A 58-year-old man presents with acute unilateral left leg swelling, pain, and warmth 5 days after total knee replacement surgery. Compression ultrasound is performed. The structure marked **B** in the diagram shows a non-compressible common femoral vein with intraluminal thrombus. Which of the following best describes the pathophysiologic mechanism underlying this finding in the context of his recent orthopedic surgery?
A. Inherited thrombophilia (Factor V Leiden) unmasked by surgical stress
B. Endothelial injury from surgical trauma combined with prolonged venous stasis from immobilization
C. Platelet dysfunction secondary to perioperative aspirin use
D. Acquired hypercoagulability from malignancy-related tissue factor release
Explanation
Why "Endothelial injury from surgical trauma combined with prolonged venous stasis from immobilization" is right
The clinical anchor directly identifies DVT as forming via Virchow's triad. In the post-orthopedic surgery setting, the two dominant mechanisms are endothelial injury (from surgical trauma, especially hip/knee replacement) and venous stasis (from immobilization and reduced mobility post-operatively). These two factors together create the prothrombotic milieu that led to the non-compressible thrombus at B (common femoral vein). The CHEST and ESC guidelines emphasize that orthopedic surgery is a major transient risk factor for DVT precisely because it triggers both limbs of this pathophysiologic triad. The failure of compression at B on ultrasound is the hallmark sonographic sign of DVT formation.
Why each distractor is wrong
Inherited thrombophilia (Factor V Leiden) unmasked by surgical stress: While Factor V Leiden is the most common inherited thrombophilia and can contribute to DVT risk, it is not the primary mechanism in post-operative DVT. Most post-surgical DVTs occur in patients without inherited thrombophilias; the surgery itself is sufficient. This would be a secondary consideration, not the main pathophysiologic driver in this acute post-operative context.
Acquired hypercoagulability from malignancy-related tissue factor release: There is no clinical evidence of malignancy in this patient. Cancer-associated thrombosis (Trousseau's syndrome) is a specific subset of VTE pathophysiology relevant to adenocarcinomas, not to routine post-operative DVT. This is an incorrect mechanism for the clinical scenario presented.
Platelet dysfunction secondary to perioperative aspirin use: Perioperative aspirin does not cause platelet dysfunction in the prothrombotic direction; if anything, it reduces thrombotic risk. DVT pathophysiology is driven by stasis and endothelial injury, not by platelet dysfunction. This is mechanistically incorrect.
High-YieldNEET PG
Orthopedic surgery (hip/knee replacement) is a major transient DVT risk factor because it combines endothelial injury + immobilization-induced stasis; both are essential components of Virchow's triad and explain why post-operative DVT is common and why prophylaxis is mandatory.
