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EMBOLISM
Ikram Ullah
M.Phil MLSc
EMBOLISM
 An embolus is an intravascular solid, liquid, or gaseous mass
that is carried by the blood to a site distant from its point of
origin
 The vast majority of emboli derive from a dislodged
thrombus—hence the term thromboembolism.
 Less common types of emboli include fat droplets, bubbles of
air or nitrogen, atherosclerotic debris (cholesterol emboli),
tumor fragments, bits of bone marrow, and amniotic fluid.
 The primary consequence of systemic embolization is ischemic
necrosis (infarction) of downstream tissues
 While embolization in the pulmonary circulation leads to
hypoxia, hypotension, and right-sided heart failure.
Pulmonary Thromboembolism
Fragmented thrombi from DVTs are carried
through progressively larger channels and usually
pass through the right side of the heart before
arresting in the pulmonary vasculature
Depending on size, a PE can occlude the main
pulmonary artery, lodge at the bifurcation of the
right and left pulmonary arteries (saddle embolus),
or pass into the smaller, branching arterioles
Rarely, an embolus passes through an atrial or
ventricular defect and enters the systemic
circulation (paradoxical embolism).
Clinical and pathologic features of PE
Most pulmonary emboli (60% to 80%) are small and
clinically silent
At the other end of the spectrum, a large embolus
that blocks a major pulmonary artery can cause
sudden death
Embolic obstruction of medium-sized arteries and
subsequent rupture of capillaries rendered anoxic can
cause pulmonary hemorrhage.
Such embolization does not usually cause pulmonary
infarction since the area also receives blood through
an intact bronchial circulation (dual circulation)
However, a similar embolus in the setting of left-
sided cardiac failure (and diminished bronchial
artery perfusion) can lead to a pulmonary infarct.
Embolism to small end-arteriolar pulmonary
branches usually causes infarction.
Multiple emboli occurring over time can cause
pulmonary hypertension and right ventricular
failure (cor pulmonale).
Systemic Thromboembolism
Most systemic emboli (80%) arise from
intracardiac mural thrombi
Two thirds are associated with left ventricular
infarcts and another 25% with dilated left atria
The remainder originate from aortic aneurysms,
thrombi overlying ulcerated atherosclerotic
plaques,
Fragmented valvular vegetations or the venous
system (paradoxical emboli); 10% to 15% of
systemic emboli are of unknown origin
By contrast with venous emboli, which lodge
primarily in the lung, arterial emboli can travel
virtually anywhere
Common arteriolar embolization sites include the
lower extremities (75%) and central nervous
system (10%); intestines, kidneys, and spleen are
less common targets.
The consequences of embolization depend on the
caliber of the occluded vessel, the collateral
supply, and the affected tissue’s vulnerability to
anoxia
Arterial emboli often lodge in end arteries and
cause infarction.
Fat Embolism
Soft tissue crush injury or rupture of marrow
vascular sinusoids (long bone fracture) releases
microscopic fat globules into the circulation
Fat and marrow emboli are common incidental
findings after vigorous cardiopulmonary
resuscitation but probably are of little clinical
consequence
Similarily, although fat and marrow embolism
occurs in some 90% of individuals with severe
skeletal injuries, less than 10% show any clinical
findings
However, a minority of patients develop a
symptomatic fat embolism syndrome characterized
by pulmonary insufficiency, neurologic symptoms,
anemia, thrombocytopenia, and a diffuse petechial
rash, which is fatal in 10% of cases
The pathogenesis of fat emboli syndrome involves
both mechanical obstruction and biochemical
injury
Fat microemboli occlude pulmonary and cerebral
microvasculature, both directly and by triggering
platelet aggregation
Amniotic Fluid Embolism
Amniotic fluid embolism is an uncommon, grave
complication of labor and the immediate
postpartum period (1 in 40,000 deliveries)
The mortality rate approaches 80%, making it the
most common cause of maternal death
It accounts for 10% of maternal deaths in the
United States, while 85% of survivors suffer some
form of permanent neurologic deficit
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 disseminated
intravascular coagulation secondary to release of
thrombogenic substances from amniotic fluid
The underlying cause is entry of amniotic fluid (and
its contents) into the maternal circulation via tears
in the placental membranes and/or uterine vein
rupture
Air Embolism
Gas bubbles within the circulation can coalesce
and obstruct vascular flow and cause distal
ischemic injury
Thus, a small volume of air trapped in a coronary
artery during bypass surgery
Or introduced into the cerebral arterial circulation
by neurosurgery performed in an upright “sitting
position” can occlude flow, with dire consequences
A particular form of gas embolism called
decompression sickness is caused by sudden
changes in atmospheric pressure
 Rapid formation of gas bubbles within skeletal muscles
and supporting tissues in and about joints is
responsible for the painful condition called “the bends”
 Gas bubbles in the pulmonary vasculature cause
edema, hemorrhages, and focal atelectasis or
emphysema, leading to respiratory distress, the so-
called chokes
 Acute decompression sickness is treated by placing
affected persons in a high-pressure chamber, to force
the gas back into solution
 Subsequent slow decompression permits gradual gas
resorption and exhalation so that obstructive bubbles
do not re-form
Embolism

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Embolism

  • 2. EMBOLISM  An embolus is an intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin  The vast majority of emboli derive from a dislodged thrombus—hence the term thromboembolism.  Less common types of emboli include fat droplets, bubbles of air or nitrogen, atherosclerotic debris (cholesterol emboli), tumor fragments, bits of bone marrow, and amniotic fluid.  The primary consequence of systemic embolization is ischemic necrosis (infarction) of downstream tissues  While embolization in the pulmonary circulation leads to hypoxia, hypotension, and right-sided heart failure.
  • 3. Pulmonary Thromboembolism Fragmented thrombi from DVTs are carried through progressively larger channels and usually pass through the right side of the heart before arresting in the pulmonary vasculature Depending on size, a PE can occlude the main pulmonary artery, lodge at the bifurcation of the right and left pulmonary arteries (saddle embolus), or pass into the smaller, branching arterioles Rarely, an embolus passes through an atrial or ventricular defect and enters the systemic circulation (paradoxical embolism).
  • 4.
  • 5. Clinical and pathologic features of PE Most pulmonary emboli (60% to 80%) are small and clinically silent At the other end of the spectrum, a large embolus that blocks a major pulmonary artery can cause sudden death Embolic obstruction of medium-sized arteries and subsequent rupture of capillaries rendered anoxic can cause pulmonary hemorrhage. Such embolization does not usually cause pulmonary infarction since the area also receives blood through an intact bronchial circulation (dual circulation)
  • 6. However, a similar embolus in the setting of left- sided cardiac failure (and diminished bronchial artery perfusion) can lead to a pulmonary infarct. Embolism to small end-arteriolar pulmonary branches usually causes infarction. Multiple emboli occurring over time can cause pulmonary hypertension and right ventricular failure (cor pulmonale).
  • 7. Systemic Thromboembolism Most systemic emboli (80%) arise from intracardiac mural thrombi Two thirds are associated with left ventricular infarcts and another 25% with dilated left atria The remainder originate from aortic aneurysms, thrombi overlying ulcerated atherosclerotic plaques, Fragmented valvular vegetations or the venous system (paradoxical emboli); 10% to 15% of systemic emboli are of unknown origin
  • 8. By contrast with venous emboli, which lodge primarily in the lung, arterial emboli can travel virtually anywhere Common arteriolar embolization sites include the lower extremities (75%) and central nervous system (10%); intestines, kidneys, and spleen are less common targets. The consequences of embolization depend on the caliber of the occluded vessel, the collateral supply, and the affected tissue’s vulnerability to anoxia Arterial emboli often lodge in end arteries and cause infarction.
  • 9. Fat Embolism Soft tissue crush injury or rupture of marrow vascular sinusoids (long bone fracture) releases microscopic fat globules into the circulation Fat and marrow emboli are common incidental findings after vigorous cardiopulmonary resuscitation but probably are of little clinical consequence Similarily, although fat and marrow embolism occurs in some 90% of individuals with severe skeletal injuries, less than 10% show any clinical findings
  • 10. However, a minority of patients develop a symptomatic fat embolism syndrome characterized by pulmonary insufficiency, neurologic symptoms, anemia, thrombocytopenia, and a diffuse petechial rash, which is fatal in 10% of cases The pathogenesis of fat emboli syndrome involves both mechanical obstruction and biochemical injury Fat microemboli occlude pulmonary and cerebral microvasculature, both directly and by triggering platelet aggregation
  • 11. Amniotic Fluid Embolism Amniotic fluid embolism is an uncommon, grave complication of labor and the immediate postpartum period (1 in 40,000 deliveries) The mortality rate approaches 80%, making it the most common cause of maternal death It accounts for 10% of maternal deaths in the United States, while 85% of survivors suffer some form of permanent neurologic deficit Onset is characterized by sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures and coma
  • 12. If the patient survives the initial crisis, pulmonary edema typically develops, along with disseminated intravascular coagulation secondary to release of thrombogenic substances from amniotic fluid The underlying cause is entry of amniotic fluid (and its contents) into the maternal circulation via tears in the placental membranes and/or uterine vein rupture
  • 13. Air Embolism Gas bubbles within the circulation can coalesce and obstruct vascular flow and cause distal ischemic injury Thus, a small volume of air trapped in a coronary artery during bypass surgery Or introduced into the cerebral arterial circulation by neurosurgery performed in an upright “sitting position” can occlude flow, with dire consequences A particular form of gas embolism called decompression sickness is caused by sudden changes in atmospheric pressure
  • 14.  Rapid formation of gas bubbles within skeletal muscles and supporting tissues in and about joints is responsible for the painful condition called “the bends”  Gas bubbles in the pulmonary vasculature cause edema, hemorrhages, and focal atelectasis or emphysema, leading to respiratory distress, the so- called chokes  Acute decompression sickness is treated by placing affected persons in a high-pressure chamber, to force the gas back into solution  Subsequent slow decompression permits gradual gas resorption and exhalation so that obstructive bubbles do not re-form