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	<title>Gastroenterology Education and CPD for trainees and specialists &#187; Pancreaticobiliary</title>
	<atom:link href="https://www.gastrotraining.com/category/pancreaticobiliary/feed" rel="self" type="application/rss+xml" />
	<link>https://www.gastrotraining.com</link>
	<description>Largest online gastroenterology, hepatology and endoscopy education and training resource with histology, x-ray images, videos, gastro calculators, and MCQs.</description>
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		<title>Percutaneous Transhepatic Cholangiography</title>
		<link>https://www.gastrotraining.com/ptc-endoscopy/percutaneous-transhepatic-cholangiography</link>
		<comments>https://www.gastrotraining.com/ptc-endoscopy/percutaneous-transhepatic-cholangiography#comments</comments>
		<pubDate>Sun, 08 May 2011 08:13:51 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[PTC]]></category>
		<category><![CDATA[PTC Endoscopy]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=6215</guid>
		<description><![CDATA[For biliary decompression/ biliary stenting when ERCP fails (classically hilar tumour). Some units prefer PTC over ERCP for Hilar obstructions In CBD stone disease- when ERCP is unsuccessful- PTC is carried out first and then a Rendezvous ERCP is carried out Steps: Patient is placed on supine position and draped aseptically after cleaning the site [...]]]></description>
				<content:encoded><![CDATA[<ol>
<li>For biliary decompression/ biliary stenting when ERCP fails (classically hilar tumour). Some units prefer PTC over ERCP for Hilar obstructions</li>
<li>In CBD stone disease- when ERCP is unsuccessful- PTC is carried out first and then a Rendezvous ERCP is carried out</li>
</ol>
<p>Steps:</p>
<ol>
<li>Patient is      placed on supine position and draped aseptically after cleaning the site</li>
<li>US probe is covered with aseptic      plastic sheath and so is the image intensifier</li>
<li>Radiologist/interventionist  is also dressed aseptically with gown      over lead apron (also leaded sterile gloves)</li>
<li>Patient is      given both local anaesthesia +/- IV sedation (fentanyl/midazolam)</li>
<li>Anticipated      needle tract is anaesthetized and a 3mm stab of the skin is made</li>
<li>Under US      guidance a dilated left/right biliary radicle is punctured with a 22G      Chiba needle ( part of Neff set &#8211; Chiba needle, dilator and .018      guidewire)  and the position is      checked by injecting contrast (through a connecting tubing) with the      patient breath holding in mid inspiration</li>
<li>Once      position is confirmed a 0.018 guidewire (platinum tipped to ensure      visibility on fluoroscopy) is advanced and then the Chiba needle is withdrawn a dilator is      passed to dilate the tract through the liver capsule. Wire is changed to      0.038 guidewire and dilator is withdrawn</li>
</ol>
<p>Cholangiogram showing a hilar stricture (above the coiled appearance of the cystic duct)</p>
<p>Same patient with an external-internal drain in situ beside a metal biliary stent across the stricture (also note distended gall bladder in the second picture)</p>
<ol>
<li>A biliary      manipulation catheter (BMC) is threaded over the guidewire and guidewire      is changed to Hydrophilic Terumo wire to cross the stricture.</li>
<li>Once the      stricture is crossed then guidewire is advanced to the distal duodenum      followed by the BMC catheter- position confirmed by contrast in the small      bowel.</li>
<li>Then BMC      catheter is withdrawn and 7.5F angio sheath is introduced over the      guidewire</li>
<li>Guidewire      is changed to Amplatz superstiff/stiff guidewire.</li>
<li>Then a      metal biliary stent is placed across the stricture and deployed</li>
<li>The metal      stent may need to be further dilated with an angio balloon (inflated      across the stricture).</li>
<li>Normally an      8F catheter is also kept to drain externally to ensure access and faster      drainage.</li>
<li>The      external drainage catheter can be closed off after 48hours (if LFT’s are      improving and repeat imaging shows decompressed biliary system) and may be      removed after a further period of observation. While removing the external      catheter, the hole in the liver capsule is sealed of by injecting gel.</li>
<li>If in      doubt about sepsis and cholangitis- before a stent is placed- biliary tree      is decompressed thoroughly by placing an external-internal (EI) drain. An      EI drain will have a loop in the duodenum outside ampulla and draining holes      above the stricture (the technique to ensure that &#8211; a guidewire is passed      through the EI drain- when it catches the hole on further pushing it      buckles- on screening it ensures that buckle is above the stricture). Bile      will collect in the external bag as well as will flow in the duodenum.      Clipping the external drain ensures bile flows predominantly internally.</li>
<li>For      biliary stone disease-Rendezvous procedure: After initial      external-internal drainage, a guidewire is passed again in to the duodenum      and EI drain is withdrawn. This is a very long guidewire- as it needs to      come out through ampulla and then be able to be fed through the accessory      channel of the ERCP scope (duodenoscope)</li>
<li>The      duodenoscope is introduced and a snare is used to grab the tip of the guidewire      and pulled back through the accessory channel.</li>
<li>Then the      sphincterotome is passed over the guidewire into the biliary tree. Once      position is secure- external guidewire is withdrawn and fresh guidewire is      passed through accessory port into the biliary system.</li>
</ol>
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		</item>
		<item>
		<title>Sphincter of Oddi (SO) dysfunction</title>
		<link>https://www.gastrotraining.com/pancreaticobiliary/sphincter-of-oddi/sphincter-of-oddi-dysfunction</link>
		<comments>https://www.gastrotraining.com/pancreaticobiliary/sphincter-of-oddi/sphincter-of-oddi-dysfunction#comments</comments>
		<pubDate>Fri, 30 Jul 2010 07:25:26 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[Sphincter of Oddi dysfunction]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=1885</guid>
		<description><![CDATA[Discuss the SO dysfunction? The SO is a muscle that encircles the confluence of the distal common bile duct and the pancreatic duct as they penetrate the wall of the duodenum. The term &#8220;sphincter of Oddi&#8221; dysfunction is used to describe a clinical syndrome of biliary or pancreatic obstruction related to mechanical or functional abnormalities [...]]]></description>
				<content:encoded><![CDATA[<p><strong>Discuss the SO dysfunction?</strong></p>
<ul>
<li>The SO is a muscle that encircles the confluence of the distal common bile duct and the pancreatic duct as they penetrate the wall of the duodenum.</li>
<li>The term &#8220;sphincter of Oddi&#8221; dysfunction is used to describe a clinical syndrome of biliary or pancreatic obstruction related to mechanical or functional abnormalities of the sphincter of Oddi.</li>
<li>SO dysfunction may be caused by SO stenosis (due to inflammation and scarring from pancreatitis, passage of gallstones, infection etc) or SO dyskinesia (functional obstruction of SO, leading to intermittent biliary obstruction).</li>
<li>The prevalence of SO dysfunction is difficult to estimate.</li>
</ul>
<p><strong><br />
Discuss the clinical features of SO dysfunction?</strong><br />
SO dysfunction can cause biliary pain and pancreatitis.</p>
<p><strong>Discuss the types of SO dysfunction?</strong></p>
<p>The Rome III consensus statement classifies SO dysfunction into 3 types.<br />
<strong><br />
Type I patients (Definite SOD dysfunction)</strong></p>
<ul>
<li>Biliary-type pain;</li>
<li>Abnormal aminotransferases, bilirubin or alkaline phosphatase &gt;2 times normal values documented on two or more occasions and a</li>
<li>Dilated bile duct greater than 8 mm diameter on ultrasound.</li>
<li>Majority have manometric evidence of biliary SOD. However, it is unnecessary.</li>
<li>Type I patients benefit from sphincterotomy in 90%.</li>
</ul>
<p><strong>Type II patients (Presumptive SOD dysfunction)</strong></p>
<ul>
<li>Biliary-type pain and</li>
<li>One of the previously mentioned laboratory or imaging abnormalities.</li>
<li>Up to 60% patients may have manometric evidence of biliary SOD .Manometry is essential before considering sphincterotomy.</li>
<li>Type II benefit from sphincterotomy if basal pressure are elevated on manometry.</li>
<li>Some experts recommend empiric sphincterotomy in such patients, a strategy that was supported by a cost-effectiveness analysis.</li>
</ul>
<p><strong>Type III patients (Possible SOD dysfunction)</strong></p>
<ul>
<li>Recurrent biliary-type pain and</li>
<li>Have none of the previously mentioned laboratory or imaging criteria.</li>
<li>Variable number of these patients have manometric evidence of biliary SOD. Manometry is essential if intervention is contemplated</li>
<li>Group III benefit from sphincterotomy in only 50% if abnormal manometry</li>
<li>Pharmacologic trials should be tried with PPI, GTN, calcium channel blockers etc before considering SO manometry.</li>
</ul>
<p><strong>Discuss evaluation of SO dysfunction?</strong></p>
<ul>
<li>These patients are a diagnostic challenge. Invasive procedures should be avoided in such patients if possible. ERCP with manometry and sphincterotomy should preferably be done at specialist centres.</li>
<li>Functional bowel diseases such as dyspepsia or irritable bowel syndrome should be considered in the differential diagnosis.</li>
<li>If SO dysfunction is clinically suspected, some experts recommend obtaining a gallbladder ejection fraction to determine whether the gallbladder may be the source of symptoms. They recommend laparoscopic cholecystectomy for those who have an ejection fraction &lt;40 percent.</li>
<li>For patients who have undergone cholecystectomy- Liver and pancreatic biochemical tests are recommended followed by ultrasound, MRCP and then ERCP with SO manometry as needed. Choledochoscintigraphy may be a useful test before undertaking SO manometry.</li>
</ul>
<p><strong><br />
Discuss evaluation of suspected pancreatic SOD? </strong><br />
Diagnostic evaluation suggested in the Rome III consensus statements suggest the following in patients presenting with pain episodes associated with an elevated amylase/lipase.</p>
<ul>
<li>Exclude structural abnormalities like microlithiasis or pancreas divisum by USS, CT, EUS, MRCP or ERCP depending upon the patients&#8217; clinical picture.</li>
<li>If the above are negative,ERCP with bile analysis and SO manometry may be indicated as needed.</li>
</ul>
]]></content:encoded>
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		</item>
		<item>
		<title>Mirizzi syndrome</title>
		<link>https://www.gastrotraining.com/pancreaticobiliary/mirizzi-syndrome/mirizzi-syndrome</link>
		<comments>https://www.gastrotraining.com/pancreaticobiliary/mirizzi-syndrome/mirizzi-syndrome#comments</comments>
		<pubDate>Fri, 30 Jul 2010 07:21:36 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[Mirizzi syndrome]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=1882</guid>
		<description><![CDATA[Discuss Mirizzi syndrome? It refers to common hepatic duct obstruction caused by an extrinsic compression from an impacted stone in the cystic duct or Hartmann’s pouch. It presents with obstructive jaundice, RUQ pain and fever USS/CT will show gall stones and dilation of the biliary system above the level of gall bladder neck. ERCP and [...]]]></description>
				<content:encoded><![CDATA[<p><span style="text-decoration: underline;"><strong></strong></span><strong>Discuss Mirizzi syndrome?</strong><br />
It refers to common hepatic duct obstruction caused by an extrinsic compression from an impacted stone in the cystic duct or Hartmann’s pouch.<br />
It presents with obstructive jaundice, RUQ pain and fever<br />
USS/CT will show gall stones and dilation of the biliary system above the level of gall bladder neck.<br />
ERCP and biliary stenting may be needed in patients with jaundice or cholangitis. Surgery is the mainstay of treatment.<br />
Recognition of Mirizzi syndrome is of particular importance because surgery in its presence is associated with an increased incidence of bile duct injury at surgery; indeed the syndrome has been cited as a trap in the surgery of gallstones.</p>
]]></content:encoded>
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		<item>
		<title>Complications of Laparoscopic cholecystectomy</title>
		<link>https://www.gastrotraining.com/pancreaticobiliary/cholecystectomy/cholecystectomy</link>
		<comments>https://www.gastrotraining.com/pancreaticobiliary/cholecystectomy/cholecystectomy#comments</comments>
		<pubDate>Fri, 30 Jul 2010 07:19:04 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[Cholecystectomy]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=1877</guid>
		<description><![CDATA[Discuss the complications of laparoscopic cholecystectomy? Serious complications can occur in 2.6 percent. A study of laparoscopic cholecystectomies reported the following types and frequencies of major complications: bleeding (0.11 to 1.97 percent), abscess (0.14 to 0.3 percent), bile leak (0.3 to 0.9 percent), biliary injury (0.26 to 0.6 percent), and bowel injury (0.14 to 0.35 [...]]]></description>
				<content:encoded><![CDATA[<p><strong>Discuss the complications of laparoscopic cholecystectomy?</strong><br />
Serious complications can occur in 2.6 percent.<br />
A study of laparoscopic cholecystectomies reported the following types and frequencies of major complications: bleeding (0.11 to 1.97 percent), abscess (0.14 to 0.3 percent), bile leak (0.3 to 0.9 percent), biliary injury (0.26 to 0.6 percent), and bowel injury (0.14 to 0.35 percent)<br />
<strong>Biliary leak</strong><br />
Major biliary leakage is usually seen 2 to 10 days postcholecystectomy. Affected patients typically present with fever, abdominal pain, and/or bilious ascites. Jaundice is usually mild. Leukocytosis and abnormal liver function tests are common. Bilirubin will be mildly elevated as the body reabsorbs third-spaced bile.<br />
An initial USS helps to define the extent of bile leak.  Bile leaks can present as localised collection or diffuse peritonitis. CT scan can define the collections better. Large loculated collections may need to be percutaneously drained by the radiologist.<br />
MRCP offers a non-invasive method of diagnosing a bile leak, identifying the source of the leak<br />
Significant biliary leaks can be managed by biliary stent inserted at the time of the ERCP to decrease pressure in the proximal biliary system. The stent is subsequently removed if the patient is asymptomatic and the liver function tests are normal and there is no ongoing leak at the follow-up ERCP.<br />
Some bile duct injuries present late with biliary strictures<br />
<strong>Bleeding complications</strong> — bleeding can occur from three distinct sites &#8211; the liver, arterial sources (cystic artery), or port insertion sites.<br />
<strong>Bowel injury</strong> — patients may present with trocar site pain, abdominal distention or sepsis typically within 96 hours of the procedure<br />
<strong>Ref</strong></p>
<ol>
<li><a href="http://www.ajronline.org/cgi/content/full/191/3/794" target="_blank">Thurley PD et al. Laparoscopic cholecystectomy: postoperative imaging. AJR Am J Roentgenol. 2008 Sep; 191(3):794-801.</a></li>
</ol>
]]></content:encoded>
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		<item>
		<title>Common Bile Duct Stones (CBDS)</title>
		<link>https://www.gastrotraining.com/pancreaticobiliary/cbd-stones/cbd-stones</link>
		<comments>https://www.gastrotraining.com/pancreaticobiliary/cbd-stones/cbd-stones#comments</comments>
		<pubDate>Fri, 30 Jul 2010 07:17:16 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[CBD stones]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=1874</guid>
		<description><![CDATA[Discuss common bile duct stones? The natural history of secondary CBDS (stones that slip from gallbladder in to CBD) is not well understood. What is clear is that when ductal stones do become symptomatic the consequences are often serious and can include pain, partial or complete biliary obstruction, cholangitis, hepatic abscesses or pancreatitis. Chronic obstruction [...]]]></description>
				<content:encoded><![CDATA[<p><strong>Discuss common bile duct stones?</strong></p>
<p>The natural history of secondary CBDS (stones that slip from gallbladder in to CBD) is not well understood. What is clear is that when ductal stones do become symptomatic the<br />
consequences are often serious and can include pain, partial or complete biliary obstruction, cholangitis, hepatic abscesses or pancreatitis. Chronic obstruction may also cause secondary biliary cirrhosis and portal hypertension. It is thus recommended that CBDS always need extraction. This applies even in cases where cirrhosis has developed, as reversal of hepatic fibrosis has been observed following relief of chronic biliary obstruction<br />
<strong><br />
Discuss the investigations for CBD stones?</strong></p>
<ul>
<li>Transabdominal USS is not very sensitive</li>
<li>EUS and MR are both highly effective for confirming the presence of CBDS. Prospective studies has failed to show a statistically significant difference in performance when the two modalities are compared, though for small CBD stones EUS may still be more sensitive. Choice of test therefore depends on local expertise.</li>
<li>CT scan- recent studies suggest helical CT can diagnose CBDS with sensitivity and specificity that is comparable to MR cholangiography</li>
</ul>
<p><strong>Discuss the endoscopic treatment of CBDS?</strong></p>
<p>ERCP can be used to provide definitive or temporary treatment of CBDS. ERCP is reserved for patients with confirmed or high suspicion of CBDS. ERCP should not be used as a diagnostic test.<br />
Biliary sphincterotomy (BS) followed by stone extraction using a basket or balloon catheter represents standard endoscopic therapy for CBDS.<br />
It is important that endoscopists ensure adequate biliary drainage is achieved in patients with CBDS that have not been extracted.  Bacterial contamination of bile is common in<br />
patients with CBDS and incomplete duct clearance may therefore place patients at risk of cholangitis. It is therefore important that a biliary stent be inserted where stones cannot be extracted. The short-term use of an endoscopic biliary stent followed by further ERCP or surgery has been shown to be a safe management option in this setting. In contrast the use of a biliary stent as sole treatment for CBDS should be restricted to a selected group of patients with limited life expectancy and/or prohibitive surgical risk.</p>
<p>BS can be safely performed on patients taking aspirin or non-steroidal anti-inflammatory drugs. Administration of low dose heparin should not be considered a contraindication to BS. Where possible, newer anti-platelet agents such as clopidogrel<br />
should be stopped 7–10 days prior to BS.<br />
PS- Patients with acute cholangitis who fail to respond to antibiotic therapy or who have signs of septic shock require urgent biliary decompression. Biliary sphincterotomy, supplemented by stenting or stone extraction, is therefore indicated.<br />
<strong><br />
Discuss the surgical treatment of CBDS?</strong><br />
Surgical treatment of CBDS occurs in the setting of concurrent laparoscopic cholecystectomy.<br />
Patients with CBDS undergoing laparoscopic cholecystectomy may be managed by laparoscopic common bile duct exploration (LCBDE) at the time of surgery, or undergo<br />
peri-operative ERCP. There is no evidence of a difference in efficacy, morbidity or mortality when these approaches are compared, though LCBDE is associated with a shorter hospital<br />
stay. The two approaches are considered equally valid treatment options.</p>
<p><strong>Discuss cholecystectomy for CBDS?</strong></p>
<p>Cholecystectomy is recommended for all patients with CBDS and symptomatic gallbladder stones, unless there are specific reasons for considering surgery inappropriate</p>
<p>In patients with CBDS cholecystectomy may be performed routinely or reserved for those who develop recurrent biliary symptoms following ERCP.  Randomised control studies comparing these two approaches suggest 15–37% of patients whose gallbladder is left in situ will develop symptoms that require cholecystectomy during a follow-up period ranging from an average of 17 months to over 5 years. Recurrent symptoms following ESE are most likely to be reported by younger, surgically fit patients with radiologically proven gallstones.<br />
Deferred laparoscopic cholecystectomy in this group is associated with higher rates of conversion to open surgery and a greater risk of surgical complication.</p>
<p>Therefore in patients with CBDS and gallstones endoscopic stone extraction as sole<br />
treatment should be avoided unless there are patient related factors that make cholecystectomy inappropriate.</p>
<p><strong>Discuss the complications of ERCP? </strong><br />
Post-ERCP pancreatitis- 1.5%<br />
Gastrointestinal haemorrhage- 0.9 (1.5% of BS patients)<br />
Cholangitis- 1.1%<br />
Duodenal perforation- 0.4%<br />
Miscellaneous, including cardio respiratory- 1.4%</p>
<p><strong><br />
Ref</strong></p>
<ol>
<li><a href="http://www.bsg.org.uk/clinical-guidelines/pancreatic/guidelines-on-the-management-of-common-bile-duct-stones-cbds.html" target="_blank">British Society of Gastroenterology guidelines on the management of common bile duct stones</a></li>
<li><a href="http://www.ncbi.nlm.nih.gov/pubmed/17145737" target="_blank">Williams EJ et al. Are we meeting the standards set for endoscopy? Results of a large-scale prospective survey of endoscopic retrograde cholangio-pancreatograph practice. Gut. 2007 Jun;56(6):821-9.</a></li>
</ol>
]]></content:encoded>
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		</item>
		<item>
		<title>Cholelithiasis (Gallstones)</title>
		<link>https://www.gastrotraining.com/pancreaticobiliary/cholelithiasis/cholelithiasis</link>
		<comments>https://www.gastrotraining.com/pancreaticobiliary/cholelithiasis/cholelithiasis#comments</comments>
		<pubDate>Fri, 30 Jul 2010 07:14:55 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[Cholelithiasis]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=1872</guid>
		<description><![CDATA[Discuss cholelithiasis? Gallstones are fairly common (20% of women and 8% of men), however less than 50% of those with gallstones actually have symptoms, and fewer than 10% develop potentially life-threatening complications. Discuss the clinical presentations of cholelithiasis? Biliary colic typically described as postprandial epigastric or RUQ pain (steady, non paroxysmal pain, rapidly increases in [...]]]></description>
				<content:encoded><![CDATA[<p><strong>Discuss cholelithiasis?</strong></p>
<p>Gallstones are fairly common (20% of women and 8% of men), however less than 50% of those with gallstones actually have symptoms, and fewer than 10% develop potentially life-threatening complications.</p>
<p><strong>Discuss the clinical presentations of cholelithiasis?</strong></p>
<p><strong>Biliary colic</strong> typically described as postprandial epigastric or RUQ pain (steady, non paroxysmal pain, rapidly increases in intensity then plateaus), sometimes radiating to the interscapular region or up to the right shoulder. The pain may last from several minutes to several hours (usually less than 4 hours). Intense pain is often accompanied by nausea and vomiting. Occasionally, the pain may be in the left upper quadrant.<br />
Biliary colic is usually caused by the gallbladder contracting due to a fatty meal, forcing a stone against the gallbladder outlet or cystic duct opening, and leading to increased intra gallbladder pressure and pain. The stones often fall back from the cystic duct as the gallbladder relaxes. In most patients the pain is not very severe. There is not much to find on physical examination.</p>
<p><strong>Acute cholecystitis</strong>-patients with acute cholecystitis experience severe pain that persists for several hours (6hrs or more), until they finally seek help at a local emergency department. Whereas in biliary colic the cystic duct obstruction is transient, in acute cholecystitis it is persistent. Persistent cystic duct obstruction, in combination with chemical irritants in the bile, results in inflammation and edema of the gallbladder wall. Nausea and vomiting are common. Physical examination usually reveals marked tenderness in the right upper quadrant, often associated with a definite mass or fullness. Murphy’s sign is positive. Fever and local peritoneal signs are common.</p>
<p><strong>Gallstone pancreatitis</strong> (see acute pancreatitis)<br />
<strong><br />
Choledocholithiasis and cholangitis</strong>- presents with fever, jaundice and pain.<br />
<strong><br />
Gallstone ileus</strong>- is caused by impaction of a gallstone in the ileum after being passed through a biliary-enteric fistula. It presents with episodic sub acute obstruction in an elderly female. The mainstay of treatment is removal of the obstructing stone after resuscitating the patient.</p>
<p><strong>Discuss the investigations for cholelithiasis?</strong><br />
<strong><br />
USS</strong>- is the investigation of choice for suspected gall stones. Positive findings include stones, thickening of the gallbladder wall, pericholecystic fluid, and a positive Murphy sign on contact with the ultrasonographic probe. These findings are particularly indicative of acute cholecystitis.<br />
<strong>Computed tomography</strong> is not as accurate as USS in detecting gallstones since most stones are isodense with bile and thus not visible on CT scanning. CT can be useful in patients in whom medical therapy is being considered since the presence of calcifications within gallstones (readily apparent on CT) makes it unlikely that such therapy will be successful.<br />
<strong>MRCP</strong> &#8211; when stones in CBD are suspected.<br />
<strong>CT cholangiography</strong>- is indicated in patients with suspected choledocholithiasis when MRI is contraindicated. The technique involves an injection of contrast that is excreted in bile as the patient is imaged in the CT scanner. The test relies upon the excretion of contrast in bile.  Obstructive jaundice is a relative contraindication. In general, it is not possible to obtain good images of the biliary tree if the bilirubin is twice the upper limit of the normal range. This technique can give excellent pictures of the biliary tree but will not show the gallbladder at all unless the cystic duct is patent – and hence is less useful in cases of biliary colic or cholecystitis.</p>
<p><strong>Discuss the management of cholelithiasis?</strong></p>
<p>Asymptomatic gallstones do not need any treatment.<br />
Laparoscopic cholecystectomy is now the gold standard in the treatment of symptomatic gallbladder disease. It is effective and safe, with low rates of complications and mortality (&lt;0.1%).</p>
<p><strong>Discuss cholecystectomy in cirrhotic patients? </strong><br />
Patients with symptomatic gallstones and compensated cirrhosis (i.e., Child’s class A or B) should be considered for a cholecystectomy. In a meta-analysis of six studies comparing outcomes after cholecystectomy in patients with and without cirrhosis, patients with cirrhosis had no significant difference in mortality rate. However, overall complications such as liver bleeding and new onset ascites were higher in patients with cirrhosis compared with those without cirrhosis (21 versus 8 percent, respectively). Although the studies on cholecystectomy in patients with Child class C cirrhosis are not large enough to yield significant results, unacceptably high mortality rates have been reported. Therefore, it is generally agreed that a more conservative approach is warranted in patients with Child class C cirrhosis and symptomatic gallstone disease, directing treatment toward improving their liver function before cholecystectomy.<br />
<strong><br />
Discuss the nonsurgical treatment of gallstone disease?</strong><br />
Oral dissolution therapy using 10 mg per kg per day of ursodeoxycholic acid (UDCA) can be used in patients unfit or unwilling to undergo surgery. This treatment is suitable for small cholesterol rich stones without any calcification and good gallbladder function. Treatment may be required for up to 2 years depending on the size of the stone. Gallstone recurrence is a disadvantage of this treatment; approximately 25 percent of patients develop recurrent gallstones within five years.<br />
Extracorporeal shockwave lithotripsy (ESWL) may be used with UDCA in patients with stones too large for dissolution therapy.</p>
<p><strong>Ref</strong></p>
<ol>
<li><a href="http://www.ccjm.org/content/69/12/977.long" target="_blank">David P. Vogt. Gallbladder disease: An update on diagnosis and treatment. Cleveland clinic of journal of medicine. Vol 69 No 12</a></li>
</ol>
<div id="_mcePaste" style="overflow: hidden; position: absolute; left: -10000px; top: 171px; width: 1px; height: 1px;">Cholelithiasis (Gallstones)<br />
Discuss cholelithiasis?</p>
<p>Gallstones are fairly common (20% of women and 8% of men), however less than 50% of those with gallstones actually have symptoms, and fewer than 10% develop potentially life-threatening complications.</p>
<p>Discuss the clinical presentations of cholelithiasis?</p>
<p>Biliary colic typically described as postprandial epigastric or RUQ pain (steady, non paroxysmal pain, rapidly increases in intensity then plateaus), sometimes radiating to the interscapular region or up to the right shoulder. The pain may last from several minutes to several hours (usually less than 4 hours). Intense pain is often accompanied by nausea and vomiting. Occasionally, the pain may be in the left upper quadrant.<br />
Biliary colic is usually caused by the gallbladder contracting due to a fatty meal, forcing a stone against the gallbladder outlet or cystic duct opening, and leading to increased intra gallbladder pressure and pain. The stones often fall back from the cystic duct as the gallbladder relaxes. In most patients the pain is not very severe. There is not much to find on physical examination.</p>
<p>Acute cholecystitis-patients with acute cholecystitis experience severe pain that persists for several hours (6hrs or more), until they finally seek help at a local emergency department. Whereas in biliary colic the cystic duct obstruction is transient, in acute cholecystitis it is persistent. Persistent cystic duct obstruction, in combination with chemical irritants in the bile, results in inflammation and edema of the gallbladder wall. Nausea and vomiting are common. Physical examination usually reveals marked tenderness in the right upper quadrant, often associated with a definite mass or fullness. Murphy’s sign is positive. Fever and local peritoneal signs are common.</p>
<p>Gallstone pancreatitis (see acute pancreatitis)</p>
<p>Choledocholithiasis and cholangitis- presents with fever, jaundice and pain.</p>
<p>Gallstone ileus- is caused by impaction of a gallstone in the ileum after being passed through a biliary-enteric fistula. It presents with episodic sub acute obstruction in an elderly female. The mainstay of treatment is removal of the obstructing stone after resuscitating the patient.</p>
<p>Discuss the investigations for cholelithiasis?</p>
<p>USS- is the investigation of choice for suspected gall stones. Positive findings include stones, thickening of the gallbladder wall, pericholecystic fluid, and a positive Murphy sign on contact with the ultrasonographic probe. These findings are particularly indicative of acute cholecystitis.<br />
Computed tomography is not as accurate as USS in detecting gallstones since most stones are isodense with bile and thus not visible on CT scanning. CT can be useful in patients in whom medical therapy is being considered since the presence of calcifications within gallstones (readily apparent on CT) makes it unlikely that such therapy will be successful.<br />
MRCP &#8211; when stones in CBD are suspected.<br />
CT cholangiography- is indicated in patients with suspected choledocholithiasis when MRI is contraindicated. The technique involves an injection of contrast that is excreted in bile as the patient is imaged in the CT scanner. The test relies upon the excretion of contrast in bile.  Obstructive jaundice is a relative contraindication. In general, it is not possible to obtain good images of the biliary tree if the bilirubin is twice the upper limit of the normal range. This technique can give excellent pictures of the biliary tree but will not show the gallbladder at all unless the cystic duct is patent – and hence is less useful in cases of biliary colic or cholecystitis.</p>
<p>Discuss the management of cholelithiasis?</p>
<p>Asymptomatic gallstones do not need any treatment.<br />
Laparoscopic cholecystectomy is now the gold standard in the treatment of symptomatic gallbladder disease. It is effective and safe, with low rates of complications and mortality (&lt;0.1%).</p>
<p>Discuss cholecystectomy in cirrhotic patients?<br />
Patients with symptomatic gallstones and compensated cirrhosis (i.e., Child’s class A or B) should be considered for a cholecystectomy. In a meta-analysis of six studies comparing outcomes after cholecystectomy in patients with and without cirrhosis, patients with cirrhosis had no significant difference in mortality rate. However, overall complications such as liver bleeding and new onset ascites were higher in patients with cirrhosis compared with those without cirrhosis (21 versus 8 percent, respectively). Although the studies on cholecystectomy in patients with Child class C cirrhosis are not large enough to yield significant results, unacceptably high mortality rates have been reported. Therefore, it is generally agreed that a more conservative approach is warranted in patients with Child class C cirrhosis and symptomatic gallstone disease, directing treatment toward improving their liver function before cholecystectomy.</p>
<p>Discuss the nonsurgical treatment of gallstone disease?<br />
Oral dissolution therapy using 10 mg per kg per day of ursodeoxycholic acid (UDCA) can be used in patients unfit or unwilling to undergo surgery. This treatment is suitable for small cholesterol rich stones without any calcification and good gallbladder function. Treatment may be required for up to 2 years depending on the size of the stone. Gallstone recurrence is a disadvantage of this treatment; approximately 25 percent of patients develop recurrent gallstones within five years.<br />
Extracorporeal shockwave lithotripsy (ESWL) may be used with UDCA in patients with stones too large for dissolution therapy.</p>
<p>Ref<br />
David P. Vogt. Gallbladder disease: An update on diagnosis and treatment. Cleveland clinic of journal of medicine. Vol 69 No 12</p>
<p>http://www.ccjm.org/content/69/12/977.long</p>
</div>
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		<title>Biliary dyskinesia</title>
		<link>https://www.gastrotraining.com/pancreaticobiliary/biliary-dyskinesia/biliary-dyskinesia</link>
		<comments>https://www.gastrotraining.com/pancreaticobiliary/biliary-dyskinesia/biliary-dyskinesia#comments</comments>
		<pubDate>Fri, 30 Jul 2010 07:08:43 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[Biliary dyskinesia]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=1867</guid>
		<description><![CDATA[Discuss biliary dyskinesia? Some patients present with typical biliary colic but without gallstones on ultrasonography.  These patients either have small stones (microlithiasis) or sludge that were missed on conventional imaging studies or other causes of biliary symptoms unrelated to gallstones such as sphincter of Oddi dysfunction, dyspepsia, irritable bowel syndrome or biliary dyskinesia. Discuss the [...]]]></description>
				<content:encoded><![CDATA[<p><strong>Discuss biliary dyskinesia?</strong></p>
<p>Some patients present with typical biliary colic but without gallstones on ultrasonography.  These patients either have small stones (microlithiasis) or sludge that were missed on conventional imaging studies or other causes of biliary symptoms unrelated to gallstones such as sphincter of Oddi dysfunction, dyspepsia, irritable bowel syndrome or biliary dyskinesia.<br />
<strong><br />
Discuss the diagnosis?</strong></p>
<ul>
<li>Exclude other causes as above. An OGD is usually performed to exclude peptic ulcer, reflux or gastritis.</li>
<li>EUS may help to exclude microlithiasis</li>
<li>Cholescintigraphy or HIDA scan- In this technique, the radio labelled tracer (HIDA or hepatobiliary imino diacetic acid) is injected intravenously and excreted in bile. Images are obtained using the gamma camera over a period of time and can be relied upon as functional images. The gallbladder ejection fraction can be computed and compared to the normal range.  Biliary dyskinesia was defined by a gallbladder ejection fraction of less than 50 percent on HIDA scan in conjunction with typical clinical symptoms.</li>
</ul>
<p><strong>Discuss the treatment?</strong></p>
<p>An abnormal gallbladder emptying (measured as the gallbladder ejection fraction) has been proposed as an indication that cholecystectomy would help relieve symptoms of typical biliary pain in patients without gallstones or sludge on imaging studies. A number of reports have described surgical outcomes in patients with abnormal gallbladder contractility as assessed by a HIDA scan. However the results are conflicting. Thus a low gallbladder ejection fraction is not a reliable indicator of clinical outcomes. Thus, the differential diagnosis in these patients with a low gallbladder ejection fraction should still include functional dyspepsia, irritable bowel syndrome, small intestinal bacterial overgrowth, and sphincter of Oddi dysfunction, all of which should be considered before recommending a cholecystectomy.</p>
<p><strong>Ref</strong></p>
<ol>
<li><a href="http://www.ccjm.org/content/69/12/977.long" target="_blank">David P. Vogt. Gallbladder disease: An update on diagnosis and treatment. Cleveland clinic of journal of medicine. Vol 69 No 12</a></li>
</ol>
<div id="_mcePaste" style="overflow: hidden; position: absolute; left: -10000px; top: 137px; width: 1px; height: 1px;">Biliary dyskinesia</div>
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		<title>Acute Cholecystitis</title>
		<link>https://www.gastrotraining.com/pancreaticobiliary/acute-cholecystitis/acute-cholecystitis</link>
		<comments>https://www.gastrotraining.com/pancreaticobiliary/acute-cholecystitis/acute-cholecystitis#comments</comments>
		<pubDate>Fri, 30 Jul 2010 07:07:15 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[Acute cholecystitis]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=1864</guid>
		<description><![CDATA[Discuss acute cholecystitis? Patients with acute cholecystitis experience severe pain that persists for several hours (6hrs or more), until they finally seek help at a local emergency department. Whereas in biliary colic the cystic duct obstruction is transient, in acute cholecystitis it is persistent. Persistent cystic duct obstruction, in combination with chemical irritants in the [...]]]></description>
				<content:encoded><![CDATA[<p><strong>Discuss acute cholecystitis?</strong><br />
Patients with acute cholecystitis experience severe pain that persists for several hours (6hrs or more), until they finally seek help at a local emergency department. Whereas in biliary colic the cystic duct obstruction is transient, in acute cholecystitis it is persistent. Persistent cystic duct obstruction, in combination with chemical irritants in the bile, results in inflammation and edema of the gallbladder wall. Nausea and vomiting are common.</p>
<p>Physical examination usually reveals marked tenderness in the right upper quadrant, often associated with a definite mass or fullness. Murphy’s sign is positive. Fever and local peritoneal signs are common.</p>
<p><strong>Discuss the diagnosis?</strong><br />
Diagnosis is suspected based on the clinical presentation above.<br />
<strong>Blood tests</strong> reveal leukocytosis with neutrophilia. A mild elevation in bilirubin, liver enzymes and amylase occur even in the absence of cholangitis or choledocholithiasis. These abnormalities may be due to the passage of small stones, sludge, or pus.<br />
<strong>USS</strong>- is the investigation of choice. Positive findings particularly indicative of acute cholecystitis are stones, thickening of the gallbladder wall, pericholecystic fluid, and a positive Murphy sign on contact with the ultrasonographic probe.<br />
<strong><br />
Cholescintigraphy (HIDA scan) </strong>- may be needed if the diagnosis remains uncertain following USS. It has no role in the diagnosis of gallstones but is very useful in excluding acute cholecystitis in patients who present with acute biliary colic. The test is positive if the gallbladder does not visualize which is invariably due to cystic duct obstruction, usually from edema associated with acute cholecystitis or an obstructing stone.</p>
<p><strong>Discuss the treatment?</strong></p>
<ul>
<li>Supportive care- Fluid and electrolyte correction and pain relief</li>
<li>Antibiotics- most patients with acute cholecystitis are given antibiotics, although clear evidence of benefit is lacking.</li>
<li>Cholecystectomy-
<ul>
<li>Patients who are at low-risk (ASA classes I and II) benefit from early cholecystectomy during the same hospital admission. Several studies have indicated that cholecystectomy performed for low surgical risk patients during the initial hospitalization can reduce morbidity and costs</li>
<li>High-risk patients — Patients who are in ASA classes III, IV, or V have a surgical mortality ranging from 5 to 27 percent, and are considered high-risk for cholecystectomy. In such patients, treatment should be aimed at stabilizing symptoms only. They are discharged once stable.</li>
</ul>
</li>
</ul>
<p><strong>Discuss the complications of acute cholecystitis?</strong><br />
The symptoms of cholecystitis may abate spontaneously within 7 to 10 days. However, complications rates are alarmingly high with this approach; hence treatment should be started on an emergent basis. He complications of acute cholecystitis are:</p>
<ul>
<li><strong>Gangrenous cholecystitis</strong> is the most common complication of cholecystitis especially in elderly and diabetics.</li>
<li><strong>Perforation of the gallbladder</strong> usually occurs after the development of gangrene. It may lead to a localised abscess or lead to a generalized peritonitis.</li>
<li><strong>Cholecystoenteric</strong> <strong>fistula</strong> may result from perforation of the gallbladder directly into the duodenum or jejunum.</li>
<li><strong>Gallstone ileus</strong> — Passage of a gallstone through a cholecystoenteric fistula may lead to the development of mechanical bowel obstruction, usually in the terminal ileum (gallstone ileus)</li>
</ul>
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		<title>Acute acalculous cholecystitis</title>
		<link>https://www.gastrotraining.com/pancreaticobiliary/acalculous-cholecystitis</link>
		<comments>https://www.gastrotraining.com/pancreaticobiliary/acalculous-cholecystitis#comments</comments>
		<pubDate>Fri, 30 Jul 2010 06:59:52 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[Acalculous cholecystitis]]></category>
		<category><![CDATA[Pancreaticobiliary]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=1861</guid>
		<description><![CDATA[Discuss acute acalculous cholecystitis? It generally occurs in critically ill patients but can occur in ambulatory patients too. It can rapidly progress to gangrene and perforation, since the pathophysiologic process appears to be transmural infarction of the gallbladder wall rather than inflammatory changes associated with stones. Discuss the clinical features of acalculous cholecystitis? Abdominal pain, [...]]]></description>
				<content:encoded><![CDATA[<p><strong>Discuss acute acalculous cholecystitis?</strong><br />
It generally occurs in critically ill patients but can occur in ambulatory patients too. It can rapidly progress to gangrene and perforation, since the pathophysiologic process appears to be transmural infarction of the gallbladder wall rather than inflammatory changes associated with stones.<br />
<strong>Discuss the clinical features of acalculous cholecystitis?</strong></p>
<p>Abdominal pain, fever, and RUQ tenderness or signs of local peritoneal irritation. Almost all have abnormal liver function tests and leukocytosis.</p>
<p><strong>Discuss the diagnosis?</strong><br />
USS and CT scan<br />
<strong>Discuss the treatment?</strong><br />
Treatments for acute acalculous cholecystitis include percutaneous cholecystostomy, open<br />
cholecystostomy, and cholecystectomy (depending on the general condition of the patient).<br />
Even though acute acalculous cholecystitis may result from infarction of the gallbladder wall,<br />
decompression of the gallbladder by placement of a cholecystostomy tube may be sufficient<br />
to control the inflammatory process.<br />
If cholecystectomy is necessary, the degree of inflammation and induration usually precludes the laparoscopic approach.<br />
The mortality rate is 50% if surgery is not performed. The mortality rate associated with surgical intervention in these patients ranges from 6% to 9%, which is significantly higher than with calculous disease. The mortality is related primarily to the patient’s overall condition.</p>
<p><strong>Ref</strong></p>
<ol>
<li><a href="http://www.ccjm.org/content/69/12/977.long" target="_blank">David P. Vogt. Gallbladder disease: An update on diagnosis and treatment. Cleveland clinic of journal of medicine. Vol 69 No 12</a></li>
</ol>
<p><a href="http://www.ccjm.org/content/69/12/977.long" target="_blank"> </a></p>
]]></content:encoded>
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		<title>Pancreatic pseudocysts (PP)</title>
		<link>https://www.gastrotraining.com/pancreaticobiliary/pancreatic-pseudocysts/pancreatic-pseudocysts</link>
		<comments>https://www.gastrotraining.com/pancreaticobiliary/pancreatic-pseudocysts/pancreatic-pseudocysts#comments</comments>
		<pubDate>Fri, 30 Jul 2010 06:50:46 +0000</pubDate>
		<dc:creator>Gastro Training</dc:creator>
				<category><![CDATA[Pancreatic Pseudocysts]]></category>

		<guid isPermaLink="false">http://www.gastrotraining.com/?p=1855</guid>
		<description><![CDATA[Discuss pancreatic pseudocysts? Pancreatic pseudocysts are complications of acute or chronic pancreatitis. Pseudocysts are localized fluid collection that is rich in amylase and other pancreatic enzymes and is surrounded by a wall of fibrous tissue that is not lined by epithelium. What are the different types of pseudocysts? D’Egidio and Schein define three distinct types [...]]]></description>
				<content:encoded><![CDATA[<p><strong>Discuss pancreatic pseudocysts?</strong></p>
<p>Pancreatic pseudocysts are complications of acute or chronic pancreatitis. Pseudocysts are localized fluid collection that is rich in amylase and other pancreatic enzymes and is surrounded by a wall of fibrous tissue that is not lined by epithelium.<br />
<strong><br />
What are the different types of pseudocysts?</strong></p>
<p>D’Egidio and Schein define three distinct types of pseudocysts.</p>
<ul>
<li>Type I, or acute “post-necrotic” pseudocysts that occur after an episode of acute pancreatitis and are associated with normal duct anatomy, and rarely communicate with the pancreatic duct.</li>
<li>Type II, also post-necrotic pseudocysts, which occurs after an episode of acute-on-chronic pancreatitis (the pancreatic duct is diseased, but not strictured, and there is often a duct-pseudocyst communication).</li>
<li>Type III, defined as “retention” pseudocysts, occur with chronic pancreatitis and are uniformly associated with duct stricture and pseudocyst duct communication.</li>
</ul>
<p><strong>Discuss the aetiology of pseudocysts?</strong></p>
<p>Pseudocysts seems to form from disruptions of the pancreatic duct due to pancreatitis<br />
or trauma followed by extravasation of pancreatic secretions. Majority of patients with pseudocysts have demonstrable connections between the cyst and the pancreatic duct. In other patients, an inflammatory reaction most likely sealed the connection so that it is<br />
not demonstrable.<br />
<strong><br />
Discuss the clinical features of pseudocysts?</strong></p>
<p>They can be asymptomatic or present with one of the complications. The most common symptoms are nausea, vomiting and abdominal pain.</p>
<p><strong>Discuss the complications of pseudocyst?</strong></p>
<ul>
<li>Infection</li>
<li>Obstruction- luminal (gastric- causing n&amp;v), vascular (splenic or portal vein thrombosis giving rise to gastric varices) or biliary (may present with obstructive jaundice or cholangitis)</li>
<li>Bleeding- from pseudo aneurysms can present as an acute intra- or retroperitoneal bleed. Pseudo aneurysms are treated by angiographic embolization.</li>
<li>Rupture of the pseudocyst in the GIT or peritoneum or the vasculature</li>
</ul>
<p><strong>Discuss the diagnosis of pseudocyst?</strong><br />
Diagnosis is by USS or CT scan.<br />
Once a pancreatic cyst is diagnosed, a pseudocyst will need to be differentiated from other cystic lesions like cystic neoplasm, a benign or an incidental cyst. The clues which favour a pseudocyst are: evidence of chronic pancreatitis, preceding h/o acute pancreatitis, extra pancreatic location, communication with PD and high fluid amylase content.  EUS and analysis of the aspirated cyst fluid may help differentiate pseudocysts from cystic tumours of the pancreas</p>
<p><strong>Discuss the management of pancreatic pseudocyst?</strong></p>
<p>40% of pts with pancreatitis will have acute fluid collection. 80% of them resolve on their own- hence only follow up scan needed in 3-4 weeks after discharge. 20% will go on form a pseudocyst. 50% of these pseudocysts will stabilise or disappear and the other 50% will be clinically relevant.</p>
<p>Initial management consists of supportive care. Persistent symptoms and the development of complications warrant invasive intervention.</p>
<p><strong>What are the indications for intervention in pancreatic pseudocyst? </strong></p>
<p>Absolute size of 6cm is no longer a sole indication for intervention. However, treatment is needed if they are causing symptoms or if there is any sign of complications like infection, obstruction or bleeding.<br />
<strong><br />
How do you choose an appropriate therapy?<br />
</strong><br />
Pseudocysts can be treated by various methods: surgical, percutaneous or endoscopic.  There are no randomized trials comparing any of these approaches. As a result, the management varies based on local expertise but in general endoscopic drainage is becoming the preferred approach.</p>
<ul>
<li>Percutaneous- using USS, a pigtail is catheter is placed percutaneously in the fluid cavity and the fluid drained. The catheter stays in till the fluid output becomes minimal. This may take weeks. This method has a high risk of infection and a success rate of only 50% for successful resolution of the cyst. Unsuccessful drainages are usually caused by large ductal leaks.</li>
<li>Surgical- drainage is achieved by providing a communication between the pseudocyst and the stomach or the small bowel. This approach to drainage is often reserved for those patients that cannot tolerate or have failed percutaneous or endoscopic drainage.</li>
<li>Endoscopic drainage- has become the preferred therapeutic approach. Drainage is accomplished with either a transpapillary approach with ERCP or direct drainage across the stomach or duodenal wall. A transpapillary approach is used when the pseudocyst communicates with the main pancreatic duct. A transgastric or transduodenal approach is used (with EUS) when the pseudocyst is directly adjacent to the gastroduodenal wall. A distance between the gastric or duodenal wall and cyst wall of more than 1 cm or the presence of large intervening vessels or varices are relative contraindications for endoscopic drainage</li>
</ul>
<p><strong><br />
Discuss the supportive medical care for pancreatic pseudocysts?</strong></p>
<ul>
<li>Low fat diet</li>
<li>The logic of octreotide therapy for pancreatic pseudocyst is that it will decrease pancreatic secretions and aid in pseudocyst resolution. However, this strategy has not been rigorously tested.</li>
<li>Most pseudocysts tend to resolve with supportive medical care.</li>
</ul>
<p><strong>Ref</strong></p>
<ol>
<li><a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2653285/?tool=pubmed" target="_blank">Habashi S, Draganov PV.Pancreatic pseudocyst. World J Gastroenterol. 2009 Jan 7; 15(1):38-47</a></li>
</ol>
<p><a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2653285/?tool=pubmed" target="_blank"> </a></p>
<p>?</p>
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