Fig. 13.24 Largesaddleembolusfromthefemoralveinlyingastridethemainleftandrightpulmonaryarteries.(Courtesy of Dr. Linda Margraf, Department of Pathology, University of Texas Southwestern Medical School, Dallas, Texas.)
The clinical consequences of pulmonary thromboembolism are summarized as follows: • Most (60% to 80%) are clinically silent because they are small; the bronchial circulation sustains the viability of the affected lung parenchyma, and the embolic mass is rapidly removed by fibrinolytic activity.
Fig. 13.25 Asmall,roughlywedge-shapedhemorrhagicpulmonaryinfarctofrecentoccurrence.
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In 5% of cases, death, acute right-sided heart failure, or cardiovascular collapse (shock) occurs suddenly. Massive pulmonary embolism is one of the few causes of virtually instantaneous death. These severe consequences typically happen when more than 60% of the total pulmonary vasculature is obstructed by a large embolus or multiple simultaneous small emboli.
Obstruction of small to medium pulmonary branches (10% to 15% of cases) causes pulmonary infarction if some element of circulatory insufficiency also is present. Typically, individuals who sustain infarctions present with dyspnea.
In a small but significant subset of patients (accounting for <3% of cases), recurrent “showers” of emboli lead to pulmonary hypertension, chronic right-sided heart failure, and, in time, pulmonary vascular sclerosis with progressively worsening of dyspnea.
Emboli usually resolve after the initial acute event, as endogenous fibrinolytic activity often leads to their complete dissolution. However, in the presence of an underlying predisposing factor, a small, innocuous embolus may presage a larger one, and patients who have experienced one pulmonary embolism have a 30% chance of developing a second. Prophylactic therapy may include anticoagulation, early ambulation for postoperative and postparturient patients, application of elastic stockings, intermittent pneumatic calf compression, and isometric leg exercises for bedridden patients. Those who develop pulmonary embolism are given anti-coagulation therapy. Patients with massive pulmonary embolism who are hemodynamically unstable (shock, acute right heart failure) are candidates for thrombolytic therapy.
Nonthrombotic pulmonary emboli come in several uncommon but potentially lethal forms, such as air, fat, and amniotic fluid embolism (Chapter 4). Intravenous drug abuse often is associated with foreign body embolism in the pulmonary microvasculature; the presence of magnesium trisilicate (talc) in the intravenous mixture elicits a granulomatous response within the interstitium or pulmonary arteries. Involvement of the interstitium may lead to fibrosis, while vascular involvement leads to pulmonary hypertension. Residual talc crystals can be demonstrated within the granulomas using polarized light. Bone marrow embolism (denoted by the presence of hematopoietic and fat elements within a pulmonary artery) can occur after massive trauma and in patients with bone infarction secondary to sickle cell anemia.
Almostalllargepulmonaryarterythrombiareembolicinorigin,usuallyarisingfromthedeepveinsofthelowerleg.
Riskfactorsincludeprolongedbedrest,kneeorhipsurgery,severetrauma,congestiveheartfailure,useoforalcontraceptives(especiallythosewithhighestrogencontent),disseminatedcancer,andgeneticcausesofhypercoagulability.
Mostemboli(60%to80%)areclinicallysilent;aminority(5%,typicallylarge“saddleemboli”)causeacuteright-sidedheartfailure,shock,orsuddendeath;andtheremaindercausepulmonaryinfarction.