liver transplantation partⅡ
DESCRIPTION
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. - PowerPoint PPT PresentationTRANSCRIPT
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