<?xml version="1.0" encoding="UTF-8"?>
<rss version="2.0"
	xmlns:content="http://purl.org/rss/1.0/modules/content/"
	xmlns:wfw="http://wellformedweb.org/CommentAPI/"
	xmlns:dc="http://purl.org/dc/elements/1.1/"
	xmlns:atom="http://www.w3.org/2005/Atom"
	xmlns:sy="http://purl.org/rss/1.0/modules/syndication/"
	xmlns:slash="http://purl.org/rss/1.0/modules/slash/"
	>

<channel>
	<title>SurgeryProcedure.info &#187; Search Results  &#187;  spleen injury with blood behind heart</title>
	<atom:link href="http://surgeryprocedure.info/?s=spleen%20injury%20with%20blood%20behind%20heart&#038;feed=rss2" rel="self" type="application/rss+xml" />
	<link>http://surgeryprocedure.info</link>
	<description>Questions and Answers About Surgery From Diagnosis to Recovery</description>
	<lastBuildDate>Fri, 07 Aug 2009 14:58:08 +0000</lastBuildDate>
	<generator>http://wordpress.org/?v=2.8.5</generator>
	<language>en</language>
	<sy:updatePeriod>hourly</sy:updatePeriod>
	<sy:updateFrequency>1</sy:updateFrequency>
			<item>
		<title>Hepatic &amp; Biliary Trauma. Operative Management Of Liver Injury</title>
		<link>http://surgeryprocedure.info/trauma/hepatic-biliary-trauma-operative-management-of-liver-injury</link>
		<comments>http://surgeryprocedure.info/trauma/hepatic-biliary-trauma-operative-management-of-liver-injury#comments</comments>
		<pubDate>Tue, 07 Jul 2009 20:49:37 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[TRAUMA]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/?p=158</guid>
		<description><![CDATA[OPERATIVE MANAGEMENT OF LIVER INJURY
11. How are acute liver injuries classified? 	
Show answer
Liver wounds are generally graded on a scale of I to VI according the depth of parenchymal laceration and involvement of the hepatic veins or retrohepatic portion of the inferior vena cava. Optimal methods of obtaining hemostasis vary with the severity of the [...]]]></description>
			<content:encoded><![CDATA[<p><strong>OPERATIVE MANAGEMENT OF LIVER INJURY</strong></p>
<blockquote><p><strong>11. How are acute liver injuries classified? </strong>	</p></blockquote>
<p>Show answer<br />
Liver wounds are generally graded on a scale of I to VI according the depth of parenchymal laceration and involvement of the hepatic veins or retrohepatic portion of the inferior vena cava. Optimal methods of obtaining hemostasis vary with the severity of the injury.<br />
<span id="more-158"></span></p>
<blockquote><p><strong>12. Do all patients with a traumatic liver injury require surgery? </strong></p></blockquote>
<p>	Show answer<br />
No. Nonoperative treatment is the standard for victims of blunt trauma who remain hemodynamically stable (approximately 85% of patients). One third of such patients require blood transfusions, but if the volume exceeds 6 units in the first 24 hours, angiography should be done. CT scan should be repeated in 5-7 days for grade IV and V injuries. Complications, including perihepatic infection, biloma, and hemobilia, have been reported in 10% of nonoperative patients.</p>
<blockquote><p><strong>13. What are the options for temporary control of significant hemorrhage in victims of hepatic trauma?</strong> 	</p></blockquote>
<p>Show answer<br />
Ongoing hemorrhage leads to the vicious cycle of acidosis, hypothermia, and coagulopathy. Manual compression, perihepatic packing, and the Pringle maneuver are the most effective temporary strategies.</p>
<blockquote><p><strong>14. What is the Pringle maneuver?</strong> </p></blockquote>
<p>	Show answer<br />
The Pringle maneuver is a manual or vascular clamp occlusion of the hepatoduodenal ligament to interrupt blood flow into the liver. Included in the hepatoduodenal ligament are the hepatic artery, portal vein, and common bile duct. Failure of the Pringle maneuver to control liver hemorrhage suggests either (1) injury to the retrohepatic vena cava or hepatic vein or (2) arterial supply from an aberrant right or left hepatic artery (see question 9).</p>
<blockquote><p><strong>15. What is the finger fracture technique?</strong> 	</p></blockquote>
<p>Show answer<br />
Finger fracture hepatotomy or tractotomy is the method of exposing bleeding points deep within liver lacerations by blunt dissection. Pushing apart the liver parenchyma enables points to be identified and ligated. This method is most commonly required for penetrating injuries.</p>
<blockquote><p><strong>16. What is the role of selective hepatic artery ligation in securing hemostasis in patients with a major liver injury? 	</strong></p></blockquote>
<p>Show answer </p>
<p>Deep lacerations of the right or left hepatic lobe may result in bleeding that cannot be completely controlled by suture ligation of specific bleeding points within the liver parenchyma. In this situation, either the right or left artery can be ligated for control of the bleeding with little risk of ischemic liver necrosis.</p>
<blockquote><p><strong>17. Why is retrohepatic vena caval laceration lethal?</strong> </p></blockquote>
<p>	Show answer<br />
Exposure requires either extensive hepatotomy, extensive mobilization of the right lobe, or right lobectomy, or transection of the vena cava. The large caliber and high flow of the inferior vena cava results in massive hemorrhage during surgical exposure, whereas clamping of the inferior vena cava often results in hypotension attributable to an abrupt decrease in venous return to the heart.</p>
<blockquote><p><strong>18. What is the physiologic rationale for use of a shunt in attempted repair of retrohepatic vena caval injuries?</strong> </p></blockquote>
<p>	Show answer<br />
Hemorrhage control requires maintenance of venous return to the heart while both antegrade and retrograde bleeding through the laceration is stopped. These requirements are met by shunting blood through a tube spanning the laceration between the right atrium and lower inferior vena cava.</p>
<blockquote><p><strong>19. What is the intrahepatic balloon tamponading device? </strong>	</p></blockquote>
<p>Show answer<br />
For transhepatic penetrating injuries, a 1-inch Penrose drain is sutured around a red rubber catheter. This forms a long balloon that is threaded through the bleeding liver injury and inflated with contrast media through a stopcock in the red rubber catheter. The balloon tamponades liver hemorrhage. The catheter is brought out through the abdominal wall, deflated, and removed 24-48 hours later.</p>
<blockquote><p><strong>20. What are the indications for perihepatic packing?</strong> </p></blockquote>
<p>	Show answer<br />
Liver packing with planned reoperation for definitive treatment of injuries in patients who have hypothermia, acidosis, and coagulopathies is a life-saving maneuver. Laparotomy pads (> 20) are packed around the liver to compress and control hemorrhage. The skin of the abdomen is then closed with towel clips (abbreviated laparotomy), and the patient&#8217;s metabolic abnormalities are corrected with planned reoperation within 24 hours.</p>
<blockquote><p><strong>21. What is the abdominal compartment syndrome? </strong>	</p></blockquote>
<p>Show answer<br />
The abdominal compartment syndrome is a potentially lethal complication of perihepatic packing. It may occur when intraabdominal pressure exceeds 20 cmH2O. Intraabdominal pressure increases because of bowel and liver edema secondary to ischemia and reperfusion injury or continued hemorrhage into the abdominal cavity. As pressure increases beyond 20 cmH2O, venous return, cardiac output, and urine output decrease, but ventilatory pressures increase. Patients must return promptly to the operating room for decompression of the abdomen. A manometer attached to the Foley catheter is useful in following intraabdominal pressure.</p>
]]></content:encoded>
			<wfw:commentRss>http://surgeryprocedure.info/trauma/hepatic-biliary-trauma-operative-management-of-liver-injury/feed</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Lower Urinary Tract Injury &amp; Pelvic Trauma</title>
		<link>http://surgeryprocedure.info/trauma/lower-urinary-tract-injury-pelvic-trauma</link>
		<comments>http://surgeryprocedure.info/trauma/lower-urinary-tract-injury-pelvic-trauma#comments</comments>
		<pubDate>Wed, 08 Jul 2009 06:46:19 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[TRAUMA]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/?p=177</guid>
		<description><![CDATA[31 LOWER URINARY TRACT INJURY AND PELVIC TRAUMA
Fernando J. Kim M.D., Siam Oottamasathien M.D.

1. What are the causes of bladder injury?
 	Show answer
Iatrogenic manipulation and penetrating or blunt trauma. Because of the rich detrusor blood supply, bladder injury is usually accompanied by hematuria. Other signs may include suprapubic pain, inability to void, or incomplete recovery [...]]]></description>
			<content:encoded><![CDATA[<p><strong>31 LOWER URINARY TRACT INJURY AND PELVIC TRAUMA<br />
Fernando J. Kim M.D., Siam Oottamasathien M.D.<br />
</strong></p>
<blockquote><p><strong>1. What are the causes of bladder injury?</strong></p></blockquote>
<p> 	Show answer<br />
Iatrogenic manipulation and penetrating or blunt trauma. Because of the rich detrusor blood supply, bladder injury is usually accompanied by hematuria. Other signs may include suprapubic pain, inability to void, or incomplete recovery of catheter irrigation.<br />
<span id="more-177"></span></p>
<blockquote><p>2. <strong>What types of bladder injury may occur with blunt trauma? </strong>	</p></blockquote>
<p>Show answer<br />
Laceration or perforation may be either intra- or extraperitoneal. Hematuria with a normal cystogram defines bladder contusion in the absence of upper tract injury. Extraperitoneal injuries constitute the majority of bladder trauma and tend to concentrate at the bladder base or parasymphyseal area. These can be managed conservatively with urinary catheter drainage for at least 10 days. Intraperitoneal (IP) ruptures typically occur when the bladder is distended at the time of trauma, causing a blowout of the dome of a bladder. IP vesical rupture should be surgically repaired using a two-layer closure with absorbable sutures and placement of suprapubic and urethral catheters.<br />
<em><strong>KEY POINTS: MANAGEMENT OF BLADDER INJURY DUE TO BLUNT TRAUMA</strong></p>
<p>   1. Diagnose with CT cystography and retrograde cystourethrography.<br />
   2. Extraperitoneal injuries are more common and may be managed conservatively with a Foley catheter for 10 days.<br />
   3. Intraperitoneal injuries are more likely if the bladder is distended at the time of injury; they require surgical repair with suprapubic and Foley drainage postoperatively.</em></p>
<blockquote><p><strong>3. What is the likelihood of a bladder injury in patients with a fractured pelvis? </strong>	</p></blockquote>
<p>Show answer<br />
Extraperitoneal bladder injury occurs in 10% of all pelvic fractures. Conversely, approximately 85% of blunt bladder injury is associated with pelvic fracture. Bladder injuries occur more often with parasymphyseal pubic arch fractures and more often with bilateral than unilateral fractures. Isolated ramus fractures produce bladder laceration in 10% of cases.</p>
<blockquote><p><strong>4. How is bladder injury evaluated? </strong>	</p></blockquote>
<p>Show answer<br />
Both computed tomography (CT) cystography and retrograde cystourethrography provide great diagnostic accuracy for bladder rupture. The bladder should be filled under gravity with a total of 300-400 mL of a 50% dilution of standard radiocontrast agent using the Foley catheter. Films should include anteroposterior, lateral, and oblique views. Finally, a postvoid film should be obtained. When renal or distal ureteral injury is suspected, upper tract imaging (intravenous pyelogram [IVP] or CT scan) should precede the cystogram.</p>
<blockquote><p><strong>5. What are the retrograde cystourethrographic patterns of bladder injury? 	</strong></p></blockquote>
<p>Show answer<br />
Extraperitoneal injury allows contrast agent to escape adjacent to the symphysis, but it is confined to the bladder base by the intact peritoneum. Intraperitoneal extravasation produces a &#8220;sunburst&#8221; appearance from the bladder dome, which may collect in the paracolic gutters, outline loops of bowel, or pool under the liver or spleen. It is pivotal to obtain postvoid films.</p>
<blockquote><p><strong>6. How is bladder rupture managed? </strong></p></blockquote>
<p>	Show answer<br />
Extraperitoneal lacerations can be managed with an indwelling catheter for 7-10 days, at which time cystogram usually confirms resolution of extravasation. Intraperitoneal lacerations require operative repair. Bladder contusion requires catheter drainage until gross bleeding has subsided.</p>
<blockquote><p><strong>7. When should urethral injury be investigated? </strong>	</p></blockquote>
<p>Show answer<br />
The mechanism of injury (e.g., crushing or deceleration/impact, straddle injuries) and associated trauma (e.g., pelvic fracture), blood at the meatus, penile or scrotal swelling and ecchymosis, upward prostatic displacement on digital rectal examination, and inability to void or to pass a urethral catheter (do not try this) should be investigated.</p>
<blockquote><p><strong>8. When a patient presents with a pelvic fracture, is concomitant urethral injury a major concern? </strong>	</p></blockquote>
<p>Show answer<br />
Yes. Urethral trauma occurs in 10% of pelvic fractures; it is more common with anterior disruption of the pelvic ring, including 20% of unilateral and 50% of bilateral parasymphyseal fractures. Posterior (prostatomembranous) avulsion is associated with potentially disabling sequelae and requirements for complex and challenging operative corrections. In contrast, more distal urethral injuries avoid impotence and incontinence issues and are more surgically accessible.</p>
<blockquote><p><strong>9. How is urethral injury best assessed? </strong></p></blockquote>
<p>	Show answer<br />
Retrograde urethrography must always be performed before inserting a Foley catheter. Incomplete urethral transection produces local contrast dye extravasation and bladder opacification. Total avulsion produces extensive local extravasation, and no contrast dye gets into the bladder. Incomplete transection is more common with anterior (50%) than posterior (10%) urethral injuries.</p>
<blockquote><p><strong>10. How is urethral injury managed? </strong>	</p></blockquote>
<p>Show answer<br />
For incomplete transection regardless of site, either catheter stenting across the defect or diversion by suprapubic cystostomy permits resolution. With complete urethral transection, the bladder should be decompressed initially via suprapubic cystostomy. Early restoration of continuity by placement of a bridging urethral catheter should be performed endoscopically. A bridging catheter reduces complex scarring and avoids subsequent surgery in many patients.</p>
<blockquote><p><strong>11. What are the complications of urethral injury? 	</strong></p></blockquote>
<p>Show answer<br />
Strictures, incontinence, and impotence (associated with traumatic prostatic displacement). Iatrogenic complications are associated with retropubic dissection.</p>
<blockquote><p><strong>12. What is the differential diagnosis in blunt scrotal trauma?</strong></p></blockquote>
<p> 	Show answer<br />
Testicular rupture, hematocele, scrotal hematoma, intratesticular hematoma, and testicular torsion. Ultrasonography helps sort this out.</p>
<blockquote><p><strong>13. What is the sonographic sign of testicular rupture? </strong>	</p></blockquote>
<p>Show answer<br />
The sign is loss of the normal homogenous echo texture of the testicle, with areas of irregular hyper- or hypoechogenicity.</p>
<blockquote><p><strong>14. How are patients with acute testicular rupture managed?</strong> </p></blockquote>
<p>	Show answer<br />
Management includes surgical exploration and debridement of extruded, nonviable tubules and evacuation of the hematoma. After proper hemostasis is achieved, the tunica albuginea should be closed with running absorbable suture.</p>
<blockquote><p><strong>15. What is the most common cause of penile fractures? </strong>	</p></blockquote>
<p>Show answer<br />
Penile fracture is a rupture of the corpus cavernosum, most commonly associated with sexual intercourse, masturbation, or an abnormally forced bending of the erect penis. Characteristically the patient hears a popping sound, followed by pain and detumescence.</p>
<blockquote><p><strong>16. What are the physical examinations findings with a penile fracture? 	</strong></p></blockquote>
<p>Show answer<br />
Injury to the tunica albuginea causes formation of hematoma and deviation of the shaft to the opposite side of injury. If Buck&#8217;s fascia is intact, the hematoma will be confined to the penis; disruption of Buck&#8217;s fascia allows spread of the hematoma under Colles&#8217; and Scarpa&#8217;s fascia onto the perineum and abdominal wall.</p>
<blockquote><p><strong>17. How are penile fractures managed?</strong> </p></blockquote>
<p>	Show answer<br />
Surgically. A retrograde urethrogram should be performed when urethral injury is suspected. Closure of the defect (or defects) along the tunica albuginea and evacuation of hematoma are performed after degloving the penis.</p>
<blockquote><p><strong>18. In penile amputation injuries, how should the amputated portion of the penis be preserved for transport? </strong></p></blockquote>
<p>	Show answer<br />
The amputated portion of the penis should be wrapped in saline-soaked gauze, placed in a plastic bag with ice slush surrounding the bag.</p>
<blockquote><p><strong>19. How is major scrotal skin loss managed? </strong>	</p></blockquote>
<p>Show answer<br />
If primary repair is not possible, meshed split-thickness skin grafts may be used to cover the testis. When delayed repair is necessary, thigh pouches should be created until permanent reconstruction is feasible.</p>
<blockquote><p><strong>20. A 50-year-old woman complains of urine leakage from her vagina after a hysterectomy. What is the most likely diagnosis? </strong>	</p></blockquote>
<p>Show answer<br />
Unrecognized bladder injury during hysterectomy with subsequent urine extravasation into the surgical field and drainage via the vaginal cuff suture line leads to formation of vesicovaginal fistula.</p>
<blockquote><p><strong>21. What is the best time to repair a vesicovaginal fistula secondary to an uncomplicated hysterectomy? </strong>	</p></blockquote>
<p>Show answer<br />
Although 3-6 months after injury has been recommeded in the past, early repair can be successful if there is minimal inflammation and there are no complicating factors.</p>
<p><strong><br />
References</strong><br />
WEB SITES<br />
<a href="http://www.east.org/tpg/GUmgmt.pdf"><br />
   1. http://www.east.org/tpg/GUmgmt.pdf</a><br />
   <a href="http://www.acssurgery.com/abstracts/acs/acs0510.htm">2. http://www.acssurgery.com/abstracts/acs/acs0510.htm</a></p>
<p>BIBLIOGRAPHY<br />
1. Armstrong PA, Litscher LJ, Key DW, McCarthy MC: Management strategies for genitourinary trauma. Hosp Phys 34:19-25, 1998.<br />
2. Jacob TD, Gruen GS, Udekwu AO, Peitzman AB: Pelvic fracture. Surg Rounds (Aug):583, 1993.<br />
3. Jordan GH: Lower Genitourinary Tract Trauma and Male External Genital Trauma (Nonpenetrating Injuries, Penetrating Injuries, and Avulsion Injuries). In American Urological Association Update Series, Vol. XIX, Lesson 11, part 2. Baltimore, American Urological Association, 2000.<br />
4. Kim FJ: Urologic trauma. In Feliciano DV, Moore EE, Mattox KL (eds): Trauma Companion Handbook, 4th ed. New York, McGraw-Hill, 2002.<br />
5. McAninch JW: Traumatic and Reconstructive Urology. Philadelphia, W.B. Saunders, 1996.<br />
6. Peterson NE: Current management of urethral injuries. In Rous S (ed): 1998 Urology Annual. New York, Appleton-Century-Crofts, 1988, pp 143-179.<br />
7. Peterson NE: Traumatic posterior urethral avulsion. Mongr Urol 7:61, 1986.<br />
8. Spirnak JP: Pelvic fracture and injury to the lower urinary tract. Surg Clin North Am 68:1057, 1988. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=3051452&#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=3051452">Similar articles</a></p>
]]></content:encoded>
			<wfw:commentRss>http://surgeryprocedure.info/trauma/lower-urinary-tract-injury-pelvic-trauma/feed</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Pancreatic &amp; Duodenal Injury</title>
		<link>http://surgeryprocedure.info/trauma/pancreatic-duodenal-injury</link>
		<comments>http://surgeryprocedure.info/trauma/pancreatic-duodenal-injury#comments</comments>
		<pubDate>Tue, 07 Jul 2009 21:07:37 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[TRAUMA]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/?p=165</guid>
		<description><![CDATA[27 PANCREATIC AND DUODENAL INJURY
Caesar M. Ursic M.D.

1. How common are pancreatic injuries? 	
Show answer
The pancreas is not commonly injured because of its protected retroperitoneal position, and thus accounts for only 8% of all penetrating and 2% of all blunt visceral injuries.

2. What other injuries are typically associated with penetrating pancreatic trauma? 	
Show answer
Liver injury [...]]]></description>
			<content:encoded><![CDATA[<p><strong>27 PANCREATIC AND DUODENAL INJURY<br />
Caesar M. Ursic M.D.<br />
</strong></p>
<blockquote><p><strong>1. How common are pancreatic injuries?</strong> 	</p></blockquote>
<p>Show answer<br />
The pancreas is not commonly injured because of its protected retroperitoneal position, and thus accounts for only 8% of all penetrating and 2% of all blunt visceral injuries.<br />
<span id="more-165"></span></p>
<blockquote><p><strong>2. What other injuries are typically associated with penetrating pancreatic trauma? </strong>	</p></blockquote>
<p>Show answer<br />
Liver injury is the most frequent concomitant injury, with a reported incidence of ≤ 50%. Other commonly associated injuries include the stomach (40%), large abdominal vessels such as the aorta and vena cava (40%), spleen (25%), kidneys (2%), and duodenum (20%).</p>
<blockquote><p><strong>3. How are pancreatic injuries diagnosed and staged preoperatively?</strong> 	</p></blockquote>
<p>Show answer<br />
Preoperatively, computed tomography with intravenous contrast enhancement may actually demonstrate a transected pancreas or major destruction of portions of the gland and has a high positive predictive value; however, it suffers from a low negative predictive value (i.e., it may miss even big injuries). Ultrasound does not consistently image the retroperitoneum adequately and is often hampered by overlying bowel gas. Elevated serum amylase concentrations are nonspecific for pancreatic injury and can be normal in a high proportion of patients shown subsequently to harbor significant injuries to the gland. Diagnostic peritoneal lavage is also unreliable. Short of mandatory exploration, there are no universally reliable methods to assure early diagnosis of significant pancreatic injuries. Surgeons must pay particular attention to the mechanism of injury and subtle signs and symptoms of the physical examination and combine them with data obtained from imaging studies.</p>
<blockquote><p><strong>4. What are some of the commonly used surgical options for the treatment of pancreatic injuries? </strong></p></blockquote>
<p>	Show answer<br />
Most low-grade penetrating and blunt injuries to the pancreas are adequately treated by closed suction drains placed at surgery. First, the integrity of the main pancreatic duct should be evaluated, either by direct inspection or by intraoperative pancreatography. Distal duct injuries (defined as those occurring to the left of the superior mesenteric vessels) are treated with distal pancreatectomy, with or without splenectomy, and closed drainage of the pancreatic stump. Preservation of the spleen is preferable. Injuries to the proximal portion of the gland that do not involve the main duct are treated with closed suction drainage. Injury to the pancreatic duct in the head or neck of the pancreas may require resection of significant portions of distal pancreas. If more than 80% of the gland is removed, the risk of endocrine and exocrine pancreatic insufficiency is high. Try to preserve distal glandular tissue by incorporating it into a Roux-en-Y pancreaticojejunostomy. With severe pancreatic head destruction, instances involving significant injuries to the duodenum and distal biliary structures may require a pancreaticoduodenectomy (i.e., Whipple procedure). Recent reports of successful nonoperative management of complete pancreatic transections in pediatric patients may shift the approach to these injuries away from resection, although the current standard of care remains surgical.</p>
<p><em><strong>KEY POINTS: SURGICAL OPTIONS FOR PANCREATIC INJURIES</strong></p>
<p>   1. Low-grade injuries are treated with simple closed suction drainage at the time of celiotomy.<br />
   2. In unstable patients, debride, obtain hemostasis, and drain. Deal with the resultant fistula at a later time.<br />
   3. If ductal injury is suspected in a stable patient, visualize with ERCP or cholangiogram.<br />
   4. If ductal injury is present in the head or neck of the pancreas, ligate proximally and attempt to preserve pancreatic tissue with Roux-en-Y pancreaticojejunostomy.<br />
   5. Always place a jejunal feeding tube.</em></p>
<blockquote><p><strong>5. Is an elevated serum amylase level diagnostic of pancreatic trauma? </strong>	</p></blockquote>
<p>Show answer<br />
No. Up to 40% of patients who have sustained significant pancreatic injury do not show elevations in their initial serum amylase level. There appears to be a slightly higher positive predictive value if the elevated amylase level is obtained more than 3 hours after the patient&#8217;s injury, although elevated amylase is common with trauma not involving the pancreas. Up to 40% of patients sustaining isolated head trauma can present with serum hyperamylasemia, which is unrelated to pancreatic injury.</p>
<blockquote><p><strong>6. How do blunt pancreatic injuries differ in children and adults? </strong></p></blockquote>
<p>	Show answer<br />
Adult pancreatic injury is usually either penetrating (e.g., stab and gunshot wounds) or high-speed blunt forces (e.g., motor vehicular crashes). Children usually present after direct blows to the epigastrium, typically from bicycle handlebars, which compress the pancreas between the anterior surface of the thoracic spine and the handlebar, often resulting in complete glandular transection.</p>
<blockquote><p><strong>7. What is the optimal route of nutritional supplementation after a major pancreatic injury?</strong> </p></blockquote>
<p>	Show answer<br />
Direct feeding into the stomach is contraindicated because it stimulates pancreatic exocrine secretion and aggravates healing, potentiating secondary pancreatitis and pancreatic fistulas formation. Postpyloric enteral nutrition can be delivered safely and effectively via a feeding jejunostomy tube placed at the completion of the abdominal exploration and pancreatic repair.</p>
<blockquote><p><strong>8. Describe the common complications of pancreatic injuries.</strong> </p></blockquote>
<p>	Show answer<br />
Complications are common. The two most common are pancreatic fistulas and intraabdominal abscesses. Other problems are pancreatitis, pancreatic pseudocyst, and pancreatic hemorrhage. Most patients who die after sustaining injuries to the pancreas do so as a result of late complications and not from the pancreatic injury itself.</p>
<blockquote><p><strong>9. What is the role of computed tomography (CT) scanning in diagnosing blunt duodenal injuries? </strong>	</p></blockquote>
<p>Show answer<br />
Although CT is an excellent tool for visualizing solid organ injuries, CT is less useful with injuries to hollow organs such as the duodenum. Even the addition of an oral contrast agent to the study does not seem to improve the diagnostic yield. Subtle signs of duodenal injury on CT scans include periduodenal edema or fluid and retroduodenal air, which usually indicates a duodenal rupture and spillage of small amounts of intralumenal contents into the retroperitoneum.</p>
<blockquote><p><strong>10. What is the importance of the Kocher maneuver? </strong>	</p></blockquote>
<p>Show answer </p>
<p>In 1903, Kocher described what has now become a routine maneuver during the exploratory celiotomy to visualize and repair injuries to the duodenum, distal common bile duct, and pancreatic head. The avascular lateral peritoneal attachments to the duodenum are incised sharply; then the duodenal sweep is elevated and reflected medially, allowing for inspection and palpation of its posterior surface as well as of the head of the pancreas.</p>
<blockquote><p><strong>11. What are the four portions of the duodenum and their surgical relationships?</strong> 	</p></blockquote>
<p>Show answer<br />
The first portion of the duodenum starts at the pylorus (intraperitoneally) and passes backward (retroperitoneally) toward the gallbladder (the remainder of the duodenum is retroperitoneal). The second portion descends 7-8 cm and is anterior to the vena cava. The left border of the duodenum is attached to the head of the pancreas, at the site where the common bile and pancreatic ducts enter; it shares a common blood supply with the head of the pancreas through the pancreaticoduodenal arcades. The third portion of the duodenum turns horizontally to the left, with its cranial surface in contact with the uncinate process of the pancreas, and passes posterior to the superior mesenteric artery and vein. The fourth portion continues to the left, ascending slightly and crossing the spine anterior to the aorta, where it is fixed to the suspensory ligament of Treitz at the duodenojejunal flexure.</p>
<blockquote><p><strong>12. How are duodenal injuries classified?</strong> </p></blockquote>
<p>	Show answer<br />
An organ injury scale has been adopted that allows for standardized descriptions of duodenal injuries, which extend from grade I (least severe) to grade V (most severe). The grading of duodenal injuries assists surgeons in selecting the appropriate surgical procedure for the repair or reconstruction of these frequently complex injuries. (See Table 27-1).<br />
<strong>Table 27-1. GRADES OF PANCREATIC INJURY</strong></p>
<table width="100%" border=1 cellpadding=2 bordercolor="#c0c0c0" cellspacing=2 bgcolor="#ffffff">
<tr valign=top>
<td width=39><font size=2 color="#000000" face="Arial"></p>
<div><b>Grade</b></div>
<p></font>
</td>
<td width=74><font size=2 color="#000000" face="Arial"></p>
<div><b> Injury</b></div>
<p></font>
</td>
<td width=404><font size=2 color="#000000" face="Arial"></p>
<div><b> Description</b></div>
<p></font>
</td>
</tr>
<tr valign=top>
<td width=39><font size=2 color="#000000" face="Arial"></p>
<div>I</div>
<p></font>
</td>
<td width=74><font size=2 color="#000000" face="Arial"></p>
<div>Hematoma</div>
<p></font>
</td>
<td width=404><font size=2 color="#000000" face="Arial"></p>
<div>Involving single portion of duodenum</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td width=39>
</td>
<td width=74><font size=2 color="#000000" face="Arial"></p>
<div>Laceration</div>
<p></font>
</td>
<td width=404><font size=2 color="#000000" face="Arial"></p>
<div>Partial thickness; no perforation</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td width=39><font size=2 color="#000000" face="Arial"></p>
<div>II</div>
<p></font>
</td>
<td width=74><font size=2 color="#000000" face="Arial"></p>
<div>Hematoma</div>
<p></font>
</td>
<td width=404><font size=2 color="#000000" face="Arial"></p>
<div>Involving more than one portion</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td width=39>
</td>
<td width=74><font size=2 color="#000000" face="Arial"></p>
<div>Laceration</div>
<p></font>
</td>
<td width=404><font size=2 color="#000000" face="Arial"></p>
<div>Disruption &lt; 50% of circumference</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td width=39><font size=2 color="#000000" face="Arial"></p>
<div>III</div>
<p></font>
</td>
<td width=74><font size=2 color="#000000" face="Arial"></p>
<div>Laceration</div>
<p></font>
</td>
<td width=404><font size=2 color="#000000" face="Arial"></p>
<div>Disruption 50-75% circumference of D2 or disruption of 50-100% of D1, D3, D4</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td width=39><font size=2 color="#000000" face="Arial"></p>
<div>IV</div>
<p></font>
</td>
<td width=74><font size=2 color="#000000" face="Arial"></p>
<div>Laceration</div>
<p></font>
</td>
<td width=404><font size=2 color="#000000" face="Arial"></p>
<div>Disruption &gt; 75% of D2 or involving ampulla or distal common bile duct</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td width=39><font size=2 color="#000000" face="Arial"></p>
<div>V</div>
<p></font>
</td>
<td width=74><font size=2 color="#000000" face="Arial"></p>
<div>Laceration</div>
<p></font>
</td>
<td width=404><font size=2 color="#000000" face="Arial"></p>
<div>Massive disruption of duodenopancreatic complex</div>
<p></font>
</td>
</tr>
<tr valign=top>
<td width=39>
</td>
<td width=74><font size=2 color="#000000" face="Arial"></p>
<div>Vascular</div>
<p></font>
</td>
<td width=404><font size=2 color="#000000" face="Arial"></p>
<div>Devascularization of duodenum</div>
<p></font>
</td>
</tr>
</table>
<p>D1, D2, D3, and D4 refer to the portions of the duodenum (i.e., first through fourth).</p>
<blockquote><p><strong>13. What are the main surgical options for penetrating duodenal injuries?</strong> </p></blockquote>
<p>	Show answer<br />
Most simple lacerations can be repaired primarily. Complex lacerations with devitalized margins or lacerations that involve > 50% of the duodenal circumference require debridement of margins and re-anastomosis of the divided ends. If tension on the suture line is anticipated because of extensive tissue loss, adjunctive techniques such as Roux-en-Y duodenojejunostomy or pyloric exclusion are more appropriate. Protection of a duodenal repair is best assured by a tube duodenostomy and generous external drainage. With severe duodenal injury that involves distal biliary structures and the pancreatic head, a pancreaticoduodenectomy (i.e., Whipple procedure) may be the most appropriate option.</p>
<p><strong>References</strong><br />
WEB SITE<br />
<a href="http://www.acs.surgery.com/abstracts/acs/acs0507.htm">http://www.acs.surgery.com/abstracts/acs/acs0507.htm</a></p>
<p>BIBLIOGRAPHY<br />
1. Asensio JA, Demetriades D, Hanpeter DE, et al: Management of pancreatic injuries. Curr Probl Surg 36:325-419, 1999.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10410646&#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=10410646"> Similar articles</a><br />
2. Ilahi O, Bochicchio GV, Scalea TM: Efficacy of computed tomography in the diagnosis of pancreatic injury in adult blunt trauma patients: A single-institutional study. Am Surg 68:704-707, 2002. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=12206605&#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=12206605">Similar articles</a><br />
3. Ivatury RR, Nallathambi M, Gaudino J, et al: Penetrating duodenal injuries. Analysis of 100 consecutive cases. Ann Surg 202:153-158, 1985.<br />
4. Jobst MA, Canty TG Sr, Lynch FP: Management of pancreatic injury in pediatric blunt abdominal trauma. J Pediatr Surg 34:818-823, 1999. Medline <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=10359187">Similar articles </a><a href="http://dx.doi.org/10.1016/S0022-3468%2899%2990379-2">Full article</a><br />
5. Moore EE, Cogbill T, Malangoni M, et al: Organ injury scaling II: Pancreas, duodenum, small bowel, colon, and rectum. J Trauma 30:1427, 1990. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=2231822&#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=2231822">Similar articles</a><br />
6. Patel SV, Spencer JA, el-Hansani S, Sheridan MB: Imaging of pancreatic trauma. Br J Radiol 71:985-990, 1998.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10195019&#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=10195019">Similar articles</a><br />
7. Patton J, Lyden S, Croce M, et al: Pancreatic trauma: a simplified management guideline. J Trauma 43:234-239, 1997.<br />
8. Takishima T, Sugimoto K, Hirata M, et al: Serum amylase level on admission in the diagnosis of blunt injury to the pancreas: Its significance and limitations. Ann Surg 226:70-76, 1997. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=9242340">Similar articles</a> <a href="http://dx.doi.org/10.1097/00000658-199707000-00010">Full article</a><br />
9. Vasquez JC, Coimbra R, Hoyt DB, et al: Management of penetrating pancreatic trauma: An 11-year experience of a level-1 trauma center. Injury 32:753-759, 2001. Full article<br />
10. Wales PW, Shuckett B, Kim PC: Long-term outcome after nonoperative management of complete traumatic pancreatic transaction in children. J Pediatr Surg 36:823-827, 2001. 1. Young PR Jr, Meredith JW, Baker CC, et al: Pancreatic injuries resulting from penetrating trauma: A multi-institution review. Am Surg 64:838-843, 1998. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9731810&#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=9731810">Similar articles</a></p>
]]></content:encoded>
			<wfw:commentRss>http://surgeryprocedure.info/trauma/pancreatic-duodenal-injury/feed</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<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>
]]></content:encoded>
			<wfw:commentRss>http://surgeryprocedure.info/transplantation/heart-transplantation/feed</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Hepatic &amp; Biliary Trauma. Biliary Tract Injury</title>
		<link>http://surgeryprocedure.info/trauma/hepatic-biliary-trauma-biliary-tract-injury</link>
		<comments>http://surgeryprocedure.info/trauma/hepatic-biliary-trauma-biliary-tract-injury#comments</comments>
		<pubDate>Tue, 07 Jul 2009 20:53:29 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[TRAUMA]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/?p=160</guid>
		<description><![CDATA[BILIARY TRACT INJURY
22. Why are complications associated with bile duct leaks? 	
Show answer
Bilomas (i.e., collections of bile) frequently become infected and may result in lethal peritonitis. Biliopleural fistula, a communication between the biliary system and pleural cavity, persists because of the relative negative pressure in the thorax and may result in a bile empyema.

23. What [...]]]></description>
			<content:encoded><![CDATA[<p><strong>BILIARY TRACT INJURY</strong></p>
<blockquote><p><strong>22. Why are complications associated with bile duct leaks? 	</strong></p></blockquote>
<p>Show answer<br />
Bilomas (i.e., collections of bile) frequently become infected and may result in lethal peritonitis. Biliopleural fistula, a communication between the biliary system and pleural cavity, persists because of the relative negative pressure in the thorax and may result in a bile empyema.</p>
<p><span id="more-160"></span></p>
<blockquote><p><strong>23. What is the initial management of an established bile leak? 	</strong></p></blockquote>
<p>Show answer<br />
Endoscopic transampullary stenting frequently allows spontaneous resolution of bile duct injuries. Extensive injuries require hepaticojejunostomy for reconstruction.</p>
<p><strong>References</strong><br />
WEB SITES</p>
<p>   <a href="http://www.acssurgery.com/abstracts/acs/acs0506.htm">1. http://www.acssurgery.com/abstracts/acs/acs0506.htm</a><br />
  <a href="http://www.acssurgery.com/abstracts/acs/acs0508.htm"> 2. http://www.acssurgery.com/abstracts/acs/acs0508.htm</a></p>
<p>BIBLIOGRAPHY<br />
1. Croce MA, Fabian TC, Menke PG, et al: Nonoperative management of blunt hepatic trauma is the treatment of choice for hemodynamically stable patients. Ann Surg 221:744-753, 1995. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=7794078&#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=7794078">Similar articles</a><br />
2. Gaines BA, Ford HR: Abdominal and pelvic trauma in children. Crit Care Med 30(suppl):S416-S423, 2002.<br />
3. Hiatt JR, Gabbay J, Busutill RW: Surgical anatomy of the hepatic arteries in 1000 cases. Ann Surg 220:50-52, 1994.<br />
4. Meldrum DR, Moore FA, Moore EE, et al: Cardiopulmonary hazards of perihepatic packing for major liver injury. Am J Surg 170:537-540, 1995. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=7491996&#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=7491996">Similar articles</a> <a href="http://dx.doi.org/10.1016/S0002-9610%2899%2980011-7">Full article</a><br />
5. Meredith JW, Young JR, Bowling J, Roboussin D: Nonoperative management of adult blunt hepatic trauma: The exception or the rule? J Trauma 36:529-534, 1994.<a href="http://dx.doi.org/10.1016/S0002-9610%2899%2980011-7"> Full article</a><br />
6. Moore EE: Staged laparotomy for the hypothermia, acidosis, and coagulopathy syndrome. Am J Surg 172:405-410, 1996.<br />
7. Moore EE, Cogbill TH, Malangoni MA, et al: Organ injury scaling. Surg Clin North Am 75:293-303, 1995.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=7899999&#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=7899999">Similar articles</a><br />
8. Pachter HL, Hofstetter SR: The current status of nonoperative management of adult blunt hepatic injuries. Am J Surg 169:442-454, 1995.<br />
9. Poggetti RS, Moore EE, Moore FA, et al: Balloon tamponade for bilobar transfixing hepatic gunshot wounds. J Trauma 33:694-697, 1992.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=1464918&#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=1464918">Similar articles</a><br />
10. Sheik-Gafoor M, Singh B, Moodley J: Traumatic thoracobiliary fistula: Report of a case with an overview of current diagnostic and therapeutic options. J Trauma 45:819-821, 1998.<br />
11. Tai NR, Boffard KD, Goosen J, Plani F: A 10-year experience of complex liver trauma. Br J Surg 89:1532-1537, 2002.<br />
12. Verous M, Cillo U, Brolese A, et al: Blunt liver injury: From non-operative management to liver transplantation. Injury 34:181-186, 2003.</p>
]]></content:encoded>
			<wfw:commentRss>http://surgeryprocedure.info/trauma/hepatic-biliary-trauma-biliary-tract-injury/feed</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Traumatic Brain Injury</title>
		<link>http://surgeryprocedure.info/trauma/traumatic-brain-injury</link>
		<comments>http://surgeryprocedure.info/trauma/traumatic-brain-injury#comments</comments>
		<pubDate>Tue, 07 Jul 2009 18:00:07 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[TRAUMA]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/?p=127</guid>
		<description><![CDATA[18 TRAUMATIC BRAIN INJURY
J. Paul Elliott M.D., Sanjay Misra M.D.

1. Is traumatic brain injury (TBI) a common problem? 
	Show answer
Yes. In the United States, 1 in 12 deaths is due to injury. One third of traumatic deaths are associated with TBI. Of deaths resulting from motor vehicle accidents, 60% are due to brain injury. Even [...]]]></description>
			<content:encoded><![CDATA[<p><strong>18 TRAUMATIC BRAIN INJURY<br />
J. Paul Elliott M.D., Sanjay Misra M.D.</strong></p>
<blockquote><p>
<strong>1. Is traumatic brain injury (TBI) a common problem? </strong></p></blockquote>
<p>	Show answer<br />
Yes. In the United States, 1 in 12 deaths is due to injury. One third of traumatic deaths are associated with TBI. Of deaths resulting from motor vehicle accidents, 60% are due to brain injury. Even more common is minor TBI, which accounts for 75% of admissions for head trauma.</p>
<p><span id="more-127"></span></p>
<blockquote><p><strong>2. What is a concussion? </strong>	</p></blockquote>
<p>Show answer<br />
The relatively common occurrence of transient loss of neurologic function without macroscopic brain abnormality. Concussion is on one end of a spectrum that extends to coma. The Glasgow Coma Scale (GCS) score is used to categorize brain injuries as follows: mild, 14-15; moderate, 9-13; and severe, ≤ 8.</p>
<blockquote><p><strong>3. How is the GCS score derived?</strong> </p></blockquote>
<p>	Show answer<br />
The GCS is a means of identifying change in neurologic status. Its principal strengths are ease of use and reproducibility among observers. It is a 15-point scale; 15 is the best score, and 3 is the worst. The score is derived from the addition of the three individual components: best eye-opening response (1-4 points), best verbal response (1-5 points), and best motor response (1-6 points). The GCS is insensitive to pupillary response and focality. A patient with a perfect score of 15 may have hemiparesis and a life-threatening lesion.</p>
<blockquote><p><strong>4. When should a neurosurgeon be consulted?</strong></p></blockquote>
<p> 	Show answer<br />
For patients with loss of consciousness and subsequent neurologic abnormality or abnormality on computed tomography (CT) scan. These patients usually but not always have a GCS score ≤ 13.</p>
<blockquote><p><strong>5. How does one initially assess the brain-injured patient? </strong>	</p></blockquote>
<p>Show answer<br />
Just like any trauma patient. The first steps are assessment of the ABCs (airway, breathing, circulation) and rapid physiologic resuscitation. The neurologic examination is crucial. The initial examination includes (1) level of consciousness, (2) pupillary examination, and (3) motor examination. Repetition of the neurologic examination is also crucial. If deterioration is missed and appropriate treatment is not initiated quickly, irreversible brain injury may result. Finally, watch for concurrent cervical spine injury.</p>
<blockquote><p><strong>6. What takes priority in a hypotensive patient with TBI?</strong> </p></blockquote>
<p>	Show answer<br />
Hypotension in patients with head injury frequently accompanies other injuries. Do not assume that hypotension is due to the brain injury alone. Hypotension resulting from brain injury is a terminal event.</p>
<blockquote><p><strong>7. What is the significance of anisocoria in a patient with a decreased level of consciousness? </strong></p></blockquote>
<p>	Show answer </p>
<p>Anisocoria (unequal pupils) is a true neurologic emergency. Commonly a mass lesion (e.g., subdural or epidural hematoma, contusion, or diffuse swelling of one hemisphere) leads to uncal herniation and stretching of the ipsilateral third nerve. Time is crucial. Give mannitol, get a CT scan, and proceed with surgical decompression (if possible).</p>
<blockquote><p><strong>8. What if the larger pupil is reactive? 	</strong></p></blockquote>
<p>Show answer<br />
If the larger pupil is reactive, the third cranial nerve is functioning. Think of Horner&#8217;s syndrome (miosis, ptosis, and anhydrosis) on the other side. This syndrome may be due to injury to the sympathetic nerves traveling with the carotid artery in the neck. Consider evaluation (angiography) for a carotid dissection.</p>
<blockquote><p><strong>9. Are terms such as semicomatose nonsense?</strong> </p></blockquote>
<p>	Show answer<br />
Yes. Patients are alert (like medical students and surgeons), lethargic (like internists, in whom arousal is maintained by verbal interaction), obtunded (like hospital administrators, who require constant mechanical stimulation to maintain arousal), or comatose (like most deans, in whom neither verbal nor mechanical stimulation elicits arousal). Change in level of consciousness is often the first sign of increasing intracranial pressure (ICP); it is also the most poorly documented part of the neurologic examination. Document all findings!</p>
<blockquote><p><strong>10. How is motor response tested? </strong>	</p></blockquote>
<p>Show answer<br />
Ascertain the ability to follow commands by asking the patient to hold up fingers and move his or her arms and legs. If the patient does not follow commands (he or she may be a dean), test response to painful central stimulus. Localization of painful stimulus is confirmed by the patient&#8217;s hand reaching toward a sternal rub. The patient may be in even bigger trouble if in response to pain he or she exhibits flexor posturing (decorticate), extensor posturing (decerebrate), or no response. Flexor posturing indicates a high brainstem injury, and extensor posturing is associated with low brainstem dysfunction. The patient with no motor response may have a cervical spine injury.</p>
<blockquote><p><strong>11. What is the significance of periorbital ecchymosis (raccoon eyes) and ecchymosis over the mastoid (Battle&#8217;s sign)? </strong>	</p></blockquote>
<p>Show answer<br />
In the absence of direct trauma to the eyes or mastoid regions, periorbital ecchymosis and ecchymosis over the mastoid are reliable signs of basilar skull fractures. Of patients with basilar skull fractures, 10% have cerebrospinal fluid (CSF) leaks, including rhinorrhea or otorrhea. Persistent CSF leaks are associated with meningitis.</p>
<blockquote><p><strong>12. Should scalp lacerations be explored in the emergency department?</strong> </p></blockquote>
<p>	Show answer<br />
Yes-but gently. You want to know whether there is an underlying fracture. A laceration over a linear nondisplaced fracture can be cleaned and closed. If CSF or brain tissue is evident in the wound or if a depressed fracture is identified, surgical intervention is required to debride the wound and to close any dural tears. If you are worried, get a head CT scan.</p>
<blockquote><p><strong>13. Which patients need CT scans of the head? </strong></p></blockquote>
<p>	Show answer<br />
The CT scan is used partly as a triage tool with minor brain injuries and can be cost-effective compared with admission to the intensive care unit for observation. Conversely, patients with focality on examination do not proceed to the operating room without a CT scan.</p>
<blockquote><p><strong>14. What are the common traumatic surgical lesions?</strong></p></blockquote>
<p> 	Show answer<br />
If the ventricles are large (ventriculomegaly), a ventriculostomy can drain excessive CSF. Epidural hematomas (from arterial bleeding), subdural hematomas (from venous bleeding), and intraparenchymal hematomas with significant mass effect should be surgically evacuated. A depressed skull fracture or foreign body (e.g., a bullet) also requires a trip to the operating room.</p>
<blockquote><p><strong><br />
15. When is ICP monitoring indicated?</strong> </p></blockquote>
</blockquote>
<p>	Show answer<br />
When the neurologic examination becomes insensitive (when the patient is unconscious) to changes in ICP. It also may be indicated when there is known brain injury and the patient will be under general anesthesia for a surgical procedure for an extended period.</p>
<blockquote><p><strong>16. Describe the initial treatment of patients with a suspected increase in ICP.</strong> </p></blockquote>
<p>	Show answer<br />
The brain, similar to every other organ, must have adequate blood flow and oxygen delivery. The ABCs come first. Systolic blood pressures < 90 mmHg and Pao2 < 60 mmHg are correlated significantly with poor outcomes in patients with TBI. Keep the systolic blood pressure > 100 mmHg and avoid hypoxia.</p>
<blockquote><p><strong>17. Should all patients with elevated ICP be hyperventilated? 	</strong></p></blockquote>
<p>Show answer<br />
Decreasing the Pco2 is the most rapidly effective treatment for elevated ICP. The goal is usually a Pco2 of 30-35 mmHg. Any patient with a depressed level of consciousness and inability to protect the airway should be intubated. Before a CT scan is obtained, patients thought to have a mass lesion by neurologic examination should be hyperventilated until definitive treatment is achieved. Avoid chronic hyperventilation, which can cause ischemic brain injury.</p>
<blockquote><p><strong>18. In hemodynamically stable patients, how do you decrease ICP? </strong>	</p></blockquote>
<p>Show answer<br />
Mannitol, 1 g/kg, as an IV bolus. Also be sure the cervical collar is not obstructing venous outflow through the jugular system.<br />
<em><strong>KEY POINTS: INDICATIONS FOR BLOOD TRANSFUSION IN THE TRAUMA BAY</strong></p>
<p>   1. An unstable adult patient who does not respond to 2 L of &#8220;wide open&#8221; crystalloid infusion should receive uncrossed, O-negative packed red cells.<br />
   2. For pediatric patients, give 20 mL/kg of lactate Ringer&#8217;s by bolus; then repeat if necessary.<br />
   3. If the pediatric patient does not respond to lactate Ringer&#8217;s, proceed to transfuse 10 mL/kg uncrossed, O-negative packed red cells.<br />
   4. Do not wait for type-specific blood in the unstable patient who is not responding to crystalloid resuscitation.</em></p>
<blockquote><p><strong>19. What is the end point of diuresis?</strong></p></blockquote>
<p> 	Show answer<br />
Serum sodium of 150 mEq/L and serum osmolarity of 320 mOsm are usually the upper limits of diuresis. Blood volume should be maintained with colloids to help form an osmotic gradient between the extravascular and the intravascular spaces. Anticipate intravascular hypovolemia, and treat with colloids and blood products as necessary.<br />
<</p>
<blockquote><p>strong>20. What is the significance of cerebral perfusion pressure (CPP)?</strong></p></blockquote>
<p> 	Show answer<br />
CPP is the difference between mean arterial pressure (MAP) and ICP:</p>
<p>CPP = MAP &#8211; ICP</p>
<p>CPP is important. Neurologic outcome is best in patients with CPPs in the 60s-70s. Some patients require treatment with pressors to maintain the CPP; if CPP is < 60 mmHg, you may be creating a dean.</p>
<blockquote><p><strong>21. Why should all children with TBI be undressed and examined thoroughly? </strong></p></blockquote>
<p>	Show answer<br />
Half of children suffering nonaccidental trauma (child abuse) have TBI.</p>
<blockquote><p><strong>22. Should posttraumatic seizures be treated prophylactically?</strong> </p></blockquote>
<p>	Show answer<br />
Patients with brain parenchymal abnormalities on CT scan after head injury may benefit from 1 week of antiseizure prophylaxis. Early seizures can increase the metabolic demand of the injured brain and adversely affect ICP. Of patients who have seizures within the first 7 days of injury, 10% also have late seizures. Prevention of early seizures does not reduce the incidence of late seizures, however.</p>
<blockquote><p><strong>23. Which coagulopathy is associated with severe brain injury?</strong> </p></blockquote>
<p>	Show answer<br />
Disseminated intravascular coagulation. The presumed mechanism is massive release of thromboplastin from the injured brain into the circulation. The serum levels of fibrin degradation products roughly correlate with the extent of brain parenchymal injury. All severely brain-injured patients should be evaluated with prothrombin time, partial thromboplastin time, platelet counts, and fibrinogen levels.</p>
<blockquote><p><strong>24. What other medical complications may result from severe head injury?</strong> 	</p></blockquote>
<p>Show answer<br />
Diabetes insipidus (DI) secondary to the inadequate secretion of antidiuretic hormone is caused by injury to the pituitary or hypothalamic tracts. The kidney is unable to decrease free water loss. Usually the urine output is > 200 mL/hr, and the urine specific gravity is < 1.003. The serum sodium may rise precipitously if DI is not treated promptly. The treatment of choice in trauma is IV infusion of synthetic vasopressin (Pitressin), which has a 20-minute half-life and can be titrated to produce the appropriate urine output. Because most trauma-induced DI is self-limited, long-term 1-deamino-8-d-arginine vasopressin (DDAVP), which has a 12-hour half-life, is not necessary.</p>
<blockquote><p><strong>25. If a patient is awake with significant neurologic symptoms but no abnormality on CT scan, what are the likely explanations?</strong></p></blockquote>
<p> 	Show answer<br />
A spinal cord injury or carotid or vertebral artery dissection.</p>
<blockquote><p><strong>26. Are gunshot wounds that cross the midline of the brain uniformly fatal?</strong></p></blockquote>
<p> 	Show answer<br />
No (although such a wound killed Lincoln). The tract that the bullet takes is important, but so is the energy that it imparts to the brain.</p>
<blockquote><p><strong>27. What is the significance of concussion?</strong> </p></blockquote>
<p>	Show answer<br />
In most studies of minor TBI, > 50% of patients have complaints of headache, fatigue, dizziness, irritability, and alterations of cognition and short-term memory. It is important to alert the patient to the likelihood of developing these symptoms. The neurobehavioral problems significantly affect patients&#8217; lives. The symptoms usually resolve within 3-6 months after injury.</p>
<blockquote><p><strong>28. Can patients with minor TBIs be discharged from the emergency department?</strong></p></blockquote>
<p> 	Show answer<br />
Patients whose examination (including short-term memory) returns to normal and who have a normal head CT scan can be discharged to home if they are accompanied by a responsible person.</p>
<blockquote><p><strong>29. Is brain injury permanent? Is the outcome always poor?</strong></p></blockquote>
<p> 	Show answer<br />
No and no. Brain injury occurs in two phases. The primary injury occurs at the moment of impact. Secondary injury is preventable and treatable. Examples include hypoxia, hypotension, elevated ICP, and decreased perfusion to the brain secondary to ischemia, brain swelling, and expanding mass lesions. Rapid surgical management and avoidance of secondary injury improve outcome. Although previously it was believed that the brain was not capable of repair, it is now clear that neuronal repair and reorganization occur after injury.</p>
<p><strong>References</strong><br />
WEB SITES</p>
<p>  <a href="http://www.acssurgery.com/abstracts/acs/acs0501.htm"> 1. http://www.acssurgery.com/abstracts/acs/acs0501.htm</a><br />
   <a href="http://www.surgery.ucsf.edu/eastbaytrauma/Protocols/ER%20protocol%20pages/closedheadinjury.htm">2. http://www.surgery.ucsf.edu/eastbaytrauma/Protocols/ER%20protocol%20pages/closedheadinjury.htm</a><br />
  <a href="http://www.ascsurgery.com/abstracts/acs/acs0612.htm"> 3. http://www.ascsurgery.com/abstracts/acs/acs0612.htm</a></p>
<p>BIBLIOGRAPHY<br />
1. Brain Trauma Foundation: Management and Prognosis of Severe Traumatic Brain Injury. New York, Brain Trauma Foundation, 2000. Available at www.braintrauma.org.<br />
2. Mazzola CA, Adelman PD: Critical care management of head trauma in children. Crit Care Med 30:S393-S401, 2002.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=12528780&#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=12528780">Similar articles</a><br />
3. Narayan RK, Michel ME, Ansell B, et al: Clinical trials in head injury. J Neurotrauma 19:503-557, 2002. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=12042091&#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=12042091">Similar articles</a> <a href="http://dx.doi.org/10.1097/00004045-200208000-00007">Full article</a><br />
4. Narayan RK, Wilberger JE, Povlishock JT: Neurotrauma. New York, McGraw-Hill, 1996. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=12042091&#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=12042091">Similar articles </a><a href="http://dx.doi.org/10.1097/00004045-200208000-00007">Full article</a><br />
5. Shaw NA: The neurophysiology of concussion. Prog Neurobiol 67:281-344, 2002. </p>
]]></content:encoded>
			<wfw:commentRss>http://surgeryprocedure.info/trauma/traumatic-brain-injury/feed</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Risks Of Bloodborne Disease</title>
		<link>http://surgeryprocedure.info/health-care/risks-of-bloodborne-disease</link>
		<comments>http://surgeryprocedure.info/health-care/risks-of-bloodborne-disease#comments</comments>
		<pubDate>Tue, 14 Jul 2009 17:34:02 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[HEALTH CARE]]></category>

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

 	Show answer
In developed nations with mature blood banking systems, by far the most common transfusion-acquired infections are hepatitis from the hepatitis B (HBV) and C (HCV) viruses. Other less commonly transmitted agents include the [...]]]></description>
			<content:encoded><![CDATA[<p><strong>101 RISKS OF BLOODBORNE DISEASE<br />
Caesar M. Ursic M.D., Doru I. E. Georgescu M.D.</strong></p>
<blockquote><p><strong>1. What infectious diseases are transmissible via blood transfusion?</strong></p></blockquote>
<p><span id="more-487"></span><br />
 	Show answer<br />
In developed nations with mature blood banking systems, by far the most common transfusion-acquired infections are hepatitis from the hepatitis B (HBV) and C (HCV) viruses. Other less commonly transmitted agents include the human immunodeficiency virus (HIV) and cytomegalovirus (CMV). Even rarer but still occasionally reported bloodborne infections are parasitic diseases such as malaria (genus, Plasmodium), babesiosis (genus, Babesium), Chagas disease (Trypanasoma cruzi), toxoplasmosis (Toxoplasma gondii), the lymphomas and leukemias caused by the human T-cell lymphotropic virus (HTLV-I), and infectious mononucleosis (Epstein-Barr virus). Bacterial contaminations are also rare but possible, especially in platelet preparations that are stored at room temperature. This may result in a toxic shock-like syndrome, the risk of which has been estimated as equivalent to the risk of HIV transmission.</p>
<blockquote><p><strong>2. What are the estimated risks of HBV, HCV, and HIV transmission by blood transfusion in the United States? 	</strong></p></blockquote>
<p>Show answer </p>
<p><img src="http://surgeryprocedure.info/http://surgeryprocedure.info/wp-content/uploads/2009/07/411.jpg" alt="4" title="4" width="716" height="100" class="alignright size-full wp-image-488" /></p>
<blockquote><p><strong>3. Which bloodborne pathogens pose a risk to surgeons? </strong> </p></blockquote>
<p>	Show answer<br />
Although the epidemic of HIV has increased general concern about bloodborne pathogens, the prevalence of hepatitis C virus (HCV) throughout North America has led to a shift of emphasis from HIV to hepatitis. Hepatitis B is an occupational risk in surgery, but vaccinations and a relatively efficient post-exposure protocol have reduced the consequences of contamination with HBV. Surgeons in the United States care for more patients with chronic hepatitis C than with chronic hepatitis B, and no vaccine is available for HCV infection. Although the rate of seroconversion for hepatitis C is 10% versus 30% for hepatitis B, when acute infection occurs, there is a much higher chance of developing chronic hepatitis (50% versus 10%) after HCV infection. Thus, HCV infection is the greatest threat to surgeons.</p>
<blockquote><p><strong>4. What is the risk to health care workers of exposure to HBV? </strong></p></blockquote>
<p>	Show answer<br />
The number of new infections in 2001 has dropped to approximately 78,000 from the estimated yearly incidence of 260,000 in the 1980s. At present, 1.25 million U.S. residents have chronic hepatitis B, with the highest prevalence occurring among 20-49-year-old individuals. Thirty percent of percutaneous hollow needle exposures are followed by acute infection. Thirty percent of hepatitis B cases are clinically occult, and ≤ 10% of infected people remain viral carriers for life. Many carriers are asymptomatic and suffer no active liver disease, although they are potentially infectious to others. Twenty-five percent of HBV-infected individuals eventually die from hepatic diseases.</p>
<blockquote><p><strong>5. What is the risk to health care workers of exposure to HCV?</strong></p></blockquote>
<p> 	Show answer<br />
The number of new infections in 2001 was 25,000, down from 240,000 per year in the 1980s. Currently, 3.9 million (1.8%) U.S. residents have HCV infection, of whom 2.7 million are infected chronically. The risk of seroconversion from a percutaneous hollow needle injury is 10%, but 90% of acute infections result in the chronic carrier state, which is typically asymptomatic. Although these data are still controversial, 50% of HCV infected patients will develop cirrhosis, and 50% of these patients will develop a hepatoma.</p>
<blockquote><p><strong>6. What is the risk to health care workers of exposure to HIV?</strong> </p></blockquote>
<p>	Show answer<br />
The risk of HIV seroconversion after percutaneous inoculation with HIV-contaminated blood is approximately 0.3%. Risk of infection also appears to be greater when the source of the blood is a terminally or severely ill patient. The U.S. Centers for Disease Control and Prevention (CDC) reports that 57 health care workers in the U.S. have been documented as seroconverting to HIV as a result of an occupational exposure to the virus. The majority of these individuals were either nurses (n = 24) or laboratory workers (n = 19); physicians accounted for only six of these cases. The routes of infection were percutaneous (puncture or cutting wounds) in 84% of the cases. Thus, the risk appears small relative to the large number of exposures that have probably occurred since the onset of the epidemic in the early 1980s. The CDC also reports that as of January 1, 1998, there has been no documented transmission of HIV infection from a patient to a surgeon secondary to occupational exposure.</p>
<blockquote><p><strong>7. How well does hepatitis B vaccination protect against the disease?</strong></p></blockquote>
<p> 	Show answer<br />
Effective protection against hepatitis B correlates positively with post-immunization anti-hepatitis B surface antibody (anti-HBs) serum titers of ≥ 10 mIU/mL. These titers are achieved in 95% of young, healthy recipients of the standard three-dose immunization regimen, and the actual protective efficacy (i.e., ability of the vaccine to prevent the disease) is estimated to approach 100% in these individuals. Although about 50% of successfully vaccinated adults demonstrate a decrease in their anti-HBs levels to nondetectable levels by 10 years, continued immunologic protection is thought to persist via the amnestic humoral response. Because of the persistence of this &#8220;immune memory&#8221; to the viral antigen, healthy individuals appear to enjoy lifelong protection after vaccination and do not require booster doses. A bivalent vaccine immunizing against both hepatitis A and B was approved in 2001 by the U.S. Food and Drug Administration for individuals 18 years of age and older, and it is as successful as the monovalent vaccine in conferring protection from the HBV infection with the added benefit of protecting against hepatitis A viral infection.</p>
<blockquote><p><strong>8. Are patients at risk of infection from surgeons who are infected with HBV? </strong></p></blockquote>
<p>	Show answer<br />
Transmission of hepatitis B infection from surgeons to patients has been documented. Surgeons who are at risk for transmitting infection to patients are generally positive for the e-antigen of hepatitis B. The e-antigen is a degradation product of the nucleocapsid of the virus and represents active viral replication within the liver. People who test positive for the e-antigen have high viral titers and are quite infectious. The large number of documented transmissions of HBV to patients by surgical providers is particularly troublesome and may require restriction of clinical privileges. Furthermore, a recent report from England documented transmission of HBV infection from surgeons to patients even when the surgeon was negative for the e-antigen.</p>
<blockquote><p><strong>9. What is the proper response after percutaneous exposure to a patient with known hepatitis B? </strong>	</p></blockquote>
<p>Show answer<br />
This depends on the provider&#8217;s vaccination status. Older individuals show a tendency to mount a weaker or delayed immunologic response as measured by peak serum titers of anti-HBs. If the provider has been vaccinated and has a positive antibody titer, no additional response is necessary. If the provider has not been vaccinated and is negative for antibodies to HBV or if the provider completed the series of vaccinations but exhibited a weak or absent antibody titer, then he or she should receive a dose of hepatitis B immunoglobulin and begin the hepatitis B vaccination series. For surgeons who were successfully immunized against HBV in the past, neither routine booster doses nor routine immunity status surveillance is recommended.</p>
<blockquote><p><strong>10. What are the recommendations for hepatitis C immunization?</strong> </p></blockquote>
<p>	Show answer<br />
There is currently no effective vaccine available against HCV. Immunoglobulin for HCV does not confer protection. Using universal barrier precautions remains the best strategy.</p>
<blockquote><p><strong>11. Does laparoscopic surgery minimize the risk of HIV contamination?</strong></p></blockquote>
<p> 	Show answer<br />
The laparoscopic technique reduces exposure to blood products and sharp instruments; however, the risks are different. The evacuation of the pneumoperitoneum during laparoscopic procedures releases aerosolized HIV-infected blood and peritoneal fluid into the operative suite. Evacuation of the pneumoperitoneum into a closed system diminishes this exposure.</p>
<blockquote><p><strong>12. Is double gloving an effective method of protection?</strong> 	</p></blockquote>
<p>Show answer<br />
Although double gloving may not prevent percutaneous injury, it clearly reduces blood exposure. The contact rates between blood and the surgeon&#8217;s skin are decreased by 70% when the surgeon wears two pairs of gloves. Whereas outer glove perforation occurs in 25% of cases, inner glove perforation occurs in only 10% of cases (surgeons, 8.7%; assistants, 3.7%). The longer the procedure, the more frequent are inner glove perforations. The nondominant index finger is the most common target.</p>
<blockquote><p><strong>13. Are eye splash injuries a major threat to surgeons? 	</strong></p></blockquote>
<p>Show answer<br />
A CDC study demonstrated that approximately 13% of documented HIV transmissions occurred by mucocutaneous contact. Eye splash injuries during surgery are often underestimated, although they are the easiest type of contact to prevent. A recent study examined 160 eye shields used by surgeons and assistants. All operations lasted ≥ 30 minutes. The shields were inspected for macroscopic splashes and then tested for microscopic splashes. Forty-four percent of the shields tested positive for blood. The surgeon was aware of a spray in only 8% of cases. The splashes were macroscopically visible in only 16% of cases. The risk of eye splashes was higher for surgeons than for assistants and increased with the length of the operation. The type of operation also proved to be a determining factor; vascular surgery and orthopedic surgery had the higher risks for eye splash injuries. Eye protection should be mandatory.</p>
<blockquote><p><strong>14. What is the surgeons&#8217; rate of exposure to blood and body fluids?</strong></p></blockquote>
<p> 	Show answer<br />
Percutaneous blood exposure occurs in 1.2-5.6% of surgical cases and mucocutaneous blood contact in 6.4-50.4%. The discrepancy among reported rates reflects differences in data collection, procedures performed, surgical technique, and degree of precautions. No health care worker has ever been infected through exposure of intact skin to blood and body fluids. However, transmission of HIV after mucocutaneous contact with HIV-infected blood has been reported. The risk of contamination is real for all personnel in the operating room, but it is much higher for surgeons and first assistants, who account for 80% of all body contamination and 65% of injuries.</p>
<blockquote><p><strong>15. Again, what are the seroconversion rates for HIV and HBV exposure?</strong> 	</p></blockquote>
<p>Show answer<br />
Seroconversion rates from a hollow needle stick are 0.3% for HIV and 30% for HBV.</p>
<blockquote><p><strong>16. What is the lifetime occupational risk of HIV infection for surgeons?</strong> </p></blockquote>
<p>	Show answer </p>
<p>The risk of HIV infection for a surgeon can be calculated by obtaining the product of HIV seroprevalence in surgical patients (0.32-50.00%), percutaneous injury rate (1.2-6.0%), and seroconversion rate (0.29-0.50%). The calculated risk per case of acquiring HIV ranges from 0.11 per million to 66 per million. Assuming that a surgeon performs 350 operations per year over a 30-year career, the estimated lifetime cumulative risk ranges from 0.12% to 50.0%, depending on the variables. Several assumptions are inherent in this calculation:</p>
<p>    * The formula assumes a constant HIV prevalence, but it is estimated that the prevalence increases by 4.0-8.6% annually in the United States.<br />
    * The formula assumes that exposure to HIV-infected blood occurs only through percutaneous injuries, disregarding the risk caused by mucocutaneous exposure.<br />
    * The formula assumes that whereas every operation carries the same risk, the risk varies with the length of procedure and amount of blood loss.<br />
    * The formula assumes that the risk per case is the same for a trauma surgeon in center city Detroit and a plastic surgeon in Beverly Hills.</p>
<p>Clearly, these assumptions are imprecise.</p>
<blockquote><p><strong>17. Are there effective methods to reduce the risk of transmission of bloodborne diseases to surgeons?</strong> </p></blockquote>
<p>	Show answer<br />
For HBV infection, in addition to universal precautions, a highly effective vaccine is available, but it is not used as much as it should be. Most surgeons who are 45 years or older have not been vaccinated. A precisely defined postexposure protocol is also available. For HCV and HIV infections, the most pragmatic approach is to lower the rate of percutaneous and mucocutaneous injuries by observing barrier precautions and using safe surgical technique.<br />
Finally, prompt response to blood exposure is required. Contamination of the hands or arms is best dealt with by immediate rescrubbing. If this is not practical, the area should be irrigated with povidone iodine, and rescrubbing should be accomplished soon thereafter.</p>
<p><strong>References</strong><br />
BIBLIOGRAPHY<br />
1. Barrie PS, Patchen Dellinger E, Dougherty SH, Fink MP: Assessment of hepatitis B virus immunization status among North American surgeons. Arch Surg 129:27-32, 1994.<br />
2. Bell DM: Occupational risk of human immunodeficiency virus infection in healthcare workers: An overview. Am J Med 102(suppl 5B):81S-85S, 1997.<br />
3. Cardo DM, Culver DH, Ciescielski CA, et al: A case-control study of HIV seroconversion in healthcare workers after percutaneous exposure. N Engl J Med 337:1485-1490, 1997. Medline <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=9366579">Similar articles </a><a href="http://dx.doi.org/10.1056/NEJM199711203372101">Full article</a><br />
4. Dodd RY, Notari EP, Stramer SL: Current prevalence and incidence of infectious disease markers and estimated window-period risk in the American Red Cross blood donor population. Transfusion 42:975-979, 2002. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=12385406&#038;dopt=Abstract">Medline</a> Similar articles <a href="http://dx.doi.org/10.1046/j.1537-2995.2002.00174.x">Full article</a><br />
5. Eubanks S, Newman L, Lucas G: Reduction of HIV transmission during laparoscopic procedures. Surg Laparosc Endosc 3:2-5, 1993.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=8258065&#038;dopt=Abstract"> Medline </a><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=8258065">Similar articles</a><br />
6. Fry DE: Blood-borne diseases in 1998. Bull Am Coll Surg 83:13-18, 1998.<br />
7. Gerberding JL: Reducing occupational risk of HIV infection. Hosp Pract 113-110, 115-118, 1991.<br />
8. Klein HG: Allogenic transfusion risks in the surgical patient. Am J Surg 317:242-245, 1995.<br />
9. Koff RS: Hepatitis A, hepatitis B, and combination hepatitis vaccines for immunoprophylaxis: An update. Digest Dis Sci 47:1183-1194, 2002. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=12064790&#038;dopt=Abstract">Medline </a><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=12064790">Similar articles</a> Full article<br />
10. Lin EY, Brunicardi C: HIV infection and surgeons. World J Surg 18:753-757, 1994. Medline <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=7975695">Similar articles </a><a href="http://dx.doi.org/10.1007/BF00298922">Full article</a><br />
11. Marasco S, Woods S: The risk of eye splash injuries in surgery. Aust N Z J Surg 68:785-787, 1998. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9814742&#038;dopt=Abstract">Medline </a><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=9814742">Similar articles</a><br />
12. Megan J, Patterson M, Novak CB, et al: Surgeons&#8217; concern and practices of protection against bloodborne pathogens. Ann Surg 228:266-272, 1998.<br />
13. Pietrabissa A, Merigliano S, Montorsi M, et al: Reducing the occupational risk of infections for the surgeons: Multicentric national survey on more than 15,000 surgical procedures. World J Surg 21:573-578, 1997.<a href="http://dx.doi.org/10.1007/s002689900275"> Full article</a><br />
14. Schreiber GB, Busch MP, Kleinman SH, et al: The risk of transfusion-transmitted viral infections: The retrovirus epidemiology donor study. N Engl J Med 334:1685-1690, 1996. Medline Similar articles Full article<br />
15. Szmuness W, Stevens CE, Harley EJ, et al: Hepatitis B vaccine: Demonstration of efficacy in a controlled clinical trial in a high-risk population in the United States. N Engl J Med 303:833-841, 1980. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=6997738&#038;dopt=Abstract">Medline </a><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=6997738">Similar articles</a></p>
]]></content:encoded>
			<wfw:commentRss>http://surgeryprocedure.info/health-care/risks-of-bloodborne-disease/feed</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Why Get Arterial Blood Gases?</title>
		<link>http://surgeryprocedure.info/general-topics/why-get-arterial-blood-gases</link>
		<comments>http://surgeryprocedure.info/general-topics/why-get-arterial-blood-gases#comments</comments>
		<pubDate>Mon, 06 Jul 2009 20:05:02 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[GENERAL TOPICS]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/?p=43</guid>
		<description><![CDATA[6 WHY GET ARTERIAL BLOOD GASES?
Alden H. Harken M.D.
1. Is breathing really overrated? 
	Show answer
It may be. A Japanese yoga master survived just fine breathing once per minute for an hour (see reference 1)!
2. Mr. O&#8217;Flaherty has just undergone an inguinal herniorrhaphy under local anesthesia. The recovery room nurse asks permission to sedate him. She [...]]]></description>
			<content:encoded><![CDATA[<p><strong>6 WHY GET ARTERIAL BLOOD GASES?<br />
Alden H. Harken M.D.</strong></p>
<blockquote><p><strong>1. Is breathing really overrated?</strong> </p></blockquote>
<p>	Show answer<br />
It may be. A Japanese yoga master survived just fine breathing once per minute for an hour (see reference 1)!</p>
<blockquote><p><strong>2. Mr. O&#8217;Flaherty has just undergone an inguinal herniorrhaphy under local anesthesia. The recovery room nurse asks permission to sedate him. She says that he is confused and unruly and keeps trying to get out of bed. Is it safe to sedate Mr. O&#8217;Flaherty? </strong>	</p></blockquote>
<p>Show answer<br />
No. A confused, agitated patient in the recovery room or surgical intensive care unit (SICU) must be recognized as acutely hypoxemic until proved otherwise.</p>
<blockquote><p><strong>3. Mr. O&#8217;Flaherty is moved to the SICU, and at 2:00 a.m. the SICU nurse calls to report that he has a Po2 of 148 mmHg on facemask oxygen. Is it okay to roll over and go back to sleep? </strong>	</p></blockquote>
<p><span id="more-43"></span><br />
Show answer<br />
No. More information is needed.</p>
<blockquote><p><strong>4. You glance at the abandoned cup of coffee sitting on your well-worn copy of Surgical Secrets. What is the Po2 of that cup of coffee?</strong> </p></blockquote>
<p>	Show answer<br />
148 mmHg.</p>
<blockquote><p><strong>5. How can Mr. O&#8217;Flaherty and the coffee have the same Po2? </strong>	</p></blockquote>
<p>Show answer<br />
The abandoned coffee presumably has had time to equilibrate completely with atmospheric gas. At sea level, the barometric pressure is 760 mmHg. To obtain the partial pressure of oxygen in the coffee, subtract water vapor pressure (47 mmHg) and multiply by the concentration of oxygen (20.8%) in the atmosphere:</p>
<p><strong>PO2 = (760-47) x 20.8% &#8211; 148 mmHg</strong></p>
<blockquote><p>
<strong>6. What is the difference between Mr. O&#8217;Flaherty&#8217;s and the coffee&#8217;s Po2? </strong>	</p></blockquote>
<p>Show answer<br />
Nothing. Both represent the partial pressure of oxygen in fluid. A complete set of blood gases is necessary.</p>
<blockquote><p><strong>7. What constitutes a complete set of blood gases? 	</strong></p></blockquote>
<p>Show answer </p>
<p>    * Po2<br />
    * Pco2<br />
    * pH<br />
    * Hemoglobin saturation<br />
    * Hemoglobin concentration</p>
<blockquote><p><strong>8. If Mr. O&#8217;Flaherty and the coffee have the same Po2, how would Mr. O&#8217;Flaherty do if he were exchange-transfused with coffee? </strong></p></blockquote>
<p>	Show answer<br />
Badly.</p>
<blockquote><p><strong>9. Why?</strong> 	</p></blockquote>
<p>Show answer<br />
Although the oxygen tensions are the same, the amount of oxygen in blood is vastly greater.</p>
<blockquote><p><strong>10. How does one quantitate the amount of oxygen in blood? </strong>	</p></blockquote>
<p>Show answer<br />
Arterial oxygen content (CaO2) is quantitated as mL of oxygen/100 mL of blood. (Watch out: Almost all other concentrations traditionally are provided per mL or per L-not per 100 mL.) Because mL of oxygen is a volume in 100 mL of blood, these units frequently are abbreviated as vol %.</p>
<blockquote><p><strong>11. Why is blood thicker than coffee (or wine)?</strong> </p></blockquote>
<p>	Show answer<br />
Because hemoglobin binds a huge <strong>amount</strong> of oxygen. A total of 10 g of fully saturated hemoglobin (hematocrit about 30%) binds 13.4 mL of oxygen, whereas 100 mL of plasma at a Po2 of 100 mmHg contains only 0.3 mL of oxygen.</p>
<blockquote><p><strong>12. Does the position of the oxyhemoglobin dissociation curve make any difference?</strong> </p></blockquote>
<p>	Show answer </p>
<p>    * An increase in Pco2<br />
    * An increase in hydrogen ion concentrations<strong> (not pH)</strong><br />
    * An increase in temperature</p>
<p>All shift the oxyhemoglobin curve to the right; that is, oxygen is released more easily in the tissues. Within physiologic limits, however, Mae West probably said it best: &#8220;There is less to this than meets the eye.&#8221;<br />
<em><strong>KEY POINTS: MEDIATORS OF OXYHEMOGLOBIN DISSOCIATION CURVE</strong></p>
<p><strong>Right Shift 	Left Shift</strong></p>
<p>   1. Increase in Pco2<br />
   2. Increase in [H+], lower pH<br />
   3. Increase in temperature stored<br />
   4. Increase in 2,3-DPG</p>
<p>   1. Decrease in [H+], higher pH<br />
   2. Higher altitudes/elevation<br />
   3. Decrease in 2,3-DPG (e.g., at 4 wk blood maintains no DPG)</em></p>
<blockquote><p><strong>13. If Cao2 or ultimately systemic oxygen delivery (cardiac output x Cao2) is what the surgeon really wants to know, why does the nurse report Mr. O&#8217;Flaherty&#8217;s Po2 instead of his Cao2 at 2:00 a.m.?</strong> </p></blockquote>
<p>	Show answer<br />
No one knows.</p>
<blockquote><p><strong>14. What is the fastest and most practical method of increasing Mr. O&#8217;Flaherty&#8217;s Cao2? </strong>	</p></blockquote>
<p>Show answer<br />
Transfusion of red blood cells. The patient&#8217;s Cao2 is increased by 25% with transfusion from a hemoglobin concentration of 8 to 10 g/dL. The patient&#8217;s arterial oxygen content is affected negligibly by an increase in arterial Po2 from 100 to 200 mmHg (hemoglobin is fully saturated in both instances).</p>
<blockquote><p><strong>15. What is a transfusion trigger?</strong></p></blockquote>
<p> 	Show answer </p>
<p>The hematocrit at which a patient is automatically transfused. This is not a useful concept. The NIH Consensus Conference, drawing data from Jehovah&#8217;s Witnesses, patients with renal failure, and monkeys concluded that it is not necessary to transfuse a patient until the hematocrit is 21%. Traditional surgical dogma mandates a hematocrit >30%. When the patient is in trouble, however, authorities in surgical critical care encourage transfusion to a hematocrit of 45% to optimize systemic oxygen delivery.</p>
<blockquote><p><strong>16. What governs respiratory drive?</strong></p></blockquote>
<p> 	Show answer<br />
Pco2 and pH are inextricably intertwined by the Henderson-Hasselbalch equation. By juggling this equation in the cerebrospinal fluid (CSF) of goats, it is clear that CSF hydrogen ion concentration (not Pco2) controls respiratory drive. This distinction is not clinically important, however. What is important is that if a person becomes acidotic either with diabetic ketoacidosis or by running up a flight of stairs, minute ventilation (VE) is increased.</p>
<blockquote><p><strong>17. How tight is respiratory control? Or, if you hold your breath for 1 minute, how much do you want to breathe</strong>?</p></blockquote>
<p> 	Show answer<br />
A lot (unless you are a yoga master approaching nirvana).</p>
<blockquote><p><strong>18. After 60 seconds of apnea, what happens to Paco2? </strong>	</p></blockquote>
<p>Show answer<br />
It increases only from 40 to 47 mmHg. Tiny changes in Pco2 (and pH) translate into a huge respiratory stimulus. Normally, respiratory compensation for metabolic acidosis is tight.</p>
<blockquote><p><strong>19. Define base excess. 	</strong></p></blockquote>
<p>Show answer<br />
Base excess is a poor man&#8217;s indicator of the metabolic component of acid-base disorders. After correcting the Pco2 to 40 mmHg, the base excess or base deficit is touted as an indirect measure of serum lactate. Although many parameters directing volume resuscitation in shock are more practical and direct (see Chapter 3), base deficit has been advertised as helpful. The base excess or deficit is calculated from the Sigaard-Anderson nomogram in the blood gas laboratory. Normally, there is no base excess or deficit. Acid-base status is &#8220;just right.&#8221;</p>
<p><strong>References</strong><br />
BIBLIOGRAPHY<br />
1. Dekerle J, Baron B, Dupont L, et al: Maximal lactate steady state, respiratory compensation threshold, and critical power. Eur J Appl Physiol 89:280-288, 2003.<br />
2. Miyamura M, Nishimura K, Ishida K, et al: Is a man able to breathe once a minute for an hour? The effect of yoga exercises on blood gases. Jpn J Physiol 52:313, 2002.<br />
3. Tada T, Hashimoto F, Matsushita Y, et al: Study of life satisfaction and quality of life of patients receiving home oxygen therapy. J Med Invest 50:55-63, 2003. </p>
]]></content:encoded>
			<wfw:commentRss>http://surgeryprocedure.info/general-topics/why-get-arterial-blood-gases/feed</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<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>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/top-search/queries-5</guid>
		<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>
			<content:encoded><![CDATA[<p><span id="more-566"></span>
<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>
<li><a href="http://surgeryprocedure.info/search/pilonoidal+sinus">pilonoidal sinus</a></li>
<li><a href="http://surgeryprocedure.info/search/gatorade+spleen">gatorade spleen</a></li>
<li><a href="http://surgeryprocedure.info/search/urinary+tract+surgery">urinary+tract+surgery</a></li>
<li><a href="http://surgeryprocedure.info/search/CHRONIC+INTESTIONAL+PSEUDOOBSTRUCTION">CHRONIC INTESTIONAL PSEUDOOBSTRUCTION</a></li>
<li><a href="http://surgeryprocedure.info/search/rocky+davis+incision">rocky davis incision</a></li>
<li><a href="http://surgeryprocedure.info/search/urinary+tract+trauma">urinary tract trauma</a></li>
<li><a href="http://surgeryprocedure.info/search/caput+medusae+dilated+veins">caput medusae dilated veins</a></li>
<li><a href="http://surgeryprocedure.info/search/spleen+injury+with+blood+behind+heart">spleen injury with blood behind heart</a></li>
<li><a href="http://surgeryprocedure.info/search/bleeding+caput+medusa">bleeding caput medusa</a></li>
<li><a href="http://surgeryprocedure.info/search/hernia+mesh+neuroma">hernia mesh neuroma</a></li>
<li><a href="http://surgeryprocedure.info/search/neuroma+hernia">neuroma+hernia</a></li>
<li><a href="http://surgeryprocedure.info/search/mesh+rejection">mesh rejection</a></li>
<li><a href="http://surgeryprocedure.info/search/emphysema+necessitans">emphysema necessitans</a></li>
<li><a href="http://surgeryprocedure.info/search/Infant+Testicle">Infant Testicle</a></li>
<li><a href="http://surgeryprocedure.info/search/blakemore+tube">blakemore+tube</a></li>
<li><a href="http://surgeryprocedure.info/search/spleen+injury">spleen injury</a></li>
</ul>
<p><!--more--></p>
]]></content:encoded>
			<wfw:commentRss>http://surgeryprocedure.info/top-search/queries-5/feed</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Queries 2</title>
		<link>http://surgeryprocedure.info/top-search/queries-2</link>
		<comments>http://surgeryprocedure.info/top-search/queries-2#comments</comments>
		<pubDate>Wed, 05 Aug 2009 07:03:41 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Uncategorized]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/?page_id=544</guid>
		<description><![CDATA[

Postoperative fever workup
opss sepsis 14 days
solitary pulmonary nodule breast cancer patient
honeymoon period bochdalek
relation between breathlessness and total thyroidectomy
colon surgery diverticulitis
Hematest-positive NGT
nonoperative management of spleen injury
when is the parental nutrion discontinued
grading for splenic laceration
having a solitary nodule with calcium flecks
how many milliequivalents in gatorade


]]></description>
			<content:encoded><![CDATA[<p><span id="more-544"></span>
<ul>
<li><a href="http://surgeryprocedure.info/search/Postoperative+fever+workup">Postoperative fever workup</a></li>
<li><a href="http://surgeryprocedure.info/search/opss+sepsis+14+days">opss sepsis 14 days</a></li>
<li><a href="http://surgeryprocedure.info/search/solitary+pulmonary+nodule+breast+cancer+patient">solitary pulmonary nodule breast cancer patient</a></li>
<li><a href="http://surgeryprocedure.info/search/honeymoon+period+bochdalek">honeymoon period bochdalek</a></li>
<li><a href="http://surgeryprocedure.info/search/relation+between+breathlessness+and+total+thyroidectomy">relation between breathlessness and total thyroidectomy</a></li>
<li><a href="http://surgeryprocedure.info/search/colon+surgery+diverticulitis">colon surgery diverticulitis</a></li>
<li><a href="http://surgeryprocedure.info/search/Hematest-positive+NGT">Hematest-positive NGT</a></li>
<li><a href="http://surgeryprocedure.info/search/nonoperative+management+of+spleen+injury">nonoperative management of spleen injury</a></li>
<li><a href="http://surgeryprocedure.info/search/when+is+the+parental+nutrion+discontinued">when is the parental nutrion discontinued</a></li>
<li><a href="http://surgeryprocedure.info/search/grading+for+splenic+laceration">grading for splenic laceration</a></li>
<li><a href="http://surgeryprocedure.info/search/having+a+solitary+nodule+with+calcium+flecks">having a solitary nodule with calcium flecks</a></li>
<li><a href="http://surgeryprocedure.info/search/how+many+milliequivalents+in+gatorade">how many milliequivalents in gatorade</a></ul>
</li>
<p><!--more--></p>
]]></content:encoded>
			<wfw:commentRss>http://surgeryprocedure.info/top-search/queries-2/feed</wfw:commentRss>
		<slash:comments>0</slash:comments>
		</item>
	</channel>
</rss>
