Thrombus (blood clot): formation, structure, and clinical significance

Composition and how thrombi form

Thrombus formation is the end result of the coagulation cascade and platelets working together to produce a stable plug. Typical components include:

• Aggregated platelets that adhere to the damaged vessel wall.
• Fibrin strands that create a mesh, produced by the coagulation system often referred to as coagulation.
• Entrapped blood cells such as red blood cells and leukocytes.

The material of a thrombus is sometimes called cruor in older texts. Formation typically begins when the endothelial surface is disrupted or when blood flow and composition change in ways that favor clotting.

Physiologic role and pathological consequences

Thrombi serve an essential hemostatic role after injury by sealing breaks in vessels and allowing tissue repair. However, when clots occur inappropriately within intact vessels it is referred to as thrombosis. A pathological thrombus can reduce or block blood flow, causing ischemia of downstream tissues. Pieces may detach and travel as emboli, lodging in distant vessels.

Clinically, thrombi are important in disorders such as deep vein thrombosis, pulmonary embolism, myocardial infarction and ischemic stroke. Diagnosis may use imaging and blood tests of coagulation, while prevention and treatment include anticoagulant and antiplatelet drugs, mechanical measures, or procedures to remove or dissolve clots.

Notable distinctions include the difference between a mural thrombus (attached to a vessel wall), a red thrombus rich in erythrocytes, and a white thrombus rich in platelets. Over time some thrombi can be organized by ingrowth of tissue, become recanalized, or undergo lysis. Understanding when a thrombus is protective and when it becomes pathological is central to preventing and managing cardiovascular and thromboembolic disease.