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	<title>SurgeryProcedure.info &#187; Search Results  &#187;  hernia mesh rejection symptoms</title>
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		<title>Inguinal Hernia. Controversies</title>
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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>Queries 5</title>
		<link>http://surgeryprocedure.info/top-search/queries-5</link>
		<comments>http://surgeryprocedure.info/top-search/queries-5#comments</comments>
		<pubDate>Mon, 21 Sep 2009 06:21:43 +0000</pubDate>
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				<category><![CDATA[Uncategorized]]></category>

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		<description><![CDATA[

sengstaken blakemore tube
hernia mesh rejection symptoms
fissurotomy
lasix sandwich
anal+fissurotomy
sengstaken blakemore
empyema necessitans
sengstaken-blakemore
Space of Bogros Bhernia
anal fissurotomy
esophageal varices
shalyajanya nadi vrana
penetrating neck carotid artery
pilonoidal sinus
gatorade spleen
urinary+tract+surgery
CHRONIC INTESTIONAL PSEUDOOBSTRUCTION
rocky davis incision
urinary tract trauma
caput medusae dilated veins
spleen injury with blood behind heart
bleeding caput medusa
hernia mesh neuroma
neuroma+hernia
mesh rejection
emphysema necessitans
Infant Testicle
blakemore+tube
spleen injury


]]></description>
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<ul>
<li><a href="http://surgeryprocedure.info/search/sengstaken-blakemore+tube">sengstaken blakemore tube</a></li>
<li><a href="http://surgeryprocedure.info/search/hernia+mesh+rejection+symptoms">hernia mesh rejection symptoms</a></li>
<li><a href="http://surgeryprocedure.info/search/fissurotomy">fissurotomy</a></li>
<li><a href="http://surgeryprocedure.info/search/lasix+sandwich">lasix sandwich</a></li>
<li><a href="http://surgeryprocedure.info/search/anal+fissurotomy">anal+fissurotomy</a></li>
<li><a href="http://surgeryprocedure.info/search/sengstaken+blakemore">sengstaken blakemore</a></li>
<li><a href="http://surgeryprocedure.info/search/empyema+necessitans">empyema necessitans</a></li>
<li><a href="http://surgeryprocedure.info/search/sengstaken-blakemore">sengstaken-blakemore</a></li>
<li><a href="http://surgeryprocedure.info/search/Space+of+Bogros+hernia">Space of Bogros Bhernia</a></li>
<li><a href="http://surgeryprocedure.info/search/anal+fissurotomy">anal fissurotomy</a></li>
<li><a href="http://surgeryprocedure.info/search/esophageal+varices">esophageal varices</a></li>
<li><a href="http://surgeryprocedure.info/search/shalyajanya+nadi+vrana">shalyajanya nadi vrana</a></li>
<li><a href="http://surgeryprocedure.info/search/penetrating+neck+carotid+artery">penetrating neck carotid artery</a></li>
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<li><a href="http://surgeryprocedure.info/search/rocky+davis+incision">rocky davis incision</a></li>
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		<title>Queries 3</title>
		<link>http://surgeryprocedure.info/top-search/queries-3</link>
		<comments>http://surgeryprocedure.info/top-search/queries-3#comments</comments>
		<pubDate>Fri, 14 Aug 2009 18:10:27 +0000</pubDate>
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sengstaken blakemore tube
blakemore tube
post splenectomy leukocytosis
esophageal varices
abdominal trauma hematoma,calcium nodule
dextrose
colon benign obstruction web
forum for people with imperforate anus
barium enema in neonates
disease of anorectal
empyema necessitans
penetrating neck trauma management asymptomatic
open abdominal surgery in cirrhotic patients
what is stump pressure?
suturing facial laceration
surgically correctable causes of hypertension
solution dakin sinus pilonidale
rejection of hernia mesh neuroma formation
albumin and Lasix sandwich


]]></description>
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<ul>
<li><a href="http://surgeryprocedure.info/search/sengstaken+blakemore+tube">sengstaken blakemore tube</a></li>
<li><a href="http://surgeryprocedure.info/search/blakemore+tube">blakemore tube</a></li>
<li><a href="http://surgeryprocedure.info/search/post+splenectomy+leukocytosis">post splenectomy leukocytosis</a></li>
<li><a href="http://surgeryprocedure.info/search/esophageal+varices">esophageal varices</a></li>
<li><a href="http://surgeryprocedure.info/search/abdominal+trauma+hematoma+calcium+nodule">abdominal trauma hematoma,calcium nodule</a></li>
<li><a href="http://surgeryprocedure.info/search/dextrose">dextrose</a></li>
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<li><a href="http://surgeryprocedure.info/search/barium+enema+in+neonates">barium enema in neonates</a></li>
<li><a href="http://surgeryprocedure.info/search/disease+of+anorectal">disease of anorectal</a></li>
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<li><a href="http://surgeryprocedure.info/search/open+abdominal+surgery+in+cirrhotic+patients">open abdominal surgery in cirrhotic patients</a></li>
<li><a href="http://surgeryprocedure.info/search/what+is+stump+pressure?">what is stump pressure?</a></li>
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<li><a href="http://surgeryprocedure.info/search/albumin+and+Lasix+sandwich">albumin and Lasix sandwich</a></ul>
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		<title>Gastroesophageal Reflux Disease</title>
		<link>http://surgeryprocedure.info/abdominal-surgery/gastroesophageal-reflux-disease</link>
		<comments>http://surgeryprocedure.info/abdominal-surgery/gastroesophageal-reflux-disease#comments</comments>
		<pubDate>Wed, 08 Jul 2009 17:44:40 +0000</pubDate>
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				<category><![CDATA[ABDOMINAL SURGERY]]></category>

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		<description><![CDATA[43 GASTROESOPHAGEAL REFLUX DISEASE
Michael E. Fenoglio M.D., Lawrence W. Norton M.D.
1. What symptoms suggest gastroesophageal reflux disease (GERD)? 	
Show answer
Substernal burning after meals or at night, associated occasionally with regurgitation of gastric juices, is one symptom. Discomfort is relieved by standing or sitting. Dysphagia, a late complication of GERD, is caused by mucosal edema or [...]]]></description>
			<content:encoded><![CDATA[<p><strong>43 GASTROESOPHAGEAL REFLUX DISEASE<br />
Michael E. Fenoglio M.D., Lawrence W. Norton M.D.</strong></p>
<blockquote><p><strong>1. What symptoms suggest gastroesophageal reflux disease (GERD)? 	</strong></p></blockquote>
<p>Show answer<br />
Substernal burning after meals or at night, associated occasionally with regurgitation of gastric juices, is one symptom. Discomfort is relieved by standing or sitting. Dysphagia, a late complication of GERD, is caused by mucosal edema or stricture of the distal esophagus. However, no symptom is specific for GERD, and therapeutic decisions should not be made on symptoms alone.<br />
<span id="more-229"></span></p>
<blockquote><p><strong>2. What is the difference between heartburn and GERD? </strong></p></blockquote>
<p>	Show answer<br />
Heartburn is a lay term for mild, intermittent reflux of gastric content into the esophagus without tissue injury. It is relatively common among adults. GERD implies esophagitis with varying degrees of erythema, edema, and friability of the distal esophageal mucosa. It occurs in 10% of the population.</p>
<blockquote><p><strong>3. What causes GERD?</strong> </p></blockquote>
<p>	Show answer<br />
The underlying abnormality of GERD is functional incompetence of the lower esophageal sphincter (LES), which allows gastric acid, bile, and digestive enzymes to damage the unprotected esophageal mucosa. Achalasia, scleroderma, and other esophageal motility disorders are sometimes associated with GERD.</p>
<blockquote><p><strong>4. Is hiatal hernia an essential defect in patients with GERD?</strong> </p></blockquote>
<p>	Show answer<br />
No. Not all patients with GERD have a hiatal hernia, and not all patients with a hiatal hernia have GERD. A total of 50% of patients with GERD have an associated hiatal hernia.</p>
<blockquote><p><strong>5. What studies are useful to diagnose GERD? </strong>	</p></blockquote>
<p>Show answer<br />
Endoscopy with biopsy is essential in diagnosing GERD. Barium swallow with or without fluoroscopy can diagnose reflux but cannot identify esophagitis. Twenty-four-hour esophageal pH testing associates reflux with symptoms and is useful in some patients. Gastric secretory or gastric emptying tests are occasionally helpful. Manometry of the esophagus and LES is required whenever an esophageal motility disorder is suspected and before any surgical intervention.</p>
<blockquote><p><strong>6. What is the initial management of a patient suspected of having GERD? </strong>	</p></blockquote>
<p>Show answer </p>
<p>    * Change diet to avoid foods known to induce reflux (e.g., chocolate, alcohol, and coffee).<br />
    * Avoid large meals before bedtime.<br />
    * Stop smoking.<br />
    * Do not wear tight, binding clothes.<br />
    * Elevate the head of the bed 4-5 inches.<br />
    * Take antacids when symptomatic.<br />
    * Weight loss can be very effective in reducing GERD symptoms.</p>
<blockquote><p><strong>7. If initial treatment fails, what should be recommended? </strong></p></blockquote>
<p>	Show answer<br />
About 50% of patients show significant healing with H2 blockers, but only 10% of these patients remain healed 1 year later. Metoclopramide promotes gastric emptying but rarely relieves symptoms consistently in the absence of acid reduction.</p>
<p><em><strong>KEY POINTS: DIAGNOSTIC WORK-UP OF GERD</strong></p>
<p>   1. Underlying anatomic abnormality may cause functional incompetence of the lower esophageal sphincter (LES).<br />
   2. Endoscopy and biopsy are paramount in diagnosis.<br />
   3. Swallow studies delineate possible anatomic causes.<br />
   4. 24-hour pH monitoring can link reflux to patient&#8217;s symptoms.<br />
   5. Manometry of the LES is required if esophageal motility disorder is suspected.</em></p>
<blockquote><p><strong>8. What is the role of proton pump inhibitor (PPI) in GERD?</strong> </p></blockquote>
<p> 	Show answer<br />
PPIs (omeprazole and others) irreversibly inhibit the parietal cell hydrogen ion pump and are > 80% successful in healing severe erosive esophagitis. Two thirds of patients who continue the medication remain healed. A concern in prolonged PPI therapy is hypergastrinemia secondary to alkalinization of the antrum. Gastrin is trophic to gastrointestinal mucosa, but the initial fear of induced neoplasia has not been borne out by follow-up studies.</p>
<blockquote><p><strong>9. When should operation for GERD be recommended? 	</strong></p></blockquote>
<p>Show answer<br />
Failure of nonoperative (medical) therapy is the primary indication for surgery. Noncompliance with prescribed treatment is a frequent cause of failure and even stricture unresponsive to dilation. With PPIs, most patients&#8217; symptoms can be controlled for long periods of time. Current recommendations for surgical intervention include: (1) failed medical therapy (e.g., intractable disease, intolerance or allergy to medications, noncompliance, and recurrence of symptoms while on medical therapy), (2) complications (e.g., stricture, respiratory symptoms, medicosocial changes, and premalignant mucosal changes), (3) patient preference (e.g., cost-long-term medical prescriptions can be expensive-or lifestyle issues).</p>
<blockquote><p><strong>10. What is the goal of surgical treatment? 	</strong></p></blockquote>
<p>Show answer<br />
Operations for GERD attempt to prevent reflux by mechanically increasing LES pressure and, in most procedures, to restore a sufficient length of distal esophagus to the high-pressure zone of the abdomen. Hiatal hernia, when present, is reduced simultaneously.</p>
<blockquote><p><strong>11. What procedures can accomplish this goal and how do they do it? </strong></p></blockquote>
<p>	Show answer </p>
<p>   1. <strong>In the Nissen fundoplication,</strong> which is used in > 95% of patients, the fundus of the stomach is mobilized, wrapped around the distal esophagus posteriorly, and secured to itself anteriorly (i.e., 360-degree wrap). The procedure alters the angle of the gastroesophageal junction and maintains the distal esophagus within the abdomen to prevent reflux. The operation is performed transabdominally by either laparotomy or laparoscopy. (See Figure 43-1.)<br />
   2. <strong>The Belsey Mark IV operation</strong> accomplishes the same anatomic changes but is done via a thoracotomy. (See Figure 43-2.)<br />
   3. <strong>The Hill gastropexy </strong>restores the esophagus to the abdominal cavity by securing the gastric cardia to the preaortic fascia. (See Figure 43-3.)<br />
   4. <strong>The Toupet (partial) fundoplication </strong>is used in patients who have associated motility disorders. Because the wrap is not circumferential, the incidence of postoperative dysphagia is significantly reduced with this partial wrap compared with a full 360-degree wrap (Nissen fundoplication). However, long-term durability may not be as good as with a Nissen fundoplication. This operation can be done transabdominally by either laparotomy or laparoscopy. (See Figure 43-4.)</p>
<p><img src="http://img3.raidpic.com/603.43.1.jpg" /></p>
<p><strong>Figure 43-1 In the Nissen fundoplication, which is used in > 95% of patients, the fundus of the stomach is mobilized, wrapped around the distal esophagus posteriorly, and secured to itself anteriorly (i.e., 360° wrap). The procedure alters the angle of the GE junction and maintains the distal esophagus within the abdomen to prevent reflux. The operation is performed transabdominally by either laparotomy or laparoscopy.</strong></p>
<p><img src="http://img7.raidpic.com/663.43.2.jpg" /></p>
<p><strong>Figure 43-2 The Belsey Mark IV operation accomplishes the same anatomic changes as the Nissen fundoplication but is done via a thoracotomy.</strong></p>
<p><img src="http://img3.raidpic.com/163.43.3.jpg" /></p>
<p><strong>Figure 43-3 The Hill gastropexy restores the esophagus to the abdominal cavity by securing the gastric cardia to the preaortic fascia.</strong></p>
<p><img src="http://img2.raidpic.com/323.43.4.jpg" /></p>
<p><strong>Figure 43-4 The Toupet (partial) fundoplication is used in patients who have associated motility disorders. Because the wrap is not circumferential, the incidence of postoperative dysphagia is significantly reduced with this partial wrap compared with a full 360° wrap (Nissen fundoplication). However, long-term durability may not be as good as with a Nissen fundoplication. This operation can be done transabdominally by either laparotomy or laparoscopy.</strong></p>
<blockquote><p><strong><br />
12. What are the success rates for such procedures? </strong></p></blockquote>
<p>	Show answer<br />
All of the procedures described in question 11 eliminate GERD in almost 90% of patients who are followed for </p>
<blockquote><p><strong>10 years. But the Nissen fundoplication wins in comparison studies. Recurrent symptoms should be thoroughly worked up because they are frequently associated with other disorders and not recurrent GERD.<br />
13. What are the long-term complications of such procedures?</strong> </p></blockquote>
<p>	Show answer<br />
The repair may fail, with recurrence of reflux, after any of these operations. Incorrect placement or slippage of the stomach wrap can complicate Nissen fundoplication and the Belsey Mark IV procedure. Dysphagia and the inability to belch (i.e., gas-bloat syndrome) result from too tight a wrap.</p>
<blockquote><p><strong>14. How can stricture from GERD be managed?</strong> </p></blockquote>
<p>	Show answer<br />
Pliable (unfixed) strictures can be dilated. Fixed strictures require surgical repair. A Thal patch expands the stricture by interposing a piece of stomach.</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>
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		<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>Heart Transplantation</title>
		<link>http://surgeryprocedure.info/transplantation/heart-transplantation</link>
		<comments>http://surgeryprocedure.info/transplantation/heart-transplantation#comments</comments>
		<pubDate>Tue, 14 Jul 2009 16:37:28 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[TRANSPLANTATION]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/?p=456</guid>
		<description><![CDATA[91 HEART TRANSPLANTATION
Daniel R. Meldrum M.D., Azad Raiesdana M.D., Jeffrey A. Breall M.D., John W. Brown M.D.
1. Who performed the first experimental heart-lung transplant?
 	Show answer
Alexis Carrel, a French-born American surgeon, developed the vascular techniques required for heart-lung transplantation and performed the first experimental heart-lung transplant in 1907. He transplanted the lungs, heart, aorta, and [...]]]></description>
			<content:encoded><![CDATA[<p><strong>91 HEART TRANSPLANTATION<br />
Daniel R. Meldrum M.D., Azad Raiesdana M.D., Jeffrey A. Breall M.D., John W. Brown M.D.</strong></p>
<blockquote><p><strong>1. Who performed the first experimental heart-lung transplant?</strong></p></blockquote>
<p> 	Show answer<br />
Alexis Carrel, a French-born American surgeon, developed the vascular techniques required for heart-lung transplantation and performed the first experimental heart-lung transplant in 1907. He transplanted the lungs, heart, aorta, and vena cava of a 1-week-old cat into the neck of a large adult cat. For devising the technique of vascular anastomosis and other outstanding accomplishments, Carrel received the Nobel Prize in 1912 (the first Nobel Prize awarded to a scientist working in an American laboratory).<br />
<span id="more-456"></span></p>
<blockquote><p><strong>2. Who performed the first successful experimental heart-lung transplant?</strong></p></blockquote>
<p> 	Show answer<br />
V.P. Demikhov performed the first successful heart-lung transplant in a dog in 1962.</p>
<blockquote><p>3<strong>. Who developed the surgical strategy required for human heart transplantation?</strong> </p></blockquote>
<p>	Show answer<br />
Norman Shumway.</p>
<blockquote><p><strong>4. Who performed the first human heart transplant? When? </strong>	</p></blockquote>
<p>Show answer<br />
C.N. Bernard performed the first human heart transplant in December, 1967 (in Capetown, South Africa, after visiting Dr. Shumway), although Dr. Shumway set the stage by developing the technique in animals. Shumway and the Stanford group performed the first heart transplant in the United States and accomplished the first successful clinical series.</p>
<blockquote><p><strong>5. Who performed the first successful heart-lung transplant? When? </strong>	</p></blockquote>
<p>Show answer<br />
Dr. Bruce Reitz at Stanford in 1981 on a 21-year-old woman with pulmonary hypertension secondary to an atrial septal defect.</p>
<blockquote><p><strong>6. How many heart transplants are performed annually? Is the number increasing or decreasing?</strong></p></blockquote>
<p> 	Show answer<br />
In 1983 approximately 300 heart transplants were performed worldwide. By 1988, the number had rapidly increased to approximately 3000 and remains relatively stable between 3500 and 4000.</p>
<blockquote><p><strong>7. What anastomoses (surgical connections) must be performed for a combined heart and lungs transplant?</strong></p></blockquote>
<p> 	Show answer<br />
The operation requires only a right atrial-to-cava (inflow) anastomosis and an aortic (outflow) anastomosis with a connection at the trachea. Heart-lung transplant is less complicated (fewer anastomoses) than heart transplant alone, which may explain why heart-lung transplant was attempted first.<br />
8. What anastomoses must be performed for a heart transplant? 	Show answer<br />
Left atrial, right atrial, aortic, and pulmonary arterial.</p>
<blockquote><p><strong>9. Who is an acceptable cardiac donor?</strong> </p></blockquote>
<p>	Show answer </p>
<p>Acceptable cardiac donors meet the following criteria:</p>
<p>   1. Requirements for brain death<br />
   2. Consent from next of kin<br />
   3. ABO blood group compatibility with recipient<br />
   4. Within 20% of the same size as recipient<br />
   5. Absence of history of cardiac disease<br />
   6. Normal echocardiogram (ventricular wall motion)<br />
   7. Normal heart by inspection during organ recovery</p>
<blockquote><p><strong>10. Who is an acceptable cardiac recipient?</strong></p></blockquote>
<p> 	Show answer<br />
Although selection criteria are evolving as a result of improved techniques and outcomes, the following criteria are standard: age between newborn and 65 years; irremediable New York Heart Association Functional Class IV cardiac disease; normal renal, hepatic, pulmonary, and central nervous system function; pulmonary vascular resistance < 6-8 Wood units; and absence of malignancy, infection, recent pulmonary infarction, and severe peripheral vascular or cerebrovascular disease. Diabetes is a relative contraindication; the steroids used in posttransplant immunosuppression make diabetes difficult to manage. Also, normal psychological status has proven to be important.</p>
<blockquote><p><strong>11. What are the most common indications for heart transplant in adults and in children?</strong></p></blockquote>
<p> 	Show answer<br />
In adults, coronary artery disease (ischemic cardiomyopathy) and idiopathic cardiomyopathy each account for approximately 45% of transplants.<br />
In children, congenital heart disease and cardiomyopathy are most common, with hypoplastic left heart being the most common congenital malformation requiring heart transplantation.</p>
<blockquote><p><strong>12. What percentage of potential recipients (on the transplant list) die while waiting for a heart transplant?</strong> </p></blockquote>
<p>	Show answer<br />
20%.</p>
<blockquote><p><strong>13. At what point does donor heart ischemic time influence mortality?</strong> </p></blockquote>
<p>	Show answer<br />
Donor heart ischemic time > 6 hours definitely increases mortality. Ischemic times between 4 and 6 hours stun the donor heart. Most transplant teams try to keep ischemic times (from donor harvest to perfusion in the recipient) to < 4 hours.</p>
<blockquote><p><strong>14. Who pioneered hypothermic myocardial preservation? </strong>	</p></blockquote>
<p>Show answer<br />
Henry Swan at the University of Colorado. He submerged anesthetized children in a bathtub of ice water before cardiac procedures.</p>
<blockquote><p><strong>15. How is cardiac allograft rejection prevented?</strong> 	</p></blockquote>
<p>Show answer<br />
Pharmacologically induced immunosuppression is performed by using one of two protocols. The first is triple therapy, which combines cyclosporine, azathioprine, and prednisone. The second major protocol incorporates the monoclonal antibody OKT3 into the triple therapy protocol. OKT3 is substituted for cyclosporine for the first 2 weeks after transplant.</p>
<blockquote><p><strong>16. What is OKT3? 	</strong></p></blockquote>
<p>Show answer<br />
OKT3 is a mouse monoclonal antibody that binds to and blocks the T-cell CD3 receptor. A monoclonal antibody is an antibody generated from the clones of a single cell. For instance, a single B cell, which recognizes the CD3 receptor as an antigen (foreign), is immortalized in cell culture and produces the monoclonal antibody in limitless supply. The CD3 receptor, which is common to all T cells, is important for antigen recognition and T-cell activation; therefore, OKT3 is highly immunosuppressive.<br />
<em><strong>KEY POINTS: CRITERIA FOR ACCEPTABLE HEART DONORS</strong></p>
<p>   1. Donors must meet the criteria for brain death.<br />
   2. Consent from donor&#8217;s next of kin.<br />
   3. ABO blood group compatibility with recipient.<br />
   4. Donor must be within 20% of same size as recipient.<br />
   5. Donor must have no history of cardiac disease and a normal echocardiogram.<br />
   6. Donor heart must appear normal by inspection during organ recovery.</em></p>
<blockquote><p><strong><br />
17. What complications are associated with the use of OKT3? </strong></p></blockquote>
<p>	Show answer<br />
OKT3 may have severe side effects, including pulmonary edema and high fevers, that result from transient cytokine release, which may occur when OKT3 binds to the T-cell activation site. Because OKT3 is an antigen (an antibody from a different species [i.e., a mouse]), patients develop anti-OKT3 antibodies fairly quickly; the result is that OKT3 can only be used to treat one rejection episode. Severe side effects occur in < 5% of patients.</p>
<blockquote><p><strong>18. Does HLA mismatch influence the incidence of rejection after heart transplantation? Is HLA typing routinely performed before heart transplantation? </strong>	</p></blockquote>
<p>Show answer<br />
Yes and no. In a multi-institutional, multivariate analysis of 1719 cardiac transplant recipients by Jarcho et al., HLA mismatch increased the incidence of rejection. However, HLA typing is not routinely done before heart transplantation because it takes too long. In addition, with three of six mismatches, there was still only a trend toward increased rejection-related deaths (P = 0.14). If longer organ preservation times can be achieved, donor/recipient HLA matching will become feasible and should improve survival rates. Again, ABO blood group compatibility does influence graft survival.</p>
<blockquote><p><strong>19. What are the major complications of heart transplantation? </strong></p></blockquote>
<p>	Show answer </p>
<p>    * Allograft rejection (days to weeks)<br />
    * Infection (months)<br />
    * Transplant coronary artery disease (years)</p>
<blockquote><p><strong>20. What is the incidence of transplant coronary artery disease? What are the risk factors? </strong>	</p></blockquote>
<p>Show answer<br />
Nearly 50% of patients have angiographic evidence of coronary artery disease by 5 years after transplant. However, only approximately 10% develop at least 70% stenosis (hemodynamically significant stenosis). Severe stenosis is highly predictive of the need for retransplantation. Risk factors for transplant coronary artery disease include male gender of the donor or recipient, older donor age, and donor hypertension.</p>
<blockquote><p><strong>21. How is cardiac allograft rejection diagnosed? </strong>	</p></blockquote>
<p>Show answer<br />
Clinical suspicion is raised by new-onset cardiac arrhythmia, fever, or hypotension. Diagnosis depends on endomyocardial biopsy, which is performed at regular intervals to detect histologic evidence of rejection before signs or symptoms occur. Radionuclide ventriculography and echocardiography are useful adjuncts in following the hemodynamic manifestations of rejection. Electrocardiography itself is not very sensitive in the diagnosis of rejection.</p>
<blockquote><p>
<strong>22. Are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (&#8221;statin&#8221; drugs) generally recommended for post-cardiac transplant patients? </strong></p></blockquote>
<p>	Show answer<br />
Yes. Hypercholesterolemia is common after transplantation, and HMG-CoA reductase inhibitors reduce the development of the diffuse atherosclerosis that tends to occur in transplanted hearts. In addition, statins have an early effect on mortality, which suggests that these drugs may also have immunosuppressive effects.</p>
<blockquote><p><strong>23. What are ventricular assist devices (VADs)? </strong></p></blockquote>
<p>	Show answer<br />
These devices are designed to unload either the right (RVAD) or left (LVAD) ventricle while supporting the pulmonary or systemic circulation. Patients with these VADs may be ambulatory, and the devices may be worn for weeks to months. VADs may be used as a bridge to transplant (when the patient is listed for transplantation) or as destination therapy (when no transplant is planned).</p>
<blockquote><p><strong>24. What is the most serious complication of transvenous endomyocardial biopsy?</strong> </p></blockquote>
<p>	Show answer<br />
Cardiac perforation occurs in 0.5% of cases. This can rapidly lead to tamponade and circulatory collapse.</p>
<blockquote><p><strong>25. What is the typical infection pattern for a posttransplant patient? 	</strong></p></blockquote>
<p>Show answer </p>
<p>    * First postoperative month: conventional bacterial pathogens encountered in surgical patients<br />
    * 1-4 months: opportunistic pathogens, especially cytomegalovirus<br />
    * >4 months: both conventional and opportunistic infections</p>
<blockquote><p><strong>26. Is the transplanted heart denervated?</strong> </p></blockquote>
<p>	Show answer<br />
Initially, yes, but it is believed that partial reinnervation begins within 1 year. Because of this, the heart&#8217;s anatomically mediated reflexes are blunted (e.g., higher resting heart rate because of decreased or absent vagal tone).</p>
<blockquote><p><strong>27. Can one heart be successfully transplanted twice? </strong>	</p></blockquote>
<p>Show answer<br />
Yes. Meiser et al. transplanted the same heart a second time on March 19, 1991, 42 hours after the initial transplantation. Second transplant of the same heart has since been reported by others.</p>
<blockquote><p><strong>28. What is &#8220;domino heart transplant&#8221;? </strong>	</p></blockquote>
<p>Show answer<br />
The good heart from a heart-lung recipient is transplanted into a patient requiring a heart transplant. Some patients with primary lung dysfunction have secondary irreversible cardiac dysfunction (i.e., Eisenmenger&#8217;s syndrome); others, however, such as patients with cystic fibrosis, have good cardiac function. Patients with good cardiac function may serve as donors and increase the donor pool.</p>
<blockquote><p><strong>29. Is the heart capable of making tumor necrosis factor (TNF)? What does TNF have to do with heart transplantation? </strong></p></blockquote>
<p>	Show answer<br />
TNF, typically described as a macrophage- or monocyte-derived inflammatory cytokine, is also produced in large quantities by the heart. TNF released by the heart after ischemia-reperfusion probably contributes to immediate injury (dysfunction) and possibly to later rejection. Anti-TNF strategies are intuitively promising (but undocumented) therapeutic strategies.</p>
<blockquote><p><strong>30. What is the overall 30-day mortality rate after heart transplant? What is the breakdown in mortality between adult and pediatric patients?</strong></p></blockquote>
<p> 	Show answer<br />
The registry of the International Society for Heart and Lung Transplantation, which has data for approximately 45,000 heart transplants, has recorded a 30-day mortality rate of 10%. The 30-day mortality rate for adult recipients is about 8%; for pediatric recipients, it is slightly higher.</p>
<blockquote><p><strong>31. What are the 5- and 10-year actuarial survival rates for heart transplant recipients? 	</strong></p></blockquote>
<p>Show answer </p>
<blockquote><p><strong>75% and 50%, respectively (and the quality of life is dramatically improved).<br />
32. What work remains to be done in heart transplantation? 	</strong></p></blockquote>
<p>Show answer<br />
The future of heart transplantation is bright. Knowledge gained in experimental myocardial ischemia-reperfusion injury and protection is accelerating. New, exciting ways to manipulate myocardial immunology (e.g., signal transduction, gene therapy, chimerism) will further extend donor ischemic times and improve postoperative myocardial function and graft tolerance. Ultimately, genetic alteration of donor hearts will increase the donor pool.</p>
<p><strong><br />
References</strong><br />
WEB SITE<br />
<a href="http://www.transplantation-soc.org/">http://www.transplantation-soc.org</a><br />
BIBLIOGRAPHY<br />
1. Hosenpud JD, Bennett LE, Keck BM, et al: The Registry of the International Society for Heart and Lung Transplantation: Eighteenth official report-2001. J Heart Lung Transplant 20:805-815, 2001.<br />
2. Kobashigawa JA: Advances in immunosuppression for heart transplantation. Adv Card Surg 10:155-174, 1998. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9917904&#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=9917904">Similar articles</a><br />
3. Kupiec-Weglinski JW: Graft rejection in sensitized recipients. Ann Transplant 1:34-40, 1996. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9869935&#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=9869935">Similar articles</a><br />
4. Kuvin JT, Kimmelstiel CD: Infectious causes of atherosclerosis. Am Heart J 137:216-226, 1999. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9924154&#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=9924154">Similar articles</a><br />
5. Leier CV, Binkley PF: Parenteral inotropic support for advanced congestive heart failure. Prog Cardiovasc Dis 41:207-224, 1998.<br />
6. Meldrum DR: Tumor necrosis factor in the heart [review]. Am J Physiol 274:R577, 1998. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=9530222">Medline</a> <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9530222&#038;dopt=Abstract">Similar articles</a><br />
7. Meldrum DR, Dinarello CA, Meng X, et al: Ischemic preconditioning decreases post-ischemic myocardial TNF: Potential ultimate effector mechanism of preconditioning. Circulation 98:II214-II218, 1998.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9852905&#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=9852905">Similar articles</a><br />
8. Mindan JP, Panizo A: Pathology of heart transplant. Curr Top Pathol 92:137-165, 1999.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=9919809"> Similar articles</a><br />
9. Orbaek Andersen H: Heart allograft vascular disease: An obliterative vascular disease in transplanted hearts. Atherosclerosis 142:243-263, 1999. Medline Similar articles<br />
10. Pillai R, Bando K, Schueler S, et al: Leukocyte depletion results in excellent heart-lung function after 12 hours of storage. Ann Thorac Surg 50:211-214, 1990. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10030375&#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=10030375">Similar articles</a><br />
11. Reardon MJ, Letsou GV, Anderson JE, et al: Orthotopic cardiac transplantation after minimally invasive direct coronary artery bypass. J Thorac Cardiovasc Surg 117:390-391, 1999.<br />
12. Spann JC, Van Meter C: Cardiac transplantation. Surg Clin North Am 78:679-690, 1998. Medline Similar articles</p>
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		<title></title>
		<link>http://surgeryprocedure.info/transplantation/457</link>
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		<pubDate>Mon, 13 Jul 2009 19:31:37 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[TRANSPLANTATION]]></category>

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		<description><![CDATA[91 HEART TRANSPLANTATION
Daniel R. Meldrum M.D., Azad Raiesdana M.D., Jeffrey A. Breall M.D., John W. Brown M.D.
1. Who performed the first experimental heart-lung transplant? 	
Show answer
Alexis Carrel, a French-born American surgeon, developed the vascular techniques required for heart-lung transplantation and performed the first experimental heart-lung transplant in 1907. He transplanted the lungs, heart, aorta, and [...]]]></description>
			<content:encoded><![CDATA[<p><strong>91 HEART TRANSPLANTATION<br />
Daniel R. Meldrum M.D., Azad Raiesdana M.D., Jeffrey A. Breall M.D., John W. Brown M.D.</strong></p>
<blockquote><p><strong>1. Who performed the first experimental heart-lung transplant? </strong>	</p></blockquote>
<p>Show answer<br />
Alexis Carrel, a French-born American surgeon, developed the vascular techniques required for heart-lung transplantation and performed the first experimental heart-lung transplant in 1907. He transplanted the lungs, heart, aorta, and vena cava of a 1-week-old cat into the neck of a large adult cat. For devising the technique of vascular anastomosis and other outstanding accomplishments, Carrel received the Nobel Prize in 1912 (the first Nobel Prize awarded to a scientist working in an American laboratory).<br />
<span id="more-457"></span><br />
<!--more--></p>
<blockquote><p><strong>2. Who performed the first successful experimental heart-lung transplant? 	</strong></p></blockquote>
<p>Show answer<br />
V.P. Demikhov performed the first successful heart-lung transplant in a dog in 1962.</p>
<blockquote><p><strong>3. Who developed the surgical strategy required for human heart transplantation? 	</strong></p></blockquote>
<p>Show answer<br />
Norman Shumway.</p>
<blockquote><p><strong>4. Who performed the first human heart transplant? When? </strong></p></blockquote>
<p>	Show answer<br />
C.N. Bernard performed the first human heart transplant in December, 1967 (in Capetown, South Africa, after visiting Dr. Shumway), although Dr. Shumway set the stage by developing the technique in animals. Shumway and the Stanford group performed the first heart transplant in the United States and accomplished the first successful clinical series.</p>
<blockquote><p><strong>5. Who performed the first successful heart-lung transplant? When? </strong></p></blockquote>
<p>	Show answer<br />
Dr. Bruce Reitz at Stanford in 1981 on a 21-year-old woman with pulmonary hypertension secondary to an atrial septal defect.</p>
<blockquote><p><strong>6. How many heart transplants are performed annually? Is the number increasing or decreasing?</strong></p></blockquote>
<p> 	Show answer<br />
In 1983 approximately 300 heart transplants were performed worldwide. By 1988, the number had rapidly increased to approximately 3000 and remains relatively stable between 3500 and 4000.</p>
<blockquote><p><strong>7. What anastomoses (surgical connections) must be performed for a combined heart and lungs transplant? </strong>	</p></blockquote>
<p>Show answer<br />
The operation requires only a right atrial-to-cava (inflow) anastomosis and an aortic (outflow) anastomosis with a connection at the trachea. Heart-lung transplant is less complicated (fewer anastomoses) than heart transplant alone, which may explain why heart-lung transplant was attempted first.</p>
<blockquote><p><strong>8. What anastomoses must be performed for a heart transplant?</strong> 	</p></blockquote>
<p>Show answer<br />
Left atrial, right atrial, aortic, and pulmonary arterial.</p>
<blockquote><p><strong>9. Who is an acceptable cardiac donor? </strong>	</p></blockquote>
<p>Show answer </p>
<p>Acceptable cardiac donors meet the following criteria:</p>
<p>   1. Requirements for brain death<br />
   2. Consent from next of kin<br />
   3. ABO blood group compatibility with recipient<br />
   4. Within 20% of the same size as recipient<br />
   5. Absence of history of cardiac disease<br />
   6. Normal echocardiogram (ventricular wall motion)<br />
   7. Normal heart by inspection during organ recovery</p>
<blockquote><p><strong>10. Who is an acceptable cardiac recipient? </strong></p></blockquote>
<p>	Show answer<br />
Although selection criteria are evolving as a result of improved techniques and outcomes, the following criteria are standard: age between newborn and 65 years; irremediable New York Heart Association Functional Class IV cardiac disease; normal renal, hepatic, pulmonary, and central nervous system function; pulmonary vascular resistance < 6-8 Wood units; and absence of malignancy, infection, recent pulmonary infarction, and severe peripheral vascular or cerebrovascular disease. Diabetes is a relative contraindication; the steroids used in posttransplant immunosuppression make diabetes difficult to manage. Also, normal psychological status has proven to be important.</p>
<blockquote><p><strong>11. What are the most common indications for heart transplant in adults and in children? </strong>	</p></blockquote>
<p>Show answer<br />
In adults, coronary artery disease (ischemic cardiomyopathy) and idiopathic cardiomyopathy each account for approximately 45% of transplants.<br />
In children, congenital heart disease and cardiomyopathy are most common, with hypoplastic left heart being the most common congenital malformation requiring heart transplantation.</p>
<blockquote><p><strong>12. What percentage of potential recipients (on the transplant list) die while waiting for a heart transplant?</strong></p></blockquote>
<p> 	Show answer<br />
20%.</p>
<blockquote><p><strong>13. At what point does donor heart ischemic time influence mortality?</strong> </p></blockquote>
<p>	Show answer<br />
Donor heart ischemic time > 6 hours definitely increases mortality. Ischemic times between 4 and 6 hours stun the donor heart. Most transplant teams try to keep ischemic times (from donor harvest to perfusion in the recipient) to < 4 hours.</p>
<blockquote><p><strong>14. Who pioneered hypothermic myocardial preservation?</strong></p></blockquote>
<p> 	Show answer<br />
Henry Swan at the University of Colorado. He submerged anesthetized children in a bathtub of ice water before cardiac procedures.</p>
<blockquote><p><strong>15. How is cardiac allograft rejection prevented? </strong>	</p></blockquote>
<p>Show answer<br />
Pharmacologically induced immunosuppression is performed by using one of two protocols. The first is triple therapy, which combines cyclosporine, azathioprine, and prednisone. The second major protocol incorporates the monoclonal antibody OKT3 into the triple therapy protocol. OKT3 is substituted for cyclosporine for the first 2 weeks after transplant.</p>
<blockquote><p><strong>16. What is OKT3? 	</strong></p></blockquote>
<p>Show answer<br />
OKT3 is a mouse monoclonal antibody that binds to and blocks the T-cell CD3 receptor. A monoclonal antibody is an antibody generated from the clones of a single cell. For instance, a single B cell, which recognizes the CD3 receptor as an antigen (foreign), is immortalized in cell culture and produces the monoclonal antibody in limitless supply. The CD3 receptor, which is common to all T cells, is important for antigen recognition and T-cell activation; therefore, OKT3 is highly immunosuppressive.<br />
<em><br />
<strong>KEY POINTS: CRITERIA FOR ACCEPTABLE HEART DONORS</strong></p>
<p>   1. Donors must meet the criteria for brain death.<br />
   2. Consent from donor&#8217;s next of kin.<br />
   3. ABO blood group compatibility with recipient.<br />
   4. Donor must be within 20% of same size as recipient.<br />
   5. Donor must have no history of cardiac disease and a normal echocardiogram.<br />
   6. Donor heart must appear normal by inspection during organ recovery.</em></p>
<blockquote><p>
<strong>17. What complications are associated with the use of OKT3? 	</strong></p></blockquote>
<p>Show answer<br />
OKT3 may have severe side effects, including pulmonary edema and high fevers, that result from transient cytokine release, which may occur when OKT3 binds to the T-cell activation site. Because OKT3 is an antigen (an antibody from a different species [i.e., a mouse]), patients develop anti-OKT3 antibodies fairly quickly; the result is that OKT3 can only be used to treat one rejection episode. Severe side effects occur in < 5% of patients.</p>
<blockquote><p><strong>18. Does HLA mismatch influence the incidence of rejection after heart transplantation? Is HLA typing routinely performed before heart transplantation? 	</strong></p></blockquote>
<p>Show answer<br />
Yes and no. In a multi-institutional, multivariate analysis of 1719 cardiac transplant recipients by Jarcho et al., HLA mismatch increased the incidence of rejection. However, HLA typing is not routinely done before heart transplantation because it takes too long. In addition, with three of six mismatches, there was still only a trend toward increased rejection-related deaths (P = 0.14). If longer organ preservation times can be achieved, donor/recipient HLA matching will become feasible and should improve survival rates. Again, ABO blood group compatibility does influence graft survival.</p>
<blockquote><p><strong>19. What are the major complications of heart transplantation?</strong> </p></blockquote>
<p>	Show answer </p>
<p>    * Allograft rejection (days to weeks)<br />
    * Infection (months)<br />
    * Transplant coronary artery disease (years)</p>
<blockquote><p><strong>20. What is the incidence of transplant coronary artery disease? What are the risk factors? </strong></p></blockquote>
<p>	Show answer<br />
Nearly 50% of patients have angiographic evidence of coronary artery disease by 5 years after transplant. However, only approximately 10% develop at least 70% stenosis (hemodynamically significant stenosis). Severe stenosis is highly predictive of the need for retransplantation. Risk factors for transplant coronary artery disease include male gender of the donor or recipient, older donor age, and donor hypertension.</p>
<blockquote><p><strong>21. How is cardiac allograft rejection diagnosed? 	</strong></p></blockquote>
<p>Show answer<br />
Clinical suspicion is raised by new-onset cardiac arrhythmia, fever, or hypotension. Diagnosis depends on endomyocardial biopsy, which is performed at regular intervals to detect histologic evidence of rejection before signs or symptoms occur. Radionuclide ventriculography and echocardiography are useful adjuncts in following the hemodynamic manifestations of rejection. Electrocardiography itself is not very sensitive in the diagnosis of rejection.</p>
<blockquote><p><strong>22. Are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (&#8221;statin&#8221; drugs) generally recommended for post-cardiac transplant patients? 	</strong</p></blockquote>
<p>>Show answer<br />
Yes. Hypercholesterolemia is common after transplantation, and HMG-CoA reductase inhibitors reduce the development of the diffuse atherosclerosis that tends to occur in transplanted hearts. In addition, statins have an early effect on mortality, which suggests that these drugs may also have immunosuppressive effects.</p>
<blockquote><p><strong>23. What are ventricular assist devices (VADs)?</strong> 	</p></blockquote>
<p>Show answer<br />
These devices are designed to unload either the right (RVAD) or left (LVAD) ventricle while supporting the pulmonary or systemic circulation. Patients with these VADs may be ambulatory, and the devices may be worn for weeks to months. VADs may be used as a bridge to transplant (when the patient is listed for transplantation) or as destination therapy (when no transplant is planned).</p>
<blockquote><p><strong>24. What is the most serious complication of transvenous endomyocardial biopsy? </strong>	</p></blockquote>
<p>Show answer<br />
Cardiac perforation occurs in 0.5% of cases. This can rapidly lead to tamponade and circulatory collapse.</p>
<blockquote><p><strong>25. What is the typical infection pattern for a posttransplant patient?</strong> 	</p></blockquote>
<p>Show answer </p>
<p>    * First postoperative month: conventional bacterial pathogens encountered in surgical patients<br />
    * 1-4 months: opportunistic pathogens, especially cytomegalovirus<br />
    * >4 months: both conventional and opportunistic infections</p>
<blockquote><p><strong>26. Is the transplanted heart denervated? 	</strong></p></blockquote>
<p>Show answer<br />
Initially, yes, but it is believed that partial reinnervation begins within 1 year. Because of this, the heart&#8217;s anatomically mediated reflexes are blunted (e.g., higher resting heart rate because of decreased or absent vagal tone).</p>
<blockquote><p><strong>27. Can one heart be successfully transplanted twice?</strong></p></blockquote>
<p> 	Show answer<br />
Yes. Meiser et al. transplanted the same heart a second time on March 19, 1991, 42 hours after the initial transplantation. Second transplant of the same heart has since been reported by others.</p>
<blockquote><p><strong>28. What is &#8220;domino heart transplant&#8221;? </strong>	</p></blockquote>
<p>Show answer<br />
The good heart from a heart-lung recipient is transplanted into a patient requiring a heart transplant. Some patients with primary lung dysfunction have secondary irreversible cardiac dysfunction (i.e., Eisenmenger&#8217;s syndrome); others, however, such as patients with cystic fibrosis, have good cardiac function. Patients with good cardiac function may serve as donors and increase the donor pool.</p>
<p><strong><br />
<blockquote>29. Is the heart capable of making tumor necrosis factor (TNF)? What does TNF have to do with heart transplantation? 	</p></blockquote>
<p></strong></p>
<p>Show answer<br />
TNF, typically described as a macrophage- or monocyte-derived inflammatory cytokine, is also produced in large quantities by the heart. TNF released by the heart after ischemia-reperfusion probably contributes to immediate injury (dysfunction) and possibly to later rejection. Anti-TNF strategies are intuitively promising (but undocumented) therapeutic strategies.</p>
<blockquote><p><strong>30. What is the overall 30-day mortality rate after heart transplant? What is the breakdown in mortality between adult and pediatric patients? </strong>	</p></blockquote>
<p>Show answer<br />
The registry of the International Society for Heart and Lung Transplantation, which has data for approximately 45,000 heart transplants, has recorded a 30-day mortality rate of 10%. The 30-day mortality rate for adult recipients is about 8%; for pediatric recipients, it is slightly higher.</p>
<blockquote><p><strong>31. What are the 5- and 10-year actuarial survival rates for heart transplant recipients? 	</strong></p></blockquote>
<p>Show answer<br />
75% and 50%, respectively (and the quality of life is dramatically improved).</p>
<blockquote><p><strong>32. What work remains to be done in heart transplantation?</strong> </p></blockquote>
<p>	Show answer<br />
The future of heart transplantation is bright. Knowledge gained in experimental myocardial ischemia-reperfusion injury and protection is accelerating. New, exciting ways to manipulate myocardial immunology (e.g., signal transduction, gene therapy, chimerism) will further extend donor ischemic times and improve postoperative myocardial function and graft tolerance. Ultimately, genetic alteration of donor hearts will increase the donor pool.</p>
<p><strong>References</strong><br />
WEB SITE<br />
<a href="http://www.transplantation-soc.org/">http://www.transplantation-soc.org</a><br />
BIBLIOGRAPHY<br />
1. Hosenpud JD, Bennett LE, Keck BM, et al: The Registry of the International Society for Heart and Lung Transplantation: Eighteenth official report-2001. J Heart Lung Transplant 20:805-815, 2001.<br />
2. Kobashigawa JA: Advances in immunosuppression for heart transplantation. Adv Card Surg 10:155-174, 1998. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9917904&#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=9917904"> Similar articles</a><br />
3. Kupiec-Weglinski JW: Graft rejection in sensitized recipients. Ann Transplant 1:34-40, 1996.<br />
4. Kuvin JT, Kimmelstiel CD: Infectious causes of atherosclerosis. Am Heart J 137:216-226, 1999. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9924154&#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=9924154">Similar articles</a><br />
5. Leier CV, Binkley PF: Parenteral inotropic support for advanced congestive heart failure. Prog Cardiovasc Dis 41:207-224, 1998.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9872607&#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=9872607"> Similar articles</a><br />
6. Meldrum DR: Tumor necrosis factor in the heart [review]. Am J Physiol 274:R577, 1998.<br />
7. Meldrum DR, Dinarello CA, Meng X, et al: Ischemic preconditioning decreases post-ischemic myocardial TNF: Potential ultimate effector mechanism of preconditioning. Circulation 98:II214-II218, 1998. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9852905&#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=9852905">Similar articles</a><br />
8. Mindan JP, Panizo A: Pathology of heart transplant. Curr Top Pathol 92:137-165, 1999.<br />
9. Orbaek Andersen H: Heart allograft vascular disease: An obliterative vascular disease in transplanted hearts. Atherosclerosis 142:243-263, 1999. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10030375&#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=10030375"> Similar articles</a><br />
10. Pillai R, Bando K, Schueler S, et al: Leukocyte depletion results in excellent heart-lung function after 12 hours of storage. Ann Thorac Surg 50:211-214, 1990.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=2383105&#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=2383105">Similar articles</a><br />
11. Reardon MJ, Letsou GV, Anderson JE, et al: Orthotopic cardiac transplantation after minimally invasive direct coronary artery bypass. J Thorac Cardiovasc Surg 117:390-391, 1999.<br />
12. Spann JC, Van Meter C: Cardiac transplantation. Surg Clin North Am 78:679-690, 1998. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9891570&#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=9891570">Similar articles</a></p>
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		<title>Surgical Infectious Disease. Prophylaxis</title>
		<link>http://surgeryprocedure.info/general-topics/surgical-infectious-disease-prophylaxis</link>
		<comments>http://surgeryprocedure.info/general-topics/surgical-infectious-disease-prophylaxis#comments</comments>
		<pubDate>Tue, 07 Jul 2009 07:31:13 +0000</pubDate>
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				<category><![CDATA[GENERAL TOPICS]]></category>

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		<description><![CDATA[PROPHYLAXIS 
17. Should systemic antibiotic prophylaxis be used in elective colon resection? 	
Show answer
Yes, beyond any statistical shadow of a doubt. At least two dozen clinical trials have been carried out using placebo controls against a variety of antibiotics, principally those active against at least the anaerobic-predominant flora, and nearly all have shown a reduction [...]]]></description>
			<content:encoded><![CDATA[<p><strong>PROPHYLAXIS </strong></p>
<blockquote><p><strong>17. Should systemic antibiotic prophylaxis be used in elective colon resection? 	</strong></p></blockquote>
<p>Show answer<br />
Yes, beyond any statistical shadow of a doubt. At least two dozen clinical trials have been carried out using placebo controls against a variety of antibiotics, principally those active against at least the anaerobic-predominant flora, and nearly all have shown a reduction in infectious complications in the antibiotic group. Never again should this point need repeating, and no patient should be placed at risk when systemic antibiotic prophylaxis has been established as the standard of care. No new clinical trials against placebo in this group of patients with known risk can be performed ethically given the confirmed risk reduction.<br />
Other risk groups (e.g., cesarean section after membrane rupture) besides patients undergoing colon resection have been standardized by trials in large patient populations and have shown similar risk reduction. The benefit of prophylaxis has been demonstrated. In other groups of patients that cannot be standardized because of unusual contamination factors or unique factors of host resistance impairment, guidelines for rational prophylaxis should follow similar principles.<br />
<span id="more-111"></span></p>
<blockquote><p><strong>18. Are two prophylactic doses better than one in preventing infection? Are three doses better still?</strong></p></blockquote>
<p> 	Show answer<br />
Only one dose of prophylactic antibiotic can be proved, beyond statistical or clinical doubt, to be efficacious-the dose in systemic circulation at the time of the inoculum. Whether the dose needs to be repeated one or more times during the 24 hours after the inoculum depends on the blood levels of the drug, which are largely a function of protein binding and clearance rate. We also know for sure that 10 days of the same prophylactic drug that is efficacious if given immediately before the inoculum results in a higher risk of infection than no antibiotic at all.<br />
<em><strong>KEY POINTS: PREOPERATIVE ANTIBIOTIC PROPHYLAXIS</strong></p>
<p>   1. Timing of administration is the most important factor.<br />
   2. Dose 30 minutes before incision so that antibiotic is circulating before the inoculum.<br />
   3. No evidence supports continuation of prophylaxis beyond 24 hours.</em></p>
<blockquote><p><strong>19. What factors determine the timing of antibiotic administration under the criteria of prophylaxis?</strong></p></blockquote>
<p> 	Show answer<br />
The one immutable principle has been set out above-the most important element in timing of prophylaxis is that the drug be circulating before the inoculum. When should it stop? When the reduction in infection risk is no longer provable and before continued use will defeat the prophylactic purpose (as explained above). To summarize with an arbitrary <em>rule of thumb: there is no justification for prophylactic antibiotic 24 hours after the inoculum of an invasive procedure.</em></p>
<p>What does this rule imply? Should we not continue prophylaxis for weeks to cover the presence of a prosthetic hip joint? Presumably, the prosthetic hip will be in the patient for many years-but surely you do not argue that the antibiotic should continue on a daily basis as long as the hip is in place! What is &#8220;prophylaxed&#8221; is not the prosthetic hip but the procedure of implantation. And it is not only implantation that poses a risk to the patient with a prosthesis-so does hemorrhoidectomy done years later, for which prophylaxis is made mandatory by the presence of the hip prosthesis.<br />
The prosthetic or rheumatic heart valve is a risk, but the indication for the use of prophylactic antibiotics is an invasive procedure-a root canal is an example in which an inoculum is unavoidable. <em>Operations are covered by prophylactic antibiotics;</em> the conditions that are risk factors during the operation are not.</p>
<blockquote><p><strong>20. To be safe, why not administer prophylactic antibiotics to all patients undergoing any kind of operation?</strong></p></blockquote>
<p> 	Show answer<br />
Can you give me the indication for a prophylactic antibiotic in a patient undergoing a clean elective surgical procedure that implants no prosthesis, such as hernia repair?<br />
&#8220;Sure,&#8221; one of my brighter students once responded, &#8220;the patient who has a serious impairment in host response, such as acute granulocytic leukemia in blast crisis.&#8221;<br />
I responded, &#8220;Why on earth are you fixing his hernia? That is a clean error [hopefully not a clean kill] in surgical judgment that has nothing to do with antibiotics at all. A patient with that degree of host impairment does not undergo an elective surgical procedure.&#8221;<br />
<strong>Rule of thumb:</strong> <em>If you can provide the indication for a prophylactic antibiotic to cover a clean elective nonprosthetic operation for a patient, you have provided the contraindication for the operation.</p>
<p></em></p>
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