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Liver Transplantation PartⅡ

Liver Transplantation PartⅡ. Presented by SC 林 麟 SC 梁祥光 Supervised by R3 陳建宇 V 詹光政. Intraoperative physiologic changes in liver transplantation. Plasma glucose concentration Acid-Base alteration Plasma potassium concentration Blood Coagulation. Plasma glucose concentration.

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Liver Transplantation PartⅡ

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  1. Liver TransplantationPartⅡ Presented by SC 林 麟SC 梁祥光 Supervised by R3 陳建宇 V 詹光政

  2. Intraoperative physiologic changes in liver transplantation • Plasma glucose concentration • Acid-Base alteration • Plasma potassium concentration • Blood Coagulation

  3. Plasma glucose concentration • The role of liver in glucose metabolism- glycogen storage v.s glycogenolysis - gluconeogenesis • Hypoglycemia may complicate the anhepatic phase of liver transplantation.

  4. Mean plasma glucose concentration during three phases of liver transplantation ~Mayo Clin Proc 64:241-245,1989

  5. Intraoperative hyperglycemia • Stress response to surgery • Anesthesia • Hypothermia • Corticosteroid • Infusion of blood product

  6. Abrupt increase in plasma glucose after reperfusion • Influx of the remaining preservation solution into systemic circulation • Release of intracellular glucose from ischemic hepatocyte • Insufficient hepatic glycogenesis • Suppression of insulin response

  7. Hormonal control of glucose metabolism during liver transplantation • Hyperglycemia is not accompanied by appropriate hormonal changes. • The releases of catecholamines in response to stress may block insulin release and insulin function. ~Transplantation proceedings, Vol.21, No3(Jun), 1989:p3529

  8. Acid-base alteration A= induction; B= dissection; C= anhepatic; D= reperfusion;E= gallbladder anastomosis; F= skin closure; G= end of procedure ~Anesth Analg 1985; 64:108-16

  9. Acid-base alteration • Acid metabolite from rapid transfusion • Stagnation of blood flow below diaphragm • Decreased BP and reduced tissue perfusion • Reduced hepatic clearance of acidic substance • Hypothermia • Metabolites from the donor liver after reperfusion

  10. Plasma potassium concentration What factors influence [K+] in OLT patient • Pre-operative: ↓ [K+] - diuretics therapy inadequate intake loss from vomiting /diarrhea ↑[K+] - renal dysfunction • Intra-operative: ↑[K+] - inadequate renal function large volume blood transfusion

  11. Plasma potassium concentration • Stable throughout the early part of operation • A dramatic but transient ↑[K+] after reperfusion • A gradual decrease in [K+] after introduction of the new liver. ~Anesth Analg 1985; 64:108-16

  12. Acute hyperkalemia after reperfusion－influx of potassium from donor liver • Elevated T wave and arrhythmia • Myocardial depression, cardiac arrest • May contributed to subsequent postreperfusion syndrome • The potassium is taken up by the donor liver and cells of the body later in the neohepatic phase.

  13. Pathophysiological mechanisms of hyperkalemia in orthotopic liver transplantation (Anesth Analg 2000; 91:1351-5) Recipient • SerumK+, serum lactate, and CI during anhepatic phase were independent and significant factors that could predict serum K+ concentration 1-min postrevascularization.. • Metabolic acidosis caused by lower cardiac output and decreased liver lactate uptake may explain ↑[K+] just before revascularization. Donor • [K+] just after revascularization does not correlate with the extent of preservation injury of the graft liver or the duration of cold ischemia. • K+ derived from the preservation solution might be the important donor-related factor causing hyperkalemia.

  14. Blood coagulation

  15. Blood coagulation • The PT and aPTT lengthen significantly at early stage Ⅲ(reperfusion) and returen toward normal by the end of the operation. • FactorsⅡ, Ⅶ, Ⅸ, Ⅹ, XII, fall during the anhepatic period, reaching their nadirs early in stageⅢ, and then return to baseline. • FactorsⅠ,Ⅴ,Ⅷ start to fall earlier and have made lesser recovery. • The curve of factor XI is almost flat. • ELT(euglobulin lysis time) decreased rapidly and were significantly different from baseline. ~Hepatology Vol.9, No.5, pp.710-714, 1989

  16. Blood coagulation • Activation of fibrinolysis in late anhepatic phase causes the destruction of susceptible coagulation factors(Ⅰ,Ⅴ,Ⅷ ) and concomitant prolongation of aPTT early in reperfusion phase. • Activation of fibrinolysis process • Release of plasminogen activator(t-PA) from vascular endothelium • Reduced hepatic clearance of t-PA during anhepatic phase • Inhibition of t-PA inhibitor by protein C • Acidosis/ hypothermia / catecholamines ~Anesth Analg 1994; 78:382-99

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