Clevenger B, Mallett SV. Transfusion and coagulation management in liver transplantation. World J Gastroenterol 2014; 20(20): 6146-6158 [PMID: 24876736 DOI: 10.3748/wjg.v20.i20.6146]
Corresponding Author of This Article
Susan V Mallett, MBBS, FRCA, Consultant Anaesthetist, Department of Anaesthesia, Royal Free NHS Foundation Trust, Pond Street, London NW3 2QG, United Kingdom. susan.mallett@nhs.net
Research Domain of This Article
Transplantation
Article-Type of This Article
Topic Highlight
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. May 28, 2014; 20(20): 6146-6158 Published online May 28, 2014. doi: 10.3748/wjg.v20.i20.6146
Table 1 Risks of transfusion
General risks
Transfusion related immunomodulation
Accumulation of immune mediators in stored blood
Transfusion associated circulatory overload
Acute left ventricular failure or congestive cardiac failure
Transfusion related acute lung injury
Capillary leak and neutrophil extravasation and activation caused by: Immune mediated: Donor antibodies react with recipient white blood cells, forming leukoagglutinate that become trapped in the lung Non-immune mediated: Endothelium suffers initial insult (e.g., sepsis, surgery or trauma), attracting neutrophils that are activated by biologically active compounds in stored blood
Haemolytic transfusion reactions
Immediate: Donor membrane antigens react with antibodies against these present in recipient plasma
Delayed: Alloimmunised recipient with specific antibodies respond to re-exposure to antigen positive red blood cells
Acute non haemolytic transfusion reactions
Febrile: Donor leucocyte antigens react with recipient white cell antibodies
Allergic: Soluble donor antigens react in an already sensitised recipient
Post-transfusion purpura
Previous sensitisation produces antibodies which attach donor platelet antigens and additionally destroy their own platelets
Transfusion associated graft vs host disease
Donor lymphocytes proliferate within immunocompromised recipient, attacking host cells as ‘‘foreign’’
Infection
Bacterial 1:2000-1:500000
Viral: hepatitis B 1:450000; hepatitis C 1:32000000; HIV 1:5000000; human T-cell leukaemia virus 1:12500000
Table 2 Alterations in both anti- and pro- haemostatic dynamics in liver disease
Thrombocytopaenia Platelet function defects Increased nitric oxide and prostacyclin Low levels of factors II, V, VII, IX, X, XI Vitamin K deficiency Low levels of alpha 2 anti-plasmin, factor XIII, thrombin activatable fibrinolysis inhibitor Elevated t-PA Dysfibrinogenaemia
Surgical technical difficulty Portal hypertension Oesophago-gastric venous distension secondary to compression and vascular clamping
Prolonged R time Decreased alpha-angle Reduced MA
Anhepatic
Reduced coagulation factor synthesis Reduced clearance of t-PA
Duration greater than 45 min
Increased lysis
Reperfusion
‘‘Heparin like effect’’ Platelet entrapment in sinusoids of donor liver Reduction of all coagulation factors Decreased PAI-1 Decreased antifibrinolytic factors Hyper-fibrinolysis
Acidosis Hypothermia
Virtually ‘‘flat’’ native trace with prolonged R time and significantly reduced MA Heparinase trace required Lysis
Post reperfusion
Accelerated t-PA release Thrombocytopaenia (balanced by increased activation)
Delayed graft function
MA reduced
Table 4 Parameters of viscoelastic tests - thromboelastography/rotational thromboelastometry
Parameter
TEG®
ROTEM®
Description
Clotting time
R
CT
Relates to concentration of soluble clotting factors in the plasma, the period of initial fibrin formation (time to reach 2 mm amplitude on the tracing)
Clot kinetics
K (K value) (min)
CFT
Measure the kinetics of clot formation
Measures the speed to reach a specific level of clot strength (period for amplitude to increase from 2 to 20 mm)
Alpha angle (angle in degrees) (°)
Alpha
Measures the rate of clot formation, reflects rate of fibrin build up and cross-linking (angle between a tangent to the tracing at 2 mm amplitude and the horizontal midline)
Clot strength
MA (mm)
MCF
Represents the ultimate strength of the clot (platelets and fibrin), maximum dynamic properties of fibrin and platelet bonding via GPIIb/IIIa receptors (greatest vertical width of tracing)
Clot stability
LY30
CLI
Relates to clot stability and lysis, measures the rate of amplitude reduction from MA at 30 min (in per cent)
Citation: Clevenger B, Mallett SV. Transfusion and coagulation management in liver transplantation. World J Gastroenterol 2014; 20(20): 6146-6158