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	<title>SurgeryProcedure.info &#187; Search Results  &#187;  CHRONIC INTESTIONAL PSEUDOOBSTRUCTION</title>
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		<title>Diagnosis &amp; Therapy of Chronic Pancreatitis</title>
		<link>http://surgeryprocedure.info/abdominal-surgery/diagnosis-therapy-of-chronic-pancreatitis</link>
		<comments>http://surgeryprocedure.info/abdominal-surgery/diagnosis-therapy-of-chronic-pancreatitis#comments</comments>
		<pubDate>Wed, 08 Jul 2009 14:25:31 +0000</pubDate>
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		<description><![CDATA[41 DIAGNOSIS AND THERAPY OF CHRONIC PANCREATITIS
Clay Cothren M.D., Jon M. Burch M.D.
1. What is chronic pancreatitis? 	
Show answer
The classic syndrome consists of smoldering abdominal pain and evidence of pancreatic insufficiency. Histologically, chronic inflammation results in destruction of the functioning endocrine and exocrine pancreatic cells.

2. What is the most common cause? 	
Show answer
Alcohol abuse accounts [...]]]></description>
			<content:encoded><![CDATA[<p><strong>41 DIAGNOSIS AND THERAPY OF CHRONIC PANCREATITIS<br />
Clay Cothren M.D., Jon M. Burch M.D.</strong></p>
<blockquote><p><strong>1. What is chronic pancreatitis?</strong> 	</p></blockquote>
<p>Show answer<br />
The classic syndrome consists of smoldering abdominal pain and evidence of pancreatic insufficiency. Histologically, chronic inflammation results in destruction of the functioning endocrine and exocrine pancreatic cells.<br />
<span id="more-215"></span></p>
<blockquote><p><strong>2. What is the most common cause? </strong>	</p></blockquote>
<p>Show answer<br />
Alcohol abuse accounts for 75% of cases.</p>
<blockquote><p><strong>3. Is chronic pancreatitis the result of acute pancreatitis?</strong> </p></blockquote>
<p>	Show answer<br />
Patients may not have had acute pancreatitis, although alcoholism is common to both. One hypothesis is the inflammation from recurrent bouts of acute pancreatitis causes interstitial acinar fibrosis with secondary dilatation of the main pancreatic duct. The average age for chronic pancreatitis is paradoxically 13 years less than for acute disease.</p>
<blockquote><p><strong>KEY POINTS: CHRONIC PANCREATITIS</strong></p>
<p>   1. 75% of cases are due to alcohol abuse.<br />
   2. Symptoms include smoldering abdominal pain and evidence of pancreatic insufficiency (diabetes, steatorrhea).<br />
   3. 30% of patients may not mount hyperamylasemia due to &#8220;burned-out&#8221; pancreas.<br />
   4. Common complications include pseudocyst, abscess, fistula, obstructive jaundice, malnutrition.</p></blockquote>
<blockquote><p><strong>4. What are the signs of pancreatic insufficiency? </strong>	</p></blockquote>
<p>Show answer<br />
Insulin-dependent diabetes mellitus (found in up to 30% of patients) and steatorrhea (in 25%).</p>
<blockquote><p><strong>5. How much of the pancreas must be destroyed before diabetes develops? </strong>	</p></blockquote>
<p>Show answer<br />
Approximately 90%.</p>
<blockquote><p><strong>6. What is steatorrhea? How does one confirm the diagnosis?</strong> </p></blockquote>
<p>	Show answer<br />
Steatorrhea is soft, greasy, foul-smelling stools. A 72-hour fecal fat analysis may be done to confirm the diagnosis. The D-xylose test shows normal results, and the Schilling test is not sensitive for pancreatic insufficiency. Patients with steatorrhea are treated with a variable combination of low-fat diets, pancreatic enzymes, antacids, and cimetidine.</p>
<blockquote><p><strong>7. Is serum amylase elevated in patients with chronic pancreatitis? </strong>	</p></blockquote>
<p>Show answer<br />
No. The serum amylase level is usually normal in cases of &#8220;burned-out&#8221; pancreatitis.</p>
<blockquote><p><strong>8. What are the complications of chronic pancreatitis?</strong> 	</p></blockquote>
<p>Show answer<br />
Pancreatic pseudocyst, abscess, or fistula may occur. Obstruction of the biliary tree with resultant jaundice may be caused by areas of fibrosis. Malnutrition and narcotic addiction are more likely to coexist than actual complications of pancreatic insufficiency.</p>
<blockquote><p><strong>9. What is a possible source of upper gastrointestinal bleeding (UGIB) in a patient with chronic pancreatitis?</strong></p></blockquote>
<p> 	Show answer<br />
Although gastritis and peptic ulcer disease are more common causes of UGIB, splenic vein thrombosis with associated gastric varices and hypersplenism also should be considered. (Your attending will love this answer!)</p>
<blockquote><p><strong>10. What is the &#8220;chain of lakes&#8221;? </strong>	</p></blockquote>
<p>Show answer<br />
In performing endoscopic retrograde cholangiopancreatography (ERCP), contrast dye is introduced directly into the pancreatic duct; sequential areas of narrowing followed by dilatation of the duct cause the appearance of a &#8220;string of beads&#8221; or &#8220;chain of lakes.&#8221;</p>
<blockquote><p><strong>11. What are the indications for surgery? </strong>	</p></blockquote>
<p>Show answer<br />
There are no steadfast rules. Relative indications include unabating pain refractory to medical management, a dilated main pancreatic duct, biliary or gastric outlet obstruction, pancreas divisum, and suspicion of malignancy.</p>
<blockquote><p><strong>12. Which operative procedures are commonly performed? </strong>	</p></blockquote>
<p>Show answer<br />
The Peustow procedure (a lateral Rouxen-Y pancreaticojejunostomy) lays the Roux limb of bowel directly upon the &#8220;chain of lakes&#8221; duct to provide longitudinal head-to-tail drainage. Distal pancreatectomy may be used for isolated distal disease or retrograde drainage into a pancreaticojejunostomy. A modified Whipple operation (i.e., pancreaticoduodenectomy) can also remove a nonfunctioning but painful pancreas.</p>
<blockquote><p><strong>13. What is the result of such operations? </strong>	</p></blockquote>
<p>Show answer<br />
Pain relief occurs in 70% of patients at the end of 1 year and in 50% of patients at the end of 5 years.</p>
<p><strong>References</strong><br />
WEB SITES</p>
<p><a href="http://www.emedicinehealth.com/articles/10597-1.asp">   1. http://www.emedicinehealth.com/articles/10597-1.asp</a><br />
   <a href="http://www.ascsurgery.com/abstracts/acs/acs0304.htm">2. http://www.ascsurgery.com/abstracts/acs/acs0304.htm</a></p>
<p>BIBLIOGRAPHY<br />
1. American Gastroenterological Association: AGA technical review: Treatment of pain in chronic pancreatitis. Gastroenterology 115:765-776, 1998.<br />
2. Beger HG, Schlosser W, et al: The surgical management of chronic pancreatitis: Duodenum-preserving pancreatectomy. Adv Surg 32:87-104, 1999. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9891740&#038;dopt=Abstract">Medline </a><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=9891740">Similar articles</a><br />
3. Fernandezdel Castillo C, Rattner DW, Warshaw AL: Standards for pancreatic resection in the 1990s. Arch Surg 130:295-300, 1995.<br />
4. Mergener K, Baillie J: Chronic pancreatitis. N Engl J Med 332:1379-1385, 1995.<br />
5. Steer ML, Waxman I, Freedman S: Chronic pancreatitis. N Engl J Med 332:1482-1490, 1995. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=7739686&#038;dopt=Abstract">Medline </a><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=7739686">Similar articles</a> <a href="http://dx.doi.org/10.1056/NEJM199506013322206">Full article</a><br />
6. Wiersema M: Diagnosing chronic pancreatitis: Shades of gray. Gastrointest Endosc 48:102-106, 1998. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9684680&#038;dopt=Abstract">Medline</a> <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=9684680">Similar articles</a></p>
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		<title>Queries 5</title>
		<link>http://surgeryprocedure.info/top-search/queries-5</link>
		<comments>http://surgeryprocedure.info/top-search/queries-5#comments</comments>
		<pubDate>Mon, 21 Sep 2009 06:21:43 +0000</pubDate>
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sengstaken blakemore tube
hernia mesh rejection symptoms
fissurotomy
lasix sandwich
anal+fissurotomy
sengstaken blakemore
empyema necessitans
sengstaken-blakemore
Space of Bogros Bhernia
anal fissurotomy
esophageal varices
shalyajanya nadi vrana
penetrating neck carotid artery
pilonoidal sinus
gatorade spleen
urinary+tract+surgery
CHRONIC INTESTIONAL PSEUDOOBSTRUCTION
rocky davis incision
urinary tract trauma
caput medusae dilated veins
spleen injury with blood behind heart
bleeding caput medusa
hernia mesh neuroma
neuroma+hernia
mesh rejection
emphysema necessitans
Infant Testicle
blakemore+tube
spleen injury


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<li><a href="http://surgeryprocedure.info/search/sengstaken+blakemore">sengstaken blakemore</a></li>
<li><a href="http://surgeryprocedure.info/search/empyema+necessitans">empyema necessitans</a></li>
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<li><a href="http://surgeryprocedure.info/search/Space+of+Bogros+hernia">Space of Bogros Bhernia</a></li>
<li><a href="http://surgeryprocedure.info/search/anal+fissurotomy">anal fissurotomy</a></li>
<li><a href="http://surgeryprocedure.info/search/esophageal+varices">esophageal varices</a></li>
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		<title>Acute Large Bowel Obstruction</title>
		<link>http://surgeryprocedure.info/abdominal-surgery/acute-large-bowel-obstruction</link>
		<comments>http://surgeryprocedure.info/abdominal-surgery/acute-large-bowel-obstruction#comments</comments>
		<pubDate>Wed, 08 Jul 2009 20:29:47 +0000</pubDate>
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		<description><![CDATA[49 ACUTE LARGE BOWEL OBSTRUCTION
Elizabeth C. Brew M.D.
1. What are the mechanical causes of large bowel obstruction?
 	Show answer
The three most common mechanical causes are carcinoma (50%), volvulus (15%), and diverticular disease (10%). Extrinsic compression from metastatic carcinoma is another cause of obstruction. Less frequent causes include stricture, hernia, intussusception, benign tumor, and fecal impaction.

2. [...]]]></description>
			<content:encoded><![CDATA[<p><strong>49 ACUTE LARGE BOWEL OBSTRUCTION<br />
Elizabeth C. Brew M.D.</strong></p>
<blockquote><p><strong>1. What are the mechanical causes of large bowel obstruction?</strong></p></blockquote>
<p> 	Show answer<br />
The three most common mechanical causes are carcinoma (50%), volvulus (15%), and diverticular disease (10%). Extrinsic compression from metastatic carcinoma is another cause of obstruction. Less frequent causes include stricture, hernia, intussusception, benign tumor, and fecal impaction.<br />
<span id="more-255"></span></p>
<blockquote><p><strong>2. How is the diagnosis made? </strong>	</p></blockquote>
<p>Show answer </p>
<p>   1. The patient complains of crampy abdominal pain and bloating. Nausea and vomiting occur later in large bowel obstruction and may be feculent. An acute onset of symptoms is more consistent with volvulus compared with the gradual development of obstructive complaints from patients with colon carcinoma.<br />
   2. Physical examination reveals abdominal distention and high-pitched bowel sounds. Rectal examination may reveal an obstructing rectal cancer or evidence of fecal impaction. Absence of bowel sounds and localized tenderness may be signs of peritonitis. Progression of symptoms accompanied by a high fever or tachycardia requires immediate operative attention.<br />
   3. Flat and upright abdominal radiographs reveal dilated colon proximal to the obstruction. An upright chest radiograph may show free air under the diaphragm if a perforation has occurred.</p>
<blockquote><p><strong>3. How is the diagnosis confirmed? </strong>	</p></blockquote>
<p>Show answer<br />
A contrast enema (barium or water-soluble contrast) is necessary to delineate the level and nature of an obstruction. A volvulus can be identified by a &#8220;bird&#8217;s beak&#8221; narrowing at the neck of the volvulus. Sigmoidoscopy or colonoscopy is an essential part of the evaluation; it allows visualization of the colon and may be therapeutic in the case of a sigmoid volvulus.</p>
<blockquote><p><strong>4. What is the role of computed tomography (CT) scanning in the diagnosis of large bowel obstruction?</strong> </p></blockquote>
<p>	Show answer<br />
CT scans may be valuable in distinguishing between mechanical obstruction or pseudo-obstruction. It can help with the diagnosis of diverticulitis or colon carcinoma. However, plain radiographs, colonoscopy, and physical examination exceed the benefits of CT scanning in the evaluation of large bowel obstruction.</p>
<blockquote><p><strong>5. Why is tenderness in the right lower quadrant (RLQ) important? </strong>	</p></blockquote>
<p>Show answer<br />
The cecum is the area that is most likely to perforate. When the cecum reaches 15 cm at its widest diameter, the tension on the wall is so great that decompression is essential to prevent perforation. The larger diameter of the cecum causes more tension of the cecal wall at the same intraluminal pressure (law of Laplace). The other area at risk for perforation is the site of a primary colon cancer.</p>
<blockquote><p><strong>6. Where is the obstructing cancer usually located? </strong>	</p></blockquote>
<p>Show answer<br />
Most obstructing colorectal carcinomas occur in the splenic flexure, descending colon, or hepatic flexure. In contrast, lesions of the right colon usually present with occult bleeding. Cecal and rectal cancers are uncommon causes of obstruction.</p>
<p><em><strong>KEY POINTS: CAUSES OF LARGE BOWEL OBSTRUCTION</strong></p>
<p>   1. Carcinoma: most common cause: 50%<br />
   2. Volvulus: 15%<br />
   3. Diverticular disease: 10%<br />
   4. Stricture, hernia, intussusception, fecal impaction: 25%</em></p>
<blockquote><p><strong>7. What is a volvulus? Where is it located? </strong></p></blockquote>
<p> 	Show answer<br />
A volvulus is an abnormal rotation of the colon on an axis formed by its mesentery and occurs either in the sigmoid colon (75%) or cecum (25%). Sigmoid volvulus occurs in an older population when chronic constipation causes the sigmoid colon to elongate and become redundant. Cecal volvulus requires a hypermobile cecum as a result of incomplete embryologic fixation of the ascending colon.</p>
<blockquote><p><strong>8. When is surgery indicated?</strong></p></blockquote>
<p> 	Show answer<br />
Surgery is performed early in colon obstruction. Urgent laparotomy is necessary in patients with suspected perforation or ischemia. Danger signs are quiet abdomen, RLQ tenderness, and increasing pain. The patient&#8217;s cardiopulmonary status should be assessed and optimized preoperatively. It is essential to correct dehydration and administer perioperative antibiotics. Marking of possible stoma sites and deep venous thrombosis prophylaxis are other important preoperative considerations.</p>
<blockquote><p><strong>9. Which operation should be performed for a large bowel obstruction?</strong></p></blockquote>
<p> 	Show answer<br />
The traditional procedure for a large bowel obstruction has been a decompressing colostomy. However, careful assessment of the patient&#8217;s condition, viability of the bowel, location of the obstruction, and absence of intra-abdominal contamination often allow resection with or without a primary anastomosis. In fact, an initial diverting colostomy has not been shown to have any survival advantage and incurs the risk of further surgeries.<br />
An obstructing carcinoma may be resected satisfactorily under emergency conditions in 90% of patients. Carcinomas of the right and transverse colon (proximal to the splenic flexure) are routinely treated with resection and primary anastomosis. Recently, obstructing cancers of the descending colon have been treated either with resection and colostomy or intraoperative lavage followed by resection and primary anastomosis. Techniques for nonoperative decompression of the colon, such as balloon dilation, laser therapy, and stent placement, are under investigation. Theoretically, these techniques will allow palliation, bowel preparation, and elective colon resection.<br />
A volvulus should be reduced and resected. Reduction of a sigmoid volvulus can be achieved nonoperatively by sigmoidoscopy or hydrostatic decompression with a contrast enema. The recurrence rate of volvulus after simple nonoperative reduction is 75%. Surgical therapy includes detorsion with colopexy or sigmoid colectomy. Cecal volvulus can be treated similarly with nonoperative decompression, cecopexy, or surgical resection.<br />
The optimal treatment of diverticular disease is initial bowel rest; intravenous antibiotics; and percutaneous abscess drainage, if necessary. Colon resection and primary anastomosis can be performed after adequate bowel preparation.</p>
<blockquote><p><strong>10. What are the nonmechanical causes of large bowel obstruction?</strong></p></blockquote>
<p> 	Show answer<br />
Paralytic ileus (i.e., colonic pseudoobstruction) or toxic megacolon.</p>
<blockquote><p><strong>11. What is Ogilvie&#8217;s syndrome? 	</strong></p></blockquote>
<p>Show answer<br />
Ogilvie&#8217;s syndrome is an acute paralytic (adynamic) ileus or pseudoobstruction (i.e., enormous dilation of the colon without a mechanical distal obstructing lesion). Patients present with a massively dilated abdomen and a small amount of pain. Nonoperative management, including bowel rest, intravenous fluids, and gentle enemas, is the therapy of choice. Gastrografin enema or colonoscopy is diagnostic and therapeutic. Neostigmine is another treatment modality in patients with colons > 10 cm in diameter.</p>
<blockquote><p><strong>12. What is toxic megacolon? </strong>	</p></blockquote>
<p>Show answer<br />
Toxic megacolon is dilatation of the entire colon secondary to acute inflammatory bowel disease. The disease is manifested by acute onset of abdominal pain, distention, and sepsis. Initial therapy includes intravenous fluid resuscitation, nasogastric decompression, and broad-spectrum antibiotics. If symptoms do not resolve within a few hours, the patient requires an operation to avoid perforation. Surgical therapy most often consists of an emergency abdominal colectomy with formation of an ileostomy.</p>
<p><strong>References</strong><br />
WEB SITE<br />
<a href="http://www.emedicine.com/emerg/topic65.htm">http://www.emedicine.com/emerg/topic65.htm</a><br />
BIBLIOGRAPHY<br />
1. Adler DG, Baron TH: Endoscopic palliation of colorectal cancer. Hematol Oncol Clin North Am 16:1015-1029, 2002. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=12418060&#038;dopt=Abstract">Medline</a> <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=12418060">Similar articles</a><br />
2. Dauphine CE, Tan P, Beart RW Jr, et al: Placement of self-expanding metal stents for acute malignant large-bowel obstruction: A collective review. Ann Surg Oncol 9:574-579, 2002. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=12095974&#038;dopt=Abstract">Medline </a><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=12095974">Similar articles</a><a href="http://dx.doi.org/10.1245/aso.2002.9.6.574"> Full article</a><br />
3. Frager D: Intestional obstruction: Role of CT. Gastroenterol Clin North Am 31:777-799, 2002. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=12481731&#038;dopt=Abstract">Medline</a> <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=12481731">Similar articles</a><br />
4. Lopez-Kostner F, Hool GR, Lavery IC: Management and causes of acute large-bowel obstruction. Surg Clin North Am 77:1265-1290, 1997. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9431339&#038;dopt=Abstract">Medline</a> <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=9431339">Similar articles</a><br />
5. Murray JJ, Schoetz DJ, Coller JA, et al: Intraoperative colonic lavage and primary anastomosis in nonelective colon resection. Dis Colon Rectum 34:527-531, 1991.<br />
6. Paran H, Silverberg D, Mayo A: Treatment of acute colonic pseudo-obstruction with neostigmine. J Am Coll Surg 190(3):315-318, 2000.<br />
7. Tan SG, Nambiar R, Rauff A, et al: Primary resection and anastomosis in obstructed descending colon due to cancer. Arch Surg 126:748-751, 1991. </p>
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		<title>Intestinal Ischemia. Controversies</title>
		<link>http://surgeryprocedure.info/abdominal-surgery/intestinal-ischemia-controversies</link>
		<comments>http://surgeryprocedure.info/abdominal-surgery/intestinal-ischemia-controversies#comments</comments>
		<pubDate>Wed, 08 Jul 2009 20:11:58 +0000</pubDate>
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				<category><![CDATA[ABDOMINAL SURGERY]]></category>

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		<description><![CDATA[CONTROVERSIES
30. What is celiac compression syndrome (Dunbar&#8217;s syndrome)? 	
Show answer
Celiac compression is a rare and controversial disorder most commonly described in women (female-to-male ratio = 4:1) between the ages of 20 and 50 years. Patients appear to suffer from chronic mesenteric ischemia without angiographic evidence of atherosclerotic disease. The mechanical compression is believed to be [...]]]></description>
			<content:encoded><![CDATA[<p><strong>CONTROVERSIES</strong></p>
<blockquote><p><strong>30. What is celiac compression syndrome (Dunbar&#8217;s syndrome)? 	</strong></p></blockquote>
<p>Show answer<br />
Celiac compression is a rare and controversial disorder most commonly described in women (female-to-male ratio = 4:1) between the ages of 20 and 50 years. Patients appear to suffer from chronic mesenteric ischemia without angiographic evidence of atherosclerotic disease. The mechanical compression is believed to be caused by the left crus of the diaphragm (i.e., marginal arcuate ligament), and diagnosis occasionally is confirmed by demonstrating transient celiac compression during expiration. The associated pain is the result of a complicated and still heavily debated redirection of flow (foregut steal) away from the SMA. Effective treatment has required not only release of the compression but also bypass to improve the likelihood of pain resolution.<br />
<span id="more-251"></span></p>
<blockquote><p><strong>31. Which is the preferred treatment for chronic mesenteric ischemia, antegrade or retrograde visceral artery bypass? Is it necessary to reconstruct more than one mesenteric vessel? 	</strong></p></blockquote>
<p>Show answer<br />
As they apply to intestinal bypass, the terms antegrade and retrograde refer to the origin of the graft from the aorta as either proximal to the celiac axis or distal to the SMA, respectively. The stated advantages of antegrade bypass are less kinking of the graft and possibly better blood flow characteristics. The disadvantages are that supraceliac exposure is technically more difficult and clamping may result in renal or spinal cord ischemia. Retrograde bypass grafts are more difficult to position to avoid kinking.<br />
Recent series suggest that the results for single- or multiple-vessel reconstruction in either antegrade or retrograde fashion are excellent, with symptom-free survival rates > 90% at 5 years.</p>
<blockquote><p><strong>32. What is the role of percutaneous transluminal angioplasty (PTA) in chronic mesenteric ischemia? 	</strong></p></blockquote>
<p>Show answer<br />
The endovascular treatment of chronic mesenteric ischemia is a relatively new technique. The obvious avoidance of surgery is an important advantage, but the rare complications of dissection and embolus can be devastating in arterial beds without adequate collaterals. Success rates approximate 70%; restenosis and recurrent symptoms are reported in 50% of patients. No prospective trials have compared PTA with arterial bypass; however, retrospective reviews suggest that initial results with either technique are similar with regard to morbidity, death, and recurrent stenosis. However, symptom recurrence rates are higher with PTA.</p>
<p><strong>References</strong><br />
WEB SITE<br />
http://www.emedicine.com/emerg/topic311.htm<br />
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BIBLIOGRAPHY<br />
1. Fisher DF Jr, Fry WJ: Collateral mesenteric circulation. Surg Gynecol Obstet 164:487-492, 1987. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=3554567&#038;dopt=Abstract">Medline</a> <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=3554567">Similar articles</a><br />
2. Gewertz BL, Schwartz LB: Mesenteric ischemia. Surg Clin North Am 77:275-502, 1997.<br />
3. Hallisey MJ, Deschaine J, Illescas FF, et al: Angioplasty for the treatment of visceral ischemia. J Vasc Interv Radiol 6:785-791, 1995.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=8541685&#038;dopt=Abstract"> Medline</a> <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=8541685">Similar articles</a><br />
4. Kasirajan K, O&#8217;Hara PJ, Gray BH, et al: Chronic mesenteric ischemia: Open surgery versus percutaneous angioplasty and stenting. J Vasc Surg 33:63-71, 2001.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=11137925&#038;dopt=Abstract"> Medline </a><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=11137925">Similar articles</a> <a href="http://dx.doi.org/10.1067/mva.2001.111808">Full article</a><br />
5. Kazmers A: Operative management of acute mesenteric ischemia. Ann Vasc Surg 12:187-197, 1998. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9514240&#038;dopt=Abstract">Medline</a><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=9514240"> Similar articles</a><a href="http://dx.doi.org/10.1007/s100169900139"> Full article</a><br />
6. Kazmers A: Operative management of chronic mesenteric ischemia. Ann Vasc Surg 12:299-308, 1998.<br />
7. Park WM, Cherry KJ Jr, Chua HK, et al: Current results of open revascularization for chronic mesenteric ischemia: a standard for comparison. J Vasc Surg 35:853-859, 2002. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=12021698&#038;dopt=Abstract">Medline</a> <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=12021698">Similar articles </a><br />
8. Taylor LM: Management of visceral ischemic syndromes. In Rutherford RB (ed): Vascular Surgery, 5th ed. Philadelphia, W.B. Saunders, 2000</p>
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		<title>Inflammatory Bowel Disease</title>
		<link>http://surgeryprocedure.info/abdominal-surgery/inflammatory-bowel-disease</link>
		<comments>http://surgeryprocedure.info/abdominal-surgery/inflammatory-bowel-disease#comments</comments>
		<pubDate>Wed, 08 Jul 2009 20:35:22 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[ABDOMINAL SURGERY]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/?p=257</guid>
		<description><![CDATA[50 INFLAMMATORY BOWEL DISEASE
Anthony J. LaPorta M.D., Gilbert Hermann M.D.
1. What two clinical entities encompass the diagnosis of inflammatory bowel disease? 
	Show answer
Crohn&#8217;s disease and ulcerative colitis (acute or chronic).
2. Although the two diseases often overlap, they usually can be distinguished by clinical criteria. What are the major clinical differences? 	
Show answer
Rectal bleeding is unusual [...]]]></description>
			<content:encoded><![CDATA[<p><strong>50 INFLAMMATORY BOWEL DISEASE<br />
Anthony J. LaPorta M.D., Gilbert Hermann M.D.</strong></p>
<blockquote><p><strong>1. What two clinical entities encompass the diagnosis of inflammatory bowel disease?</strong> </p></blockquote>
<p>	Show answer<br />
Crohn&#8217;s disease and ulcerative colitis (acute or chronic).</p>
<blockquote><p><strong>2. Although the two diseases often overlap, they usually can be distinguished by clinical criteria. What are the major clinical differences? </strong>	</p></blockquote>
<p>Show answer<br />
Rectal bleeding is unusual in Crohn&#8217;s disease but common in chronic ulcerative colitis. An abdominal mass and anal complications (fissure, fistula) are more common in Crohn&#8217;s disease.<br />
<span id="more-257"></span></p>
<blockquote><p><strong>3. What are the major radiologic differences between the two diseases? </strong>	</p></blockquote>
<p>Show answer<br />
Terminal ileal involvement, skip areas, internal fistulas, and &#8220;thumb printing&#8221; are rare or absent in chronic ulcerative colitis but common in Crohn&#8217;s disease.</p>
<blockquote><p><strong>4. What are the major histologic differences? 	</strong></p></blockquote>
<p>Show answer<br />
Granulomas in the intestinal wall and adjacent lymph nodes are absent in ulcerative colitis but occur in 60% of patients with Crohn&#8217;s disease. The inflammatory process in Crohn&#8217;s disease involves the entire bowel wall. In ulcerative colitis, the inflammation usually is limited to the mucosa and submucosa.</p>
<blockquote><p><strong>5. Although Crohn&#8217;s disease may affect the gastrointestinal (GI) tract from the pharynx to the anus, what are the most common clinical patterns of GI involvement? </strong></p></blockquote>
<p>	Show answer<br />
Small bowel only: 28%; both ileum and colon (ileocolitis): 41%; and colon only: 27%. Crohn&#8217;s involvement of the colon is also called Crohn&#8217;s colitis or granulomatous colitis.</p>
<blockquote><p><strong>6. Crohn&#8217;s colitis and ulcerative colitis are often difficult to distinguish clinically. What are the major differences at colonoscopy?</strong> </p></blockquote>
<p>	Show answer<br />
Crohn&#8217;s disease is focal and predominantly right sided. The mucosa has a cobblestone appearance with transverse ulcerations in affected areas. Biopsies reveal transmural disease with possible focal granulomas. On colonoscopy, chronic ulcerative colitis may appear as a diffuse disease. However, if only a portion of the colon is involved, it is on the left side and almost always involves the rectum. Pathologic changes involve the mucosa and submucosa.</p>
<blockquote><p><strong>7. What are the major indications for surgery in Crohn&#8217;s disease?</strong> </p></blockquote>
<p>	Show answer<br />
It depends on the site of involvement. Enterocutaneous or enteroenteral fistulas (controversial), abscess, and intestinal obstruction are the most common surgical indications for small intestinal and ileocolic types. Perianal disease, medical failure, ileocolic fistulas, and abscess formation are the most common indicators for surgery in Crohn&#8217;s colitis.</p>
<blockquote><p><strong>8. What are the major indications for surgery in ulcerative colitis?</strong></p></blockquote>
<p> 	Show answer<br />
Medical intractability (including failure to thrive in children, diarrhea, weight loss, and abdominal pain), toxic megacolon with or without perforation, and concern about the development of colonic cancer (controversial, but real).</p>
<p><em><strong>KEY POINTS: DIFFERENCES BETWEEN CROHN&#8217;S DISEASE AND ULCERATIVE COLITIS</strong></p>
<p>   1. Rectal bleeding is uncommon in Crohn&#8217;s disease but common in chronic ulcerative colitis.<br />
   2. Terminal ileal involvement, skip areas, internal fistulas, and &#8220;thumb printing&#8221; are common in Crohn&#8217;s disease but rare or absent in chronic ulcerative colitis.<br />
   3. In ulcerative colitis, the inflammation is usually limited to the mucosa and submucosa, whereas in Crohn&#8217;s disease it involves the entire bowel wall.</em></p>
<blockquote><p><strong>9. What is the surgical treatment of ulcerative colitis?</strong> </p></blockquote>
<p>	Show answer<br />
Total colectomy with ileoanal pouch anastomosis is the standard. A total colectomy with a Brooke ileostomy was the classic surgical approach and is still applicable in some situations. A Kock (continent) pouch can be used for younger (age < 55 years) patients who do not wish to wear an ileostomy bag or who have lost their ileoanal pouch. Ileorectal anastomosis has been advocated by some (controversial), but this leaves disease behind.</p>
<blockquote><p><strong>10. What are the surgical procedures for the complications of Crohn&#8217;s disease?</strong> 	</p></blockquote>
<p>Show answer<br />
Complications requiring surgery are usually corrected by removing all areas of bowel involved in the complication. Strictureplasty as opposed to resection is now preferred in selected cases of small bowel obstruction. When resection is necessary, grossly clear margins are satisfactory. Skip areas should be preserved unless they are directly adjacent to resected intestine.</p>
<blockquote><p><strong>11. What should the patient be told about the possibility of recurrence after surgery? </strong>	</p></blockquote>
<p>Show answer<br />
With chronic ulcerative colitis, surgery is definitive and curative. With Crohn&#8217;s disease, however, the aim of surgery is to treat the complications (i.e., obstruction and sepsis). Recurrence of Crohn&#8217;s disease can be expected in a high percentage of cases if the patient is followed long enough. Small bowel recurrence after total colectomy for Crohn&#8217;s colitis does occur.</p>
<blockquote><p><strong>12. How do you evaluate the placement of a stoma? </strong></p></blockquote>
<p>	Show answer<br />
The location of a stoma is a major factor in patient morbidity. Placement is optimal at the summit of the infraumbilical bulge within the rectus muscle. This is usually within a triangle formed by lines between the umbilicus to the anterior superior iliac spine, umbilicus to the pubis, and the inguinal ligament. All scars and creases should be avoided.</p>
<blockquote><p><strong>13. Does Crohn&#8217;s disease have a genetic basis? </strong>	</p></blockquote>
<p>Show answer<br />
The patients described by Crohn et al. in the original article were a 14-year-old boy and his 32-year-old sister. Genetic studies have identified two loci, IBD1 and IBD2 on chromosomes 16 and 12, respectively, that are linked to inflammatory bowel disease. New data suggest that these mutations affect the innate bacterial reaction to lipopolysaccharides, leading to an exaggerated immune response, causing the tissue damage in Crohn&#8217;s disease. Similar studies also have links to chromosomes 14q and 6p.</p>
<blockquote><p><strong>14. What is the difference between an enteroclysis and a small bowel follow-through?</strong> 	</p></blockquote>
<p>Show answer </p>
<p>Enteroclysis is a procedure performed by a radiologist with a catheter placed at the duodenal-jejunal junction. Because the rate of barium entering the intestine and thus distention of the intestine can be controlled, this study provides a superior demonstration of the luminal contour, valvulae conniventes, and mucosal surface. Thus, it is superior to the small bowel follow-through for the evaluation of short obstructing lesions but is a technically more demanding procedure for the radiologist and the patient.</p>
<blockquote><p><strong>15. What is a Brooke ileostomy? </strong>	</p></blockquote>
<p>Show answer<br />
The Brooke ileostomy is the &#8220;rosebud&#8221; or full-thickness ileostomy folded over on itself for approximately 1 cm above the skin. This prevents the erosion of the skin and high-output serositis that is common with an ostomy that is flush with the skin.</p>
<blockquote><p><strong>16. What is pouchitis, and which patients are likely to have it? 	</strong></p></blockquote>
<p>Show answer<br />
Pouchitis is an inflammation of indeterminate origin, possibly related to bacterial overgrowth, that occurs in the ileal pouch after ileal-pouch anal anastomosis. This complication is common (25%) when this procedure is performed for ulcerative colitis, but it is rare when this same procedure is performed for familial polyposis. Patients with pouchitis are effectively treated with metronidazole, ciprofloxacin, or 5-amino salicylic acid. They rarely require ileal diversion or pouch excision.</p>
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		<title>Noninvasive Vascular Diagnostic Laboratory. Venous Disease</title>
		<link>http://surgeryprocedure.info/vascular-surgery/noninvasive-vascular-diagnostic-laboratory-venous-disease</link>
		<comments>http://surgeryprocedure.info/vascular-surgery/noninvasive-vascular-diagnostic-laboratory-venous-disease#comments</comments>
		<pubDate>Fri, 10 Jul 2009 08:27:24 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[VASCULAR SURGERY]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/?p=356</guid>
		<description><![CDATA[VENOUS DISEASE
7. What noninvasive test is used to diagnose acute DVT? 	
Show answer
Duplex ultrasound has replaced venous occlusion plethysmography as the accepted standard. Colorflow duplex is useful because it helps to identify small veins from the muscle and fascial layers. The ultrasound assessment involves the following steps:

   1. Examine the vein for echogenic [...]]]></description>
			<content:encoded><![CDATA[<p><strong>VENOUS DISEASE</strong></p>
<blockquote><p><strong>7. What noninvasive test is used to diagnose acute DVT? 	</strong></p></blockquote>
<p>Show answer<br />
Duplex ultrasound has replaced venous occlusion plethysmography as the accepted standard. Colorflow duplex is useful because it helps to identify small veins from the muscle and fascial layers. The ultrasound assessment involves the following steps:<br />
<span id="more-356"></span><br />
   1. Examine the vein for echogenic thrombus.<br />
   2. Compress the vein, using pressure on the ultrasound probe, looking for complete collapse. Inability to compress the vein suggests thrombosis. Partial compression suggests partial thrombosis.<br />
   3. A Doppler signal from the vein that is phasic with respiration suggests no proximal occlusive thrombus. A signal that is spontaneously present but nonphasic suggests flow around an occlusion via small collateral veins. Absence of a Doppler signal in the vein suggests absence of flow.</p>
<blockquote><p><strong><br />
8. Can duplex ultrasound be used for surveillance in patients at high risk for DVT? </strong></p></blockquote>
<p>	Show answer<br />
Diagnosis of DVT in asymptomatic patients presents a dilemma. The sensitivity of duplex ultrasound is reduced from the reported 95% to < 80% for above-knee detection of DVT in asymptomatic patients. Calf DVT detection is much worse, with sensitivities as low as 20% in many reported series. However, serial contrast venography, although more specific, is not a practical surveillance strategy.</p>
<blockquote><p><strong>9. Does venous occlusion plethysmography still have a role in the assessment of DVT?</strong> </p></blockquote>
<p>	Show answer<br />
Yes. Venous occlusion plethysmography or impedance plethysmography (IPG) has high sensitivity and specificity in detecting occlusive thrombi above the knee, particularly for iliofemoral occlusive thrombi (95%). Because IPG provides functional information about deep venous outflow from the legs, it provides diagnosis of nonvisualized caval or iliac thrombosis, diagnosis of recurrent acute proximal thrombosis superimposed on chronic thrombosis, and functional evaluation of residual or chronic outflow obstruction (venous claudication).</p>
<blockquote><p><strong>10. What noninvasive tests are useful for evaluation of venous incompetence?</strong></p></blockquote>
<p> 	Show answer<br />
Doppler ultrasound can detect venous reflux in the deep veins of the legs and in the greater and lesser saphenous veins. With experience, the test can be done using a simple Doppler (continuous wave versus pulsed Doppler), but duplex ultrasound is often used to facilitate identification of the vein segments and valves and to position a pulsed Doppler sample reliably. Some laboratories measure the duration of reflux during controlled proximal compression as an indicator of severity of valve incompetence, but unless a valvuloplasty or valve transposition is planned for the identified incompetent valve, such specific measures appear to have little clinical utility.</p>
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		</item>
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		<title>Inflammatory Bowel Disease. Controversies</title>
		<link>http://surgeryprocedure.info/abdominal-surgery/inflammatory-bowel-disease-controversies</link>
		<comments>http://surgeryprocedure.info/abdominal-surgery/inflammatory-bowel-disease-controversies#comments</comments>
		<pubDate>Wed, 08 Jul 2009 20:42:53 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[ABDOMINAL SURGERY]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/?p=259</guid>
		<description><![CDATA[CONTROVERSIES
17. Should all patients with enteroenteral fistulas secondary to Crohn&#8217;s disease have surgery when the fistula is discovered? 	
Show answer
For: Such patients ultimately do poorly, develop further intraperitoneal septic complications, and almost always require surgery.
Against: Many of these patients do well without operative treatment until they develop symptoms. It is fine to wait for symptoms.

18. [...]]]></description>
			<content:encoded><![CDATA[<p><strong>CONTROVERSIES</strong></p>
<blockquote><p><strong>17. Should all patients with enteroenteral fistulas secondary to Crohn&#8217;s disease have surgery when the fistula is discovered?</strong> 	</p></blockquote>
<p>Show answer<br />
For: Such patients ultimately do poorly, develop further intraperitoneal septic complications, and almost always require surgery.<br />
Against: Many of these patients do well without operative treatment until they develop symptoms. It is fine to wait for symptoms.<br />
<span id="more-259"></span></p>
<blockquote><p><strong>18. Should all patients with ulcerative colitis that is documented for 10 years, whether the disease is active or not, undergo a colectomy to avoid the risk of carcinoma of the colon? </strong>	</p></blockquote>
<p>Show answer<br />
For: The risk of colon cancer in ulcerative colitis increases by approximately 1% per year 10 years after the diagnosis.<br />
Against: Using surveillance colonoscopy and biopsy, only patients whose colons show dysplastic changes need a colectomy.</p>
<blockquote><p><strong>19. Is ileorectal anastomosis an acceptable operation after colectomy for ulcerative colitis?</strong></p></blockquote>
<p> 	Show answer<br />
For: The patients have reasonably normal bowel habits and avoid the complications associated with anal reconstructive procedures.<br />
Against: At least 50% of patients eventually require reoperation for recurrence of disease. The remaining rectum also may be a site for the development of cancer.</p>
<blockquote><p><strong>20. Is standard (Brooke) ileostomy a good way to handle the terminal ileum after total colectomy for chronic ulcerative colitis?</strong></p></blockquote>
<p> 	Show answer<br />
For: The complication rate is very low. More than 90% of patients lead satisfactory lives.<br />
Against: Psychosocial and sexual problems are associated with the use of external appliances, particularly in the teenage group, among whom chronic ulcerative colitis is quite common.</p>
<blockquote><p><strong>21. Is the continent Kock pouch a good procedure after colectomy for chronic ulcerative colitis? </strong>	</p></blockquote>
<p>Show answer<br />
For: It avoids use of an external appliance and is quite easy to manage.<br />
Against: Approximately 25% of all patients who have a Kock pouch require a revision due to slippage of the valve mechanism, thus rendering the pouch incontinent.</p>
<blockquote><p><strong>22. Is an ileoanal anastomosis with a surgically constructed ileoanal reservoir a good operation after colectomy for chronic ulcerative colitis? </strong>	</p></blockquote>
<p>Show answer<br />
For: It avoids external appliances or ostomies, so it is well accepted by patients. Currently, this is the most commonly performed operation after colectomy.<br />
Against: It is more difficult technically to construct; thus, the complication rate is higher. The average number of bowel movements is five per day, and there may be soilage at night. Pouchitis remains a problem.</p>
<blockquote><p><strong>23. Do all ileal pouch anal anastomoses require a temporary diverting ileostomy? </strong>	</p></blockquote>
<p>Show answer<br />
For: The diverting ileostomy protects the reservoir and its suture lines by diverting the fecal stream until it is healed, thus lowering the complication rate.<br />
Against: The triple-stapled ileal pouch anal anastomosis has a low complication rate and low rate of small bowel obstruction. Thus, avoidance of the diverting ileostomy returns the patient to a functional life sooner.</p>
<p><strong>References</strong><br />
BIBLIOGRAPHY<br />
1. Duerr RH: The genetics of inflammatory bowel disease. Gastroenterol Clin North Am 31:63-76, 2002. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=12122744&#038;dopt=Abstract">Medline</a> <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=12122744">Similar articles</a><br />
2. Farouk R: Functional outcomes after ileal pouch-anal anastomosis for chronic ulcerative colitis. Ann Surg 231:919-926, 2000.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10816636&#038;dopt=Abstract"> Medline</a><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=10816636"> Similar articles</a><a href="http://dx.doi.org/10.1097/00000658-200006000-00017"> Full article</a><br />
3. Fazio V: Current status of surgery for inflammatory bowel disease. Digestion 59:470-480, 1998. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9705532&#038;dopt=Abstract">Medline</a><br />
4. Heuschen UA, Hinz U, Allemeyer EH, et al: One- or two-state procedure for restorative protocolectomy: Rationale for a surgical strategy in ulcerative colitis. Ann Surg 234:788-794, 2001. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=11729385&#038;dopt=Abstract">Medline</a> <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=11729385">Similar articles</a><a href="http://dx.doi.org/10.1097/00000658-200112000-00010"> Full article</a><br />
5. Hurst RD, Michelassi F: Strictureplasty for Crohn&#8217;s disease: Techniques and long term results. World J Surg 22:359-363, 1998.<br />
6. Present DH, Rutgeerts P Targan S, et al: Infliximab for the treatment of fistulas in patients with Crohn&#8217;s disease. N Engl J Med 340:1398-1405, 1999. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=9523517">Similar articles </a><a href="http://dx.doi.org/10.1007/s002689900397">Full article</a><br />
7. Solomon MJ, Schmitz M: Cancer and inflammatory bowel disease: Bias, epidemiology, surveillance, and treatment. World Surg 22:352-358, 1998. <a href="http://dx.doi.org/10.1007/s002689900396">Full article</a><br />
8. Stocchi L, Pemberton JH: Pouch and pouchitis. Gastroenterol Clin North Am 30:223-241, 2001. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=11394032&#038;dopt=Abstract">Medline</a> <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=11394032">Similar articles</a><br />
9. Sugerman HJ: Ileal pouch anal anastomosis without ileal diverson. Ann Surg 232:530-541, 2000. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10998651&#038;dopt=Abstract">Medline </a><br />
10. Wolff BG: Factors determining recurrence following surgery for Crohn&#8217;s disease. World J Surg 22:364-369, 1998.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9523518&#038;dopt=Abstract"> Medline</a> <a href="http://dx.doi.org/10.1007/s002689900398">Similar articles</a> <a href="http://dx.doi.org/10.1007/s002689900398">Full article</a></p>
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		<item>
		<title>Anorectal Disease. Pilonidal Sinus Disease</title>
		<link>http://surgeryprocedure.info/abdominal-surgery/anorectal-disease-pilonidal-sinus-disease</link>
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		<pubDate>Thu, 09 Jul 2009 07:32:17 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[ABDOMINAL SURGERY]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/?p=282</guid>
		<description><![CDATA[PILONIDAL SINUS DISEASE
29. What is the most common clinical presentation of a pilonidal sinus? 	
Show answer
Pain and swelling in the sacrococcygeal region, which typically are associated with a (sometimes several) chronic draining sinus tract.

30. Is pilonidal disease acquired or congenital? 	
Show answer
Acquired. Hair follicles in the midline sacrococcygeal area enlarge and become infected, resulting in [...]]]></description>
			<content:encoded><![CDATA[<p><strong>PILONIDAL SINUS DISEASE</strong></p>
<blockquote><p><strong>29. What is the most common clinical presentation of a pilonidal sinus? </strong>	</p></blockquote>
<p>Show answer<br />
Pain and swelling in the sacrococcygeal region, which typically are associated with a (sometimes several) chronic draining sinus tract.<br />
<span id="more-282"></span></p>
<blockquote><p><strong>30. Is pilonidal disease acquired or congenital?</strong> 	</p></blockquote>
<p>Show answer<br />
Acquired. Hair follicles in the midline sacrococcygeal area enlarge and become infected, resulting in an abscess.</p>
<blockquote><p><strong>31. How is acute pilonidal abscess treated? </strong></p></blockquote>
<p>	Show answer<br />
Incision and drainage (like a fistula in ano, it is necessary to excise the whole tract).</p>
<blockquote><p><strong>32. What is the definitive therapy for pilonidal disease?</strong> </p></blockquote>
<p>	Show answer<br />
Excision of the entire pilonidal cavity and associated sinus tracts down to the fascia with primary or delayed closure.</p>
<blockquote><p><strong>33. What theory explains the rarity of pilonidal disease after age 40 years?</strong> </p></blockquote>
<p>	Show answer<br />
Changes in body habitus.</p>
<p><strong>References</strong><br />
BIBLIOGRAPHY<br />
1. Beck DE, Wexner SD (eds): Fundamentals of Anorectal Surgery. Philadelphia, W.B. Saunders, 1998.<br />
2. Cho DV: Endosonographic criteria for an internal opening of fistula-in-ano. Dis Colon Rectum 42:515-518, 1999.<br />
3. Cintron JR, Park JJ, Orsay CP, et al: Repair of fistulas-in ano using fibrin adhesive: Long-term follow-up. Dis Colon Rectum 43:944-949, 2000. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10910240&#038;dopt=Abstract">Medline </a><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=10910240">Similar articles</a><br />
4. Corman ML: Anal fistula. In Corman ML: Colon and Rectal Surgery, 4th ed. Philadelphia, Lippincott-Raven, 1998, pp 238-271.<br />
5. Hodgkin W: Pilonidal sinus disease. J Wound Care 7:481-483, 1998.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9887741&#038;dopt=Abstract"> Medline</a> <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=9887741">Similar articles</a><br />
6. Law WL, Chu KW: Triple rubber band ligation for hemorrhoids: Prospective randomized trial of local anesthetic injection. Dis Colon Rectum 42:363-366, 1999. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10223757&#038;dopt=Abstract">Medline </a><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=10223757">Similar articles</a><br />
7. Park JJ, Cintron JR, Orsay CP, et al: Repair of chronic anorectal fistulae using commercial fibrin sealant. Arch Surg 135:166-169, 2000.<br />
8. Sentovich SM: Fibrin glue for all anal fistulas. J Gastrointest Surg 5:158-161, 2001. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=11331478&#038;dopt=Abstract">Medline </a><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=11331478">Similar articles</a> <a href="http://dx.doi.org/10.1016/S1091-255X%2801%2980028-7">Full article</a></p>
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		<title>Properties In Evaluation Of The Acute Abdomen. Lab Stadies</title>
		<link>http://surgeryprocedure.info/general-topics/properties-in-evaluation-of-the-acute-abdomen-lab-stadies</link>
		<comments>http://surgeryprocedure.info/general-topics/properties-in-evaluation-of-the-acute-abdomen-lab-stadies#comments</comments>
		<pubDate>Tue, 07 Jul 2009 07:11:15 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[GENERAL TOPICS]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/?p=103</guid>
		<description><![CDATA[LABORATORY STUDIES

15. How is a complete blood count helpful? 

	Show answer 
   1. Hematocrit. If the hematocrit is high (> 45%), the patient is most likely dry or may have chronic obstructive pulmonary disease. If it is low (< 30%), the patient probably has a more chronic disease (associated with blood loss-always do [...]]]></description>
			<content:encoded><![CDATA[<p><strong>LABORATORY STUDIES</strong></p>
<p><strong><br />
<blockquote>15. How is a complete blood count helpful? </p></blockquote>
<p></strong></p>
<p>	Show answer </p>
<p>  <strong> 1. Hematocrit.</strong> If the hematocrit is high (> 45%), the patient is most likely dry or may have chronic obstructive pulmonary disease. If it is low (< 30%), the patient probably has a more chronic disease (associated with blood loss-always do a rectal and test the stool for blood).<br />
   <b>2. White blood cell count.</b> It takes hours for inflammation to release cytokines and elevate the white blood cell count. A normal white blood cell count is entirely consistent with significant abdominal trouble.<span id="more-103"></span></p>
<blockquote><p><strong>16. Is urinalysis necessary?</strong> </p></blockquote>
<p>	Show answer<br />
Yes. White blood cells in the urine may redirect attention to the diagnosis of pyelonephritis or cystitis. Hematuria points to renal or ureteral stones. Because an inflamed appendix may lie directly on the right ureter, red and white blood cells may be found in the urine of patients with appendicitis.</p>
<blockquote><p><strong>17. What is a &#8220;three-way of the abdomen&#8221;?</strong></p></blockquote>
<p> 	Show answer </p>
<p>   <strong>1. Upright chest radiograph.</strong> Look for free air under the diaphragm (perforated viscus) and pneumonia or pneumothorax.<br />
   <strong>2. Upright abdomen.</strong> Look for free air under the diaphragm and air-fluid levels (intestinal obstruction). Remember to look for sigmoid or rectal air (partial obstruction).<br />
   <strong>3. Supine abdomen.</strong> This radiograph tells nothing.</p>
<p>Most ureteral stones can be visualized. Only 10% of gallstones are radiopaque, and appendiceal fecaliths are rarely noted.<br />
Honors: Air in the biliary system indicates a biliary-enteric fistula; this in association with intestinal air-fluid levels makes the diagnosis of gallstone ileus.<br />
<em><strong>KEY POINTS: RADIOGRAPHIC EVALUATION FOR THE ACUTE ADBOMEN</strong></p>
<p>   1. May assist in diagnostic evaluation but should not supplant physical exam in evaluaton of an acute abdomen.<br />
   2. Three-way of the abdomen: look for free air under the diaphragm, intrathoracic pathology, air-fluid levels, dilated alimentary canal, distal air in rectum.<br />
   3. Ultrasound: useful for biliary, ob-gyn, and vascular assessments; may note intraperitoneal or retroperitoneal fluid collections.<br />
   4. Computed tomography: increasing use in clinical arena, with excellent visualization of abdominal structures. Drawbacks: cost, radiation exposure.</em></p>
<blockquote><p><strong>18. What is a sentinel loop? </strong></p></blockquote>
<p>	Show answer<br />
Except in children (who swallow everything, including air), small bowel gas is always pathologic. A single loop of small bowel gas adjacent to an inflamed organ (e.g., the pancreas) may point to the diseased organ.</p>
<blockquote><p><strong>19. Is ultrasound valuable? </strong></p></blockquote>
<p>	Show answer<br />
Yes, if the working diagnosis is cholecystitis, gallstones, ectopic pregnancy, ovarian cyst, abdominal aortic aneurysm, or intraperitoneal/retroperitoneal fluid.</p>
<blockquote><p><strong>20. Is abdominal computed tomography (CT) valuable? </strong></p></blockquote>
<p>	Show answer<br />
Yes, if the working diagnosis is an intra-abdominal abscess (sigmoid diverticulitis), pancreatitis, retroperitoneal bleeding (leaking abdominal aortic aneurysm; this patient should have gone straight to the operating room), or intrahepatic or splenic pathology.</p>
<blockquote><p><strong>21. What is a double-contrast CT scan?</strong></p></blockquote>
<p> 	Show answer<br />
The bowel is delineated with barium or Gastrografin. The blood vessels are delineated with an iodinated vascular dye. The CT scan precisely displays the abdominal contents relative to vascular and intestinal landmarks. Contrast CT of pancreatitis is valuable to assess zones of perfusion or necrosis.</p>
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		<title>MITRAL REGURGITATION</title>
		<link>http://surgeryprocedure.info/cardiothoracic-surgery/mitral-regurgitation</link>
		<comments>http://surgeryprocedure.info/cardiothoracic-surgery/mitral-regurgitation#comments</comments>
		<pubDate>Fri, 10 Jul 2009 18:51:41 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[CARDIOTHORACIC SURGERY]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/?p=373</guid>
		<description><![CDATA[76 MITRAL REGURGITATION
David A. Fullerton M.D., Glenn J.R. Whitman M.D.
1. List the causes of mitral regurgitation.
 	Show answer 
    * Rheumatic fever
    * Endocarditis
    * Ruptured chordae tendineae
    * Senile mitral annular calcification
    * Papillary muscle dysfunction from ischemia
  [...]]]></description>
			<content:encoded><![CDATA[<p><strong>76 MITRAL REGURGITATION<br />
David A. Fullerton M.D., Glenn J.R. Whitman M.D.</strong></p>
<blockquote><p><strong>1. List the causes of mitral regurgitation.</strong></p></blockquote>
<p> 	Show answer </p>
<p>    * Rheumatic fever<br />
    * Endocarditis<br />
    * Ruptured chordae tendineae<br />
    * Senile mitral annular calcification<br />
    * Papillary muscle dysfunction from ischemia<br />
    * Annular dilatation from left ventricular dilation<br />
<span id="more-373"></span></p>
<blockquote><p><strong>2. What is the pathophysiology of mitral regurgitation? </strong></p></blockquote>
<p>	Show answer<br />
The left ventricle ejects blood via two routes: (1) antegrade, through the aortic valve, or (2) retrograde, through the mitral valve. The amount of each stroke volume ejected retrograde into the left atrium is the regurgitant fraction. To compensate for the regurgitant fraction, the left ventricle must increase its total stroke volume. This ultimately produces volume overload of the left ventricle and leads to ventricular dysfunction.</p>
<blockquote><p><strong>3. What are the symptoms of mitral regurgitation?</strong></p></blockquote>
<p> 	Show answer<br />
Dyspnea on exertion and loss of exercise tolerance are the symptoms of heart failure.</p>
<blockquote><p><strong>4. What determines left atrial pressure in mitral regurgitation?</strong></p></blockquote>
<p> 	Show answer<br />
The compliance of the left atrium.</p>
<blockquote><p><strong>5. Why does acute mitral regurgitation cause severe symptoms?</strong></p></blockquote>
<p> 	Show answer<br />
With acute mitral regurgitation, the normal left atrium is noncompliant. Hence, left atrial pressure increases rapidly, flooding the lungs (i.e., congestive heart failure) and causing severe symptoms. Conversely, chronic mitral regurgitation is associated with progressive dilatation of the left atrium. With increased left atrial compliance, the left atrial pressure may not increase.</p>
<blockquote><p><strong>6. What hemodynamic conditions exacerbate mitral regurgitation? </strong></p></blockquote>
<p>	Show answer<br />
Increased left ventricular afterload: Increased systemic arterial blood pressure increases the impedance against which the left ventricle must pump to eject blood antegrade. The regurgitant fraction is therefore increased (more blood goes backwards through the mitral valve).<br />
Tachycardia: Because mitral regurgitation occurs during systole, tachycardia (i.e., more systoles per minute) increases the regurgitant fraction.<br />
Volume overload: Left ventricular distension secondary to volume overload stretches the mitral anulus, impairs coaptation of the mitral valve leaflets, and increases mitral regurgitation.</p>
<blockquote><p><strong>7. What is the murmur of mitral regurgitation?</strong></p></blockquote>
<p> 	Show answer<br />
A holosystolic murmur is best heard at the apex with radiation to the left axilla.</p>
<blockquote><p><strong>8. How is the diagnosis confirmed?</strong></p></blockquote>
<p> 	Show answer<br />
By color Doppler echocardiography, especially transesophageal echocardiography (TEE; the left atrium lies right on the esophagus). The regurgitant jet may be accurately visualized and quantitated. Echocardiography also allows determination of the anatomic abnormality of the mitral valve apparatus that is responsible for the regurgitation.</p>
<blockquote><p><strong>9. What is the medical therapy for mitral regurgitation?</strong></p></blockquote>
<p> 	Show answer </p>
<p>    * Afterload reduction with angiotensin-converting enzyme (ACE) inhibitors<br />
    * Diuretics (furosemide) for lower left ventricular preload<br />
    * Digoxin provides ventricular rate control for patients in atrial fibrillation<br />
    * Warfarin (Coumadin) is used for patients in atrial fibrillation</p>
<blockquote><p><strong>10. What are the indications for surgery in patients with mitral regurgitation?</strong></p></blockquote>
<p> 	Show answer </p>
<p>    * Severe mitral regurgitation, especially with a ruptured chordae tendineae<br />
    * Symptoms despite medical therapy<br />
    * Progressive mitral regurgitation by echocardiography<br />
    * Deteriorating left ventricular systolic function. Because mitral regurgitation lowers the total impedance of left ventricular ejection (much of each stroke volume escapes via the low resistance mitral valvular &#8220;back door&#8221;), the left ventricular ejection fraction (LVEF) should be greater than normal in the presence of mitral regurgitation. An LVEF < 55% in the presence of mitral regurgitation suggests left ventricular dysfunction.<br />
    * Pulmonary artery pressure increases with exercise</p>
<p><em><strong>KEY POINTS: MITRAL REGURGITATION</strong></p>
<p>   1. The symptoms are dyspnea on exertion and loss of exercise tolerance.<br />
   2. The murmur of mitral regurgitation is a holosystolic murmur heard best at the apex with radiation to the left axilla.<br />
   3. Mitral valve regurgitation is corrected with mitral valve repair or mitral valve replacement.<br />
   4. Mitral valve repair is preferable to replacement because of lower operative mortality rates, less risk of thromboembolism, less risk of endocarditis, better long-term left ventricular function, and less need (if any) for chronic anticoagulation.<br />
   5. Repair also avoids prosthetic valve-related complications.</em></p>
<blockquote><p><strong>11. How is mitral regurgitation corrected?</strong></p></blockquote>
<p> 	Show answer<br />
Mitral valve repair. Mitral valve repair is the preferred surgical procedure. This preserves the mitral apparatus, maintaining the continuity between the left ventricular muscle and the mitral anulus via the chordae tendineae. Loss of this continuity by resection of the apparatus places the left ventricle at a mechanical disadvantage that over time leads to left ventricular dilatation and dysfunction.<br />
Mitral valve replacement. An inability to repair the regurgitant valve mandates replacement. If replacement is necessary, efforts should be made to preserve the posterior leaflet of the mitral valve. In most series, mitral valve replacement is required in < 30% of cases.</p>
<blockquote><p><strong>12. Why is it preferable to repair rather than replace the mitral valve?</strong></p></blockquote>
<p> 	Show answer </p>
<p>    * Lower operative mortality<br />
    * Less risk of thromboembolism<br />
    * Less risk of endocarditis<br />
    * Less need (if any) for chronic anticoagulation<br />
    * Better long-term left ventricular function<br />
    * Avoids valve-related complications</p>
<blockquote><p><strong>13. How is the mitral valve repaired?</strong></p></blockquote>
<p> 	Show answer<br />
The redundant portion(s) of the valve leaflet(s) is resected, the leaflet is reapproximated, and the mitral anulus is plicated and reinforced with a prosthetic anuloplasty ring. The anuloplasty ring is sewn around the perimeter of the anulus on the left atrial side of the valve. In so doing, the mitral leaflets are supported by competent chordae tendineae, and the circumference of the mitral anulus is decreased. Competency of the repaired valve is assessed intraoperatively using TEE.</p>
<blockquote><p><strong>14. What is the operative mortality of mitral valve repair versus mitral valve replacement? </strong>	</p></blockquote>
<p>Show answer<br />
Repair: 2%; replacement: 6%.</p>
<blockquote><p><strong>15. How durable are mitral valve repairs?</strong></p></blockquote>
<p> 	Show answer<br />
The risk of requiring another mitral valve operation is approximately 2% per year.</p>
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