2. Def: 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.
3. Almost all emboli represent some
part of a dislodged thrombus
Unless specified embolism means
Thromboembolism
4. Rare forms of emboli
droplets of fat
bubbles of air or nitrogen
Cholesterol emboli from AS debri
tumor fragments
bits of bone marrow, or even
foreign bodies such as bullets
5. Effect of embolus
Occlusion
Emboli lodge in vessels too small to permit
further passage, resulting in partial or
complete vascular occlusion
7. Clinical outcome
Depends on: the site of origin &
the site of lodgment
The clinical outcomes are best
understood from the standpoint of
whether emboli lodge in the pulmonary
or systemic circulations.
9. PULMONARY
THROMBOEMBOLISM
•Incidence of 20 to 25 per 100,000 hospitalized patients
•In more than 95% of instances, venous emboli originate from deep
leg vein thrombi
•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
•in general, the patient who has had one pulmonary embolus is at
high risk of having more.
•Rarely, an embolus may pass through an interatrial or
interventricular defect to gain access to the systemic circulation
(paradoxical embolism)
10. • Most pulmonary emboli (60% to 80%) are clinically silent because they are
small. With time, they undergo organization and are incorporated into the
vascular wall in some cases, organization of the thromboembolus leaves
behind a delicate, bridging fibrous web.
• Sudden death, right heart 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 may result in pulmonary
hemorrhage but usually does not cause pulmonary infarction because of the
dual blood flow into the area from the bronchial circulation. A similar
embolus in the setting of left-sided cardiac failure (i.e., with sluggish
bronchial artery flow), however, may result in a large infarct.
• Embolic obstruction of small end-arteriolar pulmonary branches usually
does result in associated infarction.
• Multiple emboli over time may cause pulmonary hypertension with right
heart failure.
PULMONARY
THROMBOEMBOLISM
11. Consequences of Pul.embolism
• The morphologic consequences depend on the
size of the embolic mass and the general state
of the circulation
• Large emboli - Sudden death often ensues -
acute cor pulmonale (ECG-elecromechanical
dissociation)
• Smaller emboli
– with good CVS – hemorrhages
resorption & reconstitution of
the preexisting architecture
– with CVS compromise - 10% infarction
12. Here is large pulmonary
thromboembolus seen in cross
section of this lung. The
typical source for such
thromboemboli is from large
veins in the legs and pelvis.
13.
14. Figure 4-17 Large
embolus derived from a
lower extremity deep
venous thrombosis and
now impacted in a
pulmonary artery branch
18. Non thrombotic forms of pul.emboli
• uncommon but potentially lethal
• air (may be iatrogenic)
• bone marrow (after trauma and bone
marrow necrosis in sickle cell patients)
• fat (trauma and surgery)
• amniotic fluid (during parturition) and
• foreign bodies (in I/V drug abusers)
19. SYSTEMIC THROMBOEMBOLISM
• refers to emboli travelling within the
arterial circulation
• Common source: Mural thrombi in heart
(80%)
• Less common source: Aorta (AS,
Aneurysm)
21. SYSTEMIC THROMBOEMBOLISM
The major sites for arteriolar embolization
• Lower extremities (75%) and
• Brain (10%)
• the intestines, kidneys, spleen, and upper
extremities involved to a lesser extent
22. SYSTEMIC THROMBOEMBOLISM
The consequences of systemic emboli
depend on:
the extent of collateral vascular supply in the
affected tissue
the tissue's vulnerability to ischemia and
the caliber of the vessel occluded
in general, arterial emboli cause infarction of
tissues downstream of the obstructed
vessel
23. Tissues supplied by end-arteries
without significant collateral
supplies will be the most
susceptible.
Obstruction of blood supply
leads to ischemia which when
prolonged leads to necrosis and
atrophy.
Where there is reperfusion after
ischemic necrosis the tissues will
show a hemorrhagic necrosis.
Where there is infection by
Clostridia (gram positive bacilli),
gangrene sets in.
24. FAT EMBOLISM
• Presence of microscopic fat globules in
the circulation
• Causes: # of long bones
Soft tissue trauma
Burns
25. FAT EMBOLISM
Fat embolism syndrome is characterized by
pulmonary insufficiency,
neurologic symptoms,
anemia, and
Thrombocytopenia
Symptoms:
typically begin 1 to 3 days after injury,
sudden onset of tachypnea, dyspnea, and
tachycardia
26. FAT EMBOLISM
Fat embolism syndrome: Pathogenesis
mechanical obstruction and
biochemical injury
Fat globule platelet complexes
Fat globule RBC complexes
Release of FFA > toxic injury to endothelium >
inflammation > further damage to the vessels
27. FAT EMBOLISM
Demonstration of fat embolism in
specimens:
By means of frozen sections
Routine processing dissolves fat
28. Figure 4-18 Bone marrow embolus in the pulmonary circulation. The
cleared vacuoles represent marrow fat that is now impacted in a distal
vessel along with the cellular hematopoietic precursors.
29. AIR EMBOLISM
• Gas bubbles within the circulation can
obstruct vascular flow
• Entry of gas into circulation occurs during
Obstetric procedures
Chest wall injury
30. AIR EMBOLISM
Dose: should be > 100ml to produce
any clinical effect
Bubbles act like physical obstructions and
may coalesce to form frothy masses
sufficiently large to occlude major vessels
31. AIR EMBOLISM
Decompression sickness:
Scuba and deep sea divers,
underwater construction workers, and
individuals in unpressurized aircraft
Gas: Nitrogen
Clinically: bends, chokes, ischemia, infarction
Treatment: slow decompression
Caisson disease: chronic form of decompression
sickness
32. AMNIOTIC FLUID EMBOLISM
Uncommon complication of laborUncommon complication of labor
Has a mortality rate of 20% to 40%
Clinically: sudden severe dyspnea, cyanosis, and
hypotensive shock, followed by seizures and coma
Pathogenesis: DIC
The underlying cause: infusion of amniotic fluid or fetal
tissue into the maternal circulation via a tear in the
placental membranes or rupture of uterine veins
The classic findings: the presence in the pulmonary
microcirculation of squamous cells shed from fetal skin,
lanugo hair, fat from vernix caseosa, and mucin derived
from the fetal respiratory or gastrointestinal tract
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:
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 instances, venous emboli originate from deep leg vein thrombi
They are carried through progressively larger channels and usually pass through the right side of the heart into 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. 4-17 ). Frequently, there are multiple emboli, perhaps sequentially or as a shower of smaller emboli from a single large mass; in general, the patient who has had one pulmonary embolus is at high risk of having more. Rarely, an embolus may pass through an interatrial or interventricular defect to gain access to the systemic circulation (paradoxical embolism). A more complete discussion of pulmonary emboli is presented in Chapter 15 ; an overview is offered here.[43][44]
The morphologic consequences of embolic occlusion of the pulmonary arteries depend on the size of the embolic mass and the general state of the circulation. Large emboli may impact in the main pulmonary artery or its major branches or lodge at the bifurcation as a saddle embolus ( Fig. 15-27 ). Sudden death often ensues, owing largely to the blockage of blood flow through the lungs. Death may also be caused by acute failure of the right side of the heart (acute cor pulmonale). Smaller emboli can travel out into the more peripheral vessels, where they may cause infarction. In patients with adequate cardiovascular function, the bronchial arterial supply can often sustain the lung parenchyma despite obstruction to the pulmonary arterial system. Under these circumstances, hemorrhages may occur, but there is no infarction of the underlying lung parenchyma. Only about 10% of emboli actually cause infarction. Although the underlying pulmonary architecture may be obscured by the suffusion of blood, hemorrhages are distinguished by the preservation of the pulmonary alveolar architecture; in such cases, resorption of the blood permits reconstitution of the preexisting architecture
====================
A large pulmonary embolus is one of the few causes of virtually instantaneous death. During cardiopulmonary resuscitation in such instances, the patient frequently is said to have electromechanical dissociation, in which the electrocardiogram has a rhythm but no pulses are palpated because of the massive blockage of blood in the systemic venous circulation.
Here is another large pulmonary thromboembolus seen in cross section of this lung. The typical source for such thromboemboli is from large veins in the legs and pelvis.
This pulmonary thromboembolus is occluding the main pulmonary artery. Persons who are immobilized for weeks are at greatest risk. The patient can experience sudden onset of shortness of breath. Death may occur within minutes.
Figure 4-17 Large embolus derived from a lower extremity deep venous thrombosis and now impacted in a pulmonary artery branch
A pulmonary thromboembolus travels from a large vein in the leg up the inferior vena cava to the main pulmonary arteries as they branch. Such thrombi embolize most often from large veins in the legs and pelvis where thrombi form with stasis.
This is the microscopic appearance of a pulmonary embolus (PE) in a major pulmonary artery branch
Figure 4-14 Mural thrombi. A, Thrombus in the left and right ventricular apices, overlying a white fibrous scar. B, Laminated thrombus in a dilated abdominal aortic aneurysm.
The major sites for arteriolar embolization are the lower extremities (75%) and the brain (10%), with the intestines, kidneys, spleen, and upper extremities involved to a lesser extent.
The major sites for arteriolar embolization are the lower extremities (75%) and the brain (10%), with the intestines, kidneys, spleen, and upper extremities involved to a lesser extent.
Figure 4-18 Bone marrow embolus in the pulmonary circulation. The cleared vacuoles represent marrow fat that is now impacted in a distal vessel along with the cellular hematopoietic precursors
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 of 20% to 40%, and as other obstetric complications (e.g., eclampsia, pulmonary embolism) have been better managed, amniotic fluid embolism has become an important cause of maternal mortality. 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) DIC, owing to release of thrombogenic substances from amniotic fluid.[51][52]
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. The classic findings are therefore the presence in the pulmonary microcirculation of squamous cells shed from fetal skin, lanugo hair, fat from vernix caseosa, and mucin derived from the fetal respiratory or gastrointestinal tract. There is also marked pulmonary edema and changes of diffuse alveolar damage ( Chapter 15 ) as well as systemic fibrin thrombi indicative of DIC.