Changes

The contact activator used in the ACT test triggers the intrinsic pathway, and so ACT allows assessment of the intrinsic and common pathways. ACT will therefore be prolonged when factors I, II, V, VIII, IX, X, XI or XII are deficient or abnormal, such as in DIC, liver disease, vitamin K antagonist toxicosis or haemophilia A or B². Thrombocytopenia may also increase ACT.

The contact activator used in the ACT test triggers the intrinsic pathway, and so ACT allows assessment of the intrinsic and common pathways. ACT will therefore be prolonged when factors I, II, V, VIII, IX, X, XI or XII are deficient or abnormal, such as in DIC, liver disease, vitamin K antagonist toxicosis or haemophilia A or B². Thrombocytopenia may also increase ACT.

===PT===

===Prothrombin Time===

2:The prothrombin time (PT) is measured by an automated analyzer and there are some new point of care

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.  

machines now available that allow this and APTT to be measured on an emergency basis. The prothrombin time

is a measure of the extrinsic and common coagulation pathways. It will be prolonged by deficiency or

abnormalities in coagulation factors VII, X, II or I. Disease processes expected to prolong the PT include Vitamin

K antagonists, liver disease and DIC.

The PT measures the time necessary to generate fibrin after activation of factor VII. It measures the integrity of the "extrinsic" and "common" pathways (factors VII, V, X, prothrombin, and fibrinogen).

A prolonged PT may reflect either factor deficiency or a circulating inhibitor of coagulation. Repeating the test using a mix of test plasma and "normal" plasma can help differentiate these possibilities³. PT is more sensitive than APTT for factor deficiencies.

It will be prolonged by deficiency or

abnormalities in coagulation factors VII, X, II or I. Disease processes expected to prolong the PT include Vitamin

 

K antagonists, liver disease and DIC.

As with the interpretation of a prolonged aPTT, a prolonged PT may reflect either factor deficiency or a circulating inhibitor of coagulation. The distinction is made by repeating the test after a 1:1 mix with normal plasma.

Inherited deficiency of factor VII is a rare bleeding disorder characterized by a prolonged PT and a normal aPTT. The PT completely corrects when mixed with normal plasma. Acquired deficiencies are usually related to liver disease, warfarin therapy, or depletion secondary to consumptive coagulopathy, severe bleeding, or massive transfusion.

Inherited deficiency of factor VII is a rare bleeding disorder characterized by a prolonged PT and a normal aPTT. The PT completely corrects when mixed with normal plasma. Acquired deficiencies are usually related to liver disease, warfarin therapy, or depletion secondary to consumptive coagulopathy, severe bleeding, or massive transfusion.