Deep vein thrombosis and pulmonary embolism: Pathology review

Hannah is a 42 year old woman who came to the emergency department due to pain in her right calf.

She reports flying from Japan back to the United States 2 days ago.

She denies fever, chills, or history of trauma to the leg.

She reports a 25 pack year smoking history for 20 years, and she takes oral contraceptive pills.

On physical examination, she is stable, and her BMI is 32.

Her right leg is shown in this image.

On laboratory investigation, her D-dimer levels are elevated.

Deep vein thrombosis, or DVT and pulmonary embolism, or PE are a spectrum of clinical manifestations that result from venous thromboembolism.

The pathogenesis and risk factors of both DVT and PE centers around Virchow’s triad, that is; stasis of blood flow, hypercoagulability, and endothelial injury.

Board exams like to test your ability to identify a PE by using scenarios that promote venous stasis such as paralysis after a stroke, the postoperative period, as well as long drives or flights.

People with varicose veins are also at risk of DVT, because incompetent venous valves prevent proper venous outflow, causing stasis.

An interesting risk factor is pregnancy, where the enlarged uterus may compress the iliac veins, causing stasis of venous outflow.

Another similar cause is May-Thurner syndrome where the left iliac vein gets sandwiched between the right iliac artery anteriorly and the lumbar vertebrae posteriorly, which also leads to venous stasis.

Now, the coagulation system is normally balancing clot formation and clot lysis.

Hypercoagulability occurs is when the scale is tipped towards clot formation.

This may be genetic, such as factor V Leiden, or antithrombin III deficiency.