body versus antrum versus pan-gastritis) should be thrown into the equation when deciding on surveillance gastroscopy. Of course, geographical location and family history are also important factors that determine the decision to endoscopically surveille or not.

I am adding the seminal prospective study from 2001 on Helicobacter pylori infection and development of gastric cancer done by Naomi Uemura et al. This study gives us some insight on some factors to consider when considering surveillance gastroscopy.

The key finding of this study was that gastric cancer developed in persons infected with H. pylori but not in uninfected persons.

Additionally, those with histologic findings of severe gastric atrophy, corpus-predominant gastritis, or intestinal metaplasia were at highest risk.

Importantly, persons with H. pylori infection and non-ulcer dyspepsia, gastric ulcers, or gastric hyperplastic polyps were also at risk, but those with duodenal ulcers are not.

Summary and results of study:

In this study the authors prospectively studied 1526 Japanese patients who had duodenal ulcers, gastric ulcers, gastric hyperplasia, or non-ulcer dyspepsia at the time of enrollment; 1246 had H. pylori infection and 280 did not. The mean follow-up was 7.8 years (range, 1.0 to 10.6). Patients underwent endoscopy with biopsy at enrollment and then between one and three years after enrollment. H. pylori infection was assessed by histologic examination, serologic testing, and rapid urease tests and was defined by a positive result on any of these tests.

A total of 36 gastric cancers were found, with 23 intestinal-type and 13 diffuse- type cancers. Among the patients with H. pylori infection, those with severe gastric atrophy, corpus- predominant gastritis, and intestinal metaplasia were at significantly higher risk for gastric cancer. Gastric cancers were detected in 21 (4.7 percent) of the 445 patients with non-ulcer dyspepsia, 10 (3.4 percent) of the 297 with gastric ulcers, 5 (2.2 percent) of the 229 with gastric hyperplastic polyps, and none of the 275 with duodenal ulcers.

(N Engl J Med 2001; 345:784-9)

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Giant Prolapsing Gastric Polyp

Fri, 26 Jan 2024 00:00:00 GMT

Case

A 75-year old male with iron deficiency anemia underwent upper endoscopy. A pedunculated lesion prolapsing into the bulb across the pylorus was found. With some difficulties the lesion was "brought back" into the stomach and the head of the tumor had ulcerated surface with contact bleeding.

Since the patient was currently on ASA and clopidogrel, several biopsies were taken. He is probably a poor surgical candidate. CT scan was negative for enlarged regional lymph nodes and distant metastases.

Would you consider endoscopic removal in such case hoping for negative resection margin, despite ulcerated surface and iron-deficiency anemia indicating malignant transformation or send him for surgery? What factors would affect your decision for this lesion?

Analysis of Case

This giant prolapsing polyp is likely hyperplastic. The other important differential diagnosis is inflammatory polyp, especially the so-called Vanek tumor. Less commonly, these lesions are mesenchymal or lymphoid in origin or are cancerous (e.g. adenocarcinoma).This polyps result in intermittent obstruction and anemia or frank GI bleeding. Because of the constant prolapse their surface erodes and becomes „ugly-looking“, mimicking malignancy. If the polyps are hyperplastic, they have more chances of harboring malignancy if larger than 10 mm.This polyp is definitely > 10 mm.What would make me resect this lesion endoscopically?1. The polyp has a nice base and a long stalk (it’s more of an elongated base, due to constant bouncing back and forth).2. This nice base allows for nice submucosal injection of saline-epinephrine mix.3. The location is also ideal for controlled resection.4. If the lesion is resected and no malignancy is found or if the submucosal invasion is minimal and the margins are broad (R0), the patient is cured. And also cured from the bleeding. If there is invasive tumor, the resection was also helpful for diagnostic purposes and further therapeutic planning.5. This lesion is ideally resected using ESD or ESD-Hybrid technique. I would not proceed with a polypectomy as the stomach is highly vascularized and these lesions tend to harbor huge vessels. The risk of bleeding would be too high. That’s why performing a controlled resection, step-by-step is better.6. Pre-resection endoscopic ultrasound is highly recommended. EUS may be very helpful determining infiltration. If there is deep infiltration I would not resect endoscopically. In the absence of EUS I would do a CT of the abdomen, if the kidney function is fine.

Case presented by Dr. Stefan Mitev and discussed by Prof. Klaus Mönkemüller

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Granular Cell Tumor (GCT)

Fri, 26 Jan 2024 00:00:00 GMT

Although some guidelines dichotomize the decision to resect granular cell tumors (also called Abrikosoff's tumor) based on presence or absence of symptoms, others, including ourselves support the decision to resect based in histological criteria.

Let's not forget that GCT can be malignant from the outset, regardless of their size or presence of symptoms. Indeed, GCT are classified as malignant, benign and indeterminate. Furthermore, 2% of benign GCT progress to malignancy.

Thus, I like to use the classification of Fanburg-Smith (see table), which takes various histological features into consideration, such as tumor necrosis, spindle cells, vesicular nuclei with prominent nucleoli, mitotic activity (>2 mitosis/10 high-power fields), high nucleocytoplasmic ration, nuclear pleomorphism.

I am enclosing a table (from ref. No 2) comparing three classification systems to highlight that necrosis and mitotic activity are used in all of them to risk-stratify the lesion.

When you’re ready, here are 2 ways I can help you:

▶️ (FREE) Watch my YouTube videos

References:

Aksoy S, Abali H, Kilickap S, Harputluoglu H, Erman M. Metastatic granular cell tumor: a case report and review of the literature. Acta Oncol. 2006;45:91–4.
Salaouatchi M, T, De Breucker S, Rouvière H, et al. A Rare Case of a Metastatic Malignant Abrikossoff Tumor. Case Rep Oncol 2021:1868-1875.

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Handling Post-Operative Common Bile Duct Leaks

Fri, 26 Jan 2024 00:00:00 GMT

This middle-aged patient with diabetes mellitus underwent open cholecystectomy for an emphysematous gallbladder and presented 72-hours later with abdominal pain.

How would you treat this bile leak?

The most common recommendation is to perform a biliary sphincterotomy. Many experts also use a plastic stent alone or in combination with biliary sphincterotomy. Although it is commonly believed that placing a short-length stent is enough, we always take a good look at the type of leak, it’s size and location, and then decide on the length of the plastic stent. High volume leaks, or those associated with a big defect, tortuous bile duct or proximal location require a stent to be extending from proximal location, and extending across the papilla.

I encourage you to read the expert commentary by Interventional Endoscopist Thomas Kröner, MD from the USA.

Dr. Kröner:

The key to handling biliary leaks lies in thinking about the fact that bile will always flows through the path of least resistance. Bearing this in mind, we consider the “four pressure systems” that factor into a leak:

a) the biliary ductal system’s (with an intact ampulla is ~15mmHg),

b) the intra-abdominal (~6mmHg),

c) the bowel’s (~5mmHg), and

d) the outside world’s (technically 0mmHg).

This means that in a bile leak scenario we have “bilio-athmospheric” (between the bile duct and outside world through the drain), the “bilio-abdominal or peritionel” (between the bile ducts and the intraabdominal cavity through the leak), and “bilio-enteric” (between the bile duct and the bowel through the ampulla) pressure gradients.The objective of a leak treatment will be for the bilioenteric gradient to be favored by “equalizing” the pressures between the biliary ductal system and the bowel, which is performed doing a sphincterotomy +/- stenting, as suggested by our colleagues in the discussion. This new gradient or “assistance to the bilioenteric drainage” would in theory be more favorable than the “bilioabdominal” gradient.However, another important point is to never forget the importance of the role the external drain plays. If this drain is still wide-open and immediately adjacent to the leak, the most favorable gradient for bile flow could still be the “bilio-athmospheric” one, even after sphincterotomy and possible stenting. Therefore, careful retraction of the drain a good 4-6cm from the site of the leak is recommended. This will theoretically now favor the bilioenteric route once again.

How Does Clostridioides Difficile Lead to Massive Leukocytosis?

Fri, 26 Jan 2024 00:00:00 GMT

In clinical practice, all practicing endoscopists see and treat patients with C. difficile infection (CDI). One of the criteria for the severity of CDI is leukocytosis (1). Indeed, the leukocytosis in CDI can be so bad, that occasionally it’s called “leukemoid reaction”.

Let’s look at two classic clinical studies evaluating this issue. In a prospective study looking conditions associated with leukocytosis in hospitalized patients Wanahita et al found that of 53% of 400 inpatients with WBC counts of more than15,000 cells/mm3 had infection (2). Of these 207 patients, 97 (47%) had pneumonia, 60 (29%) had urinary tract infection, 34 (16%) had soft-tissue infection, and 34 (16%) had C. difficile infection. Importantly, CDI was present in 25% of patients with WBC counts of >30,000 cells/mm3 (2). In another prospective study looking into patients with unexplained leukocytosis, C. difficile infection was found to be the main culprit (3)

How does C. difficile cause leukocytosis?

During physiological circumstances, 95% of granulocytes reside in the bone marrow. Of the neutrophils in the blood half are circulating and half are marginated (4). Stress induces marinated granulocytes to enter the main circulation. Soon after toxin exposure in the colon, lots of neutrophils migrate there. Although a significant number comes from demarginalization, most originate from the bone marrow. How? We know that under basal conditions granulocyte colony-stimulating factor (G-CSF) is an essential regulator of neutrophil release from the bone marrow (5). In an elegant study looking into inpatients with CDI, asymptomatic carriage, or non-CDI diarrhea the investigators found that CDI lead to significant higher increase of cytokines (IL-1, IL-6, TNF-alpha) and G-CSF (granulocyte colony stimulating factor), as compared to non-CDI patients.

So, it’s this extra secretion of G-CSF that stimulates the bone marrow to release granulocytes and move them to the circulation, often causing a leukemoid reaction.

If you encounter patients with leukocytosis, think of CDI, and if they have CDI, let’s watch out closer, as these patients have a higher risk of complications.

References:

1. Zar FA, Bakkanagari SR, Moorthi KM, Davis MB. A comparison of vancomycin and metronidazole for the treatment of Clostridium difficile-associated diarrhea, stratified by disease severity. Clin Infect Dis. 2007 Aug 1;45(3):302-7. doi: 10.1086/519265. Epub 2007 Jun 19. PMID: 17599306.

2. Wanahita A, Goldsmith EA, Musher DM. Conditions associated with leukocytosis in a tertiary care hospital, with particular attention to the role of infection caused by clostridium difficile. Clin Infect Dis. 2002 Jun 15;34(12):1585-92. doi: 10.1086/340536. Epub 2002 May 23. PMID: 12032893.

3. Wanahita A, Goldsmith EA, Marino BJ, Musher DM. Clostridium difficile infection in patients with unexplained leukocytosis. Am J Med. 2003 Nov;115(7):543-6. doi: 10.1016/s0002-9343(03)00420-0. PMID: 14599633.

4. ATHENS JW, RAAB SO, HAAB OP, MAUER AM, ASHENBRUCKER H, CARTWRIGHT GE, WINTROBE MM. Leukokinetic studies. III. The distribution of granulocytes in the blood of normal subjects. J Clin Invest. 1961 Jan;40(1):159-64. doi: 10.1172/JCI104230. PMID: 13684959; PMCID: PMC290701.

5. Semerad CL, Liu F, Gregory AD, Stumpf K, Link DC. G-CSF is an essential regulator of neutrophil trafficking from the bone marrow to the blood. Immunity. 2002 Oct;17(4):413-23. doi: 10.1016/s1074-7613(02)00424-7. PMID: 12387736.

Kelly CP, Chen X, Williams D, Xu H, Cuddemi CA, Daugherty K, Barrett C, Miller M, Foussadier A, Lantz A, Banz A, Pollock NR. Host Immune Markers Distinguish Clostridioides difficile Infection From Asymptomatic Carriage and Non-C. difficile Diarrhea. Clin Infect Dis. 2020 Mar 3;70(6):1083-1093. doi: 10.1093/cid/ciz330. PMID: 31211839; PMCID: PMC82044

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Inflammatory Fibroid Polyps (IFP) or Vanek Tumors of the GI Tract

Fri, 26 Jan 2024 00:00:00 GMT

The images show Vanek tumors of the duodenum (left) and the stomach (right) (Stomach photo by @patholwaker)

Inflammatory fibroid polyps (IFP) or "Vanek tumors" are rare submucosal lesions arising from a reactive, benign granuloma-like process of the GI tract (1). This tumor is most commonly located in the stomach (70%), ileum (29%) and colon (6%) (2-4). Other locations such as esophagus, duodenum, ileum and gallbladder account each to 1% (1-3).

Patients with these tumors may present with abdominal pain, bleeding and obstructive signs. Diagnosis is made by histology. However, the endoscopic findings often show a submucosal lesion that is ulcerated or an elevated ulcer, such as these cases.

On histology the main characteristics are the presence of spindle cells, accompanied by vascular and fibroblastic proliferation and eosinophilic infiltration (2-4). Immunohistochemistry is important to distinguish IFP or Vanek tumors from GIST. Whereas GIST are CD-117 and DOG-1 positive, IFPs are CD-34 and Vimentin-positive, but NEGATIVE for CD-117, c-kit, DOG-1, S-100, desmin, ALK, and IgG4. Treatment generally consists of endoscopic or surgical resection of the lesion (5, 6).

Further reading:

Garmpis N, Damaskos C, Garmpi A, et al. Inflammatory Fibroid Polyp of the Gastrointestinal Tract: A Systematic Review for a Benign Tumor. In Vivo. 2021;35(1):81-93.
Kawai A, Matsumoto H, Haruma K, et al. Rare case of gastric inflammatory fibroid polyp located at the fornix of the stomach and mimicking gastric cancer: a case report. Surg Case Rep. 2020;6:292.

3. Wysocki AP, Taylor G, Windsor JA. Inflammatory fibroid polyps of the duodenum: a review of the literature. Dig Surg 2007;24:162-168.

4. Vanek J. Gastric submucosal granuloma with eosinophilic infiltration. Am J Pathol 1949;25:397–411.

5. Shimura T, Kataoka H, Sasaki M, et al. Rectal inflammatory fibroid polyp resected with endoscopic submucosal dissection. Intern Med 2008;47:2029–2031.

6. Akbulut S. Intussusception due to inflammatory fibroid polyp: a case report and comprehensive literature review. World J Gastro 2012;18:5745–5752.

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Introducing “This vs That”, a Training Atlas to Improve Your Endoscopic Diagnostic Skills

Fri, 26 Jan 2024 00:00:00 GMT

This vs That Digital Flashcards. Never be confused by similar GI diseases again! Flashcards for diseases that every endoscopist must know! Grab yours by clicking here.

What Is the Diagnosis of This Rectal Polyp?

This is no simple polyp. And too often, there is a tendency to instinctively diagnose a “lipoma”. It is not.

“This versus That”:

Whenever one sees a lesion like this (panel A) in the rectum or rectosigmoid area, it is a carcinoid (neuroendocrine tumor) until proven otherwise.

Note the round appearance and yellowish color with smooth mucosal pattern. Importantly, the pit pattern is Kudo type I, but the vascular pattern is Sano type 2, much different than that of a plain hyperplastic polyp. Why? Because carcinoid is a highly vascularized submucosal tumor.

Another possibility is a granular cell tumor (B), but these tumors are much less common than carcinoids.

Endoscopic ultrasound (EUS) may assist in evaluating the lesion.

Another great trick is injecting the submucosa. The lesion will not rise well. This is an important diagnostic step, as it will differentiate between mucosal and submucosal lesions.

In addition, submucosal injection will assist during the subsequent endoscopic resection of the lesion using either EMR or ESD techniques.

Never try to resect these lesions using plain snare polypectomy, as this technique often results in incomplete resection and stress for the patient and endoscopist, as the patient needs follow-up with resection of a scar with tumor remnant.

Get all 20 This vs That Flashcards by clicking here

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Is Endoscopic Submucosal Dissection (ESD) Ready to Enter Center-Stage for the Resection of Large Colorectal Polyps?

Fri, 26 Jan 2024 00:00:00 GMT

In this article, we'll dive into:

The game-changing results of a massive Japanese study involving over 1,800 colorectal lesions
Why ESD has been slow to catch on globally, despite its advantages
The impressive long-term survival rates that might make you rethink your approach to large polyps
How this technique could dramatically reduce the need for invasive surgeries

Endoscopic submucosal dissection (ESD) is a treatment for superficial tumors, pre-cancerous, and early cancerous lesions in the gaintestinal (GI) tract [1, 2]. This endoscopically-guided minimal invasive, surgical technique was first developed in Japan back in the late 1990s [3, 4]. However, the initial concept of endoscopic removal of colorectal polyps dates back to 1971 when Dehyle et al. reported on using a novel diathermy snare [5]. Soon thereafter, Dehyle et al reported on the concept of resection of sessile colon polyps after creating a submucosal cushion with injection [6]. The concept of advanced endoscopic mucosal resection (EMR) was born. Interestingly, the reason for introducing injection-assisted polypectomy was to prevent colon perforations, which were happening quite often at that time using standard snare resection techniques [6]. Thus, a concept introduced to prevent colon perforation became a method to increase the chances of in-toto and R0 resection. Later on, submucosal injection became the basis of EMR, ESD, tunneling and third-space techniques.

Despite the advantages of ESD over other resection techniques for early colon neoplasia, this technique has been slow to enter clinical practice in many parts of the world. Whereas technical factors and acquisition of skills may be one reason for this, a big argument still hindering its more widespread acceptance was the lack of large, prospective observational outcome studies.

The solution to this knowledge gap is provided now by the Colorectal ESD Activation Team of Japan (CREATE-J), consisting of 20 academic or tertiary institutions in Japan [7]. CREATE-J designed a prospective, large-scale, multicenter cohort trial of colorectal ESD to address this aspect in an elegant and overwhelming study, enrolling 1740 consecutive patients 1814 colorectal epithelial neoplasms ≥ 20 mm who underwent ESD between February 2013 and January 2015. The patients were followed intensively during a 5-year follow-up. In the 1814 cases, the mean tumor diameter was 32.4 mm, and more than half of the lesions (55.5%) were located in the right colon. Most tumors (n=1612), 88.9% were LST. En bloc resection was achieved in 1759 (97.0%) lesions, whereas piecemeal resection was required in 35 (1.9 %) lesions. Only twenty (1.1%) ESD procedures were discontinued due to technical difficulties or severe intraoperative adverse events. The 5-year OS, DSS, and intestinal preservation rates were 93.6%, 99.6%, and 88.6%, respectively. The authors concluded that a favorable long-term prognosis indicates that ESD can be the standard treatment for large colorectal epithelial neoplasms (7).

In summary, this seminal study has shown that ESD is safe and efficient to resect advanced colonic neoplastic lesions, with low complication rates and excellent long-term outcomes. The authors placed the finger in the wound and showed us that ESD is should probably the standard of care for dealing with larger colorectal lesions.

How does this study affect our practice?

It is evident that ESD is an efficient technique to achieve complete resection of large colorectal lesions. Second, the favorable results a very large, prospective follow-up study now underscore the clinical efficacy of this resection method. Based on this findings, it is our opinion that ESD or hybrid ESD-EMR should be considered the key standard for resection of larger colorectal lesions. Ideally, a prospective, randomized study comparing ESD to piecemeal-EMR should be performed.

Happy to take questions on this study in the comments section below

References:

1. Saito Y, Fujii T, Kondo H, et al. Endoscopic treatment for laterally spreading tumors in the colon. Endoscopy. 2001;33(8):682–686.

2. Bhatt A, Abe S, Kumaravel A, Vargo J, Saito Y. Indications and Techniques for Endoscopic Submucosal Dissection. Am J Gastroenterol. 2015;110:784-91.

3. Lee EJ, Lee JB, Lee SH, et al. Endoscopic submucosal dissection for colorectal tumors--1,000 colorectal ESD cases: one specialized institute's experiences. Surg Endosc 2013;27:31-9.

4. Yamada M, Saito Y, Takamaru H, et al. Long-term clinical outcomes of endoscopic submucosal dissection for colorectal neoplasms in 423 cases: a retrospective study. Endoscopy 2017;49:233-242.

5. Deyhle P, Seuberth K, Jenny S et al. Endoscopic polypectomy in the proximal colon. Endoscopy 1971; 3: 103 – 105

6. Dehyle P, Largiadér F, Jenny S, Fumagalli I. A method for endoscopic electroresection of sessile colonic polyps. Endoscopy 1973;5:38-40.

7. Ohata K, Kobayashi N, Sakai E, et al. Long-Term Outcomes After Endoscopic Submucosal Dissection for Large Colorectal Epithelial Neoplasms: A Prospective, Multicenter, Cohort Trial from Japan. Gastroenterology. 2022 Jul 8:S0016-5085(22)00751-X. doi: 10.1053/j.gastro.2022.07.002. Epub ahead of print. PMID: 35810779.

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Journal Club

Fri, 26 Jan 2024 00:00:00 GMT

Paper discussion: Endoscopic mucosal resection combined with hybrid argon plasma coagulation to prevent recurrence of large nonpedunculated colorectal polyps (Motchum et al GIE 2022) https://giejournal.org/retrieve/pii/S0016510722017692)

In contrast to Japan, Korea and other Eastern countries, endoscopic mucosal dissection (EMR) is considered to be the standard of care for resecting colorectal non-polypoid lesions larger than 20 mm in most Western countries. Unfortunately, EMR, especially piecemal-EMR, is associated with high post-resection recurrence rates of up to 21% (1-4). Argon plasma coagulation (APC) has been shown to reduce recurrence rates after piecemeal EMR. A novel ablative method, hybrid APC (h-APC) encompasses submucosal injection and application of APC. The hope being that submucosal injection is going to prevent perforation when applying APC.

In a two-center, prospective case series Motchum et al enrolled 84 patients with 101 non-polypoid lesions larger than 20 mm during a 2-year period (5). The lesions measuring a median of 30 mm (range 20 to 60 mm) were resected using piecemal EMR and afterwards treated with h-APC. Patients were scheduled for follow-up colonoscopy at 4-6 months after the intervention. The authors found that the recurrence rate was 2.2%, with 13% complications, of which almost a third were severe (n = 4 patients, 3.6%) (5). An additional patient had a perforation during index EMR and was excluded from the study.

This data is quite encouraging and the efficacy almost matches that of endoscopic submucosal dissection. Although one could be encouraged to add h-APC to the armamentarium of techniques to decrease post-EMR polyp recurrence, it is important to recognize that the study has several potential drawbacks.

First it was non-controlled, non-randomized. Ideally, this new method should have been compared to an established technique such as STSC (6).
Second, the study was non-standardized. It was left at the discretion of the endoscopist how to apply h-APC. Some endoscopists applied APC at the borders and base and others just at the borders. The definition of border was also unclear, as it was defined an area extending 3 to 5 mm beyond the resection line. Furthermore, a total of seven different snares from three different manufacturers were used, ranging from 10 mm to 27 mm in diameter.
Third, lots of patients were lost to follow-up (n=7).
Fourth, the settings (0,8 liters flow, 40 W, effect 2) appeared somewhat “stiff”, as only this one setting was used for right and left colon lesions. In the study there were more than 85% of lesions coming from the proximal colon. But what about this large laterally-spreading tumors located in the distal colon, and especially the rectum. Do these settings suffice to ablate the remaining tumoral tissue?
And fifth, on follow-up only 74 out of 84 patients underwent biopsy of the resection site. This may overestimate the “efficacy” rate of h-APC.

In sum, this open-label, two-center case series showed that h-APC is feasible and appears to have promising efficacy in decreasing polyp resection after piecemeal EMR. But this study also underscores the fact that traditional piecemeal EMR is an insufficient technique to completely resect colorectal polyps larger than 20 mm. Otherwise we would not need to continue evaluating ablative techniques to deal with neoplastic tissue left-overs (R1 or incomplete resection).

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Liver Tests and Ratios – a Practical Summary

Fri, 26 Jan 2024 00:00:00 GMT

Knowledge of liver tests are essential for the daily practice of gastroenterology and endoscopy. The response of the liver to various types of injury varies and is often reflected by differentiated elevation of different liver tests.

Classic examples are a ratio of 2:1 of AST:ALT in alcohol-induced liver injury, however, with AST rarely surpassing 50 IU/L, unless there is an additional insult, such as acetaminophen.

Also, often we are called to the intensive care unit to evaluate patients with massive elevations of transaminases, often in the 10,000s. In these situations think ischemic hepatitis! This is usually confirmed by a marked elevation of LDH.

One of the most common misdiagnosis in the emergency room department in patient with abdominal pain and elevated liver tests is “hepatitis”, when indeed a patient has choledocolithiasis. In this scenario, the ALT can elevate several-fold, of course, wrongly mimicking “hepatitis”.

I hope this summary of liver tests, rations and some other liver-related values is useful for your practice. Of course, this list just represent a broad collection of data, based on clinical experience and literature review, especially for GI board preparation and does not constitute a certified guideline. Please feel free to add, correct and comment as needed. I am happy to receive feedback to continue expanding this list.

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LAMS vs Plastic Stents in Infected Pancreatic Necrosis

Fri, 26 Jan 2024 00:00:00 GMT

Lumen-apposing metal stents (LAMS) have larger lumen and are supposed to drain better. In this comparative study, the need for further necrosectomy was the same for LAMS or plastic stents. It was not a head-to-head comparative study.

The authors compared the results from the TENSION trial (plastic stents only) versus an ongoing LAMS trial. Nonetheless, the data seems clinically significant and the data appears compelling.

It is time to step back and realize that LAMS are not a panacea for complex pancreatic necrosis and that these collections mandate a continued and close observation and intervention approach.

When dealing with complex pancreatic necrosis, there is no time to place a stent and then "sit back and relax".

On: Boxhoorn L, et al. Comparison of lumen-apposing metal stents versus double-pigtail plastic stents for infected necrotising pancreatitis. Gut. 2022 Jun 14:gutjnl-2021-325632. doi: 10.1136/gutjnl-2021-325632. Epub ahead of print.

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Master the Art of Endoscopy Tattoos

Fri, 26 Jan 2024 00:00:00 GMT

�🌟 Welcome to the Practicing Endoscopist Newsletter!

In this edition, we're sharing valuable insights from our latest Five-Minute Friday’s series, where we reveal the secret to perfecting the India ink tattooing technique in endoscopy.

Learn how to create flawless India ink tattoos for accurate lesion identification and improved patient outcomes.

💡 5 Key Tips for the Perfect India Ink Tattoo

1. Choose the right needle and prime it with normal saline. The normal saline will fill-in the dead space within the needle channel and is the essential part of this technique.

2. Advance needle through the scope and choose a spot for injection, usually 3 cm proximal to the tumor. NEVER inject below a polyp as ink will create a fibrotic reaction and impede proper removal of the polyp.

The next figure shows an ideal injection to mark the location of a small bowel gastrointestinal tumor.

3. Placement of needle in relation to mucosa. Opt for an oblique, if possible, almost tangential position rather than a squared angle position one for more accurate submucosal tattooing. Injecting into the peritoneum will result in spillage, irritation and creation of reactive granulomas and nodules, which may mimic infection, tumor or endometriosis.

4. Create a submucosal cushion with the saline inside of the needle. The India ink syringe is connected to the needle and injected slowly. This pushes the saline out of the needle, to form a cushion before the ink arrives, to prevent intraperitoneal injection and ensure a localized tattoo.

5. Use the right amount of ink. Typically, half to one milliliters of India ink is sufficient to create a clear and lasting tattoo.

Additional reading:

Colonoscopic Tattoo Dye Spillage Mimics Endometriosis on Laparoscopy - Journal of Minimally Invasive Gynecology (jmig.org)

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Mastering the Use of Hemoclips (Through-The-Scope-Clips)

Fri, 26 Jan 2024 00:00:00 GMT

Hemoclips, originally designed for hemostasis, are versatile tools that have revolutionized various endoscopic procedures.

1. Understanding Hemoclips

Hemoclips are multifaceted tools that currently are used beyond their original purpose of hemostasis, and therefore we will refer to them as “clips”.These clips are now employed for closing perforations, post-resectiondefects, marking, and attaching devices such as stents and feeding tubes. For instance, in a procedure involving a gastric, esophageal or colon perforation, clips can effectively seal the defect, preventing further complications. Figure 1 shows several clinical applications of clips. A. Duodenal ulcer with visible vessel. B. Clip being pushed towards the lesion. C. Released clip closing the duodenal ulcer. D. Clipped Mallory Weiss tear. E. Large post-resection defect in the cecum. F. Complete prophylactic closure of the defect. G. Perforation of the cecum during endoscopic resection of fibrotic polyp. H. Complete closure of the defect with clips.

Hemoclips are indeed a testament to medical innovation.

2. The Anatomy and Deployment Clips

Understanding the anatomy and mechanisms of action of clips is crucial to their effective use.

Clips consist of stem with two arms with distal teeth. The arms can vary in shape and number (yellow arrows). The length of the shaft or stem (green arrow) holding the arms can also differ, impacting their use in tight areas like small bowel strictures or esophageal stenosis. For example, a longer shaft in a small bowel stricture or esophagus could exacerbate the condition, as it would be rubbing the mucosa on the opposite site. Figure 1D shows a clip with “short” stem, and still, the stem’s end may still rub the opposite mucosa. A clip with long stem would have been inappropriate in this situation. Therefore, understanding the clip's anatomy can guide its appropriate selection and use.

3. Advancing and Applying Clips

The advancement and application of through-the-scope clips require precision and care.

When first advancing the clip into the working channel of the scope, it's crucial to hold close to the tip to avoid bending the arm. Once the clip has been pushed through the working channel and is at the tip of the scope, it should be gently pushed out, opened, and pulled back towards the scope (Figure 1B). For instance, when addressing a bleeding lesion, the clip should be open and advanced towards the lesion by moving the endoscope. At the final moment, once the clip is close to the target vessel or defect to be closed, the clip should be pushed out with the hand (Figure 1B), then closed and released by the assistant (Figure 1C).

Proper knowledge, handling and application of clips can significantly improve patient outcomes.

Remember, the mastery of clips lies in understanding their anatomy, their mechanics, knowing how to deploy them, and applying them with precision. With practice, you can harness the full potential of these versatile tools to improve patient care.

Mechanism of action of PCABs (Potasium-Competitive Acid Blockers)

Fri, 26 Jan 2024 00:00:00 GMT

Background:

Conventional proton pump inhibitors (PPIs) are the main first-line therapy to treat acid-related disorders (1). However, they have a number of limitations including slow onset of action, influence by cytochrome P450 polymorphisms, unsatisfactory effects at night, and instability in acidic conditions (1). Potassium-competitive acid blockers (P-CABs) induce a rapid, long-lasting, and reversible inhibition of the gastric hydrogen potassium ATPase, the proton pump of the stomach (1). These agents have a faster onset of action than PPIs, and they have a more sustained action in inhibiting acid secretion. Thus, they represent a new option to treat acid-related disorders. Herby we summarize the mechanism of action of PCABs.

Key Aspects:

- Proton pumps (H1, K1-ATPase) are stored in tubulovesicles in the cytoplasm of parietal cells and are kept in an inactive state.

- Activation of proton pumps occurs after their insertion into the extracytoplasmic secretory canalicular membrane at the luminal border.

- PPIs bind to cysteines located on the exposed site of active proton pumps, blocking exchange of hydrogen and potassium ions (yellow arrow).

- However, PPIs require an acidic environment for activation.

- PCABs bind reversibly to K+ ions and block the H+, K+ ATPase enzyme, thus preventing acid production. PCABs block the access of potassium ions to the potassium-binding site of the pump.

- Importantly, PCAB (Potassium Competitive Acid Blocker) accumulation and binding are NOT pH-dependent, allowing PCABs to bind to both inactive and active proton pumps (red arrow).

Ref:

1. Oshima T, Miwa H. Potent Potassium-competitive Acid Blockers: A New Era for the Treatment of Acid-related Diseases. J Neurogastroenterol Motil. 2018 Jul 30;24(3):334-344.

2. Laine L, et al. Pharmacodynamics and Pharmacokinetics of the Potassium-Competitive Acid Blocker Vonoprazan and the Proton Pump Inhibitor Lansoprazole in US Subjects. Am J Gastroenterol;2022:117:1158-1161

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Mid-GI bleeding of Obscure Cause due to a Cavernous Lymphangioma

Fri, 26 Jan 2024 00:00:00 GMT

Honorary Professor, Universidad de La República, Montevideo, Uruguay

Visiting Professor, Faculty of Medicine, University of Belgrade, Serbia

Case presentation:

A 32-year-old patient presented with melena and drop in hemoglobin (9 gr/dl). During double balloon enteroscopy a 3 cm yellowish, polypoid lesion with a depressed center was found in the proximal jejunum.

An India Ink tattoo mark was placed to facilitate its recognition during subsequent operative segmental small bowel resection.

Discussion:

Cavernous lymphangiomas are uncommon benign tumors found intra-abdominally, close to the mesentery or in the small bowel.

Small bowel lymphangiomas can cause gross or occult (obscure) gastrointestinal hemorrhage, anemia, abdominal pain, and/or small bowel obstruction. Endoscopists should be aware of this rare tumor and its ileus due to endoscopic features. Cavernous lymphangiomas may endoscopically mimic neuroendocrine tumors. The ideal treatment is complete resection, as incomplete excision may result in recurrence. There are reports on endoscopic therapy using argon plasma coagulation, injection of sclerosants and endoscopic resection. However, those endoscopic options should be mainly used in small lesions, for palliative purposes or in circumstances when a surgical intervention is not feasible.

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Multiple Polypoid Sigmoid Colon Lesions

Fri, 26 Jan 2024 00:00:00 GMT

An elderly patient presented with abdominal pain, diarrhea and fever. A colonoscopy was performed about 10 days after the initial symptoms had improved. At that point the main indication for colonoscopy was the presence of mild hematochezia. What is the diagnosis?

When discovering polypoid lesions in the colon, the endoscopist should characterize those. How many polypoid lesions are present? What is the colonic distribution? How does the mucosa appear? Do the polypoid lesions express a “pit pattern”? What is the color of the lesions? Are there any associated findings? What is the consistency of the lesions?

In this case there were about 20 to 25 polypoid lesions ranging from 10 to 30 mm in size located in the sigmoid colon. The mucosa overlying the lesion was normal without any specific pit pattern or ulcerations. However, some areas of erythema were present on few of them. The polypoid lesions were soft and appeared as “blebs”. There were no other associated mucosal findings.

Answer: Pneumatosis coli

This is the characteristic endoscopic and descriptive appearance of multiple gaseous cysts inside the bowel wall or pneumatosis coli, also known as pneumatosis cystoides intestinalis or pneumatosis intestinalis, whereas the latter mainly refers to small bowel involvement.

Pneumatosis can present in children, usually in premature infants, as a consequence of the life-threatening condition necrotizing enterocolitis. In adults there are life-threatening and “benign” forms. Life-threatening pneumatosis can originate from ischemia, bowel obstruction, enterocolitis, toxic megacolon and collagen vascular diseases (1). Benign etiologies include COPD, transient ischemic colitis, gastroenteritis, collagen vascular diseases, acquired immunodeficiency syndrome and organ transplantation. Importantly, the benignity of the pneumatosis does mainly depend on the clinical presentation of the patient, as many of the etiologies are not certainly “benign”.

As you noticed, there are lots of potential etiologies, indicating that the mechanism of injury must be different. These mechanism for bleb formation include: a) pulmonary disease leading to pneumomediastinum with gas travelling or tracking through the peri- mesenteric vessels to the gut, b) bacterial gas production (during gastroenteritis), c) disarrangement of the microbioma with dysbiosis and promotion of gas-forming organisms, d) local mucosal damage due to toxins, drugs and hormones, and e) ischemia with gas entrapment following regeneration of the epithelium and submucosa.

Histology is usually not needed for the diagnosis. The outcome of pneumatosis cystoides intestinalis depends on the primary diagnosis. In the present case, the triggering event (transient ischemic colitis or gastroenteritis) had already subsided and the patient was doing well. Therefore, no additional endoscopic or medical therapy was instituted.

References:

1. Ho LM, Paulson EK, Thompson WM. Pneumatosis intestinalis in the adult: benign to life-threatening causes. (2007) AJR. American journal of roentgenology. 188 (6): 1604-13. doi:10.2214/AJR.06.1309

2. Jacob T, Paracha M, Penna M, et al. Pneumatosis coli mimicking colorectal cancer. Case Rep Surg. 2014;2014:428989. doi: 10.1155/2014/428989. Epub 2014 Oct 7. PMID: 25400972; PMCID: PMC4220578.

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New Guidelines From the ASGE for Diagnosis and Management of Eosinophilic Esophagitis

Fri, 26 Jan 2024 00:00:00 GMT

Question:

A 25-year- old patient presents with acute meat impaction. After removing the food bolus, would you biopsy to rule out eosinophilic esophagitis?

The new guidelines for the diagnosis and management for eosinophilic esophagitis are out. Let’s see what they say. I have prepared a list of key takeaways.

Answer to the above question:

Yes, biopsies during index endoscopy for removal of food impaction are recommended. Of course, removing a food impaction may be challenging and often, this procedure is done in the middle of the night and, in also unsedated patients. Thus, if the patient is feeling uncomfortable and has nausea and retching, prolonging the procedure to obtain enough biopsies may not be wise. However, a follow-up procedure to obtain biopsies is indicated.

Key Takeaways:

Bx at index EGD (even if the EGD was done for food impaction) (see my comment)
Obtain at least 6 biopsy samples, from the distal and mid/proximal esophagus
Even if esophagus appears quite normal, if suspicious if EoE, biopsies are mandatory
Response to therapy is based on endoscopy, thus repeated EGD is important, especially when adjusting medications or diet
Dilation is important in the presence of dysphagia
When dilating, the endpoints are mucosal laceration or disruption or reaching the target diameter
Gradual and repeated dilations may be necessary to reach a target diameter of 16m.

For more information: Aceves S, et al.Endoscopic approach to eosinophilic esophagitis: American Society for Gastrointestinal Endoscopy Consensus Conference. Gastrointest Endosc 2022:96;576-592

https://www.giejournal.org/action/showPdf?pii=S0016-5107%2822%2901725-4

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Optimal Use of Variable Stiffness Colonoscopes

Fri, 26 Jan 2024 00:00:00 GMT

What is the optimal way to use variable stiffness colonoscopes in difficult colonoscopies? Have you had any adverse events?

Variable stiffness is a wonderful addition to colonoscopes, especially pediatric colonoscopes, which I use for most colonoscopies in the hospital where I have these scopes. At my other hospital we have a different scope brand (Fujifilm), which are also wonderful scopes. Variable stiffness is especially useful in floppy colons, elongated sigmoid colon and long colons that make turns in the pelvis. I advise to use variable stiffness mode in a “dynamic” fashion, meaning that once you feel there is some “floppyness” or you are about to enter the transverse coming from the descending colon, you apply more stiffness. Once you have mastered the area, it’s advisable to remove the stiffness and allow the colon to move into your scope (to “accordion”) into the scope. Do not apply variable stiffness while the scope is torqued or in alpha or reverse alpha loop, as this may increase the chances of laceration, but mainly may impede you advancing as you “lock” your scope in a twisted position. Also, do not start insertion in the rectum with a stiffened scope. The scope should be floppy when it is pushed from rectum to recto-sigmoid and sigmoid colon. I also like to use variable stiffness when located at the hepatic flexure. That “final” stiffening of the scope “straightens” the transverse and splenic flexure, adding the last needed push for the scope tip to conquer the hepatic flexure and reach the cecum. Once in the cecum I take the stiffness off and continue travel to the ileum.

What do you think of the Long Term POEM success?

There is little long-term data. So far, we know that a significant amount of patients develop severe reflux esophagitis and stricturing esophageal disease. I still think that POEM is a good alternative for patients who are poor surgical candidates, but am still not 100% convinced that it's the only therapy for achalasia, especially with much more long-term data from surgical interventions such as Heller myotomy.

Peroral endoscopic myotomy (POEM). POEM is one the most significant progresses in interventional gastrointestinal endoscopy. The elemental concept of POEM is the performance of endoscopy between the muscle layer and the submucosa. As endoscopy is not performed endoluminally nor in the Peritoneum, pleural or mediastinal spaces it is properly called “third-space endoscopy” or submucosal tunneling pro- cedure. The figure shows the essential steps for POEM, including proper creation of a submucosal cushion, incision of the mucosa and submu- cosa, endoscopic dissection and tunneling through the submucosal layer and final endoscopic myotomy. As expected submucosal tunneling techniques are also useful to perform resection of submucosal and muscular tumors per-oral endoscpic tumor excision (POET) and submucosal tunneling endoscopic resection (STER).

Ref.: 1. Inoue and Maydeo. Endoscopy 2019; 51: 1010–1012

What are the Palisade Veins?

Fri, 26 Jan 2024 00:00:00 GMT

The palisade vessels are tiny capillaries (or veins) located in the distal submucosa of the esophagus and are quite important to distinguish esophagus from stomach. Whereas in most countries endoscopists use the beginning of the proximal gastric folds to determine the location of the gastopesophageal junction, in Japan and other astern countries, but also many Western experts, use the palisade vessels as a marker of the GEJ. I first learned about the palisade veins about 10 years after finishing my gastroenterology training. The gastroesophageal junction is such an interesting transition zone, which continues to surpise us. Although the palisade veins are mostly known to be helpful for defining the GEJ, there are additional pathophysiological aspects that make this vessels quite important. Let’s ask Prof. Roy Soetikno explain us another pearl about the palisade vessels

Prof. Soetikno:

Let me try to answer. The palisade vessels are the linear vessels at the (esophago-gastric) EG junction. These vessels are in the mucosa and most importantly they give rise to esophageal varices.

These vessels are in the mucosa to provide continuous circulation of that area. This is because the diaphragm would intermittently pinch the m. propria during expiration and detour pathways are needed to ensure circulation.

Normally, the lower part of the palisade vessels drain caudad and the rest cephalad. But with portal hypertension the flow becomes caudad throughout. The diameter of the vessels will increase as the pressure goes up. With time, a bunch of dilated vessels become clustered and give rise to a column of varix.

At higher Portal V - HV pressure gradient, bleeding occurs as one of the vessels burst.

The point of bursting is usually within 3 cm of the SCJ where there is a weak point in the dilated palisade vessels.

Thus banding should be done in that area only. The column of varices in the mid and sometimes proximal esophagus are in the submuosa layers as they are not from the palisade vessels. They usually don’t bleed. Banding them actually may cause iatrogenic bleeding as it may be difficult to cause a complete occlusion.

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Superior Mesenteric Artery Syndrome

Fri, 26 Jan 2024 00:00:00 GMT

Superior mesenteric artery syndrome (SMAS) depicts the rare phenomena of the third (or horizontal) portion of the duodenum being compressed between the superior mesenteric artery (SMA) and abdominal aorta (AA), resulting in proximal small bowel obstruction (1-4). SMAS was first described as a case report by Carl von Rokitansky in 1842, and later expanded upon–with regards to pathophysiology and diagnostic findings–by David Wilkie in 1927. SMAS has also been referred to as Wilkie’s syndrome or aorto-mesenteric compass syndrome (1,3,4).

Typically, a mesenteric fat pad separates the SMA and AA thereby preventing constriction of the third portion of the duodenum by these structures. Thus, factors which impact the anatomical balance of these structures lead to a decrease in SMA-AA angle and distance–ultimately allowing for duodenal compression. One example would be significant weight loss as this decreases the proportion of mesenteric fat present. Numerous etiologies can cause this such as: hypermetabolic state (e.g., drug-induced, burn-related trauma), diet disorders (e.g., anorexia nervosa), malabsorptive disease (e.g., celiac disease, crohn’s disease), or cachexia-inducing conditions (e.g., malignancy, tuberculosis, AIDS) (1-4).

There are conflicting reports with regards to an accurate prevalence of SMAS; however, the reported incidence has been approximated, via radiographic studies, to 0.013%-0.780% (1), with other reports narrowing this range to 0.1%-0.3% (3). A recent SMAS review by Oka et al (2023) reported a median age of 23 years old with an interquartile range of 16-39 but did acknowledge the recent literature reporting an increasing number of SMAS cases in the elderly. As etiology of SMAS can vary greatly between cases, so too can the affected age (1). In terms of gender, SMAS has been shown to affect females more than males with a ratio of 3:2 (1,3).

In terms of clinical presentation, signs/symptoms of SMAS are often vague and/or non-specific and can be either acute or chronic. Symptoms can include nausea, vomiting, epi-gastric pain, abdominal distention, weight loss, early satiety, post-prandial discomfort. Of note, both the epigastric pain and post-prandial discomfort are likely to be position dependent where-in a supine position aggravates these symptoms while a left lateral decubitus position alleviates these symptoms. SMAS can have an acute or chronic presentation, presenting with obstructive features including nausea/vomiting, poor oral intake, gastric dilation, and weight loss. Since SMAS is highly variable in its presentation, it can easily be overlooked often leading to delays in diagnosis with potentially fatal complications. A high index of clinical suspicion is needed to ensure proper identification/diagnosis (1-4). Gastrointestinal mucosal injury/damage has been reported as a common complication with a reported rate of 25-59%, often secondary to several mechanisms (e.g., retained or refluxed peptic and/or bile acid, increased intraluminal pressure) (1,3). If not treated in a proper timeframe or manner, this may lead to sequalae such as pneumoperitoneum, emphysema, portal venous gas, or necrosis. Less dire complications such as elevations in pancreatic enzymes and/or acute pancreatitis can also occur (1).

A diagnosis of SMAS consists of both clinical symptomatology and associated imaging findings of duodenal obstruction. Multiple modalities can be utilized to assess for SMAS (e.g., CT, US, MRI, EUS); however, the most beneficial modality would be CT imaging as it can not only confirm SMAS in multiple views (Figure 1), but also provide supporting data such as SMA-AA angle/distance and/or identify the aforementioned complications of SMAS. On CT imaging, the standard SMA-AA angle, distance typically ranges from 38-65 degrees and 10-33 mm, respectively (1,3). Unal et al (2005) determined that the cutoff values of 22 degrees (SMA-AA angle) and 8 mm (SMA-AA distance) for SMAS had 42.8% sensitivity/ 100% specificity and 100% sensitivity/100% specificity–respectively. Abdominal US has been shown to be an effective modality in diagnosing SMAS. In recent literature, the use of EUS has become more commonplace as it can not only confirm duodenal compression but also now measure both SMA-AA angle and distance (1).

It is worthwhile to mention that SMAS can, at times, present alongside additional vascular compression syndromes. Most commonly, this being nutcracker syndrome (left renal vein compression between the SMA and AA) based on the anatomical location (Figure 2). Another example would be celiac axis compression syndrome which occurs due to compression of the celiac artery by the median arcuate ligament (1).

Besides the initial clinical stabilization, fluid resuscitation and electrolyte repletion, the treatment of SMAS relies chiefly on nutritional support. Often patients are not able to tolerate oral diet, so alternate methods of delivery of nutrition into the gut are utilized which may include placement of a naso-jejunal feeding tube. Conservative approaches using patient positioning (e.g. left lateral decubitus) have been suggested, however, have limited clinical utility and often do not translate into clinical benefit. Unfortunately, many will fail conservative therapy and require more aggressive therapy along the lines of surgical or other alternative invasive intervention (1-4).

Previously, traditional open bypass surgery was done but with the advent of minimally invasive techniques, laparoscopic duodenojejunostomy is the current preferred procedure for SMAS due to its high success rate and improved overall outcomes (3,4). In the recent literature, endoscopic ultrasound-guided (EUS) gastroenterostomy or more specifically EUS gastrojejunostomy has been done for SMAS treatment with positive results–showcasing the ever-expanding application of EUS based procedures (1).

In summary, prompt and accurate diagnosis remains a challenge owing to the non-specific nature of this condition, thus requiring a high index of clinical suspicion. Abdominal cross-sectional imaging remains the gold standard for diagnosis currently. Due to advancement in minimally invasive techniques, endoscopists have an even greater degree of impact in management of patients with this syndrome and continue to serve as a vital part of the care management team.

References:

Oka A, Awoniyi M, Hasegawa N, et al. Superior mesenteric artery syndrome: Diagnosis and management. World J Clin Cases. 2023;11(15):3369-3384.
Sinagra E, Raimondo D, Albano D, et al. Superior Mesenteric Artery Syndrome: Clinical, Endoscopic, and Radiological Findings. Gastroenterol Res Pract. 2018;2018:1937416. Published 2018 Aug 27.
Van Horne N, Jackson JP. Superior Mesenteric Artery Syndrome. [Updated 2023 Jul 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482209/
Sabry A, Shaalan R, Kahlin C, Elhoofy A. Superior Mesenteric Artery Syndrome Managed with Laparoscopic Duodenojejunostomy. Minim Invasive Surg. 2022;2022:4607440. Published 2022 Aug 3.
Unal B, Aktaş A, Kemal G, et al. Superior mesenteric artery syndrome: CT and ultrasonography findings. Diagn Interv Radiol. 2005;11(2):90-95.

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The ESD-EMR Hybrid or Pre-Cutting EMR Endoscopic Resection Technique

Fri, 26 Jan 2024 00:00:00 GMT

Traditionally, flat colorectal non-polypoid lesions have been resected using endoic submucosal dissection (ESD), endoscopic mucosal resection (EMR) or piecemeal EMR techniques. In addition, smaller, flat serrated lesions may be hard to catch and resect using polypectomy snares. These lesions have a slippery surface and often it is frustrating to see how the snare only catches a piece of the polyp or completely slips off.

Here we show you a technique to improve complete entrapment and resection colorectal, esophageal and stomach lesions. This technique of incision and resection is a hybrid ESD-EMR technique. Some experts also refer to it “precutting” EMR, as an incision is made around the lesion before the final resection takes places. This incision creates a groove where the snare can be perfectly placed for subsequent EMR. However, often, in addition to just incising around the lesion, we also perform submucosal dissection to decrease the size of the base that needs to be ensnared (see lipoma case, figure 2)

Our technique involves using a) submucosal injection, and b) just a snare. After we create the submucosal cushion (Fig. 1a and Fig 1b) we make a circumferential incision around the lesion just using the tip of the snare (Fig. 1 c and Fig 1 d). Usually, a 1-2 mm snare tip exposure is sufficient to achieve nice incision and submucosal dissection (Fig 1 c). Once the entire lesion has been circumferentially incised (Fig. 1 e), the snare is placed around the lesion and resection using EMR is achieved (Fig. 1 e and Fig 1f). This technique improves the R0 resection of the lateral aspect of the polyp. And if sufficient submucosal cushion has been injected, a nice R0 vertical resection is achieved as well. This technique is also useful to resect larger lesions, including lipomas (Figure 2), granular cell tumors of the esophagus, and small gastric mucosal neoplasia and submucosal lesions, such as ectopic pancreas or GIST. Very importantly, if the lesion is situated in a hard location, or you cannot see or control the entire circumferential incision, we proceed to use additional equipment such as IT-knife, which has a ceramic tip that prevents the transmission of energy beyond the tip of the knife and thus, there is less chances of perforation. In sum, here we show you a technique of advanced endoscopic resection or hybrid ESD-EMR technique using a simple needle and a snare.

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The MIRacle Sign

Fri, 26 Jan 2024 00:00:00 GMT

Adil S. Mir MD FACP; Klaus Mönkemüller MD, PhD, FASGE, FJGES

Virginia Tech Carilion School of Medicine, Roanoke, VA, USA

Upper gastrointestinal (GI) endoscopy or esophagogastroduodenoscopy (EGD) continues to be an extremely useful diagnostic tool for perspicuous macroscopic findings. Besides, attention to detail remains of utmost significance in deciphering clinical clues to rather uncommon pathophysiology. Herein, we describe an observation and endoscopically inducible sign which could be a potential clue to diagnose borderline or overt gut ischemia.

We describe the case of an 81-year-old male patient with pertinent history of multiple medical comorbidities including gastroesophageal reflux disease, coronary artery disease, hypertension, diabetes mellitus, hyperlipidemia, congestive heart failure and history of deep venous thrombosis. Pertinent surgical history included the history of gastric volvulus requiring laparoscopic para-esophageal hernia repair and percutaneous endoscopic gastro-jejunostomy (PEG-J) tube placement about 1 month prior. The patient was admitted for the management of generalized weakness, nausea, electrolyte abnormalities, poor oral intake, and dehydration after he accidentally dislodged his PEG-J tube. After detailed risk and benefit discussions, the GI team was consulted, and the patient underwent endoscopic replacement of the same with gastropexy and placement of two suture-stays. Pertinent findings during EGD included scar at the previous gastrostomy site, fundic gastritis with/and likely worsened by retention of gastric contents, and severe reflux esophagitis (LA grade D).

During the procedure, on entering the stomach with the standard EGD scope, the mucosa was noted to be grossly normal appearing and well perfused (Image 1: A). It was noted that progressive inflation of the stomach lead to sequential increasing pallor which was more pronounced at the top of the gastric mucosal folds (Image 1: B, C, D respectively). After the PEG tube was placed and the stomach decompressed, the gastric folds were noted to return to the normal appearing perfused salmon-pink mucosal color (Image 1: E). Carbon dioxide was used for inflation during this procedure. Throughout the procedure the patient’s vitals remained stable, without any documented hypotension..

Image 1: (A) Normal appearing perfused gastric mucosa on entering the stomach with an EGD scope; (B) Minimal blanching starts to appear (arrowhead); (C) Mucosal blanching with gastric inflation most pronounced on the top of the gastric folds (arrowhead); (D) Blanching starts to improve with deflation (arrowhead); (E) Blanching resolved with full deflation after completion of the procedure.

This ‘miraculously’ inducible phenomenon of reversible blanching of the gastric mucosa, most conspicuous at the top of the mucosal folds, appearing with inflation and disappearing with deflation, during the same procedure remains of clinical interest. We intend to give this sign the name of a miracle ‘The MIRacle sign’ after the name of the coining author.

Although gastric mucosal pallor or white mucosa during endoscopy has been described as a potential pointer to a diagnosis of chronic mesenteric ischemia, the phenomenon of endoscopic inducibility and reversibility during the same exam has not been described in detail [1,2]. Eliciting this sign during endoscopy should prompt the clinician to work up further causes of gastric/intestinal ischemia especially in patients with pertinent vascular history. Cross sectional imaging with angiography should be considered in such cases.

One of the very few signs that are inducible during endoscopy, such as esophageal rings in reflux and eosinophilic esophagitis or “cat scratch colon” in collagenous colitis, the MIRacle sign may potentially serve as an important diagnostic pointer in the appropriate patient population. It is possible that in a susceptible patient with underlying significant vascular or cardiac disease, progressive gastric inflation with carbon dioxide or air may transiently compromise the blood supply of the already borderline perfused stomach. We theorize this may either happen by virtue of microvascular compression from increased intragastric pressure or potentially worsening the take-off angle of the major vessels arising from the aorta, or both. Of course, whitening of the mucosa may appearduring epinephrine injection, but it is a patchy phenomenon, and it does not appear and disappear during endoscopy.

The MIRacle sign may further potentially serve as an indirect sign for the assessment of gastric vascular perfusion. Further studies are needed to determine and describe the scientific basis of this rather intriguing and puzzling phenomenon.

References:

Tsay CJ, Protiva P. Chronic Mesenteric Ischemia with Peristaltic Blanching. Am J Gastroenterol. 2021 May 1;116(5):870.
Ichita C, Sasaki A, Isogai N, Sumida C, Nishino T, Kubota J, Shionoya K, Kimura K. White gastric mucosa during endoscopy as a new endoscopic feature of chronic ischemic gastritis: A case report. DEN Open. 2022 Dec 13;3(1):e192.

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Tip for Inspection of the Papilla of Vater Using Distal Transparent Cap

Fri, 26 Jan 2024 00:00:00 GMT

Question:

Answer:

New Videos

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Tips for Management of Colon Polyps with Thick and/or Long Stalks Using Endoloop

Fri, 26 Jan 2024 00:00:00 GMT

Pedunculated polyps (Paris 0-Ip) with thick and long stalk (Figure 1) pose a resection challenge as the pedicle usually has one or more big arteries and thus, the risk of intra- or post-polypectomy bleeding is increased. Therefore, pre-resection or post-resection interventions to prevent post-polypectomy bleeding are mandatory. These include clipping, injection, using endoloop or a combination of some of them.

In dealing with 0-Ip lesions, our approach is pre-resection endoloop placement. While endoloops may resemble snares, their endoscopic handling is different because they can't be opened and closed as easily. We pass the catheter with the endoloop proximal to the polyp head, slowly expose the loop, and then carefully place it on the polyp head.

In the 0-Ip lesions shown here we proceeded with pre-resection endoloop placement. Although endoloops look like a snare, endoscopic handling is different, as these cannot be opened and closed at will (Figure 2A). Thus, we like to pass the catheter with the endoloop proximal to the polyp head (Figure 2B), expose (“open”) the loop slowly and then pull scope with the opened loop proximally, slowly allowing for the loop to place itself on the polyp head. Once the endoloop can be clearly seen “under” the polyp head and around the stalk we wiggle the scope and or the loop-catheter to go as proximal to the stalk base. We like to tighten and place the loop about 10 mm above the base (Figure 2C).

When the assistant tightens the loop using the “pushing ring or band”, the endoscopist must gently, and minimally push the scope towards the stalk, staying close to the “field of action”. After tightening of the loop with the pushing band has occurred, the endoscopist starts pulling catheter through the working channel of the scope, using the right hand, while the assistant does the final release of the loop, pushing it out. At that moment, the long tail of the attached loop becomes visible and the polyp head starts changing color, acquiring a bluish discoloration (Figure 3A). Once the polyp has a purplish color we proceed with endoscopic resection in three steps: a) closing the snare and holding tight for about 30 seconds (this induces physiologic coagulation); b) applying a short burst of coagulation current; and c) applying cutting current (here we prefer the computer-controlled Endocut current) (Figure 3B). The resection process is the same when using clips, except that careful attention must be paid not to capture any the loop with the electrosurgical snare. Figure 3C shows on the importance of cutting well below the neoplastic tissue, to ensure complete resection (R0). Also, notice how cutting well below the polyp head, also ensure resection of neoplastic tissue extending into the stalk (Figure 3C).

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Tips for Post-EMR Bleeding for Lesions Located at the Anal Verge or Distal Rectum

Fri, 26 Jan 2024 00:00:00 GMT

This polyp is located on the anal verge, right proximal to the dentate line. What would you do?

A. Endoscopic band ligation

B. Refer to colorectal surgeon or proctologist

C. Resect using regular snare

D. Resect using EMR technique

E. Other

Answer

Polyps or polypoid lesions located close to the dentate line may represent a challenge for endoscopic resection. However, careful delineation and injection of submucosal cushion can lead to safe and effective endoscopic resection. Tips for post-EMR bleeding for lesions located at the anal verge or distal rectum: a) you can tamponade using your finger, b) other measures such as oxidized cellulose (or toilet paper = cellulose) also are effective for hemostasis. If you use clips always look at the dentate line, which must be avoided as it has a very rich nerve ending and clipping there will lead to lots of pain.

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Treating Upper Gastrointestinal Bleeding: An Update on Endoscopic Techniques

Fri, 26 Jan 2024 00:00:00 GMT

Upper gastrointestinal (GI) bleeding encompasses hemorrhage anywhere from the esophagus to the distal duodenum due to myriad etiologies including peptic ulcers, tumors, vascular malformations, esophageal varices, hemosuccus pancreaticus and trauma. Acute upper GI bleeding is a common reason for hospitalization, carrying a mortality rate of up to 10% (1)(1). Endoscopy serves as a powerful tool in both diagnosing and treating the source of GI hemorrhage through relatively non-invasive approaches. This article delves into the latest devices and techniques now available in the endoscopist's toolkit for tackling gastrointestinal bleeding.

Know Your Lesions

Identifying the specific lesion responsible for hemorrhage is the critical first step in managing GI bleeding. The spectrum of potential culprits includes (Figure 1):

Gastric antral vascular ectasia (GAVE) – this refers to dilated, tortuous vessels in the antral mucosa, which can ooze chronically and present as iron deficiency anemia. There are several subtypes ranging from linear striped vessels, to a diffuse honeycomb pattern, to discrete nodular lesions. Giant gastric folds and mixed morphologies also occur. 
Peptic ulcers – these can arise anywhere from the esophagus to the duodenum, but the majority localize to the stomach and duodenal bulb. Bleeding ulcers often localize to the posterior duodenal wall, presenting a challenge to target therapeutically. Ulcers can also form at gastrojejunal anastomoses after gastric bypass surgery.
Tumors – both benign and malignant tumors of the stomach, duodenum, or colon can erode into underlying vessels and cause acute hemorrhage. Cancers of the GI tract are a common culprit.
Dieulafoy’s lesion – this refers to abnormal subsurface arteries that protrude through tiny mucosal defects, typically in the proximal stomach, and lead to pulsatile bleeding.
Post-surgical bleeding – this can be seen after anastomoses, gastric resections, bariatric surgery, endoscopic submucosal dissection (ESD), and other procedures. Failure of suture lines is a frequent cause.

Risk Stratification

The Forrest classification stratifies lesions based on endoscopic characteristics and correlated risk of recurrent bleeding if not treated (Figure 1). For example, a spurting arterial bleed (Forrest Ia) carries a 90-100% risk of continued hemorrhage, while an ulcer with a pigmented flat spot (Forrest IIc) has only a 10-20% rebleeding risk (2,3). This provides valuable prognostic information to triage lesions requiring urgent therapy.

Traditional Therapies 

Endoscopists have several established therapies to manage GI bleeding (Figure 3):

Injection therapy – injecting dilute epinephrine or saline into and around the bleeding site constricts vessels and slows bleeding. Fibrin glue and other inert agents can also be injected.
Clipping – endoscopic clips provide direct mechanical compression of bleeding lesions. They come in various sizes with differing properties. Often several overlapping clips are required for definitive hemostasis.
Thermal coagulation – using electrocautery devices to apply targeted thermal energy to the bleeding site induces vessel thrombosis and tissue necrosis to stop hemorrhage.
Combination therapy – no single modality is universally successful, thus combining epinephrine injection followed by application of clips or thermal energy improves outcomes.

Novel Mechanical Approaches

Several innovative mechanical tools have recently expanded the GI bleed management arsenal:

Over-the-scope clips (OTSC) – these contain superelastic nitinol alloy that allows the clip ends to be flattened into an “open bear trap” configuration (Figure 4). When deployed, the preloaded clip achieves excellent compression across a broad region of tissue. Studies show OTSC achieves hemostasis comparable to surgery for severe bleeding.
Endoscopic suturing – devices like the OverStitch permit endoscopic placement of suture with access to hard-to-reach areas. This allows direct ligation of bleeding lesions.
Vascular embolization – interventional radiologists can inject coils, gel foam, particles, or liquids into bleeding vessels to induce targeted vascular occlusion under fluoroscopic guidance.
Oxidized cellulose – substances like Surgicel applied topically interact with blood to accelerate clot formation for hemorrhage control.

Topical Hemostatic Agents

”Contact-free” modalities have emerged as another option for refractory bleeding:

Hemospray – this bentonite powder is a naturally occurring aluminum phyllosilicate clay (similar to kaolin). This mineral powder rapidly aggregates into a cohesive barrier when sprayed onto bleeding tissue. It is deployed through a catheter passed down the endoscope. Hemospray was non-inferior to standard therapy in a randomized trial of peptic ulcer hemorrhage.
Purastat - composed of peptides that form a viscous gel, Purastat works by forming a self-assembling nanofiber matrix that provides mechanical tamponade upon application to the hemorrhage site. 
Other powders – additional substances like TC-325 and EndoCclot work via similar mechanisms to promote rapid clot formation.

Technical Tips and Tricks

Several techniques can improve visualization and precision:

Distal transparent attachments – transparent caps and hoods fitted to the endoscope tip help retract mucosal folds, stabilize the scope position, expose bleeding lesions, provide compression hemostasis, and target hemostatic utensil onto the lesion (Figure 5)
Overtubes – these provide stability and permit repeated access to bleeding sites.
Unique positions – adjusting scope positioning and angles can permit targeting of hard-to-reach hemorrhages.
Traction-countertraction – applying targeted tension to tissues allows focused application of hemostatic therapy precisely on the bleeding vessel. In conclusion, management of GI bleeding has advanced tremendously in recent years, with both new technologies and innovative techniques expanding the endoscopist’s armamentarium (4-61,2). The future of GI bleed care will likely involve personalized endoscopy (Figure 6) using a diverse palette of options tailored to each clinical scenario. As devices and strategies continue evolving, outcomes for this common and potentially fatal condition will continue to improve.

References:

Hearnshaw, S. A., Logan, R. F., Lowe, D., Travis, S. P., Murphy, M. F., & Palmer, K. R. (2011). Acute upper gastrointestinal bleeding in the UK: patient characteristics, diagnoses and outcomes in the 2007 UK audit. Gut, 60(10), 1327–1335. https://doi.org/10.1136/gut.2010.228437
Laine, L., & Peterson, W. L. (1994). Bleeding peptic ulcer. The New England journal of medicine, 331(11), 717–727. https://doi.org/10.1056/NEJM199409153311107
Hadzibulic, E., Govedarica, S. (2007). Significance of Forest Classification, Rockall’s and Blatchford’s Risk Scoring System in Prediction of Rebleeding in Peptic Ulcer Disease. Acta Medica Medianae, 46(4), 38-43.
Mönkemüller, K., & Soehendra, N. (2019). Endoscopic treatments for gastrointestinal bleeding: a story of cleverness and success. Endoscopy, 51(1), 5–6. https://doi.org/10.1055/a-0790-8509
Mönkemüller, K., Martínez-Alcalá, A., Schmidt, A. R., & Kratt, T. (2020). The Use of the Over the Scope Clips Beyond Its Standard Use: A Pictorial Description. Gastrointestinal endoscopy clinics of North America, 30(1), 41–74. https://doi.org/10.1016/j.giec.2019.09.003
Martínez-Alcalá, A., & Mönkemüller, K. (2018). Emerging Endoscopic Treatments for Nonvariceal Upper Gastrointestinal Hemorrhage. Gastrointestinal endoscopy clinics of North America, 28(3), 307–320. https://doi.org/10.1016/j.giec.2018.02.004

This manuscript is based on a transcript of a lecture given by KM during the Dominican Congress of Gastroenterology, 2023

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Ulcerations of the Intestines in Patient with Multiple Endocrine Neoplasia (MEN) Type 2b

Fri, 26 Jan 2024 00:00:00 GMT

Presented by Prof. Adrian Canavesi:

Middle-aged patient 42 with MEN IIb syndrome, s/p thyroidectomy about 10 years ago for medullary thyroid cancer, s/p bilateral adrenalectomy due to pheochromocytoma one year later. Since then, taking hydrocortisone and fludrocortisone. About 5 years underwent subtotal colectomy due to intestinal obstruction and megacolon. Immunohistochemistry was performed, being positive for S100, which was diagnostic of intestinal ganglioneuromatosis.

She was recently admitted due to hematochezia but no abdominal pain, no fever, no weight loss, no night sweats.

Push enteroscopy was unremarkable. However, ileocolonoscopy to 60 cm proximal to the ileocolic anastomosis shows dilated small bowel with multiple ulcers between 5 and 30 mm that tend to converge in some sectors, with congested edges and a deep bottom with fibrin; healthy surrounding mucosa.

What is your differential diagnosis?

Discussion by Klaus Mönkemüller:

Diffuse intestinal ganglineuromatosis can present sporadically or in association with von Recklinghausen disease (neurofibromatosis) or MEN2b, such as in your case.

The salient aspects of these ulcers are their depth and location. In cases of intestinal or colonic atonia or paralysis one must always think of stasis-ulcers (similar to stercoral ulcer). The location and linearity of the lesions also remind me of Zuckerberg or colon single strip sign (CSSS) in ischemic colitis, including the type associated with ingestion of NSAIDs, although these ulcers are in the small bowel. Thus, NSAID-induced ulcers must be ruled out.

Deep ulcers also should make one think of cytomegalovirus colitis, or tuberculosis, especially in a patient who is immunosupressed or taking steroids. Crohn's disease is always a consideration when small bowel ulcers are present, and also CMUSE (cryptogenic, multifocal ulcerative and stenosing enteritis).

MEN 1 is usually associated with gastrinoma, gastric hyperchloridia and diffuse small bowel ulcers. MEN2b is not generally associated with gastrinoma, but it is associated with hyperrparathroidism, which in turn leads to gastric hypersecretion, and eventual enteric ulcers.

Lastly, in systemic ganglioneuromatosis there is a diffuse infiltration of the submucosa by nerve fibres and ganglion cells that can be so exuberant, leading to deep ulcerations of the mucosa, submucosa, which may reach the muscular propria. I think this will be the final diagnosis in this case.

Biopsies will be very important, of course including special stains for cytomegalovirus, tuberculosis and nerve and spindle cells (e.g. calretinin, synaptophysin, S-100).

In addition, would obtain serum tests for tuberculosis (quantiferon), parathyroid-hormone (PTH) level, calcium, skin PPD, chest x-ray.

A CT of the abdomen or MRI would be helpful to determine the amount of transmural inflammation, extent of the disease, and presence or absence of lymph nodes.

Final Diagnosis: infiltrating intestinal ganglioneuromatosis.

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Understanding Cronkhite-Canada Syndrome

Fri, 26 Jan 2024 00:00:00 GMT

Cronkhite-Canada Syndrome (CCS) is a rare, non-inherited gastrointestinal condition of unknown etiology, often presenting as a diagnostic challenge with multiple symptoms, which may be vague and non-specific.

Case presentation:

A 48-year-old woman presented with chronic diarrhea and loss of taste. On the clinical exam she appeared pale, had brittle nails, and had partial hair loss. She was found to have severe iron deficiency anemia.

Colonoscopy showed multiple reddish, edematous mucosal streaks and polyps and pseudopolyps ranging from 5 to about 20 mm (Figure 1).

On EGD the stomach was characterized by enlarged mucosal folds, pseudoplyps (Figure 2) and duodenal mucosal atrophy (Figure 3)

Histology showed the below findings (see figure 4 A,B).

Main Point No. 1: Clinical Presentation

CCS often manifests in middle-aged adults with a distinctive set of symptoms.

Chronic diarrhea, loss of taste, and weight loss are common, coupled with iron deficiency anemia, likely due to malabsorption resulting from GI mucosal atrophy. This malabsorption may extend to physical changes such as alopecia, brittle nails, and dystrophic changes of the skin. For instance, the patient in our case displayed these symptoms, accentuating how CCS's unique symptomology can clue in a sharp diagnostician.

Main Point No. 2: Gastrointestinal Findings

CCS is characterized by distinct GI findings that aid in its identification. Pseudopolyps, red streaks, patchy atrophy, and unusual villi shapes, like those seen in our patient's colonoscopy and endoscopy, are typical. Additionally, patients often exhibit significant inflammation and lymphocytic infiltration in the lamina propria. Recognizing these GI markers is crucial for practitioners suspecting CCS.

Main Point No. 3: Risks and Prognosis

CCS is associated with significant health risks, mandating vigilant follow-up. Patients with CCS have a higher risk for developing gastric adenocarcinoma and other GI cancers. For instance, men are slightly more prone to CCS than women, with a ratio of 3:2, emphasizing the importance of regular monitoring and early intervention to manage these risks effectively.

Main Point No. 4: Treatment Approaches

Although there's no established treatment for CCS, some strategies have shown promising results.

Therapeutic approaches include systemic corticosteroids, antibiotics (particularly for eradicating Helicobacter pylori), and prolonged zinc supplementation. Some patients have experienced complete healing following these treatments, which underscores the potential for individualized management strategies.

Knowledge is power. The better we understand Cronkhite-Canada Syndrome, the more capable we are in recognizing, diagnosing, and managing this rare condition. Don't forget: every symptom counts in piecing together the diagnostic puzzle.

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Unusual Bile Duct Problems: The Sump Syndrome

Fri, 26 Jan 2024 00:00:00 GMT

Welcome to 6,136 motivated endoscopists!

The Sump Syndrome

In the past, performing a side-to-side anastomosis of the bile duct to the duodenum (choledocoduodenostomy) was a quite common operation. This operation is now seldomly performed, but we still patients who underwent it.
The “Sump syndrome” is a rare complication of a side-to-side choledochoduodenostomy that usually presents with obstructive jaundice or ascending cholangitis.
Sump syndrome develops due to the accumulation of food and debris entering through the choledocoduodenostomy and being collected inside of the distal bile duct.
The debris cannot be excreted through the papilla due to malfunction of the sphincter of Oddi, as the main orifice of bile excretion into the duodenum is the choledocoduodenostomy, which is the path of least resistance.
At one point there is so much “dirt” inside the bile duct that obstruction and infection (cholangitis) ensue.
Treatment is easy: biliary sphincterotomy with cleansing of the bile ducts.
However, knowledge of this condition is essential for proper recognition and treatment. Lack of knowledge of the sump syndrome condition may lead to incomplete or failed ERCP and persistent cholangitis or choledocolithiasis.

Reader Poll

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Do You Use CO2 and Water Immersion in Diagnostic Colonoscopies on a Daily Basis?

Fri, 26 Jan 2024 00:00:00 GMT

Do You Use CO2 and Water Immersion in Diagnostic Colonoscopies on a Daily Basis?

Yes. And Yes.

Using CO2 is a great for colonoscopy for several reasons: a) improved patient tolerability, b) improved cecal intubation rate, c) improves therapeutic possibilities as the colon does not get distended as much as compared to plain air, thus keeping the lesion at a better position and also decreasing chances of perforation. The latter is based on the “balloon-effect”. The more a balloon (colon) is inflated the higher the chances of laceration and perforation. Also, the more a balloon or colon is inflated, the thinner its wall becomes. Thus, when snaring a polyp of a distended colon, the chances of damage (perforation and burn) are increased.
Regarding water 💧 or hydro/colonoscopy, there are many pros: a) less colon distinction and thus improved patient tolerability, b) cleaning the colon of remnant debris, c) stimulating the colon to move onto the scope (yes, water does stimulate colon motility), d) ability to perform underwater inspection and also resection of lesions, e) less chance of electrosurgical damage (as water disperses the electricity applied to the polyp base), f) flushing water facilitates ileum intubation.

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Water Assisted-Colonoscopy (WAC or Hydrocolonoscopy)

Fri, 26 Jan 2024 00:00:00 GMT

Water immersion or assisted technique for colonoscopy (WAC) insertion has been noted to help reduce pain and occasionally makes difficult colonoscopies somewhat easier by straightening out the colon and reducing angulations (1, 2). WAC has been gathering interest in recent years due to high-quality studies offering evidence of the benefits of WAC to both the endoscopist and the patient (3-5). Water exchange may be superior to water immersion in minimizing colonoscopy discomfort and in increasing adenoma detection rates. The benefits of WAC arise from two principal mechanisms:

(I) Use of water exerts a gravitational effect and reduces colonic elongation, thereby reducing loop formation, procedure discomfort and sedation requirements (1-3).

(II) Water irrigation improves mucosal views and can increase adenoma detection rates (ADR) (4).

The concept of keeping the lumen minimally distended with water appears to reduce angulations in the colon and facilitate advancement with less looping of the instrument. Compared with air insufflation, both water immersion and water exchange significantly reduce colonoscopy pain. Importantly, WAC does not compromise any other aspects of colonoscopy; for example, the procedure does not take longer with the water method (1-4).

In our practice we often perform “partial” WAC. This method consists of using water preferentially over CO2 during colonoscopy. Here we use the best of both worlds, water to traverse tight angulations, prevent elongation of the colon and clean the mucosal surface, and CO2 to open the lumen and flatten the folds when looking for colon polyps. With modern colonoscopes that allow for easy suctioning and generous use of water with the incorporated waterjet, the quality of the colonoscopy can be greatly improved using this hybrid, dynamic technique.

Furthermore, using lots of water during colonoscopy is essential to clean the mucosal surface and remove debris to improve detection of colorectal adenomas. Lastly, we want to emphasize that water is also is advantageous to perform some resections (“underwater endoscopic mucosal resection”) and is essential to clean the wound surface during and after polypectomy.

In sum, water is essential during colonoscopy, and can be used as the primary colon distention method (WAC) or as a hybrid dynamic tool to improve the results of colonoscopy.

Further reading:

1. Friedland S. The water immersion technique for colonoscopy insertion. Gastroenterol Hepatol (N Y). 2010;6(9):555-6.

2. Siau K, Beintaris I. My approach to water-assisted colonoscopy. Frontline Gastroenterology 2019;10:194-197.

3. Leung CW, Kaltenbach T, Soetikno R, Wu KK, Leung FW, Friedland S. Water immersion versus standard colonoscopy insertion technique: randomized trial shows promise for minimal sedation. Endoscopy. 2010;42:557–563.

4. Leung JW, Mann SK, Siao-Salera R, et al. A randomized, controlled comparison of warm water infusion in lieu of air insufflation versus air insufflation for aiding colonoscopy insertion in sedated patients undergoing colorectal cancer screening and surveillance. Gastrointest Endosc. 2009;70:505–510.

5. Fuccio L , Frazzoni L , Hassan C , et al. Water exchange colonoscopy increases adenoma detection rate: a systematic review with network meta-analysis of randomized controlled studies. Gastrointest Endosc 2018;88:589–97.

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What is a Phrygian (Cap) Gallbladder?

Fri, 26 Jan 2024 00:00:00 GMT

A phrygian cap gallbladder is a congenital anomaly of the gallbladder with an incidence of 4%. It can simulate a mass in the liver during hepatobiliary imaging and is sometimes mistaken for pathology. A Phrygian cap, however, has no pathological significance and normally causes no symptoms.

The gallbladder is a pear-shaped organ measuring about 7 cm long and 3 cm wide and is located on the undersurface of the liver. Variations of the gallbladder include anomalies of form, location or number of gallbladders. A phrygian cap is the most common congenital abnormality of the gallbladder with an incidence of 4%. Although it can simulate a mass in the liver on radiological imaging studies, it does not have any pathological significance, and there is no need for cholecystectomy, unless it causes symptoms such as biliary colic or cholecystitis (1).

The phrygian cap has many symbolic meanings and is represented in art, politics, sports, TV and many national flags and coins.

1. van Kamp MJ, Bouman DE, Steenvoorde P, Klaase JM. A phrygian cap. Case Rep Gastroenterol. 2013;7(2):347-351.

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Where Does the Measurement "Fr" (French) Come From, and What Does It Mean?

Fri, 26 Jan 2024 00:00:00 GMT

Every day in the endoscopy unit we use instruments and accessories with measures in “French” (Fr). In Germany we refer to the “French measurement” as “Ch, Charr or Charrière”. Who was Charrière? Joseph-Frédéric-Benoît Charrière (1803-1876) was a Swiss-French artisan medical instrument designer who created a panoply of surgical products, mostly used in urology, but he also developed, scissors, syringes, forceps, and non-rebreathing systems for administering anesthesia (1, 2).

To be useful, the products had to be reproducible and follow standards for keeping the same size. Charrière devised a famous system of gauging, known as the Charrière or “French” gauge system, which is still used today. It has uniform increments between gauge sizes; a third of a millimeter equates one Ch, Charr or French: i.e. 1 Charr [French] = 0.333 mm.

In essence, one increment on the French scale is equal to 1/3 millimeter, e.g. 10 Fr catheter is 10 x 0.33 mm = 3,33 mm in caliber.

Good to know! If you are using a gastroscope with a 2.8 mm working channel, it’s impossible to pass a delivery device, stent or pushing catheter larger than 8 Fr. Most delivery systems for self-expanding metal stents (SEMS) used to palliate gastric outlet, small bowel and colonic obstruction are 10 Fr. Therefore, you can deploy these SEMS only using scopes with a large enough working channel, for example colonoscope or duodenoscope (see figure below).

However, if you don’t have a scope with a large enough channel, there are always tricks to pass thicker catheters or stent to the target lesion or position using overtubes or guidewires like shown in this example:

Just multiple 1 Fr x 0,33 = 0,33 mm

1 Fr is 0.33 mm

2 Fr is 0,66 mm

3 Fr is 1 mm

4 Fr is 1.33 mm

5 Fr is 1.67 mm

6 Fr is 2 mm

7 Fr is 2.33 mm

8 Fr is 2.67 mm

9 Fr is 3 mm

10 Fr is 3.33 mm

12 Fr is 4 mm

14 Fr is 4.67 mm

16 Fr is 5.33 mm

20 Fr is 6.66 mm

Fig. legend: Balloon-assisted endoscopic retrograde cholangiopancreatography. a Magnetic resonance cholangiopancreatography revealed a tight distal bile duct stricture (yellow arrow). b Tight opening of the hepaticojejunostomy. c Balloon dilation of the hepaticojejunostomy. d The balloon-assisted enteroscopy overtube worked as a giant working channel. The wire was left inside, connecting the bile ducts to the operator. The operator then advanced a fully covered metal stent, over-the-wire and through-the-overtube, using radiological guidance, and then successfully inserted the stent inside the bile duct (3).

Ref:

Bowen DK, Wan J, Engel R, Lyon RP, Dielubanza E, Bloom DA. Sounds and Charrière: the rest of the story. J Pediatr Urol. 2014;10(6):1106-10. doi: 10.1016/j.jpurol.2014.04.010.
Iserson KV. J.-F.-B. Charrière: the man behind the "French" gauge. J Emerg Med. 1987;5(6):545-8. doi: 10.1016/0736-4679(87)90218-6.
Hewitt BA, Jovanovic I, Martínez-Alcalá A, Kröner PT, D'Assunçao M, Mönkemüller K. Insertion of fully covered self-expandable metal stent during balloon-assisted ERCP in patient with surgically altered upper gastrointestinal anatomy. Endoscopy. 2018;50(1):E20-E21. doi: 10.1055/s-0043-1196

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Zenker

Fri, 26 Jan 2024 00:00:00 GMT

An elderly man presented with dysphagia to solids. The patient also complained of partially digested food drooling out of his mouth while he slept. A barium esophagogram revealed a 40-mm posterior protrusion at the level of the proximal cervical esophagus. On EGD a diverticulum was seen.

Zenker's diverticulum, also known as pharyngeal pouch, is really a pseudodiverticulum, as it only contains mucosa and submucosa and does not involve all the layers of the esophageal. This pseudodiverticulum results from posterior herniation of esophageal mucosa into Killian's triangle, an area of least resistance situated above the upper esophageal sphincter (cricopharyngeal muscle) and below the inferior pharyngeal constrictor muscle.

Symptoms of Zenker’s diverticulum are dysphagia, and the pooling of food within the diverticulum, which can cause bad breath, frequent regurgitation and aspiration pneumonia.

Treatment consists of a surgical transcervical diverticulectomy without myotomy, diverticulopexy or endoscopic myotomy of the septum (i.e. longitudinal incision and dissection into the anterior septum). A myotomy can be accomplished using rigid or flexible endoscopes. Nowadays, most myotomies are performed by interventional endoscopists and ear nose and throat (ENT) specialists.

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The Practicing Endoscopist

Diagnosis at First Sight: Gastric Adenoma

References

How Would You Remove This Pedunculated Polyp (Paris 0-Ip, Kudo IIIL)?

Question

Answer

Post-Prandial Thoracic Pain and Pre-Syncopal Symptoms: Watch Out for Roemheld Syndrome

Clinical History

Endoscopic and Physiologic Findings

Endoscopic Technique

Discussion

References

Ménétrier Disease: A Diagnostic Challenge of Enlarged Gastric Folds

Endoscopic Findings

Endoscopic Technique

Discussion

References

Gastric Adenoma Resection in a Patient with Lynch Syndrome

Endoscopic Findings

Endoscopic Technique

Discussion

References

Gastrointestinal Manifestations of Systemic Sclerosis

Final Diagnosis

Patient Demographics

Clinical History

Endoscopic Findings

Endoscopic Technique

Discussion

Key Learning Points

References

Acetic Acid Chromoendoscopy in Barrett Esophagus for Dysplasia Detection

Endoscopic Findings

Endoscopic Technique

Discussion

References

Endoscopic Balloon Dilation of a Benign Duodenal Stenosis

Endoscopic Findings

Endoscopic Technique

Discussion

References

Endoscopic Placement of a Self-Expanding Metal Stent for Obstructing Sigmoid Diverticulitis

Endoscopic Findings

Endoscopic Technique

Discussion

References

Hyperplastic Duodenal Polyp in Portal Hypertensive Gastrointestinal Disease

Final Diagnosis

Patient Demographics

Clinical History

Endoscopic Findings

Endoscopic Technique

Discussion

Key Learning Points

References

Pseudo-Mirizzi on ERCP: A Warning Sign for Vanishing Calot Syndrome

Clinical History

Endoscopic Findings

Endoscopic Technique

Discussion

References

Endoscopic Findings of Eosinophilic Esophagitis: A Case Report

Abstract

★ Key Clinical Takeaways

Clinical History

Endoscopic Findings

Discussion

References

Conflict of Interest

When to Perform Endoscopy or Radiological Tests in Patients with Unresponsive Celiac Disease?

Alerting findings on endoscopy

Signs on x-ray

References

Upper Esophageal Stenosis, Microcytic Anemia, and Plummer-Vinson Syndrome

Final Diagnosis

Patient Demographics

Clinical History

Endoscopic Findings

Endoscopic Technique

Discussion