1. Coagulation Assessment

11-15 seconds

• Time it takes to produce fibrin polymers after adding thromboplastin and calcium

• Thromboplastin is a laboratory reagent that contains tissue factor and phospholipids.

• Common

• Extrinsic

• Increased in:

  • Vitamin K deficiency

  • Impaired coagulation factor production (e.g., in cirrhosis)

  • Factor VII deficiency

  • DIC

• Monitoring of vitamin K antagonist therapy (INR)

0.9 - 1.1

• Derived from PT, but calculated by comparing the laboratory-specific PT to a standardized PT

• Measured using a standardized tissue factor reagent

Common and Extrinsic

• Increased in:

  • Vitamin K deficiency

  • Impaired coagulation factor production (e.g., in cirrhosis)

  • Factor VII deficiency

  • DIC

• Monitoring of vitamin K antagonist therapy (INR)

25-40 sec

• Time it takes to produce fibrin polymers after adding phospholipids

Intrinsic, Common

• Prolonged in:

  • Hemophilia

  • Vitamin K deficiency

  • DIC

  • Possibly in von Willebrand disease

  • SLE (if lupus anticoagulant is present)

• Monitoring of unfractionated heparin (UFH) therapy

• < 2 seconds deviation from control

• Usually 14–19 seconds

• Time it takes to produce fibrin polymers after adding thrombin

Common only

• Test for fibrinogen deficiency

• Monitoring of heparin therapy (as an alternative) and fibrinolytic therapy

14-24 seconds

• Time it takes to produce fibrin polymers after adding reptilase

• Reptilase catalyzes the conversion of fibrinogen to fibrin, but not the formation of fibrin polymers. The resulting fibrin degrades quickly in living organisms, preventing thrombus formation. The persistent conversion of fibrinogen to fibrin, however, causes a fibrin deficiency that can be used therapeutically to prevent thrombus and embolus formation.

Common only

Unlike thrombin time, reptilase time is not affected by heparin or hirudin therapy, as reptilase is unaffected by antithrombin. Reptilase time increases in cases of fibrinogen deficiency or if fibrinogen or fibrin degradation products are present.

Bleeding time: amount of time it takes for a bleeding to stop after a small skin puncture

The reference range depends on the testing protocol and is typically 2–7 minutes.

• Prolonged in disorders of primary hemostasis (thrombocytopenia and platelet dysfunction)

• Not routinely performed

• Anti-factor Xa assay: used to monitor certain anticoagulant therapies

  • Low molecular weight heparin (LMWH) or fondaparinux therapy in patients with impaired renal function

  • Unfractionated heparin (UFH) therapy if aPTT is inconclusive (e.g., due to coagulation factor deficiency or heparin antibodies)

• D-dimer: fibrin degradation product that correlates with activity of coagulation and fibrinolysis

  • High sensitivity: Increased serum D-dimer levels occur in deep vein thrombosis (DVT), pulmonary embolism (PE), and disseminated intravascular coagulation.

  • Low specificity: Elevation can also occur due to other conditions, including malignancies, infection, pregnancy, renal insufficiency, or surgical procedures.

• Ristocetin cofactor assay: measures the ability of von Willebrand factor (vWF) to agglutinate platelets

  • Ristocetin: antibiotic that activates vWF, which then binds to glycoprotein Ib on platelets

  • Interpretation: If ristocetin is added to blood lacking vWF (or the vWF receptor), platelets will not aggregate.

    • Von Willebrand disease (↓ vWF)

      • Failure of platelet aggregation or a ristocetin cofactor level < 30 IU/dL that corrects with the addition of normal plasma

      • Normal platelet aggregation in response to other agonists such as ADP, epinephrine, collagen, and thrombin

    • Bernard-Soulier syndrome (↓ vWF receptor on platelets)

      • Failure of platelet aggregation or a ristocetin cofactor level < 30 IU/dL that does not correct with the addition of normal plasma

      • Normal platelet aggregation in response to other agonists such as ADP, epinephrine, collagen, and thrombin

    • Glanzmann thrombasthenia

      • Normal platelet aggregation in response to ristocetin

      • Failure of platelet aggregation in response to other agonists such as ADP, epinephrine, collagen, and thrombin

full blood assay that assesses the formation, stability, and dissolution of a thrombus alongside PT and aPTT

• Clot observation test: simple method of point-of-care testing to assess coagulation, especially if hyperfibrinolysis is suspected

  • Procedure: A small amount of blood is collected in a test tube and examined macroscopically after a few minutes.

  • Interpretation

    • Stable thrombus formation : normal coagulation

    • No thrombi formation: severely impaired coagulation (e.g., in DIC)

    • Formation of an unstable thrombus that dissolves quickly: hyperfibrinolysis

• Rumpel-Leede test: detects primary hemostasis disorders and increased dermal capillary fragility

  • Procedure: A tourniquet is applied to the upper arm and the cuff is inflated to a pressure that is midway between the patient's systolic and diastolic blood pressure. After 5 minutes, the tourniquet is removed and the cubital pit and forearm are examined for petechiae.

  • Interpretation

    • Test is positive if ≥ 10 petechiae appear per square inch.

    • Positive test results occur in:

      • Dengue hemorrhagic fever

      • Disorders affecting primary hemostasis (e.g., thrombocytopenia)

      • Increased capillary fragility (e.g., prolonged steroid use, scurvy)

      • Vascular hemorrhagic diathesis (Osler-Weber-Rendu disease, IgA vasculitis)

      • Scarlet fever