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	<channel>
		<title>The Digital Atlas of Video Education - Gastroenterology</title>
		<link>http://daveproject.org/</link>
		<description> The DAVE Project - Gastroenterology  is a collection of teaching tools. The focus is gastrointestinal endoscopic video clips and presentations using the full spectrum 
		endoscopic imaging supported by pathologic, radiologic, and surgical images. Physicians are able to submit, for consideration, new entries to enrich and expand the atlas. 
		</description>
		<language>en-us</language>
		<webMaster>dcollier@daveproject.org (Dan Collier)</webMaster>
		<ttl>60</ttl>
		<copyright>Copyright held by original authors. Released under a Creative Commons license.</copyright>
		
			<item>
				<title>Intussuception in Peutz-Jegher Syndrom</title>
				<pubDate>Thu, 21 Jan 2010 03:01:33 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=889</guid>
				<description><![CDATA[A 30 year old woman with Peutz-Jegher syndrome presented with nausea, vomiting and crampy left abdominal pain. She had undergone multiple abdominal surgeries since child hood for intussuception of the small bowel due to large hamartomatous polyps. Her physical exam was remarkable for tachycardia, hyperpigmented spots on her lips  and an abdomen tender to deep palpation with no rebound tenderness. 

A computer tomography of the abdomen and pelvis showed gastric polyps and dilated loops of bowel with obstruction from large polypoid lesions. A target sign was present.

After the benefits and risks of surgery were explained to the patient, she elected endoscopy with double balloon enteroscopy with polypectomy to avoid surgery and maintain small bowel function.

Both upper and lower endoscopy were performed. 

Upon entry into the stomach, multiple large polypoid lesions were found throughout the stomach as well as duodenum. The larger polyps had a pedunculated appearance. Using monopolar cautery they were carefully removed.

A colonoscopy with double balloon enteroscopy showed multiple large polypoid lesions throughout the visualized small bowel, causing intussuception. Air was carefully insufflated. Polyps greater than 1 centimeter were snared using monopolar cautery.

According to the current limited data from case series, up to 68% of adults with Peutz-Jegher syndrome undergo laparotomy by the time they are 18 years of age. Of those, 39% undergo repeat laparatomy within 5 years. Removal of small bowel polyps larger than 1cm during laparotomy, a technique referred to as &#8220;clean sweep&#8221;, delays the need for repeat laparotomy.

Histopathology of polypoid lesions showed arborizing pattern with smooth muscle fibers consistent with Hamartomatous Polyps.

Our case demonstrates endoscopy with double balloon enteroscopy with removal of large polyps is a feasible alternative to laparotomy for intussuception.

References

&diams;	Giardiello FM, Trimbath JD.  Peutz-Jeghers Syndrome and Management Recommendations. Clinical Gastroenterology and Hepatology 2006; 4:408-415.
&diams;	Hines R, Philp C, Hyer W, et al. Complications of Childhood Peutz-Jeghers Syndrome: Implications for Pediatric Screening.  Journal of Paediatric Gastroenterology and Nutrition 2004;39: 219-220.]]></description>
				<dc:creator>Mike Babineaux, MD,, University of Texas Medical Branch, Gabriel Lee, MD,, University of Texas Medical Branch, Andrew W. DuPont, M.D., Assistant Professor of Medicine, University of Texas Medical Branch</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=889</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/evca.i.pol.pjs.pec.5.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=889" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/pjs-intussuception.jpg</media:thumbnail>
				<media:people role="producer">Mike Babineaux, MD,, University of Texas Medical Branch, Gabriel Lee, MD,, University of Texas Medical Branch, Andrew W. DuPont, M.D., Assistant Professor of Medicine, University of Texas Medical Branch</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[A 30 year old woman with Peutz-Jegher syndrome presented with nausea, vomiting and crampy left abdominal pain. She had undergone multiple abdominal surgeries since child hood for intussuception of the small bowel due to large hamartomatous polyps. Her physical exam was remarkable for tachycardia, hyperpigmented spots on her lips  and an abdomen tender to deep palpation with no rebound tenderness. 

A computer tomography of the abdomen and pelvis showed gastric polyps and dilated loops of bowel with obstruction from large polypoid lesions. A target sign was present.

After the benefits and risks of surgery were explained to the patient, she elected endoscopy with double balloon enteroscopy with polypectomy to avoid surgery and maintain small bowel function.

Both upper and lower endoscopy were performed. 

Upon entry into the stomach, multiple large polypoid lesions were found throughout the stomach as well as duodenum. The larger polyps had a pedunculated appearance. Using monopolar cautery they were carefully removed.

A colonoscopy with double balloon enteroscopy showed multiple large polypoid lesions throughout the visualized small bowel, causing intussuception. Air was carefully insufflated. Polyps greater than 1 centimeter were snared using monopolar cautery.

According to the current limited data from case series, up to 68% of adults with Peutz-Jegher syndrome undergo laparotomy by the time they are 18 years of age. Of those, 39% undergo repeat laparatomy within 5 years. Removal of small bowel polyps larger than 1cm during laparotomy, a technique referred to as &#8220;clean sweep&#8221;, delays the need for repeat laparotomy.

Histopathology of polypoid lesions showed arborizing pattern with smooth muscle fibers consistent with Hamartomatous Polyps.

Our case demonstrates endoscopy with double balloon enteroscopy with removal of large polyps is a feasible alternative to laparotomy for intussuception.

References

&diams;	Giardiello FM, Trimbath JD.  Peutz-Jeghers Syndrome and Management Recommendations. Clinical Gastroenterology and Hepatology 2006; 4:408-415.
&diams;	Hines R, Philp C, Hyer W, et al. Complications of Childhood Peutz-Jeghers Syndrome: Implications for Pediatric Screening.  Journal of Paediatric Gastroenterology and Nutrition 2004;39: 219-220.]]></media:text>
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			<item>
				<title>Duodenum - Endoscopic Management of a Windsock Diveticulum</title>
				<pubDate>Tue, 19 Jan 2010 04:01:09 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=785</guid>
				<description><![CDATA[A 24 year old female was referred for complaints intermittent nausea and vomiting and weight loss. The upper GI barium study demonstrates an enlarged diverticulum in the second portion of the duodenum. A thin radiolucent stripe is seen around the diverticulum which has been described as the halo sign. Upper endoscopy is performed which identifies a large diverticulum which intermittently obstructs the duodenal lumen. The endoscopic appearance is consistent with a windsock diverticulum. This intraluminal diverticulum is thought to result from incomplete recanalization of the duodenum during embryological development and with complete obstruction, symptoms present during childhood. In contrast, when there is a small aperture in the duodenum, patients may initially remain asymptomatic. However, the duodenal web that is present is stretched over time by peristalsis resulting in the development of an intraluminal diverticulum. As the diverticulum increases in size, it may cause intermittent obstruction or even pancreatitis. In contrast to diverticula located elsewhere in the gastrointestinal tract, these diverticula are lined on both sides by intestinal mucosa. Symptoms of nausea and vomiting can often be relieved if the narrow duodenal lumen is opened. 
In this video, we present the endoscopic management of a windsock diverticulum using the needle knife sphincterotome. Initially, the narrow lumen of the duodenum is located adjacent to the diverticulum. The endoscope is advanced through his aperture into the distal duodenum. The guidewire is placed across this opening and a 10 French by 10 cm pigtail stent is subsequently deployed. Placement of the stent allows the endoscopist to easily locate the aperture, which may be difficult during the case. Next, the major papilla is identified. If visualization of the major papilla during the endoscopy, is difficult, a pancreatic stent can be placed to mark its location. This was not required in this patient. Next, the first endoscopic clip is placed. This clip is placed on the opposite wall of the papilla and along the diverticular rim. Subsequently, a second clip is deployed. 
These clips are used to define the plane of resection for the needle knife incision. The needle knife is placed between the two endoscopic clips. Note that the direction of the incision is away from the major papilla and towards the diverticular rim. A series of short incisions are made for a total length of approximately 10 mm. Next two endoscopic clips will be placed at the extent of the prior incision. These clips identify where the next needle knife incision should be made. After placement of the clips, the needle knife is again used. In a direction towards the diverticulum, the diverticulotomy is extended until its total length is approximately 2 cm. The dilating balloon is then used to evaluate the diverticulotomy size. The balloon is fully inflated to 20mm and there is no resistance identified in the area of the prior stenosis. Both the endoscope and balloon pass through the diverticulotomy site. The pigtail catheter is removed and the procedure is complete.]]></description>
				<dc:creator>Rajesh N. Keswani, MD,, Washington University, Steven A. Edmundowicz, MD,, Washington University</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=785</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/evca.d.div.obs.cli.nif.1oo.ke0508us.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=785" playerHeight="480" playerWidth="320" expression="full"></media:content>
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				<media:people role="producer">Rajesh N. Keswani, MD,, Washington University, Steven A. Edmundowicz, MD,, Washington University</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[A 24 year old female was referred for complaints intermittent nausea and vomiting and weight loss. The upper GI barium study demonstrates an enlarged diverticulum in the second portion of the duodenum. A thin radiolucent stripe is seen around the diverticulum which has been described as the halo sign. Upper endoscopy is performed which identifies a large diverticulum which intermittently obstructs the duodenal lumen. The endoscopic appearance is consistent with a windsock diverticulum. This intraluminal diverticulum is thought to result from incomplete recanalization of the duodenum during embryological development and with complete obstruction, symptoms present during childhood. In contrast, when there is a small aperture in the duodenum, patients may initially remain asymptomatic. However, the duodenal web that is present is stretched over time by peristalsis resulting in the development of an intraluminal diverticulum. As the diverticulum increases in size, it may cause intermittent obstruction or even pancreatitis. In contrast to diverticula located elsewhere in the gastrointestinal tract, these diverticula are lined on both sides by intestinal mucosa. Symptoms of nausea and vomiting can often be relieved if the narrow duodenal lumen is opened. 
In this video, we present the endoscopic management of a windsock diverticulum using the needle knife sphincterotome. Initially, the narrow lumen of the duodenum is located adjacent to the diverticulum. The endoscope is advanced through his aperture into the distal duodenum. The guidewire is placed across this opening and a 10 French by 10 cm pigtail stent is subsequently deployed. Placement of the stent allows the endoscopist to easily locate the aperture, which may be difficult during the case. Next, the major papilla is identified. If visualization of the major papilla during the endoscopy, is difficult, a pancreatic stent can be placed to mark its location. This was not required in this patient. Next, the first endoscopic clip is placed. This clip is placed on the opposite wall of the papilla and along the diverticular rim. Subsequently, a second clip is deployed. 
These clips are used to define the plane of resection for the needle knife incision. The needle knife is placed between the two endoscopic clips. Note that the direction of the incision is away from the major papilla and towards the diverticular rim. A series of short incisions are made for a total length of approximately 10 mm. Next two endoscopic clips will be placed at the extent of the prior incision. These clips identify where the next needle knife incision should be made. After placement of the clips, the needle knife is again used. In a direction towards the diverticulum, the diverticulotomy is extended until its total length is approximately 2 cm. The dilating balloon is then used to evaluate the diverticulotomy size. The balloon is fully inflated to 20mm and there is no resistance identified in the area of the prior stenosis. Both the endoscope and balloon pass through the diverticulotomy site. The pigtail catheter is removed and the procedure is complete.]]></media:text>
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			</item>
			
			<item>
				<title>Intestine - EUS of an Appendiceal Adenoma</title>
				<pubDate>Wed, 13 Jan 2010 06:01:52 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=820</guid>
				<description><![CDATA[On routine examination of the cecum during screening colonoscopy, a 76 year-old man is noted to have a small amount of polypoid tissue extruding from the appendiceal orifice. The lesion is submerged in water and a 20 MHz, high-frequency, EUS probe is used for further evaluation.  EUS allows for easy sonographic identification of the polyp. The bright white, hyperechoic portions of the colonic wall correspond to the submucosal layer; thus making this polyp a superficial, mucosal-based lesion. The polyp is then grasped with a standard biopsy forceps in order to expose all points of involvement within the appendiceal lumen for complete inspection.]]></description>
				<dc:creator>Jonathan M Buscaglia, MD, Instructor of Medicine, Johns Hopkins Medical Center</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=820</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/evca.i.apx.oo.oo.eus.0903bu.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=820" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/vlcsnap-14933305.jpg</media:thumbnail>
				<media:people role="producer">Jonathan M Buscaglia, MD, Instructor of Medicine, Johns Hopkins Medical Center</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[On routine examination of the cecum during screening colonoscopy, a 76 year-old man is noted to have a small amount of polypoid tissue extruding from the appendiceal orifice. The lesion is submerged in water and a 20 MHz, high-frequency, EUS probe is used for further evaluation.  EUS allows for easy sonographic identification of the polyp. The bright white, hyperechoic portions of the colonic wall correspond to the submucosal layer; thus making this polyp a superficial, mucosal-based lesion. The polyp is then grasped with a standard biopsy forceps in order to expose all points of involvement within the appendiceal lumen for complete inspection.]]></media:text>
				<enclosure url="http://daveproject.org/media/videos/512k/480x320/flash/evca.i.apx.oo.oo.eus.0903bu.mpg.flv" type="video/x-flash"  length="54321" />
			</item>
			
			<item>
				<title>Pure Wire Guided Cannulation of the Bile Duct Using a Loop-tip Guidewire</title>
				<pubDate>Tue, 08 Dec 2009 05:12:08 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=888</guid>
				<description><![CDATA[In this video we will present two cases discussing the technique of bile duct access with pure wire guided cannulation using a loop tip guide wire.  For pure wire guided cannulation, a sphincterotome is recommended.  We should stay slightly away from the papilla so that papilla is clearly visualized and using the bow of sphincterotome the guide wire can be advanced in a cephalad direction over the septum in the direction of the bile duct.  Loop-tip guidewire is a 0.035 inch guide wire with an atraumatic tip . The loop at end prevents dissection of the tissue and prevents puncturing of pancreatic duct.  The radio-opacity of the guide wire tells us the duct accessed without injecting contrast.  Also, the guide wire has enough stiffness for adequate pushing force.  This schematic diagram shows how the bow of the sphincterotome is used to get an upward angulation. 
This is a 21-year-old female patient who presented with right upper quadrant abdominal pain with abnormal liver enzymes.  Right upper quadrant sonogram showed gall stones and a dilated bile duct.  Here you can visualize the papilla.  Once the sphincterotome is in the duodenum; the guide wire is moved to make sure there is free movement.  Using the bow of the sphincterotome the guide wire is directed towards the bile duct and advanced over the septum. A few extra minutes are spent to angulate the wire towards the bile duct.  Fluoroscopically the guide wire can be seen passing into the bile duct.  Subsequently the sphincterotome can be slowly advanced over the guide wire into the bile duct to complete the therapy. 
In another example; a 79 year old patient presented with obstructed jaundice from a pancreatic head mass.  A normal appearing prominent papilla is visualized. The sphincterotome is advanced and the guide wire is moved to assess for free movement.  Again, staying away from the papilla the bow of the sphincterotome is used to align in the direction of the bile duct.  Using the movement of the wheels and  the bow of the tome, the tip of the sphincterotome is aligned in the direction of the bile duct.  Once adequate angle is achieved the guide wire is slowly advanced over the septum into the bile duct.  The direction of the guide wire is confirmed with fluoroscopy.  The sphincterotome is advanced over the guide wire into the bile duct and contrast is injected and therapy completed.  These two cases illustrate a simple and effective technique of bile duct access using a loop tip guide wire and technique of pure wire guided cannulation.]]></description>
				<dc:creator>Kapil Gupta, M.D., Assistant Professor of Medicine, Hennepin County Medical Center, University of Minnesota</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=888</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/evca.p.can.guide.wire.pa0912us.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=888" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/gupta078_AT_umn.edu-Looptip-1.jpg</media:thumbnail>
				<media:people role="producer">Kapil Gupta, M.D., Assistant Professor of Medicine, Hennepin County Medical Center, University of Minnesota</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[In this video we will present two cases discussing the technique of bile duct access with pure wire guided cannulation using a loop tip guide wire.  For pure wire guided cannulation, a sphincterotome is recommended.  We should stay slightly away from the papilla so that papilla is clearly visualized and using the bow of sphincterotome the guide wire can be advanced in a cephalad direction over the septum in the direction of the bile duct.  Loop-tip guidewire is a 0.035 inch guide wire with an atraumatic tip . The loop at end prevents dissection of the tissue and prevents puncturing of pancreatic duct.  The radio-opacity of the guide wire tells us the duct accessed without injecting contrast.  Also, the guide wire has enough stiffness for adequate pushing force.  This schematic diagram shows how the bow of the sphincterotome is used to get an upward angulation. 
This is a 21-year-old female patient who presented with right upper quadrant abdominal pain with abnormal liver enzymes.  Right upper quadrant sonogram showed gall stones and a dilated bile duct.  Here you can visualize the papilla.  Once the sphincterotome is in the duodenum; the guide wire is moved to make sure there is free movement.  Using the bow of the sphincterotome the guide wire is directed towards the bile duct and advanced over the septum. A few extra minutes are spent to angulate the wire towards the bile duct.  Fluoroscopically the guide wire can be seen passing into the bile duct.  Subsequently the sphincterotome can be slowly advanced over the guide wire into the bile duct to complete the therapy. 
In another example; a 79 year old patient presented with obstructed jaundice from a pancreatic head mass.  A normal appearing prominent papilla is visualized. The sphincterotome is advanced and the guide wire is moved to assess for free movement.  Again, staying away from the papilla the bow of the sphincterotome is used to align in the direction of the bile duct.  Using the movement of the wheels and  the bow of the tome, the tip of the sphincterotome is aligned in the direction of the bile duct.  Once adequate angle is achieved the guide wire is slowly advanced over the septum into the bile duct.  The direction of the guide wire is confirmed with fluoroscopy.  The sphincterotome is advanced over the guide wire into the bile duct and contrast is injected and therapy completed.  These two cases illustrate a simple and effective technique of bile duct access using a loop tip guide wire and technique of pure wire guided cannulation.]]></media:text>
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			</item>
			
			<item>
				<title>Large Diameter Balloon Dilation for Removal of Bile Duct Stone</title>
				<pubDate>Fri, 20 Nov 2009 11:11:33 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=887</guid>
				<description><![CDATA[83 year old male with multiple co-morbidities presented with fever, abnormal liver enzymes and dilated common bile duct (CBD) up to 15 mm in size on abdominal CT scan and elevated international normalized ratio (INR).  A pull type sphincterotome was used to cannulate the common bile duct.  After the slight adjustment, the sphincterotome was advanced freely without any resistance into the common bile duct and the cholangiogram was obtained.  
 Here we see a large common bile duct stone on the cholangiogram.  This stone was approximately 15 mm in size.  A small biliary sphincterotomy was performed using the endocut current.  We used controlled radial expansion (CRE) balloon over the guidewire to dilate the biliary orifice.  We inflated the CRE balloon up to 12 mm and was kept in position for approximately 30 seconds.  The cholangiogram is showing the gradual expansion of the CRE balloon in the common bile duct.  Then the balloon was inflated up to 15 mm and was kept in position for another 30 seconds.  This view shows the inflated CRE balloon up to 15 mm.  Slight capillary oozing was seen at the site of biliary sphincteroplasty.  This was most likely due to elevated INR of the patient.  A mechanical lithotripsy basket was used to remove the CBD stones.  This cholangiogram shows two CBD stones within the lithotripsy basket.  These CBD stones were removed without any difficulty from the common bile duct.]]></description>
				<dc:creator>Manmeet Padda, MD, Advanced Endoscopy Fellow, Yale University, Uzma Siddiqui, M.D., Assistant Professor of Medicine, Yale University, Harry Aslanian, M.D., Associate Professor of Medicine, Yale University, Priya A. Jamidar, MD, Professor of Medicine, Director of Endoscopy, Yale University</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=887</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/evca.p.bal.dil.stn.pa0911.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=887" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/evca.p.bal.dil.stn.pa0911-1.jpg</media:thumbnail>
				<media:people role="producer">Manmeet Padda, MD, Advanced Endoscopy Fellow, Yale University, Uzma Siddiqui, M.D., Assistant Professor of Medicine, Yale University, Harry Aslanian, M.D., Associate Professor of Medicine, Yale University, Priya A. Jamidar, MD, Professor of Medicine, Director of Endoscopy, Yale University</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[83 year old male with multiple co-morbidities presented with fever, abnormal liver enzymes and dilated common bile duct (CBD) up to 15 mm in size on abdominal CT scan and elevated international normalized ratio (INR).  A pull type sphincterotome was used to cannulate the common bile duct.  After the slight adjustment, the sphincterotome was advanced freely without any resistance into the common bile duct and the cholangiogram was obtained.  
 Here we see a large common bile duct stone on the cholangiogram.  This stone was approximately 15 mm in size.  A small biliary sphincterotomy was performed using the endocut current.  We used controlled radial expansion (CRE) balloon over the guidewire to dilate the biliary orifice.  We inflated the CRE balloon up to 12 mm and was kept in position for approximately 30 seconds.  The cholangiogram is showing the gradual expansion of the CRE balloon in the common bile duct.  Then the balloon was inflated up to 15 mm and was kept in position for another 30 seconds.  This view shows the inflated CRE balloon up to 15 mm.  Slight capillary oozing was seen at the site of biliary sphincteroplasty.  This was most likely due to elevated INR of the patient.  A mechanical lithotripsy basket was used to remove the CBD stones.  This cholangiogram shows two CBD stones within the lithotripsy basket.  These CBD stones were removed without any difficulty from the common bile duct.]]></media:text>
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			<item>
				<title>EUS FNA of a Pancreatic Neuroendocrine Tumor</title>
				<pubDate>Fri, 20 Nov 2009 10:11:39 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=886</guid>
				<description><![CDATA[A 67 year old man was referred for an EUS of an incidental pancreatic mass lesion. 
His past medical history included a colorectal cancer resected 18 year ago. He was admitted to the hospital 1 month prior to the EUS for one episode of melaena. He had no weight loss and was otherwise well. He had a normal gastroscopy and colonoscopy  and a capsule endoscopy showed a small bowel polyp. To further investigate this polyp the patient had a CT abdomen that did not show the polyp but that revealed a 1.6 cm well defined mass in the neck of the pancreas (figure 1,2).

On EUS a well defined 1.6 cm homogenous hypoechoic mass with a central calcification was seen in the neck of the pancreas. The pancreatic duct was mildly dilated in the body and tail. There were no enlarged lymph nodes and the liver was normal. Fine needle aspiration biopsy was performed using a 25FG needle ( 3 passes) (video1 ). The cytological smears were highly cellular with discohesive sheets of small cells with high nuclear:cytoplasmic ratio, limited eccentric cytoplasm, round to pleiomophic nucleai and a mix of fine and coarse cromatin (figure 3). These features were suggestive of a neuroendocrine tumor. On immuno-histochemistry the cells were CAM5.2, pankeratin (weak), chromogranin and synaptophysin positive and cytokeratin 7, cytokeratin 20, cytokeratin 5/6 and S100 negative (figure 4). These findings confirmed the diagnosis of a pancreatic neuroendocrine tumour. The patient underwent a somastostatin receptor scintigraphy that showed a solitary increased uptake in the neck of the pancreas. Currently the patient is awaiting surgery.


EUS is an excellent method of diagnosing NET with an accuracy between 83%-93% (1,2) The typical EUS appearance of NET is that of a well defined round, homogeneous, hypoechoic lesion within the pancreas. Calcifications may suggest the presence of psammoma bodies, pathognomonic for somatostatinoma (3).  Rarely, NET may also appear isoechoic or cystic, the cystic NET representing 8% in recently published series (4). The most helpful cytologic finding for the diagnosis of NET is a richly cellular sample with a monotonous, poorly cohesive population of small or medium-sized cells with granular chromatin and plasmacytoid morphology (5). 

1.  Anderson M.A., Carpenter S., Thompson N.W., et al:  Endoscopic ultrasound is highly accurate and directs management in patients with neuroendocrine tumors of the pancreas.  Am J Gastroenterol 95. 2271-2277.2000
2.  Ardengh J.C., Andrade de Paulo G., et al:  EUS-guided FNA in the diagnosis of pancreatic neuroendocrine tumors before surgery.  Gastrointest Endosc 60. 378-384.2004
3.  Patel K. K, Kang Kim M. Neuroendocrine tumors of the pancreas: endoscopic diagnosis.
Curr Opin Gastroenterol. 2008;24(5):638-642.
4.  Jani N, Khalid A, Kaushik N, et al. EUS-guided FNA diagnosis of pancreatic endocrine tumors: new trends identified. Gastrointest Endosc 2008; 67:44-50.
5. Chatzipantelis P, Salla C , et all.  Endoscopic Ultrasound-guided Fine-Needle Aspiration Cytology of Pancreatic Neuroendocrine Tumors : A Study of 48 Cases. Cancer, 2008,  vol. 114, no4, pp. 255-262]]></description>
				<dc:creator>Alina Stoita, MBBS, Advanced Trainee in Gastroenterology, St Vincent&#39;s Hospital Sydney, Australia, David Williams, MBBS, Head of Department of Gastroenterology, St Vincent&#39;s Hospital Sydney, Australia</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=886</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/evca.p.eus.fna.mas.sto0911.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=886" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/Fig 1 Lesion in the neck of the pancreas on CT.jpg</media:thumbnail>
				<media:people role="producer">Alina Stoita, MBBS, Advanced Trainee in Gastroenterology, St Vincent&#39;s Hospital Sydney, Australia, David Williams, MBBS, Head of Department of Gastroenterology, St Vincent&#39;s Hospital Sydney, Australia</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[A 67 year old man was referred for an EUS of an incidental pancreatic mass lesion. 
His past medical history included a colorectal cancer resected 18 year ago. He was admitted to the hospital 1 month prior to the EUS for one episode of melaena. He had no weight loss and was otherwise well. He had a normal gastroscopy and colonoscopy  and a capsule endoscopy showed a small bowel polyp. To further investigate this polyp the patient had a CT abdomen that did not show the polyp but that revealed a 1.6 cm well defined mass in the neck of the pancreas (figure 1,2).

On EUS a well defined 1.6 cm homogenous hypoechoic mass with a central calcification was seen in the neck of the pancreas. The pancreatic duct was mildly dilated in the body and tail. There were no enlarged lymph nodes and the liver was normal. Fine needle aspiration biopsy was performed using a 25FG needle ( 3 passes) (video1 ). The cytological smears were highly cellular with discohesive sheets of small cells with high nuclear:cytoplasmic ratio, limited eccentric cytoplasm, round to pleiomophic nucleai and a mix of fine and coarse cromatin (figure 3). These features were suggestive of a neuroendocrine tumor. On immuno-histochemistry the cells were CAM5.2, pankeratin (weak), chromogranin and synaptophysin positive and cytokeratin 7, cytokeratin 20, cytokeratin 5/6 and S100 negative (figure 4). These findings confirmed the diagnosis of a pancreatic neuroendocrine tumour. The patient underwent a somastostatin receptor scintigraphy that showed a solitary increased uptake in the neck of the pancreas. Currently the patient is awaiting surgery.


EUS is an excellent method of diagnosing NET with an accuracy between 83%-93% (1,2) The typical EUS appearance of NET is that of a well defined round, homogeneous, hypoechoic lesion within the pancreas. Calcifications may suggest the presence of psammoma bodies, pathognomonic for somatostatinoma (3).  Rarely, NET may also appear isoechoic or cystic, the cystic NET representing 8% in recently published series (4). The most helpful cytologic finding for the diagnosis of NET is a richly cellular sample with a monotonous, poorly cohesive population of small or medium-sized cells with granular chromatin and plasmacytoid morphology (5). 

1.  Anderson M.A., Carpenter S., Thompson N.W., et al:  Endoscopic ultrasound is highly accurate and directs management in patients with neuroendocrine tumors of the pancreas.  Am J Gastroenterol 95. 2271-2277.2000
2.  Ardengh J.C., Andrade de Paulo G., et al:  EUS-guided FNA in the diagnosis of pancreatic neuroendocrine tumors before surgery.  Gastrointest Endosc 60. 378-384.2004
3.  Patel K. K, Kang Kim M. Neuroendocrine tumors of the pancreas: endoscopic diagnosis.
Curr Opin Gastroenterol. 2008;24(5):638-642.
4.  Jani N, Khalid A, Kaushik N, et al. EUS-guided FNA diagnosis of pancreatic endocrine tumors: new trends identified. Gastrointest Endosc 2008; 67:44-50.
5. Chatzipantelis P, Salla C , et all.  Endoscopic Ultrasound-guided Fine-Needle Aspiration Cytology of Pancreatic Neuroendocrine Tumors : A Study of 48 Cases. Cancer, 2008,  vol. 114, no4, pp. 255-262]]></media:text>
				<enclosure url="http://daveproject.org/media/videos/512k/480x320/flash/evca.p.eus.fna.mas.sto0911.mpg.flv" type="video/x-flash"  length="54321" />
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				<title>Pancreatic Sphincterotomy and Stent Placement for a Communicating Pseudocyst</title>
				<pubDate>Fri, 20 Nov 2009 10:11:16 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=885</guid>
				<description><![CDATA[ERCP is attempted for transpapillary drainage of a communicating pseudocyst.  Cannulation of the pancreatic orifice is performed using a standard sphincterotome. Injection pancreatogram reveals a gush of contrast extravasating from the main pancreatic duct. A large amount of contrast is seen pooling behind the endoscope. A decision is made to perform a pancreatic sphincterotomy and place a pancreatic duct stent.  Using a guidewire technique, the sphincterotome cutting wire is positioned in the 12 o&#39;clock to 1 o&#39;clock position to cut the pancreatic portion of the sphincter of Oddi.  In order to expose more of the intraduodenal portion of the sphincter muscle, the sphincterotome is contracted, or bowed, within the proximal pancreatic duct while simultaneously withdrawing the instrument to pull the sphincter out from the duodenal wall. In doing so, more of the pancreatic sphincter can be splayed to achieve a larger sphincterotomy. After sphincterotomy, the sphincterotome is exchanged over the guidewire. A 5-French, 3 cm pancreatic duct stent is placed to facilitate drainage of cyst fluid out the pancreatic duct orifice.]]></description>
				<dc:creator>Jonathan M Buscaglia, MD, Instructor of Medicine, Johns Hopkins Medical Center, Anthony Kalloo, M.D., Chief of Gastroenterology, Johns Hopkins Medical Center</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=885</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/evca.p.es.stent.bu0910.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=885" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/evca.p.es.stent.bu0910.jpg</media:thumbnail>
				<media:people role="producer">Jonathan M Buscaglia, MD, Instructor of Medicine, Johns Hopkins Medical Center, Anthony Kalloo, M.D., Chief of Gastroenterology, Johns Hopkins Medical Center</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[ERCP is attempted for transpapillary drainage of a communicating pseudocyst.  Cannulation of the pancreatic orifice is performed using a standard sphincterotome. Injection pancreatogram reveals a gush of contrast extravasating from the main pancreatic duct. A large amount of contrast is seen pooling behind the endoscope. A decision is made to perform a pancreatic sphincterotomy and place a pancreatic duct stent.  Using a guidewire technique, the sphincterotome cutting wire is positioned in the 12 o&#39;clock to 1 o&#39;clock position to cut the pancreatic portion of the sphincter of Oddi.  In order to expose more of the intraduodenal portion of the sphincter muscle, the sphincterotome is contracted, or bowed, within the proximal pancreatic duct while simultaneously withdrawing the instrument to pull the sphincter out from the duodenal wall. In doing so, more of the pancreatic sphincter can be splayed to achieve a larger sphincterotomy. After sphincterotomy, the sphincterotome is exchanged over the guidewire. A 5-French, 3 cm pancreatic duct stent is placed to facilitate drainage of cyst fluid out the pancreatic duct orifice.]]></media:text>
				<enclosure url="http://daveproject.org/media/videos/512k/480x320/flash/evca.p.es.stent.bu0910.mpg.flv" type="video/x-flash"  length="54321" />
			</item>
			
			<item>
				<title>EUS for Staging of Rectal Cancer</title>
				<pubDate>Mon, 09 Nov 2009 06:11:57 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=884</guid>
				<description><![CDATA[A 72 year-old man is found to have a rectal adenocarcinoma on screening colonoscopy. CT scan of the abdomen and pelvis is performed and shows evidence of rectal wall thickening without associated lymphadenopathy. Subsequent PET scan shows increased activity in the rectum only. Staging pull-through EUS examination is then performed. Radial imaging at 7.5 MHz shows clear identification of the bladder. Upon pull-through with the EUS scope, the rectal wall is identified showing the muscularis propria and a thickened submucosal space suggesting tumor involvement. The tumor appears to extend through the muscularis propria, shown here at the 6 o&#39;clock position. As the probe is withdrawn further, there is easy identification of the seminal vesicles. Upon withdrawal of the EUS scope towards the anal verge, the prostate gland is identified at the 11 o&#39;clock position. There is a clear interface between the rectal wall and the prostate gland. No lymphadenopathy is seen as the scope is finally pulled through the anus. An upper endoscope is then introduced through the tumor to the proximal tumor border. A 22-gauge sclerotherapy needle is then used to inject a total of 3 cc&#39;s of India Ink, or tattoo agent, in a submucosal bleb-like fashion in order to mark the proximal tumor border for possible surgical resection of this lesion. Final tumor stage: T3N0Mx.]]></description>
				<dc:creator>Jonathan M Buscaglia, MD, Instructor of Medicine, Johns Hopkins Medical Center</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=884</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/evca.c.eus.0910bu.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=884" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/EUS T3 image.BMP</media:thumbnail>
				<media:people role="producer">Jonathan M Buscaglia, MD, Instructor of Medicine, Johns Hopkins Medical Center</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[A 72 year-old man is found to have a rectal adenocarcinoma on screening colonoscopy. CT scan of the abdomen and pelvis is performed and shows evidence of rectal wall thickening without associated lymphadenopathy. Subsequent PET scan shows increased activity in the rectum only. Staging pull-through EUS examination is then performed. Radial imaging at 7.5 MHz shows clear identification of the bladder. Upon pull-through with the EUS scope, the rectal wall is identified showing the muscularis propria and a thickened submucosal space suggesting tumor involvement. The tumor appears to extend through the muscularis propria, shown here at the 6 o&#39;clock position. As the probe is withdrawn further, there is easy identification of the seminal vesicles. Upon withdrawal of the EUS scope towards the anal verge, the prostate gland is identified at the 11 o&#39;clock position. There is a clear interface between the rectal wall and the prostate gland. No lymphadenopathy is seen as the scope is finally pulled through the anus. An upper endoscope is then introduced through the tumor to the proximal tumor border. A 22-gauge sclerotherapy needle is then used to inject a total of 3 cc&#39;s of India Ink, or tattoo agent, in a submucosal bleb-like fashion in order to mark the proximal tumor border for possible surgical resection of this lesion. Final tumor stage: T3N0Mx.]]></media:text>
				<enclosure url="http://daveproject.org/media/videos/512k/480x320/flash/evca.c.eus.0910bu.mpg.flv" type="video/x-flash"  length="54321" />
			</item>
			
			<item>
				<title>Transgastric Endoscopic Necrosectomy for Walled-Off Pancreatic Necrosis</title>
				<pubDate>Wed, 28 Oct 2009 05:10:48 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=883</guid>
				<description><![CDATA[The patient is a 61 year-old gentleman with multiple medical problems, including end stage renal disease requiring a deceased donor kidney transplant, who developed walled-off pancreatic necrosis four months after an episode of severe gallstone pancreatitis. 

He developed progressive anorexia, early satiety, and post-prandial nausea, leading to profound weight loss despite nutritional supplementation and pancreatic enzyme replacement. 

Abdominal computed tomography (CT) scan revealed a 15 cm x 5 cm collection of necrotic debris and gas replacing the majority of the pancreatic parenchyma. 

A prolonged trial of percutaneous drainage failed to resolve the collection and resulted in a pancreatic-percutaneous fistula.  Because of the patient&#39;s multiple comorbidities, compromised nutritional state, and suboptimal functional status, a formal surgical necrosectomy was deferred. After discussion of the risks, benefits, and alternatives, he elected to proceed with a transgastric endoscopic necrosectomy.

The steps involved in performing a transgastric necrosectomy are: 

1) EUS-guided transgastric puncture into the necrosis followed by passage of a guidewire into the cavity.

2) Over the guidewire, electrosurgical current is delivered through a needle-knife cannula to establish a tract.

3) Pneumatic dilators are used to sequentially dilate the tract over the guidewire.

4) The necrosis cavity is entered with a standard gastroscope.

5) Flexible endoscopic instruments are used to debride necrotic tissue.

6) In the event multiple sessions are necessary, the tract is maintained for future debridement by placing multiple double pigtail stents.

With the curved-linear array echoendoscope in the antrum of the stomach, the necrosis cavity was identified endosonographically. After using Doppler to exclude an intervening blood vessel, a 19-gauge fine needle aspiration (FNA) needle was advanced into the cavity under endoscopic ulrasound (EUS) guidance. Through the needle, a hydrophilic guidewire was then passed into the cavity and coiled. Over this guidewire, a needle knife cannula was used to establish a tract between the lumen of the stomach and the necrosis cavity.

After withdrawing the needle knife, the echoendoscope was exchanged for a standard upper endoscope over the wire. Subsequently, wire-guided, through-the-scope pneumatic dilators were used to sequentially dilate the tract. In this particular case, the tract was dilated to a maximum diameter of 15 mm.  The final dilation was performed alongside the wire. 

The necrosis cavity was then entered with the standard gastroscope. After briefly exploring the cavity, mechanical debridement is initiated. Multiple endoscopic devices, including jumbo forceps, foreign body graspers, and an endoscopic net were used to grasp necrotic tissue and remove it from the cavity into the stomach lumen. In this case, resecting morsels of necrotic tissue with a hot snare and transferring these pieces into the stomach with a two-pronged grasper was most effective. 

The quantity of necrosis within the cavity was such that multiple prolonged sessions were necessary for complete debridement. In between sessions, the tract connecting the gastric lumen to the necrosis cavity was maintained by placing three 10 french double pigtail plastic stents. The necrosectomies were performed at 3-4 week intervals. The patient was given five days of oral fluoroquinolones after each procedure.

After the second session, the patient&#39;s symptoms improved substantially and his oral intake increased, leading to weight gain. After four sessions, a very small amount of necrotic tissue remained and all further intervention resulted in oozing from the cavity wall, suggesting viability. A repeat CT scan confirmed the near-complete resolution of pancreatic necrosis and the double pigtail stents were removed.

He remains asymptomatic 3 months after completion of the necrosectomy.]]></description>
				<dc:creator>B. Joseph Elmunzer, MD,, University of Michigan, Amaar Ghazale, MD,, University of Michigan, Akbar K. Waljee, MD,, University of Michigan, Craig M. Womeldorph MD,, University of Michigan</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=883</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/badihe_endoscopic-necrosectomy.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=883" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/thumbnail photo.BMP</media:thumbnail>
				<media:people role="producer">B. Joseph Elmunzer, MD,, University of Michigan, Amaar Ghazale, MD,, University of Michigan, Akbar K. Waljee, MD,, University of Michigan, Craig M. Womeldorph MD,, University of Michigan</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[The patient is a 61 year-old gentleman with multiple medical problems, including end stage renal disease requiring a deceased donor kidney transplant, who developed walled-off pancreatic necrosis four months after an episode of severe gallstone pancreatitis. 

He developed progressive anorexia, early satiety, and post-prandial nausea, leading to profound weight loss despite nutritional supplementation and pancreatic enzyme replacement. 

Abdominal computed tomography (CT) scan revealed a 15 cm x 5 cm collection of necrotic debris and gas replacing the majority of the pancreatic parenchyma. 

A prolonged trial of percutaneous drainage failed to resolve the collection and resulted in a pancreatic-percutaneous fistula.  Because of the patient&#39;s multiple comorbidities, compromised nutritional state, and suboptimal functional status, a formal surgical necrosectomy was deferred. After discussion of the risks, benefits, and alternatives, he elected to proceed with a transgastric endoscopic necrosectomy.

The steps involved in performing a transgastric necrosectomy are: 

1) EUS-guided transgastric puncture into the necrosis followed by passage of a guidewire into the cavity.

2) Over the guidewire, electrosurgical current is delivered through a needle-knife cannula to establish a tract.

3) Pneumatic dilators are used to sequentially dilate the tract over the guidewire.

4) The necrosis cavity is entered with a standard gastroscope.

5) Flexible endoscopic instruments are used to debride necrotic tissue.

6) In the event multiple sessions are necessary, the tract is maintained for future debridement by placing multiple double pigtail stents.

With the curved-linear array echoendoscope in the antrum of the stomach, the necrosis cavity was identified endosonographically. After using Doppler to exclude an intervening blood vessel, a 19-gauge fine needle aspiration (FNA) needle was advanced into the cavity under endoscopic ulrasound (EUS) guidance. Through the needle, a hydrophilic guidewire was then passed into the cavity and coiled. Over this guidewire, a needle knife cannula was used to establish a tract between the lumen of the stomach and the necrosis cavity.

After withdrawing the needle knife, the echoendoscope was exchanged for a standard upper endoscope over the wire. Subsequently, wire-guided, through-the-scope pneumatic dilators were used to sequentially dilate the tract. In this particular case, the tract was dilated to a maximum diameter of 15 mm.  The final dilation was performed alongside the wire. 

The necrosis cavity was then entered with the standard gastroscope. After briefly exploring the cavity, mechanical debridement is initiated. Multiple endoscopic devices, including jumbo forceps, foreign body graspers, and an endoscopic net were used to grasp necrotic tissue and remove it from the cavity into the stomach lumen. In this case, resecting morsels of necrotic tissue with a hot snare and transferring these pieces into the stomach with a two-pronged grasper was most effective. 

The quantity of necrosis within the cavity was such that multiple prolonged sessions were necessary for complete debridement. In between sessions, the tract connecting the gastric lumen to the necrosis cavity was maintained by placing three 10 french double pigtail plastic stents. The necrosectomies were performed at 3-4 week intervals. The patient was given five days of oral fluoroquinolones after each procedure.

After the second session, the patient&#39;s symptoms improved substantially and his oral intake increased, leading to weight gain. After four sessions, a very small amount of necrotic tissue remained and all further intervention resulted in oozing from the cavity wall, suggesting viability. A repeat CT scan confirmed the near-complete resolution of pancreatic necrosis and the double pigtail stents were removed.

He remains asymptomatic 3 months after completion of the necrosectomy.]]></media:text>
				<enclosure url="http://daveproject.org/media/videos/512k/480x320/flash/badihe_endoscopic-necrosectomy.mpg.flv" type="video/x-flash"  length="54321" />
			</item>
			
			<item>
				<title>Esophagus - Band Ligation of Actively Bleeding Gastroesophageal Varices</title>
				<pubDate>Wed, 28 Oct 2009 05:10:12 EST</pubDate>
				<guid>http://dave1.mgh.harvard.edu/viewfilms.cfm?film_id=715</guid>
				<description><![CDATA[A 53-year old female with hepatitis C, alcohol abuse, and child C cirrhosis presented with hematemesis for one day.  Vital signs on admission were a blood pressure of 100/66 and heart rate of 110.  Laboratory results were hemoglobin: 10 g/dL, platelets: 89,000, and INR: 2.8.  She had a previous history of esophageal varices without any bleeding or history of variceal banding.  Initial management consisted of packed red blood cells, IV Octreotide, a proton pump inhibitor, antibiotics, fresh frozen plasma, vitamin K, Erythromycin.  Emergent endoscopy was undertaken.  
	As the scope enters the gastroesophageal junction, an actively spurting vessel is seen at 2 o&#39;clock on the screen in the cardia.  Here is the retroflexed view also showing bleeding from the cardia.  After evaluation of the rest of the stomach and duodenum to rule out concurrent lesions, the scope is now repositioned and the GE junction is evaluated with a direct head on view.  The scope was urgently removed from the patient, a banding device mounted, and the patient&#39;s esophagus reintubated.  A band ligator is carefully positioned to show a &#8220;red out&#8221; which is due to the blood spurting on the lens of the endoscope as well as the suction applied.  After banding in the cardia, the varices in the esophagus are banded in a distal to proximal manner.
Sarin classified gastric varices into gastroesophageal varices type I where they extend into the lesser curvature, gastroesophageal varices type 2 where they extend to the fundus.  Isolated gastric varices type I which are only found in the fundus, and isolated gastric varices type 2 which have extensions to ectopic areas in the stomach or duodenum.
The management of gastric variceal bleeding can be subdivided into acute bleeding and secondary prophylaxis.
There is limited literature on the management of gastric varices, but the most current recommendations are: gastroesophageal varices may be managed like esophageal varices with band ligation.  Isolated gastric varices should be managed with endoscopic variceal obturation with N-butyl&#8211;cyanoacrylate injection when available.  Otherwise, endoscopic variceal ligation is an option.  Isolated gastric varices secondary to splenic vein thrombosis should be treated with splenectomy when possible.  TIPS should be considered in uncontrolled fundic varices and rebleeding varices despite multiple therapies.
Treatment with IV proton pump inhibitor appears in some studies to have a reduction in rebleeding rates.  Unlike esophageal varices, there are no studies to recommend the routine use of Terlipressin or Octreotide.  Antibiotics is also recommended for Spontaneous Bacterial Peritonitis prophylaxis.
Secondary prophylaxis against rebleeding includes a repeat endoscopy in two to three weeks and TIPSS or balloon occluded retrograde transvenous obliteration (BRTO) in the presence of gastrorenal shunts.]]></description>
				<dc:creator>Lauren Layer, Medical Student, University of Texas Medical Branch, Sathya Jaganmohan, MD, GI Fellow, University of Texas Medical Branch, Gottumukkala S. Raju, M.D., Director of Endoscopy, Center for Endoscopic Research, Training and Innovation, University of Texas Medical Branch, Andrew W. DuPont, M.D., Assistant Professor of Medicine, University of Texas Medical Branch</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=715</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/jaganmohan.band.lig.varic.ra200801f.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=715" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/uvs090308-0011.jpg</media:thumbnail>
				<media:people role="producer">Lauren Layer, Medical Student, University of Texas Medical Branch, Sathya Jaganmohan, MD, GI Fellow, University of Texas Medical Branch, Gottumukkala S. Raju, M.D., Director of Endoscopy, Center for Endoscopic Research, Training and Innovation, University of Texas Medical Branch, Andrew W. DuPont, M.D., Assistant Professor of Medicine, University of Texas Medical Branch</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[A 53-year old female with hepatitis C, alcohol abuse, and child C cirrhosis presented with hematemesis for one day.  Vital signs on admission were a blood pressure of 100/66 and heart rate of 110.  Laboratory results were hemoglobin: 10 g/dL, platelets: 89,000, and INR: 2.8.  She had a previous history of esophageal varices without any bleeding or history of variceal banding.  Initial management consisted of packed red blood cells, IV Octreotide, a proton pump inhibitor, antibiotics, fresh frozen plasma, vitamin K, Erythromycin.  Emergent endoscopy was undertaken.  
	As the scope enters the gastroesophageal junction, an actively spurting vessel is seen at 2 o&#39;clock on the screen in the cardia.  Here is the retroflexed view also showing bleeding from the cardia.  After evaluation of the rest of the stomach and duodenum to rule out concurrent lesions, the scope is now repositioned and the GE junction is evaluated with a direct head on view.  The scope was urgently removed from the patient, a banding device mounted, and the patient&#39;s esophagus reintubated.  A band ligator is carefully positioned to show a &#8220;red out&#8221; which is due to the blood spurting on the lens of the endoscope as well as the suction applied.  After banding in the cardia, the varices in the esophagus are banded in a distal to proximal manner.
Sarin classified gastric varices into gastroesophageal varices type I where they extend into the lesser curvature, gastroesophageal varices type 2 where they extend to the fundus.  Isolated gastric varices type I which are only found in the fundus, and isolated gastric varices type 2 which have extensions to ectopic areas in the stomach or duodenum.
The management of gastric variceal bleeding can be subdivided into acute bleeding and secondary prophylaxis.
There is limited literature on the management of gastric varices, but the most current recommendations are: gastroesophageal varices may be managed like esophageal varices with band ligation.  Isolated gastric varices should be managed with endoscopic variceal obturation with N-butyl&#8211;cyanoacrylate injection when available.  Otherwise, endoscopic variceal ligation is an option.  Isolated gastric varices secondary to splenic vein thrombosis should be treated with splenectomy when possible.  TIPS should be considered in uncontrolled fundic varices and rebleeding varices despite multiple therapies.
Treatment with IV proton pump inhibitor appears in some studies to have a reduction in rebleeding rates.  Unlike esophageal varices, there are no studies to recommend the routine use of Terlipressin or Octreotide.  Antibiotics is also recommended for Spontaneous Bacterial Peritonitis prophylaxis.
Secondary prophylaxis against rebleeding includes a repeat endoscopy in two to three weeks and TIPSS or balloon occluded retrograde transvenous obliteration (BRTO) in the presence of gastrorenal shunts.]]></media:text>
				<enclosure url="http://daveproject.org/media/videos/512k/480x320/flash/jaganmohan.band.lig.varic.ra200801f.mpg.flv" type="video/x-flash"  length="54321" />
			</item>
			
			<item>
				<title>Pseudomelanosis</title>
				<pubDate>Wed, 21 Oct 2009 08:10:15 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=882</guid>
				<description><![CDATA[During a routine endoscopy for Barrett&#39;s related dysplasia surveillance, this mucosal abnormality was identified.  
On endoscopy, these pigmented areas of mucosa in the antrum, pylorus, and duodenum were seen. This is the classic endoscopic finding of pseudomelanosis of the gastrointestinal tract, whose features include a brownish-black pigmentation of the mucosa in a non-inflamed, random, speckled pattern. There is no apparent associated mucosal thickening or other defects.
Pseudomelanosis has been observed to occur anywhere along the length of the gastrointestinal tract. The pigment of pseudomelanosis has not been completely characterized although ferrous sulfide is commonly found on staining. A recent case series demonstrated that the majority of these patients are taking oral iron therapy, and as well as antihypertensive medication.  A history of renal insufficiency is also common.
This pattern is similar to the finding of melanosis coli in right colon as seen here. With both clinical syndromes the pigmentation is found in lamina propria macrophages.  The pigmentation in melanosis coli, however, is in the form of lipofucschin, which is a degradation product of anthracine metabolites commonly taken in the form of oral cathartics in the management of chronic constipation. 
The diagnosis is of pseudomelanosis may be confirmed on biopsy.  Low power view of the duodenal lamina propria demonstrates villi with darkly pigmented cells admixed with inflammatory cells and vessels. The pigment  appears to be confined to histiocytes within the lamina propria and does not involve the epithelium. 
On higher magnification, the pigment is noted to be granular,  black,  and fairly uniform.
Pseudo-melanosis may be more subtle as was seen as an incidental finding in this second example during a routine colonoscopy. Here a faint brownish pigmentation can be observed in the terminal ileal mucosa in an otherwise unremarkable exam.  
It has been proposed that the sulfides present in various diuretics such as hydrochlorothiazide and furosemide can bind to oral iron, resulting in the pigmented deposition seen here. It is noteworthy that this patient&#39;s lengthy medication list included both oral iron replacement therapy as well as furosemide. The iron deposition seen in pseudomelanosis does not suggest either an iron overload state or any metabolic abnormality, nor does the iron need to be treated with chelation therapy.]]></description>
				<dc:creator>Mohammad Bilal,, Harvard Medical School, David G. Forcione, M.D., Instructor in Medicine, Harvard Medical School, Massachusetts General Hospital, Peter B. Kelsey, M.D., Assistant Professor of Medicine, Harvard Medical School, Massachusetts General Hospital</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=882</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/evca.i.pig.ooo.ooo.bio.1op.br060613.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=882" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/jpeg.i.pig.ooo.ooo.bio.1oo.br060613.jpg</media:thumbnail>
				<media:people role="producer">Mohammad Bilal,, Harvard Medical School, David G. Forcione, M.D., Instructor in Medicine, Harvard Medical School, Massachusetts General Hospital, Peter B. Kelsey, M.D., Assistant Professor of Medicine, Harvard Medical School, Massachusetts General Hospital</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[During a routine endoscopy for Barrett&#39;s related dysplasia surveillance, this mucosal abnormality was identified.  
On endoscopy, these pigmented areas of mucosa in the antrum, pylorus, and duodenum were seen. This is the classic endoscopic finding of pseudomelanosis of the gastrointestinal tract, whose features include a brownish-black pigmentation of the mucosa in a non-inflamed, random, speckled pattern. There is no apparent associated mucosal thickening or other defects.
Pseudomelanosis has been observed to occur anywhere along the length of the gastrointestinal tract. The pigment of pseudomelanosis has not been completely characterized although ferrous sulfide is commonly found on staining. A recent case series demonstrated that the majority of these patients are taking oral iron therapy, and as well as antihypertensive medication.  A history of renal insufficiency is also common.
This pattern is similar to the finding of melanosis coli in right colon as seen here. With both clinical syndromes the pigmentation is found in lamina propria macrophages.  The pigmentation in melanosis coli, however, is in the form of lipofucschin, which is a degradation product of anthracine metabolites commonly taken in the form of oral cathartics in the management of chronic constipation. 
The diagnosis is of pseudomelanosis may be confirmed on biopsy.  Low power view of the duodenal lamina propria demonstrates villi with darkly pigmented cells admixed with inflammatory cells and vessels. The pigment  appears to be confined to histiocytes within the lamina propria and does not involve the epithelium. 
On higher magnification, the pigment is noted to be granular,  black,  and fairly uniform.
Pseudo-melanosis may be more subtle as was seen as an incidental finding in this second example during a routine colonoscopy. Here a faint brownish pigmentation can be observed in the terminal ileal mucosa in an otherwise unremarkable exam.  
It has been proposed that the sulfides present in various diuretics such as hydrochlorothiazide and furosemide can bind to oral iron, resulting in the pigmented deposition seen here. It is noteworthy that this patient&#39;s lengthy medication list included both oral iron replacement therapy as well as furosemide. The iron deposition seen in pseudomelanosis does not suggest either an iron overload state or any metabolic abnormality, nor does the iron need to be treated with chelation therapy.]]></media:text>
				<enclosure url="http://daveproject.org/media/videos/512k/480x320/flash/evca.i.pig.ooo.ooo.bio.1op.br060613.mpg.flv" type="video/x-flash"  length="54321" />
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			<item>
				<title>Case Study: Endoscopic Ultrasound (EUS) Guided-Celiac Plexus Neurolysis (CPN)</title>
				<pubDate>Mon, 19 Oct 2009 12:10:26 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=881</guid>
				<description><![CDATA[<br/>
Author: Mohamad A. Eloubeidi, M.D., M.H.S., F.A.C.P., F.A.C.G. FASGE
Associate Professor of Medicine and Pathology Director, Endoscopic Ultrasound Program Co-Director Pancreatico-biliary Center 

Institution: University of Alabama at Birmingham 
Department of Medicine 
Division of Gastroenterology/Hepatology 


Statement of COI: Dr. Eloubeidi reports no conflicts of interests relating to this video presentation 

A 62 year old lady with pancreatic cancer was diagnosed two weeks ago at our center by EUS-guided FNA. We started her on Loretab but unfortunately it did not help her pain. During her last examination by EUS and by CT scan of the abdomen there is clear evidence of involvement of the celiac artery and therefore she is not amenable for surgical resection. We counseled her regarding the need for celiac plexus neurolysis (CPN) and she&#39;s here today to undergo CPN. Many studies published to date suggest that EUS-guided CPN is really helpful in the setting of pancreatic cancer pain  and leads to success in about 70-80% of the patients. It is a safe procedure performed on outpatient basis under conscious sedation. We have given our patient a low dose of Demerol, and Verset, and we used low dose Ketamine as an adjunct to sedation. Typically we insert the echo endoscope to the level of the celiac artery where the injection is performed at its base. The echo endoscope is inserted in the patient esophagus. It was a smooth intubation. When the echoendoscope is at about 35 cm from the incisors we switch to ultrasound. The landmark we look for is really the descending aorta at about 35-40 centimeters from the incisors. The descending aorta is a tubular organ as you see here with color Doppler ultrasound. Once you identify the aorta you push forward with the echo endoscope until you find the first branching artery and that&#39;s the celiac artery. 

To confirm further it would be nice to demonstrate the superior mesenteric artery as you can see in this image back to back. This way you are sure you are performing the celiac neurolysis in the right area. Also for confirmatory purposes we perform color Doppler sonography to identify further the celiac artery and to be sure that there are no intervening vessels in the way. The arrow actually is a good location and estimation of where I need my needle to be to initiate the injection. I am currently using the CPN needle it&#39;s a  20 gauge needle. I think the advantages are clear with using it. In comparison to the 22 gauge needle I think we can do a quicker and faster injection. I think I crossed the wall of the stomach here and then we&#39;re going to aspirate to ensure we don&#39;t have any blood return. We are performing the injection, again it&#39;s all at the tip of the arrow- you see the needle in place. That actually created a nice cushion for us to inject the alcohol. Now here we better be sure of the needle placement since the alcohol will create a hyperechoic shadow that will block the view as you see in this image. As you see the injections really quick with this fenestrated needle we used 6ccs of bupivacaine and we injected 20 ccs of absolute alcohol in this area. We withdraw the needle from the scope and at this time the procedure is terminated.]]></description>
				<dc:creator>Mohamad A. Eloubeidi, MD, Associate Professor of Medicine and Pathology, University of Alabama at Birmingham</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=881</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/evca.p.pancCA.cpn.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=881" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/vlcsnap-2009-10-17-08h18m12s233.jpg</media:thumbnail>
				<media:people role="producer">Mohamad A. Eloubeidi, MD, Associate Professor of Medicine and Pathology, University of Alabama at Birmingham</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[<br/>
Author: Mohamad A. Eloubeidi, M.D., M.H.S., F.A.C.P., F.A.C.G. FASGE
Associate Professor of Medicine and Pathology Director, Endoscopic Ultrasound Program Co-Director Pancreatico-biliary Center 

Institution: University of Alabama at Birmingham 
Department of Medicine 
Division of Gastroenterology/Hepatology 


Statement of COI: Dr. Eloubeidi reports no conflicts of interests relating to this video presentation 

A 62 year old lady with pancreatic cancer was diagnosed two weeks ago at our center by EUS-guided FNA. We started her on Loretab but unfortunately it did not help her pain. During her last examination by EUS and by CT scan of the abdomen there is clear evidence of involvement of the celiac artery and therefore she is not amenable for surgical resection. We counseled her regarding the need for celiac plexus neurolysis (CPN) and she&#39;s here today to undergo CPN. Many studies published to date suggest that EUS-guided CPN is really helpful in the setting of pancreatic cancer pain  and leads to success in about 70-80% of the patients. It is a safe procedure performed on outpatient basis under conscious sedation. We have given our patient a low dose of Demerol, and Verset, and we used low dose Ketamine as an adjunct to sedation. Typically we insert the echo endoscope to the level of the celiac artery where the injection is performed at its base. The echo endoscope is inserted in the patient esophagus. It was a smooth intubation. When the echoendoscope is at about 35 cm from the incisors we switch to ultrasound. The landmark we look for is really the descending aorta at about 35-40 centimeters from the incisors. The descending aorta is a tubular organ as you see here with color Doppler ultrasound. Once you identify the aorta you push forward with the echo endoscope until you find the first branching artery and that&#39;s the celiac artery. 

To confirm further it would be nice to demonstrate the superior mesenteric artery as you can see in this image back to back. This way you are sure you are performing the celiac neurolysis in the right area. Also for confirmatory purposes we perform color Doppler sonography to identify further the celiac artery and to be sure that there are no intervening vessels in the way. The arrow actually is a good location and estimation of where I need my needle to be to initiate the injection. I am currently using the CPN needle it&#39;s a  20 gauge needle. I think the advantages are clear with using it. In comparison to the 22 gauge needle I think we can do a quicker and faster injection. I think I crossed the wall of the stomach here and then we&#39;re going to aspirate to ensure we don&#39;t have any blood return. We are performing the injection, again it&#39;s all at the tip of the arrow- you see the needle in place. That actually created a nice cushion for us to inject the alcohol. Now here we better be sure of the needle placement since the alcohol will create a hyperechoic shadow that will block the view as you see in this image. As you see the injections really quick with this fenestrated needle we used 6ccs of bupivacaine and we injected 20 ccs of absolute alcohol in this area. We withdraw the needle from the scope and at this time the procedure is terminated.]]></media:text>
				<enclosure url="http://daveproject.org/media/videos/512k/480x320/flash/evca.p.pancCA.cpn.mpg.flv" type="video/x-flash"  length="54321" />
			</item>
			
			<item>
				<title>Pancreas - Advancing the Principles of Minimally Invasive Surgical Therapy: A Percutaneous, Combined IR / Flexible Endoscopic Pancreatic Necrosectomy</title>
				<pubDate>Thu, 20 Aug 2009 02:08:39 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=879</guid>
				<description><![CDATA[Our video aims to review the combined interventional radiographic and endoscopic techniques used to perform a percutaneous retroperitoneal necrosectomy in a patient with severe necrotizing pancreatitis.  The five minimally invasive tenants of the procedure will be demonstrated:
&diams;	Using interventional techniques to establish a retroperitoneal access site that will allow repeated endoscopic access.
&diams;	Inspect and lavage infected tissue under direct endoscopic guidance to soften the site for debridement.  
&diams;	Demonstrate debridement of necrotic tissue using a combination of snare polypectomy, rat-tooth forceps, and Roth net extraction.
&diams;	Once adequate debridement has been completed, Malencott drains are left in place in the access tract to allow residual fluid and tissue collection.
&diams;	And finally, demonstrate radiographic and clinical improvement following necrosectomy.
This preoperative CT scan demonstrates extensive multiloculated cystic fluid collections within the left retroperitoneum with small pockets of air, as indicated by the red arrows.  The location of these retroperitoneal cystic collections made it difficult for conventional transgastric endoscopic access.
After the patient is placed in the right lateral position, a previously placed percutaneous drainage tube is removed over wire, and the tract is dilated over a balloon stent.  A nine millimeter Pentax endoscope is passed through the overtube into the perinephric area with almost immediate expulsion of purulent material, as shown in the video in the upper left corner.
On the fluoroscopic view, the proximity of the endoscope can be seen between the  previously placed transgastric stent is visible.  Using standard snare polypectomy technique, large sections of necrotic debris are removed through the access tract.
In between snare removals, the tissue is irrigated with multiple flushes of sterile saline and aspirated to expose the underlying adherent debris.
Here we demonstrate the utility of the rat-tooth forceps in breaking up large sections of necrotic debris.  The device is carefully thrust back and forth to break sections that do not readily break free following snare polypectomy or saline flush.
A readily available Roth net is shown here removing sections of tissue that are too large or too adherent to come through the access catheter.  Roth net extraction allowed for larger sections of tissue removal.  
As evidenced here, visibility is often compromised, requiring delicacy and skill to be practiced while performing the separate techniques of the endoscopic necrosectomy.
At the completion of the necrosectomy, a Malencott drain is left in place to allow residual drainage of the necrotic debris over time.
The five week post-operative CT scan demonstrates interval decrease of the peripancreatic and the left retroperitoneal fluid collection, as shown here.
The red arrow designates placement of the Malencott drainage catheter.

In summary endoscopic intervention is effective in resolving collections of pancreatic necrosis that cannot be readily accessed by a transluminal approach.  
Percutaneous access sites can be adequately dilated to achieve sufficient access for percutaneous endoscopy.  Percutaneous endoscopy can be performed either directly or as demonstrated in this case, via a nephrostomy tube.
The goal of therapy should always be complete removal of necrosum for best outcome.  All three patients who underwent percutaneous necrosectomy at our institution have done well.
In conclusion, percutaneous endoscopic necrosectomy can be complementary to standard transluminal therapy in the management of complicated peri-pancreatic necrotic collections.]]></description>
				<dc:creator>Matthew T. Moyer, MD, MS, Clinical Instructor, Penn State Milton S. Hershey Medical Center, Arnab Biswas, DO,, Penn State Milton S. Hershey Medical Center, Abraham Mathew, MD, Associate Professor, Penn State Milton S. Hershey Medical Center, Frank C. Lynch, MD, , Associate Professor of Radiology and Surgery, Penn State Milton S. Hershey Medical Center, Leslie B. Scorza, MD, Assistant Professor of Radiology, Surgery &amp; Medicine, Penn State Milton S. Hershey Medical Center</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=879</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/evca.p.per.panc.necro.moyer.0908us.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=879" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/moyer-1.jpg</media:thumbnail>
				<media:people role="producer">Matthew T. Moyer, MD, MS, Clinical Instructor, Penn State Milton S. Hershey Medical Center, Arnab Biswas, DO,, Penn State Milton S. Hershey Medical Center, Abraham Mathew, MD, Associate Professor, Penn State Milton S. Hershey Medical Center, Frank C. Lynch, MD, , Associate Professor of Radiology and Surgery, Penn State Milton S. Hershey Medical Center, Leslie B. Scorza, MD, Assistant Professor of Radiology, Surgery &amp; Medicine, Penn State Milton S. Hershey Medical Center</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[Our video aims to review the combined interventional radiographic and endoscopic techniques used to perform a percutaneous retroperitoneal necrosectomy in a patient with severe necrotizing pancreatitis.  The five minimally invasive tenants of the procedure will be demonstrated:
&diams;	Using interventional techniques to establish a retroperitoneal access site that will allow repeated endoscopic access.
&diams;	Inspect and lavage infected tissue under direct endoscopic guidance to soften the site for debridement.  
&diams;	Demonstrate debridement of necrotic tissue using a combination of snare polypectomy, rat-tooth forceps, and Roth net extraction.
&diams;	Once adequate debridement has been completed, Malencott drains are left in place in the access tract to allow residual fluid and tissue collection.
&diams;	And finally, demonstrate radiographic and clinical improvement following necrosectomy.
This preoperative CT scan demonstrates extensive multiloculated cystic fluid collections within the left retroperitoneum with small pockets of air, as indicated by the red arrows.  The location of these retroperitoneal cystic collections made it difficult for conventional transgastric endoscopic access.
After the patient is placed in the right lateral position, a previously placed percutaneous drainage tube is removed over wire, and the tract is dilated over a balloon stent.  A nine millimeter Pentax endoscope is passed through the overtube into the perinephric area with almost immediate expulsion of purulent material, as shown in the video in the upper left corner.
On the fluoroscopic view, the proximity of the endoscope can be seen between the  previously placed transgastric stent is visible.  Using standard snare polypectomy technique, large sections of necrotic debris are removed through the access tract.
In between snare removals, the tissue is irrigated with multiple flushes of sterile saline and aspirated to expose the underlying adherent debris.
Here we demonstrate the utility of the rat-tooth forceps in breaking up large sections of necrotic debris.  The device is carefully thrust back and forth to break sections that do not readily break free following snare polypectomy or saline flush.
A readily available Roth net is shown here removing sections of tissue that are too large or too adherent to come through the access catheter.  Roth net extraction allowed for larger sections of tissue removal.  
As evidenced here, visibility is often compromised, requiring delicacy and skill to be practiced while performing the separate techniques of the endoscopic necrosectomy.
At the completion of the necrosectomy, a Malencott drain is left in place to allow residual drainage of the necrotic debris over time.
The five week post-operative CT scan demonstrates interval decrease of the peripancreatic and the left retroperitoneal fluid collection, as shown here.
The red arrow designates placement of the Malencott drainage catheter.

In summary endoscopic intervention is effective in resolving collections of pancreatic necrosis that cannot be readily accessed by a transluminal approach.  
Percutaneous access sites can be adequately dilated to achieve sufficient access for percutaneous endoscopy.  Percutaneous endoscopy can be performed either directly or as demonstrated in this case, via a nephrostomy tube.
The goal of therapy should always be complete removal of necrosum for best outcome.  All three patients who underwent percutaneous necrosectomy at our institution have done well.
In conclusion, percutaneous endoscopic necrosectomy can be complementary to standard transluminal therapy in the management of complicated peri-pancreatic necrotic collections.]]></media:text>
				<enclosure url="http://daveproject.org/media/videos/512k/480x320/flash/evca.p.per.panc.necro.moyer.0908us.mpg.flv" type="video/x-flash"  length="54321" />
			</item>
			
			<item>
				<title>Intestine - Total Gastrectomy with Esophagojejunostomy</title>
				<pubDate>Thu, 20 Aug 2009 02:08:47 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=880</guid>
				<description><![CDATA[The following video demonstrates the medical management of total gastrectomy with esophagojejunostomy. 
These are the two different types of esophago jejunostomies. This is a simple Roux-en-Y esophagojejunostomy. It has a short blind loop and a patent loop of jejunum.
We will now see the endoscopic view of a simple Roux-en-Y esophagojejunostomy in a 73 year old female patient who underwent total gastrectomy for the management of gastric adenocarcinoma.

The scope is introduced into the esophagus. One can see the esophago-jejunal anastomosis with the blind loop on the left and the patent loop on the right. Initial attempt was made to explore the blind loop followed by exploring the patent loop of jejunum. Here the endoscope is pushed through the patent loop followed by its withdrawal.
Total gastrectomy is indicated in the management of patients with gastric cancer, gastric sarcoma and gastric lymphoma. The procedure of total gastrectomy can be done either by laparotomy or by laparoscopy. Upto 3% of people may develop life threatening complications and around 20% may develop other serious complications.
All the complications arising as a result of total gastrectomy can be grouped as Post-gastrectomy syndrome.
The basic functions of the stomach are storage of the food and digestion of the food. As a result of the loss of these two basic functions, patients after total gastrectomy exhibit two major types of disturbances. Nutritional Intolerance which is due to loss of the storage function of the stomach  and Nutritional deficiency due to loss of the digestive capacity. Nutritional intolerance may present either as Dumping syndrome or Fat maldigestion.

We will now look in detail about the Dumping syndrome which is a result of the loss of gastric reservoir resulting in the rapid emptying of hyper osmolar contents into the small bowel causing fluid shifts. Depending on the time of the onset of symptoms, dumping syndrome can be classified as either early-onset type or the late-onset type.  Early-onset manifests within 15-30 minutes after a meal. This is due to the hyperosmolarity of food entering the small bowel leading to fluid shifts into the small bowel lumen resulting in its rapid distension and an increase in the frequency of its contractions. Late-onset dumping syndrome occurs 2-3 hours after a meal and is due to reactive hypoglycemia which is a result of hyperglycemia and subsequent hyperinsulinemia. Patients present with Post prandial weakness, flushing, dizziness and sweating as a result of the fluid shifts and hypoglycemia. 
Management of the patients with dumping syndrome includes counseling the patients about eating smaller meals at frequent intervals to prevent the hypoglycemia, to limit the fluid intake along with the meal and to eat food rich in proteins and fibers and also to avoid foods with high carbohydrates as they exacerbate both the early and late onset types.

Fat maldigestion is a result of the faster transit time, decreased enzyme production and larger food particles entering the small bowel preventing the proper mixing of enzymes leading to reduced digestion of ingested fats.  The management of these patients include supplementing them with pancreatic enzymes and advising them to take a low fat diet. 

Nutritional deficiencies can manifest either as   Anemia or metabolic bone disease. Anemia can be either megaloblastic or microcytic. Megaloblastic anemia is due to deficiency of Vitamin b12 as a result of absent intrinsic factor requires for its absorption and a deficiency of folic acid due to impaired absorption and digestion. Oral or parenteral supplementation of B12 and 5 mg of folic acid is given to prevent megaloblastic anemia. Microcytic anemia is due to inadequate iron absorption as a result of loss of gastric acidity. 200 mg of elemental iron daily is prescribed along with advising the patient to eat iron-containing foods and take vitamin C supplements which have been shown to enhance iron absorption. 

Metabolic bone disease is due to lack  of calcium and Vitamin D because of altered digestion and absorption. Patients manifest with fractures from osteoporosis, osteopenia and osteomalacia. The management of these patients includes regular monitoring of the Vitamin D levels and also the bone mineral density by DEXA scans and prescribing 500 mg of calcium TID and 800IU of Vit D daily.]]></description>
				<dc:creator>Chandra S. Dasari, MD,, MD Anderson Cancer Center, Gottumukkala S. Raju, M.D., Professor of Medicine, MD Anderson Cancer Center</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=880</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/evca.i.surg.stom.eja.med.manag.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=880" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/evca.i.surg.stom.eja.med.manag.jpg</media:thumbnail>
				<media:people role="producer">Chandra S. Dasari, MD,, MD Anderson Cancer Center, Gottumukkala S. Raju, M.D., Professor of Medicine, MD Anderson Cancer Center</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[The following video demonstrates the medical management of total gastrectomy with esophagojejunostomy. 
These are the two different types of esophago jejunostomies. This is a simple Roux-en-Y esophagojejunostomy. It has a short blind loop and a patent loop of jejunum.
We will now see the endoscopic view of a simple Roux-en-Y esophagojejunostomy in a 73 year old female patient who underwent total gastrectomy for the management of gastric adenocarcinoma.

The scope is introduced into the esophagus. One can see the esophago-jejunal anastomosis with the blind loop on the left and the patent loop on the right. Initial attempt was made to explore the blind loop followed by exploring the patent loop of jejunum. Here the endoscope is pushed through the patent loop followed by its withdrawal.
Total gastrectomy is indicated in the management of patients with gastric cancer, gastric sarcoma and gastric lymphoma. The procedure of total gastrectomy can be done either by laparotomy or by laparoscopy. Upto 3% of people may develop life threatening complications and around 20% may develop other serious complications.
All the complications arising as a result of total gastrectomy can be grouped as Post-gastrectomy syndrome.
The basic functions of the stomach are storage of the food and digestion of the food. As a result of the loss of these two basic functions, patients after total gastrectomy exhibit two major types of disturbances. Nutritional Intolerance which is due to loss of the storage function of the stomach  and Nutritional deficiency due to loss of the digestive capacity. Nutritional intolerance may present either as Dumping syndrome or Fat maldigestion.

We will now look in detail about the Dumping syndrome which is a result of the loss of gastric reservoir resulting in the rapid emptying of hyper osmolar contents into the small bowel causing fluid shifts. Depending on the time of the onset of symptoms, dumping syndrome can be classified as either early-onset type or the late-onset type.  Early-onset manifests within 15-30 minutes after a meal. This is due to the hyperosmolarity of food entering the small bowel leading to fluid shifts into the small bowel lumen resulting in its rapid distension and an increase in the frequency of its contractions. Late-onset dumping syndrome occurs 2-3 hours after a meal and is due to reactive hypoglycemia which is a result of hyperglycemia and subsequent hyperinsulinemia. Patients present with Post prandial weakness, flushing, dizziness and sweating as a result of the fluid shifts and hypoglycemia. 
Management of the patients with dumping syndrome includes counseling the patients about eating smaller meals at frequent intervals to prevent the hypoglycemia, to limit the fluid intake along with the meal and to eat food rich in proteins and fibers and also to avoid foods with high carbohydrates as they exacerbate both the early and late onset types.

Fat maldigestion is a result of the faster transit time, decreased enzyme production and larger food particles entering the small bowel preventing the proper mixing of enzymes leading to reduced digestion of ingested fats.  The management of these patients include supplementing them with pancreatic enzymes and advising them to take a low fat diet. 

Nutritional deficiencies can manifest either as   Anemia or metabolic bone disease. Anemia can be either megaloblastic or microcytic. Megaloblastic anemia is due to deficiency of Vitamin b12 as a result of absent intrinsic factor requires for its absorption and a deficiency of folic acid due to impaired absorption and digestion. Oral or parenteral supplementation of B12 and 5 mg of folic acid is given to prevent megaloblastic anemia. Microcytic anemia is due to inadequate iron absorption as a result of loss of gastric acidity. 200 mg of elemental iron daily is prescribed along with advising the patient to eat iron-containing foods and take vitamin C supplements which have been shown to enhance iron absorption. 

Metabolic bone disease is due to lack  of calcium and Vitamin D because of altered digestion and absorption. Patients manifest with fractures from osteoporosis, osteopenia and osteomalacia. The management of these patients includes regular monitoring of the Vitamin D levels and also the bone mineral density by DEXA scans and prescribing 500 mg of calcium TID and 800IU of Vit D daily.]]></media:text>
				<enclosure url="http://daveproject.org/media/videos/512k/480x320/flash/evca.i.surg.stom.eja.med.manag.mpg.flv" type="video/x-flash"  length="54321" />
			</item>
			
			<item>
				<title>Biliary - Multiple Liver Microabscesses in Malignant Biliary Obstruction; EUS view</title>
				<pubDate>Wed, 12 Aug 2009 12:08:17 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=878</guid>
				<description><![CDATA[Our case is a 75 year old male who presented with obstructive jaundice, fever, and leukocytosis with bandemia.  CT scan of the abdomen showed common bile duct and pancreatic duct dilation.  There was a large pancreatic mass seen along with multiple liver lesions.  Here in the abdominal CT scan the red arrows are pointing at multiple small loculated fluid collections.  Here you see the distal common bile duct with a markedly thickened wall and just below the bile duct is the portal vein.  As the common bile duct is followed distally it becomes obstructed by the pancreatic head mass.  The mass appeared hypechoic and irregular with measurements of approximately 4 cm x 3 cm.  EUS guided fine needle aspiration of this mass proved it to be an adenocarcinoma.  
	Here you see the sonographic imaging of the left lobe of the liver.  There are multiple, anechoic spaces dispersed throughout the parenchyma.  The anechoic nature of the liver lesions indicates that they are fluid filled and therefore this sonographic appearance will be consistent with microabscesses.  There were also markedly dilated intrahepatic bile ducts consistent with biliary obstruction and here the arrow points towards a thickened intrahepatic bile duct wall.  Again, as the liver is scanned, you can see multiple anechoic liver lesions dispersed throughout the parenchyma.  These would be more consistent with microabscesses than with metastatic picture.  Typically, metastatic lesions in the liver appear more solid in appearance and have a hypo, hyper or isoechoic appearance.  Our patient underwent percutaneous drainage of one of the fluid collections in the liver.  Purulent material was aspirated and diagnosis of hepatic abscesses was confirmed. The patient was treated with broad-spectrum intravenous antibiotics.  
	The annual incidence of liver abscesses is approximately 2.3 cases per 100,000 populations.  There is slight predominance in males and risk factor includes diabetes, hepatobiliary or pancreatic malignancy and liver transplant.  Management includes CT or US guided drainage and broad spectrum antibiotics.  [Editor&#39;s note:  In the management of patients with liver abscesses and cholangitis in the setting of malignant obstruction, draining the biliary tree either endoscopically or percutaneously is an important therapeutic maneuver to complement abscess drainage and antibiotics.]]]></description>
				<dc:creator>Manmeet Padda, MD, Advanced Endoscopy Fellow, Yale University, Uzma Siddiqui, M.D., Assistant Professor of Medicine, Yale University</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=878</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/Padda.rev.2009.07.08.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=878" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/uvs090708-002.BMP</media:thumbnail>
				<media:people role="producer">Manmeet Padda, MD, Advanced Endoscopy Fellow, Yale University, Uzma Siddiqui, M.D., Assistant Professor of Medicine, Yale University</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[Our case is a 75 year old male who presented with obstructive jaundice, fever, and leukocytosis with bandemia.  CT scan of the abdomen showed common bile duct and pancreatic duct dilation.  There was a large pancreatic mass seen along with multiple liver lesions.  Here in the abdominal CT scan the red arrows are pointing at multiple small loculated fluid collections.  Here you see the distal common bile duct with a markedly thickened wall and just below the bile duct is the portal vein.  As the common bile duct is followed distally it becomes obstructed by the pancreatic head mass.  The mass appeared hypechoic and irregular with measurements of approximately 4 cm x 3 cm.  EUS guided fine needle aspiration of this mass proved it to be an adenocarcinoma.  
	Here you see the sonographic imaging of the left lobe of the liver.  There are multiple, anechoic spaces dispersed throughout the parenchyma.  The anechoic nature of the liver lesions indicates that they are fluid filled and therefore this sonographic appearance will be consistent with microabscesses.  There were also markedly dilated intrahepatic bile ducts consistent with biliary obstruction and here the arrow points towards a thickened intrahepatic bile duct wall.  Again, as the liver is scanned, you can see multiple anechoic liver lesions dispersed throughout the parenchyma.  These would be more consistent with microabscesses than with metastatic picture.  Typically, metastatic lesions in the liver appear more solid in appearance and have a hypo, hyper or isoechoic appearance.  Our patient underwent percutaneous drainage of one of the fluid collections in the liver.  Purulent material was aspirated and diagnosis of hepatic abscesses was confirmed. The patient was treated with broad-spectrum intravenous antibiotics.  
	The annual incidence of liver abscesses is approximately 2.3 cases per 100,000 populations.  There is slight predominance in males and risk factor includes diabetes, hepatobiliary or pancreatic malignancy and liver transplant.  Management includes CT or US guided drainage and broad spectrum antibiotics.  [Editor&#39;s note:  In the management of patients with liver abscesses and cholangitis in the setting of malignant obstruction, draining the biliary tree either endoscopically or percutaneously is an important therapeutic maneuver to complement abscess drainage and antibiotics.]]]></media:text>
				<enclosure url="http://daveproject.org/media/videos/512k/480x320/flash/Padda.rev.2009.07.08.mpg.flv" type="video/x-flash"  length="54321" />
			</item>
			
			<item>
				<title>Racial and Ethnic Disparities in Liver Disease</title>
				<pubDate>Wed, 08 Jul 2009 03:07:53 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=877</guid>
				<description><![CDATA[Dr Andrea Reid, Gastroenterology Program Director at Massachusetts General Hospital, presented clinical grand rounds on the topic of "Racial and Ethnic Disparities in Liver Disease". Issues discussed include hepatitis B, hepatitis C, NAFLD, hepatocellular carcinoma, and liver transplantation. The lecture was recorded June 23, 2009.]]></description>
				<dc:creator>Andrea E. Reid, MD, MPH, Assistant Professor of Medicine, Harvard Medical School</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=877</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/reid_cgr_20090623.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=877" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/reid_cgr_20090623.jpg</media:thumbnail>
				<media:people role="producer">Andrea E. Reid, MD, MPH, Assistant Professor of Medicine, Harvard Medical School</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[Dr Andrea Reid, Gastroenterology Program Director at Massachusetts General Hospital, presented clinical grand rounds on the topic of "Racial and Ethnic Disparities in Liver Disease". Issues discussed include hepatitis B, hepatitis C, NAFLD, hepatocellular carcinoma, and liver transplantation. The lecture was recorded June 23, 2009.]]></media:text>
				<enclosure url="http://daveproject.org/media/videos/512k/480x320/flash/reid_cgr_20090623.flv" type="video/x-flash"  length="54321" />
			</item>
			
			<item>
				<title>NOTES Transrectal Rectosigmoid Resection</title>
				<pubDate>Wed, 08 Jul 2009 02:07:13 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=876</guid>
				<description><![CDATA[Dr Patricia Sylla, Instructor in Surgery at Massachusetts General Hospital, delivered clinical grand rounds at the MGH GI Unit on the topic of transrectal rectosigmoid resection via NOTES. The lecture was recorded May 19, 2009.]]></description>
				<dc:creator>Patricia Sylla, MD, Instructor in Surgery, Massachusetts General Hospital</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=876</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/sylla_cgr_20090519.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=876" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/sylla_cgr_20090519.jpg</media:thumbnail>
				<media:people role="producer">Patricia Sylla, MD, Instructor in Surgery, Massachusetts General Hospital</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[Dr Patricia Sylla, Instructor in Surgery at Massachusetts General Hospital, delivered clinical grand rounds at the MGH GI Unit on the topic of transrectal rectosigmoid resection via NOTES. The lecture was recorded May 19, 2009.]]></media:text>
				<enclosure url="http://daveproject.org/media/videos/512k/480x320/flash/sylla_cgr_20090519.flv" type="video/x-flash"  length="54321" />
			</item>
			
			<item>
				<title>Duodenum - Leaking Roof Concept of Duodenal Ulcers</title>
				<pubDate>Tue, 07 Jul 2009 04:07:56 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=875</guid>
				<description><![CDATA[The following video demonstrates the endoscopic view of a duodenal ulcer and a look at its pathogenesis by reviewing The leaking roof concept by C. S. Goodwin.

The most important causative factor for a duodenal ulcer is Helicobacter pylori.

Endoscopic view of a DU. The endoscope is in the duodenum. Retracting the scope from the second part of the duodenum slowly into the duodenal bulb showed an ulcer in the first part of the duodenum. Biopsies taken from this ulcer were positive for H pylori infection.

C. S. Goodwin published the Leaking roof concept explaining the pathogenesis of a DU in The Lancet in 1988. He compared the duodenum to a house with an intact roof. Any breech in the roof allows the leakage of acid rain resulting in the formation of an ulcer.
We will now look in detail the series of events leading to the formation of a DU according to the leaking roof concept. Gastric hypermotility along with the hyperacidity are the initiative factors which lead to the gastric metaplasia of the duodenum. H pylori which normally infects the gastric antrum producing antral gastritis invades the gastric metaplasia of the duodenum to produce duodenitis. H pylori damages the microvilli and the cytoskelatal webs and also disrupts the intercellular bridges. It also depletes the mucin by producing a protease and a lipase. Acid and pepsin leak through this damaged mucin roof and precipitate erosions and ulcerations leading to the formation of a DU. Other mucin disrupting factors also contribute to this. 

The principles of management of a patient with DU is therefore based on the precipitating causes. To repair the roof by treating H pylori and to prevent the acid rain by using proton pump inhibitors.]]></description>
				<dc:creator>Chandra S. Dasari, MD,, MD Anderson Cancer Center, Gottumukkala S. Raju, M.D., Professor of Medicine, MD Anderson Cancer Center</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=875</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/evca.d.leak.roof.dasari.ra0907.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=875" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/evca.d.leak.roof.dasari.ra0907.jpg</media:thumbnail>
				<media:people role="producer">Chandra S. Dasari, MD,, MD Anderson Cancer Center, Gottumukkala S. Raju, M.D., Professor of Medicine, MD Anderson Cancer Center</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[The following video demonstrates the endoscopic view of a duodenal ulcer and a look at its pathogenesis by reviewing The leaking roof concept by C. S. Goodwin.

The most important causative factor for a duodenal ulcer is Helicobacter pylori.

Endoscopic view of a DU. The endoscope is in the duodenum. Retracting the scope from the second part of the duodenum slowly into the duodenal bulb showed an ulcer in the first part of the duodenum. Biopsies taken from this ulcer were positive for H pylori infection.

C. S. Goodwin published the Leaking roof concept explaining the pathogenesis of a DU in The Lancet in 1988. He compared the duodenum to a house with an intact roof. Any breech in the roof allows the leakage of acid rain resulting in the formation of an ulcer.
We will now look in detail the series of events leading to the formation of a DU according to the leaking roof concept. Gastric hypermotility along with the hyperacidity are the initiative factors which lead to the gastric metaplasia of the duodenum. H pylori which normally infects the gastric antrum producing antral gastritis invades the gastric metaplasia of the duodenum to produce duodenitis. H pylori damages the microvilli and the cytoskelatal webs and also disrupts the intercellular bridges. It also depletes the mucin by producing a protease and a lipase. Acid and pepsin leak through this damaged mucin roof and precipitate erosions and ulcerations leading to the formation of a DU. Other mucin disrupting factors also contribute to this. 

The principles of management of a patient with DU is therefore based on the precipitating causes. To repair the roof by treating H pylori and to prevent the acid rain by using proton pump inhibitors.]]></media:text>
				<enclosure url="http://daveproject.org/media/videos/512k/480x320/flash/evca.d.leak.roof.dasari.ra0907.mpg.flv" type="video/x-flash"  length="54321" />
			</item>
			
			<item>
				<title>Endoscopic Resection of Distal Bile Duct Mass</title>
				<pubDate>Mon, 01 Jun 2009 01:06:56 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=866</guid>
				<description><![CDATA[<br/>
1.	This video demonstrated a case of endoscopic resection of a distal bile duct mass.
2.	A 76-yr old patient with recurrent cholangitis under went EUS for evaluation of a dilated bile duct. 
3.	At EUS, a hyperechoic mass was seen in the distal CBD consistent with a polyp.
4.	An ERCP was undertaken to evaluate the mass by intraductal ultrasound.
5.	Cholangiogram confirmed the presence of a distal CBD mass.
6.	At intraductal ultrasound, a dilated CBD was seen with a hyperechoic polypoid mass sparing the deep muscle layers.
7.	A biliary sphincterotomy was undertaken and extended up to the duct-duodenal junction.
8.	A stone retrieval balloon was then advanced into the bile duct and the inflated balloon was pulled.
9.	The bile duct mass was then gently extracted by pulling the balloon.
10.	Using a polypectomy snare, the mass was resected by administration of electrocautery.
11.	Using a net, the mass was retrieved successfully.
12.	The resected bile duct mass measured 2 cms.
13.	On histopathology, the resected mass was diagnosed to be a pyogenic granuloma of the bile duct that has not been previously reported. 
14.	At 6-month follow-up, the patient was doing well without any symptom recurrence.]]></description>
				<dc:creator>Shyam S. Varadarajulu, MD,, University of Alabama at Birmingham</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=866</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/P_40_VTS_01_1.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=866" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/P_40_VTS_01_1-1.jpg</media:thumbnail>
				<media:people role="producer">Shyam S. Varadarajulu, MD,, University of Alabama at Birmingham</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[<br/>
1.	This video demonstrated a case of endoscopic resection of a distal bile duct mass.
2.	A 76-yr old patient with recurrent cholangitis under went EUS for evaluation of a dilated bile duct. 
3.	At EUS, a hyperechoic mass was seen in the distal CBD consistent with a polyp.
4.	An ERCP was undertaken to evaluate the mass by intraductal ultrasound.
5.	Cholangiogram confirmed the presence of a distal CBD mass.
6.	At intraductal ultrasound, a dilated CBD was seen with a hyperechoic polypoid mass sparing the deep muscle layers.
7.	A biliary sphincterotomy was undertaken and extended up to the duct-duodenal junction.
8.	A stone retrieval balloon was then advanced into the bile duct and the inflated balloon was pulled.
9.	The bile duct mass was then gently extracted by pulling the balloon.
10.	Using a polypectomy snare, the mass was resected by administration of electrocautery.
11.	Using a net, the mass was retrieved successfully.
12.	The resected bile duct mass measured 2 cms.
13.	On histopathology, the resected mass was diagnosed to be a pyogenic granuloma of the bile duct that has not been previously reported. 
14.	At 6-month follow-up, the patient was doing well without any symptom recurrence.]]></media:text>
				<enclosure url="http://daveproject.org/media/videos/512k/480x320/flash/P_40_VTS_01_1.mpg.flv" type="video/x-flash"  length="54321" />
			</item>
			
			<item>
				<title>Direct Peroral Cholangioscopy in the Management of Refractory Stone Disease</title>
				<pubDate>Mon, 01 Jun 2009 01:06:55 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=865</guid>
				<description><![CDATA[Direct, peroral cholangioscopy in the management of refractory stone disease, presented by Gregory Cote, Steven Edmundowicz, Sreenivasa Jonnalagadda and Riad Azar. Cholangioscopy allows direct visualization of the bile duct; this has been used to distinguish malignant from benign bile duct lesions, as wall as in the management of complicated choledocholithiasis by allowing direct visualization for electrohydraulic lithotripsy, or EHL.

Traditional mother-daughter systems are limited by the need for two experienced endoscipists, poor visualization and the absence of a meaningful working channel. Single operator, fiberoptic cholangioscopy allows for four-way deflection and continuous irrigation, but the optical resolution remains inferior to standard endoscopic images. Direct, peroral cholangioscopy involves intubation of the biliary orifice using standard endoscopes. Wire guided cannulation has been described using and ultraslim 5.9 mm upper endoscope. Our group has recently reported a similar technique using a retrieval balloon to pull a standard gastroscope into the common hepatic duct. 

We will present two cases where direct peroral cholangioscopy facilitated management of complicated bile duct stones. The first patient is a 50 year old woman who initially presented with acute onset of right quadrant abdominal pain and jaundice. MRCP demonstrated a large stone occluding the common hepatic duct. On initial ERCP, attempts to extract the stone sing retrieval balloons and a lithotripsy basket were unsuccessful. To distinguish an obstruction common hepatic duct stone from Mirizzi syndrome, she returned for cholangioscopy and probable EHL.

A guidewire is left in the proximal hepatic duct. An 8.8 mm gastroscope, preloaded with a retrieval balloon, is then advanced over the guidewire to the level of major papilla. The balloon, shown under fluoroscopy, was inflated above the stone and used to stabilize the position of the gastroscope, allowing it to be reduced into the common bile duct. This generates a remarkably high resolution image the depicting the stone obstructing the cystic duct orifice and causing extrinsic compression on the common hepatic duct consistent with Mirizzi syndrome. As a result of the scope&#39;s tenuous position once the balloon was withdrawn, EHL could not be performed through the gastroscope. Single operator, fiberoptic cholangioscopy was used to direct EHL. Note the inferior image quality of the fiberoptic cholangioscope compared to the initial high resolution picture. EHL fragmented the obstructing stone, permitting balloon extraction in a piecemeal fashion. After two sessions of EHL, there was no evidence if biliary obstruction. In summary, direct peroral Cholangioscopy clarified the diagnosis of Mirizzi syndrome prior to successful treatment using EHL through fiberoptic Cholangioscopy.

Our second example is an 84 year old woman who presented with recurrent epigastric pain and jaundice at a nearby hospital. ERCP demonstrated multiple filling defects in the common bile duct, but attempts at stone extraction using retrieval balloons and baskets were unsuccessful. Repeat ERCP at our institution demonstrated multiple filling defects. Mechanical lithotripsy was performed on two occasions, but the largest stone persisted. She returned for cholangioscopy with the intention of performing EHL.

 In this case, the 8.8mm gastroscope directly visualized a distal filling defect through a widely patent biliary orifice. To facilitate direct cholangioscopy, balloon sphincteroplasty using an 18mm balloon is used to dilate the biliary orifice. This permits direct cannulation of the bile duct with the gastroscope. Once oriented, a long and flat stone is clearly visualized extending from the common hepatic duct to the lever of the bifurcation. Initial attempts to remove the stone using a large retrieval balloon are unsuccessful, flipping the stone from its original orientation. Since no retrieval baskets were available that fit through the working channel of the gastroscope, a retrieval net is carefully opened above the stone. The net is used to grasp the stone under direct visualization. The gastroscope is removed from the patient, bringing the 22 mm stone intact.

The gastroscope is advanced to the duodenum, where the biliary orifice is easily cannulated a second time. Fluoroscopy demonstrates the movement of the gastroscope as it is reduced to first examine the base of the cystic duct before advancing into the proximal common hepatic duct. Multiple 5 to 10mm stones persist, so the net is again used to retrieve several of these stones at a time. Several of these are released in the stomach, however, the larger stone material is trapped within the net, mandating the removal through the oropharynx. 

This process is repeated until a total of eight stones, each measuring at least 5mm, are extracted. Clearance of stones is confirmed on balloon occlusion cholangiogram and sweep using an oversized retrieval balloon.

To our knowledge, this is the first reported example of a retrieval net being used for stone extraction under direct visualization using peroral cholangioscopy.

Limitations of this technique must be considered, particularly the difficulty in maintaining a stable scope position to allow for further diagnostic ant therapeutic intervention. Further, direct cannulation of the bile duct often requires a markedly dilated common duct and balloon sphincteroplasty. Use of an overtube with a smaller diameter endoscope may address these issues.

Thank you to the ASGE video editing scholarship program.]]></description>
				<dc:creator>Gregory A. Cote, MD, MS,, University of Washington</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=865</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/P_31_R2_Cholangioscopy.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=865" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/P_31_R2_Cholangioscopy-1.jpg</media:thumbnail>
				<media:people role="producer">Gregory A. Cote, MD, MS,, University of Washington</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[Direct, peroral cholangioscopy in the management of refractory stone disease, presented by Gregory Cote, Steven Edmundowicz, Sreenivasa Jonnalagadda and Riad Azar. Cholangioscopy allows direct visualization of the bile duct; this has been used to distinguish malignant from benign bile duct lesions, as wall as in the management of complicated choledocholithiasis by allowing direct visualization for electrohydraulic lithotripsy, or EHL.

Traditional mother-daughter systems are limited by the need for two experienced endoscipists, poor visualization and the absence of a meaningful working channel. Single operator, fiberoptic cholangioscopy allows for four-way deflection and continuous irrigation, but the optical resolution remains inferior to standard endoscopic images. Direct, peroral cholangioscopy involves intubation of the biliary orifice using standard endoscopes. Wire guided cannulation has been described using and ultraslim 5.9 mm upper endoscope. Our group has recently reported a similar technique using a retrieval balloon to pull a standard gastroscope into the common hepatic duct. 

We will present two cases where direct peroral cholangioscopy facilitated management of complicated bile duct stones. The first patient is a 50 year old woman who initially presented with acute onset of right quadrant abdominal pain and jaundice. MRCP demonstrated a large stone occluding the common hepatic duct. On initial ERCP, attempts to extract the stone sing retrieval balloons and a lithotripsy basket were unsuccessful. To distinguish an obstruction common hepatic duct stone from Mirizzi syndrome, she returned for cholangioscopy and probable EHL.

A guidewire is left in the proximal hepatic duct. An 8.8 mm gastroscope, preloaded with a retrieval balloon, is then advanced over the guidewire to the level of major papilla. The balloon, shown under fluoroscopy, was inflated above the stone and used to stabilize the position of the gastroscope, allowing it to be reduced into the common bile duct. This generates a remarkably high resolution image the depicting the stone obstructing the cystic duct orifice and causing extrinsic compression on the common hepatic duct consistent with Mirizzi syndrome. As a result of the scope&#39;s tenuous position once the balloon was withdrawn, EHL could not be performed through the gastroscope. Single operator, fiberoptic cholangioscopy was used to direct EHL. Note the inferior image quality of the fiberoptic cholangioscope compared to the initial high resolution picture. EHL fragmented the obstructing stone, permitting balloon extraction in a piecemeal fashion. After two sessions of EHL, there was no evidence if biliary obstruction. In summary, direct peroral Cholangioscopy clarified the diagnosis of Mirizzi syndrome prior to successful treatment using EHL through fiberoptic Cholangioscopy.

Our second example is an 84 year old woman who presented with recurrent epigastric pain and jaundice at a nearby hospital. ERCP demonstrated multiple filling defects in the common bile duct, but attempts at stone extraction using retrieval balloons and baskets were unsuccessful. Repeat ERCP at our institution demonstrated multiple filling defects. Mechanical lithotripsy was performed on two occasions, but the largest stone persisted. She returned for cholangioscopy with the intention of performing EHL.

 In this case, the 8.8mm gastroscope directly visualized a distal filling defect through a widely patent biliary orifice. To facilitate direct cholangioscopy, balloon sphincteroplasty using an 18mm balloon is used to dilate the biliary orifice. This permits direct cannulation of the bile duct with the gastroscope. Once oriented, a long and flat stone is clearly visualized extending from the common hepatic duct to the lever of the bifurcation. Initial attempts to remove the stone using a large retrieval balloon are unsuccessful, flipping the stone from its original orientation. Since no retrieval baskets were available that fit through the working channel of the gastroscope, a retrieval net is carefully opened above the stone. The net is used to grasp the stone under direct visualization. The gastroscope is removed from the patient, bringing the 22 mm stone intact.

The gastroscope is advanced to the duodenum, where the biliary orifice is easily cannulated a second time. Fluoroscopy demonstrates the movement of the gastroscope as it is reduced to first examine the base of the cystic duct before advancing into the proximal common hepatic duct. Multiple 5 to 10mm stones persist, so the net is again used to retrieve several of these stones at a time. Several of these are released in the stomach, however, the larger stone material is trapped within the net, mandating the removal through the oropharynx. 

This process is repeated until a total of eight stones, each measuring at least 5mm, are extracted. Clearance of stones is confirmed on balloon occlusion cholangiogram and sweep using an oversized retrieval balloon.

To our knowledge, this is the first reported example of a retrieval net being used for stone extraction under direct visualization using peroral cholangioscopy.

Limitations of this technique must be considered, particularly the difficulty in maintaining a stable scope position to allow for further diagnostic ant therapeutic intervention. Further, direct cannulation of the bile duct often requires a markedly dilated common duct and balloon sphincteroplasty. Use of an overtube with a smaller diameter endoscope may address these issues.

Thank you to the ASGE video editing scholarship program.]]></media:text>
				<enclosure url="http://daveproject.org/media/videos/512k/480x320/flash/P_31_R2_Cholangioscopy.mpg.flv" type="video/x-flash"  length="54321" />
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			<item>
				<title>Pancreatic Balloon Sphincteroplasty For Removal of Large Radiolucent Pancreatic Stones</title>
				<pubDate>Mon, 01 Jun 2009 01:06:54 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=864</guid>
				<description><![CDATA[We describe here a technique of endoscopy large balloon sphincteroplasty for removing large radiolucent pancreatic stones. A 18Yrs old male patient with symptomatic large radiolucent pancreatic stones underwent a MRCP and then an ERCP for stone extraction.
ERCP was started in left lateral position with a normal cannula for cannulating the pancreatic duct. After turning the patient in the supine position a pancreatogram was obtained which showed large stones occupying the pancreatic duct with a uniformly dilated duct. A sphincterotomy was then carried out of the pancreatic sphincter using a double lumen sphincterotome with the cut being carried some where between 12 to 2&#39;oclock direction. The sphicterotomy was done in a step by step manner using a blended endocut current and as the cut was being progressed there was a flow of pancreatic juice with some floating whitish pancreatic stones coming out from the pancreatic duct. The cut was extended until the entire bulging position of the ampulla was cut and until the biliary and duodenal junction was reached. After making a complete cut a controlled radial expansion (CRE) balloon of 12-15mms was inserted by the side of the guide wire inside the dilated pancreatic duct an the pancreatic sphincter was dilated up to 13mm.
After dilation once the balloon removed there was a gush of pelt up pancreatic juice and some floating stones after which a stone extraction balloon was inserted right till the tail of the pancreas and some of the stones which were in the head and body of the pancreas were removed by gentle sweep of the balloon in the axis of the pancreatic duct. Two or three times the balloon had to be passed inside and pulled out for achieving complete ductal clearance. As the stoned were large inspite of the large balloon sphincteroplasty a gentle but firm push of the endoscope with the balloon inside was required to pull some of the stones out an there by the achieve a complete ductal clearance. Because of large balloon sphincteroplasty even the big stones which were located inside the pancreatic duct could be taken out by repeated sweeps of the stone extraction balloon catheter without the need of performing a intraductal lithotripsy. A pancreaotography done after the stone removal showed that most of the large stones were removed in a single sitting of balloon sphincteroplasty after which a temporary 7 Fr. Stent was placed inside for continued and enhanced pancreatic ductal drainage. The patients was followed up after three months and the stent was removed and the duct checked and the patient had been completely asymptomatic at six months follow up after stent removal.]]></description>
				<dc:creator>Amit P. Maydeo, MD,, Institute of Advanced Endoscopy</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=864</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/P_30_VTS_01_1.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=864" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/P_30_VTS_01_11.jpg</media:thumbnail>
				<media:people role="producer">Amit P. Maydeo, MD,, Institute of Advanced Endoscopy</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[We describe here a technique of endoscopy large balloon sphincteroplasty for removing large radiolucent pancreatic stones. A 18Yrs old male patient with symptomatic large radiolucent pancreatic stones underwent a MRCP and then an ERCP for stone extraction.
ERCP was started in left lateral position with a normal cannula for cannulating the pancreatic duct. After turning the patient in the supine position a pancreatogram was obtained which showed large stones occupying the pancreatic duct with a uniformly dilated duct. A sphincterotomy was then carried out of the pancreatic sphincter using a double lumen sphincterotome with the cut being carried some where between 12 to 2&#39;oclock direction. The sphicterotomy was done in a step by step manner using a blended endocut current and as the cut was being progressed there was a flow of pancreatic juice with some floating whitish pancreatic stones coming out from the pancreatic duct. The cut was extended until the entire bulging position of the ampulla was cut and until the biliary and duodenal junction was reached. After making a complete cut a controlled radial expansion (CRE) balloon of 12-15mms was inserted by the side of the guide wire inside the dilated pancreatic duct an the pancreatic sphincter was dilated up to 13mm.
After dilation once the balloon removed there was a gush of pelt up pancreatic juice and some floating stones after which a stone extraction balloon was inserted right till the tail of the pancreas and some of the stones which were in the head and body of the pancreas were removed by gentle sweep of the balloon in the axis of the pancreatic duct. Two or three times the balloon had to be passed inside and pulled out for achieving complete ductal clearance. As the stoned were large inspite of the large balloon sphincteroplasty a gentle but firm push of the endoscope with the balloon inside was required to pull some of the stones out an there by the achieve a complete ductal clearance. Because of large balloon sphincteroplasty even the big stones which were located inside the pancreatic duct could be taken out by repeated sweeps of the stone extraction balloon catheter without the need of performing a intraductal lithotripsy. A pancreaotography done after the stone removal showed that most of the large stones were removed in a single sitting of balloon sphincteroplasty after which a temporary 7 Fr. Stent was placed inside for continued and enhanced pancreatic ductal drainage. The patients was followed up after three months and the stent was removed and the duct checked and the patient had been completely asymptomatic at six months follow up after stent removal.]]></media:text>
				<enclosure url="http://daveproject.org/media/videos/512k/480x320/flash/P_30_VTS_01_1.mpg.flv" type="video/x-flash"  length="54321" />
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			<item>
				<title>Endoscopic Anastomosis Between the Cystic Duct Stump and a Severed Aberrant Right Hepatic Duct</title>
				<pubDate>Mon, 01 Jun 2009 01:06:53 EST</pubDate>
				<guid>http://daveproject.org/viewfilms.cfm?film_id=863</guid>
				<description><![CDATA[A 57 year old patient underwent cholecystectomy and colonic resection for a neoplasm in November 2007. Post operative course was complicated by a post-operative biliary leak.

An ERCP was performed and showed a complete transaction of posterolateral sectorial bile duct.

Fistula output reduced significantly after a percutaneous drainage of the severed duct but a low volume leak eventually persisted after 15 days. Patient was referred to our Endoscopy Unit for the endoscopic treatment.

The severed duct stump was not identified in ERCP.

Therefore, the cystic duct stump was cannulated and very stiff guide-wire was used to reopen the cystic duct stump.

A diagnostic catheter was advanced and the stiff guide-wire was exchanged with a fully hydrophilic soft-angle-tip guide-wire. The guide-wire was gently maneuvered with back &#8211;and &#8211;fro and torch movement to pass through the CD stump into the peritoneum and therefore into the severed duct.

Once again cholangiography demonstrated leak from the aberrant duct.

The percutaneous tube was withdrawn.

A 4mm balloon was advanced over the wire and inflated to dilate the cystic stump and the new path between the cystic duct and the aberrant duct.

A guiding catheter was pushed into the postero-lateral bile duct and therefore a 10F 12cm long stent was placed to create an anastomosis between the severed duct and cystic duct stump.

Bile leak stopped immediately. Cholangiography after 24 hours did not demonstrate any contrast leak. The PTC tube and the sub hepatic drain were removed.

The stent was let in place for three months. At ERCP a long and tight stricture was observed, without any contrast leaks. Patient underwent re-stenting for an additional 3 months.

The stent was eventually removed, without any prior cholangiography.

This kind approach should not be generalized for all patients with post-operative major biliary lesions and should not be considered only as a rescue measure for the management of biliary leaks.

A long stricture is likely to be present at the level of the &#8220;anastomosis&#8221; between the cystic duct stump and the posterolateral duct.

Such a stricture is unlikely to be successfully treated endoscopically. Surgery will be scheduled in case of recurrent cholangitis.]]></description>
				<dc:creator>Guido Costamagna, MD,, Catholic University, Rome</dc:creator>
				<link>http://daveproject.org/viewfilms.cfm?film_id=863</link>
				<media:content url="http://daveproject.org/media/videos/512k/480x320/flash/P_27_Costamagna.mpg.flv" type="video/x-flash" playerUrl="http://daveproject.org/ViewFilms.cfm?film_id=863" playerHeight="480" playerWidth="320" expression="full"></media:content>
				<media:thumbnail height="180" width="120">http://daveproject.org/media/images/clip_img/180x120/P_27_Costamagna.jpg</media:thumbnail>
				<media:people role="producer">Guido Costamagna, MD,, Catholic University, Rome</media:people>
				<media:category>Science : Educational Resources : Gastroenterology</media:category>
				<creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license>
				<media:text><![CDATA[A 57 year old patient underwent cholecystectomy and colonic resection for a neoplasm in November 2007. Post operative course was complicated by a post-operative biliary leak.

An ERCP was performed and showed a complete transaction of posterolateral sectorial bile duct.

Fistula output reduced significantly after a percutaneous drainage of the severed duct but a low volume leak eventually persisted after 15 days. Patient was referred to our Endoscopy Unit for the endoscopic treatment.

The severed duct stump was not identified in ERCP.

Therefore, the cystic duct stump was cannulated and very stiff guide-wire was used to reopen the cystic duct stump.

A diagnostic catheter was advanced and the stiff guide-wire was exchanged with a fully hydrophilic soft-angle-tip guide-wire. The guide-wire was gently maneuvered with back &#8211;and &#8211;fro and torch movement to pass through the CD stump into the peritoneum and therefore into the severed duct.

Once again cholangiography demonstrated leak from the aberrant duct.

The percutaneous tube was withdrawn.

A 4mm balloon was advanced over the wire and inflated to dilate the cystic stump and the new path between the cystic duct and the aberrant duct.

A guiding catheter was pushed into the postero-lateral bile duct and therefore a 10F 12cm long stent was placed to create an anastomosis between the severed duct and cystic duct stump.

Bile leak stopped immediately. Cholangiography after 24 hours did not demonstrate any contrast leak. The PTC tube and the sub hepatic drain were removed.

The stent was let in place for three months. At ERCP a long and tight stricture was observed, without any contrast leaks. Patient underwent re-stenting for an additional 3 months.

The stent was eventually removed, without any prior cholangiography.

This kind approach should not be generalized for all patients with post-operative major biliary lesions and should not be considered only as a rescue measure for the management of biliary leaks.

A long stricture is likely to be present at the level of the &#8220;anastomosis&#8221; between the cystic duct stump and the posterolateral duct.

Such a stricture is unlikely to be successfully treated endoscopically. Surgery will be scheduled in case of recurrent cholangitis.]]></media:text>
				<enclosure url="http://daveproject.org/media/videos/512k/480x320/flash/P_27_Costamagna.mpg.flv" type="video/x-flash"  length="54321" />
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