22 June 2011
1:17 AM | 
Posted by
Dr.Proxy
Thromboelastometry monitoring (rotation thromboelastometry) is different to conventional tests of blood coagulation, which look at isolated stages of blood clotting in plasma. The thromboelastograph looks at the whole process of blood coagulation using whole blood. The measurement is displayed as a graph from the beginning of clot formation to fibrinolysis. It measures the time taken for the clot to form - i.e. the kinetics of clot formation and the tensile strength of the clot. The blood clot has both viscous and elastic properties and it is the elastic shear properties of the clot that the thromboelastograph measures.
Classical thromboelastometry is performed by filling a cuvette with native whole blood and lowering a pin suspended by a torsion wire into the sample. The cup is rotated through 4° 45’ over 10 seconds with a 1 second rest period at each end. The torque of the cup is transmitted to the pin through the sample in the cup. The width of the tracing is proportional to the magnitude of the elastic shear modulus of the sample. Liquid blood has little or no torque so there will be no deflection even when the viscosity is high. As the blood clots and fibrin strands begin to form between the cup and the pin, the motion of the cup is transmitted to the pin.
The pin is guided by a ball bearing ensuring that all movement is limited to rotation. The movement of the pin is detected by an optical detection system and is transmitted to and processed by a computer with specific software. Results obtained by thromboelastometry are dependent on the activity of the plasma coagulation system, platelet function, fibrinolysis and many factors which influence these interactions, including several drugs.
Many limitations of classical thromboelastometry are overcome by the innovative rotation thrombelastometry (ROTEM®). Data obtained with ROTEM® correlate well with classical thromboelastometry (Calatzis et. al, 1996).
In ROTEM®, the pin (sensor) is fixed onto the tip of a rotating shaft, which is guided by a high precision ball bearing system. The shaft rotates back and forth (+/- 4.75 °; cycle time 10/min). It is connected with a spring for the measurement of elasticity. The exact position of the axis is detected by the reflection of light by a small mirror that is attached to the shaft.
The loss of the elasticity upon clotting of the sample leads to a change in the rotation of the shaft. This is detected by a CCD array and the data are analysed by a computer.
This opto-mechanical detection method provides a good protection against the impact of vibrations and mechanical shocks.
Clotting time (CT) or reaction time( R time)
The time from the start of the curve until it reaches 1 mm wide
This is the time taken to form fibrin. Prolonged with clotting factor deficiencies, anticoagulants and thrombocytopaenia.
Clot formation time (CFT) or K time
The time taken for the graph to widen from 1 mm to 20 mm. This is dependent on fibrinogen and platelets.
Maximum clot firmness (MCF )or maximum amplitude
This is the width of the curve at the widest point. This is affected by platelet function and number and fibrinogen.
Alpha angle
This is the angle measured between the midline of the tracing and a line drawn from the 1 mm point tangential to the curve.
The alpha value and CFT indicate the rate of increase of elastic shear modulus in the sample – i.e. how fast the clot structure is forming.
This is abnormal in the presence of clotting factor deficiencies, platelet dysfunction, thrombocytopenia and hypofibrinogenaemia.
Fibrinolysis
This is measured as a decrease in amplitude from the maximum. If there is a substantial decrease – i.e. more than 15% – then this is an indication of fibrinolysis taking place.
Advantages of thromboelastometry
Real time production of a trace Heparinase modification allows the diagnosis of excess heparin as a cause of long R time. Fibrinolysis may be demonstrated by the lysis times at 30 and 60 minutes. A normal trace in a bleeding patient suggests a surgical source. Repeated tests can monitor the progress of intervention.Cardiac surgery
Cardiac surgery has become an area, in which application of thrombelastometry has contributed significantly to an optimisation of therapy.
Except for surgical bleeding, the most often observed problems arise from:
the management of heparin dosage and of protamine chloride
hyperfibrinolysis
dilution
haemostasis disorders by plasma expanders and hypothermia
consumption of coagulation factors and platelets
activation of coagulation and hyperfibrinolysis
other drug effects
A differentiation of surgical bleeding from a true haemostasis disorder is important and influences therapeutic strategies. Thromboelastometry analysis is able to characterise the majority of relevant haemostasis disorders within a few minutes. This is not only a benefit for the outcome of the patient but also an economical advantage. Interventions can be made faster, and often with fewer blood products or other expensive therapies.
Except for surgical bleeding, the most often observed problems arise from:
the management of heparin dosage and of protamine chloride hyperfibrinolysis dilution haemostasis disorders by plasma expanders and hypothermia consumption of coagulation factors and platelets activation of coagulation and hyperfibrinolysis other drug effects A differentiation of surgical bleeding from a true haemostasis disorder is important and influences therapeutic strategies. Thromboelastometry analysis is able to characterise the majority of relevant haemostasis disorders within a few minutes. This is not only a benefit for the outcome of the patient but also an economical advantage. Interventions can be made faster, and often with fewer blood products or other expensive therapies.
Bleeding disorders
Coagulation assays may sometimes generate results which do not reflect the clinical situation. Pathological prothrombin time or activated partial thromboplastin time results initiate additional tests which can often not be performed in the same location. This delays therapeutic decisions, may postpone surgery and increases costs. Thromboelastometry is sensitive for factor XIII and reflects any disturbances in fibrinogen polymerisation or the interaction between fibrinogen and platelets much better than clotting assays, and should be used in those cases.
In some cases of haemophilia, especially with inhibitors, ROTEM® has been successfully used in order to manage substitution therapy with factor VIIa, which is difficult to manage with clotting assays. Also, for other cases of haemophilia, thromboelastometry may give a better picture on the clot stability than clotting tests, which are sometimes subject to interference by lupus anticoagulants.
In some cases of haemophilia, especially with inhibitors, ROTEM® has been successfully used in order to manage substitution therapy with factor VIIa, which is difficult to manage with clotting assays. Also, for other cases of haemophilia, thromboelastometry may give a better picture on the clot stability than clotting tests, which are sometimes subject to interference by lupus anticoagulants.
Alterations of the normal thromboelastographic pattern can give information about:
The coagulation factor activation - R value The coagulation factor amplification - k value and alpha angle The platelet aggregation - maximal amplitude Fibrinolysis - amplitude 60 minutes after maximum Platelet adhesion to the collagen matrix is not assessedOverview
Examples of thromboelastometry
Example 1
No clot formation due to very low factor levels or a heparin effect.
Example 2
A: No coagulation at all – due to whole blood from a heparinised patient
A: No coagulation at all – due to whole blood from a heparinised patient
B: Normal curve – due to whole blood after the addition of heparinase.
Example 3
Prolonged R value suggesting factor deficiency or possibly a minimal heparin effect.
Example 4
Normal coagulation profile with adequate reversal of heparin by protamine. This is confirmed by the second trace with heparinase added.
Example 5
Small alpha angle and small maximal amplitude with weak clot formation. This may be due to thrombocytopenia or hypofibrinogenaemia.
Example 6
Short R value, borderline maximal amplitude. There is significant clot lysis due to poor platelet function and fibrinolysis.
Example 7
Elongated R value, k value not readable, small alpha angle and small maximal amplitude. Due to technical error in thrombelastograph processing or severe coagulopathy.
Example 8
Short R value, short k value, large alpha angle and large maximal amplitude. No fibrinolysis evident, possibly due to aggressive replacement of factors, e.g. platelet rich plasma or chronic hypercoagulable states.
-------------------------( References )-------------------------
Thrombelastography: a review article
Mallett SV, Cox DJA
Comparison of Thrombelastography and Platelet Aggregometry
Tuman KJ, McCarthy RJ, Patel RV, Ivankovich AD
Anesthesiology 1991; 75: A 433 (no medline abstract)
Heparinase-guided thrombelastography in an anticoagulated parturient.
Abrahamson DC, Abouleish EI, Pivalizza EG, Luehr SL, Myers T Phillips MD
Thrombelastography Changes in Pre-Eclampsia and Eclampsia
Orlikowski CEP, Rocke DA, Murray WB, Gouws E, Moodley J, Kenoyer DG, Byrne S
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1 comments:
It cleaves highly sulphated polysaccharide chains in presence of 2-O-sulfated α-L-idopyranosyluronic acid and β-D-glucopyranosyluronic acid residues of polysaccharides. Heparinase
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