The document discusses different types of embolism. An embolism is a blockage of a blood vessel by an object that travels through the bloodstream. There are several types defined by the material causing the blockage (e.g. fat, air), origin (e.g. cardiac, arterial), and location (e.g. venous, pulmonary). Pulmonary embolism is a common and potentially fatal type where an embolism occurs in the pulmonary arteries. Risk factors, signs and symptoms, diagnostic tests, and treatment methods are described for pulmonary embolism specifically.

1. EMBOLISM
Dr. Shailaja Kupati
19th August 2014

2. CONTENTS
• Definition Of Embolism
• History
• Pathophysiology
• Types Of Embolism
• Venous Embolism
• Arterial Embolism
• Therapeutic embolisation
• Summary
• REFERENCES

3. Definition Of Embolism
• Almost all emboli represent some part of
dislodged thrombus – thromboembolism
• Emboli can lodge anywhere in vascular tree and
cause partial or complete vascular occlusion and
lead to ischemic necrosis
“An Embolism is sudden blockage of
venous or arterial circulation by any
material that can lodge in blood vessel
and obstruct its lumen”

4. History
• In 1948, the term Embolus coined by
Rudolf Virchow.
• He described the objects lodge in blood
vessels.
• The phenomenon of embolisation of
cholesterol was first recognized by the
Danish pathologist Dr. Peter Ludvig
Panum and published in 1862.
• American pathologist Dr. Curtis M.
Flory,in 1945 described eroded
atheroma is the source of emboli.
• The word Embolism comes from Greek,
meaning “Interposition.”

5. Depending upon the matter in the emboli
Types Of Embolism
• Detached thrombi
• Athromatous material
• Tumor cell clumps
• Tissue fragments
• Parasites
• Bacterial clumps
• Foreign bodies
• Fat globules
• Amniotic fluid
• Bone marrow
Solid Liquid
• Air and nitrogen
bubbles
Gases

6. Depending upon the matter in the emboli infected
Or not infected
Types Of Embolism ….
• When sterile • When infected
Bland Septic

7. Depending upon the source of emboli
Types Of Embolism ….
• Emboli originating
from left atrium and
atrial appendages
• Vegetations of
endocarditis
• In the systemic
arteries
Cardiac Emboli Arterial Emboli
• In pulmonary
arteries
Venous Emboli
Lymphatic Emboli

8. Depending upon the flow of the blood
Types Of Embolism ….
• An embolus which is
carried from the
venous side of
circulation to arterial
side or vice versa
• An embolus which
travels against the
flow of blood like
metastatic deposit
in spine from ca.
prostate
Paradoxical Retrograde

9. Effect Of Embolism
• The effects depends on
• Nature of embolus-Septic emboli cause septic
infarct or mycotic aneurysm, If the embolus
contains tumor cells – metastasis will be
produced
• Size of vessel that is blocked-Obstruction of the
large sized artery may cause sudden death

10. Effect Of Embolism ….
• Nature of organ whose blood supply has been
blocked-eg : microscopic emboli in the brain
can cause transient ischemic attacks
• Amount of collateral circulation available
• The bland emboli cause mechanical obstruction
of blood supply

11. Venous Embolism
• Source of venous embolism, most of the times
– DVT
– Cavernous Veins
– Pelvic Veins
– Pulmonary Artery

12. Pulmonary Embolism
• Incidence
– 2 to 4/1000 Hospitalized patients in US.
• Risk factors
– Venous stasis
– Age
– OCP’s
– Surgery
– Pregnancy
– Malignancy
– Immobilization(ICU patients)
• 95% originate from DVT

13. • Depending on size of embolus may occlude
– Main Pulmonary artery, straddle the pulmonary
bifurcation called as saddle embolus
– An embolus can pass inter atrial or ventricular
defect,gain access to systemic circulation this is
called as Paradoxical embolus.
• Not only mechanical obstruction by emboli but also
local release of 5-hydroxytryptamine cause collapse,
produces bronchospasm.
• Heparin reduces bronchospasm & further platelet depositio

15. Clinical Feature
• Most are clinically silent
• Dyspnoea
• Chest pain
• Syncope
• Tachycardia
• Respiratory crackles
• Right heart failure, sudden death
• Compromised bronchial artery flow result in infarction
• Multiple emboli over time may cause pulmonary HTN
and RVF

16. Clinically pulmonary embolism can be classified as –
• Massive pulmonary embolism resulting in sudden
death or severe strain on right ventricle
• Medium sized embolism giving rise to pulmonary
infarction
• Silent embolism with little or no clinical effects
• Recurrent embolism leading to chronic rise in
pulmonary artery pressure and lead to congestive
cardiac failure (cor pulmonale)

17. Fate of emboli
• After 12 hrs a layer of fibrin is seen covering the embolus
• Within 24 hrs edema of media and neutrophilic infiltration of the
vessel is seen
• Experimental studies have shown that
– The emboli retract during first few hours which allow blood flow
around the embolus
– Which may wash loose embolic material that become impacted
farther down the arterial tree
• At 24 hrs.
– Embolus is covered with endothelial like cells
• After a week
– Clefts lined by endothelium appear in large embolus and fibrous tissue
invade the thrombus first at its point of attachment
• By two or three weeks
– The thrombus is finely adherent to the arterial wall and undergone
recanalization with fibrous tissue surrounding new vascular channels

18. • In pulmonary infarction – lower lobes
are more often affected
• The infarcted portion is solid, dull red,
raised and sharply demarcated
• A fibrinous pleurisy is present and
small pleural effusion is seen
• Histologically there may be true
necrosis or the alveolar walls appear
viable but the air spaces are filled with
blood

19. Diagnosis of PE
• Wells score for prediction of PE.
• A total score
>6 : Indicates a high probability of a PE
2−6 : Moderate probability
<2 : Low probability.
Parameter Score
Clinically suspected DVT 3
Alternative diagnosis less likely than PE 3
Rapid heart rate 1.5
Immobilization within past 4 weeks 1.5
History of DVT 1.5
Haemoptysis 1
Malignancy 1
DVT, deep vein thrombosis; PE, pulmonary embolism.

20. • Leukocytosis
• Plasma D dimer assay is plasmin mediated fibrin
degradation product, elevated levels imply that fibrin
has formed and undergone proteiolysis.
Normal value-Less than 500ng/ml. It is also increased
in MI,pneumonia,sepsis,cancer and 2 nd 3rd trimister
of pregnancy.
• ABG analysis hypoxemia,hypocapnia
• Biomarkers- Troponine ,brain natriuretic peptide
Investigations

21. • Imaging:
• chest x ray-pulmonary
infarction may show
Hampton’s hump,
• ventilation perfusion
scan.
• Pulmonary angiography is the gold standard
investigation

22. Management algorithm for PE

24. Treatment of pulmonary embolism
• Anticoagulation-(parenteral )unfractionated
heparin,LMWH, fundofarinux
after 4 to 5 days oral anticoagulants like warfarin.
• Complications of anticoagulants- life threatening
intra cranial hemorrhage.
• HIT can be treated by direct thrombin inhibitors.
• Duration of anticoagulation-PE with major surgeries-
3 to 6 m of anticoagulation.

25. Treatment…..
• Maintain adequate hydration
• Fibrinolysis
• IVC filters-Inserted via the blood
vessels femoral vein,internal jugular vein.
• the American College of
Chest Physicians
recommended IVC filters
for those with
contraindications to
anticoagulation.

26. • Pulmonary embolectomy: Emboli can be
removed by using Fogarty catheter.
• Surgically the surgeon will make a cut in the
affected artery and the foreign body
causing the blockage will be sucked out in a
process known as aspiration

27. Prevention
• Early immobilisation in post operative patients.
• Avoid travelling for 3 to 4 wks after surgery.
• Daily use of below knee 30-40 mmHg vascular
stockings.
• Compression devices are inflatable and work in
similar way, expanding at regular intervals to
squeeze legs and encourage the flow of blood.
• Life style modifications-regular exercise, low fat diet
quit smoking.
• Pharmacological prophylaxis.

29. Pulmonary infarction
• Embolic obstruction of medium sized arteries can
result in hemorrhage but not infarction its due to
lungs has got dual blood supply,intact bronchial
circulation continues to perfuse affected area.
• However similar setting in LHF,compromised
bronchial artery flow result in infarction.
• Pulmonary infarction is more frequent in those
with additional cardiac or pulmonary disease
• The infarcts are generally pyramidal, with
the base of the pyramid on the pleural
surface

30. The pulmonary infarct is
classically hemorrhagic and
appears as a raised, red-blue
area in the early stages . Often,
the apposed pleural surface is
covered by a fibrinous exudate.
The red cells begin to lyse
within 48 hours, and the infarct
becomes paler and eventually
red-brown as hemosiderin is
produced. With the passage of
time, fibrous replacement
begins at the margins as a gray-
white peripheral zone and
eventually converts the infarct
into a contracted scar

31. Pulmonary embolus can be distinguished from a post-
mortem clot by the presence of the lines of Zahn in the
thrombus.
They have visible and microscopic alternating layers
(laminations) of platelets mixed with fibrin, which appear
lighter, and darker layers of red blood cells.
Their presence implies thrombosis at a site of rapid blood
flow that happened before death.

32. Difference between post mortem
clot and thromboembolus
• Post mortem clot – it is moist, shiny and gelatinous
• Loosely inserted in pulmonary trunks
• Shape confirms to that of situation where it is found
• On withdrawal a cast of pulmonary tree is
obtained
Massive thromboembolus –
• Dry, friable and granular
• Ripples of platelet may be visible on its
surface
• The shape of embolus does not confirm to that of surrounding
• Very tightly inserted in pulmonary tree so removal is difficult

33. Arterial Thromboembolism
• Most of them arise from intracardiac mural thrombi.
• 2/3rd associated with left ventricular wall infarcts
• 1/3rd are associated with left atrial dilatation and
fibrillation.
• Other originate from aortic aneurysm, fragmentation of
valvular vegetation.

34. Major sites for arterial embolism
SOURCES

35. Pathogenesis of arterial
thrombus
An arterial thrombus attached to a vessel wall is
initially soft, friable, and dark red, with fine alternating
bands of yellowish platelets and fibrin, the lines of
Zahn .
• Lysis- owing to the potent thrombolytic activity of
the blood.
• Propagation - because a thrombus serves as a focus
for further thrombosis.

36. • Organization-the eventual invasion of connective
tissue elements involved in repair , which causes
a thrombus to become firm and grayish white.
• Canalization-by which new lumina lined by
endothelial cells form in an organized thrombus.
• Embolization-when part or all of the thrombus
becomes dislodged, travels through the
circulation, and lodges in a blood vessel some
distance from the site of thrombus formation.

37. Arterial Air Embolism
• Gas bubbles within circulation can coalesce to form frothy masses
that obstruct Vascular flow.
• This can occur during coronary bypass surgery,angiography,in
cerebral circulation in neurosurgery,otolaryngeal surgery in sitting
position,dialysis,during MTP,while creating pneumoperitonium(lap
Surgeries)
• More then 100cc of air is required to have clinical effect.

38. Effects of venous air embolism depends on –
• Amount of air introduced into circulation
• Rapidity of entry of air
• Position of patient
• General condition of patient
If the death from pulmonary air embolism is
suspected, the heart and pulmonary artery
should be opened under water

39. Decompression Sickness
• Occurs when individual experience sudden decrease in
atmospheric pressure
• Also known as divers disease or caisson’s disease
• Seen in- Scuba and deep sea divers, under water
construction workers
• Persons exposed to increase atm pressure ,during
descent large amount of inert Gas(nitrogen or helium)
are dissolved in bodily fluids, when diver ascends gas
released from solution.

40. Decompression Sickness …
• 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
• 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
• In chronic form the foci of ischemic necrosis is seen
throughout the body

41. The effects of decompression sickness
depend on –
• Depth or altitude reached
• Duration of exposure to altered
pressure
• Rate of ascent or descent
• General condition of the individual

42. Decompression Sickness …
• In chronic form ischemic necrosis is seen throughout
the body,
The features include
• Avascular necrosis of bone
• Neurological symptoms : Paraesthesia, Paraplegia
• Lung involvement : Dyspnea, Non productive cough
and chest pain
• Skin manifestation : Itching, Patchy erythema,
Cyanosis
• Lipid vacuoles in liver and pancreas

43. Treatment
• All cases of decompression sickness is
treated by 100% OXYGEN, untill
hyperbaric oxygen therapy provided.
• This will force the gas bubbles back
into circulation, this will lead to
gradual resorption and exhalation of
dissolved gases so that obstructive
bubbles donot reform.

44. Fat Embolism
• Impaction of microscopic fat globules with or
without marrow elements in pulmonary vasculature
• Etiology-
• Traumatic causes
– Trauma to bones
– Trauma to soft tissue
• Non traumatic causes
Extensive burns, DM, fatty liver, pancreatitis, sickle
cell anaemia, decompression sickness, extrinsic fat or
oil introduced in circulation

45. Fat Embolism Syndrome
• Characterized by
• Pulmonary insufficiency
• Neurological symptoms
• Anemia(Hemolysis)
• Thrombocytopenia(due to adhesion of platelets to
fat globules)
• In severe cases
• Patient become comatose within few hrs.
• Dies within 1-2 days

46. Pathology
• Pathology is not only mechanical obstruction
but also release of free fatty acids from fat
globules exacerbate local toxic injury to
endothelium.
• Fat microemboli and associated red
cells,platelet aggregate can occlude pulm and
cerebral microvasculature.
• Release of free radicle,protease and eicosanoid
release complete vascular aasault.

47. Pathogenesis
• The following mechanisms are proposed to explain the
pathogenesis
• Mechanical theory
– Mobilization of fluid fat may occur following trauma to long bones
• Emulsion instability theory
– Fat emboli are formed by aggregation of plasma lipids due to
disturbance in natural emulsification of fat
• Intravascular coagulation theory
– In stress, release of some factors activate DIC and aggregation of fat
emboli

49. Systemic fat embolism
• When the fat globules pass from pulmonary circulation and
enter into systemic circulation and then lodged in the capillaries
of the organs like brain, kidney, skin etc.
• Brain
• Petechial hemorrhage is seen on laptomeninges
• Petechial hemorrhage is also seen in white matter
• Microscopically – microinfarct of brain, edema and
hemorrhage are seen
• Kidney
• Fat emboli are seen in glomerular capillaries.
• Skin, conjunctiva, retina and serosal surfaces are also
affected

50. Systemic fat embolism …
• On investigations
• Platelet count is low
• Serum calcium is low
• Urine shows presence of fat
• Bone marrow embolism
Seen after vigorous cardiac resuscitation,
when there is fracture of the ribs, and sternum

51. Amniotic Fluid Embolism
• It refers to entry of amniotic fluid into maternal
circulation through open uterine and cervical
veins
• It is an ominous complication of labour and
immediate post partum period
• Underlying cause is infusion of amniotic fluid or
fetal tissue into maternal circulation via a tear in
the placental membrane or ruptured uterine
veins
• Seen 1 in 40,000 deliveries and mortality rate is
up to 80%

53. Amniotic Fluid Embolism …
• Classical findings include
• Presence of squamous cells
• Lunigo hairs
• Fat from vernix caseosa
• Mucin in the maternal pulmonary
vasculature
• Other findings are
• Marked pulmonary edema
• Diffuse alveolar damage
• Presence of fibrin thrombi in vascular beds

54. Amniotic Fluid Embolism …
Complications of amnitic fluid
embolism after survival from
acute episode

55. Tumor Embolism
• Malignant tumor cells invade the local blood vessels and may
form tumor emboli
• It is transported elsewhere and produce metastatic tumor
deposits
• It may be carried by lymphatics also
• The majority of these emboli are destroyed and only a small
percentage develop in metastatic deposits
• Multiple small tumor emboli initiate consumption coagulopathy
• Seen in clear cell carcinoma of kidney, carcinoma of lung and in
malignant melanoma

57. Cholesterol embolism
In people who have extensive
atherosclerosis (narrowed
arteries due to a build-up of
cholesterol), small pieces of
cholesterol can sometimes
break away from the side of a
blood vessel, resulting in an
embolism. Also called as
Atheroembolism.

58. It consist of cholesterol crystals, hyaline debris,
and calcified material ,
Produce foreign body reaction at the site of
lodgment
Effects of atheroembolism
Ischemia, atrophy and necrosis of tissue
Infarcts in the organs affected,Gangrene in
lower limbs,hypertension

59. Clinical features
• Fever, muscle pain, loss of appetite.
severe pain.
• Embolism to the legs causes
mottled appearance and purple
discoloration of the toes
• If kidney is involved then
hypertension,electrolyte disturbance
• CNS-headache, stroke
• Spinal chord-paraparesis,cauda equina
syndrome, loss of control over bladder
etc.

60. Cholesterol Embolism …
• When the kidneys are involved, the disease is
referred to as atheroembolic renal disease
(AERD)
Diagnosis
• Eosinophil count is increased
• CRP and ESR will be elevated
• Abnormal liver enzymes
• If kidneys involved then urea creatinine will be
elevated,casts may be seen
• Complement level estimation –decreased in
cholesterol embolism, where as increased in
vasculitis.

61. • cholesterol embolus
showing characteristic
cholesterol clefts
(biconvex white
spaces) and a giant
cell reaction.
• Generally symptomatic, i.e. it deals with the
symptoms and complications but cannot reverse the
phenomenon itself.
• In kidney failure resulting from cholesterol crystal
emboli, statins have been shown to halve the risk of
requiring hemodialysis
Treatment
Histopathology

62. C Cholesterol emboli
• Usually occurs intact vessel wall-
from atheromatous plaque
• Cholesterol clefts seen
• Filipin is fluorescent stain highly
Specific for cholesterol
Fat emboli
• Occurs after trauma such as
long bone fractures
• Vacualated spaces seen

63. Miscellaneous emboli
Fo Foreign body embolism:
• Result from many materials introduced into
body that can embolise to the lung.iv drug
abusers inject themselves with impure
preparations of narcotics “Fillers’’. usually corn
starch and talc used as fillers..
• Polythene tubing may embolise during cardiac
catheterization
• Fragments of broken valve prosthesis can also
embolise

64. • The insoluble additives lodge in arterioles
and small muscular arteries where they
cause thrombosis and proliferation of intimal
cells,they often migrate into perivascular
space and elicit foreign body reaction.
• Cotton and cellulose fibers are reported
in autopsy findings in patients died after
cardiac operations.

65. Red cell aggregate
• Blockage of small vessels by aggregates of red
cells is commonly seen in infection and trauma.
• This condition is also called sludging.
• Red cell aggregation also occur in the exposed
limbs when cold autohaemagglutinins are
present. This is the cause of Raynaud’s
phenomenon seen in patients with acquired
hemolytic anaemia of cold antibody type .

66. • Micro emboli
• Are sometimes seen in retinal vessels and by
plugging them produce microinfarcts
• Some of these bodies are made of athromatous
material and others are platelet aggregate or
fibrin derived.
• During open heart surgery emboli is made of
calcium, silicon or fat

67. In the eye they are blamed for
transient attack of unilateral
blindness (Amaurosis fugax)

68. Parasites
• Various parasites and their ova are
carried by blood stream.
• Schistosomes and their ova may lodge in
the branches of portal veins in liver and
induce pipe stem type fibrosis
E embolism
• This is seen in individuals who sits for long
time in front of computers.

69. Therapeutic embolisation
• Introduction of emboli into vessels supplying
tumors,vascular abnormalities and sites of bleeding.
• Emboli used Gelfoam,muscle,silastic balls,silicon
balloons,steel coils and Cyanocrylalate glue.
• Kidney, liver, G I tract are common sites where
therapeutic embolisation is used.

70. Summary
• Venous emboli are most common form of emboli.
• Almost all venous emboli are from thrombus
especially from DVT.
• Pulmonary embolism is most common cause of death
after major orthopedic surgery,and it is most common
non obstetric cause of post partum death.
• Arterial emboli especially large emboli leads to
infarction of vital organs and cause
permanent disability.

71. References
• Robins and cotran pathalogical basis of diseases,8th
edition
• Anderson’s pathology, Ivan Damjanov. James Linder. 10th
edition.
• Muir’s Textbook of pathology, David A levison, Robin
Reid.14th edition.
• Rubin’s pathology, Emanuel Rubin, Howard M reisner,5th
edition
• Walter and Israel general pathology ,7th edition
• Harrison’s principles of internal medicine, 18th edition
• Internet sources.