Abstract
Since Virchow's autopsy studies in the mid-1800s, it has generally been believed that
pulmonary embolism (PE) originated from the embolization of fibrin fragments from
a deep venous thrombosis (DVT). However, a DVT is often not found in patients with
PE (up to 50% of cases). Could fibrin form in the pulmonary vessels without coming
from the periphery? In this review, the authors will try to support the hypothesis
that a pulmonary thrombosis (PT) may develop. They will do so through different clinical
models related to some pathological conditions such as pneumonia, chronic obstructive
pulmonary disease (COPD), and asthma, all of which show a close relationship between
local inflammation and activation of blood coagulation, two defensive systems that
may lead to fibrin deposition in the lungs, thus recognizing the possibility that
PT may be a newly recognized entity. An increased risk for PE has been demonstrated
in these conditions. Sickle cell disease and assisted reproductive technologies are
other very different conditions in which an increased risk for PE has been found.
Gaucher's disease is a rare hereditary condition in which the hemostatic system could
have a role in the pathogenesis of pulmonary hypertension, which complicates the course
of the disease. In particular, the increased risk for PT, common to all these conditions,
deserves attention when a patient presents with sudden dyspnea, an unexpected COPD
exacerbation, or severe sudden asthmatic dyspnea. As a consequence, prediction scores
for venous thromboembolism could be revised.
Keywords
pulmonary embolism - pulmonary thrombosis - pneumonia - chronic obstructive pulmonary
disease - asthma - sickle cell disease - Gaucher's disease
