TEG Interpretation

Thromboelastography (TEG) is a viscoelastic test: it measures the physical strength of a clot as it forms, matures, and breaks down in whole blood, rather than isolating a single factor the way PT/INR or PTT do. A pin (TEG 5000) or an oscillating fluid meniscus (TEG 6s) tracks resistance over time as fibrin strands form and platelets cross-link them, producing the characteristic spindle-shaped tracing.¹ Because it evaluates the whole clotting cascade — factors, fibrinogen, platelets, and fibrinolysis — in one test, TEG enables goal-directed, product-specific transfusion rather than empiric ratio-based resuscitation.²

Two generations of hardware exist side by side in most systems today: the older TEG 5000 (a single kaolin-activated cup-and-pin channel per run) and the newer TEG 6s (a disposable four-channel microfluidic cartridge). They report overlapping but not identical parameter sets — this guide covers both, and how to translate between them.

The five classic parameters, mapped onto the actual spindle shape

Every downstream parameter is really just a labeled point on this one curve — worth anchoring visually before the tables below turn it into numbers.

Single kaolin-activated channel · cup-and-pin mechanical detection · the five parameters most clinicians learned first

The TEG 5000 reports five core parameters from a single kaolin-activated trace. Each maps to a specific deficiency and a specific blood product, which is what makes TEG useful as a bedside, goal-directed tool rather than a lab curiosity.

Trauma-specific thresholds refine these ranges: an R time beyond roughly twice normal predicts massive transfusion need, and an LY30 above 3% in the injured patient (a lower bar than the general reference range) identifies clinically significant hyperfibrinolysis warranting antifibrinolytic therapy.³

Disposable four-channel cartridge · optical detection · runs multiple activators in parallel from one draw

The TEG 6s replaces the mechanical cup-and-pin with a microfluidic cartridge and optical detection of clot-driven resonance, requiring a single ~400 µL citrated blood transfer instead of manual pipetting across separate cups.⁴ Because the cartridge runs four channels in parallel from one sample, it reports a fuller hemostatic picture per draw than a single TEG 5000 run — most notably, a dedicated functional fibrinogen channel that the classic model lacks.

The CFF channel is the key structural advance: by pharmacologically blocking platelet contribution with a GPIIb/IIIa antagonist, its MA correlates directly with Clauss fibrinogen concentration, giving a true isolated fibrinogen readout that the TEG 5000's alpha angle could only approximate.⁵ The CK/CKH pairing similarly enables direct heparin detection: comparing CK-R to CKH-R (kaolin alone versus kaolin plus heparin-neutralizing heparinase) isolates a heparin effect that a single TEG 5000 trace cannot resolve on its own.

*Ranges as printed on the manufacturer's 07-604-US (Global Hemostasis-HN) result display. Ranges differ by cartridge and by each lab's validation; use the ranges your lab reports.¹⁰

Not every TEG 6s run reports every channel · the cartridge decides what you can and can't see

A specialized add-on assay, ordered separately from the standard panel

Standard TEG channels fully activate platelets with kaolin or tissue factor, so a maximal thrombin-driven clot forms regardless of whether the patient is taking aspirin or a P2Y12 inhibitor — routine MA cannot see antiplatelet drug effect. Platelet Mapping (TEG-PM) resolves this with two additional heparinized channels that isolate platelet contribution by agonist.

Percent platelet inhibition is calculated as: 100 − [(MA_agonist − MA_Fibrin) ÷ (MA_Thrombin − MA_Fibrin) × 100].⁶

Which TEG 6s channel replaces which TEG 5000 parameter

Numerical values are not directly interchangeable between platforms: head-to-head comparison during liver transplantation found considerable inter-device variability despite both systems measuring the same underlying physiology, so trend a patient on one platform rather than converting a TEG 5000 result to a TEG 6s threshold or vice versa.⁴

Same physiology, different vendor, different assay names — common outside North American trauma centers

Rotational thromboelastometry (ROTEM) assesses the same underlying clot physiology as TEG using a rotating-pin rather than cup-and-pin or optical mechanism, with its own reagent-named assays and parameter labels.¹

APTEM is the one assay with no direct TEG analog: it re-runs EXTEM with an antifibrinolytic added to the sample. If APTEM normalizes an abnormal EXTEM tracing, that confirms the abnormality was hyperfibrinolysis rather than a factor or platelet defect, supporting a decision to give TXA.

Applies to either result model — treat the deficiency the abnormal parameter names

The numbers are only as good as the sample and the technique behind them

Because pre-analytical variables move the numbers as much as real pathology does, trend the tracing against the clinical picture rather than treating an isolated abnormal value in a vacuum.²

Non-pregnant, non-cirrhotic reference ranges do not always apply

Pregnancy. Normal pregnancy is a physiologic hypercoagulable state — a shorter R, steeper alpha angle, and higher MA than non-pregnant reference ranges, driven by rising factor and fibrinogen levels and reduced fibrinolytic activity. In postpartum hemorrhage, fibrinogen is the first factor to fall to a critical level and the strongest single predictor of progression to severe hemorrhage, which is why obstetric protocols increasingly trend fibrinogen (via CFF-MA or FIBTEM) rather than waiting on standard coags.⁹

Cirrhosis / chronic liver disease. Conventional coagulation tests (INR, platelet count) overstate bleeding risk in cirrhosis because they only capture the loss of pro-coagulant factors, ignoring the parallel loss of anticoagulant proteins (protein C, protein S) and elevated von Willebrand factor that "rebalance" hemostasis at a lower overall set point.⁸ TEG/ROTEM better reflect this rebalanced state and have been used to reduce unnecessary pre-procedure FFP transfusion in cirrhotic patients — but neither test reliably captures the qualitative platelet defects or portal-hypertension-driven hyperfibrinolysis also common in advanced liver disease, so clinical correlation still matters.

Pediatric and neonatal. Developmental hemostasis means normal ranges shift meaningfully with age. Apply age-specific pediatric reference ranges rather than the adult cutoffs presented in this guide.