Short explanation:
A prolonged R time that is normalised with heparinase suggests residual heparin effect. FFP would not necessarily reverse this. In the stable patient protamine sulphate is a suitable treatment, urgent re-exploration is not yet indicated. Clamping the drains could be fatal. Heparinase is not currently used.
Long explanation:
Thromboelastography (sometimes known as TEG – this is a registered trademark) measures the visco-elastic properties of whole blood during, and after clot formation. This real-time profiling provides a global assessment of haemostatic function from initiation to early fibrinolysis. It can thus be used to guide therapy and blood product transfusion.
The thromboelastogram is interpreted using the following measurements:
The trace produced is actually a single trace, but with a mirror image reflected about it's 'y-axis' midpoint.
The R (reaction time) is the time from the start of the test until the width of the trace is 1mm. This represents the time until fibrin is formed. This is prolonged in clotting factor deficiency, anticoagulants and thrombocytopenia
The K time follows the R time, and is the time until the amplitude reaches 20mm. It represents the rate of reaction, and is dependent on both platelets and fibrinogen
The α angle is the angle created by a tangent to the curve at the R time and the midline. It is a measure of the rate of clot formation, and is affected by deficiency in number or function of any aspect of the haemostatic mechanism.
The MA (maximum amplitude) is the maximum width of the curve. It is a measure of the overall strength of clot formed, and is dependent on the platelet numbers and function, and the fibrin that links them.
LY30 (30 minute lysis) or EPL (Estimated Percent Lysis) is a the rate of decline of the curve to baseline. It can be used to determine the stability of the clot (if rapid, indicates significant fibrinolysis)
In the given example, a prolonged R time that corrects with heparinase (an enzyme which inactivates heparin) is likely to be as a result of residual heparin effect. This can be rapidly ameliorated by giving protamine, which should be readily available in the above situation. It is important to note that protamine has been documented, paradoxically, to have adverse effects on both coagulation and platelet function, so it is important not to give an excessive dose. Giving FFP here would not necessarily correct this. Clamping the drains could result in tamponade and therefore is dangerous. Heparinase would reverse the abnormality, if less effectively than protamine, but it's use is not currently recommended. Initiation of cardiopulmonary bypass following heparinase utilisation would require potentially massive doses of heparin. Ultimately this patient may require blood product transfusion, and potentially even return to theatre, but initial therapy with protamine is the most appropriate early management.
Mallet SV, Cox DJA: Thrombelastography; a Review Article. Br J Anaes 1992; 69: 307-313(s)
Willmott, CHA. Arrowsmith, JE. Point of Care Testing. In Klein A, Vuylsteke A and Nashef SAM eds. Core Topics in Cardiothoracic Critical Care. Cambridge, Cambridge University Press. 2008. 117-126
Short explanation:
A prolonged R time that is normalised with heparinase suggests residual heparin effect. FFP would not necessarily reverse this. In the stable patient protamine sulphate is a suitable treatment, urgent re-exploration is not yet indicated. Clamping the drains could be fatal. Heparinase is not currently used.
Long explanation:
Thromboelastography (sometimes known as TEG – this is a registered trademark) measures the visco-elastic properties of whole blood during, and after clot formation. This real-time profiling provides a global assessment of haemostatic function from initiation to early fibrinolysis. It can thus be used to guide therapy and blood product transfusion.
The thromboelastogram is interpreted using the following measurements:
The trace produced is actually a single trace, but with a mirror image reflected about it's 'y-axis' midpoint.
The R (reaction time) is the time from the start of the test until the width of the trace is 1mm. This represents the time until fibrin is formed. This is prolonged in clotting factor deficiency, anticoagulants and thrombocytopenia
The K time follows the R time, and is the time until the amplitude reaches 20mm. It represents the rate of reaction, and is dependent on both platelets and fibrinogen
The α angle is the angle created by a tangent to the curve at the R time and the midline. It is a measure of the rate of clot formation, and is affected by deficiency in number or function of any aspect of the haemostatic mechanism.
The MA (maximum amplitude) is the maximum width of the curve. It is a measure of the overall strength of clot formed, and is dependent on the platelet numbers and function, and the fibrin that links them.
LY30 (30 minute lysis) or EPL (Estimated Percent Lysis) is a the rate of decline of the curve to baseline. It can be used to determine the stability of the clot (if rapid, indicates significant fibrinolysis)
In the given example, a prolonged R time that corrects with heparinase (an enzyme which inactivates heparin) is likely to be as a result of residual heparin effect. This can be rapidly ameliorated by giving protamine, which should be readily available in the above situation. It is important to note that protamine has been documented, paradoxically, to have adverse effects on both coagulation and platelet function, so it is important not to give an excessive dose. Giving FFP here would not necessarily correct this. Clamping the drains could result in tamponade and therefore is dangerous. Heparinase would reverse the abnormality, if less effectively than protamine, but it's use is not currently recommended. Initiation of cardiopulmonary bypass following heparinase utilisation would require potentially massive doses of heparin. Ultimately this patient may require blood product transfusion, and potentially even return to theatre, but initial therapy with protamine is the most appropriate early management.
Mallet SV, Cox DJA: Thrombelastography; a Review Article. Br J Anaes 1992; 69: 307-313(s)
Willmott, CHA. Arrowsmith, JE. Point of Care Testing. In Klein A, Vuylsteke A and Nashef SAM eds. Core Topics in Cardiothoracic Critical Care. Cambridge, Cambridge University Press. 2008. 117-126