Thrombosis and Embolism
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Direct answer
Thrombosis is the formation of a solid mass (thrombus) from blood constituents within the circulation during life, governed by Virchow's triad — endothelial injury, abnormal blood flow (stasis or turbulence) and hypercoagulability. An embolus is any detached intravascular mass, solid, liquid or gaseous, carried by the blood to a point distant from its origin; thromboembolism accounts for the vast majority of embolic events.
What you must remember
- Arterial thrombi are pale, platelet-rich masses forming on injured or atherosclerotic endothelium under high flow; their laminated lines of Zahn (alternating platelet-fibrin and red-cell layers) prove formation during life.
- Venous thrombi are red, coagulation-rich and form in stagnation, classically in the deep veins of the calf and popliteal region; leg venous thrombosis above the knee is the classic source of pulmonary embolism.
- Hypercoagulability includes inherited states such as factor V Leiden, prothrombin and protein C, S and antithrombin deficiencies, and acquired states — surgery, immobility, malignancy (Trousseau syndrome), pregnancy, oral contraceptives and nephrotic syndrome.
- Lines of Zahn distinguish an antemortem thrombus from a post-mortem clot, which is gelatinous, unattached and separates into "chicken fat" and "currant jelly" layers.
- Thromboembolism: pulmonary embolism presents with sudden dyspnoea, pleuritic chest pain, haemoptysis and, with large saddle emboli, sudden death; a paradoxical embolus crosses a patent foramen ovale to reach the systemic circulation.
- Non-thrombotic emboli: fat embolism syndrome one to three days after long-bone fracture (respiratory distress, cerebral signs, thrombocytopenia and petechiae); decompression sickness from nitrogen bubbles (the "bends", treated with hyperbaric oxygen); amniotic fluid embolism during labour causing abrupt hypoxia, hypotension and disseminated intravascular coagulation; tumour and atherosclerotic cholesterol emboli.
- Fates of a thrombus: propagation, embolisation, dissolution by fibrinolysis, and organisation with recanalisation; prophylaxis in hospitalised patients uses low-molecular-weight heparin and early ambulation.
Common confusion
The commonest error is equating embolism with infarction. An embolus lodges where vessel size no longer permits passage, but infarction follows only when collateral supply is inadequate — dual blood flow protects lung and liver. Also keep thrombus and embolus straight: the thrombus is the attached clot, the embolus is the detached traveller.
Exam-focused takeaway
Theory answers should state Virchow's triad with examples, contrast arterial and venous thrombi, list embolus varieties with their settings, and describe the fates of a thrombus. Viva examiners ask the significance of lines of Zahn and why venous thrombosis targets the legs. MCQs pair fat embolism with long-bone fractures and petechiae, amniotic fluid embolism with disseminated intravascular coagulation, Trousseau with malignancy and factor V Leiden with inherited thrombophilia.
Frequently asked questions
What is Virchow's triad?
Endothelial injury, abnormal blood flow (stasis or turbulence) and hypercoagulability of blood — the three forces that favour thrombus formation.
How does an antemortem thrombus differ from a post-mortem clot?
The thrombus is firm, attached and shows lines of Zahn; a post-mortem clot is gelatinous, unattached and lacks lamination.
What is paradoxical embolism?
A venous thrombus crossing a patent foramen ovale or other right-to-left shunt to occlude a systemic artery, causing stroke or limb ischaemia.
When does fat embolism syndrome appear and how?
Typically 24 to 72 hours after long-bone fracture or orthopaedic surgery, with respiratory distress, confusion, thrombocytopenia and a petechial rash.
What are the possible fates of a thrombus?
Propagation, embolisation, dissolution by fibrinolysis, and organisation with recanalisation to restore partial flow.