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	<title>SurgeryProcedure.info &#187; Search Results  &#187;  rejection of hernia mesh neuroma formation</title>
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		<title>Inguinal Hernia. Controversies</title>
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		<pubDate>Thu, 09 Jul 2009 08:12:40 +0000</pubDate>
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				<category><![CDATA[ABDOMINAL SURGERY]]></category>

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		<description><![CDATA[CONTROVERSIES
36. What are some of the anatomic issues related to inguinal hernias?
 	Show answer
At issue is the iliopubic tract, which is central to the Anson/McVay anatomic description of the inguinal area and featured in the McVay Cooper&#8217;s ligament repair. Although the McVay repair is used in England, the iliopubic tract is not referred to or [...]]]></description>
			<content:encoded><![CDATA[<p><strong>CONTROVERSIES</strong></p>
<blockquote><p><strong>36. What are some of the anatomic issues related to inguinal hernias?</strong></p></blockquote>
<p> 	Show answer<br />
At issue is the iliopubic tract, which is central to the Anson/McVay anatomic description of the inguinal area and featured in the McVay Cooper&#8217;s ligament repair. Although the McVay repair is used in England, the iliopubic tract is not referred to or described in English anatomic texts.<br />
<span id="more-290"></span><br />
The term conjoined tendon, although commonly used, is considered by many to be anatomically inaccurate and misleading. The internal oblique and transversus abdominis muscles that make up the conjoined tendon are obvious and can be used surgically either alone or together. The tendinous edge of the transversus abdominis muscle and the tendinous edge of the internal oblique muscle start at their insertion on the pubic tubercle and course laterally and superiorly to the medial edge of the internal ring. At this point, the tendinous elements diminish, leaving only muscle tissues, and continue laterally and superiorly to their origins.<br />
Whether the lacunar ligament or the iliopubic tract defines the medial border of the femoral canal is controversial. The compromise position is that the iliopubic tract is the border whereas in the normal unstretched state, the lacunar ligament (Gimbernat&#8217;s ligament) is the border in the presence of hernia (stretched state). At surgery it is enough to say that a palpable, visible curved ligament is present and used in some femoral repairs.</p>
<blockquote><p><strong>37. What are some surgical issues in the repair of inguinal hernias?</strong></p></blockquote>
<p> 	Show answer </p>
<p>The controversy over implanting mesh, as in the Lichtenstein repair, has been resolved in favor of mesh. Another controversy concerns the use of the laparoscope for hernia repair. A further issue is intra-abdominal or preperitoneal placement of mesh. At present, most surgeons accept laparoscopic repair as an alternative for preperitoneal hernia repair. The indications for a preperitoneal approach to hernia repair are still being defined, although the preperitoneal approach is acceptable for repair of recurrent hernia and unusually large or difficult hernias. The preperitoneal approach is used with increasing frequency for repair of femoral hernias. The repair should be appropriate to the circumstance of the hernia. Thus, hernia location and size as well as the patient&#8217;s age, general condition, and recurrence status should be factored into the strategy of repair.</p>
<p><strong><br />
References</strong><br />
BIBLIOGRAPHY<br />
1. Avisse C, Delattre JF, Flament JB: The inguinal rings. Surg Clin North Am 80:49-69, 2000.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10685144&#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=10685144">Similar articles</a><br />
2. Avisse C, Delattre JF, Flament JB: The inguinofemoral area from a laparoscopic standpoint. History, anatomy, and surgical applications. Surg Clin North Am 80:35-48, 2000. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10685143&#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=10685143">Similar articles</a><br />
3. Bendavid R, Howarth D: Transversalis fascia rediscovered. Surg Clin North Am 80:25-33, 2000. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10685142&#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=10685142">Similar articles</a><br />
4. Collaboration EH: Laparoscopic compared with open methods of groin hernia repair: Systematic review of randomized controlled trials. Br J Surg 87:860-867, 2000. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10931019&#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=10931019">Similar articles</a><a href="http://dx.doi.org/10.1046/j.1365-2168.2000.01540.x"> Full article</a><br />
5. Collaboration EH: Mesh compared with non-mesh methods of open groin hernia repair. Systematic review of randomized controlled trials. Br J Surg 87:854-859, 2000.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10931018&#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=10931018">Similar articles</a> <a href="http://dx.doi.org/10.1046/j.1365-2168.2000.01539.x">Full article</a></p>
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		<title>Inguinal Hernia</title>
		<link>http://surgeryprocedure.info/abdominal-surgery/inguinal-hernia</link>
		<comments>http://surgeryprocedure.info/abdominal-surgery/inguinal-hernia#comments</comments>
		<pubDate>Thu, 09 Jul 2009 07:46:44 +0000</pubDate>
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				<category><![CDATA[ABDOMINAL SURGERY]]></category>

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		<description><![CDATA[56 INGUINAL HERNIA
Gregory P. Victorino M.D., Jyoti Arya M.D., James Bascom M.D.
1. &#8220;Groin&#8221; hernia refers to which three hernias? 	
Show answer
Direct and indirect inguinal hernias and femoral hernias.

2. Francois Poupart, a French surgeon and anatomist (1616-1708), described a ligament that bears his name. What is the anatomic name of the Poupart ligament?
 	Show answer
Inguinal ligament, [...]]]></description>
			<content:encoded><![CDATA[<p><strong>56 INGUINAL HERNIA<br />
Gregory P. Victorino M.D., Jyoti Arya M.D., James Bascom M.D.</strong></p>
<blockquote><p><strong>1. &#8220;Groin&#8221; hernia refers to which three hernias? </strong>	</p></blockquote>
<p>Show answer<br />
Direct and indirect inguinal hernias and femoral hernias.<br />
<span id="more-285"></span></p>
<blockquote><p><strong>2. Francois Poupart, a French surgeon and anatomist (1616-1708), described a ligament that bears his name. What is the anatomic name of the Poupart ligament?</strong></p></blockquote>
<p> 	Show answer<br />
Inguinal ligament, which is a key element in most groin hernia repair.</p>
<blockquote><p><strong>3. Franz K. Hesselbach, a German surgeon and anatomist (1759-1816), described a triangle that is the common site of direct hernias. What are the anatomic margins of Hesselbach&#8217;s triangle?</strong></p></blockquote>
<p> 	Show answer<br />
The triangle is defined inferiorly by the inguinal ligament, superiorly by the inferior epigastric vessels, and medially by the rectus fascia. The transversalis fascia forms the floor of the triangle. The original description used Cooper&#8217;s ligament as the inferior limit but because of the common use of the anterior approach to hernias, the more apparent inguinal ligament was substituted as the inferior limit of the triangle. With the increasing use of preperitoneal approaches to hernia repair, Cooper&#8217;s ligament is again much more apparent and useful as an anatomic touchstone.</p>
<blockquote><p><strong>4. Sir Astley Paston Cooper, an English surgeon and anatomist (1768-1841), described a ligament bearing his name. What is the anatomic name for the ligament and the proper name of Cooper&#8217;s ligament repair? </strong>	</p></blockquote>
<p>Show answer<br />
The anatomic name of Cooper&#8217;s ligament is iliopectineal ligament. The Cooper&#8217;s ligament repair or McVay repair was popularized by Chester McVay (1911-1987). With Barry Aston, professor of anatomy at Northwestern University, McVay provided the modern description of the groin anatomy.</p>
<blockquote><p><strong>5. Antonio de Gimbernat, a Spanish surgeon and anatomist (1734-1816), had his interesting name attached to the lacunar ligament, which marks the medial margin of a groin area opening. What is the opening? What hernia protrudes into this opening?</strong> </p></blockquote>
<p>	Show answer<br />
The opening is the femoral canal, which is defined medially by the lacunar ligament, anteriorly by the inguinal ligament, posteriorly by the pectineal fascia, and laterally by the femoral vein. A femoral hernia protrudes into the femoral canal.</p>
<blockquote><p><strong>6. Indirect inguinal hernia (particularly in children) and hydrocele are associated with which congenital abnormality? </strong>	</p></blockquote>
<p>Show answer<br />
Persistence of an open processus vaginalis, in the case of a hernia, allows descent of bowel into the inguinal canal. With fluid accumulation, partial obstruction presents as a hydrocele of the spermatic cord.</p>
<blockquote><p><strong>7. What are the diagnostic criteria for hernia in an infant or child? </strong>	</p></blockquote>
<p>Show answer </p>
<p>    * Inguinal, scrotal, or labial lump that may or may not be reducible<br />
    * History of a lump seen by a health care provider<br />
    * History of a lump seen by the mother<br />
    * The &#8220;silk sign&#8221; (the feeling of rubbing together two surfaces of silk cloth when gently rubbing together the two surfaces of a hernia sac)<br />
    * An incarceration sometimes felt on rectal examination</p>
<blockquote><p><strong>8. What can be done to reduce an incarcerated hernia in an infant or child?</strong> </p></blockquote>
<p>	Show answer<br />
The four-point program is easier said than done, but it is worth the effort:</p>
<p>   1. Sedate the patient.<br />
   2. Place the patient in the Trendelenburg position.<br />
   3. Apply a cold pack (over petroleum gauze to avoid skin injury) in inguinal area.<br />
   4. In the absence of spontaneous reduction-and if the patient is quiet-use gentle manipulation.</p>
<blockquote><p><strong>9. How often can incarceration be successfully reduced? What should be done next? </strong></p></blockquote>
<p>	Show answer<br />
About 80% of incarcerated hernias can be reduced in children; in adults, the percentage is lower. Despite the fact that 80-90% of inguinal hernias occur in boys, most incarcerations occur in girls. The hernia should be repaired electively within a few days after incarceration. The 20% of hernias that are still incarcerated are operated immediately.</p>
<blockquote><p><strong>10. What is a Bassini repair? </strong></p></blockquote>
<p>	Show answer<br />
The Bassini repair sutures together the conjoined tendon and the shelving edge of the inguinal ligament up to the internal ring (Figure 56-1). This classic procedure, introduced in 1887 at the Italian Society of Surgery in Genoa, revolutionized hernia repair. Until recently, it has been the standard of repair. After graduation from medical school and while fighting for Italian independence, Eduardo Bassini (1844-1924) was bayoneted in the groin and, as a prisoner, was hospitalized for months with a fecal fistula.</p>
<p><img src="http://img3.raidpic.com/193.56.1.jpg" /></p>
<p><strong>Figure 56-1 The standard right inguinal hernia repair using the conjoined tendon and inguinal ligament.</strong></p>
<blockquote><p><strong>11. What is the recurrence rate with indirect and direct hernias that have been repaired with classic Bassini repair technique?</strong> </p></blockquote>
<p>	Show answer<br />
Over a follow-up period of 50 years, the recurrence rate of adult indirect hernias is 5-10%; of direct hernias, 15-30%.</p>
<blockquote><p><strong>12. Describe a McVay hernia repair. </strong></p></blockquote>
<p>	Show answer<br />
The line of interrupted sutures starts at a the pubic tubercle and joins the tendinous arch of the transversus abdominis muscle to Cooper&#8217;s ligament up to the femoral canal. At this point, two or three transitional sutures are placed from Cooper&#8217;s ligament to the anterior femoral fascia, effectively closing the medial extreme of the femoral canal. The final set of sutures joins the transversus abdominis arch and the anterior femoral fascia. The stitches usually incorporate the inguinal ligament at the upper limit of the repair, the site of the new internal inguinal ring and cord structures. About 15 years ago, McVay described laying in a mesh patch and stitching it, at its periphery, to the same anatomic structures. This application of mesh closely resembles the Lichtenstein repair (see question 17), except that it uses Cooper&#8217;s ligament.</p>
<blockquote><p><strong>13. For what type of hernias is the McVay Cooper&#8217;s ligament repair most useful? 	</strong></p></blockquote>
<p>Show answer<br />
Femoral and direct hernias.</p>
<blockquote><p><strong>14. What is the Shouldice repair? 	</strong></p></blockquote>
<p>Show answer<br />
The Shouldice repair, popularized at the Shouldice Clinic near Toronto, imbricates or overlays the transversalis fascia and conjoined tendon with four continuous lines, using two fine-wire sutures. The suture tract runs from the pubic tubercle to a new internal ring. Care is taken with the inferior epigastric vessels. The result is layered approximation of the conjoined tendon to the inguinal ligament tract.</p>
<blockquote><p><strong>15. What is the reported recurrence rate for the Shouldice repair? </strong></p></blockquote>
<p>	Show answer<br />
The recurrence rate is 1%, the lowest reported rate for nonmesh repairs of inguinal hernias in adults.</p>
<blockquote><p><strong>16. For what type of groin hernia is the Shouldice repair not appropriate?</strong></p></blockquote>
<p> 	Show answer<br />
Femoral hernia.</p>
<blockquote><p><strong>17. Describe the Lichtenstein repair. </strong></p></blockquote>
<p>	Show answer<br />
The Lichtenstein repair consists of a sutured patch of polypropylene mesh (Marlex, C.R. Bard, Inc., Covington, GA) that covers Hesselbach&#8217;s triangle and the indirect hernia area. It is considered a tension-free repair because the mesh is sutured in place without pulling ligaments or tissues together as in all other repairs. The mesh is divided at its upper end to wrap closely around the spermatic cord and its associated structures in the normal position of the internal inguinal canal. The Lichtenstein procedure is rapidly becoming the most widely used repair of adult inguinal hernia. The reported recurrence rate is < 1%.</p>
<blockquote><p><strong>18. What are the advantages of using the Marlex mesh?</strong></p></blockquote>
<p> 	Show answer<br />
Central to acceptance and success of the Lichtenstein hernia repair has been the development of and experience with the Marlex mesh. The monofilament mesh is strong, inert, and resistant to infection. The interstices are rapidly and completely infiltrated with fibroblasts, and the mesh is not subject to deterioration, rejection, or fragmentation. (See Figure 56-2.)</p>
<blockquote><p><strong>19. For what groin area is the Lichtenstein repair not appropriate?</strong></p></blockquote>
<p><img src="http://img7.raidpic.com/483.56.2.jpg" /></p>
<p><strong>Figure 56-2 The Marlex mesh repair of a right inguinal hernia. Note that the same structures are used but not brought together; thus, the name of the &#8220;tension-free&#8221; repair.</strong></p>
<blockquote><p><strong>20. Which type of repair is acceptable for the femoral hernia?</strong></p></blockquote>
<p> 	Show answer<br />
Several different repairs can be used. Mesh in the form of a plug can be inserted into the femoral canal and fixed in place. A McVay Cooper&#8217;s ligament repair can be done. A preperitoneal approach to the hernia can be used to suture or plug the defect. A suture repair or a sartorius facial flap applied from below the inguinal ligament in a femoral approach also may be used. The preperitoneal approach is increasingly used for complicated inguinal and femoral hernias.</p>
<blockquote><p><strong>21. What is the preperitoneal or Stoppa procedure?</strong></p></blockquote>
<p> 	Show answer<br />
The preperitoneal or Stoppa procedure is a groin hernia repair on the internal side of the abdominal wall between the peritoneum and fascial surfaces that do not open into the peritoneal cavity. The anatomic landmarks are very different and initially quite challenging to surgeons accustomed to the external abdominal wall approach. The technique is suited for recurrent hernias in which scarring and obliterated anatomy increase the risk of cord injury and recurrence. Other problems such as large hernias and femoral hernias are corrected with this approach. Conceptually, the laparoscopic hernia repair uses the same approach. (See Figure 56-3.)</p>
<blockquote><p><strong>22. Where are the spaces of Retzius and Bogros? Why are they increasingly important?</strong> 	</p></blockquote>
<p>Show answer<br />
Retzius&#8217; space is between the pubis and the urinary bladder. Bogros&#8217; space is between the peritoneum and the fascia and muscle planes on the posterior aspect of the abdominal wall below the umbilicus and down to Cooper&#8217;s ligament. Laterally, the space goes to the iliac spines. In either the open Stoppa procedure or the laparoscopic preperitoneal repair, the spaces of Retzius and Bogros are developed for mesh placement and surgical exposure.</p>
<blockquote><p><strong>23. How tight around the spermatic cord should a surgically fashioned, internal inguinal ring be? </strong></p></blockquote>
<p>	Show answer<br />
About 5 mm, which http://surgeryprocedure.info/wp-admin/media-upload.php?post_id=285&#038;type=image&#038;TB_iframe=true&#038;width=640&#038;height=525<br />
Add an Imageis less than a fingertip and more than a forceps tip.</p>
<p><img src="http://img7.raidpic.com/253.56.3.jpg" /><br />
<img src="http://img2.raidpic.com/253.56.3.jpg "></p>
<p><strong>Figure 56-3 The different appearance and landmarks are seen in the anterior view (above) and the posterior view (below) of the inguinal-femoral area. In the posterior view the importance of the inferior epigastric vessels, bladder, and Cooper&#8217;s ligament as anatomic landmarks is apparent</strong>.</p>
<blockquote><p><strong>24. What is the common fascial defect of larger indirect and all direct inguinal hernias</strong>? 	</p></blockquote>
<p>Show answer<br />
Weakness or attenuation of the transversalis fascia.</p>
<blockquote><p><strong>25. On examination, the femoral hernia may be confused with what other inguinal hernia? </strong>	</p></blockquote>
<p>Show answer<br />
The femoral hernia may be confused with a direct inguinal hernia because of the tendency of the femoral hernia to present at the lateral edge of the inguinal ligament.</p>
<p><em><strong>KEY POINTS: TYPES OF INGUINAL HERNIA REPAIR</strong></p>
<p>   1. The Bassini repair sutures together the conjoined tendon and the shelving edge of the inguinal ligament up to the internal ring.<br />
   2. The McVay repair is most useful for femoral and direct hernias.<br />
   3. The Shouldice repair imbricates the transversalis fascia and conjoined tendon with four continuous lines, using two fine-wire sutures (not appropriate for femoral hernias).<br />
   4. The Lichtenstein repair consists of a sutured patch of polyprolene mesh that covers Hesselbach&#8217;s triangle and the indirect hernia sac.</em></p>
<blockquote><p><strong><br />
26. What is the difference between an incarcerated and a strangulated hernia?</strong> </p></blockquote>
<p>	Show answer<br />
<strong>Incarcerated: </strong>structures in the hernia sac still have a good blood supply but are stuck in the sac because of adhesions or a narrow neck of the hernia sac.<br />
<strong>Strangulated:</strong> herniated structures, such as bowel or omentum, have lost their blood supply because of anatomic constriction at the neck of the hernia. The herniated, ischemic tissue is, therefore, in various stages of gangrenous changes. Strangulated hernias are surgical emergencies.</p>
<blockquote><p><strong>27. What operation is done for an uncomplicated indirect infant hernia? 	</strong></p></blockquote>
<p>Show answer<br />
High ligation of the hernia sac.</p>
<blockquote><p><strong>28. What operation is done for an uncomplicated indirect hernia in young adults?</strong> </p></blockquote>
<p>	Show answer<br />
The appropriate operation consists of high ligation and possibly one or two stitches in the transversalis fascia to tighten the internal ring. This is the basic Marcy technique, developed by Henry Orlando Marcy (1837-1924); it is smaller and more anatomically focused than the Bassini repair.</p>
<blockquote><p><strong>29. What operation is done for an uncomplicated but sizable direct hernia in elderly adults?</strong></p></blockquote>
<p> 	Show answer<br />
Traditionally, the Bassini or McVay repair was chosen. More recently, because of the low recurrence rate, the Shouldice or Lichtenstein repair is favored.</p>
<blockquote><p><strong>30. What organ systems should be reviewed with particular care in the work-up of patients with hernia (especially elderly patients with recent onset of hernia)?</strong> </p></blockquote>
<p>	Show answer<br />
The gastrointestinal, urinary, and pulmonary systems should be reviewed with particular care. One is looking for causes of chronic strain or sudden forces that may have induced the hernia. Straining during defecation or urination, unusual coughing, or difficulty with breathing, if corrected, may be of great value to the patient and reduce the chance of recurrent hernia.</p>
<blockquote><p><strong>31. What is a sliding hernia? </strong>	</p></blockquote>
<p>Show answer<br />
A sliding hernia is formed when a retroperitoneal organ protrudes (herniates) outside the abdominal cavity in such a manner that the organ itself and the overlying peritoneal surface constitute a side of the hernia sac.</p>
<blockquote><p><strong>32. What organs can be found in sliding hernias?</strong></p></blockquote>
<p> 	Show answer </p>
<p>    * Colon<br />
    * Cecum<br />
    * Appendix<br />
    * Ovary<br />
    * Bladder<br />
    * Fallopian tubes<br />
    * Uterus (rare)</p>
<blockquote><p><strong>33. What are common operative and postoperative complications of hernia repairs? </strong>	</p></blockquote>
<p>Show answer<br />
<strong>Intraoperative complications</strong></p>
<p>    * Injury to the spermatic cord, especially in children<br />
    * Injury to the spermatic vessels, resulting in atrophy or acute necrosis of testes<br />
    * Injury to the ilioinguinal nerve, genitofemoral nerve, and lateral femoral cutaneous nerve (the lateral femoral cutaneous nerve is uniquely vulnerable in laparoscopic and properitoneal procedures)<br />
    * Injury to the femoral vessels</p>
<p><strong>Postoperative complications</strong></p>
<p>    * Infection-high risk in children with diaper rash and patients with bowel injury or necrosis<br />
    * Hematoma-should resolve in time<br />
    * Nerve injury-the nerve is not always divided and, with time, may improve. If pain persists, try lidocaine block for both diagnosis and treatment. If a nerve block is not successful, one may consider reexploration to free the nerve from scar or to excise a postsurgical neuroma.</p>
<blockquote><p><strong>34. What are the common sites of hernia recurrence? 	</strong></p></blockquote>
<p>Show answer<br />
Direct hernias often recur at the pubic tubercle. Indirect hernias recur at the internal ring. The cause is usually related to poorly placed or insufficient stitches. Other possible causes include infection, poor tissue, poor collagen formation, or too much tension at the surgical suture line. A single line of repair under moderate tension fails in a significant number of patients, regardless of adequacy of repair or healing process. Tension is almost always bad in surgery.</p>
<blockquote><p><strong>35. How long should the patient avoid heavy lifting after a hernia repair? </strong>	</p></blockquote>
<p>Show answer<br />
The standard advice for decades has been 6 weeks. The current advice varies from no limitation with the Lichtenstein or preperitoneal repairs to 6 weeks for a Bassini repair. The self-limitation of pain is an excellent guide.</p>
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		<title>Congenital Diaphragmatic Hernia</title>
		<link>http://surgeryprocedure.info/pediatric-surgery/congenital-diaphragmatic-hernia</link>
		<comments>http://surgeryprocedure.info/pediatric-surgery/congenital-diaphragmatic-hernia#comments</comments>
		<pubDate>Sat, 11 Jul 2009 19:48:29 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[PEDIATRIC SURGERY]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/?p=415</guid>
		<description><![CDATA[86 CONGENITAL DIAPHRAGMATIC HERNIA
Denis D. Bensard M.D., Richard J. Hendrickson M.D.
1. What is the most common type of congenital diaphragmatic hernia (CDH)? 	
Show answer
Congenital abnormalities of the diaphragm include a posterolateral defect (Bochdalek hernia), an anteromedial defect (Morgagni hernia), or the eventration (central weakening) of the diaphragm. The Bochdalek hernia is the most common variant [...]]]></description>
			<content:encoded><![CDATA[<p><strong>86 CONGENITAL DIAPHRAGMATIC HERNIA<br />
Denis D. Bensard M.D., Richard J. Hendrickson M.D.</strong></p>
<blockquote><p><strong>1. What is the most common type of congenital diaphragmatic hernia (CDH)? </strong>	</p></blockquote>
<p>Show answer<br />
Congenital abnormalities of the diaphragm include a posterolateral defect (Bochdalek hernia), an anteromedial defect (Morgagni hernia), or the eventration (central weakening) of the diaphragm. The Bochdalek hernia is the most common variant and generally occurs on the left (80%). Approximately 20% occur on the right, and < 1% are bilateral.<br />
<span id="more-415"></span></p>
<blockquote><p><strong>2. What signs and symptoms suggest CDH? </strong>	</p></blockquote>
<p>Show answer<br />
Neonatal respiratory distress is the most common manifestation of CDH caused by associated lung maldevelopment. At birth or shortly thereafter, the infant develops severe dyspnea, retractions, and cyanosis. On physical examination, breath sounds are diminished on the ipsilateral side, heart sounds can be heard more easily in the contralateral chest, and the abdomen is scaphoid because of the herniation of abdominal viscera into the chest. Mediastinal shift may result impairing venous return and cardiac output.</p>
<blockquote><p><strong>3. How is the diagnosis confirmed? 	</strong></p></blockquote>
<p>Show answer<br />
A chest radiograph demonstrates multiple loops of air-filled intestine in the ipsilateral thorax. If a chest radiograph is obtained before entry of significant amounts of air into the bowel, a confusing pattern of mediastinal shift, cardiac displacement, and opacification of the hemithorax may be observed. Insertion of a nasogastric tube followed by repeat chest radiograph often demonstrates the tube (i.e., stomach) in the chest and confirms the diagnosis.</p>
<blockquote><p><strong>4. Are other anomalies associated with CDH?</strong> </p></blockquote>
<p>	Show answer<br />
Fifty percent of infants with CDH have associated anomalies. Fewer than 10% of patients with multiple major concurrent anomalies survive. Excluding intestinal malrotation and pulmonary hypoplasia, cardiac anomalies (63%) are the most frequent, followed by genitourinary (23%), gastrointestinal (17%), central nervous system (14%), and other pulmonary (5%) anomalies.</p>
<blockquote><p><strong>5. What therapeutic measures should be initiated before transport or operation? </strong></p></blockquote>
<p>	Show answer<br />
Perhaps the easiest and most effective palliative intervention is decompression of the stomach with a nasogastric tube, which prevents further distention of the bowel and lung compression. Endotracheal intubation permits adequate ventilation and oxygenation. Ventilatory pressures are kept low (< 30 mmHg), and the infant is ventilated at a rapid rate (40-60 breaths/min) to avoid barotrauma. Venous access and fluid resuscitation complete preliminary resuscitation.</p>
<blockquote><p><strong>6. What is the &#8220;honeymoon period&#8221;? 	</strong></p></blockquote>
<p>Show answer<br />
The honeymoon period describes the interval of time in which a neonate demonstrates adequate oxygenation and ventilation in the absence of maximal medical therapy. Regardless of subsequent deterioration, a honeymoon period suggests that pulmonary function is compatible with survival.<br />
<strong>7. Describe the operative approach. </strong>	Show answer </p>
<p>CDH results in a physiologic derangement of the lungs that is not reversed by surgical reconstruction of the diaphragm. Thus, repair of CDH is not a surgical emergency. The infant must be stabilized before surgical repair is attempted. A transabdominal approach allows reduction of the herniated abdominal viscera from the chest, repair of the diaphgramatic defect without obstructed vision or tension, correction of malrotation, and stretching of the abdominal cavity or creation of a ventral hernia with a prosthetic patch if the reduced viscera are not easily accomodated in the abdomen.</p>
<blockquote><p><strong>8. What is the most feared complication of diaphragmatic hernia?</strong></p></blockquote>
<p> 	Show answer<br />
The most feared complication is persistent fetal circulation (PFC). In CDH, one or both lungs are hypoplastic, the pulmonary vascular bed is reduced, and the pulmonary arteries exhibit thickened muscular walls that are hyperreactive. Newborns with CDH are particularly prone to the development of pulmonary hypertension. PFC arises from a sustained increase in pulmonary artery pressure. Blood is shunted away from the lungs, and the unoxygenated blood is diverted to the systemic circulation (right-to-left shunt) through the patent ductus arteriosus and patent foramen ovale. PFC results in hypoxemia, profound acidosis, and shock. PFC is triggered by acidosis, hypercarbia, and hypoxia, all potent vasoconstrictors of the pulmonary circulation.</p>
<blockquote><p><strong>9. Is PFC correctable? If so, how? </strong>	</p></blockquote>
<p>Show answer<br />
Yes. Various strategies are used to prevent or reverse PFC:</p>
<p>   1. Monitoring: Oximetry or arterial sampling (preductal in the right upper extremity; postductal in the lower extremity) permits early detection of shunting of unoxygenated blood to the systemic circulation.<br />
   2. Ventilation: Hypercarbia is corrected by mechanical ventilation; adequate sedation; and, if necessary, pharmacologic paralysis.<br />
   3. Oxygenation: Hypoxemia is corrected by adequate ventilation and high concentrations of inspired oxygen (generally FiO2 = 100%).<br />
   4. Resuscitation: Metabolic acidosis is managed by restoring adequate tissue perfusion (intravenous fluids or blood, inotropes, and sodium bicarbonate).<br />
   5. Rescue: Salvage therapies include administration of pulmonary vasodilators via the ventilatory circuit (nitric oxide) or systemic circulation (priscoline, prostaglandin E2), high-frequency ventilation, and extracorporeal membrane oxygenation (ECMO).</p>
<blockquote><p><strong>10. What is the survival rate for patients with CDH? </strong>	</p></blockquote>
<p>Show answer<br />
The overall survival rate is 60%. The major determinants of survival are the degree of pulmonary hypoplasia and associated major congenital anomalies. Among infants surviving the early newborn period without significant lung dysfunction, the survival rate approaches 100%.</p>
<blockquote><p><strong>11. Does in utero intervention have a role in the treatment of patients with CDH?</strong></p></blockquote>
<p> 	Show answer<br />
To date, fetal surgery for CDH remains experimental. In a prospective trial reported in 1997, the results of intrauterine repair of CDH were compared with conventional postnatal surgery with similar outcome. The investigators concluded that because open fetal surgery does not improve survival or outcome, prenatally diagnosed CDH should be treated postnatally.</p>
<p><strong>References</strong><br />
BIBLIOGRAPHY<br />
1. Clark RH, Hardin WD, Hirschl RB, et al: Current surgical management of congenital diaphragmatic hernia: A report from the congenital diaphragmatic hernia study group. J Pediatr Surg 33:1004-1009, 1998. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9694085&#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=9694085">Similar articles</a><br />
2. Fauza DO, Wilson JM: Congenital diaphragmatic hernia and associated anomalies: Their incidence, identification, and impact on prognosis. J Pediatr Surg 29:1113-1117, 1994. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=7965516&#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=7965516">Similar articles </a><br />
3. Harrison MR, Adzick NS, Bullard KM, et al: Correction of congenital diaphragmatic hernia in utero VII: A prospective trial. J Pediatr Surg 32:1637-1642, 1997.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9396545&#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=9396545">Similar articles</a><a href="http://dx.doi.org/10.1016/S0022-3468%2897%2990472-3"> Full article</a><br />
4. Nobuhara KK, Lund DP, Mitchell J, et al: Long-term outlook for survivors of congenital diaphragmatic hernia. Clin Perinatol 23:873-887, 1996.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=8982576&#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=8982576">Similar articles</a><br />
5. Weber TR, Kountzman B, Dillon PA, et al: Improved survival in congenital diaphragmatic hernia with evolving therapeutic strategies. Arch Surg 133:498-503, 1998.</p>
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		<title>Properties In Evaluation Of The Acute Abdomen</title>
		<link>http://surgeryprocedure.info/general-topics/properties-in-evaluation-of-the-acute-abdomen</link>
		<comments>http://surgeryprocedure.info/general-topics/properties-in-evaluation-of-the-acute-abdomen#comments</comments>
		<pubDate>Tue, 07 Jul 2009 07:04:30 +0000</pubDate>
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				<category><![CDATA[GENERAL TOPICS]]></category>

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		<description><![CDATA[14 PRIORITIES IN EVALUATION OF THE ACUTE ABDOMEN
Alden H. Harken M.D.

1. What is the surgeon&#8217;s responsibility when confronted by a patient with an acute abdomen?
 	Show answer 
   1. To identify how sick the patient is
   2. To determine whether the patient (a) needs to go directly to the operating room, [...]]]></description>
			<content:encoded><![CDATA[<p><strong>14 PRIORITIES IN EVALUATION OF THE ACUTE ABDOMEN<br />
Alden H. Harken M.D.<br />
</strong></p>
<blockquote><p><strong>1. What is the surgeon&#8217;s responsibility when confronted by a patient with an acute abdomen?</strong></p></blockquote>
<p> 	Show answer </p>
<p>   1. To identify how sick the patient is<br />
   2. To determine whether the patient (a) needs to go directly to the operating room, (b) should be admitted for resuscitation or observation, or (c) can be sent safely home</p>
<p><span id="more-98"></span></p>
<blockquote><p><strong>2. Which is the most dangerous course?</strong> </p></blockquote>
<p>	Show answer<br />
To send the patient home.</p>
<blockquote><p><strong>3. Is it important to make the diagnosis in the emergency department? </strong></p></blockquote>
<p>	Show answer<br />
No. Frequently time spent confirming a diagnosis in the emergency department is lost to inhospital resuscitation or treatment in the operating room. The only patient who needs a relatively firm diagnosis is a patient who is to be sent home.</p>
<blockquote><p><strong>4. If the essential goal is not to make the diagnosis, what should the surgeon do?</strong> 	</p></blockquote>
<p>Show answer </p>
<p>   1. Resuscitate the patient. Most patients do not eat or drink when they are getting sick. Most patients are depleted of at least several liters of fluid. Fluid depletion is worse in patients with diarrhea or vomiting.<br />
   2. Start a big IV line.<br />
   3. Replace lost electrolytes (see Chapter 7).<br />
   4. Insert a Foley catheter.<br />
   5. Examine the patient (frequently).</p>
<blockquote><p><strong>5. Are symptoms and signs uniquely misleading in any groups of patients? </strong></p></blockquote>
<p>	Show answer<br />
Yes. Watch out for the following groups:</p>
<p>    * The very young, who cannot talk.<br />
    * Diabetics, because of visceral neuropathy.<br />
    * The very old, in whom, much as in diabetics, abdominal innervation is dulled.<br />
    * Patients taking steroids, which depress inflammation and mask everything.<br />
    * Patients with immunosuppression (a heart or kidney transplant patient may act cheerful even with dead or gangrenous bowel).</p>
<blockquote><p><strong>6. Summarize the history needed.</strong> </p></blockquote>
<p>	Show answer </p>
<p>   <strong>1. The patient&#8217;s age.</strong> Neonates present with intussusception; young women present with ectopic pregnancy, pelvic inflammatory disease, and appendicitis; the elderly present with colon cancer, diverticulitis, and appendicitis.<br />
   <strong>2. Associated problems.</strong> Previous hospitalizations, prior abdominal surgery, medications, heart and lung disease? An extensive gynecologic history is valuable; however, it is probably safer to assume that all women between 12 and 40 years old are pregnant.<br />
   <strong>3. Location of abdominal pain. </strong><em>Right upper quadrant:</em> gallbladder or biliary disease, duodenal ulcer. Right flank: pyelonephritis, hepatitis. Midepigastrium: duodenal or gastric ulcer, pancreatitis, gastritis. Left upper quadrant: ruptured spleen, subdiaphragmatic abscess. Right lower quadrant: appendicitis (see Chapter 37), ectopic pregnancy, incarcerated hernia, rectus hematoma. Left lower quadrant: diverticulitis, incarcerated hernia, rectus hematoma. Note: Cancer, unless it obstructs (colon cancer), and bleeding (diverticulosis) typically do not hurt.<br />
  <strong> 4. Duration of pain. </strong><em>The pain of a perforated duodenal ulcer</em> or perforated sigmoid diverticulum is sudden, whereas the pain of pyelonephritis is gradual and persistent. The pain of intestinal obstruction is intermittent and crampy. Note: Although the surgeon is rotating through a gastrointestinal service, the patient may not know this and may present with urologic, gynecologic, or vascular pathology.</p>
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		<title>Tracheoesophageal Malformations</title>
		<link>http://surgeryprocedure.info/pediatric-surgery/tracheoesophageal-malformations</link>
		<comments>http://surgeryprocedure.info/pediatric-surgery/tracheoesophageal-malformations#comments</comments>
		<pubDate>Sat, 11 Jul 2009 19:41:17 +0000</pubDate>
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				<category><![CDATA[PEDIATRIC SURGERY]]></category>

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		<description><![CDATA[85 TRACHEOESOPHAGEAL MALFORMATIONS
Denis D. Bensard M.D., David A. Partrick M.D.
1. What are tracheoesophageal fistula (TEF) and esophageal atresia (EA)? 	
Show answer
The trachea and esophagus appear as a ventral diverticulum arising from the primitive foregut during the third week of gestation. The trachea and esophagus undergo separation by the ingrowth of ectodermal ridges during the fourth [...]]]></description>
			<content:encoded><![CDATA[<p><strong>85 TRACHEOESOPHAGEAL MALFORMATIONS<br />
Denis D. Bensard M.D., David A. Partrick M.D.</strong></p>
<blockquote><p><strong>1. What are tracheoesophageal fistula (TEF) and esophageal atresia (EA)? </strong>	</p></blockquote>
<p>Show answer<br />
The trachea and esophagus appear as a ventral diverticulum arising from the primitive foregut during the third week of gestation. The trachea and esophagus undergo separation by the ingrowth of ectodermal ridges during the fourth week of gestation. Failure of separation results in anomalous connection of the trachea to the esophagus (i.e., TEF) with or without incomplete formation of the esophagus (i.e., EA).<br />
<span id="more-411"></span></p>
<blockquote><p><strong>2. Describe the three most common variants and the relative incidence of each type</strong></p></blockquote>
<p>. 	Show answer </p>
<p>    * Proximal EA with distal TEF (&#8221;proximal pouch with distal fistula&#8221;): 85%<br />
    * Isolated EA: 10%<br />
    * TEF without EA (&#8221;H fistula&#8221;): 5%</p>
<blockquote><p>
<strong>3. What other anomalies occur with tracheoesophageal malformations?</strong></p></blockquote>
<p> 	Show answer<br />
TEF and EA result from an insult during the critical phase of embryogenesis (3-8 weeks&#8217; gestation). Up to 70% of infants with tracheoesophageal malformations suffer one or more concomitant anomalies. Cardiovascular anomalies are the most prevalent (35%), followed by anomalies of the gastrointestinal (24%), genitourinary (20%), skeletal (13%), and central nervous (10%) systems. Twenty-five percent of infants born with tracheoesophageal malformation have one or more components of the VACTERL association (see question 2 in chapter 84).</p>
<blockquote><p><strong>4. Does the presence of other anomalies alter management and outcome?</strong></p></blockquote>
<p> 	Show answer<br />
Healthy infants without concomitant anomalies generally undergo early repair with a nearly 100% survival rate, whereas infants who are severely premature or have life-threatening anomalies typically undergo delayed repair. Infants with lethal anomalies, such as trisomy 18, receive palliative care only.</p>
<blockquote><p><strong>5. Describe the clinical presentation, diagnosis, and preoperative management of patients with EA with distal TEF</strong>.</p></blockquote>
<p> 	Show answer<br />
Early in the newborn period, affected infants demonstrate excessive salivation (i.e., inability to swallow secretions), choking, or regurgitation with feeding (i.e., inability to swallow feeds). Respiratory distress quickly ensues because of aspiration of secretions or feeds from the esophageal pouch and reflux of gastric acid into the airways and lungs via the distal TEF. A nasogastric tube cannot be advanced into the stomach. The radiograph demonstrates a blind-ending proximal esophageal pouch and an air-filled stomach caused by the anomalous connection of the distal esophagus to the airway. The infant is maintained in a semi-upright position with sump catheter drainage of the proximal esophageal pouch to minimize contamination of the lungs either because of aspiration or reflux.</p>
<blockquote><p><strong>6. Describe the clinical presentation, diagnosis, and preoperative management of isolated EA. </strong>	</p></blockquote>
<p>Show answer </p>
<p>Isolated EA is associated with excessive salivation, choking, and regurgitation of feeds. The inability to pass a nasogastric tube into the stomach and a gasless abdomen apparent on radiograph suggests the diagnosis. Preoperative management is directed to the identification of associated anomalies and determination of gap length. Sump catheter drainage of the proximal esophageal pouch is maintained to minimize aspiration. Gastrostomy is generally performed within the first 24 hours of life to permit feeding and assessment of the distal esophageal length. Typically, infants with EA undergo delayed repair to permit growth of the distal esophagus and reduction of gap distance.</p>
<blockquote><p><strong>7. Describe the clinical presentation, diagnosis, and preoperative management of TEF without EA.</strong></p></blockquote>
<p> 	Show answer<br />
These infants demonstrate repeated choking or cyanotic spells with feeding caused by the reflux of feeds from the esophagus to the lungs via the anomalous tracheoesophageal connection. Older infants and children may present with recurrent bouts of pneumonia or unexplained reactive airway disease resulting from the intermittent contamination of the lungs via the fistula. Video esophagography and bronchoscopy are used to demonstrate the fistula.</p>
<blockquote><p><strong>8. How are tracheoesophageal malformations corrected surgically?</strong></p></blockquote>
<p> 	Show answer<br />
Surgical treatment entails restoration of esophageal continuity and elimination of the pathologic connection of the esophagus to the airway. Correction of EA with or without TEF requires thoracotomy, with or without ligation of TEF, and end-to-end esophageal anastomosis. The first successful procedure was performed by Cameron Haight in 1941. At 5-7 days after surgery, an esophagogram is performed; if no leak is visualized, oral feedings are started and the pleural drain is removed.<br />
TEF without EA is approached via a cervical incision, avoiding thoracotomy. The fistulous tract is divided and healthy tissue is interposed to prevent recurrence.</p>
<blockquote><p><strong>9. What are the early and late complications of surgical repair?</strong></p></blockquote>
<p><strong>Early complications</strong></p>
<table width="50%" border=1 cellpadding=2 bordercolor="#c0c0c0" cellspacing=2 bgcolor="#ffffff">
<tr valign=top>
<td><font size=2 color="#000000" face="Arial"></p>
<div>Anastomotic disruption</div>
<p></font>
</td>
<td width=35><font size=2 color="#000000" face="Arial"></p>
<div>5%</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td><font size=2 color="#000000" face="Arial"></p>
<div>Recurrent TEF</div>
<p></font>
</td>
<td width=35><font size=2 color="#000000" face="Arial"></p>
<div>5%</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td><font size=2 color="#000000" face="Arial"></p>
<div>Anastomotic leak</div>
<p></font>
</td>
<td width=35><font size=2 color="#000000" face="Arial"></p>
<div>15%</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td><font size=2 color="#000000" face="Arial"></p>
<div>Tracheomalacia</div>
<p></font>
</td>
<td width=35><font size=2 color="#000000" face="Arial"></p>
<div>15%</div>
<p></font>
</td>
</tr>
</table>
<p>Early complications are related to the basic surgical principles of wound healing. Anastomotic disruption generally results from poor blood supply and tension.<br />
<b>Late complications</b></p>
<table width="50%" border=1 cellpadding=2 bordercolor="#c0c0c0" cellspacing=2 bgcolor="#ffffff">
<tr valign=top>
<td width=213><font size=2 color="#000000" face="Arial"></p>
<div>Anastomotic stricture</div>
<p></font>
</td>
<td width=40><font size=2 color="#000000" face="Arial"></p>
<div>25%</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td width=213><font size=2 color="#000000" face="Arial"></p>
<div>Gastroesophageal reflux</div>
<p></font>
</td>
<td width=40><font size=2 color="#000000" face="Arial"></p>
<div>50%</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td width=213><font size=2 color="#000000" face="Arial"></p>
<div>Esophageal dysmotility</div>
<p></font>
</td>
<td width=40><font size=2 color="#000000" face="Arial"></p>
<div>100%</div>
<p></font>
</td>
</tr>
</table>
<p>Most strictures (50%) respond to one to three dilatations performed in the first 6 months of life. Refractory strictures require identification of associated gastroesophageal reflux (GER), which may worsen stricture formation. The frequency of GER appears related to gap length (i.e., the greater the gap distance, the greater the risk of significant GER).<br />
<em><strong>KEY POINTS: TRACHEOESOPHAGEAL MALFORMATIONS</strong></p>
<p>   1. The three most common variants are proximal esophageal atresia (EA) with distal tracheoesophageal fistula (TEE), isolated EA, and TEF without EA.<br />
   2. Early in the newborn period, affected infants demonstrate excessive salivation, choking, or regurgitation with feeding.<br />
   3. Surgical treatment entails restoration of esophageal continuity and elimination of the pathologic connection of the esophagus to the airway.</em></p>
<p><strong>References</strong><br />
BIBLIOGRAPHY<br />
1. Brown AK, Tam PK: Measurements of gap length in esophageal atresia: A simple predictor of outcome. J Am Coll Surg 182:41-45, 1996. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=8542088&#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=8542088">Similar articles</a><a href="http://dx.doi.org/10.1002/%28SICI%291096-9063%28199605%2947:1%3C41::AID-PS385%3E3.0.CO;2-N"> Full article</a><br />
2. Dunn JC, Fonkalsrud EW, Atkinson JB: Simplifying the Waterston&#8217;s stratification of infants with tracheoesophageal fistula. Am Surg 65:908-910, 1999. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10515532&#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=10515532">Similar articles</a><br />
3. Saing H, Mya GH, Cheng W: The involvement of two or more systems and the severity of associated anomalies significantly influence mortality in esophageal atresia. J Pediatr Surg 33:1596-1598, 1998. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=9856874">Similar articles</a> <a href="http://dx.doi.org/10.1016/S0022-3468%2898%2990588-7">Full article</a><br />
4. Somppi E, Tammela O, Ruuska T, et al: Outcome of patients operated on for esophageal atresia: 30 years&#8217; experience. J Pediatr Surg 33:1341-1346, 1998.<br />
5. Spitz L: Esophageal atresia: Past, present, and future. J Pediatr Surg 31:19-25, 1996. Medline Similar articles <a href="http://dx.doi.org/10.1016/S0022-3468%2896%2990313-9">Full article</a><br />
6. Torfs CP, Curry CJ, Bateson TF: Population-based study of tracheoesophageal fistula and esophageal atresia. Teratology 52:220-232, 1995. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=8632277">Medline</a></a><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=8838292&#038;dopt=Abstract"> <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=8632277">Similar articles</a><br />
7. Tovar JA, Diez Pardo JA, Murcia J, et al: Ambulatory 24-hour manometric and pH metric evidence of permanent impairment of clearance capacity in patients with esophageal atresia. J Pediatr Surg 30:1224-1231, 1995.</p>
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		<title>Congenital Cysts &amp; Sinuses Of The Neck</title>
		<link>http://surgeryprocedure.info/pediatric-surgery/congenital-cysts-sinuses-of-the-neck</link>
		<comments>http://surgeryprocedure.info/pediatric-surgery/congenital-cysts-sinuses-of-the-neck#comments</comments>
		<pubDate>Mon, 13 Jul 2009 18:44:41 +0000</pubDate>
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				<category><![CDATA[PEDIATRIC SURGERY]]></category>

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		<description><![CDATA[88 CONGENITAL CYSTS AND SINUSES OF THE NECK
Frederick M. Karrer M.D., Denis D. Bensard M.D.
1. What are branchial cleft anomalies?
 	Show answer
Cysts, sinuses, and fistulas that result from incomplete obliteration of the first, second, or third branchial clefts, and are present in early fetal development.

2. Which anomaly is the most common? 
	Show answer
Second branchial cleft [...]]]></description>
			<content:encoded><![CDATA[<p><strong>88 CONGENITAL CYSTS AND SINUSES OF THE NECK<br />
Frederick M. Karrer M.D., Denis D. Bensard M.D.</strong></p>
<blockquote><p><strong>1. What are branchial cleft anomalies?</strong></p></blockquote>
<p> 	Show answer<br />
Cysts, sinuses, and fistulas that result from incomplete obliteration of the first, second, or third branchial clefts, and are present in early fetal development.</p>
<p><span id="more-441"></span></p>
<blockquote><p><strong>2. Which anomaly is the most common? </strong></p></blockquote>
<p>	Show answer<br />
Second branchial cleft anomalies are by far the most common, presenting near the mid- to upper border of the sternocleidomastoid (SCM) muscle. First branchial remnants are less common and third clefts are quite rare. (See Table 88-1.)<br />
<strong>Table 88-1. BRANCHIAL CLEFT ANOMALIES</strong></p>
<table width="100%" border=1 cellpadding=2 bordercolor="#c0c0c0" cellspacing=2 bgcolor="#ffffff">
<tr valign=top>
<td><font size=2 color="#000000" face="Arial"></p>
<div><b>Branchial Cleft</b></div>
<p></font>
</td>
<td width=149><font size=2 color="#000000" face="Arial"></p>
<div><b>Internal Opening</b></div>
<p></font>
</td>
<td width=165><font size=2 color="#000000" face="Arial"></p>
<div><b>Exterior Opening</b></div>
<p></font>
</td>
<td width=69><font size=2 color="#000000" face="Arial"></p>
<div><b>Frequency</b></div>
<p></font>
</td>
</tr>
<tr valign=top>
<td><font size=2 color="#000000" face="Arial"></p>
<div>First</div>
<p></font>
</td>
<td width=149><font size=2 color="#000000" face="Arial"></p>
<div>External auditory canal</div>
<p></font>
</td>
<td width=165><font size=2 color="#000000" face="Arial"></p>
<div>Angle of the jaw</div>
<p></font>
</td>
<td width=69><font size=2 color="#000000" face="Arial"></p>
<div>8%</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td><font size=2 color="#000000" face="Arial"></p>
<div>Second</div>
<p></font>
</td>
<td width=149><font size=2 color="#000000" face="Arial"></p>
<div>Tonsillar fossa</div>
<p></font>
</td>
<td width=165><font size=2 color="#000000" face="Arial"></p>
<div>Anterior border of the SCM</div>
<p></font>
</td>
<td width=69><font size=2 color="#000000" face="Arial"></p>
<div>&gt; 90%</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td><font size=2 color="#000000" face="Arial"></p>
<div>Third</div>
<p></font>
</td>
<td width=149><font size=2 color="#000000" face="Arial"></p>
<div>Piriform sinus</div>
<p></font>
</td>
<td width=165><font size=2 color="#000000" face="Arial"></p>
<div>Suprasternal notch</div>
<p></font>
</td>
<td width=69><font size=2 color="#000000" face="Arial"></p>
<div>&lt; 1%</div>
<p></font>
</td>
</tr>
</table>
<blockquote><p><strong>3. How do patients with branchial cleft anomalies present?</strong> </p></blockquote>
<p>	Show answer<br />
Those with complete fistulas or sinuses present with intermittent drainage of a mucoid fluid on the neck. Patients with cysts usually present later with a mass (sterile or infected). Complete surgical excision is the treatment of choice.</p>
<blockquote><p><strong>4. What are the major operative hazards of branchial cleft remnant excision?</strong></p></blockquote>
<p> 	Show answer<br />
The second branchial cleft tracts through the bifurcation of the carotid artery. The facial nerve is in close proximity to the first branchial cleft fistula. The superior laryngeal nerve and the recurrent laryngeal nerve are both at risk in dissection of a third branchial cleft.</p>
<blockquote><p><strong>5. What is a thyroglossal duct cyst?</strong> </p></blockquote>
<p>	Show answer<br />
A thyroglossal duct cyst is the most common congenital cyst found in the neck. It is caused by failure of normal obliteration of the migration tract of the thyroid gland. Embryologically, the thyroid descends from the base of the tongue (foramen caecum) to its normal location in the low anterior neck.</p>
<blockquote><p><strong>6. How do patients with thyroglossal duct cysts present?</strong></p></blockquote>
<p> 	Show answer<br />
They present with a paramidline mass in the upper neck; if infected, they may present with fever, tenderness, and erythema.</p>
<p><em><strong>KEY POINTS: CONGENITAL CYSTS AND SINUSES OF THE NECK</strong></p>
<p>   1. The most common brachial cleft anomaly is the second brachial cleft anomaly presenting near the mid- to upper border or the sternocleidomastoid muscle.<br />
   2. A thyroglossal duct cyst is the most common congenital cyst found in the neck.<br />
   3. A cystic hygroma is a congenital lymphatic malformation that is benign an usually presents as a soft mass in the lateral neck.</em></p>
<blockquote><p><strong><br />
7. How are thyroglossal duct cysts treated?</strong></p></blockquote>
<p> 	Show answer<br />
The best treatment is complete excision of the cyst, along with the tract. Because embryologically the thyroid descends before formation of the hyoid cartilage, the tract may pass right through the hyoid. Therefore, complete tract removal requires excision of the central portion of the hyoid and dissection up to the base of the tongue (i.e., the Sistrunk procedure).</p>
<blockquote><p><strong>8. What is a cystic hygroma? 	</strong></p></blockquote>
<p>Show answer<br />
A cystic hygroma is a congenital lymphatic malformation with a predilection for the neck. It is a benign lesion that usually presents as a soft mass in the lateral neck. Excision is often challenging because the lymph cysts do not respect the fascial planes and often intertwine with the neurovascular structures in the neck. Near-total excision is the treatment of choice.</p>
<p><strong>References</strong><br />
BIBLIOGRAPHY<br />
1. Alqahtani A, Nguyen LT, Flageole H, et al: 25 years experience with lymphangioma in children. J Pediatr Surg 34:1164-1168, 1999. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10442614&#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=10442614">Similar articles </a><a href="http://dx.doi.org/10.1016/S0022-3468%2899%2990590-0">Full article</a><br />
2. Brown RL, Azizkhan RG: Pediatric head and neck lesions. Pediatr Clin North Am 45:889-905, 1998. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9728193&#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=9728193">Similar articles</a><br />
3. Kang L, Chang CH, Yu CH, et al: Prenatal detection of cystic hygroma using three-dimensional ultrasound. Ultrasound Med Biol 28:719, 2002. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=12113783&#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=12113783">Similar articles</a><br />
4. Organ GM, Organ CH Jr: Thyroid gland and surgery of the thyroglossal duct: Exercise in applied embryology. World J Surg 24:886-890, 2000.<br />
5. Smith CD: Cysts and sinuses of the neck. In O&#8217;Neill JA, Rowe MI, Grosfeld JL, et al (eds): Pediatric Surgery, 5th ed. St. Louis, Mosby, 1998, pp 757-771.<br />
6. Telander RL, Filston HC: Review of head and neck lesions in infancy and childhood. Surg Clin North Am 72:1429-1447, 1992. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=1440164&#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=1440164">Similar articles<br />
</a></p>
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		<title>Diverticular Disease Of The Colon</title>
		<link>http://surgeryprocedure.info/abdominal-surgery/diverticular-disease-of-the-colon</link>
		<comments>http://surgeryprocedure.info/abdominal-surgery/diverticular-disease-of-the-colon#comments</comments>
		<pubDate>Wed, 08 Jul 2009 20:24:53 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[ABDOMINAL SURGERY]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/?p=253</guid>
		<description><![CDATA[48 DIVERTICULAR DISEASE OF THE COLON
Gregory P. Victorino M.D., Jyoti Arya M.D., Lawrence W. Norton M.D.
1. What is a colonic diverticulum? 	
Show answer
A protrusion of mucosa and submucosa through the muscular layers of the bowel wall. It has no muscular covering. Because diverticula do not involve all layers of the bowel wall, they are really [...]]]></description>
			<content:encoded><![CDATA[<p><strong>48 DIVERTICULAR DISEASE OF THE COLON<br />
Gregory P. Victorino M.D., Jyoti Arya M.D., Lawrence W. Norton M.D.</strong></p>
<blockquote><p><strong>1. What is a colonic diverticulum? </strong>	</p></blockquote>
<p>Show answer<br />
A protrusion of mucosa and submucosa through the muscular layers of the bowel wall. It has no muscular covering. Because diverticula do not involve all layers of the bowel wall, they are really &#8220;false&#8221; diverticula. Diverticulum formation may be related either to weakness of the bowel wall at the sites of vessel perforation or to increased intraluminal pressure caused by low dietary fiber and constipation.<br />
<span id="more-253"></span></p>
<blockquote><p><strong>2. What is the difference between diverticulosis and diverticulitis?</strong> </p></blockquote>
<p>	Show answer<br />
Diverticulosis is colonic diverticula without associated inflammation. Diverticulitis is inflammation and infection. Only 15% of patients with diverticulosis develop diverticulitis.</p>
<blockquote><p><strong>3. How does a diverticulum cause pain?</strong></p></blockquote>
<p> 	Show answer<br />
Pain apparently results from perforation of the diverticulum The resulting leakage may be scant and contained within pericolic fat or extensive, involving the mesentery, other organs, or the peritoneal cavity. Sigmoid diverticulitis typically causes pain in the left lower quadrant.</p>
<blockquote><p><strong>4. Where in the colon are diverticula usually located?</strong> 	</p></blockquote>
<p>Show answer<br />
In the United States, 95% of all diverticula occur in the left colon, primarily in the sigmoid colon. Diverticula, however, may occur anywhere in the colon. In Asia, right colonic diverticula are more common.</p>
<blockquote><p><strong>5. At what age is diverticulitis most common?</strong> </p></blockquote>
<p>	Show answer<br />
The sixth or seventh decade of life. Patients younger than 50 with diverticulitis tend to have more complications. Younger patients are more likely than older patients to have right colonic diverticulitis.</p>
<blockquote><p><strong>6. What strategy may decrease diverticulitis in patients with diverticula?</strong> </p></blockquote>
<p>	Show answer<br />
A diet high in fiber. Large bulk in the colon decreases segmentation and intraluminal pressure.</p>
<blockquote><p><strong>7. What is the best imaging test for diagnosing acute diverticulitis?</strong> </p></blockquote>
<p>	Show answer<br />
Computed tomography (CT) scan, which can also diagnose local complications of diverticulitis.</p>
<blockquote><p><strong>8. What complications can result from perforation of a colonic diverticulum?</strong></p></blockquote>
<p>    *  Inflammatory phlegmon or abscess in the bowel mesentery<br />
    * Peritonitis<br />
    * Intra-abdominal abscess<br />
    * Internal fistula<br />
    * Bowel obstruction</p>
<blockquote><p><strong>9. Can diverticular disease cause bleeding? </strong></p></blockquote>
<p>	Show answer<br />
Yes. Diverticulosis (not-itis) is a common cause of lower gastrointestinal bleeding. Bleeding from diverticulitis is uncommon.</p>
<blockquote><p><strong>10. How can the site of diverticular bleeding be localized? </strong>	</p></blockquote>
<p>Show answer<br />
It is localized with angiography performed via the inferior mesenteric artery and, if necessary, the superior mesenteric artery. Tagged red blood cell studies are less useful. Colonoscopy is rarely helpful.<br />
<em><strong>KEY POINTS: LOCALIZATION OF LOWER GI BLEEDING</strong></p>
<p>   1. Common causes: diverticulosis, cancer, angiodysplasia.<br />
   2. Proctosigmoidoscopy without prep is helpful in ruling out rectal source of bleeding (more proximal bleeding lmiits the utility of endoscopy).<br />
   3. Tagged red blood cell nuclear scans are useful for slower GI bleeding (detects bleeding at 0.2-0.5 mL/min).<br />
   4. Arteriography is the preferred imaging modality because it can be therapeutic and detects bleeding at 0.5-2 mL/min.<br />
   5. Start arteriography with the IMA, then the SMA, then the celiac axis if necessary; administer vasopressin or embolize (85% success rate).</em><br />
<strong></p>
<blockquote><p>11. When should an operation be performed for a bleeding colonic diverticulum?  </strong>	</p></blockquote>
<p>Show answer<br />
Replacement of 5-6 units of blood (two thirds of a patient&#8217;s blood volume) within 24 hours and rebleeding during hospitalization are standard indications for resection of the segment of colon containing a bleeding diverticulum.</p>
<blockquote><p><strong>12. If bleeding is life threatening but cannot be localized within the colon, what treatment is required?</strong> </p></blockquote>
<p>	Show answer<br />
Subtotal colectomy with ileostomy and closure of the distal sigmoid colon at the peritoneal reflection (Hartmann&#8217;s operation) or total abdominal colectomy with ileorectal anastomosis is required.</p>
<blockquote><p><strong>13. Which three procedures may be used when perforation of the diverticulum results in an abscess? Which has the lowest operative mortality rate? </strong></p></blockquote>
<p>	Show answer </p>
<p>   1. Diverting colostomy and abscess drainage (first of three stages)<br />
   2. Resection of involved colon with proximal colostomy and distal mucous fistula or closure by Hartmann&#8217;s operation (first of two stages)<br />
   3. Resection with primary anastomosis (one stage)</p>
<p>Operative mortality is lowest after resection and proximal colostomy for fecal diversion. Despite reports of success with the one-stage procedure, most surgeons favor a safer two-stage approach for perforated diverticulitis (this strategy requires a second operation after 3 months for colostomy takedown and colonic re-anastomosis).</p>
<blockquote><p><strong>14. What is the clinical evidence of a vesicocolic or ureterocolic fistula after diverticular perforation? </strong>	</p></blockquote>
<p>Show answer<br />
Pneumaturia, fecaluria, and chronic urinary tract infections (polymicrobial).</p>
<blockquote><p><strong>15. What procedure is required to repair a vesicocolic fistula?</strong></p></blockquote>
<p> 	Show answer<br />
A staged procedure was the standard until recently. Now most patients can be treated with a single procedure that includes sigmoid resection, colonic anastomosis, and primary repair of bladder defect with absorbable suture. A Foley catheter is usually left in place for 10 days after surgery. Some viable tissue should be placed between the colonic and bladder repairs to prevent a recurrent fistula.</p>
<p><strong><br />
References</strong><br />
WEB SITE<br />
<a href="http://www.acssurgery.com/abstracts/acs/acs0327.htm">http://www.acssurgery.com/abstracts/acs/acs0327.htm</a><br />
BIBLIOGRAPHY<br />
1. Bouillot JL, Berthou JC, Champault G, et al: Elective laparoscopic colonic resection for diverticular disease: Results of a multicenter study in 179 patients. Surg Endosc 16:1320-1323, 2002. <a href="http://dx.doi.org/10.1007/s00464-001-9236-x">Full article</a><br />
2. Eijbouts QA, de Haan J, Berends F, et al: Laparoscopic elective treatment of diverticular disease. A comparison between laparoscopic-assisted and resection-facilitated techniques. Surg Endosc 14:726-730, 2000.<br />
3. Faynsod M, Stamos MJ, Arnell T, et al: A case-control study of laparoscopic versus open sigmoid colectomy for diverticulitis. Am Surg 66:841-843, 2000. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10993612&#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=10993612"> Similar articles</a><br />
4. Gooszen AW, Tollenaar RA, Geelkerken RH, et al: Prospective study of primary anastomosis following sigmoid resection for suspected acute complicated diverticular disease. Br J Surg 88:693-697, 2001. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=11350443&#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=11350443">Similar articles</a> <a href="http://dx.doi.org/10.1046/j.1365-2168.2001.01748.x">Full article</a><br />
5. Schwesinger WH, Page CP, Gaskill HV 3d, et al: Operative management of diverticular emergencies: Strategies and outcomes. Arch Surg 135:558-562, 2000. <a href="http://dx.doi.org/10.1001/archsurg.135.5.558">Full article</a><br />
6. Simpson J, Scholefield JH, Spiller RC: Pathogenesis of colonic diverticula. Br J Surg 89:546-554, 2002.<br />
7. Wolff BG, Devine RM: Surgical management of diverticulitis. Am Surg 66:153-156, 2000. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10695745&#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=10695745">Similar articles</a> <a href="http://dx.doi.org/10.1002/%28SICI%291615-1003%28200005%2929:3%3C153::AID-PAUZ153%3E3.0.CO;2-Q">Full article</a><br />
8. Young-Fadok TM, Roberts PL, Spencer MP, et al: Colonic diverticular disease. Curr Probl Surg 37:457-514, 2000. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10932672&#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=10932672">Similar articles</a></p>
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		<title>Risks Of Bloodborne Disease</title>
		<link>http://surgeryprocedure.info/health-care/risks-of-bloodborne-disease</link>
		<comments>http://surgeryprocedure.info/health-care/risks-of-bloodborne-disease#comments</comments>
		<pubDate>Tue, 14 Jul 2009 17:34:02 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[HEALTH CARE]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/?p=487</guid>
		<description><![CDATA[101 RISKS OF BLOODBORNE DISEASE
Caesar M. Ursic M.D., Doru I. E. Georgescu M.D.
1. What infectious diseases are transmissible via blood transfusion?

 	Show answer
In developed nations with mature blood banking systems, by far the most common transfusion-acquired infections are hepatitis from the hepatitis B (HBV) and C (HCV) viruses. Other less commonly transmitted agents include the [...]]]></description>
			<content:encoded><![CDATA[<p><strong>101 RISKS OF BLOODBORNE DISEASE<br />
Caesar M. Ursic M.D., Doru I. E. Georgescu M.D.</strong></p>
<blockquote><p><strong>1. What infectious diseases are transmissible via blood transfusion?</strong></p></blockquote>
<p><span id="more-487"></span><br />
 	Show answer<br />
In developed nations with mature blood banking systems, by far the most common transfusion-acquired infections are hepatitis from the hepatitis B (HBV) and C (HCV) viruses. Other less commonly transmitted agents include the human immunodeficiency virus (HIV) and cytomegalovirus (CMV). Even rarer but still occasionally reported bloodborne infections are parasitic diseases such as malaria (genus, Plasmodium), babesiosis (genus, Babesium), Chagas disease (Trypanasoma cruzi), toxoplasmosis (Toxoplasma gondii), the lymphomas and leukemias caused by the human T-cell lymphotropic virus (HTLV-I), and infectious mononucleosis (Epstein-Barr virus). Bacterial contaminations are also rare but possible, especially in platelet preparations that are stored at room temperature. This may result in a toxic shock-like syndrome, the risk of which has been estimated as equivalent to the risk of HIV transmission.</p>
<blockquote><p><strong>2. What are the estimated risks of HBV, HCV, and HIV transmission by blood transfusion in the United States? 	</strong></p></blockquote>
<p>Show answer </p>
<p><img src="http://surgeryprocedure.info/http://surgeryprocedure.info/wp-content/uploads/2009/07/411.jpg" alt="4" title="4" width="716" height="100" class="alignright size-full wp-image-488" /></p>
<blockquote><p><strong>3. Which bloodborne pathogens pose a risk to surgeons? </strong> </p></blockquote>
<p>	Show answer<br />
Although the epidemic of HIV has increased general concern about bloodborne pathogens, the prevalence of hepatitis C virus (HCV) throughout North America has led to a shift of emphasis from HIV to hepatitis. Hepatitis B is an occupational risk in surgery, but vaccinations and a relatively efficient post-exposure protocol have reduced the consequences of contamination with HBV. Surgeons in the United States care for more patients with chronic hepatitis C than with chronic hepatitis B, and no vaccine is available for HCV infection. Although the rate of seroconversion for hepatitis C is 10% versus 30% for hepatitis B, when acute infection occurs, there is a much higher chance of developing chronic hepatitis (50% versus 10%) after HCV infection. Thus, HCV infection is the greatest threat to surgeons.</p>
<blockquote><p><strong>4. What is the risk to health care workers of exposure to HBV? </strong></p></blockquote>
<p>	Show answer<br />
The number of new infections in 2001 has dropped to approximately 78,000 from the estimated yearly incidence of 260,000 in the 1980s. At present, 1.25 million U.S. residents have chronic hepatitis B, with the highest prevalence occurring among 20-49-year-old individuals. Thirty percent of percutaneous hollow needle exposures are followed by acute infection. Thirty percent of hepatitis B cases are clinically occult, and ≤ 10% of infected people remain viral carriers for life. Many carriers are asymptomatic and suffer no active liver disease, although they are potentially infectious to others. Twenty-five percent of HBV-infected individuals eventually die from hepatic diseases.</p>
<blockquote><p><strong>5. What is the risk to health care workers of exposure to HCV?</strong></p></blockquote>
<p> 	Show answer<br />
The number of new infections in 2001 was 25,000, down from 240,000 per year in the 1980s. Currently, 3.9 million (1.8%) U.S. residents have HCV infection, of whom 2.7 million are infected chronically. The risk of seroconversion from a percutaneous hollow needle injury is 10%, but 90% of acute infections result in the chronic carrier state, which is typically asymptomatic. Although these data are still controversial, 50% of HCV infected patients will develop cirrhosis, and 50% of these patients will develop a hepatoma.</p>
<blockquote><p><strong>6. What is the risk to health care workers of exposure to HIV?</strong> </p></blockquote>
<p>	Show answer<br />
The risk of HIV seroconversion after percutaneous inoculation with HIV-contaminated blood is approximately 0.3%. Risk of infection also appears to be greater when the source of the blood is a terminally or severely ill patient. The U.S. Centers for Disease Control and Prevention (CDC) reports that 57 health care workers in the U.S. have been documented as seroconverting to HIV as a result of an occupational exposure to the virus. The majority of these individuals were either nurses (n = 24) or laboratory workers (n = 19); physicians accounted for only six of these cases. The routes of infection were percutaneous (puncture or cutting wounds) in 84% of the cases. Thus, the risk appears small relative to the large number of exposures that have probably occurred since the onset of the epidemic in the early 1980s. The CDC also reports that as of January 1, 1998, there has been no documented transmission of HIV infection from a patient to a surgeon secondary to occupational exposure.</p>
<blockquote><p><strong>7. How well does hepatitis B vaccination protect against the disease?</strong></p></blockquote>
<p> 	Show answer<br />
Effective protection against hepatitis B correlates positively with post-immunization anti-hepatitis B surface antibody (anti-HBs) serum titers of ≥ 10 mIU/mL. These titers are achieved in 95% of young, healthy recipients of the standard three-dose immunization regimen, and the actual protective efficacy (i.e., ability of the vaccine to prevent the disease) is estimated to approach 100% in these individuals. Although about 50% of successfully vaccinated adults demonstrate a decrease in their anti-HBs levels to nondetectable levels by 10 years, continued immunologic protection is thought to persist via the amnestic humoral response. Because of the persistence of this &#8220;immune memory&#8221; to the viral antigen, healthy individuals appear to enjoy lifelong protection after vaccination and do not require booster doses. A bivalent vaccine immunizing against both hepatitis A and B was approved in 2001 by the U.S. Food and Drug Administration for individuals 18 years of age and older, and it is as successful as the monovalent vaccine in conferring protection from the HBV infection with the added benefit of protecting against hepatitis A viral infection.</p>
<blockquote><p><strong>8. Are patients at risk of infection from surgeons who are infected with HBV? </strong></p></blockquote>
<p>	Show answer<br />
Transmission of hepatitis B infection from surgeons to patients has been documented. Surgeons who are at risk for transmitting infection to patients are generally positive for the e-antigen of hepatitis B. The e-antigen is a degradation product of the nucleocapsid of the virus and represents active viral replication within the liver. People who test positive for the e-antigen have high viral titers and are quite infectious. The large number of documented transmissions of HBV to patients by surgical providers is particularly troublesome and may require restriction of clinical privileges. Furthermore, a recent report from England documented transmission of HBV infection from surgeons to patients even when the surgeon was negative for the e-antigen.</p>
<blockquote><p><strong>9. What is the proper response after percutaneous exposure to a patient with known hepatitis B? </strong>	</p></blockquote>
<p>Show answer<br />
This depends on the provider&#8217;s vaccination status. Older individuals show a tendency to mount a weaker or delayed immunologic response as measured by peak serum titers of anti-HBs. If the provider has been vaccinated and has a positive antibody titer, no additional response is necessary. If the provider has not been vaccinated and is negative for antibodies to HBV or if the provider completed the series of vaccinations but exhibited a weak or absent antibody titer, then he or she should receive a dose of hepatitis B immunoglobulin and begin the hepatitis B vaccination series. For surgeons who were successfully immunized against HBV in the past, neither routine booster doses nor routine immunity status surveillance is recommended.</p>
<blockquote><p><strong>10. What are the recommendations for hepatitis C immunization?</strong> </p></blockquote>
<p>	Show answer<br />
There is currently no effective vaccine available against HCV. Immunoglobulin for HCV does not confer protection. Using universal barrier precautions remains the best strategy.</p>
<blockquote><p><strong>11. Does laparoscopic surgery minimize the risk of HIV contamination?</strong></p></blockquote>
<p> 	Show answer<br />
The laparoscopic technique reduces exposure to blood products and sharp instruments; however, the risks are different. The evacuation of the pneumoperitoneum during laparoscopic procedures releases aerosolized HIV-infected blood and peritoneal fluid into the operative suite. Evacuation of the pneumoperitoneum into a closed system diminishes this exposure.</p>
<blockquote><p><strong>12. Is double gloving an effective method of protection?</strong> 	</p></blockquote>
<p>Show answer<br />
Although double gloving may not prevent percutaneous injury, it clearly reduces blood exposure. The contact rates between blood and the surgeon&#8217;s skin are decreased by 70% when the surgeon wears two pairs of gloves. Whereas outer glove perforation occurs in 25% of cases, inner glove perforation occurs in only 10% of cases (surgeons, 8.7%; assistants, 3.7%). The longer the procedure, the more frequent are inner glove perforations. The nondominant index finger is the most common target.</p>
<blockquote><p><strong>13. Are eye splash injuries a major threat to surgeons? 	</strong></p></blockquote>
<p>Show answer<br />
A CDC study demonstrated that approximately 13% of documented HIV transmissions occurred by mucocutaneous contact. Eye splash injuries during surgery are often underestimated, although they are the easiest type of contact to prevent. A recent study examined 160 eye shields used by surgeons and assistants. All operations lasted ≥ 30 minutes. The shields were inspected for macroscopic splashes and then tested for microscopic splashes. Forty-four percent of the shields tested positive for blood. The surgeon was aware of a spray in only 8% of cases. The splashes were macroscopically visible in only 16% of cases. The risk of eye splashes was higher for surgeons than for assistants and increased with the length of the operation. The type of operation also proved to be a determining factor; vascular surgery and orthopedic surgery had the higher risks for eye splash injuries. Eye protection should be mandatory.</p>
<blockquote><p><strong>14. What is the surgeons&#8217; rate of exposure to blood and body fluids?</strong></p></blockquote>
<p> 	Show answer<br />
Percutaneous blood exposure occurs in 1.2-5.6% of surgical cases and mucocutaneous blood contact in 6.4-50.4%. The discrepancy among reported rates reflects differences in data collection, procedures performed, surgical technique, and degree of precautions. No health care worker has ever been infected through exposure of intact skin to blood and body fluids. However, transmission of HIV after mucocutaneous contact with HIV-infected blood has been reported. The risk of contamination is real for all personnel in the operating room, but it is much higher for surgeons and first assistants, who account for 80% of all body contamination and 65% of injuries.</p>
<blockquote><p><strong>15. Again, what are the seroconversion rates for HIV and HBV exposure?</strong> 	</p></blockquote>
<p>Show answer<br />
Seroconversion rates from a hollow needle stick are 0.3% for HIV and 30% for HBV.</p>
<blockquote><p><strong>16. What is the lifetime occupational risk of HIV infection for surgeons?</strong> </p></blockquote>
<p>	Show answer </p>
<p>The risk of HIV infection for a surgeon can be calculated by obtaining the product of HIV seroprevalence in surgical patients (0.32-50.00%), percutaneous injury rate (1.2-6.0%), and seroconversion rate (0.29-0.50%). The calculated risk per case of acquiring HIV ranges from 0.11 per million to 66 per million. Assuming that a surgeon performs 350 operations per year over a 30-year career, the estimated lifetime cumulative risk ranges from 0.12% to 50.0%, depending on the variables. Several assumptions are inherent in this calculation:</p>
<p>    * The formula assumes a constant HIV prevalence, but it is estimated that the prevalence increases by 4.0-8.6% annually in the United States.<br />
    * The formula assumes that exposure to HIV-infected blood occurs only through percutaneous injuries, disregarding the risk caused by mucocutaneous exposure.<br />
    * The formula assumes that whereas every operation carries the same risk, the risk varies with the length of procedure and amount of blood loss.<br />
    * The formula assumes that the risk per case is the same for a trauma surgeon in center city Detroit and a plastic surgeon in Beverly Hills.</p>
<p>Clearly, these assumptions are imprecise.</p>
<blockquote><p><strong>17. Are there effective methods to reduce the risk of transmission of bloodborne diseases to surgeons?</strong> </p></blockquote>
<p>	Show answer<br />
For HBV infection, in addition to universal precautions, a highly effective vaccine is available, but it is not used as much as it should be. Most surgeons who are 45 years or older have not been vaccinated. A precisely defined postexposure protocol is also available. For HCV and HIV infections, the most pragmatic approach is to lower the rate of percutaneous and mucocutaneous injuries by observing barrier precautions and using safe surgical technique.<br />
Finally, prompt response to blood exposure is required. Contamination of the hands or arms is best dealt with by immediate rescrubbing. If this is not practical, the area should be irrigated with povidone iodine, and rescrubbing should be accomplished soon thereafter.</p>
<p><strong>References</strong><br />
BIBLIOGRAPHY<br />
1. Barrie PS, Patchen Dellinger E, Dougherty SH, Fink MP: Assessment of hepatitis B virus immunization status among North American surgeons. Arch Surg 129:27-32, 1994.<br />
2. Bell DM: Occupational risk of human immunodeficiency virus infection in healthcare workers: An overview. Am J Med 102(suppl 5B):81S-85S, 1997.<br />
3. Cardo DM, Culver DH, Ciescielski CA, et al: A case-control study of HIV seroconversion in healthcare workers after percutaneous exposure. N Engl J Med 337:1485-1490, 1997. Medline <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=9366579">Similar articles </a><a href="http://dx.doi.org/10.1056/NEJM199711203372101">Full article</a><br />
4. Dodd RY, Notari EP, Stramer SL: Current prevalence and incidence of infectious disease markers and estimated window-period risk in the American Red Cross blood donor population. Transfusion 42:975-979, 2002. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=12385406&#038;dopt=Abstract">Medline</a> Similar articles <a href="http://dx.doi.org/10.1046/j.1537-2995.2002.00174.x">Full article</a><br />
5. Eubanks S, Newman L, Lucas G: Reduction of HIV transmission during laparoscopic procedures. Surg Laparosc Endosc 3:2-5, 1993.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=8258065&#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=8258065">Similar articles</a><br />
6. Fry DE: Blood-borne diseases in 1998. Bull Am Coll Surg 83:13-18, 1998.<br />
7. Gerberding JL: Reducing occupational risk of HIV infection. Hosp Pract 113-110, 115-118, 1991.<br />
8. Klein HG: Allogenic transfusion risks in the surgical patient. Am J Surg 317:242-245, 1995.<br />
9. Koff RS: Hepatitis A, hepatitis B, and combination hepatitis vaccines for immunoprophylaxis: An update. Digest Dis Sci 47:1183-1194, 2002. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=12064790&#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=12064790">Similar articles</a> Full article<br />
10. Lin EY, Brunicardi C: HIV infection and surgeons. World J Surg 18:753-757, 1994. Medline <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=7975695">Similar articles </a><a href="http://dx.doi.org/10.1007/BF00298922">Full article</a><br />
11. Marasco S, Woods S: The risk of eye splash injuries in surgery. Aust N Z J Surg 68:785-787, 1998. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9814742&#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=9814742">Similar articles</a><br />
12. Megan J, Patterson M, Novak CB, et al: Surgeons&#8217; concern and practices of protection against bloodborne pathogens. Ann Surg 228:266-272, 1998.<br />
13. Pietrabissa A, Merigliano S, Montorsi M, et al: Reducing the occupational risk of infections for the surgeons: Multicentric national survey on more than 15,000 surgical procedures. World J Surg 21:573-578, 1997.<a href="http://dx.doi.org/10.1007/s002689900275"> Full article</a><br />
14. Schreiber GB, Busch MP, Kleinman SH, et al: The risk of transfusion-transmitted viral infections: The retrovirus epidemiology donor study. N Engl J Med 334:1685-1690, 1996. Medline Similar articles Full article<br />
15. Szmuness W, Stevens CE, Harley EJ, et al: Hepatitis B vaccine: Demonstration of efficacy in a controlled clinical trial in a high-risk population in the United States. N Engl J Med 303:833-841, 1980. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=6997738&#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=6997738">Similar articles</a></p>
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		<title>Intestinal Obstruction Of Neonates &amp; Infants</title>
		<link>http://surgeryprocedure.info/pediatric-surgery/intestinal-obstruction-of-neonates-infants</link>
		<comments>http://surgeryprocedure.info/pediatric-surgery/intestinal-obstruction-of-neonates-infants#comments</comments>
		<pubDate>Sat, 11 Jul 2009 19:13:40 +0000</pubDate>
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				<category><![CDATA[PEDIATRIC SURGERY]]></category>

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		<description><![CDATA[83 INTESTINAL OBSTRUCTION OF NEONATES AND INFANTS
Richard J. Hendrickson M.D., Denis D. Bensard M.D.
1. What signs or symptoms suggest intestinal obstruction in the neonate? 
	Show answer
Signs and symptoms vary according to the level of obstruction. Proximal intestinal obstruction leads to the early onset of bilious emesis, generally with minimal abdominal distention. In contrast, neonates with [...]]]></description>
			<content:encoded><![CDATA[<p><strong>83 INTESTINAL OBSTRUCTION OF NEONATES AND INFANTS<br />
Richard J. Hendrickson M.D., Denis D. Bensard M.D.</strong></p>
<blockquote><p><strong>1. What signs or symptoms suggest intestinal obstruction in the neonate? </strong></p></blockquote>
<p>	Show answer<br />
Signs and symptoms vary according to the level of obstruction. Proximal intestinal obstruction leads to the early onset of bilious emesis, generally with minimal abdominal distention. In contrast, neonates with distal intestinal obstruction present after the first day of life with bilious vomiting and pronounced abdominal distention. Bilious emesis should always be interrogated further in infants and children.<br />
<span id="more-405"></span></p>
<blockquote><p><strong>2. What is the differential diagnosis of intestinal obstruction in neonates?</strong></p></blockquote>
<p> 	Show answer<br />
Look for an anal opening, which eliminates the diagnosis of imperforate anus. Next obtain an abdominal radiograph. The extent of gaseous distention of the bowel implicates a proximal or distal bowel obstruction. No attempts should be made to distinguish small from large bowel obstruction.</p>
<table width="80%" border=1 cellpadding=2 bordercolor="#c0c0c0" cellspacing=2 bgcolor="#ffffff">
<tr valign=top>
<td><font size=2 color="#000000" face="Arial"></p>
<div><b>Proximal</b> (minimal bowel gas)</div>
<p></font>
</td>
<td><font size=2 color="#000000" face="Arial"></p>
<div><b>Distal </b>(significant bowel gas)</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td><font size=2 color="#000000" face="Arial"></p>
<div>Duodenal atresia, stenosis</div>
<p></font>
</td>
<td><font size=2 color="#000000" face="Arial"></p>
<div>Ileal atresia</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td><font size=2 color="#000000" face="Arial"></p>
<div>Malrotation with midgut volvulus</div>
<p></font>
</td>
<td><font size=2 color="#000000" face="Arial"></p>
<div>Meconium ileus or plug</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td><font size=2 color="#000000" face="Arial"></p>
<div>Jejunal atresia</div>
<p></font>
</td>
<td><font size=2 color="#000000" face="Arial"></p>
<div>Hirschsprung&#8217;s disease</div>
<p></font>
</td>
</tr>
</table>
<p>3. When are contrast studies of the gastrointestinal (GI) tract indicated? 	Show answer<br />
If peritonitis or pneumoperitoneum is present, proceed to exploratory laparotomy without delay. Malrotation with volvulus must be distinguished from the other cause of congenital duodenal obstruction (duodenal atresia). In this setting, upper GI is the study of choice. In volvulus, the upper GI demonstrates distention of the proximal duodenum, corkscrewing of the distal duodenum, and limited or no progression of contrast into the distal bowel. Conversely, duodenal atresia appears as a blind ending pouch in the first or second portion of the duodenum. Contrast enema is generally the preferred study in all other forms of neonatal intestinal obstruction.</p>
<table width="80%" border=1 cellpadding=2 bordercolor="#c0c0c0" cellspacing=2 bgcolor="#ffffff">
<tr valign=top>
<td width=155><font size=2 color="#000000" face="Arial"></p>
<div><b>Disorder Barium</b></div>
<p></font>
</td>
<td width=261><font size=2 color="#000000" face="Arial"></p>
<div><b>Enema</b></div>
<p></font>
</td>
</tr>
<tr valign=top>
<td width=155><font size=2 color="#000000" face="Arial"></p>
<div>Ileal atresia</div>
<p></font>
</td>
<td width=261><font size=2 color="#000000" face="Arial"></p>
<div>Microcolon; no reflux into terminal ileum</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td width=155><font size=2 color="#000000" face="Arial"></p>
<div>Meconium ileus</div>
<p></font>
</td>
<td width=261><font size=2 color="#000000" face="Arial"></p>
<div>Microcolon; reflux into terminal ileum with filling defects</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td width=155><font size=2 color="#000000" face="Arial"></p>
<div>Meconium plug</div>
<p></font>
</td>
<td width=261><font size=2 color="#000000" face="Arial"></p>
<div>Normal colon; large filling defect of left colon</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td width=155><font size=2 color="#000000" face="Arial"></p>
<div>Hirschsprung&#8217;s disease</div>
<p></font>
</td>
<td width=261><font size=2 color="#000000" face="Arial"></p>
<div>Narrowed rectosigmoid; dilated proximal colon</div>
<p></font>
</td>
</tr>
</table>
<blockquote><p><strong>4. Describe intestinal atresia.</strong> </p></blockquote>
<p>	Show answer<br />
Atresia can occur anywhere in the GI tract: duodenal (50%), jejunoileal (45%), or colonic (5%). Duodenal atresia arises from a failure of recanalization during the 8th-10th week of gestation; jejunoileal and colonic atresia are caused by an in utero mesenteric vascular accident.</p>
<blockquote><p><strong>5. Distinguish duodenal atresia from other forms of intestinal atresia.</strong></p></blockquote>
<p> 	Show answer<br />
Duodenal atresia is characterized by the onset of bilious vomiting (85% of atresia distal to the ampulla of Vater) within the first day of life; significant abdominal distention is absent. Approximately 25% of affected infants have trisomy 21. The abdominal radiograph demonstates a &#8220;double bubble&#8221; caused by the distended stomach and first or second portions of duodenum. Surgical correction is performed by duodenoduodenostomy.<br />
Jejunoileal atresia produces bilious vomiting at 2-3 days of life with moderate to severe abdominal distention. The abdominal radiograph shows dilated loops of bowel with air-fluid levels. Barium enema reveals a microcolon and no reflux of contrast into the dilated bowel. Associated anomalies are uncommon. Surgical correction involves end-to-end anastomosis with or without limited intestinal resection.<br />
Colonic atresia, similar to jejunalileal atresia, is associated with the late onset of bilious vomiting, no passage of meconium, and moderate to severe abdominal distention. The abdominal radiograph reveals dilated loops of bowel with air-fluid levels suggesting distal intestinal obstruction. Barium enema demonstrates a microcolon with a cutoff observed in a proximal colonic segment. Twenty percent of affected infants suffer an associated anomaly of the heart, musculoskeletal system, abdominal wall, or GI tract. Surgical management includes limited colonic resection with primary anastomosis.</p>
<blockquote><p><strong>6. Describe malrotation with midgut volvulus.</strong></p></blockquote>
<p> 	Show answer<br />
During the 6th-12th week of gestation, the intestine undergoes evisceration, growth, return to the abdominal cavity, and counterclockwise rotation with fixation. Malrotation is an error in both rotation and fixation. Abnormal fixation and a narrow-based mesentery predispose to twisting of the midgut on its blood supply (superior mesenteric artery), vascular occlusion (strangulation), and obstruction (malrotation with midgut volvulus). Typically, a previously well neonate or child without a history of surgery presents with bilious vomiting, abdominal distention, and variable degrees of shock. If the infant is acutely ill, no further studies are needed and surgical exploration is indicated. If the diagnosis is in question and the infant is stable, an upper GI study, not a barium enema, is performed. Surgical treatment entails four parts: (1) division of abnormal peritoneal bands, (2) correction of malrotation, (3) restoration of a broad-based mesentery, and (4) appendectomy because of the location of the cecum in the right upper quadrant.</p>
<blockquote><p><strong>7. Is midgut volvulus a surgical emergency?</strong></p></blockquote>
<p> 	Show answer<br />
Yes! The risk of strangulation caused by the rotational anomaly and abnormal peritoneal bands implies a surgical emergency. Delay places the infant at risk of losing the entire midgut and potentially dying.</p>
<blockquote><p><strong>8. What is meconium ileus (MI)? </strong></p></blockquote>
<p>	Show answer<br />
MI is the obstruction of the terminal ileum by highly viscid, tenacious meconium. MI is a complication of cystic fibrosis (CF). Fifteen percent of neonates with CF present with MI. The combination of hyperviscous mucus secreted by the abnormal intestinal glands and pancreatic insufficiency leads to abnormal meconium and obstructs the lumen of the terminal ileum. Symptoms of feeding intolerance, bilious emesis, and abdominal distention begin in the second to third days of life. Unlike most forms of neonatal intestinal obstruction, surgery is reserved for patients refractory to nonoperative treatment or complex MI (atresia, volvulus, perforation). Sixty percent of infants with simple MI can be treated successfully with Gastrografin enemas and rectal irrigation. If an operation is indicated, the objective is to remove the obstructing meconium by limited resection or enterostomy with evacuation of the meconium and irrigation of the distal bowel.</p>
<blockquote><p><strong>9. What is Hirschsprung&#8217;s disease?</strong></p></blockquote>
<p> 	Show answer<br />
In this disease, the intestine is innervated by cells originating in the neural crest. During the 5th-12th week of gestation, neural crest cells migrate in a craniocaudal direction and disperse within the wall of the intestine (intermuscular, to Auerbach&#8217;s plexus; submucosal, to Meissner&#8217;s plexus). Hirschsprung&#8217;s disease arises from the failure of normal enteric innervation. The bowel remains in a contracted, spastic state and produces a functional rather than a true mechanical obstruction. Abdominal distention, feeding intolerance, and delayed or absent meconium within the first 48 hours of life are the presenting findings in infants. Older patients suffer chronic constipation, abdominal distention, and failure to thrive. Because the disease always affects the most distal bowel (80-85% rectosigmoid) with a variable involvement of proximal bowel, barium enema demonstrates the characteristic radiographic appearance of a spastic, contracted rectum with dilated proximal bowel. Suction rectal biopsy documenting the absence of ganglion cells and presence of nerve hypertrophy confirms the diagnosis. Surgical correction is performed by excision of the aganglionic (distal colorectal) segment and coloanal anastomosis.</p>
<blockquote><p><strong>10. What is intussusception? What are the therapeutic options? </strong></p></blockquote>
<p>	Show answer<br />
Intussusception is the invagination of proximal bowel (intussusceptum) into the distal bowel (intussuscipien). Swelling, vascular compromise, and obstruction follow. Nearly two thirds of cases occur in the first 2 years of life. The cause is thought to be a result of lymphoid hyperplasia in the terminal ileum after viral infection. The diagnosis should be suspected in previously well infants, 6-9 months of age, with vomiting, crampy abdominal pain, and bloody stools. Barium or air enema is both diagnostic and therapeutic. Injection of contrast demonstrates colonic obstruction with no reflux into the proximal bowel. Controlled hydrostatic reduction with barium or air is successful in 90% of cases. If hydrostatic reduction is unsuccessful or in children with peritonitis, operative reduction is indicated. The risk of recurrent intussusception is 5% for either radiographic or surgical reduction.</p>
<blockquote><p><strong>11. What examples of neonatal obstruction can escape early detection and present later in life? </strong>	</p></blockquote>
<p>Show answer<br />
Although most conditions are identified within the first week to month of life, lesions other than atresia may be identified in children and even adults.<br />
Duodenal stenosis. Unlike duodenal atresia, stenosis results in narrowing but not complete obstruction of the duodenum. Thus, infants fed formula or pureed foods may not become symptomatic until childhood. Children with intermittent abdominal pain and symptoms of gastric outlet obstruction require an upper GI study, particularly if they have trisomy 21.<br />
Malrotation. One third of patients with malrotation are identified after the first month of life. Children present with bilious emesis and intermittent abdominal pain, and malrotation is generally identified by an upper GI series. Malrotation with midgut volvulus should be suspected in any ill child with signs of intestinal obstruction and no history of abdominal surgery.<br />
Hirschsprung&#8217;s disease. One third of patients are diagnosed after the first year of life. A long history of constipation refractory to therapy mandates rectal biopsy, particularly in patients with trisomy 21.<br />
Intussusception. One third of cases occur after age 2 years. A pathologic lead point (i.e., polyp, tumor, hematoma, Meckel&#8217;s diverticulum) is present in one third of older patients.</p>
<p><strong><br />
References</strong><br />
BIBLIOGRAPHY<br />
1. Aquino A, Domini M, Rossi C, et al: Correlation between Down&#8217;s syndrome and malformation of pediatric surgical interest. J Pediatr Surg 33:1380-1382, 1998. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9766358&#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=9766358">Similar articles</a><br />
2. Daneman A, Alton DJ, Ein S, et al: Perforation during attempted intussusception reduction in children-a comparison of perforation with barium and air. Pediatr Radiol 25:81-88, 1995. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=7596670&#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=7596670">Similar articles</a><br />
3. Godbole P, Stringer MD: Bilious vomiting in the newborn: How often is it pathologic? J Pediatr Surg 37:909-911, 2002.<br />
4. Long FR, Kramer SS, Markowitz RI, Taylor GE: Radiographic patterns of intestinal malrotation in children. Radiographics 16:547-560, 1996. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=8897623&#038;dopt=Abstract">Medline </a>S<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=8897623">imilar articles</a><br />
5. Maxson RT, Franklin PA, Wagner CW: Malrotation in the older child: Surgical management, treatment, and outcome. Am Surg 61:135-138, 1995. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=7856973&#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=7856973">Similar articles</a><br />
6. Reding R, de Ville de Goyet J, Gosseye S, et al: Hirschsprung&#8217;s disease: A 20 year experience. J Pediatr Surg 32:1221-1225, 1997. <a href="http://dx.doi.org/10.1016/S0022-3468%2897%2990686-2">Full article</a></p>
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		<title>Diagnosis &amp; Therapy of Chronic Pancreatitis</title>
		<link>http://surgeryprocedure.info/abdominal-surgery/diagnosis-therapy-of-chronic-pancreatitis</link>
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		<pubDate>Wed, 08 Jul 2009 14:25:31 +0000</pubDate>
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				<category><![CDATA[ABDOMINAL SURGERY]]></category>

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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 />
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<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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