Embolism

By-Subhrajyoti Roy

2nd Year M.B.B.S. Student(WBUHS)

Embolism:
 An embolus is a detached intravascular solid, liquid, or gaseous mass that
is carried by the blood from its point of origin to a distant site, where it
often causes tissue dysfunction or infarction.
 The vast majority of emboli are dislodged thrombi, hence the term
thromboembolism.
 Other rare emboli are composed of fat droplets, nitrogen bubbles,
atherosclerotic debris (cholesterol emboli), tumor fragments, bone marrow,
or even foreign bodies.
 Emboli travel through the blood until they encounter vessels too small to
permit further passage, causing partial or complete vascular occlusion.
 Types of Emboli
Embolism

Depending Depending Depending

Depending upon upon the upon the
upon the whether source of flow of
matter of infected or emboli blood
emboli not
Cardiac emboli
from left side of Paradoxical embolus: An embolus which
the heart is carried from the venous side of
Bland, when sterile
Solid circulation to the arterial side or vice
(Thromboemboli, versa, is called paradoxical or crossed
atheromatous embolus e.g. through patent foramen
material etc.) Arterial emboli ovale, septal defects of heart,
arteriovenous shunts in the lungs
Septic, when
Liquid infected
(Fat globules,
amniotic fluid, bone
marrow) Venous emboli
Retrograde embolus: An embolus which
travels against the flow of blood is called
retrograde embolus e.g. metastatic
Gaseous deposits in spine from prostate CA via
(air,other gases) spinal veins
Lymphatic emboli
Some important types of embolism
 Pulmonary Embolism:
i. Pulmonary emboli originate from deep venous thromboses and are the most
common form of thromboembolic disease.
ii. Incidence since the 1970s of roughly 2 to 4 per 1000 hospitalized patients in the
United States.
iii. PE causes about 100,000 deaths per year in the United States.
iv. In more than 95% of cases, PEs originates from leg DVT.
v. Course of embolus causing Pulmonary Embolism
Occlude the
main pulmonary
artery

Straddle the
Right side of the pulmonary
Fragmented heart and artery
thrombi from Larger veins depending upon bifurcation
DVTs the size of (Saddle
emboli embolus)

Pass out into the

smaller
branching
arteries.

vi. Rarely, a venous embolus passes through an interatrial or interventricular defect

and gains access to the systemic arterial circulation (paradoxical embolism).
vii. Most pulmonary emboli (60% to 80%) are clinically silent because they are small.
With time they become organized and are incorporated into the vascular wall; in
some cases organization of the thromboembolus leaves behind a delicate, ridging
fibrous web.
viii. Sudden death, right heart failure (cor pulmonale), or cardiovascular collapse occurs
when emboli obstruct 60% or more of the pulmonary circulation.
ix. Embolic obstruction of medium-sized arteries with subsequent vascular rupture
can result in pulmonary hemorrhage but usually does not cause pulmonary
infarction. This is because the lung is supplied by both the pulmonary arteries and
the bronchial arteries, and the intact bronchial circulation is usually sufficient to
perfuse the affected area. Understandably, if the bronchial arterial flow is
compromised (e.g., by left-sided cardiac failure), infarction may occur.
x. Embolic obstruction of small end-arteriolar pulmonary branches often does
produce hemorrhage or infarction.
xi. Multiple emboli over time may cause pulmonary hypertension and right ventricular
failure.

Figure- Embolus from a lower extremity deep venous thrombosis,

lodged at a pulmonary artery branchpoint.
Systemic Thromboembolism
i. Most systemic emboli (80%) arise from intracardiac mural thrombi, two thirds
of which are associated with left ventricular wall infarcts and another one
fourth withleft atrial dilation and fibrillation. The remainder originates from
aortic aneurysms, atherosclerotic plaques, valvular vegetations, or venous
thrombi (paradoxical emboli);10% to 15% are of unknown origin.
ii. Arterial emboli are in contrast to venous emboli, the vast majority of which
lodge in the lung, arterial emboli can travel to a wide variety of sites; the point
of arrest depends on the source and the relative amount of blood flow that
downstream tissues receive.
iii. The emboli are arterial and invariably cause infarction at the sites of
lodgement . These sites, in descending order of frequency are: lower
extremities (75%) or the brain (10%), internal visceral organs; the intestines,
kidneys, spleen, and upper extremities, may be involved on occasion.
iv. The consequences of systemic emboli depend on the vulnerability of the
affected tissues to ischemia, the caliber of the occluded vessel, and whether a
collateral blood supply exists; in general, however, the outcome is tissue
infarction.
Fat and Marrow Embolism
i. Microscopic fat globules—sometimes with associated hematopoietic
bone marrow—can be found in the pulmonary vasculature after fractures
of long bones or, rarely, in the setting of soft tissue trauma and burns.
Presumably these injuries rupture vascular sinusoids in the marrow or
small venules, allowing marrow or adipose tissue to herniated into the
vascular space and travel to the lung.
ii. Fat and marrow emboli are very common incidental findings after
vigorous cardiopulmonary resuscitation and are probably of no clinical
consequence. Indeed, fat embolism occursin some 90% of individuals with
severe skeletal injuries but less than 10% of such patients have any clinical
findings.
iii. Fat embolism syndrome is the term applied to the minority of patients
who become symptomatic. It is characterized by pulmonary insufficiency,
neurologic symptoms, anemia, and thrombocytopenia, and is fatal in
about 5% to 15% of cases. Typically, 1 to 3 days after injury there is a
sudden onset of tachypnea, dyspnea, and tachycardia; irritability and
restlessness can progress to delirium or coma.
iv. Thrombocytopenia is attributed to platelet adhesion to fat globules and
subsequent aggregation or splenic sequestration; anemia can result from
similar red cell aggregation and/or hemolysis.
v. A diffuse petechial rash (seen in 20% to 50% of cases) is related to rapid
onset of thrombocytopenia and can be a useful diagnostic feature.
vi. Fat microemboli and associated red cell and platelet aggregates can
occlude the pulmonary and cerebral microvasculature.
vii. Release of free fatty acids from the fat globules exacerbates the situation
by causing local toxic injury to endothelium, and platelet activation and
granulocyte recruitment (with free radical, protease, and eicosanoid
release) 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 typically requires
specialized techniques, including frozen sections and stains for fat.
Figure- Bone marrow embolus in the pulmonary circulation. The cellular elements on the left side of the
embolus are hematopoietic cells, while the cleared vacuoles represent marrow fat. The relatively
uniform red area on theright of the embolus is an early organizing thrombus.
Air Embolism
i. Gas bubbles within the circulation can coalesce to form frothy
masses that obstruct vascular flow and cause distal ischemic
injury.
ii. For example, a very small volume of air trapped in a coronary
artery during bypass surgery, or introduced into the cerebral
circulation by neurosurgery in the “sitting position,” can occlude
flow with dire consequences.
iii. A particular form of gas embolism, called decompression sickness,
occurs when individuals experience sudden decreases in
atmospheric pressure.
iv. Scuba and deep sea divers, underwater construction workers, and
individuals in unpressurized aircraft in rapid ascent are all at risk.
When air is breathed at high pressure (e.g., during a deep sea dive),
increased amounts of gas (particularly nitrogen) are dissolved in the
blood and tissues. If the diver then ascends (depressurizes) too
rapidly, the nitrogen comes out of solution in the tissues and the
blood.
v. 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
vi. In the lungs, gas bubbles in the vasculature cause edema,
hemorrhage, and focal atelectasis or emphysema, leading to a form
of respiratory distress called the chokes. A more chronic form of
decompression sickness is called caisson disease (named for the
pressurized vessels used in bridge construction; workers in these
vessels suffered both acute and chronic forms of decompression
sickness).
vii. In caisson disease, persistence of gas emboli in the skeletal system
leads to multiple foci of ischemic necrosis; the more common sites
are the femoral heads, tibia, and humeri. Individuals affected by
acute decompression sickness are treated by being placed in a
chamber under sufficiently high pressure to force the gas bubbles
back into solution. Subsequent slow decompression permits
gradual resorption and exhalation of the gases, which prevents the
obstructive bubbles from reforming.
Amniotic Fluid Embolism

i. Amniotic fluid embolism is the fifth most common cause of maternal

mortality worldwide; it accounts for roughly 10% of maternal deaths in
the United States and results in permanent neurologic deficit in as many
as 85% of survivors.
ii. Amniotic fluid embolism is an ominous complication of labor and the
immediate postpartum period.
iii. Although the incidence is only approximately 1 in 40,000 deliveries, the
mortality rate is up to 80%. The onset is characterized by sudden severe
dyspnea, cyanosis, and shock, followed by neurologic impairment ranging
from headache to seizures and coma.
iv. If the patient survives the initial crisis, pulmonary edema typically develops,
frequently accompanied by disseminated intravascular coagulation.
v. The underlying cause is the infusion of amniotic fluid or fetal tissue into the
maternal circulation via a tear in the placental membranes or rupture of
uterine veins.
vi. Classicfindings at autopsy include the presence of squamous cells shed
from fetal skin, lanugo hair, fat from vernix caseosa, and mucin derived
from the fetal respiratory or gastrointestinal tract in the maternal
pulmonary microvasculature
vii. Other findings include marked pulmonary edema, diffuse alveolar damage
and the presence of fibrin thrombi in many vascular beds due to
disseminated intravascular coagulation.
Figure-Amniotic fluid embolism. Two small pulmonary
arterioles are packed with laminated swirls of fetal
squamous cells. There is marked edema and congestion.
Elsewhere the lung contained small organizing thrombi
consistent with disseminated intravascular coagulation.
(Courtesy Dr. Beth Schwartz, Baltimore, Md.)