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	<title>SurgeryProcedure.info &#187; Search Results  &#187;  what is a fissurotomy</title>
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		<title>Anorectal Disease. Anal Fissure</title>
		<link>http://surgeryprocedure.info/abdominal-surgery/anorectal-disease-anal-fissure</link>
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		<description><![CDATA[ANAL FISSURE
14. What is the most common location for idiopathic anal fissure? 
	Show answer
90% are posterior, and 10% are anterior.
15. What are the most common symptoms of anal fissure? 
	Show answer
Tearing anal pain and bleeding with bowel movements.

16. What is the underlying pathophysiology of fissure in ano? 
	Show answer
Local trauma to the anal canal, internal [...]]]></description>
			<content:encoded><![CDATA[<p><strong>ANAL FISSURE</strong></p>
<blockquote><p><strong>14. What is the most common location for idiopathic anal fissure? </strong></p></blockquote>
<p>	Show answer<br />
90% are posterior, and 10% are anterior.</p>
<blockquote><p><strong>15. What are the most common symptoms of anal fissure?</strong> </p></blockquote>
<p>	Show answer<br />
Tearing anal pain and bleeding with bowel movements.<br />
<span id="more-277"></span></p>
<blockquote><p><strong>16. What is the underlying pathophysiology of fissure in ano? </strong></p></blockquote>
<p>	Show answer<br />
Local trauma to the anal canal, internal anal sphincter dysfunction, and ischemia.</p>
<blockquote><p><strong>17. What is the differential diagnosis for anal fissure, especially if atypical in location?</strong> </p></blockquote>
<p>	Show answer<br />
Anorectal abscess, thrombosed hemorrhoid, inflammatory bowel disease, or malignancy.</p>
<blockquote><p><strong>18. How do you best diagnose anal fissure? </strong></p></blockquote>
<p>	Show answer<br />
By clinical history and visual inspection-not by digital examination or anoscopy (which serves only to turn a friendly patient into an irate one).</p>
<blockquote><p><strong>19. What are the nonoperative treatment options?</strong> </p></blockquote>
<p>	Show answer<br />
High-fiber diet; stool-bulking agents; increased hydration; frequent, warm sitz baths; and topical agents containing anti-inflammatory agents, local anesthetics, and vasodilators (nitroglycerin).</p>
<blockquote><p><strong>20. What is the most common operation performed to treat intractable fissure in ano?</strong> </p></blockquote>
<p>	Show answer<br />
Fissurotomy with lateral internal anal sphincterotomy.<br />
<em><strong>KEY POINTS: ANAL FISSURE</strong></p>
<p>   1. Ninety percent of idiopathic anal fissures are posterior and 10% are anterior.<br />
   2. The most common symptoms are tearing anal pain and bleeding with bowel movements.<br />
   3. The diagnosis involves visual inspection-not by digital exam or anoscopy.<br />
   4. Nonoperative treatment includes high-fiber diet, warm sitz baths, and topical agents containing anti-inflammatory agents, local anesthetics, and vasodilators.<br />
   5. The most common operation is a fissurotomy with lateral internal anal sphincterotomy.</em></p>
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		<title>Top Search</title>
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		<title>Privacy Policy</title>
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LOG FILES
Like many other Web sites, http://www.surgeryprocedure.info makes use of log files. The information inside the log files includes internet [...]]]></description>
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		<title>Ethics In The Surgical Intensive Care Unit</title>
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		<pubDate>Tue, 14 Jul 2009 17:41:39 +0000</pubDate>
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				<category><![CDATA[HEALTH CARE]]></category>

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		<description><![CDATA[102 ETHICS IN THE SURGICAL INTENSIVE CARE UNIT
Ricardo J. Gonzalez M.D.
1. What are the four principles of medical ethics?
   1. Beneficence describes the active role of doing good by intervention.
   2. Nonmaleficence is equivalent to saying, &#8220;First do no harm.&#8221;
   3. Autonomy accounts for informed consent, competence, and the [...]]]></description>
			<content:encoded><![CDATA[<p><strong>102 ETHICS IN THE SURGICAL INTENSIVE CARE UNIT<br />
Ricardo J. Gonzalez M.D.</strong></p>
<blockquote><p><strong>1. What are the four principles of medical ethics?</strong></p></blockquote>
<p>   1. Beneficence describes the active role of doing good by intervention.<br />
   2. Nonmaleficence is equivalent to saying, &#8220;First do no harm.&#8221;<br />
   3. Autonomy accounts for informed consent, competence, and the patient&#8217;s right to refuse treatment and to know what&#8217;s going on.<br />
   4. Justice means that all patients should receive fair and equal care but that one patient&#8217;s care should not squander limited resources for others.<br />
<span id="more-490"></span></p>
<blockquote><p><strong>2. What is a do-not-resuscitate (DNR) order? </strong></p></blockquote>
<p>	Show answer<br />
A DNR order instructs the surgeon not to resuscitate the patient if cardiopulmonary arrest occurs; however, a DNR order is much more involved and complicated than the acronym would have you believe. DNR is not absolute.<br />
The Joint Commission for the Accreditation of Healthcare Organizations mandates that hospitals have written guidelines that promote accountability for DNR orders. All DNR orders must be documented in writing, similar to all other orders, in the appropriate section of the patient&#8217;s chart. They should specify the treatments to be withheld and treatments that the patient wishes to have implemented. Patients and families must participate in the DNR decision. Moreover, the DNR status should be discussed and reviewed with the other members of the health care team. Finally, a DNR order does not mean that the patient should be medically abandoned.</p>
<blockquote><p><strong>3. What is the difference between withdrawing and withholding support?</strong></p></blockquote>
<p> 	Show answer<br />
A decision to withdraw should not be more problematic than a decision to withhold, because one cannot be sure that an intervention will work until you try it. There is no moral or ethical distinction between withdrawal and withholding of support. Either of the two allows natural progression of disease without the interface of medical technology. The decision to withdraw or withhold support does not equate with patient death, although the probability of death may be greater. After the decision has been made, appropriate management should focus on the patient&#8217;s comfort and psychosocial support.</p>
<blockquote><p><strong>4. What is an advance directive? </strong></p></blockquote>
<p>	Show answer<br />
An advance directive is a method of delineating a competent patient&#8217;s wishes for application at a time when he or she is no longer competent. Medical management or the lack thereof can be based on the patient&#8217;s wishes rather than a perceived sense of what is best for the patient. Advance directives may be an informal document, such as a living will, or a formal legal document, such as medical durable power of attorney.</p>
<blockquote><p><strong>5. What is durable power of attorney?</strong></p></blockquote>
<p> 	Show answer<br />
A durable power of attorney is a patient-appointed proxy decision maker. The proxy decision maker becomes active as soon as the patient is no longer able to make competent medical decisions. Hence, the durable power of attorney must have been established in advance of the cognitive decline of the patient.</p>
<blockquote><p><strong>6. What is a living will?</strong></p></blockquote>
<p> 	Show answer<br />
A living will, much like a durable power of attorney, is a formal advanced directive in which a competent patient produces a pre-illness guideline for future care in accordance with his or her wishes.</p>
<blockquote><p><strong>7. What is included in informed consent?</strong></p></blockquote>
<p> 	Show answer<br />
Information about the patient&#8217;s condition as well as risks and benefits of the recommended treatment are included. Moreover, the operative and nonoperative alternatives (including no treatment) should be discussed with the patient. The patient&#8217;s understanding of the information and alternatives should be assessed as part of the informed consent. Finally, informed consent is a voluntary decision made by the patient or on behalf of the patient by a proxy decision maker.</p>
<blockquote><p><strong>8. What are futile care and medical futility?</strong> </p></blockquote>
<p>	Show answer<br />
Ultimately, old age and disease will conquer us all. The definition of medically futile or inappropriate treatment is still debated. Nonetheless, there are four main concepts of medical futility:</p>
<p>   1. Health care professionals are not required to provide physiologically futile treatment.<br />
   2. Imminent demise argues against treatment if the patient has no likelihood of survival to discharge.<br />
   3. Under the concept of lethal condition, medical care is considered futile if the patient will survive temporarily but ultimately expire as a result of the ongoing disease process.<br />
   4. Quality of life or qualitative futility argues against treatment if the patient&#8217;s quality of life is so poor that it would be unreasonable to prolong life.</p>
<p>Care must be taken, however, in making medical decisions based on futility because these decisions may lead to self-fulfilling prophecies.</p>
<blockquote><p><strong>9. What are the clinical determinants of brain death?</strong></p></blockquote>
<p> 	Show answer<br />
Many of the current concepts of brain death are based on the 1968 report from the ad hoc committee at Harvard Medical School, which called for a new neurologic definition of brain death. But it was not until 1981 that BEMAT justified the neurologic criteria of brain death by stressing the need for intact brainstem integrative function in order for a person to function as a whole. By definition, brain death requires loss of brainstem reflexes in an irreversibly comatose patient. Brain death includes loss of the pupillary, corneal, oculovestibular, oculocephalic, oropharyngeal, and respiratory reflexes for ≥ 6 hours. The patient also should undergo an apnea test, in which the pCO2 is allowed to rise to at least 60 mmHg without coexistent hypoxia. The patient should be observed for the absence of spontaneous breathing. Other ancillary tests are not essential; for example, it is not necessary to perform an intravenous radioisotope cerebral angiogram or a four-vessel contrast cerebral angiogram or to document an isoelectric (&#8221;flat&#8221;) electroencephalogram.<br />
Of note, all of the above criteria for brain death require the absence of central nervous system depression caused by barbiturates, narcotics, or hypothermia.</p>
<blockquote><p><strong>10. What is a persistent vegetative state? </strong></p></blockquote>
<p>	Show answer<br />
In a persistent vegetative state, typically seen after improvement of a comatose state, the patient lies motionless and without activity. The patient appears to be awake but does not have awareness of his or her surroundings or higher mental activity. Other names for this entity are coma vigil and akinetic mutism.</p>
<blockquote><p><strong>11. What is euthanasia?</strong> </p></blockquote>
<p>	Show answer<br />
Euthanasia requires that the physician play an active role in assisting in the death of the patient. The concepts of physician-assisted suicide and active and passive euthanasia are highly controversial. In 1992, the Society of Critical Care Medicine published the results of a survey of critical care specialists; 87% had withdrawn life-prolonging support from patients. In addition, the most recent U.S. law pertaining to assisted suicide was passed in Oregon in 1994. This law makes it legal for a physician to prescribe medication to terminally ill patients for the purpose of committing suicide.</p>
<blockquote><p><strong>12. Who should approach patients&#8217; families about organ donation? </strong></p></blockquote>
<p>	Show answer<br />
Some claim that the physician who has established good rapport with the patient&#8217;s family should raise the issue of organ donation. Others believe that the local organ procurement personnel should approach the family because they have greater interest and training in the process. The best approach is probably a combined one.</p>
<blockquote><p><strong>13. What should patients&#8217; families be told when organ donation is feasible?</strong></p></blockquote>
<p> 	Show answer<br />
The surgeon should stress that the patient has died despite an actively beating heart. The family should be questioned about the patient&#8217;s wishes regarding organ donation. All topics should be based on the concepts of informed consent. The family should be informed of the likelihood that several patients will benefit from the donated organs. The family needs to understand that there is no guarantee that the organs will be suitable for donation. They should be assured that they are not responsible for the cost of care provided after brain death is determined and that they may refuse organ donation without fear of prejudice.</p>
<blockquote><p><strong>14. What is the role of the hospital ethics committee?</strong></p></blockquote>
<p> 	Show answer<br />
The hospital ethics committee educates hospital staff members, creates policy, and provides a source of consultation.<br />
The function of education is accomplished through grand rounds, seminars, special lectures, and journal clubs. The hospital ethics committee should be viewed as an intrinsic part of the hospital community. Developed policies should be reviewed by other committees and divisions of the hospital to foster a better sense of cohesiveness when ethical and moral dilemmas arise. The consultative function of the ethics committee produces the greatest amount of controversy. In fact, many hospitals negate this function by stating that it interferes with the physician-patient relationship. The hospital ethics committee can and should provide an arena for collaboration and general ethical education within the hospital.</p>
<p><strong>References</strong><br />
BIBLIOGRAPHY<br />
1. Ad Hoc Committee of the Harvard Medical School to Examine the Definition of Brain Death: A definition of irreversible coma. JAMA 205:337-340, 1968.<br />
2. Aminoff MJ: The central nervous system. In Medical Diagnosis and Treatment. Norwalk, CT, Appleton &#038; Lange, 1996.<br />
3. Arnold RM, Siminoff LA, Frader JE: Ethical issues in organ procurement: A review for intensivists. Crit Care Med 12:29-48, 1996. <a href="http://dx.doi.org/10.1016/0022-0981%2895%2900166-2">Full article</a><br />
4. Bernat JL, Culver CM, Gert B: On the definition and criterion of death. Ann Intern Med 94:389-394, 1981. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=7224389&#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=7224389">Similar articles </a><a href="http://dx.doi.org/10.1001/archinte.94.3.389">Full article</a><br />
5. Harken AH: Enough is enough. Arch Surg 10:1061-1063, 1999. <a href="http://dx.doi.org/10.1001/archsurg.134.10.1061">Full article</a><br />
6. Kelley DF, Hoyt JW: Ethics consultation. Crit Care Med 12:49-70, 1996.<br />
7. McCollough L, Jones J, Brody B: Surgical Ethics. Oxford, Oxford University Press, 1998.<br />
8. Nyman DJ, Eidelman AL, Sprung CL: Euthanasia. Crit Care Clin 12:85-96, 1996. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=8821011&#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=8821011">Similar articles</a><br />
9. Society of Critical Care Ethics Committee: Attitudes of critical care medicine professionals concerning foregoing life-sustaining treatments. Crit Care Med 20:320-326, 1992.<br />
10. State of Oregon: ORS.251.215, The Oregon Death with Dignity Act. Official 1994 Oregon General Election Handbook, 1994, pp 121-124.<br />
11. Younger SJ: Medical futility. Crit Care Clin 12:165-178, 1996.</p>
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		<title>Risks Of Bloodborne Disease</title>
		<link>http://surgeryprocedure.info/health-care/risks-of-bloodborne-disease</link>
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		<pubDate>Tue, 14 Jul 2009 17:34:02 +0000</pubDate>
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				<category><![CDATA[HEALTH CARE]]></category>

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		<description><![CDATA[101 RISKS OF BLOODBORNE DISEASE
Caesar M. Ursic M.D., Doru I. E. Georgescu M.D.
1. What infectious diseases are transmissible via blood transfusion?

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

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		<description><![CDATA[100 CAN HEALTH CARE BE REFORMED?
Alden H. Harken M.D.
1. Is health care reform an oxymoron? 
	Show answer
Yes.
2. What is fee for service? 
	Show answer
The doctor establishes the price, and the patient agrees to pay it. This traditional system of exchange has great merit if both parties understand the value of the service provided. If either [...]]]></description>
			<content:encoded><![CDATA[<p><strong>100 CAN HEALTH CARE BE REFORMED?<br />
Alden H. Harken M.D.</strong></p>
<blockquote><p><strong>1. Is health care reform an oxymoron? </strong></p></blockquote>
<p>	Show answer<br />
Yes.</p>
<blockquote><p><strong>2. What is fee for service? </strong></p></blockquote>
<p>	Show answer<br />
The doctor establishes the price, and the patient agrees to pay it. This traditional system of exchange has great merit if both parties understand the value of the service provided. If either party (usually the patient) cannot estimate the service value, it is possible (even likely) that the doctor will honestly escalate the service value in a fashion unchecked by the patient&#8217;s perceptions. Thus, in a fee-for-service system, medical prices tend to increase.<br />
<span id="more-484"></span></p>
<blockquote><p><strong>3. What is discounted fee for service?</strong></p></blockquote>
<p> 	Show answer<br />
The patient gets together with a group of friends, and they come to the doctor with the following proposition: &#8220;Hey, Doc, you can dazzle us with your fancy medical talk, but we still think that your prices are too high. How about my pals and me will pay you 80% of what you charge us?&#8221;</p>
<blockquote><p><strong>4. Is there a difference between hospital costs and hospital charges? </strong>	</p></blockquote>
<p>Show answer<br />
Absolutely. Hospital cost is the sum of the expenses (e.g., sutures, nurses&#8217; salaries, electricity, instrumentation sterilization, Band-Aids) that are expended in suturing a laceration, for example. The hospital typically charges about twice the cost (100% markup) for repairing a cut finger. This markup is highly industry specific. Thus, whereas intensely competitive food chains may make a profit of only 1 penny on a loaf of bread, hospitals and liquor stores usually charge twice the cost.</p>
<blockquote><p><strong>5. What are fixed costs? </strong>	</p></blockquote>
<p>Show answer<br />
After accounting for light, heat, and staff (nurses, housekeepers, administrators) at a hospital but before seeing a single patient, doctors and the hospital have already spent a huge amount of money. Doctors and hospitals must pay fixed costs whether or not they provide any medical services at all.</p>
<blockquote><p><strong>6. What are actual costs?</strong> </p></blockquote>
<p>	Show answer<br />
These are the incremental costs of actually providing a service in a hospital (in addition to the fixed costs of light and heat). For example, a patient shows up in the emergency department at midnight complaining of a lump on the tip of his nose. The doctor, with characteristic erudition, says, &#8220;Yep, you have a wart on your nose,&#8221; and sends the patient home with a bill for $500. The actual cost of this encounter is obviously negligible. The patient is really paying for the fixed costs of nurses and emergency resuscitative equipment should he have a cardiac arrest.</p>
<blockquote><p><strong>7. Is hospital accounting a precisely scientific and objective analysis of financial data?</strong></p></blockquote>
<p> 	Show answer<br />
No.</p>
<blockquote><p><strong>8. What is health insurance?</strong></p></blockquote>
<p> 	Show answer<br />
Traditionally, people can purchase insurance that may pay either all or a portion of their hospital and physician charges if they become ill. Insurance companies make a profit, therefore, only if the patient stays healthy. Insurance companies have elaborate tables to predict who will get sick, and they prefer to sell policies exclusively to young, healthy individuals. This practice is termed &#8220;skimming.&#8221; The insurance company takes all of the risk-and they like to keep it low. Conversely, hospitals must cover fixed costs-and the more expensive (and more frequent) the health care that physicians provide, the better it is for the hospitals.</p>
<blockquote><p><strong>9. What are health maintenance organizations (HMOs)?</strong></p></blockquote>
<p> 	Show answer<br />
HMOs are complex systems composed, in their most comprehensive form, of hospitals, doctors plus offices, and an insurance company. HMOs contract with large groups of people (potential patients) to maintain their health. Enrollees pay a monthly fee (just like health insurance) so that all hospital and physician charges are covered if the enrollees become ill. Unlike health insurance, however, in the HMO model, hospitals and physicians get paid whether or not the enrollee gets sick. So, it is better for everyone if enrollees stay healthy-and out of the hospital.</p>
<blockquote><p><strong>10. Initially, a lot of physicians did not like HMOs. Why? </strong></p></blockquote>
<p>	Show answer<br />
Because physicians are fiercely independent. They did not want a bunch of business managers telling them how to manage patients.</p>
<blockquote><p><strong>11. Why are physicians fiercely independent?</strong></p></blockquote>
<p> 	Show answer<br />
We were probably born that way.</p>
<blockquote><p><strong>12. Is that good?</strong></p></blockquote>
<p> 	Show answer<br />
Probably not. Eventually, everyone will need to work together and not hit each other when they are mad.</p>
<blockquote><p><strong>13. Do HMO administrators really dictate how physicians manage their patients? </strong>	</p></blockquote>
<p>Show answer<br />
Yes and no. Physicians have developed medically effective and optimally efficient strategies-termed clinical pathways-for caring for many common illnesses. Although physicians must treat each patient individually, when we adhere to predetermined treatment guidelines (as encouraged by HMO administrators), patients usually get better faster and cheaper.</p>
<blockquote><p><strong>14. Do physicians follow these clinical pathways?</strong> </p></blockquote>
<p>	Show answer<br />
Traditionally, no.</p>
<blockquote><p><strong>15. What do HMO managers do?</strong></p></blockquote>
<p> 	Show answer<br />
They evaluate each physician&#8217;s utilization of expensive resources (within the predetermined clinical pathways) relative to the health of the physician&#8217;s patients.</p>
<blockquote><p><strong>16. Do physicians welcome this kind of scrutiny? </strong></p></blockquote>
<p>	Show answer<br />
No.</p>
<blockquote><p><strong>17. What is a preferred provider organization (PPO)?</strong></p></blockquote>
<p> 	Show answer<br />
A PPO is a group of doctors who have elected to remain legally independent of a hospital and insurance company (if they joined together, they would be an HMO) and, most of all, patients. But PPOs maintain their independence as physicians, even though most PPOs require administrators to coordinate programs, keep the books, and keep the doctors from hitting each other. PPOs have the perception of independence, however.</p>
<blockquote><p><strong>18. Is health care expensive? </strong></p></blockquote>
<p>	Show answer<br />
Unfortunately, yes. Physicians argue that patients pay a lot but also get a lot. In the United States, patients expect unlimited access to liver transplantation and magnetic resonance imaging (MRI) for every headache. Americans believe that fancy, expensive health care is not just a privilege-it is a right.</p>
<blockquote><p><strong>19. So what is the problem?</strong></p></blockquote>
<p> 	Show answer<br />
The chief executive officers (CEOs) of big American corporations argue that the obligatory expense of health care is driving up the cost of U.S. products and making American companies less competitive in the global market-there is more health care than steel in a new Chevrolet.</p>
<blockquote><p><strong>20. Does big business have a solution?</strong></p></blockquote>
<p> 	Show answer<br />
They think so. The CEOs still want unlimited access to the most modern health care for themselves and their families. Without sounding cynical, the CEOs want to save health care dollars spent on their employees and &#8220;other people&#8217;s families.&#8221; They want to limit access to health care, but they do not want to wield the ax personally. So they developed the idea of capitation.</p>
<blockquote><p><strong>21. What is capitation? </strong></p></blockquote>
<p>	Show answer<br />
The CEOs of large businesses come to hospitals, HMOs, or PPOs and say: &#8220;Why don&#8217;t you provide all health care for all my employees at a fixed price, say, $180 per month per head?&#8221; (hence, capitation). In this model, physicians make the decisions about who gets how much medical care (satisfying their urge for independence), but they also promise to provide all necessary medical care for a prearranged price. Thus, they take all of the risk. CEOs like this model because they can still offer health care as an employee benefit and budget the cost in advance.</p>
<blockquote><p><strong>22. Why do physicians not like capitation? </strong></p></blockquote>
<p>	Show answer<br />
All of a sudden physicians may have acquired a little more independence than they bargained for. Now they are paid in advance so that all costs of patients&#8217; health care are subtracted from the money they negotiated up front. Now they must advise against an MRI for every headache and break the news to Granny that she will not think better if they dialyze her blood urea nitrogen down to 50. This is the reverse of the good old days when physicians were rewarded if their patients got sick and stayed sick. Physicians could ply them with a smorgasbord of drugs and technologies. Now physicians are trying to control health care costs.</p>
<blockquote><p><strong>23. Is all this change good? </strong></p></blockquote>
<p>	Show answer<br />
Absolutely. Medicine has always changed-and the faster, the better. Physicians were initially attracted to medicine as an intellectually stimulating discipline because medicine and surgery evolve rapidly.</p>
<blockquote><p><strong>24. Can physicians keep up with all this change? </strong>	</p></blockquote>
<p>Show answer<br />
Absolutely.</p>
<blockquote><p><strong>25. Despite all of the medical Chicken Littles who sonorously declare that the sky is falling, is medicine (and even more clearly, surgery) still the most gratifying, stimulating, and rewarding profession</strong>?</p></blockquote>
<p> 	Show answer<br />
Absolutely.</p>
<p><strong>References</strong><br />
BIBLIOGRAPHY<br />
1. Blumenthal D: Controlling health care expenditures. N Engl J Med 344:766-769, 2001. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=11236784&#038;dopt=Abstract">Medline</a> Similar articles<a href="http://dx.doi.org/10.1056/NEJM200103083441012"> Full article</a><br />
2. Dudley RA, Luft HS: Managed care in transition. N Engl J Med 344:1087-1092, 2001. Medline <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=11287981">Similar articles</a> <a href="http://dx.doi.org/10.1056/NEJM200104053441410">Full article</a><br />
3. Fuchs VR: What&#8217;s ahead for health insurance in the United States? N Engl J Med 346:1822-1824, 2002.<br />
4. Iglehart JK: Changing health insurance trends. N Engl J Med 347:956-962, 2002.<br />
5. Schroeder SA: Prospects for expanding health insurance coverage. N Engl J Med 344:847-852, 2001. Medline <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=11248165">Similar articles</a> <a href="http://dx.doi.org/10.1056/NEJM200103153441113">Full article</a><br />
6. Wilensky GR: Medicare reform-now is the time. N Engl J Med 345:458-462, 2001. Medline <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=11496860">Similar articles</a> <a href="http://dx.doi.org/10.1056/NEJM200108093450612">Full article</a><br />
7. Wood AJ: When increased therapeutic benefit comes at increased cost. N Engl J Med 346:1819-1821, 2002. Medline <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=12050345">Similar articles </a><a href="http://dx.doi.org/10.1056/NEJM200206063462313">Full article</a><br />
8. Wright JG: Hidden barriers to improvement in the quality of health care. N Engl J Med 346:1096, 2002. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=11932485&#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=11932485">Similar articles</a></p>
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		<title>Pediatric Urology</title>
		<link>http://surgeryprocedure.info/urology/pediatric-urology</link>
		<comments>http://surgeryprocedure.info/urology/pediatric-urology#comments</comments>
		<pubDate>Tue, 14 Jul 2009 16:53:02 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[UROLOGY]]></category>

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		<description><![CDATA[99 PEDIATRIC UROLOGY
Kirstan K. Meldrum M.D., Mark P. Cain M.D.
1. A healthy 3-year-old girl develops a urinary tract infection (UTI). How should she be evaluated?
 	Show answer
After treatment of the infection, the patient should undergo a urinary tract evaluation (this recommendation stands even in a little girl after only one UTI). Evaluation includes a renal-bladder [...]]]></description>
			<content:encoded><![CDATA[<p><strong>99 PEDIATRIC UROLOGY<br />
Kirstan K. Meldrum M.D., Mark P. Cain M.D.</strong></p>
<blockquote><p><strong>1. A healthy 3-year-old girl develops a urinary tract infection (UTI). How should she be evaluated?</strong></p></blockquote>
<p> 	Show answer<br />
After treatment of the infection, the patient should undergo a urinary tract evaluation (this recommendation stands even in a little girl after only one UTI). Evaluation includes a renal-bladder sonogram and voiding cystourethrogram (VCUG). Approximately 50% of children younger than age 12 years who present with a UTI are found to have abnormalities of the genitourinary tract. The most common abnormalities identified are vesicoureteral reflux, obstructive uropathies, and neurogenic bladder.<br />
<span id="more-482"></span></p>
<blockquote><p><strong>2. What is vesicoureteral reflux (VUR) disease?</strong> </p></blockquote>
<p>	Show answer<br />
With VUR, urine refluxes from the bladder into the upper urinary tract. Primary VUR is caused by an inadequate valvular mechanism at the ureterovesical junction, presumably related to a shortened submucosal ureteral tunnel. One half of children with culture-documented UTIs have VUR.</p>
<blockquote><p><strong>3. Is VUR bad?</strong></p></blockquote>
<p> 	Show answer<br />
Sterile reflux is unlikely to cause renal damage; however, persistent reflux of infected urine leads to pyelonephritis and progressive renal scarring. Currently, renal scarring is the fourth leading cause for renal transplantation in children. The combination of VUR and elevated bladder storage pressures (e.g., neuropathic bladder or bladder outlet obstruction) is particularly harmful to the kidney.</p>
<blockquote><p><strong>4. What are the indications for surgical correction of VUR?</strong></p></blockquote>
<p> 	Show answer<br />
Reflux disappears spontaneously in many children; however, high-grade reflux, especially when bilateral, is unlikely to resolve spontaneously. Children with high-grade reflux or breakthrough UTIs despite antibiotic prophylaxis should be managed surgically. Surgical management is also appropriate in children with reflux persisting into late childhood or adolescence.</p>
<blockquote><p><strong>5. What is the most common cause of antenatal hydronephrosis? </strong></p></blockquote>
<p>	Show answer<br />
Ureteropelvic junction (UPJ) obstruction. Hydronephrosis is the most common abnormality detected on prenatal ultrasound and accounts for 50% of all prenatally detected lesions. Fifty percent of prenatal hydronephrosis, in turn, is caused by UPJ obstruction. UPJ obstruction is bilateral in approximately 20% of cases and is associated with VUR in 15% of cases.</p>
<blockquote><p><strong>6. What is the most common cause of UPJ obstruction?</strong></p></blockquote>
<p> 	Show answer<br />
Intrinsic stenosis. Less common causes include lower pole (of the kidney) crossing vessels, anomalous ureteral insertions, and peripelvic fibrosis.</p>
<blockquote><p><strong>7. Can UPJ obstruction resolve spontaneously? What are the indications for pyeloplasty? </strong></p></blockquote>
<p>	Show answer<br />
Yes, it can resolve spontaneously. Ultimately, only about 25% of children with evidence of UPJ obstruction require pyeloplasty. The indications for surgical intervention include worsening hydronephrosis, poor or declining renal function, pain, and the presence of a solitary kidney or bilateral hydronephrosis.</p>
<blockquote><p><strong>8. What is the Meyer-Weigert law? </strong>	</p></blockquote>
<p>Show answer<br />
This law refers to the position of the ureteral orifices in patients with complete ureteral duplication. Occasionally, two ureteral buds develop independently from the mesonephric duct. As the ureteral buds are absorbed into the developing bladder, the bud located in a lower position along the duct (draining the lower pole of the kidney) is carried to a more cranial and lateral position. The ureteral bud located in a higher position along the duct (draining the upper pole of the kidney) is carried to a more caudal and medial position within the bladder. Lower pole ureters are more likely to reflux because of their lateral position within the bladder; however, upper pole ureters are more frequently obstructed and are more often associated with a ureterocele.</p>
<blockquote><p><strong>9. What is a ureterocele? </strong>	</p></blockquote>
<p>Show answer<br />
A ureterocele is a cystic dilatation of the distal portion of the ureter. Ureteroceles are usually associated with the upper pole ureter of a duplicated collecting system; however, they also may develop from single ureters. They are usually ectopic (i.e., some portion of the ureterocele is positioned at the bladder neck or urethra) and frequently cause ureteral obstruction.</p>
<blockquote><p><strong>10. What is an ectopic ureter? </strong>	</p></blockquote>
<p>Show answer<br />
A ureter with an ectopic opening at the level of the bladder neck or more caudally.<br />
<em><strong>KEY POINTS: PEDIATRIC UROLOGY</strong></p>
<p>   1. The most common cause of antenatal hydronephrosis is ureteropelvic junction obstruction.<br />
   2. A ureterocele is a cystic dilatation of the distal portion of the ureter.<br />
   3. The most common location of an undescended testicle is the inguinal canal.<br />
   4. The most common cause of ambiguous genitalia in newborns is congenital adrenal hyperplasia, most commonly due to 21-hydroxylase deficiency.</em></p>
<blockquote><p><strong>11. What is the most common presenting symptom in a girl with an ectopic ureter?</strong> </p></blockquote>
<p>	Show answer<br />
Incontinence. In females, an ectopic ureter will usually drain into the bladder neck, proximal urethra, or vestibule. The orifice also may be located in the vagina (25%) and, occasionally, the uterus. When the ectopic ureteral orifice is positioned below the external sphincter or within the female genital tract, incontinence can develop.</p>
<blockquote><p><strong>12. Do boys with ectopic ureters present with incontinence?</strong></p></blockquote>
<p> 	Show answer<br />
No. The ectopic pathway in boys extends from the bladder neck through the posterior urethra to the mesonephric duct derivatives (i.e., vas deferens, epididymis, and seminal vesicle). Therefore, the ectopic ureteral orifice is always positioned above the continence mechanism.</p>
<blockquote><p><strong>13. What percentage of full-term male infants have an undescended testicle?</strong></p></blockquote>
<p> 	Show answer<br />
Three percent. This number decreases to 0.8% by age 1 year.</p>
<blockquote><p><strong>14. What is the most common location of an undescended testicle? </strong></p></blockquote>
<p>	Show answer<br />
The inguinal canal (72% of undescended testicles). The testicle also may be located in the abdomen (8%) or prescrotal area (20%). Twenty percent of undescended testicles are nonpalpable at presentation; of these, 50% are absent completely.</p>
<blockquote><p><strong>15. Why should the testicle be brought back into the scrotum?</strong> </p></blockquote>
<p>	Show answer<br />
Patients with cryptorchidism have a 40-fold increased risk of germ cell cancer compared with the normal population. Although positioning of the testicle within the scrotum does not alleviate this risk, it does permit routine, thorough testicular examination. Patients with cryptorchidism also are at risk for infertility. Histologic studies have demonstrated progressive germ cell loss in the undescended testicle beginning at age 18 months. Early orchiopexy can minimize the extent of germ cell loss and thereby decrease the chance of future infertility. In general, the higher the testicle (i.e., within the abdomen), the greater the risk of cancer and infertility.</p>
<blockquote><p><strong>16. What is the most common cause of bladder outlet obstruction in boys? In girls?</strong></p></blockquote>
<p> 	Show answer<br />
Posterior urethral valves and ureterocele, respectively.</p>
<blockquote><p><strong>17. What are the urinary manifestations of posterior urethral valves?</strong></p></blockquote>
<p> 	Show answer<br />
Posterior urethral valves are congenital leaflets of tissue that extend from the verumontanum to the anterior urethra in boys. They occur at an incidence of 1 in 8000 live male births. Posterior urethral valves cause bladder outlet obstruction, which, in turn, leads to variable degrees of bladder and renal injury. Severe obstruction may result in oligohydramnios, pulmonary hypoplasia, bladder hypertrophy, vesicoureteral reflux, hydroureteronephrosis, and renal dysplasia. Fifty percent of affected children have reflux, and 33% of them progress to end-stage renal disease.</p>
<blockquote><p><strong>18. What is a myelomeningocele? What are its urologic consequences?</strong></p></blockquote>
<p> 	Show answer<br />
A myelomeningocele is a hernial protrusion of the spinal cord and its meninges through a defect in the vertebral column. The resulting neurologic injury causes, among other problems, bladder dysfunction. Patients with myelomeningocele usually are incontinent because of detrusor hyperactivity, detrusor hypoactivity, poor bladder compliance, inadequate outlet resistance, detrusor-outlet dyssynergy, or a combination of these factors. More importantly, patients with hyperactive, high-pressure bladders may develop upper urinary tract deterioration. Life-long follow-up is necessary because the neurologic lesion can change with time. Treatment goals include maintenance of a low-pressure urinary reservoir, prevention of urinary tract infections, prevention of upper urinary tract deterioration, and the achievement of continence.</p>
<blockquote><p><strong>19. What is the most common cause of ambiguous genitalia in newborns? </strong>	</p></blockquote>
<p>Show answer<br />
Congenital adrenal hyperplasia, most commonly caused by a 21-hydroxylase deficiency.</p>
<blockquote><p><strong>20. What diagnostic evaluation should be performed in any male infant presenting with hypospadias and cryptorchidism?</strong> </p></blockquote>
<p>	Show answer<br />
The presence of cryptorchidism and hypospadias should alert the physician to the possibility of an androgenized female. A karyotype should always be obtained before urogenital reconstruction.</p>
<blockquote><p><strong>21. What is the most common solid renal mass in infancy? In childhood?</strong> </p></blockquote>
<p>	Show answer<br />
In infancy, it is congential mesoblastic nephroma. This is a benign tumor of the kidney that can be managed with surgical excision alone.<br />
In childhood, it is a Wilms&#8217; tumor. Wilms&#8217; tumor is associated with Beckwith-Wiedemann syndrome, isolated hemihypertrophy, and congenital aniridia. The most important prognostic factors are tumor stage and histology. Treatment is multimodal, consisting of surgery, chemotherapy, and radiation.</p>
<p><strong>References</strong><br />
WEB SITE<br />
<a href="http://www.transplantation-soc.org/">http://www.transplantation-soc.org</a></p>
<p>BIBLIOGRAPHY<br />
1. Baker LA, Silver RI, Docimo SG: Cryptorchidism. In Gearhart JP, Rink RC, Mouriquand PDE (eds): Pediatric Urology. Philadelphia, W.B. Saunders, 2001, pp 738-753.<br />
2. Cooper CS, Snyder HM: Ureteral duplication, ectopy, and ureteroceles. In Gearhart JP, Rink RC, Mouriquand PDE (eds): Pediatric Urology. Philadelphia, W.B. Saunders, 2001, pp 430-452.<br />
3. Dinneen MD, Duffy PG: Posterior urethral valves. Br J Urol 78:275-281, 1996. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=8813928&#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=8813928">Similar articles</a><br />
4. Docimo SG: The results of surgical therapy for cryptorchidism: A literature review and analysis. J Urol 154:1148, 1995. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=7637073&#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=7637073">Similar articles</a><br />
5. Elder JS, Peters CA, Arant BS Jr, et al: Pediatric vesicoureteral reflux guidelines panel summary report on the management of primary vesicoureteral reflux in children. J Urol 157:1846-1851, 1997.  <a href="http://dx.doi.org/10.1097/00005392-199705000-00093">Full article</a><br />
6. Gill B, Kogan S: Cryptorchidism. Current concepts. Pediatr Clin North Am 44:1211-1227, 1997. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9326959&#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=9326959">Similar articles</a><br />
7. Gunther DF, Bukowski TP: Congenital adrenal hyperplasia: A spectrum of disorders. Contemp Urol 11:52-69, 1999.<br />
8. Kirsch AJ, Escala J, Duckett JW, et al: Surgical management of the nonpalpable testis: The Children&#8217;s Hospital of Philadelphia experience. J Urol 159:1340-1343, 1998.<br />
9. Pohl HG, Rushton HG: The diagnosis and management of urinary tract infection in children. AUA Update Series 17:242-247, 1998.<br />
10. Poppas DP, Bauer SB: Urologic evaluation of the myelodysplastic child. AUA Update Series 16:282-287, 1997.<br />
11. Reddy PR, Mandell J: Ureteropelvic junction obstruction: Prenatal diagnosis; therapeutic implications. Urol Clin North Am 25:171-195, 1998.<br />
12. Snyder HM: Anomalies of the ureter. In Gillenwater JY, Grayhack JT, Howards SS, Duckett JW (eds): Adult and Pediatric Urology, 3rd ed. St. Louis, Mosby, 1996, pp 2197-2228.<br />
13. Strand WR: Urinary infection in children: Pathogenesis, bacterial virulence, and host resistance. In Gonzales ET, Bauer SB (eds): Pediatric Urology Practice. Baltimore, Lippincott Williams &#038; Wilkins, 1999, pp 433-462.</p>
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		<title>Urodynamics &amp; Voiding Dysfunction</title>
		<link>http://surgeryprocedure.info/urology/urodynamics-voiding-dysfunction</link>
		<comments>http://surgeryprocedure.info/urology/urodynamics-voiding-dysfunction#comments</comments>
		<pubDate>Tue, 14 Jul 2009 16:42:08 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[UROLOGY]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/?p=480</guid>
		<description><![CDATA[98 URODYNAMICS AND VOIDING DYSFUNCTION
Firouz Daneshgari M.D.
1. What is urodynamics?
 	Show answer
Urodynamic studies assess the functional aspects of the storage and emptying ability of the lower urinary tract (LUT). The principles of urodynamic studies originated from hydrodynamics. The components of urodynamic studies are cystometrogram, leak point pressures, urethral profile pressures, pressure-flow studies, uroflowmetry, and electromyography. [...]]]></description>
			<content:encoded><![CDATA[<p><strong>98 URODYNAMICS AND VOIDING DYSFUNCTION<br />
Firouz Daneshgari M.D.</strong></p>
<blockquote><p><strong>1. What is urodynamics?</strong></p></blockquote>
<p> 	Show answer<br />
Urodynamic studies assess the functional aspects of the storage and emptying ability of the lower urinary tract (LUT). The principles of urodynamic studies originated from hydrodynamics. The components of urodynamic studies are cystometrogram, leak point pressures, urethral profile pressures, pressure-flow studies, uroflowmetry, and electromyography. These studies have evolved into videourodynamics with the addition of fluoroscopy (i.e., video).<br />
<span id="more-480"></span></p>
<blockquote><p><strong>2. What is uroflowmetry?</strong></p></blockquote>
<p> 	Show answer<br />
Uroflowmetry is the measurement of voided urine (in milliliters) per unit of time (in seconds). The important elements of the test are voided volume (which should be > 150 mL), maximum flow rate (Qmax), and the curve of the flow (which should be bell shaped). The normal Qmax is > 20 mL/sec in men and > 25 mL/sec in women.</p>
<blockquote><p><strong>3. What is benign prostatic hyperplasia (BPH)?</strong> </p></blockquote>
<p>	Show answer<br />
BPH is benign enlargement of the prostate gland that may lead to bladder outlet obstructive symptoms in men. These symptoms have recently been termed lower urinary tract symptoms (LUTS).</p>
<blockquote><p><strong>4. What is an American Urological Association (AUA) symptom score?</strong> </p></blockquote>
<p>	Show answer<br />
It is a self-reported questionnaire developed and popularized by the AUA for the assessment of bothersome LUTS in men. This questionnaire has seven questions with a maximum score of 35. The higher the score, the more severe and bothersome the symptoms. The AUA symptom score has become an index for both the diagnosis and evaluation of treatment outcome in patients with LUTS.</p>
<blockquote><p><strong>5. What are the main functions of the LUT? </strong>	</p></blockquote>
<p>Show answer<br />
Storage and emptying of urine are the main functions. For practical purposes, all symptoms of LUT dysfunction can be categorized into the malfunction of either storing or emptying ability.</p>
<blockquote><p><strong>6. What are the control mechanisms for LUT function? </strong></p></blockquote>
<p>	Show answer<br />
The control mechanisms for LUT function are recognized as central and peripheral. The central control mechanisms consist of the cortical portion of the frontal lobe of the brain and pontine micturition center. The peripheral control mechanisms include the thoracic sympathetic and lumbar parasympathetic innervation and neuromuscular apparatus of the LUT organs.</p>
<blockquote><p><strong>7. What is the role of the autonomic nervous system in the function of the LUT? </strong></p></blockquote>
<p>	Show answer<br />
Sympathetic fibers, which originate from the T10-L2 portion of the spinal cord, innervate the bladder neck and proximal urethra. These fibers mostly control the contraction of the proximal urethra or bladder neck and relaxation of the bladder, which results in storage of urine. The parasympathetic fibers, which originate primarily from the S2-S4 portion of the spinal cord, innervate the bladder body. The parasympathetic innervation allows contraction of the bladder smooth muscle, leading to bladder emptying.</p>
<blockquote><p><strong>8. What is the role of the somatic nervous system in the function of the LUT?</strong></p></blockquote>
<p> 	Show answer<br />
Voluntary control of the striated muscle of the external urinary sphincter is controlled by the somatic nervous system. Somatic fibers are conveyed to the sphincter by the pudendal nerve.</p>
<blockquote><p><strong>9. What is bulbocavernosal reflex? 	</strong></p></blockquote>
<p>Show answer<br />
Bulbocavernosal reflex tests the integrity of peripheral neurologic control of the LUT. This reflex is elicited by stimulation of the glans penis in men or the clitoris in women, which causes contraction of the external anal sphincter or bulbocavernosus muscle. Alternatively, the reflex may be stimulated by pulling the balloon of a Foley catheter against the bladder neck. This reflex is present in all normal men and in approximately 70% of normal women. Absence of this reflex in a man is strongly suggestive of a sacral neurologic lesion.</p>
<blockquote><p><strong>10. What is the most common cause of incontinence in the geriatric population?</strong> 	</p></blockquote>
<p>Show answer<br />
The most common are transient causes, mostly external, that disrupt the fragile balance of LUT function in elderly patients and cause urinary incontinence. These causes can be recalled with the mnemonic DIAPPERS:</p>
<p>    * Delirium<br />
    * Infections<br />
    * Atrophic urethritis or vaginitis<br />
    * Pharmaceuticals<br />
    * Psychological (depression)<br />
    * Endocrine (hypercalcemia, hyperglycemia)<br />
    * Restricted mobility<br />
    * Stool impaction</p>
<p><em><strong>KEY POINTS: URODYNAMICS AND VOIDING FUNCTION</strong></p>
<p>   1. Uroflowmetry is the measurement of voided urine (in milliliters) per unit of time (in seconds).<br />
   2. Benign prostatic hypertrophy is benign enlargement of the prostate gland that may lead to bladder outlet obstructive symptoms in men.<br />
   3. The sacral roots involved in micturition physiology are S2-S4.</em></p>
<blockquote><p><strong>11. What is spinal shock? What type of urinary dysfunction does it cause?</strong> </p></blockquote>
<p>	Show answer<br />
Spinal shock is the loss of contractility of the smooth muscle below the level of spinal cord injury, leading to difficulty in bladder emptying or urinary retention. This phenomenon may last from hours to several months with a high chance of reversibility if the spinal cord injury is not permanent.</p>
<blockquote><p><strong>12. What is autonomic dysreflexia? How is it treated?</strong></p></blockquote>
<p> 	Show answer<br />
Autonomic dysreflexia results from systematic outpouring of sympathetic discharge, as in patients with spinal cord lesions at or above the T6 level. This dysreflexia is triggered by distention of the bladder or other stimulus of the bowel or LUT. It is manifested by hypertension, bradycardia, hot flush, sweating, and headache. Initial treatment consists of removal of the stimulus, such as emptying the bladder and placing the patient in a sitting position. Nifedipine or nitroprusside may be used as either prophylaxis or treatment of severe episodes. This condition may lead to significant cerebrovascular complication if untreated.</p>
<blockquote><p><strong>13. What type of bladder dysfunction is seen in diabetic patients? </strong></p></blockquote>
<p>	Show answer<br />
Diabetic cystopathy is manifested primarily as atonic bladder with difficulty in emptying caused by impaired contractility of the bladder or detrusor muscle.</p>
<blockquote><p><strong>14. What type of bladder dysfunction is seen in patients with multiple sclerosis (MS)?</strong> 	</p></blockquote>
<p>Show answer<br />
Urgency (83%), urge incontinence (75%), detrusor hyperreflexia (62%), and detrusor sphincter dyssynergia (25%) are among the most common LUT symptoms in patients with MS. Variation in symptoms depends on the site of involvement by MS. Involvement of pontine pathways (tegmentum) is associated with a much higher rate of urinary symptoms.</p>
<blockquote><p><strong>15. Which sacral roots control the micturition physiology? </strong>	</p></blockquote>
<p>Show answer<br />
S2-S4.<br />
16. What are the causes of urinary retention after abdominal or pelvic surgery? 	Show answer<br />
They are injuries or disruption of pelvic plexus innervation to the LUT.</p>
<blockquote><p><strong>17. What is Ogilvie&#8217;s syndrome? 	</strong></p></blockquote>
<p>Show answer<br />
Acute massive dilatation of the cecum and ascending and transverse colon without organic obstruction is known as Ogilvie&#8217;s syndrome. This syndrome can be seen in pelvic urologic surgeries, possibly as a result of an imbalance in parasympathetic stimulation of the colon.</p>
<blockquote><p><strong>18. What is reflex versus psychic erection?</strong></p></blockquote>
<p> 	Show answer<br />
Erection after local stimulation is termed reflex erection. The afferent nerves for reflex erection run in the pudendal nerves, and the efferent fibers are found in the S2-S4 parasympathetic outflow. The psychic erection is caused by stimulation of cerebral erotic centers. The afferent stimuli for psychic erection travel through the thoracolumbar sympathetic outflow and sacral parasympathetic fibers.</p>
<p><strong>References</strong><br />
WEB SITE<br />
<a href="http://www.transplantation-soc.org/">http://www.transplantation-soc.org</a><br />
BIBLIOGRAPHY<br />
1. Bross S, Braun PM, Michel MS, et al: Preoperatively evaluated bladder wall tension as a prognostic parameter for postoperative success after surgery for bladder outlet obstruction. Urol 61:562-566, 2003. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=12639648&#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=12639648">Similar articles </a><a href="http://dx.doi.org/10.1016/S0090-4295%2802%2902372-5">Full article</a><br />
2. Holtgrewe HL: Current trends in management of men with lower urinary tract symptoms and benign prostatic hyperplasia. Urology 51(suppl 4A):1-7, 1998.<br />
3. Litwiller SE, Forhman EM, Zimmern PE: Multiple sclerosis and the urologist. J Urol 161:743-757, 1999. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10022678&#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=10022678">Similar articles </a><a href="http://dx.doi.org/10.1097/00005392-199903000-00002">Full article</a><br />
4. Mochrer B, Carey M, Wilson D: Laparoscopic colposuspension: A systematic review. Br J Obstet Gynaecol 110:230-235, 2003.<br />
5. Resnick NM, Yalla SV: Geriatric incontinence and voiding dysfunction. In Walsh PC, Retik AB, Vaughan ED, et al (eds): Campbell&#8217;s Urology, 7th ed. Philadelphia, W.B. Saunders, 1998.<br />
6. Steers WD, Barrett DM, Wein AJ: Voiding dysfunction, diagnosis, classification and management. In Gillenwater JY, Grayhack JT, Howards SS, Duckett JW (eds): Adult and Pediatric Urology, 3rd ed. St. Louis, Mosby, 1996.<br />
7. Wang CC, Yang SS, Chen YT, Hsieh JH: Videourodynamics identifies the causes of young men with lower urinary tract symptoms and low uroflow. Eur Urol 43:386-390, 2003. </p>
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		<title>Heart Transplantation</title>
		<link>http://surgeryprocedure.info/transplantation/heart-transplantation</link>
		<comments>http://surgeryprocedure.info/transplantation/heart-transplantation#comments</comments>
		<pubDate>Tue, 14 Jul 2009 16:37:28 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[TRANSPLANTATION]]></category>

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		<description><![CDATA[91 HEART TRANSPLANTATION
Daniel R. Meldrum M.D., Azad Raiesdana M.D., Jeffrey A. Breall M.D., John W. Brown M.D.
1. Who performed the first experimental heart-lung transplant?
 	Show answer
Alexis Carrel, a French-born American surgeon, developed the vascular techniques required for heart-lung transplantation and performed the first experimental heart-lung transplant in 1907. He transplanted the lungs, heart, aorta, and [...]]]></description>
			<content:encoded><![CDATA[<p><strong>91 HEART TRANSPLANTATION<br />
Daniel R. Meldrum M.D., Azad Raiesdana M.D., Jeffrey A. Breall M.D., John W. Brown M.D.</strong></p>
<blockquote><p><strong>1. Who performed the first experimental heart-lung transplant?</strong></p></blockquote>
<p> 	Show answer<br />
Alexis Carrel, a French-born American surgeon, developed the vascular techniques required for heart-lung transplantation and performed the first experimental heart-lung transplant in 1907. He transplanted the lungs, heart, aorta, and vena cava of a 1-week-old cat into the neck of a large adult cat. For devising the technique of vascular anastomosis and other outstanding accomplishments, Carrel received the Nobel Prize in 1912 (the first Nobel Prize awarded to a scientist working in an American laboratory).<br />
<span id="more-456"></span></p>
<blockquote><p><strong>2. Who performed the first successful experimental heart-lung transplant?</strong></p></blockquote>
<p> 	Show answer<br />
V.P. Demikhov performed the first successful heart-lung transplant in a dog in 1962.</p>
<blockquote><p>3<strong>. Who developed the surgical strategy required for human heart transplantation?</strong> </p></blockquote>
<p>	Show answer<br />
Norman Shumway.</p>
<blockquote><p><strong>4. Who performed the first human heart transplant? When? </strong>	</p></blockquote>
<p>Show answer<br />
C.N. Bernard performed the first human heart transplant in December, 1967 (in Capetown, South Africa, after visiting Dr. Shumway), although Dr. Shumway set the stage by developing the technique in animals. Shumway and the Stanford group performed the first heart transplant in the United States and accomplished the first successful clinical series.</p>
<blockquote><p><strong>5. Who performed the first successful heart-lung transplant? When? </strong>	</p></blockquote>
<p>Show answer<br />
Dr. Bruce Reitz at Stanford in 1981 on a 21-year-old woman with pulmonary hypertension secondary to an atrial septal defect.</p>
<blockquote><p><strong>6. How many heart transplants are performed annually? Is the number increasing or decreasing?</strong></p></blockquote>
<p> 	Show answer<br />
In 1983 approximately 300 heart transplants were performed worldwide. By 1988, the number had rapidly increased to approximately 3000 and remains relatively stable between 3500 and 4000.</p>
<blockquote><p><strong>7. What anastomoses (surgical connections) must be performed for a combined heart and lungs transplant?</strong></p></blockquote>
<p> 	Show answer<br />
The operation requires only a right atrial-to-cava (inflow) anastomosis and an aortic (outflow) anastomosis with a connection at the trachea. Heart-lung transplant is less complicated (fewer anastomoses) than heart transplant alone, which may explain why heart-lung transplant was attempted first.<br />
8. What anastomoses must be performed for a heart transplant? 	Show answer<br />
Left atrial, right atrial, aortic, and pulmonary arterial.</p>
<blockquote><p><strong>9. Who is an acceptable cardiac donor?</strong> </p></blockquote>
<p>	Show answer </p>
<p>Acceptable cardiac donors meet the following criteria:</p>
<p>   1. Requirements for brain death<br />
   2. Consent from next of kin<br />
   3. ABO blood group compatibility with recipient<br />
   4. Within 20% of the same size as recipient<br />
   5. Absence of history of cardiac disease<br />
   6. Normal echocardiogram (ventricular wall motion)<br />
   7. Normal heart by inspection during organ recovery</p>
<blockquote><p><strong>10. Who is an acceptable cardiac recipient?</strong></p></blockquote>
<p> 	Show answer<br />
Although selection criteria are evolving as a result of improved techniques and outcomes, the following criteria are standard: age between newborn and 65 years; irremediable New York Heart Association Functional Class IV cardiac disease; normal renal, hepatic, pulmonary, and central nervous system function; pulmonary vascular resistance < 6-8 Wood units; and absence of malignancy, infection, recent pulmonary infarction, and severe peripheral vascular or cerebrovascular disease. Diabetes is a relative contraindication; the steroids used in posttransplant immunosuppression make diabetes difficult to manage. Also, normal psychological status has proven to be important.</p>
<blockquote><p><strong>11. What are the most common indications for heart transplant in adults and in children?</strong></p></blockquote>
<p> 	Show answer<br />
In adults, coronary artery disease (ischemic cardiomyopathy) and idiopathic cardiomyopathy each account for approximately 45% of transplants.<br />
In children, congenital heart disease and cardiomyopathy are most common, with hypoplastic left heart being the most common congenital malformation requiring heart transplantation.</p>
<blockquote><p><strong>12. What percentage of potential recipients (on the transplant list) die while waiting for a heart transplant?</strong> </p></blockquote>
<p>	Show answer<br />
20%.</p>
<blockquote><p><strong>13. At what point does donor heart ischemic time influence mortality?</strong> </p></blockquote>
<p>	Show answer<br />
Donor heart ischemic time > 6 hours definitely increases mortality. Ischemic times between 4 and 6 hours stun the donor heart. Most transplant teams try to keep ischemic times (from donor harvest to perfusion in the recipient) to < 4 hours.</p>
<blockquote><p><strong>14. Who pioneered hypothermic myocardial preservation? </strong>	</p></blockquote>
<p>Show answer<br />
Henry Swan at the University of Colorado. He submerged anesthetized children in a bathtub of ice water before cardiac procedures.</p>
<blockquote><p><strong>15. How is cardiac allograft rejection prevented?</strong> 	</p></blockquote>
<p>Show answer<br />
Pharmacologically induced immunosuppression is performed by using one of two protocols. The first is triple therapy, which combines cyclosporine, azathioprine, and prednisone. The second major protocol incorporates the monoclonal antibody OKT3 into the triple therapy protocol. OKT3 is substituted for cyclosporine for the first 2 weeks after transplant.</p>
<blockquote><p><strong>16. What is OKT3? 	</strong></p></blockquote>
<p>Show answer<br />
OKT3 is a mouse monoclonal antibody that binds to and blocks the T-cell CD3 receptor. A monoclonal antibody is an antibody generated from the clones of a single cell. For instance, a single B cell, which recognizes the CD3 receptor as an antigen (foreign), is immortalized in cell culture and produces the monoclonal antibody in limitless supply. The CD3 receptor, which is common to all T cells, is important for antigen recognition and T-cell activation; therefore, OKT3 is highly immunosuppressive.<br />
<em><strong>KEY POINTS: CRITERIA FOR ACCEPTABLE HEART DONORS</strong></p>
<p>   1. Donors must meet the criteria for brain death.<br />
   2. Consent from donor&#8217;s next of kin.<br />
   3. ABO blood group compatibility with recipient.<br />
   4. Donor must be within 20% of same size as recipient.<br />
   5. Donor must have no history of cardiac disease and a normal echocardiogram.<br />
   6. Donor heart must appear normal by inspection during organ recovery.</em></p>
<blockquote><p><strong><br />
17. What complications are associated with the use of OKT3? </strong></p></blockquote>
<p>	Show answer<br />
OKT3 may have severe side effects, including pulmonary edema and high fevers, that result from transient cytokine release, which may occur when OKT3 binds to the T-cell activation site. Because OKT3 is an antigen (an antibody from a different species [i.e., a mouse]), patients develop anti-OKT3 antibodies fairly quickly; the result is that OKT3 can only be used to treat one rejection episode. Severe side effects occur in < 5% of patients.</p>
<blockquote><p><strong>18. Does HLA mismatch influence the incidence of rejection after heart transplantation? Is HLA typing routinely performed before heart transplantation? </strong>	</p></blockquote>
<p>Show answer<br />
Yes and no. In a multi-institutional, multivariate analysis of 1719 cardiac transplant recipients by Jarcho et al., HLA mismatch increased the incidence of rejection. However, HLA typing is not routinely done before heart transplantation because it takes too long. In addition, with three of six mismatches, there was still only a trend toward increased rejection-related deaths (P = 0.14). If longer organ preservation times can be achieved, donor/recipient HLA matching will become feasible and should improve survival rates. Again, ABO blood group compatibility does influence graft survival.</p>
<blockquote><p><strong>19. What are the major complications of heart transplantation? </strong></p></blockquote>
<p>	Show answer </p>
<p>    * Allograft rejection (days to weeks)<br />
    * Infection (months)<br />
    * Transplant coronary artery disease (years)</p>
<blockquote><p><strong>20. What is the incidence of transplant coronary artery disease? What are the risk factors? </strong>	</p></blockquote>
<p>Show answer<br />
Nearly 50% of patients have angiographic evidence of coronary artery disease by 5 years after transplant. However, only approximately 10% develop at least 70% stenosis (hemodynamically significant stenosis). Severe stenosis is highly predictive of the need for retransplantation. Risk factors for transplant coronary artery disease include male gender of the donor or recipient, older donor age, and donor hypertension.</p>
<blockquote><p><strong>21. How is cardiac allograft rejection diagnosed? </strong>	</p></blockquote>
<p>Show answer<br />
Clinical suspicion is raised by new-onset cardiac arrhythmia, fever, or hypotension. Diagnosis depends on endomyocardial biopsy, which is performed at regular intervals to detect histologic evidence of rejection before signs or symptoms occur. Radionuclide ventriculography and echocardiography are useful adjuncts in following the hemodynamic manifestations of rejection. Electrocardiography itself is not very sensitive in the diagnosis of rejection.</p>
<blockquote><p>
<strong>22. Are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (&#8221;statin&#8221; drugs) generally recommended for post-cardiac transplant patients? </strong></p></blockquote>
<p>	Show answer<br />
Yes. Hypercholesterolemia is common after transplantation, and HMG-CoA reductase inhibitors reduce the development of the diffuse atherosclerosis that tends to occur in transplanted hearts. In addition, statins have an early effect on mortality, which suggests that these drugs may also have immunosuppressive effects.</p>
<blockquote><p><strong>23. What are ventricular assist devices (VADs)? </strong></p></blockquote>
<p>	Show answer<br />
These devices are designed to unload either the right (RVAD) or left (LVAD) ventricle while supporting the pulmonary or systemic circulation. Patients with these VADs may be ambulatory, and the devices may be worn for weeks to months. VADs may be used as a bridge to transplant (when the patient is listed for transplantation) or as destination therapy (when no transplant is planned).</p>
<blockquote><p><strong>24. What is the most serious complication of transvenous endomyocardial biopsy?</strong> </p></blockquote>
<p>	Show answer<br />
Cardiac perforation occurs in 0.5% of cases. This can rapidly lead to tamponade and circulatory collapse.</p>
<blockquote><p><strong>25. What is the typical infection pattern for a posttransplant patient? 	</strong></p></blockquote>
<p>Show answer </p>
<p>    * First postoperative month: conventional bacterial pathogens encountered in surgical patients<br />
    * 1-4 months: opportunistic pathogens, especially cytomegalovirus<br />
    * >4 months: both conventional and opportunistic infections</p>
<blockquote><p><strong>26. Is the transplanted heart denervated?</strong> </p></blockquote>
<p>	Show answer<br />
Initially, yes, but it is believed that partial reinnervation begins within 1 year. Because of this, the heart&#8217;s anatomically mediated reflexes are blunted (e.g., higher resting heart rate because of decreased or absent vagal tone).</p>
<blockquote><p><strong>27. Can one heart be successfully transplanted twice? </strong>	</p></blockquote>
<p>Show answer<br />
Yes. Meiser et al. transplanted the same heart a second time on March 19, 1991, 42 hours after the initial transplantation. Second transplant of the same heart has since been reported by others.</p>
<blockquote><p><strong>28. What is &#8220;domino heart transplant&#8221;? </strong>	</p></blockquote>
<p>Show answer<br />
The good heart from a heart-lung recipient is transplanted into a patient requiring a heart transplant. Some patients with primary lung dysfunction have secondary irreversible cardiac dysfunction (i.e., Eisenmenger&#8217;s syndrome); others, however, such as patients with cystic fibrosis, have good cardiac function. Patients with good cardiac function may serve as donors and increase the donor pool.</p>
<blockquote><p><strong>29. Is the heart capable of making tumor necrosis factor (TNF)? What does TNF have to do with heart transplantation? </strong></p></blockquote>
<p>	Show answer<br />
TNF, typically described as a macrophage- or monocyte-derived inflammatory cytokine, is also produced in large quantities by the heart. TNF released by the heart after ischemia-reperfusion probably contributes to immediate injury (dysfunction) and possibly to later rejection. Anti-TNF strategies are intuitively promising (but undocumented) therapeutic strategies.</p>
<blockquote><p><strong>30. What is the overall 30-day mortality rate after heart transplant? What is the breakdown in mortality between adult and pediatric patients?</strong></p></blockquote>
<p> 	Show answer<br />
The registry of the International Society for Heart and Lung Transplantation, which has data for approximately 45,000 heart transplants, has recorded a 30-day mortality rate of 10%. The 30-day mortality rate for adult recipients is about 8%; for pediatric recipients, it is slightly higher.</p>
<blockquote><p><strong>31. What are the 5- and 10-year actuarial survival rates for heart transplant recipients? 	</strong></p></blockquote>
<p>Show answer </p>
<blockquote><p><strong>75% and 50%, respectively (and the quality of life is dramatically improved).<br />
32. What work remains to be done in heart transplantation? 	</strong></p></blockquote>
<p>Show answer<br />
The future of heart transplantation is bright. Knowledge gained in experimental myocardial ischemia-reperfusion injury and protection is accelerating. New, exciting ways to manipulate myocardial immunology (e.g., signal transduction, gene therapy, chimerism) will further extend donor ischemic times and improve postoperative myocardial function and graft tolerance. Ultimately, genetic alteration of donor hearts will increase the donor pool.</p>
<p><strong><br />
References</strong><br />
WEB SITE<br />
<a href="http://www.transplantation-soc.org/">http://www.transplantation-soc.org</a><br />
BIBLIOGRAPHY<br />
1. Hosenpud JD, Bennett LE, Keck BM, et al: The Registry of the International Society for Heart and Lung Transplantation: Eighteenth official report-2001. J Heart Lung Transplant 20:805-815, 2001.<br />
2. Kobashigawa JA: Advances in immunosuppression for heart transplantation. Adv Card Surg 10:155-174, 1998. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9917904&#038;dopt=Abstract">Medline</a> <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=9917904">Similar articles</a><br />
3. Kupiec-Weglinski JW: Graft rejection in sensitized recipients. Ann Transplant 1:34-40, 1996. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9869935&#038;dopt=Abstract">Medline</a> <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=9869935">Similar articles</a><br />
4. Kuvin JT, Kimmelstiel CD: Infectious causes of atherosclerosis. Am Heart J 137:216-226, 1999. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9924154&#038;dopt=Abstract">Medline </a><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=9924154">Similar articles</a><br />
5. Leier CV, Binkley PF: Parenteral inotropic support for advanced congestive heart failure. Prog Cardiovasc Dis 41:207-224, 1998.<br />
6. Meldrum DR: Tumor necrosis factor in the heart [review]. Am J Physiol 274:R577, 1998. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=9530222">Medline</a> <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9530222&#038;dopt=Abstract">Similar articles</a><br />
7. Meldrum DR, Dinarello CA, Meng X, et al: Ischemic preconditioning decreases post-ischemic myocardial TNF: Potential ultimate effector mechanism of preconditioning. Circulation 98:II214-II218, 1998.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9852905&#038;dopt=Abstract"> Medline </a><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=9852905">Similar articles</a><br />
8. Mindan JP, Panizo A: Pathology of heart transplant. Curr Top Pathol 92:137-165, 1999.<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=9919809"> Similar articles</a><br />
9. Orbaek Andersen H: Heart allograft vascular disease: An obliterative vascular disease in transplanted hearts. Atherosclerosis 142:243-263, 1999. Medline Similar articles<br />
10. Pillai R, Bando K, Schueler S, et al: Leukocyte depletion results in excellent heart-lung function after 12 hours of storage. Ann Thorac Surg 50:211-214, 1990. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=10030375&#038;dopt=Abstract">Medline </a><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&#038;cmd=Display&#038;dopt=pubmed_pubmed&#038;from_uid=10030375">Similar articles</a><br />
11. Reardon MJ, Letsou GV, Anderson JE, et al: Orthotopic cardiac transplantation after minimally invasive direct coronary artery bypass. J Thorac Cardiovasc Surg 117:390-391, 1999.<br />
12. Spann JC, Van Meter C: Cardiac transplantation. Surg Clin North Am 78:679-690, 1998. Medline Similar articles</p>
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		<title>Urinary Calculus Disease. Bonus Questions</title>
		<link>http://surgeryprocedure.info/urology/urinary-calculus-disease-bonus-questions</link>
		<comments>http://surgeryprocedure.info/urology/urinary-calculus-disease-bonus-questions#comments</comments>
		<pubDate>Tue, 14 Jul 2009 16:35:52 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[UROLOGY]]></category>

		<guid isPermaLink="false">http://surgeryprocedure.info/?p=466</guid>
		<description><![CDATA[BONUS QUESTIONS
11. Is there any type of stone that cannot be seen on helical CT scan?
 	Show answer
Patients taking indinavir sulfate (Crixivan) for HIV infection can form stones from the crystals of the medication; these stones are not seen on CT scan.

12. What toxic substance can be produced by using the holmium:YAG laser on uric [...]]]></description>
			<content:encoded><![CDATA[<p><strong>BONUS QUESTIONS</strong></p>
<blockquote><p><strong>11. Is there any type of stone that cannot be seen on helical CT scan?</strong></p></blockquote>
<p> 	Show answer<br />
Patients taking indinavir sulfate (Crixivan) for HIV infection can form stones from the crystals of the medication; these stones are not seen on CT scan.<br />
<span id="more-466"></span></p>
<blockquote><p><strong>12. What toxic substance can be produced by using the holmium:YAG laser on uric acid stones?</strong></p></blockquote>
<p> 	Show answer<br />
Cyanide is produced from the uric acid. Although this sounds frightening, it is never a problem.</p>
<p><strong>References</strong><br />
WEB SITE<br />
<a href="http://www.transplantation-soc.org/"><strong>http://www.transplantation-soc.org</strong></a><br />
BIBLIOGRAPHY<br />
1. Menon M, Resnick M: Urinary lithiasis: Etiology, diagnosis and medical management. In Walsh PC, Retik AB, Vaughan ED, Wein AJ et al (eds): Campbell&#8217;s Urology, 8th ed. Philadelphia, W.B. Saunders, 2002, pp 3229-3305.<br />
2. Teichman JM, Vassar GJ, Glickman RD: Holmium: YAG lithotripsy photothermal mechanism converts uric acid calculi to cyanide. J Urol 160:320-324, 1998. <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&#038;db=PubMed&#038;list_uids=9679869&#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=9679869">Similar articles</a> <a href="http://dx.doi.org/10.1097/00005392-199808000-00005">Full article</a></p>
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