Result Interpretation

ROTEM® delta

The assessment of the ROTEM® analysis is carried out along the time axis (from left to right): A disturbed activation of coagulation is indicated by a prolonged clotting time. As causes, a factor deficiency or a heparin effect have to be considered. The comparison of INTEM and HEPTEM allows for a specific detection of a heparin effect. An abnormal clot formation is indicated by a prolonged clot formation time (CFT) and/or a reduced clot firmness (MCF). The CFT is thereby influenced more strongly by a clot polymerisation disorder than the MCF. A prolonged CFT, with at the same time normal MCF, indicates therefore
a polymerisation disorder, whereas a reduced MCF with a normal CFT rather indicates a deficiency of clottable substrate (fibrinogen and / or platelets).Fibrinolysis is detected by the lysis of the clot (ML > 15%) or by the finding of a better clot formation (shorter CFT, greater MCF) in APTEM as compared to EXTEM.
Download Booklet ROTEM® Analysis: Targeted Treatment of Acute Haemostatic Disorders

ROTEM® platelet

The assessment of the ROTEM® platelet analysis is carried out along the time axis (from left to right): A disturbed platelet aggregation is indicated by a decreased amplitude (curve). As causes, the intake of drugs that are influencing the platelet function or platelet dysfunctions due to e.g extracorporeal assist devices, surgery, or others have to be considered. Drugs which can influence the platelet aggregation are cyclooxygenase inhibitors (e.g. patient treatment with acetylsalicylic acid), GP IIb/IIIa or thrombin receptor blockers (e.g. patient treatment with GP IIb/IIIa antagonists) or ADP receptor blocker (e.g. patient treatment with thienopyridines or direct ADP receptor antagonists). With the ROTEM® platelet differential diagnosis and the tests ADPTEM, TRAPTEM and ARATEM the reason for a decreased platelet aggregation can be determined.

In summary the ROTEM® analysis provides:

  • Rapid information from the beginning of clot formation until its dissolution
  • Concentration and activity of coagulation factors (incl. F XIII)
  • Effects of anticoagulants like heparin or hirudin
  • Fibrin generation and stabilisation
  • Contribution of other drugs (e.g. plasma expanders)
  • Platelet function and aggregation
  • The balance between plasmatic and platelet derived contributions to haemostasis
  • (Hyper-) fibrinolysis

Normal patient

Result interpretation normal patient

Normal patient


Platelet deficiency

Result interpretation platelet deficiency

Fibrinogen deficiency

Result interpretation fibrinogen deficiency


Result interpretation hyperfibrinolyse

Heparin influence

Result interpretation heparin influence

ADP Receptor Blockage



Dual therapy

(e.g. Aspirin® and Clopidogrel)


GP IIb/IIIa Receptor Blockage



Cyclooxygenase Inhibition

(e.g. Aspirin®)