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

• The role of liver in glucose metabolism - glycogen storage v.s glycogenolysis - gluconeogenesis

• Hypoglycemia may complicate the anhepatic phase of liver transplantation.

Mean plasma glucose concentration during three phases of liver transplantation

~Mayo Clin Proc 64:241-245,1989

Intraoperative hyperglycemia

• Stress response to surgery

• Anesthesia

• Hypothermia

• Corticosteroid

• Infusion of blood product

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

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

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

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

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

Plasma potassium concentration

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

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.

Pathophysiological mechanisms of hyperkalemia in orthotopic liver transplantation

Recipient• Serum K+, 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.

(Anesth Analg 2000; 91:1351-5)

Blood coagulation

Blood coagulation

• The PT and aPTT lengthen significantly at early stage (reperfusion) Ⅲand returen toward normal by the end of the operation.

• Factors , , , , XII, fall during the anhepatic period, reaching Ⅱ Ⅶ Ⅸ Ⅹtheir nadirs early in stage , and then return to baseline.Ⅲ

• Factors , , start to fall earlier and have made lesser recovery.Ⅰ ⅤⅧ

• 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

Blood coagulation

• Activation of fibrinolysis in late anhepatic phase causes the destruction of susceptible coagulation factors( , , Ⅰ ⅤⅧ ) and concomitant prolongation of aPTT early in reperfusion phase.

• Activation of fibrinolysis process

Release of plasminogen activator(t-PA) from vascular endotheliumReduced hepatic clearance of t-PA during anhepatic phase

Inhibition of t-PA inhibitor by protein CAcidosis/ hypothermia / catecholamines ~Anesth Analg 1994; 78:382-99