Pulmonary embolism has an incidence of 20 to 25 per 100,000 hospitalized patients.

Although the rate of fatal pulmonary emboli (as assessed at autopsy) has declined from 6% to
2% over the last quarter century, pulmonary embolism still causes about 200,000 deaths per
year in the United States. In more than 95% of cases, venous emboli originate from deep leg
vein thrombi above the level of the knee (described above). They are carried through
progressively larger channels and pass through the right side of the heart before entering the
pulmonary vasculature. Depending on the size of the embolus, it may occlude the main
pulmonary artery, impact across the bifurcation (saddle embolus), or pass out into the smaller,
branching arterioles (Fig. 4-16). Frequently, there are multiple emboli, perhaps sequentially,
or as a shower of smaller emboli from a single large thrombus; in general, the patient who
has had one pulmonary embolus is at high risk of having more. Rarely, an embolus can pass
through an interatrial or interventricular defect, thereby entering the systemic circulation
(paradoxical embolism). The following is an overview of pulmonary emboli; see Chapter 13
for a more complete discussion.
Most pulmonary emboli (60% to 80%) are clinically silent because they are small.
They eventually become organized and become incorporated into the vascular wall; in
some cases, organization of the thromboembolus leaves behind a delicate, bridging
fibrous web.Sudden death, right ventricular failure (cor pulmonale), or cardiovascular
collapse occurs when 60% or more of the pulmonary circulation is obstructed with
emboli.Embolic obstruction of medium-sized arteries can cause pulmonary
hemorrhage but usually not pulmonary infarction because the lung has a dual blood
supply and the intact bronchial arterial circulation continues to supply blood to the
area. However, a similar embolus in the setting of left-sided cardiac failure (and
resultant sluggish bronchial artery blood flow) may result in a large infarct.Embolic
obstruction of small end-arteriolar pulmonary branches usually does result in
associated infarction.Many emboli occurring over a period of time may cause
pulmonary hypertension with right ventricular failure.
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Systemic Thromboembolism
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Systemic thromboembolism refers to emboli in the arterial circulation. Most (80%) arise from
intracardiac mural thrombi, two-thirds of which are associated with left ventricular wall
infarcts and another quarter with dilated left atria (e.g., secondary to mitral valve disease).
The remainder originate from aortic aneurysms, thrombi on ulcerated atherosclerotic plaques,
or fragmentation of valvular vegetations (Chapter 11). A very small fraction of systemic
emboli appear to arise in veins but end up in the arterial circulation, through interventricular
defects. These are called paradoxical emboli. In contrast to venous emboli, which tend to
lodge primarily in one vascular bed (the lung), arterial emboli can travel to a wide variety of
sites; the site of arrest depends on the point of origin of the thromboembolus and the relative
blood flow through the downstream tissues. The major sites for arteriolar embolization are
the lower extremities (75%) and the brain (10%), with the intestines, kidneys, and spleen
affected to a lesser extent. The consequences of embolization in a tissue depend on
vulnerability to ischemia, caliber of the occluded vessel, and the collateral blood supply; in
general, arterial embolization causes infarction of the affected tissues.
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Fat Embolism
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Microscopic fat globules can be found in the circulation after fractures of long bones (which
contain fatty marrow) or after soft-tissue trauma. Fat enters the circulation by rupture of the
marrow vascular sinusoids or rupture of venules in injured tissues. Although fat and marrow

embolism occurs in some 90% of individuals with severe skeletal injuries (Fig. 4-17), fewer
than 10% of such patients show any clinical findings. Fat embolism syndrome is
characterized by pulmonary insufficiency, neurologic symptoms, anemia, and
thrombocytopenia; it is fatal in about 10% of cases. Typically, the symptoms appear 1 to 3
days after injury, with sudden onset of tachypnea, dyspnea, and tachycardia. Neurologic
symptoms include irritability and restlessness, with progression to delirium or coma.
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The pathogenesis of fat emboli syndrome probably involves both mechanical obstruction and
biochemical injury. Fat microemboli occlude pulmonary and cerebral microvasculature;
vascular occlusion is aggravated by local platelet and erythrocyte aggregation. This pathology
is further exacerbated by free fatty acid release from the fat globules, causing local toxic
injury to endothelium. Platelet activation and recruitment of granulocytes (with free radical,
protease, and eicosanoid release; Chapter 2) complete the vascular assault. Because lipids are
dissolved out of tissue preparations by the solvents routinely used in paraffin embedding, the
microscopic demonstration of fat microglobules (i.e., in the absence of accompanying
marrow) typically requires specialized techniques, including frozen sections and fat stains.
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Air Embolism
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Gas bubbles within the circulation can obstruct vascular flow (and cause distal ischemic
injury) almost as readily as thrombotic masses can. Air may enter the circulation during
obstetric procedures or as a consequence of chest wall injury. Generally, more than 100 mL of
air are required to produce a clinical effect; bubbles can coalesce to form frothy masses
sufficiently large to occlude major vessels.
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