TEG is a relatively new modality for monitoring coagulation which is very useful during management of trauma and also in the perioperative scenario..

BASIS:

• The 2 main components of the TEG machine are a cup and a pin. Whole blood is mixed with the activating agent kaolin as well as calcium. The cup then oscillates around the pin slowly, at a rate of 6 times per minute, to mimic natural blood flow in vivo and activate the clotting cascade. As the clot forms, the torque between the cup and pin is transduced and measured, creating a curve. As the clot breaks down and torque decreases, the tracing converges to represent this. 
• The different parameters of the curve are then measured to assess current coagulation status.
• Of the 4 types of TEG assays available, the most common is the rapid TEG. The use of an activator in rapid TEG standardizes the TEG test and speeds up the rate at which clotting takes place, thus making results available more quickly.

INTERPRETATION

• R(sec): The first measurement of note is the reaction time (R time). This is the time interval from the start of the test to the initial detection of the clot. Normal R values range between 7.5 and 15 minutes. A prolonged R time may indicate hemodilution or clotting factor deficiencies. The treatment for prolonged R time is to administer FFP as it contains all factors of the coagulation cascade, without further coagulant hemodilution.  A shortening of R time (< 3 minutes) occurs in hypercoagulable states. Examples would be patients with early disseminated intravascular coagulation (DIC) or septicemia. In these situations, free thrombin is released into the circulating blood, triggering the clotting mechanisms but the patient later begins to bleed because of exhaustion of clotting factors.

• K (sec) and Angle α (°): The clot strength is measured by these 2 variables in TEG. The K value measures the interval between the R time and the time when the clot reaches 20 mm. Normal K values range between 3 and 6 minutes. Prolongation of the K value with normal platelet count  indicates inadequate amounts of fibrinogen to form fibrin. The treatment for prolonged K value is therefore to administer fibrinogen/cryoprecipitate. The α angle measures a line tangent to the slope of the curve during clot formation.The alpha angle represents the thrombin burst and conversion of fibrinogen to fibrin. Normal α value is between 45° and 55°. A longer K value causes a shallow or more acute angle (<45°), while a shorter K value causes a steeper α angle (>45 °). An angle α <45° suggests a less vigorous association of fibrin with platelets. In this case, treatment begins much higher on the coagulation cascade, with the replacement of both fibrinogen and factor VIII. Thus, these patients can be treated with the administration of cryoprecipitate. Shortening of the K-value indicates a very quick formation of clot, potentially due to hypercoagulability or inappropriate consumption of coagulation factors. A shortened K value also corresponds to a steeper α (>45°). The treatment for shortened K and steeper α is anticoagulation therapy

• MA (mm): Maximum amplitude is a measurement of maximum clot strength and provides information on both fibrinogen and platelet function. As the clot develops and increases in tensile strength due to platelet activation and binding to fibrin, the tracing increases it’s MA or appears to widen. Normal values are between 50–60 mm. 80% of the MA is derived from platelet function whereas the remaining 20% is derived from fibrin. A low MA value is indicative of low clot strength, which can be caused by decreased fibrinogen levels, low platelet counts, or decreased platelet function. (i) Paired with a prolongation of K value, this could be a sign of the need for cryoprecipitate. (ii) Administration of platelets may be avoided when a low platelet count is combined with a normal MA value (=platelet function is normal) (iii) Treatment with platelets may be indicated for patients with a low MA value (=low platelet function) and normal platelet count. (iv) High MA will occur in the setting of hyperactivity of platelets, and MA above 75 mm indicates a prothrombotic state. In this case, treating with an anticoagulant would be helpful

• Shear Elastic Modulus Strength, G value or G: is a measure of clot strength or clot firmness, and is calculated based on the amplitude value (A) until the maximum amplitude (MA) is reached. It is the single most important value of the entire assay because it represents the overall function or effectiveness of the clot. Normal G values are between 5.3 and 12.4 dynes/cm². A G value >10 dynes/cm² indicates increased risk of thrombosis. Treatment for high G is accomplished by the use of platelet inhibitors such as Clopidogrel or Aspirin. Aspirin is usually not preferred because it inhibits platelet adherence rather than platelet aggregation. A G <5 dynes/cm² places a patient at increased risk of hemorrhage

• As time progresses during the TEG assay, the tracing will remain at maximal amplitude for a period of time, after which clot lysis begins. Normally, lysis continues for a period of up to 15 minutes. A computerized algorithm automatically estimates the percentage of lysis occurring over time. This is called the Estimated Percentage of Lysis or EPL. After 30 minutes, EPL becomes EPL30 or succinctly LY30 (i.e. percentage of lysis at 30 minutes). Both the EPL and LY30 are measurements of excessive fibrinolysis since they measure the percentage decrease in amplitude after MA. An EPL between 7.5 and 15%, when accompanied by a very high G, reflects a hyperfibrinolytic and hypercoagulable state typical of patients with early DIC. A very high EPL or LY30 (>20%) may indicate the need for antifibrinolytic therapy, such as the use of transexamic acid or aminocaproic acid. LY30 is also useful for patients undergoing thrombolytic drug therapy. This can be observed by rapid curve convergence.

Ref: Thromboelastography: Clinical Application, Interpretation, and Transfusion Management, Shawn Collins et al AANA Journal Course, 2016

HOW DO WE TEST CLOTTING?

• By doing tests like aPTT, PT & INR, Platelet Count, ACT, Bleeding Time, fibrinogen and factor levels, TEG etc
• The aPTT and INR use different reagents to measure the time to form a clot in vitro after platelet-poor plasma from blood collected in a calcium chelating tube, is recalcified
• The aPTT is prolonged with the deficiency of factors of the intrinsic pathway: Fs 8,9,11,12. Also the factors involved in the common pathway (Fs 1,2,10)e.g. Heparin therapy, DIC, liver disease
• The INR is prolonged especially with deficiency of F 7; but also with deficiency of Fs 1,2,5,10 e.g.  warfarin therapy, vitamin K deficiency, DIC, liver disease
• N.B Warfarin inhibits the gamma carboxylation of vitamin K dependent factors 2,7,9,10
• BLEEDING TIME :Duke’s method: Sterilize the finger tip using rectified spirit and allow to dry. Make a sufficiently deep prick using a sterile lancet, so that blood comes out freely without squeezing. Note the time (start the stop-watch) when bleeding starts. Mop the blood by touching the finger tip with a filter paper. This is repeated every 15 seconds, each time using a fresh portion of the filter paper, till bleeding stops. Note the time (stop the stop-watch). Normal value is upto 4 minutes. 
• CLOTTING TIME: Capillary tube method: (Wright’s method). Under sterile precautions make a sufficiently deep prick in the finger tip. Note the time when bleeding starts (start the stop watch). Touch the blood drop at the finger tip using one end of the capillary tube kept tilted downwards. The tube gets easily filled by capillary action. After about two minutes start snapping off small lengths of the tube, at intervals of 15 seconds, each time noting whether the fibrin thread is formed between the snapped ends. Note the time (stop the stop watch) when the fibrin thread is first seen. Clotting time is the interval between the moment when bleeding starts and the moment when the fibrin thread is first seen.

  Normal value is 3 to 10 minutes.

• Bleeding time depends on the integrity of platelets and vessel walls, whereas clotting time depends on the availability of coagulation factors