Changes

Prothrombin time (PT) gives an assessment of the extrinsic and common pathways by measuring the time necessary to generate fibrin after activation of factor VII³. It is performed by an automated analyser² using citrated plasma^{1, 3}. Blood should therefore be collected into a sodium citrate tube if prothrombin time is to be performed. In basic terms, the test procedure involves adding thromoplastin to the patient's plasma, warming, adding calcium and recording the time taken to clot¹.

Prothrombin time (PT) gives an assessment of the extrinsic and common pathways by measuring the time necessary to generate fibrin after activation of factor VII³. It is performed by an automated analyser² using citrated plasma^{1, 3}. Blood should therefore be collected into a sodium citrate tube if prothrombin time is to be performed. In basic terms, the test procedure involves adding thromoplastin to the patient's plasma, warming, adding calcium and recording the time taken to clot¹.

A prolonged PT may reflect a factor deficiency or the presence of a circulating inhibitor of coagulation.Repeating the test using a mix of test plasma and "normal" plasma can help differentiate these possibilities: PT returns to normal limits when normal plasma is added to factor-deficient plasma, but no change is seen when this is added to plasma containing inibitors³. PT is more sensitive than APTT for factor deficiencies.  

A prolonged PT may reflect a factor deficiency or the presence of a circulating inhibitor of coagulation. Repeating the test using a mix of test plasma and "normal" plasma can help differentiate these possibilities: PT returns to normal limits when normal plasma is added to factor-deficient plasma, but no change is seen when this is added to plasma containing inibitors³. PT is more sensitive than APTT for factor deficiencies.  

PT is affected by abnormalities or deficiencies in coagulation factors I, II, VII or X, for example in DIC, liver disease, or poisoning with vitamin K antagonists. Inherited defects are possible. PT is also prolonged by the presence of circulating anticoagulants. Inhibitors are often directed at factor X or thrombin and can include fibrin degradation products or heparin³.

PT is affected by abnormalities or deficiencies in coagulation factors I, II, VII or X, for example in DIC, liver disease, or poisoning with vitamin K antagonists. Inherited defects are possible. PT is also prolonged by the presence of circulating anticoagulants. Inhibitors are often directed at factor X or thrombin and can include fibrin degradation products or heparin³.