Laboratory Tests of Hemostasis by Phase

Formation of initial platelet plugs

Platelet count

Quantifies platelet number

Platelet aggregation

Evaluates adequacy of platelet responsiveness to physiologic stimuli that activate platelets (eg, collagen, ADP, arachidonic acid)

Detects abnormal patterns in hereditary or acquired platelet functional disorders

VWF antigen

Measures total concentration of plasma VWF protein

VWF multimer composition

Evaluates distribution of VWF multimers in plasma (eg, large multimers are missing in type 2 variants of VWD)

Ristocetin-induced platelet agglutination

Used in the evaluation of patients with suspected VWD: Platelet agglutination at low concentrations of ristocetin is characteristic of type 2B VWD

Ristocetin cofactor activity

Quantifies VWF function in patient plasma using formalin-fixed test platelets.*

GP1BM assay

Uses mutated form of glycoprotein 1B affixed to beads or an ELISA plate to measure the function of VWF binding to its physiologic platelet receptor

Collagen binding assay

Uses type I and III collagen immobilized on an ELISA platelet to measure VWF functional binding to collagen

Formation of fibrin

PT

Screens for the factors in extrinsic and common pathways (factors V, VII, and X; prothrombin [II]; and fibrinogen)

aPTT

Screens for the factors in intrinsic and common pathways (prekallikrein; high molecular weight kininogen; factors XII, XI, X, IX, VIII, and V; prothrombin II]; and fibrinogen)

Specific functional assays for coagulation factors

Determines activity of the specific coagulant factor tested as a percentage of normal

Thrombin time

Evaluates the last step of coagulation (thrombin cleavage of fibrinogen to fibrin)

Is prolonged by heparin activation of antithrombin and in conditions resulting in qualitative fibrinogen abnormalities or hypofibrinogenemia

Reptilase time

Reptilase (a snake venom) also activates fibrinogen to fibrin

If reptilase time is normal and the thrombin time is prolonged, provides presumptive evidence that a plasma sample contains heparin (eg, residual heparin after extracorporeal bypass or in a sample drawn from an IV line kept open with heparin flushes) because the reptilase time is not affected by heparin activation of antithrombin

Both reptilase time and thrombin time are prolonged in patients with hypofibrinogenemia or dysfibrinogenemiaBoth reptilase time and thrombin time are prolonged in patients with hypofibrinogenemia or dysfibrinogenemia

Fibrinogen level

Quantifies plasma fibrinogen, which is increased in acute phase reactions (to infection and inflammation) and decreased in severe liver disease and severe DIC

Fibrinolysis

Clot stability during 24-hour incubation in saline and in 5M urea

Lysis of clots occurs in saline if fibrinolytic activity is excessive or in 5M urea if factor XIII is deficient

Should be performed in patients with delayed bleeding, defective wound healing, or frequent spontaneous abortions

Plasminogen activity

Quantifies plasma plasminogen, which is decreased in patients with congenital early-onset venous thromboembolism (rare). Plasminogen is also decreased in patients with excessive fibrinolysis (eg, after TPA treatment, in DIC). , which is decreased in patients with congenital early-onset venous thromboembolism (rare). Plasminogen is also decreased in patients with excessive fibrinolysis (eg, after TPA treatment, in DIC).

Alpha2-antiplasmin

Quantifies plasma level of this fibrinolysis inhibitor, which can be reduced in patients with increased fibrinolysis and excessive bleeding (rare)

Serum fibrinogen and fibrin degradation products

Screens for DIC

Fibrinogen levels decline and fibrin degradation products increase in patients with DIC

Fibrin degradation products tests have been superseded by the plasma D-dimer assay

Plasma D-dimer

D-dimers are cross-linked fragments of fibrin produced by plasmin degradation. D-dimers are measured with a monoclonal antibody latex agglutination test or with an ELISA

If high, indicates that thrombin has been generated in vivo with resultant generation of fibrin, activation of the cross-linking enzyme factor XIII, and secondary fibrinolysis

Has the practical advantage that it can be performed on citrate-containing plasma and thus, unlike the test for serum fibrin degradation products, does not require blood clotting in a special tube to prepare serum free of residual fibrinogen

Is useful in the diagnosis of DIC and in vivo thrombosis (eg, deep venous thrombosis, pulmonary embolism)