How to Interpret a Thromboelastography (TEG)

A thromboelastography (TEG) tracing is a real-time picture of how your blood clots, holds together, and eventually breaks down. Unlike standard lab tests that measure isolated pieces of the clotting process, TEG tracks the entire lifecycle of a clot in a single test, from the first strands of fibrin forming to the moment the clot dissolves. The output is a characteristic shape that widens over time, and each dimension of that shape corresponds to a specific phase of clot formation. Learning to read those dimensions is the key to interpreting the test.

What the Tracing Actually Shows

TEG works by placing a small blood sample into a cup that oscillates gently. A pin suspended in the sample detects resistance as fibrin strands form and bind the pin to the cup. As the clot strengthens, the pin moves more; as the clot breaks down, resistance fades. The machine plots this resistance over time, producing a tracing that looks like a symmetrical, elongated diamond or cigar shape when clotting is normal.

The tracing starts as a flat line (no clot), then begins to diverge as clotting kicks in, widens to a peak representing maximum clot strength, and may narrow again if the clot starts dissolving. Every clinically meaningful parameter is simply a measurement taken at a specific point on this shape. Both the TEG and its European counterpart, ROTEM, generate output by measuring changes in the viscoelastic strength of a clotting blood sample to which a constant rotational force is applied, though they use slightly different terminology for equivalent parameters.¹

The Five Core Parameters

Five numbers form the backbone of TEG interpretation. Each one maps to a different phase of clot biology, and together they tell you whether clotting is starting on time, building properly, reaching adequate strength, and staying intact.

R Time (Reaction Time)

R time measures the minutes from the start of the test until the first detectable clot begins to form. It reflects the activation of coagulation and thrombin generation, essentially the enzymatic cascade that gets clotting started.² A prolonged R time suggests that clotting factor activity is low or that an anticoagulant is interfering with the cascade. A short R time points toward a hypercoagulable state where clotting is initiating too quickly. In practical terms, a long R time is often the signal to consider fresh frozen plasma, which supplies clotting factors.

K Time (Kinetics Time)

K time picks up where R time leaves off. It measures how long it takes for the clot to reach a fixed level of firmness (typically an amplitude of 20 mm on the tracing). This reflects the speed of fibrin cross-linking and early clot buildup. A prolonged K time suggests that fibrinogen levels are low or that platelet function is impaired, because both contribute to how quickly the clot gains substance. In liver disease patients, K time correlates strongly with fibrinogen levels.³

Alpha Angle

The alpha angle is the slope of the tracing as it diverges from the baseline, measured in degrees. It represents the rate of clot strengthening. A steep angle means the clot is building rapidly; a shallow angle means clot formation is sluggish. Like K time, the alpha angle reflects the interplay of fibrinogen and platelets, and it correlates consistently with fibrinogen levels across different clinical populations.³ A low alpha angle in someone who is bleeding suggests a need for cryoprecipitate (which contains concentrated fibrinogen) or fibrinogen concentrate.

MA (Maximum Amplitude)

MA is the widest point of the tracing, measured in millimeters. It represents the absolute strength of the clot at its peak and is the single most discussed TEG parameter. MA depends on both platelets and fibrinogen working together. Research in healthy patients shows that the product of platelet count and fibrinogen concentration correlates more strongly with MA than either one alone.⁴ The relationship between platelet count and MA is linear when platelet counts are low (below about 90 × 10⁹/L), then plateaus once counts exceed roughly 100 × 10⁹/L, meaning that above a certain platelet threshold, adding more platelets does not meaningfully increase clot strength.⁴

A low MA tells you the clot is weak and may not hold up against bleeding. The clinical response depends on which contributor is deficient: if platelets are low, transfuse platelets; if fibrinogen is low, give cryoprecipitate. Some TEG assays include a functional fibrinogen channel that isolates fibrinogen’s contribution, helping clinicians distinguish between the two. A high MA, on the other hand, signals a hypercoagulable state. In patients with septic shock, an MA below 60 mm was found to be an independent predictor of disseminated intravascular coagulation, with roughly 79% sensitivity and 73% specificity.⁵

LY30 (Lysis at 30 Minutes)

LY30 measures the percentage of clot that has dissolved 30 minutes after reaching maximum amplitude. It is the primary marker for fibrinolysis, the body’s process of breaking down clots. In a healthy person, very little of the clot should dissolve in that window. When LY30 is elevated, it means the clot is being chewed apart too fast, a dangerous situation in trauma or surgery because even if you form a good clot, it will not stay intact long enough to stop bleeding.

Trauma research has identified an LY30 of 3% or greater as a critical threshold. Patients above that cutoff were far more likely to need a massive transfusion and had a dramatically higher rate of hemorrhagic death compared to those below it.⁶ At even higher LY30 levels (10% or above), the risk escalates further, and patients are significantly more likely to die, require cryoprecipitate, or need massive transfusion.⁷ An elevated LY30 is the classic trigger for giving an antifibrinolytic drug such as tranexamic acid.

Putting the Numbers Together

The real power of TEG is that these five parameters, read together, create a pattern that tells you what kind of clotting problem is present. A patient who is bleeding after surgery might show a normal R time but a very low MA. That pattern suggests the clotting cascade is working fine but the clot itself is weak, pointing toward platelet or fibrinogen deficiency rather than a need for plasma. Another patient might show a prolonged R time, normal MA, and normal LY30, suggesting a factor deficiency or anticoagulant effect that delays clot initiation but does not compromise clot strength once it forms.

Broadly, TEG tracings fall into recognizable profiles:

Normal: All parameters within reference ranges. The tracing has a classic wide-bodied cigar shape.
Hypocoagulable: Prolonged R and K times, low alpha angle and MA. The tracing is narrow and slow to develop. Common in coagulopathy from dilution, factor deficiency, or severe liver disease.
Hypercoagulable: Short R time, high alpha angle and MA. The tracing is wide and develops quickly. Seen in prothrombotic states such as postoperative patients, cancer, or pregnancy.
Fibrinolytic: The tracing widens normally but then narrows rapidly as the clot dissolves. LY30 is markedly elevated. Classic for trauma-induced fibrinolysis or during liver transplantation.

Why TEG Adds Value Over Standard Lab Tests

Conventional coagulation tests like PT/INR and aPTT have been the workhorses of hemostasis assessment for decades. They measure isolated endpoints in plasma samples, essentially asking whether clotting factors can form fibrin under controlled conditions. TEG does something fundamentally different: it tests whole blood, so platelets, red blood cells, fibrinogen, and clotting factors all interact as they would in the body.

This distinction matters in several ways. In patients with severe liver disease, PT/INR is frequently abnormal, which can create the misleading impression that they are at high bleeding risk. Yet TEG tracings in many of these patients fall within normal range, reflecting the concept of “rebalanced hemostasis” where pro- and anticoagulant deficiencies offset each other.⁸ This finding has real clinical consequences: patients with acceptable TEG results can proceed to procedures, including liver transplantation, without unnecessary blood product transfusion.

In an animal model of hemorrhagic shock and hypothermia, standard PT and aPTT failed to detect coagulation defects that TEG identified and differentiated by mechanism, making TEG the only test able to guide focused treatment of the specific clotting problem present.⁹ In cardiac surgery, TEG parameters like R time and MA predicted postoperative bleeding with fair accuracy, while no conventional test reached the same threshold.¹⁰

That said, the correlation between TEG and conventional tests is inconsistent. In liver disease patients, R time correlated only weakly with INR, while MA correlated strongly with fibrinogen levels.³ The two types of tests are measuring overlapping but distinct aspects of hemostasis, so they should be treated as complementary rather than interchangeable.

Specialized TEG Assays

Beyond the standard kaolin-activated TEG, several modified assays expand what the test can detect.

The heparinase channel runs a parallel TEG sample treated with heparinase, an enzyme that neutralizes heparin. This is critical during and after cardiac surgery, where patients receive large doses of heparin for cardiopulmonary bypass. By comparing the standard tracing with the heparinase tracing, clinicians can determine whether a prolonged R time is due to residual heparin or to an actual clotting factor deficiency. If the heparinase tracing normalizes while the standard one remains prolonged, residual heparin is the culprit and additional protamine can be given.¹¹

Platelet Mapping is a TEG modification designed to measure how effectively antiplatelet drugs are suppressing platelet activity. It uses separate channels with arachidonic acid (sensitive to aspirin’s effect) and adenosine diphosphate (sensitive to clopidogrel’s effect) to quantify the degree of platelet inhibition through each pathway.¹² In practice, though, the results overlap considerably between patients on and off antiplatelet therapy, which limits its clinical usefulness for individual decision-making.¹³

Newer TEG platforms like the TEG 6s have improved the ability to measure platelet count and function at the point of care. Studies show the TEG 6s can accurately detect platelet function inhibition when it exceeds roughly 68% as measured by laboratory platelet aggregation testing.¹⁴ The TEG 6s also shows differences from older TEG 5000 devices in fibrinolysis detection: the upper limit of normal for LY30 is lower on the 6s (about 3.2% versus 5.0%), and abnormal LY30 readings are roughly six times more common on the newer device.⁷ This means clinicians switching between platforms cannot simply apply the same cutoffs.

TEG-Guided Transfusion in Practice

One of the strongest use cases for TEG is directing blood product transfusion in real time. Instead of empirically giving fixed ratios of plasma, platelets, and red blood cells, clinicians can use the TEG tracing to identify the specific deficiency and target it. A trial comparing TEG-guided resuscitation to empirical transfusion in trauma patients found that TEG-guided care reduced 28-day mortality from about 36% to about 20%, while also reducing total blood product use and increasing ICU-free and ventilator-free days.¹⁵

Similar patterns appear across multiple surgical settings. In abdominal trauma, a goal-directed TEG protocol reduced blood product use compared to conventional transfusion management.¹⁶ In cardiac surgery, introducing TEG-directed transfusion reduced overall blood product use by over 40%, translating into significant cost savings for both patients and institutions.¹⁷ During liver transplantation, TEG has become a standard tool for guiding factor replacement and managing the fibrinolysis that commonly occurs during the procedure.¹⁸ Systematic TEG use in liver transplant patients appears to result in fewer blood products administered without increasing mortality or complications.¹⁹

Detecting Hypercoagulability and Clot Risk

TEG is not only useful for identifying bleeding problems. A tracing that is “too good” can be just as clinically important. Hypercoagulable TEG patterns (short R time, high MA, elevated G value) have been linked to increased risk of blood clots after surgery. In patients with femoral and pelvic fractures, a hypercoagulable TEG profile predicted postoperative deep vein thrombosis with an odds ratio of roughly 1.9 even after adjusting for other risk factors.²⁰ In surgical patients more broadly, an elevated G value (a mathematical derivative of MA that reflects clot strength on a different scale) was the strongest predictor of thromboembolic events, with no events occurring in patients whose TEG showed normal coagulability.²¹

Sepsis is a particularly complex scenario. TEG tracings in septic patients can show hypercoagulability, hypocoagulability, or even normal values, depending on where the patient is in the disease course.²² Early sepsis often drives a hypercoagulable state as inflammation activates the clotting system. As sepsis worsens and clotting factors are consumed, the pattern can shift toward hypocoagulability and frank DIC. Serial TEG measurements can track this progression in a way that isolated lab draws cannot.

Special Populations

Pregnancy pushes the hemostatic system toward hypercoagulability as a physiological adaptation to prepare for delivery. TEG captures this shift clearly. Research in pregnant women showed that the time to initial fibrin formation (R time) and the time to reach a certain clot strength (K time) both decreased significantly from the third trimester through the postpartum period. Meanwhile, clot lysis increased significantly after delivery, reflecting the transition back toward a less prothrombotic state.²³ These shifts mean that applying standard adult reference ranges to a pregnant patient will often falsely label her as hypercoagulable when her TEG is perfectly normal for that physiological state.

Neonates present their own interpretive challenge. Healthy newborns show accelerated clot initiation, increased clot strength, and increased fibrinolysis compared to older children and adults. Premature infants have a more hypocoagulable profile than full-term babies, but their hemostasis is still balanced, evolving toward a more procoagulant pattern during the first month of life. Critically ill neonates, by contrast, shift toward hypocoagulability compared to healthy newborns.²⁴ Cord blood samples also skew results toward hypercoagulability compared to whole blood draws, which adds another variable when interpreting neonatal TEG.

Common Pitfalls and Errors

TEG is a powerful test, but it is also sensitive to how the sample is collected and processed. A study characterizing analytical errors in TEG interpretation found several recurring problems that can mislead clinicians if not recognized.

Sample evaporation during testing can produce a falsely elevated MA, making the patient appear more hypercoagulable than they actually are. This was seen in roughly 8% of error cases in one review. Failure of the instrument’s auto-calibration before a run produced a graph that appeared falsely hypercoagulable, accounting for about 10% of errors. And using calcium chloride reagent that was more than 24 hours old produced a falsely hypocoagulable tracing or even a flat line, seen in about 7% of errors.²⁵

Beyond these technical artifacts, interpretation pitfalls include applying the wrong reference ranges. As noted in the sections above, neonates, pregnant patients, and patients on specific devices all have different normal values. A TEG tracing that looks abnormal by adult standards may be entirely appropriate for a term newborn. Similarly, the shift from TEG 5000 to TEG 6s means that LY30 thresholds established on the older platform cannot be transferred directly to the newer one without local verification. Institutions adopting a new device should validate their own reference ranges rather than defaulting to published cutoffs from a different platform.

Timing also matters. TEG is typically run on citrated blood that is recalcified before testing, and the delay between blood draw and analysis can affect results. Most protocols specify running the sample within a defined window. Samples that sit too long may show artifactually different clotting profiles. In time-sensitive environments like trauma bays and operating rooms, this means the sample needs to get to the analyzer quickly, which is one reason many institutions place TEG machines as close to the point of care as possible.

TEG in the Context of ROTEM

ROTEM (rotational thromboelastometry) is the main alternative to TEG, and clinicians will encounter both depending on the institution. The two devices measure the same fundamental property of blood (viscoelastic clot strength), but they use different mechanical approaches and different reagent systems, and their parameters have different names. TEG’s R time corresponds roughly to ROTEM’s clotting time (CT); TEG’s K time corresponds to ROTEM’s clot formation time (CFT); TEG’s alpha angle and MA correspond to ROTEM’s alpha angle and maximum clot firmness (MCF).²⁶

Despite the conceptual overlap, the numerical values from TEG and ROTEM are not directly interchangeable. A normal R time on TEG and a normal CT on ROTEM may represent different absolute numbers in minutes. Institutions use one platform or the other, and the treatment algorithms built around each use device-specific thresholds. If you are trained on TEG and move to a ROTEM-based institution, the interpretive logic is the same (same phases of clot formation, same clinical questions), but you need to learn the new parameter names and the local reference ranges rather than simply converting numbers.