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.

===(A)PTT===

===Activated Partical Thromboplastin Time===  

2:The activated partial thromboplastin time (APTT) is also measured by an automated analyzer. The APTT is a

The APTT is measures the time necessary to generate fibrin from activation of the intrinsic pathway³. It therefore assesses functionality of the components of the intrinsic and common pathways of coagulation. The test is performed on citrated plasma, and so blood should be collected into a sodium citrate tube if the APTT test is to be undertaken. Once a sample is obtained, factor XII is activated by an external agent that will not also activate factor VII, such as kaolin^{,1 3}. Since the intrinsic arm of the cascade requires platelet factors to function, the test also provides a phospholipid emuslion in place of these factors. Calcium is added, the preparation is incubated, and the time for clumping of kaolin is measured. Classically, partial thromboplastin time was measured after activation by contact with a glass tube, but use of an external activating agent in the newer, "activated" partial thromboplastin time method makes results more reliable³.

measure of the intrinsic and common coagulation pathways. Like the ACT it will be prolonged by abnormalities or

 

 

Like the ACT it will be prolonged by abnormalities or

deficiencies in factors XII, XI, IX, VIII, X, V, II or I. It is not affected by thrombocytopenia. The APTT is considered

deficiencies in factors XII, XI, IX, VIII, X, V, II or I. It is not affected by thrombocytopenia. The APTT is considered

a more sensitive test than the ACT and will become prolonged when approximately 70% of a factor is depleted in

a more sensitive test than the ACT and will become prolonged when approximately 70% of a factor is depleted in

comparison the ACT will only be prolonged when approximately 90% of a factor is depleted.

comparison the ACT will only be prolonged when approximately 90% of a factor is depleted.

This test is abnormal in the presence of reduced quantities of factors XII, IX, XI, VIII, X, V, prothrombin, and fibrinogen (all integral parts of the "intrinsic" and "common" pathway. It is usually prolonged if a patient has less than approximately 30% normal activity. It can also be abnormal in the presence of a circulating inhibitor to any of the intrinsic pathway factors. The differentiation of inhibitors from factor depletion is important and can best be accomplished by a mixing study in which patient and normal plasma are combined in a 1:1 ratio and the test is repeated on the mixed sample. If the abnormal value is corrected completely, the problem is factor deficiency. If the result does not change or the abnormality is corrected only partially, an inhibitor is present. This difference stems from the above mentioned fact that the aPTT will be normal in the presence of 50% normal activity.

This test is abnormal in the presence of reduced quantities of factors XII, IX, XI, VIII, X, V, prothrombin, and fibrinogen (all integral parts of the "intrinsic" and "common" pathway. It is usually prolonged if a patient has less than approximately 30% normal activity. It can also be abnormal in the presence of a circulating inhibitor to any of the intrinsic pathway factors. The differentiation of inhibitors from factor depletion is important and can best be accomplished by a mixing study in which patient and normal plasma are combined in a 1:1 ratio and the test is repeated on the mixed sample. If the abnormal value is corrected completely, the problem is factor deficiency. If the result does not change or the abnormality is corrected only partially, an inhibitor is present. This difference stems from the above mentioned fact that the aPTT will be normal in the presence of 50% normal activity.

The aPTT is a good screening test for inherited or acquired factor deficiencies. Inherited disorders including classic hemophilia A (factor VIII deficiency) and hemophilia B (factor IX deficiency, or Christmas disease) are well-known diseases in which the aPTT is prolonged. Other intrinsic and common pathway factors may also be congenitally absent. These conditions are rare but have been described for all factors. A number of kindreds with abnormalities of factor XII activation have been described. They are usually associated with a prolonged aPTT without clinical signs of bleeding. Acquired factor deficiency is common. Vitamin K deficiency, liver dysfunction, and iatrogenic anticoagulation with warfarin are most common. Factor depletion may also occur in the setting of disseminated intravascular coagulation (DIC), prolonged bleeding, and massive transfusion.

The aPTT is a good screening test for inherited or acquired factor deficiencies. Inherited disorders including classic hemophilia A (factor VIII deficiency) and hemophilia B (factor IX deficiency, or Christmas disease) are well-known diseases in which the aPTT is prolonged. Other intrinsic and common pathway factors may also be congenitally absent. These conditions are rare but have been described for all factors. A number of kindreds with abnormalities of factor XII activation have been described. They are usually associated with a prolonged aPTT without clinical signs of bleeding. Acquired factor deficiency is common. Vitamin K deficiency, liver dysfunction, and iatrogenic anticoagulation with warfarin are most common. Factor depletion may also occur in the setting of disseminated intravascular coagulation (DIC), prolonged bleeding, and massive transfusion.

Other inhibitors appear to be antibodies. The easiest to understand is the antibody against factor VIII in patients with hemophilia A treated with factor VIII concentrate. Inhibitors against other factors have been described with a variety of diseases that follow a variable course. When characterized, they have been immunoglobulins.

Other inhibitors appear to be antibodies. The easiest to understand is the antibody against factor VIII in patients with hemophilia A treated with factor VIII concentrate. Inhibitors against other factors have been described with a variety of diseases that follow a variable course. When characterized, they have been immunoglobulins.

Occasionally the reported value of the aPTT will be lower than normal. This "shortened" time may reflect the presence of increased levels of activated factors in context of a "hypercoagulable state." It is seen in some patients in the early stages of DIC but should not be considered diagnostic for that entity.

Occasionally the reported value of the aPTT will be lower than normal. This "shortened" time may reflect the presence of increased levels of activated factors in context of a "hypercoagulable state." It is seen in some patients in the early stages of DIC but should not be considered diagnostic for that entity.