Review Question - QID 220542

The patient has an intra-articular tibial plateau fracture and a large lipohemarthrosis, as shown in Figure A, which typically separates into three layers when supine based on density: (1) fat, (2) serum/synovial fluid, and (3) blood. Urokinase-type plasminogen activator is active within synovial fluid (layer 2) and leads to the activation of plasminogen within a joint to promote thrombolysis and prevent intra-articular clot formation (Answer 3).

The immediate response to fracture involves activation of the clotting cascade, which normally results in the formation of a fibrin clot. Within a joint, however, large fluid collections consisting of fat, serum/plasma, and blood form (Illustration A), known as lipohemarthrosis, due to the presence of specific inhibitors of the coagulation cascade within the joint. For example, urokinase-type plasminogen activator is known to be active in synovial fluid. This enzyme functions to activate plasmin from its inactive plasminogen form to allow for fibrinolysis and the prevention of fibrin-clot stabilization within the joint.

Harrold et al. reviewed the defect of blood coagulation in joints. The authors note that the observation that blood shed into synovial joints fails to clot has aroused interest for many years. Given this interest, the authors reviewed a series of studies, including animal studies, and found that the results supported the view that fibrinogenolysis is responsible for at least part of the defect of clot formation noted when blood coagulates in a synovial joint. They concluded that when blood is shed into a synovial joint the plasma fibrinogen becomes the substrate for two competing reactions, namely, conversion to fibrin by thrombin or fibrinogenolysis by plasmin, with the absence of thromboplastin in normal human joint tissues favoring fibrinogenolysis over blood clotting.

McCarty et al. reviewed the biomechanical properties of mixtures of blood and synovial fluid. The authors note that synovial fluid (SF) is a viscous ultrafiltrate of plasma that lubricates articulating joint motion. The authors found that when mixing various amounts of SF with blood, the coagulation torque profile was altered over time, decreased the final clot structure mechanical stiffness (42 to 90% decrease), and increased the fluid permeability of the clots (41 to 468-fold). They concluded that these properties of blood/SF mixtures may facilitate an understanding of the repair environment in the joint and of mechanisms of cartilage repair.

Figure A is a lateral radiograph of the knee showing an intra-articular tibial plateau fracture and a large lipohemarthrosis. Illustration A is an annotated version of this radiograph showing the layers of the lipohemarthrosis.

Incorrect Answers:
Answers 1 and 2: Layer 1 of the lipohemarthrosis consists of fat, not fibrinogen or lysed red blood cells, and does not increase her risk for intra-articular clot formation.
Answers 4 and 5: Layer 3 consists primarily of red blood cells that do not form a fibrin-linked clot given the presence of intra-articular urokinase-type plasminogen activator.