A blood clot is a semisolid mass of blood components that forms when the body's haemostatic system converts normally flowing blood into a more stable structure containing platelets, fibrin and trapped blood cells. Clotting is normally protective because it limits bleeding after blood-vessel injury. The problem arises when a clot forms unnecessarily inside an intact blood vessel or becomes large enough to obstruct normal circulation.
The medical term thrombosis refers to formation of a thrombus within the cardiovascular system, while an embolus is material that travels through the bloodstream and subsequently blocks a vessel. A thrombus can therefore remain attached to its original site or part of it can detach and become an embolus. The clinical effect depends heavily on whether the clot forms in an artery, vein, heart chamber or another vascular location.
Normal clot formation begins with haemostasis, a coordinated process involving vascular constriction, platelets and the coagulation system. When a blood vessel is injured, exposed tissue factors and subendothelial structures provide signals that cause platelets to adhere, activate and aggregate. Activated platelets release signalling molecules that recruit and stimulate additional platelets. At the same time, a series of coagulation reactions generates thrombin, an enzyme that converts soluble fibrinogen into insoluble fibrin strands.
Fibrin forms a mesh that stabilises the platelet plug and traps red and white blood cells. The resulting clot provides a temporary structural barrier that helps prevent further blood loss while tissue repair begins. This tightly regulated process normally remains localised to the site of injury.
The body also contains natural anticoagulant and fibrinolytic systems that prevent clotting from spreading unnecessarily. Antithrombin, the protein C and protein S systems, tissue factor pathway inhibitor and the vascular endothelium all contribute to limiting coagulation. Once repair has progressed, plasmin breaks down fibrin through fibrinolysis, allowing the clot to be removed. The balance between clot formation and clot removal is therefore dynamic.
Thrombosis can occur when this balance shifts towards coagulation, when blood flow becomes abnormal, when the vessel wall is activated or injured, or when the blood becomes unusually prone to clotting. This concept is central to understanding why immobility, surgery, cancer, inflammation and inherited thrombophilia can increase thrombosis risk.
Arterial and venous clots have different typical compositions and clinical consequences. Arterial thrombosis commonly develops where an atherosclerotic plaque has ruptured or become disrupted, exposing thrombogenic material and producing platelet-rich clot formation. Such a clot can obstruct coronary arteries and cause myocardial infarction or obstruct cerebral arteries and cause ischaemic stroke. Venous thrombosis tends to be strongly influenced by sluggish blood flow and activation of the coagulation system, and deep vein thrombosis is a common example. Venous thrombi can obstruct venous return and can also detach, travel through the right side of the heart and lodge in the pulmonary arteries, producing pulmonary embolism. These distinctions explain why antiplatelet drugs and anticoagulants have different primary applications.
A clot is not necessarily dangerous merely because it exists. Small clots formed as part of normal haemostasis are essential and are continuously produced and removed without causing disease. The pathological problem is inappropriate clot formation, excessive clot size, obstruction of a critical vessel or embolisation. A clot blocking a small superficial vessel may have limited consequences, whereas obstruction of a major pulmonary artery, coronary artery or cerebral artery can be life-threatening.
Similarly, a venous clot may initially cause local symptoms but become dangerous if it embolises. This distinction is why the term "blood clot" alone does not provide enough information to determine severity; its location, size, age, degree of obstruction and tendency to migrate are all relevant.
Blood clots can cause local symptoms by interfering with circulation. A DVT may produce swelling, pain, warmth and skin colour changes in the affected limb, while an arterial clot can cause sudden pain, pallor, coldness, weakness or loss of pulses downstream from the obstruction. A clot in the lungs can cause sudden breathlessness, chest pain and sometimes coughing up blood. A clot in the brain can cause neurological deficits consistent with an ischaemic stroke. A clot in a coronary artery can cause chest pain and myocardial injury. The same fundamental process, thrombosis, therefore produces very different clinical syndromes depending on the vascular territory involved.
Diagnosis of a suspected clot depends on the location and clinical context. Ultrasound is commonly used to investigate suspected DVT because it can assess venous compressibility and blood flow. CT pulmonary angiography is frequently used to investigate pulmonary embolism, while other imaging and laboratory tests can be appropriate in selected cases.
D-dimer testing detects fragments generated during fibrin breakdown and can be useful in selected patients, particularly when the clinical probability of thrombosis is not high, but an elevated result is not specific for a clot. Treatment often involves anticoagulants, which reduce the ability of blood to form or extend clots. Anticoagulants do not mechanically dissolve every existing clot immediately; rather, they prevent extension and new clot formation while the body's fibrinolytic mechanisms gradually remove thrombotic material.
Blood clots are closely connected to the concept of venous thromboembolism, abbreviated VTE, which includes DVT and pulmonary embolism. A DVT is a thrombus in a deep vein, usually of the leg or pelvis, while a pulmonary embolism occurs when thrombotic material reaches the pulmonary circulation and obstructs a pulmonary artery. The two conditions can therefore represent different stages of the same pathological process. However, not every PE originates from a detectable leg DVT, and not every DVT embolises. A clot can also arise in other sites, including the arm, abdomen or heart. Understanding the distinction between thrombosis and embolism is essential: thrombosis describes formation at a site, whereas embolism describes migration and subsequent obstruction elsewhere.
