The lungs function as a filter for blood returning from the systemic circulation and, therefore, material too large to pass through the pulmonary capillary system may become lodged in the pulmonary vasculature.
Depending on the size and composition of the embolic material, these pulmonary emboli (PEs) may be asymptomatic or may result in profound abnormalities in has exchange and hemodynamic collapse. The vast majority ever, other sources of embolic material must be considered in specific situations. Embolization of marrow fat after major trauma or orthopedic surgery), amniotic fluid(during vaginal or caesarean delivery), or air(dur the adult respiratory distress syndrome.
Sickled red blood cells or blood-borne parasites(e.g., schistosomes) as well as talc granules and cotton fibers unintentionally injected during intravenous drug use, may obstruct the pulmonary vasculature and produce progressive pulmonary hypertension. Approximately 250,000 patients each year are hospitalized for pulmonary thromboembolism in the United States alone, and the 3-month mortality rate approache originate in the deep veins of the thigh, with less common sources including the veins of upper extremities, pelvic veins, and right atrial mural thrombi. Predisposing factors for PE are similar to those for DVT, with stasis, hypercoagulability, and vessel trauma playing a central role. Increased age, smoking, and exogenous estrogen use also increase he risk of PE.
The presentation of an acute or chronic OR may be difficult to distinguish from that of other cardiopulmonary disorders; unless a high level of suspicion is maintained, the diagnosis is frequently missed.Historical features may be helpful, such as a prior history of DVT or PE, a family history of venous thrombosis, or a recent istory of immobilization(e.g., recent surgery, prolonged car trips.
The most frequent symptom dyspnea,with pleuritic chest pain and hymoptysis being less common.