Pulmonary Embolism (Hematology Perspective)

Pulmonary embolism (PE) is the obstruction of one or more pulmonary arteries by thrombus, fat, air, or amniotic fluid; the most common form is thromboembolic PE arising from deep vein thrombosis of the lower extremities or pelvis. From a hematologic standpoint PE is a manifestation of venous thromboembolism (VTE) that requires risk stratification, identification of provoking factors, and decision-making about anticoagulation.

Etiology divides into provoked PE (surgery within 3 months, immobilization, trauma, hospitalization, hormonal therapy, pregnancy, cancer, central venous catheter) and unprovoked PE which carries a substantially higher risk of recurrence and warrants extended anticoagulation. Inherited thrombophilias (factor V Leiden, prothrombin G20210A, antithrombin/protein C/S deficiency) and acquired thrombophilias (antiphospholipid syndrome, myeloproliferative neoplasms with JAK2 mutation, paroxysmal nocturnal hemoglobinuria) are searched in selected cases.

Diagnosis combines pretest probability scoring (Wells, Geneva), D-dimer in low-probability cases, and CT pulmonary angiography or V/Q scanning. Hemodynamic stratification (massive, submassive, low-risk PE) drives therapy: systemic thrombolysis or catheter-directed therapy for hemodynamic instability, anticoagulation alone for stable disease. Anticoagulation choices are direct oral anticoagulants (apixaban, rivaroxaban, dabigatran, edoxaban), low-molecular-weight heparin (especially in cancer or pregnancy), or warfarin. Duration depends on provoking context and bleeding risk: 3 months for transient provoking factors, indefinite for unprovoked PE or persistent risk such as active cancer or antiphospholipid syndrome.