Thromboelastography (TEG) is a point-of-care diagnostic test that assesses a patient’s entire blood clotting process. Unlike conventional coagulation tests that use blood plasma to analyze only the initial steps of clotting, TEG uses whole blood to measure the mechanical properties of clot formation and breakdown. This comprehensive view guides targeted therapy in high-bleeding risk environments, such as major trauma and cardiac surgery. The device creates a continuous graph, or tracing, that illustrates the strength and stability of the forming clot, which informs clinical decision-making.
Understanding the Standard TEG Tracing
The TEG device works by placing a small sample of whole blood into an oscillating cup. A pin is suspended within the sample. As the blood clots, fibrin strands and platelets attach to the pin, transmitting the clot’s mechanical force to the wire. This movement generates the graphical tracing, where the horizontal X-axis represents time and the vertical Y-axis represents amplitude, signifying the clot’s strength.
A complete tracing illustrates three phases of coagulation: latency, clot formation kinetics, and stability/lysis of the mature clot. The initial flat line reflects the time before the first fibrin strands form. The subsequent widening of the graph indicates the rapid accumulation of platelets and fibrin, which strengthens the clot. The final phase shows the clot reaching its maximum strength before the tracing may narrow, indicating clot breakdown.
Detailed Analysis of Key TEG Parameters
The reaction time, designated as the R value, represents the time from the start of the test until the initial formation of the clot reaches an amplitude of 2 millimeters. The R time reflects the activity of coagulation factors involved in initiating the clotting cascade. A normal R time is typically between 4 and 8 minutes, and a prolonged R value suggests a deficiency or impairment of these circulating clotting factors.
The K time and the Alpha Angle (α) both describe the speed of clot formation and strengthening after the initial fibrin strands have formed. The K time is the duration it takes for the clot to reach a fixed amplitude of 20 millimeters, normally between 1 and 4 minutes. The Alpha Angle is the slope between the R and K points, measuring the rate of fibrin cross-linking and platelet-fibrin interaction. Both K time and Alpha Angle are dependent on the concentration and function of fibrinogen and platelets; a short K time and a steep Alpha Angle (47° to 74°) indicate rapid clot strengthening.
The Maximum Amplitude (MA) is the greatest width of the tracing, representing the ultimate mechanical strength and stability of the mature clot. This parameter indicates the combined contribution of platelet function and fibrinogen concentration to clot strength. Platelets are the dominant component, contributing approximately 80% to the MA, with fibrinogen providing the remaining 20%. A typical normal range for the MA is 55 to 73 millimeters, and any deviation suggests an issue with the quality or quantity of these cellular and protein components.
Lysis at 30 Minutes (LY30) assesses the integrity of the formed clot by measuring the percentage of amplitude reduction 30 minutes after the maximum amplitude is achieved. This parameter quantifies the degree of fibrinolysis, or the natural breakdown of the clot. A normal LY30 value is usually less than 8%, and a significantly elevated percentage indicates hyperfibrinolysis, an excessive and premature dissolution of the clot.
Interpreting Common Clinical Patterns
A prolonged R time, where the graph remains a flat line for an extended period, indicates a Factor Deficiency or the presence of circulating anticoagulants. This pattern signifies a delay because the initial enzymatic steps of the coagulation cascade are slowed. Patients often lack sufficient plasma clotting factors necessary to begin the cascade.
A pattern characterized by a normal R time but a low Alpha Angle, prolonged K time, and a reduced MA points directly to a defect in the clot’s structure, often due to Fibrinogen Deficiency or Platelet Hypofunction. The clot initiates normally, but its formation and final strength are compromised because the building blocks, particularly fibrinogen and functional platelets, are insufficient. This results in a tracing that is slow to widen and does not reach an adequate maximum height.
Conversely, a Hypercoagulable state is identified by a compressed tracing, showing a shortened R time, a steep Alpha Angle, and an increased Maximum Amplitude. This pattern reflects an overly aggressive clotting response where the clot forms too quickly and achieves an abnormally high strength. This state is often seen in conditions like pregnancy or post-operative recovery, suggesting an increased risk for thrombotic events rather than bleeding.
A pattern indicating Hyperfibrinolysis is where the tracing achieves a normal or near-normal MA, but the width rapidly diminishes afterward. This indicates that the clot formed adequately, but the body’s clot-dissolving system is overactive, leading to premature clot breakdown. An elevated LY30 value confirms this diagnosis, which is a common cause of persistent bleeding, particularly in severe trauma.
Guiding Therapeutic Interventions
When a prolonged R time confirms a factor deficiency, treatment involves replenishing missing factors, typically using Fresh Frozen Plasma (FFP). In some cases, Prothrombin Complex Concentrate (PCC) may be used to rapidly reverse the effects of certain anticoagulants and provide concentrated clotting factors.
If the tracing shows a low Alpha Angle and a prolonged K time, indicating a lack of fibrinogen, the targeted therapy is Cryoprecipitate or a fibrinogen concentrate. These products supply the high concentration of fibrinogen needed to rapidly accelerate the clot strengthening phase.
A significantly reduced MA, pointing to poor ultimate clot strength, mandates correcting the platelet and fibrinogen components. Since platelets contribute the most to MA, a low value often directs the use of a Platelet Transfusion to increase the number of functional platelets. In the presence of platelet dysfunction, desmopressin may be considered to improve existing platelet function, while cryoprecipitate would address any concurrent fibrinogen deficit.
The signature pattern of hyperfibrinolysis, marked by a high LY30, requires intervention with an Antifibrinolytic agent, such as Tranexamic Acid (TXA). TXA works by inhibiting the breakdown of the fibrin clot, thereby stabilizing the clot structure and stopping the excessive bleeding caused by premature lysis.