Download EMBOLISM An embolus is a detached intravascular solid, liquid, or

EMBOLISM
An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site
distant from its point of origin. Virtually 99% of all emboli represent some part of a dislodged thrombus,
hence the term thromboembolism. Rare forms of emboli include fat droplets, bubbles of air or nitrogen,
atherosclerotic debris (cholesterol emboli), tumor fragments, bits of bone marrow, or foreign bodies such
as bullets. However, unless otherwise specified, an embolism should be considered to be thrombotic in
origin. Inevitably, emboli lodge in vessels too small to permit further passage, resulting in partial or
complete vascular occlusion. The consequences of thromboembolism include ischemic necrosis
(infarction) of downstream tissue. Depending on the site of origin, emboli may lodge anywhere in the
vascular tree; the clinical outcomes are best understood from the standpoint of whether emboli lodge in
the pulmonary or systemic circulations.
Pulmonary Thromboembolism
Figure 4-16 Embolus derived from a lower extremity deep venous thrombosis and now impacted in a
pulmonary artery branch.
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 leftsided 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.
Systemic Thromboembolism
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.
Fat Embolism
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.
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.
Air Embolism
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.
Figure 4-17 Bone marrow embolus in the pulmonary circulation. The cellular elements on the left side of
the embolus are hematopoietic precursors, while the cleared vacuoles represent marrow fat. The relatively
uniform red area on the right of the embolus is an early organizing thrombus.
A particular form of gas embolism, called decompression sickness, occurs when individuals are exposed
to sudden changes in atmospheric pressure. Scuba and deep-sea divers, and underwater construction
workers are at risk. When air is breathed at high pressure (e.g., during a deep-sea dive), increased
amounts of gas (particularly nitrogen) become dissolved in the blood and tissues. If the diver then ascends
(depressurizes) too rapidly, the nitrogen expands in the tissues and bubbles out of solution in the blood to
form gas emboli that can induce focal ischemia in a number of tissues, including brain and heart. The
rapid formation of gas bubbles within skeletal muscles and supporting tissues in and about joints is
responsible for the painful condition called the bends (so named in the 1880s because afflicted
individuals characteristically arched their backs in a manner reminiscent of a then-popular women's
fashion called the Grecian Bend). In the lungs, gas bubbles in the vasculature cause edema, hemorrhages,
and focal atelectasis or emphysema, leading to respiratory distress, called the chokes. A more chronic
form of decompression sickness is called caisson disease, where persistence of gas emboli in the bones
leads to multiple foci of ischemic necrosis; the heads of the femurs, tibias, and humeri are most
commonly affected.
Treating acute decompression sickness requires placing the affected individual in a compression chamber
to increase barometric pressure and force the gas bubbles back into solution. Subsequent slow
decompression theoretically permits gradual resorption and exhalation of the gases so that obstructive
bubbles do not re-form.
Amniotic Fluid Embolism
Amniotic fluid embolism is a grave but fortunately uncommon complication of labor and the immediate
postpartum period (1 in 50,000 deliveries). It has a mortality rate in excess of 20% to 40%. The onset is
characterized by sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures and
coma. If the patient survives the initial crisis, pulmonary edema typically develops, along with (in half the
patients) disseminated intravascular coagulation (DIC), due to release of thrombogenic substances from
amniotic fluid.
The underlying cause is entry of amniotic fluid (and its contents) into the maternal circulation via a tear in
the placental membranes and rupture of uterine veins. Classically, there is marked pulmonary edema and
diffuse alveolar damage (Chapter 13), with the pulmonary microcirculation containing squamous cells
shed from fetal skin, lanugo hair, fat from vernix caseosa, and mucin derived from the fetal respiratory or
gastrointestinal tracts. Systemic fibrin thrombi indicate the onset of DIC.
SUMMARY
An embolus is any detached solid, liquid, or gaseous mass carried by the blood to a site distant from its
origin; the vast majority are part of a dislodged thrombus. Pulmonary emboli derive primarily from lower
extremity deep vein thrombosis; their effect (sudden death, right heart failure, pulmonary hemorrhage, or
infarction) depends on the size of the embolus.Systemic emboli derive primarily from cardiac mural or
valvular thrombi, aortic aneurysms, or atherosclerotic plaque; whether an embolus causes tissue infarction
depends on the site of embolization and collateral circulation.