Pathophysiology: Pulmonary thromboembolism is not a disease in and of itself. Rather, it is an often fatal complication of underlying venous thrombosis. Under normal conditions, microthrombi (tiny aggregates of red cells, platelets, and fibrin) are formed and lysed continually within the venous circulatory system. This dynamic equilibrium ensures local hemostasis in response to injury without permitting uncontrolled propagation of clot. Under pathological conditions, microthrombi may escape the normal fibrinolytic system to grow and propagate. PE occurs when these propagating clots break loose and embolize to block pulmonary blood vessels.
Thrombosis in the veins is triggered by venostasis, hypercoagulability, and vessel wall inflammation. These 3 underlying causes are known as the Virchow triad. All known clinical risk factors for DVT and PE have their basis in one or more of the triad.
Patients who have undergone gynecologic surgery, those with major trauma, and those with indwelling venous catheters may have DVTs that start at any location. For other patients, lower extremity venous thrombosis nearly always starts in the calf veins, which are involved in virtually 100% of all cases of symptomatic spontaneous lower extremity DVT. Although DVT starts in the calf veins, it already has propagated above the knee in 87% of symptomatic patients before the diagnosis is made.
Studies suggest that nearly every patient with thrombus in the upper leg or thigh will have a PE if a sensitive enough test is done to look for it. Current techniques allow us to demonstrate PE in 60-80% of these patients, even though about half have no clinical symptoms to suggest PE. Thrombus in the popliteal segment of the femoral vein (the segment behind the knee) is the cause of PE in more than 60% of cases.
PE can arise from DVT anywhere in the body. Fatal PE often results from thrombus that originates in the axillary or subclavian veins (deep veins of the arm or shoulder) or in veins of the pelvis. Thrombus that forms around indwelling central venous catheters is a common cause of fatal PE.
The belief that calf vein DVT is only a minor threat is outdated and inaccurate. DVT of the calf is a significant source of PE and often causes serious morbidity or death. In fact, one third of the cases of massive PE have their only identified source in the veins of the calf. One important autopsy study showed that more than 35% of patients who died from PE had isolated calf vein thrombosis. Other studies have shown that the overall frequency of PE from DVT isolated to the small deep veins of the calf is 33-46%. Most of the time, emboli from calf veins are of smaller caliber than those from more proximal venous segments, but not all emboli from calf veins are small. Even a very narrow vein can produce a long, sinuous clot that can cause hemodynamic collapse, and approximately 40% of PEs from calf veins produce perfusion scan defects that are large or massive.
Calf emboli that are very small carry their own special risks. In a 1993 study of patients with identifiable thrombi causing paradoxical embolization through a patent foramen ovale, the source was isolated to the calf veins in 15 of 24 cases.