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1098 PART 10: The Surgical Patient

has evolved to be a valuable strategy to reduce wait list mortality and
TABLE 115-11 King’s College Criteria
more recent data suggest survival similar to recipients of livers from
Acetaminophen-induced Arterial pH <7.3 deceased donors. Given the technical challenges associated with the
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disease or living-related liver transplant, this population experiences an increased
Grade III-IV encephalopathy and rate of biliary leaks, post-operative bleeding, unplanned reexplorations,
Prothrombin time >100 s and hepatic artery thrombosis, and portal vein thrombosis. 71
Serum creatinine >3.4 mg/dL (301 µmol/L)
All other causes of liver Prothrombin time >100 s ■ CHANGES IN DONOR DEMOGRAPHIC AND MANAGEMENT
failure or Deceased Donor: The ideal graft would arise from a donor age <50,
Any three of the following: with hemodynamic stability prior to retrieval, absence of hepatobiliary
1. Age <10 or >40 years disease and severe abdominal trauma, minimal vasopressor require-
2. Etiology: non-A, non-B hepatitis, halothane hepatitis, ments, and normal creatinine. Given the critical shortage of donors
idiosyncratic drug reactions and the expanding wait list, extended criteria for organ acceptance
3. Duration of jaundice before onset of encephalopathy >7 days have increased the availability of organs. However, these grafts have
4. Prothrombin time >50 s poorer initial function and are associated with a decrease in long-
5. Serum bilirubin >18 mg/dL (308 µmol/L) term survival. Hypotension as well as vasopressor use predisposes
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O’Grady et al. 67 a liver to ischemia and is associated with early graft dysfunction.
Cold ischemic times greater than 18 hours are associated with
increased incidence of graft dysfunction, biliary complications, and
series using a cutoff of a systolic PA pressure >60 mm Hg or mean PA intrahepatic strictures; therefore, most centers will try to limit the
pressure >40 mm Hg. In our own program, patients with a mean PA cold ischemic time to less than 12 hours. 73
pressure >35 mm Hg and/or PVR >350 dynes/s/cm refractory to medi- Innovative ways to expand the donor supply include the use of
5
cal therapy are not accepted for transplantation. grafts donated after cardiac death. Favorable outcomes have been
Acute Liver Failure: Acute liver failure is characterized by rapid dete- reported with warm ischemic times of 16 to 20 minutes with some
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rioration (<26 weeks) of synthetic function and encephalopathy centers accepting ischemic times of up to 1 hour. However, primary
secondary to acute severe liver injury in the absence of known under- nonfunction is significantly higher in grafts from non-heart beating
lying liver disease. The King’s College Criteria is a prognostic model donors. Hepatitis C donors are being used in hepatitis C recipients
developed in the 1980s based on a cohort of 588 patients with acute with studies demonstrating comparable survival to a non-hepatitis C
liver failure. The decision to transplant is based on the probability graft. Many centers are accepting hepatitis C donors for hepatitis C
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of spontaneous recovery and the variables most important to predict recipients provided no significant liver damage is seen on pretrans-
outcome include the degree of encephalopathy, prothrombin time, age, plant biopsies. Split liver grafts into right and left lobes for adult and
and etiology. The King’s College Criteria are outlined in Table 115-11. child pairs, respectively is also a promising strategy to increase the
Acute liver failure developing in less than 7 days is often due to donor pool. Living-related donation has also been a strategy to expand
acetaminophen overdose, hepatitis A, and ischemia. Acute liver organ availability with great success.
failure or hepatitis B. The more subacute development of liver fail- ■ TRANSPLANT PROCEDURE
failure occurring within 28 days is often due to drug-induced liver
ure (5-26 weeks) is often caused by drugs or indeterminate causes. Deceased Donor Whole Liver Transplant: During orthotopic liver trans-
Figure 115-4 outlines the variety of etiologies that can present as plantation, anastomoses are created between the native and allograft
acute liver failure. For more on liver failure etiologies, please refer vena cava (supra- and infrahepatic), portal veins, and hepatic arteries.
to Chapter 106 on fulminant hepatic failure. Etiology is the best After blood flow is restored to the liver, the biliary tract will be recon-
indicator of prognosis for reversal without transplant with better structed either by creating an end-to-end anastomosis of the donor
outcomes seen for acetaminophen, ischemic and viral hepatitis and and recipient common ducts (using a T-tube stent) or by connecting
poor outcomes in the setting of mushroom, autoimmune, Wilson, the donor’s common duct to the recipient’s jejunum. Removal of the
and idiosyncratic drug reactions. venous clamps leads to reperfusion of the organ, and will sometimes
be associated with hemodynamic instability, coagulopathy, and elec-
Outcomes: Overall 1-year survival for adult and pediatric deceased trolyte abnormalities (particularly hyperkalemia).
donor liver transplantation is now greater than 85% with 5- and 10-year
survival at 70% and 60%, respectively. Multiple studies have demon- Living Donor Transplant: Recently, there have been a growing number
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strated the safety of living donor liver transplant (LDLT) with the largest of patients who undergo living-donor transplants. The proportion of
multicenter study reporting 1-year graft survival rates of 81%. While living-donor transplant varies from region to region. For example,
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LDLT had higher complication rates and mortality at its inception, it in Asia, almost all liver transplant procedures have involved living

Acetaminophen
Drug
Hepatitis B
Hepatitis A
Autoimmune
Ischemia
Wilson
Budd-Chiari
Pregnancy
Other
Indeterminant
FIGURE 115-4. Causes of acute liver failure (Stravitz ).
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