CONTINUING MEDICAL EDUCATION PROGRAM
JACS CME-1 Featured Article, Volume 206, March 2008 Living donor liver transplantation for acute liver failure: A 10-year experience in a single center Ikegami T, Taketomi A, Soejima Y, et al J Am Coll Surg 2008;206:412–418 Beta-blockers in isolated blunt head injury Inaba K, Teixeira PGR, David J-S, et al J Am Coll Surg 2008;206:432–438 Award to physician should claim only those credits that he/ she actually spent in the educational activity. You can earn 4 CME credits using JACS CME Online, at http://jacscme.facs.org, or you can earn 2 CME credit if you submit this page by fax (see instructions in box below). Living donor liver transplantation for acute liver failure: A 10-year experience in a single center. Ikegami T, Taketomi A, Soejima Y, et al. Beta-blockers in isolated blunt head injury. Inaba K, Teixeira PGR, David J-S, et al. Current utility of staging laparoscopy for pancreatic and peripancreatic neoplasms. White R, Winston C, Gonen M, et al. Outcomes of bacteremia in burn patients involved in combat operations overseas. Ressner RA, Murray CK, Griffith ME, et al.
Objectives: After reading the featured articles published in this issue of the Journal of the American College of Surgeons (JACS) participants in the JACS CME program should be able to demonstrate increased understanding of the material specific to the article featured and be able to apply relevant information to clinical practice. Objectives are stated at the beginning of each featured article; the questions follow with five response choices, and a critique discussing the objective. The American College of Surgeons is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to sponsor continuing medical education for physicians. The JACS CME program fulfills the ACCME essentials. The American College of Surgeons designates this educational activity for a maximum of 2 Category 1 credits toward the AMA Physician’s Recognition
Questions: Wendy Cowles Husser, MA, MPA Executive Editor, JACS 633 N Saint Clair Street, Chicago, IL 60611 312-202-5306 (ph) 312-202-5027 (fax)
[email protected]
© 2008 by the American College of Surgeons Published by Elsevier Inc.
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ISSN 1072-7515/08/$34.00 doi:10.1016/j.jamcollsurg.2007.12.004
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Continuing Medical Education Program
Living donor liver transplantation for acute liver failure: A 10-year experience in a single center
Ikegami T, Taketomi A, Soejima Y, et al J Am Coll Surg 2008;206:412–418
Learning Objectives: After study of this article, the surgeon will be able to describe the etiologies, indications and expected outcomes of living donor liver transplantation (LDLT) for acute liver failure (ALF), for offering the procedure. Question 1
Which of the following statements concerning the etiologies and pre-transplant work-ups for LDLT for ALF is correct? a) A patient with delayed onset of hepatic encephalopathy later than 10 days has the greater chance of spontaneous recovery, with little possibility for requiring LDLT. b) The leading indication of LDLT for ALF is Hepatitis B associated ALF. c) ALF with acute-on-chronic type Hepatitis B is rarely indicated for LDLT, but for medical treatments including the use of antiviral agents. d) A larger living donor graft, over 60% of graft volume standard liver volume ratio (GV/SLV), is required for LDLT indicated for ALF. e) Donor work-ups need to be started as early as possible, in order to make timely LDLT before having permanent brain injuries of an ALF recipient.
Critique: Among ALF with encephalopathy (fulminant hepatitis), acute type (the onset of hepatic encephalopathy within 10 days after the initial symptoms including jaundice, abdominal pain, general fatigue, etc) has better outcome with increased spontaneous recovery rate (50–60%). However, subacute type (the onset of encephalopathy after 10 days from the initial symptoms) has poor (10–20%) spontaneous recovery rate with increased need for liver transplantation. The causes of ALF include unknown (60%), Hepatitis B (30%), and others (10%). Among the Hepatitis B associated ALF, acute-on-chronic (25%) refers acute aggravation of chronic or cirrhotic Hepatitis B. Because of its limited baseline hepatic function and poor regenerative potential, it usually needs liver transplantation. CT findings, characteristic for chronic liver diseases including cirrhotic liver with collateral vessels, are helpful for making its diagnosis. ALF with de novo infection of Hepatitis B (50%) refers the ALF with initial Hepatitis B infection in adults due to sexual contact, needle puncture, etc. ALF from Hepatitis B
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carrier (25%) refers ALF with sudden increase of Hepatitis B virus in its carrier with normal liver function tests. The minimum LDLT graft size for ALF does not differ from those for other LDLT indications; 35–40% of GV/ SLV. Although a patient with ALF has acute critical general condition, he/she basically has healthy vital organs without characteristic features for chronic liver diseases, including portal hypertension, collateral vessels or hypersplenism. However, in order to perform timely LDLT with perfect neurological recovery, donor work-ups, especially graft volumetry, need to be started as early as possible, Question 2
Which of the following statements concerning the outcomes of LDLT for ALF is correct? a) There is no relationship between the severity of hepatic encephalopathy and the size of an ALF native liver. b) Permanent neurological deficit is less than 5% after LDLT for ALF. c) The 1-year graft and patient survival rates after LDLT for ALF is 60%. d) The major cause of graft loss after LDLT for ALF is small for size graft syndrome. e) The overall complication rate for the living donors is less than 5%.
Critique: The advanced Grade of hepatic encephalopathy in ALF is associated with severe atrophy of a native liver. Therefore, even though a patient with Grade-I or –II hepatic encephalopathy, CT finding of severe liver atrophy around 50–60% of SLV expects the acute deterioration of the neurological status and the need of liver transplantation. If the donor work-ups were completed earlier, followed by timely LDLT, the neurological outcomes after LDLT is favorable, with less than 5% chance of permanent neurological deficits. The temporary neurological complication rate is 15–20% after LDLT for ALF, and the time between LDLT and extubation is prolonged in patients with advanced encephalopathy grades. The 1-year graft and patient survival rate after LDLT for ALF is 80%, and is comparable for those for other indications of LDLT. Again, the most beneficial point of LDLT for ALF is its timely application in order to avoid brain death. The leading cause of graft loss after LDLT for ALF multiorgan failure associated with septic complications. The most significant problem in LDLT is the morbidity of donors. The overall complication rate is 35% and the rate of major one (bile duct problem which requires some intervention) is 10%.
Vol. 206, No. 3, March 2008
Beta-blockers in isolated blunt head injury
Inaba K, Teixeira PGR, David J-S, et al J Am Coll Surg 2008;206:432–438
Learning Objectives: After review of this article, the surgeon will be able describe the current understanding of the role of beta-blockade in the management of patients who have sustained Traumatic Brain Injury. Question 1
Which of the following statements concerning patients with Traumatic Brain Injury (TBI) is correct? a) Due to the rarity and excellent prognosis associated with head injuries, TBI has a minimal impact on society in North America. b) Beta-blockade has been identified as an independent protective factor for mortality in the treatment of all injured patients. c) All patients with TBI should be started immediately on Beta-blockers. d) Beta-blockade has been identified as an independent protective factor for mortality in the treatment of patients with TBI and further investigation is warranted. e) The mechanism for the protective effect of betablockade as a treatment for patients with TBI has been clearly delineated.
Critique: Traumatic brain injury (TBI) is a major cause of death and neurologic disability after blunt trauma. After TBI, there is a catecholamine surge that correlates with admission GCS, neurologic recovery as measured by the Glasgow Outcome Score, survival, length of stay and ventilator dependence. In a murine model of TBI and 2 retrospective series of human head-injured patients, beta-blockade has been demonstrated to exert a protective effect. In the current study, 1,156 patients with isolated had injury admitted to the ICU of a high-volume, level 1
Continuing Medical Education Program
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trauma center over a 90 month period were retrospectively reviewed. The patients receiving beta-blockade (18%) had a lower unadjusted mortality compared to patients not receiving beta-blockade (17% vs. 21%, p ⫽ 0.183). Stepwise logistic regression identified treatment with beta-blockade to be an independent protective factor for mortality (adjusted odds ratio: 0.54; 95% CI: 0.33–0.91; p ⫽ 0.01). Due to the retrospective design of this study, the indication for beta-blockade, the beta-selectivity of the agents utilized, duration of treatment, and titrated end-points were not controlled for. Further prospective, controlled evaluation is warranted. Question 2
Which of the following patient populations may benefit most from Beta-adrenergic Blocker treatment after Traumatic Brain Injury? a) Patients ⬍ 55 years old with severe (AIS ⱖ 4) TBI. b) Pediatric patients with severe (AIS ⱖ 4) TBI. c) Patients 19–40 years old with mild to moderate (AIS ⬍ 4) TBI. d) Pediatric patients with mild to moderate (AIS ⬍ 4) TBI. e) Patients ⱖ 55 years old with severe (AIS ⱖ 4) TBI.
Critique: The TBI population in this study was stratified utilizing the main predictors for mortality identified during the multivariable analysis: age ⱖ 55 years, severe head injury (AIS ⱖ 4) and initial GCS ⱕ 8. When comparing the odds ratio for mortality between patients exposed and not exposed to beta-blockers, elderly patients (ⱖ 55) with severe had injuries (AIS ⱖ 4) were found to have a mortality of 28% compared to 60% (Odds Ratio: 0.3;96% CI: 0.1–0.6; p ⫽ 0.001). Inserting GCS reduces the numbers in each stratum and statistical significance is not reached however a clinically significant reduction in mortality from 78% to 50% (Odds Ratio ⫽ 0.43; CI ⫽ 0.19–0.97; p ⫽ 0.1) is seen with beta-blockade.