Coagulation laboratory

Normal haemostasis involves formation of blood clots to stop bleeding from damaged vessels and activation of natural anticoagulation and fibrinolytic systems to limit clot formation to sites of injury.

Urgent Tests (should be processed with 4 hours of collection)

Analyte Specimen Type Container/Special Instructions
Clotting screen Plasma Sodium Citrate (Light Blue bottle)
D-Dimer Plasma Sodium Citrate (Light Blue bottle)
Thrombophilia Plasma/Whole blood Sodium Citrate (Light Blue bottle) - x 4 specimens / Potassium EDTA (Purple bottle) - x 1 specimen


BD Citrate blood tube – importance of 360o minimum fill indicator



Bleeding disorders

EpistaxisBleeding disorders are either the result of defects in clot formation or are due to overactive fibrinolytic systems. Conversely, hyper-coagulability disorders are caused by defects in the anticoagulant system or reflect underactive fibrinolytic systems.

Platelet disorders, coagulopathies and thrombophilia states are either acquired or inherited; - specific laboratory investigations may be used to identify the nature of the clotting disorder observed and further monitor the effectiveness of anticoagulant therapy (see the Pathology test directory for further details.)

Routine clotting tests comprise of the prothrombin time (PT,) fibrinogen, activated partial thromboplastin time (APTT,) thrombin time and D-Dimer. The clotting screen is a bundled group of tests used pre-operatively to assess bleeding risk (diathesis) and used to monitor bleeding conditions and some therapies. It tests the PT (and INR,) APTT and fibrinogen. View the current BCSH guidelines for assessing bleeding risk prior to surgery (here.) 

Normal Clotting ranges

PT 9 - 11 sec
INR Therapeutic range dependent on condition treated. Contact lab for further advice if necessary
APTT 25 - 33 sec
Fibrinogen 1.5 - 4.5 sec
D-Dimer <218 ng/mL


Prothombin Time (PT)

The PT measures the vitamin K dependant clotting pathways (extrinsic pathway) and is therefore of particular use in measuring the effect of warfarin therapy (warfarin is a vitamin K antagonist.) The prothrombin time is also used to determine if there are any deficiency in extrinsic clotting factors and is a useful liver function test. Raised PTs without cause should be investigated further.

Activated Partial Thromboplastin Time (APTT)

APTT measures the intrinsic clotting pathway and is particularly useful in monitoring heparin therapy. The APTT ratio provides the ratio ofAPPT:Normal Clotting time and is the primary calculation used to monitor heparin therapy

The APTT is also useful in detecting clotting factor deficiencies of theintrinsic pathway and can be raised in the presence of factor deficiencies and lupus anticoagulants. Raised APTTs without cause should be investigated further. The APTT ratio calculation may change from time to time and you should contact the laboratory for advice if you are calculating your own ratio. View the guidelines on the use and monitoring of heparin (here.)


Due to the potential for overestimation using the PT-derived (calculation) for measuring fibrinogen, the Clauss Fibrinogen assay is used instead by the Haematology department to provide a direct measure of fibrinogen.


During the formation of a stable clot, amino acids are excised by various enzyme cascade reactions. The D-Dimer peptide is excised from the D portion of fibrin as the clot hardens. It is therefore a useful predictor of recent clot formation. It is not specific however and can be affected by many other conditions such as rheumatoid arthritis and should only be used as a negative predictor for VTE (venous thromboembolism) i.e. a raised D-Dimer is not diagnostic of a clot formation, but a normal D-Dimer can be a used as a negative predictor of venous thrombosis.  In DIC the D-Dimer levels are often very high.

Disseminated intravascular coagulation (DIC) Guidelines

View the guidelines on the diagnosis and management of DIC (here.)

Deep vein thrombosis (DVT) Guidelines

View the guidelines for Diagnosis of deep vein thrombosis in symptomatic outpatients and the potential for clinical assessment and D-dimer assays to reduce the need for diagnostic imaging (here.)