Coagulation

TEG & ROTEM

A whole-blood picture of clot formation over time: how fast it starts, how fast it builds, how strong it gets, and whether it breaks down.

How it works

Schematic of a thromboelastograph: a pin on a torsion wire suspended in a heated cup containing 0.36 mL of whole blood that oscillates through 4°45′. — A pin hangs in a heated, oscillating cup of whole blood. As clot forms, it couples the pin to the cup — the trace widens with clot strength.

Read the trace left to right: initiation → clot building → maximum strength → breakdown. First identify the platform, cartridge/assay and sample time.

The labeled trace

Thromboelastography tracing labeled with R time, K time, alpha angle, maximum amplitude (MA), amplitude 30 minutes later (A30), and the coagulation and fibrinolysis phases. — R (reaction time) → K and α angle (clot kinetics) → MA (maximum amplitude) → A30 / LY30 (lysis 30 minutes after MA).

Phase	TEG	ROTEM	Mostly reflects	If abnormal, the team discusses…
Initiation	R time	CT	Clotting factors / thrombin generation	Long R: factor deficiency or anticoagulant. Heparin? Compare the heparinase channel (TEG CKH / ROTEM HEPTEM) → protamine; otherwise plasma or PCC.
Kinetics	K, α angle	CFT, α	Fibrin build-up, fibrinogen	Long K / low α: fibrinogen → cryoprecipitate or fibrinogen concentrate (confirm with TEG FF / ROTEM FIBTEM).
Strength	MA	MCF	Platelets (≈ 80%) + fibrinogen	Low MA with normal fibrinogen: platelets (± DDAVP).
Lysis	LY30	LI30 / ML	Fibrinolysis	High LY30: hyperfibrinolysis → tranexamic acid per pathway.

Pattern gallery

Decide what each trace suggests, then reveal. Schematic traces (CC0) — not to scale.

TEG tracing with normal timing but a reduced maximum amplitude, consistent with low or dysfunctional platelets.

Figure: Thromboelastography in low or dysfunctional platelets — Mikael Häggström, MD, CC0 1.0, via Wikimedia Commons.

1. Low MA, normal timing

TEG tracing with a shallow alpha angle and slowly widening, narrow trace, consistent with fibrinogen deficiency.

Figure: Thromboelastography in fibrinogen deficiency — Mikael Häggström, MD, CC0 1.0, via Wikimedia Commons.

2. Shallow α angle, slow build, narrow trace

TEG tracing that widens briefly and then rapidly narrows to a thin line, consistent with primary hyperfibrinolysis.

Figure: Thromboelastography in primary fibrinolysis — Mikael Häggström, MD, CC0 1.0, via Wikimedia Commons.

3. Trace builds, then collapses early

TEG tracing with a short R time and large amplitude that then tapers to a point, consistent with secondary fibrinolysis (as in DIC).

Figure: Thromboelastography in secondary fibrinolysis — Mikael Häggström, MD, CC0 1.0, via Wikimedia Commons.

4. Fast, strong clot that then tapers

TEG tracing with a short R time, steep alpha angle and very large maximum amplitude, consistent with a hypercoagulable state.

Figure: Thromboelastography in thrombosis — Mikael Häggström, MD, CC0 1.0, via Wikimedia Commons.

5. Short R, steep α, very high MA

Read this trace — quick quiz

Limitations

Variably insensitive to DOACs, antiplatelet drugs (aspirin/P2Y12 need platelet-mapping assays), von Willebrand disease, and protein C/S or antithrombin deficiency.
Run at 37 °C — may not reflect the patient’s hypothermia.
Interpret with the clinical picture, conventional labs, temperature, calcium and the local bleeding pathway. An abnormal curve never means “automatically give product X.”

Pimp questions

Pimp question 1

Which TEG parameter mostly reflects platelets?

Answer

MA (maximum amplitude) — about 80% platelet contribution, the rest fibrinogen.

Pimp question 2

A long R time in a cardiac surgery patient — what do you compare it with?

Answer

The heparinase channel. If it normalizes there, residual heparin is the cause (protamine), not factor deficiency.

Pimp question 3

Can you carry a numeric lysis value from TEG to ROTEM?

Answer

No — the platforms define and time their lysis indices differently.