2. Definition and Types
Definition-An embolus is a detached
intravascular/extravascular solid,liquid
or gaseous mass that is carried by the
blood to a site distant from its point of
origin
Varieties of emboli-intravascular-solid-
fragments of thrombi (septic/aseptic),
atherosclerotic debris
4. Types of Emboli
Types
1)Depending on matter in the emboli
2)Depending on whether they are
infected/not
3)Depending on source of emboli
4)Depending upon flow of blood,two special
types of emboli
1.Paradoxical embolus
2.Retrograde embolus
6. Pulmonary
Thromboembolism
Occlusion affects large/medium sized
pulmonary artery
95% pulmonary emboli arise in thrombi
within large deep veins of lower limbs
Pulmonary thrombosis occurs in pulmonary
atherosclerosis & pulmonary hypertension
Depending on size of embolus occlusion of
main pulmonary artery (saddle embolus) /
impact smaller arterioles-pulmonary
haemorrhage/infarction
14. Consequences of
Pulmonary Embolism
Clinical significance-60-80%-clinically silent-
resolution due to fibrinolysis
If organized, incorporated into vascular wall
With >60% obstruction-sudden death, acute
cor pulmonale/cardiovascular collapse
Over time,pulmonary hypertension with
chronic cor pulmonale & pulmonary vascular
sclerosis
15. Obstruction of medium sized arteries-
pulmonary haemorrhage
Obstruction of smaller vessels-infarction
16. Systemic
Thromboembolism-Causes
1)Causes in the heart (80%-mural
thrombus-LV infarcts, valvular disease,
vegetations, cardiomyopathy)
2)Causes in the arteries(atheroma,
aneurysm, fragmentation of valvular
vegetation)
3)Causes in the veins-lower legs,pelvic
veins,upper limb veins
28. Special stain for fat
demonstration
An oil red O stain for neutral fat (B) shows a globule of fat in a capillary. Several alveolar macrophages also stain, but the
stain is slightly browner and in small granules. This granular pigment corresponds to the lipochrome pigment just described,
which appears brown on H&E stain. Lipochrome pigment must be distinguished from the homogeneous red of fat embolism,
as seen in the capillary wall.
30. Air Embolism
Gas bubbles in circulation-vascular
obstruction-distal ischaemia
Causes
obstetric procedures
head and neck surgeries
chest wall injury
Maybe arterial or venous
>100 ccs for clinical symptoms
31. Air Embolism
Decompression sickness-scuba & deep sea
divers
Bends-painful gas bubbles in muscles & joints
Chokes-Lungs
Clinical significance- Focal ischaemia in brain
and heart
Ischaemic necrosis in heads of femurs, tibia
humeri (Caisson’s disease)
32. Amniotic Fluid Embolism
Complication of labor & immediate
postpartum period-80% mortality rate
Symptoms
Sudden dyspnea
Cyanosis
hypotensive shock
Pulmonary edema
DIC
Causes
Infusion of amniotic fluid or fetal tissue into
maternal circulation-tear in placental membranes
or rupture of uterine veins
33. Amniotic Fluid Embolism
Microscopy
Pulmonary microcirculation shows epithelial
squamous cells shed from fetal skin,lanugo
hair,fat from vernix caseosa,mucin from
fetal respiratory cells/GIT
Marked pulmonary edema
DAD
Fibrin thrombi
38. entrapment in a hernia sac
traumatic rupture of the blood supply
twisting of the vessels eg testicular
torsion or bowel volvulus
compression of the blood vessel by
oedema
45. RED INFARCTS
• venous obstruction-ovarian tumour
• loose tissues –lung
• in tissues with dual supply –lung and
small intestine
• in tissues that were previously
congested because of sluggish venous
outflow
• reperfusion
46. WHITE OR ANEMIC INFARCT
arterial occlusion in the solid organ with
end arterial circulation –heart, spleen
,kidney
solidity of the tissue
64. kidney
Image Description: The infarct is characterized by shadowy outlines
of necrotic renal parenchyma surrounded by a zone of leukocytic
infiltration and hemorrhage, appearing as a darker pink-to-orange ring
around the pale necrotic area. The infarct is wedge-shaped, with the
base at the capsular surface (mid upper field).
68. Hemosiderin pigment (brown) in cells of some of the alveolar
spaces, often in macrophages - signals breakdown of
erythrocytes. Note absence of nuclei in cells of alveolar septa -
they're dead
69. CLINICAL CORRELATIONS
• factors that effect/ influence
development of an infarct
• 1.nature of vascular supply
• 2.rate of development of occlusion
• 3.vulnerability of a given tissue to
hypoxia
• 4. blood oxygen content
