Thrombosis & embolism

Basic Science for Optometrists

2. Thrombosis Embolism
►1. Robbins pathologic Basis of Diseases – 1. Robbins pathologic Basis of Diseases –
20002000
►Pathology of Eye – GOH NaumannPathology of Eye – GOH Naumann
►Ocular Pathology – 5Ocular Pathology – 5
thth
Edition Edition
►Muir’s Textbook of PathologyMuir’s Textbook of Pathology
►InternetInternet

3. Thrombosis Embolism
►Hemostasis – Basic conceptsHemostasis – Basic concepts
►Thrombosis Thrombosis
Predisposing Factors Predisposing Factors
Basic terminologiesBasic terminologies
Morphology & Fate of ThrombiMorphology & Fate of Thrombi
►EmbolismEmbolism
Introduction ; Terms & TerminologiesIntroduction ; Terms & Terminologies
Major TypesMajor Types
►Clinical Correlation to EyeClinical Correlation to Eye
Retinal Vein OcclusionRetinal Vein Occlusion
Types of EmbolizationTypes of Embolization

4. Thrombosis Embolism
HemostasisHemostasis
►Hemostasis is a balance of two opposing Hemostasis is a balance of two opposing
forces: clot formation and dissolutionforces: clot formation and dissolution
►Major factors involved in Hemostasis:Major factors involved in Hemostasis:
Platelets, Vascular endothelium, Coagulation Platelets, Vascular endothelium, Coagulation
Process – Deposition of FibrinProcess – Deposition of Fibrin
Plasmin / Fibrinolytic system – Digests FibrinPlasmin / Fibrinolytic system – Digests Fibrin

5. Thrombosis Embolism
The 3 categories are: The 3 categories are:
( to make( to make the study easy)the study easy)
PrimaryPrimary hemostasis hemostasis
Secondary hemostasisSecondary hemostasis
Tertiary HemostasisTertiary Hemostasis

6. Thrombosis Embolism
►PrimaryPrimary hemostasis hemostasis: This is defined as the : This is defined as the
formation of the platelet plug.formation of the platelet plug.
InhibitorsInhibitors
Natural Natural prostacyclinprostacyclin and and nitric oxidenitric oxide, which are , which are
released by endothelial cells, and bradykinin. released by endothelial cells, and bradykinin.
Acquired: AspirinAcquired: Aspirin
►SecondarySecondary hemostasis hemostasis: formation of fibrin : formation of fibrin
through the coagulation cascade.through the coagulation cascade.
Inhibitors: Inhibitors: Natural : Antithrombin III Natural : Antithrombin III
AT binding to thrombin – enhanced by heparin AT binding to thrombin – enhanced by heparin
(Used to prevent thrombosis)(Used to prevent thrombosis)

7. Thrombosis Embolism
►TertiaryTertiary hemostasis: This is defined as the hemostasis: This is defined as the
formation of plasmin for breakdown of the formation of plasmin for breakdown of the
clot. clot.
Drugs that inhibit fibrinolysis include Drugs that inhibit fibrinolysis include
epsilonaminocaproic acid and tranexamic acidepsilonaminocaproic acid and tranexamic acid

8. Thrombosis Embolism
Series of overlapping processes after Series of overlapping processes after
the damage of a blood vessel:the damage of a blood vessel:
►1. Vasoconstriction1. Vasoconstriction
Platelets adhere to the damaged wall.Platelets adhere to the damaged wall.
Release SerotoninRelease Serotonin
ThromboxanesThromboxanes
►2.Platelet plug formation 2.Platelet plug formation
Release of ADPRelease of ADP
Positive feedback mechanismPositive feedback mechanism
Temporary sealTemporary seal
►3.Coagulation3.Coagulation
Positive feedback mechanismPositive feedback mechanism
Mesh of fibrin – strongMesh of fibrin – strong
Formation of Prothrombin activator by extrinsic and intrinsic Formation of Prothrombin activator by extrinsic and intrinsic
pathwaypathway

9. Thrombosis Embolism
Blood clotting factors:Blood clotting factors:
I I Fibrinogen Fibrinogen
IIII Prothrombin Prothrombin
III Tissue factorIII Tissue factor
( Thromboplastin)( Thromboplastin)
IV Calcium (CaIV Calcium (Ca
++++
))
V Labile FactorV Labile Factor
VII Stable factorVII Stable factor
VIII Antihaemophilic globulinVIII Antihaemophilic globulin
(A. H. factor A)(A. H. factor A)
IX Christmas factor IX Christmas factor
(A.H. factor B)(A.H. factor B)
X Stuart Power factorX Stuart Power factor
XI A.H. factor CXI A.H. factor C
XII Hageman factorXII Hageman factor
XIII Fibrin Stabilising FactorXIII Fibrin Stabilising Factor
►N.B.:N.B.:
There is no factor VIThere is no factor VI
Vit. K is essential for Vit. K is essential for
the synthesis of the synthesis of
factors : ii vii ix & xfactors : ii vii ix & x
Their no.s represent Their no.s represent
the order in which the order in which
they were they were
discovered.discovered.

10. Thrombosis Embolism
HemostasisHemostasis

11. Thrombosis Embolism
►4. Fibrinolysis4. Fibrinolysis
 Removing blood and healing damaged blood vesselsRemoving blood and healing damaged blood vessels
ActivatorsActivators
Plasminogen Plasminogen Plasmin Plasmin
Fibrin Fibrin Breakdown products Breakdown products

12. Thrombosis Embolism
Control Of Coagulation:Control Of Coagulation:
►1. Perfect smoothness of blood vessel lining1. Perfect smoothness of blood vessel lining
►2. Presence of natural anticoagulants like Heparin2. Presence of natural anticoagulants like Heparin
►3.Binding to Thrombin to a special thrombin 3.Binding to Thrombin to a special thrombin
receptor on the cells lining blood vessels.receptor on the cells lining blood vessels.

13. Thrombosis Embolism
ThrombosisThrombosis
►ThrombusThrombus: an aggregation of : an aggregation of
blood factors primarily blood factors primarily
platelets & fibrin with platelets & fibrin with
entrapment of cellular entrapment of cellular
elements, frequently causing elements, frequently causing
vascular obstruction at the vascular obstruction at the
point of its formationpoint of its formation
►ThrombosisThrombosis : Formation of a : Formation of a
solid or a semisolid mass from solid or a semisolid mass from
the constituents of the blood the constituents of the blood
within the vascular system within the vascular system
within life.within life.

14. Thrombosis Embolism
ThrombosisThrombosis
►PathogenesisPathogenesis
Primary influences Primary influences
predisposing to predisposing to
thrombosisthrombosis

15. Thrombosis Embolism
Endothelial InjuryEndothelial Injury
►Dominant influenceDominant influence
►Any perturbation in the Any perturbation in the
dynamic balance of the dynamic balance of the
pro and antithrombotic pro and antithrombotic
effects of the effects of the
endothelium can endothelium can
influence local clotting influence local clotting
effectseffects

16. Thrombosis Embolism
►Endothelial dysfunction d/t hemodynamic stresses Endothelial dysfunction d/t hemodynamic stresses
of hypertension, turbulent flow over scarred of hypertension, turbulent flow over scarred
valves, or bacterial endotoxinsvalves, or bacterial endotoxins
►Homocystinuria, Hypercholesterolemia, radiation Homocystinuria, Hypercholesterolemia, radiation
or products absorbed from cigarette smoke may or products absorbed from cigarette smoke may
initiate endothelial injury.initiate endothelial injury.
►Thrombosis in cardiac chambers, over ulcerated Thrombosis in cardiac chambers, over ulcerated
plaques in atherosclerotic arteries or at traumatic plaques in atherosclerotic arteries or at traumatic
or inflammatory vascular injury - largely d/t or inflammatory vascular injury - largely d/t
endothelial injury.endothelial injury.

17. Thrombosis Embolism
Endothelial EnjuryEndothelial Enjury
►Exposure of subendothelial proteinsExposure of subendothelial proteins
►Platelets adhesionPlatelets adhesion
►Prevention from blood lossPrevention from blood loss

18. Thrombosis Embolism
Excessive adhesion of platelets - BlockageExcessive adhesion of platelets - Blockage

19. Thrombosis Embolism
Alterations in Normal Blood FlowAlterations in Normal Blood Flow
( Turbulence & Stasis)( Turbulence & Stasis)
►TurbulenceTurbulence
Arterial & cardiac thrombosisArterial & cardiac thrombosis
- endothelial injury or dysfunction- endothelial injury or dysfunction
►Stasis and TurbulenceStasis and Turbulence
1.1.Disrupt laminar flow – Platelets into contact with the Disrupt laminar flow – Platelets into contact with the
endotheliumendothelium
2.2.Prevent the dilution of activated clotting factorsPrevent the dilution of activated clotting factors
3.3.Retard the inflow of clotting Factor inhibitorsRetard the inflow of clotting Factor inhibitors
4.4.Promote endothelial cell activationPromote endothelial cell activation

20. Thrombosis Embolism
Contribution of Turbulence & Stasis to Contribution of Turbulence & Stasis to
Thrombosis in Clinical Settings:Thrombosis in Clinical Settings:
►Ulcerated atherosclerotic plaques – sources of turbulenceUlcerated atherosclerotic plaques – sources of turbulence
►Abnormal aortic and arterial dilations (Aneurysms) – Abnormal aortic and arterial dilations (Aneurysms) –
Favored sites of ThrombosisFavored sites of Thrombosis
►Myocardial Infarction - regions of non-contractile Myocardial Infarction - regions of non-contractile
myocardium – stasismyocardium – stasis
: Mural Thrombi: Mural Thrombi
►Mitral valve stenosis – Left arterial dilationMitral valve stenosis – Left arterial dilation
►Hyper-viscosity syndromes cause small vessel stasis Hyper-viscosity syndromes cause small vessel stasis
and in sickle cell anemia deformed RBCs cause vascular and in sickle cell anemia deformed RBCs cause vascular
occlusionsocclusions

21. Thrombosis Embolism
HypercoagulabilityHypercoagulability
►Less contribution to thrombosisLess contribution to thrombosis
►Causes :Causes :
►
Primary (Genetic)Primary (Genetic)
►Secondary (Acquired)Secondary (Acquired)
►Inherited causes of HypercoagulabilityInherited causes of Hypercoagulability
Mutations in the factor v gene and ProthrombinMutations in the factor v gene and Prothrombin
Polymorphisms Polymorphisms
Inherited deficiency of anticoagulants such as Inherited deficiency of anticoagulants such as
Antithrombin III, Protein C or protein SAntithrombin III, Protein C or protein S

22. Thrombosis Embolism
Significances of inherited disorders:Significances of inherited disorders:
►Individually uncommonIndividually uncommon
►1. Mutations are usually co-inherited1. Mutations are usually co-inherited
►( a and b together ) > ( a + b)( a and b together ) > ( a + b)
►2.Higher risk of developing venous 2.Higher risk of developing venous
thrombosisthrombosis

23. Thrombosis Embolism
Acquired Thrombotic DiathesesAcquired Thrombotic Diatheses
►More complicated and multifactorialMore complicated and multifactorial
►Causes:Causes:
Stasis or venous injuryStasis or venous injury
Increased hepatic secretion of many coagulation Increased hepatic secretion of many coagulation
factors and reduced synthesis of antithrombin factors and reduced synthesis of antithrombin
III III
Release of procoagulant tumourRelease of procoagulant tumour

24. Thrombosis Embolism
Hypercoagulability seen with Hypercoagulability seen with
advancing age:advancing age:
►Due to Increased susceptibility to platelet Due to Increased susceptibility to platelet
aggregation aggregation
►Smoking and obesity promote Smoking and obesity promote
hypercoagulability by unknown mechanisms.hypercoagulability by unknown mechanisms.

25. Thrombosis Embolism
ThrombosisThrombosis
►Basic Terms and Terminologies:Basic Terms and Terminologies:
►Agonal Thrombus : Clot formed in the Heart during the Agonal Thrombus : Clot formed in the Heart during the
process of dyingprocess of dying
►Antemortem ThrombusAntemortem Thrombus
►Ball ThrombusBall Thrombus
►Milk ThrombusMilk Thrombus
►Parietal ThrombusParietal Thrombus
►Fibrin ThrombusFibrin Thrombus
►Hyaline ThrombusHyaline Thrombus
►Infective ThrombusInfective Thrombus
►Primary ThrombusPrimary Thrombus
►Stratified ThrombusStratified Thrombus
►Traumatic ThrombusTraumatic Thrombus

26. Thrombosis Embolism
Retinal branched vein ThrombosisRetinal branched vein Thrombosis

27. Thrombosis Embolism
►Laminated Thrombus/ Laminated Thrombus/
mixed Thrombusmixed Thrombus
►Mural ThrombusMural Thrombus
Coral ThrombusCoral Thrombus
Organized ThrombusOrganized Thrombus

28. Thrombosis Embolism
►Annular ThrombusAnnular Thrombus
►Calcified Thrombus/ Calcified Thrombus/
PhlebolithPhlebolith
►White ThrombusWhite Thrombus
►Blood plate / Platelet Blood plate / Platelet
ThrombusThrombus

29. Thrombosis Embolism
Deep Vein ThrombosisDeep Vein Thrombosis
►formation of a blood formation of a blood
clot in a deep vein. clot in a deep vein.
►It commonly affects It commonly affects
the leg veins, such as the leg veins, such as
the femoral vein or the the femoral vein or the
popliteal vein or the popliteal vein or the
deep veins of the deep veins of the
pelvis.pelvis.

30. Thrombosis Embolism
Deep Vein ThrombosisDeep Vein Thrombosis
►SIGNS AND SYMPTOMSSIGNS AND SYMPTOMS
pain, pain,
swelling swelling
redness of the leg and redness of the leg and
dilatation of the surface dilatation of the surface
veinsveins
►THERAPYTHERAPY
Anticoagulation is the usual Anticoagulation is the usual
treatmenttreatment

31. Thrombosis Embolism
PORTAL VEIN THROMBOSISPORTAL VEIN THROMBOSIS
►a form of a form of
venous venous
thrombosis thrombosis
affecting the affecting the
portal vein, portal vein,
which can lead which can lead
to portal to portal
hypertension hypertension
and reduction in and reduction in
the blood supply the blood supply
to the liver.to the liver.

32. Thrombosis Embolism
►Causes Causes
pancreatitis, cirrhosis, pancreatitis, cirrhosis,
►Treatments Treatments
anticoagulants, shunts, bypass surgery, and anticoagulants, shunts, bypass surgery, and
transplants.transplants.

33. Thrombosis Embolism
HEPATIC VEIN THROMBOSISHEPATIC VEIN THROMBOSIS
-Occlusion of hepatic vein-Occlusion of hepatic vein

34. Thrombosis Embolism
►Symptoms:Symptoms:
progressive abdominal painprogressive abdominal pain
hepatomegaly , and later the symptoms of hepatomegaly , and later the symptoms of
hepatic dysfunctionhepatic dysfunction
►Therapy:Therapy:
anticoagulant medicationanticoagulant medication

35. Thrombosis Embolism
RENAL VEIN THROMBOSISRENAL VEIN THROMBOSIS
►formation of a clot or formation of a clot or
thrombus obstructing thrombus obstructing
the renal vein, leading the renal vein, leading
to a reduction in to a reduction in
drainage of the kidney.drainage of the kidney.
►can lead to imbalances can lead to imbalances
in blood clotting factorin blood clotting factor
►SymptomsSymptoms
blood in urine blood in urine

36. Thrombosis Embolism
General Morphology / Characteristics of Arterial & General Morphology / Characteristics of Arterial &
venous Thrombivenous Thrombi
CharacteristicsCharacteristicsArterial/ CardiacArterial/ Cardiac
ThrombusThrombus
Venous/Red/Stasis/Venous/Red/Stasis/
Phlebo-thrombusPhlebo-thrombus
LocationLocation At the site of At the site of
endothelial injury or endothelial injury or
turbulenceturbulence
At the sites of At the sites of
StasisStasis
Direction Direction Retrograde dir. From Retrograde dir. From
pt. of attchmentpt. of attchment
In a directon of In a directon of
blood flowblood flow
NatureNature Usually Occlusive Usually Occlusive Almost invariably Almost invariably
occlusiveocclusive
Gray – white,Firmly Gray – white,Firmly
adhered to arterial walladhered to arterial wall
Red/stasis Red/stasis
thrombusthrombus

37. Thrombosis Embolism
Composed Composed
of:of:
Tangled mesh of Tangled mesh of
platelets, fibrin, platelets, fibrin,
erythrocytes & erythrocytes &
degenerating degenerating
leucocytesleucocytes
More enmeshed More enmeshed
erythrocyteserythrocytes
CommonCommon
sitessites
(In descending (In descending
order)order)
Coronory ArteriesCoronory Arteries
Cerebral arteriesCerebral arteries
Femoral arteriesFemoral arteries
Veins ofVeins of
Lower extremitiesLower extremities
upper extremitiesupper extremities
Less commonLess common: :
Periprostatic plexusPeriprostatic plexus
Ovarian and Peri uterine Ovarian and Peri uterine
veinsveins

38. Thrombosis Embolism
At Autopsy, post mortem clots may be At Autopsy, post mortem clots may be
confused for venous thrombi:confused for venous thrombi:
Post Mortem ClotsPost Mortem ClotsRed ThrombiRed Thrombi
Gelatinous; red cells Gelatinous; red cells
settled by gravitysettled by gravity
More enmeshed More enmeshed
erythrocytes, under erythrocytes, under
transection reveal vague transection reveal vague
strands of pale gray fibrinstrands of pale gray fibrin
Not attached to the Not attached to the
underlying wallunderlying wall
Firmer, almost always Firmer, almost always
have a point of have a point of
attachmentattachment

39. Thrombosis Embolism
Fate of Thrombus :Fate of Thrombus :
►1.1. Propagation Propagation
– – Accumulation of more platelets and fibrin; Accumulation of more platelets and fibrin;
vessel obstruction vessel obstruction
►2. 2. EmbolizationEmbolization
– – Dislodge and travel to other sitesDislodge and travel to other sites
►3.3. Dissolution Dissolution – Removed by fibrinolytic activity – Removed by fibrinolytic activity
►4. 4. Organization and recanalizationOrganization and recanalization
- May induce inflammation and fibrosis- May induce inflammation and fibrosis
- Re-establish vascular flow- Re-establish vascular flow

40. Thrombosis Embolism
Lab Tests to measure Coagulation and Lab Tests to measure Coagulation and
ThrombolysisThrombolysis
►Platelet countPlatelet count
►Bleeding timeBleeding time
►APTT (Activated Partial Thromboplastin Time)APTT (Activated Partial Thromboplastin Time)
Measure of intrinsic pathwayMeasure of intrinsic pathway
Used to monitor Heparin TherapyUsed to monitor Heparin Therapy
►Prothrombin Time – Used to measure Prothrombin Time – Used to measure
effectiveness of oral anticoagulants like warfarineffectiveness of oral anticoagulants like warfarin
►Thrombin TimeThrombin Time
►Fibrin Clot StabilityFibrin Clot Stability
►Measurement of Fibrin degradation ProductsMeasurement of Fibrin degradation Products

41. Thrombosis Embolism
EmbolismEmbolism
►Embolus:Embolus:
detached intravascular detached intravascular
solid liquid or gaseous solid liquid or gaseous
mass that is carried by the mass that is carried by the
blood to a site distant blood to a site distant
from its point of originfrom its point of origin
►Unless otherwise Unless otherwise
considered – thrombotic considered – thrombotic
in originin origin
►Results in partial or Results in partial or
complete vascular complete vascular
occlusionocclusion
►Potential consequence - Potential consequence -
InfarctionInfarction

42. Thrombosis Embolism

43. Thrombosis Embolism
Terms and TerminologiesTerms and Terminologies
►ThromboembolismThromboembolism
►Pulmonary embolismPulmonary embolism
►Air embolism – after trauma or surgical proceduresAir embolism – after trauma or surgical procedures
►Amniotic Fluid EmbolismAmniotic Fluid Embolism
►Fat / Oil embolismFat / Oil embolism
►Coronary embolism – of coronary arteriesCoronary embolism – of coronary arteries
►Crossed / Paradoxical EmbolismCrossed / Paradoxical Embolism
►Direct embolism – in the direction of the blood flowDirect embolism – in the direction of the blood flow
►Bland embolism – when thrombotic plug is composed of Bland embolism – when thrombotic plug is composed of
non-septic materialnon-septic material
►Bacillary embolism – By aggregation of bacilli.Bacillary embolism – By aggregation of bacilli.
►Bone marrow embolism : By material from a fractured Bone marrow embolism : By material from a fractured
bonebone
►Capillary Embolism – Blockage of capillaries with bacteriaCapillary Embolism – Blockage of capillaries with bacteria

44. Thrombosis Embolism
►Pulmonary embolismPulmonary embolism►Retinal Embolism – Retinal Embolism –
Central artery of the Central artery of the
retinaretina

45. Thrombosis Embolism
Cerebral embolism- Of a cerebral arteryCerebral embolism- Of a cerebral artery

46. Thrombosis Embolism
ThromboembolismThromboembolism
►A)A) Pulmonary thromboembolismPulmonary thromboembolism
Incidence : 20 – 25 / 100,000 Incidence : 20 – 25 / 100,000
hospitalized patientshospitalized patients
►In 95 % instances, - venous In 95 % instances, - venous
emboliemboli
Multiple Emboli : Pts. Who had Multiple Emboli : Pts. Who had
once – high risk of having once – high risk of having
more.more.
60 to 80 % pulmonary emboli 60 to 80 % pulmonary emboli
are silent – smallare silent – small
When > 60 % pulmonary When > 60 % pulmonary
circulation is obstructed with circulation is obstructed with
emboli, - Right Heart Failureemboli, - Right Heart Failure

47. Thrombosis Embolism
# # Effects:Effects:
Depends upon sizeDepends upon size
May occlude main pulmonary May occlude main pulmonary
artery, impact across the artery, impact across the
bifurcation (Saddle bifurcation (Saddle
embolus ) or pass out into embolus ) or pass out into
smaller branching arteriolessmaller branching arterioles
Embolic Obstruction of :Embolic Obstruction of :
►Medium sized arteryMedium sized artery::
Pulmonary haemorrhagePulmonary haemorrhage
►Small End-arteriolar pulmonary Small End-arteriolar pulmonary
branches:branches:
InfarctionInfarction
►Multiple EmboliMultiple Emboli : :
 Pulmonary hypertension Pulmonary hypertension
with right heart failurewith right heart failure

48. Thrombosis Embolism
Systemic ThromboembolismSystemic Thromboembolism
= = within the arterial circulation within the arterial circulation
►80% arise from intracardiac mural 80% arise from intracardiac mural
ThrombiThrombi
►Major sites :Major sites :
Lower extremities (75%)Lower extremities (75%)
Brain (10%)Brain (10%)
►Consequences:Consequences:
Depends upon:Depends upon:
►Extent of collatoral vascular Extent of collatoral vascular
supply in the affected tissue.supply in the affected tissue.
►Tissue’s vulnerability to ischemiaTissue’s vulnerability to ischemia
►Caliber of the vessel occluded.Caliber of the vessel occluded.
►In GeneralIn General
►Infarction to tissues downstream Infarction to tissues downstream
of the obstructed vesselof the obstructed vessel

49. Thrombosis Embolism
Fat EmbolismFat Embolism
►Fat released by marrow or Fat released by marrow or
adipose tissue injuryadipose tissue injury
►90% with severe skeletal 90% with severe skeletal
injuriesinjuries
►Fat Embiolism Syndrome:Fat Embiolism Syndrome:
Pulmonary insufficiency, Pulmonary insufficiency,
neurologic symptoms, anemia neurologic symptoms, anemia
and thrombocytopeniaand thrombocytopenia
Symptoms:Symptoms:
►Tachycardia Dyspnea Tachycardia Dyspnea
►Neurological Symptoms:Neurological Symptoms:
Irritaqbility & restlessnessIrritaqbility & restlessness
Delirium to comaDelirium to coma
►PathogenesisPathogenesis
Mechanical obstruction and Mechanical obstruction and
biochemical injurybiochemical injury

50. Thrombosis Embolism
Air EmbolismAir Embolism
►Can obstruct vascular flow Can obstruct vascular flow
– Distal ischemic Injury– Distal ischemic Injury
►EntranceEntrance
During Obstetric procedures During Obstetric procedures
As a consequence of chest As a consequence of chest
wall injury ( Usu. In excess of wall injury ( Usu. In excess of
100 cc – clinical effect)100 cc – clinical effect)

51. Thrombosis Embolism
►Decompression SicknessDecompression Sickness
Exposition to sudden Exposition to sudden
changes in atmospheric changes in atmospheric
pressurepressure
People at risk:People at risk:
►Deep sea divers, in Deep sea divers, in
unpressurized aircraft in unpressurized aircraft in
rapid descent (??)rapid descent (??)
►BendsBends
Rapid formation of gas Rapid formation of gas
bubbles with in the bubbles with in the
skeletal muscle & skeletal muscle &
supporting tissues.supporting tissues.

52. Thrombosis Embolism
►Effects:Effects:
May induce local ischemia in brain, Heart etc.May induce local ischemia in brain, Heart etc.
oedema in lungs leading to respiratory distress – oedema in lungs leading to respiratory distress –
ChokesChokes
Haemorrhages and focal atelectasis or emphysemaHaemorrhages and focal atelectasis or emphysema
►Treatment:Treatment:
Place the individual in compression chamber ( ??? )Place the individual in compression chamber ( ??? )
►Caisson DiseaseCaisson Disease
More chronic form of decompression sicknessMore chronic form of decompression sickness
Persistence of gas emboli in the skeletal system leads to Persistence of gas emboli in the skeletal system leads to
multiple foci of ischemic necrosismultiple foci of ischemic necrosis
Common sites:Common sites:
►Heads of Femur, Tibia and HumeriHeads of Femur, Tibia and Humeri

53. Thrombosis Embolism
Amniotic Fluid EmbolismAmniotic Fluid Embolism
►Grave but uncommon Grave but uncommon
complication of labor & complication of labor &
immediate postpartum immediate postpartum
periodperiod
►Underlying Cause :Underlying Cause :
Infusion of amniotic fluid or Infusion of amniotic fluid or
fetal tissue into maternal fetal tissue into maternal
circulation through a tear in circulation through a tear in
the placental membranes or the placental membranes or
rupture of uterine veinsrupture of uterine veins

54. Thrombosis Embolism
►Mortality rate 20 – 40%Mortality rate 20 – 40%
►Not managed wellNot managed well
►Onset characterized by Onset characterized by
sudden severe dyspnea, sudden severe dyspnea,
cyanosis & hypotensive cyanosis & hypotensive
shock followed by shock followed by
Seizures and comaSeizures and coma
►Marked pulmonary Marked pulmonary
edema edema
►Diffuse alveolar damageDiffuse alveolar damage
►Systemic fibrin thrombiSystemic fibrin thrombi

55. Thrombosis Embolism

56. Thrombosis Embolism
Thrombosis & EmbolismThrombosis & Embolism
►Most common causes of Occlusive Disorders Most common causes of Occlusive Disorders
of Retinaof Retina
May arise from large vessels of neck or may be May arise from large vessels of neck or may be
cardiac in origincardiac in origin
Common in pt.s with Hypertension & other Common in pt.s with Hypertension & other
cardiovascular diseasescardiovascular diseases

57. Thrombosis Embolism
Retinal Artery OcclusionRetinal Artery Occlusion
►Usu. UnilateralUsu. Unilateral
►CRAO – Obstruction at Lamina CribrosaCRAO – Obstruction at Lamina Cribrosa
BRAO – Lodgement of embolus at BRAO – Lodgement of embolus at bifurcationbifurcation
►ManagementManagement
Rx : UnsatisfactoryRx : Unsatisfactory
Immediate lowering of IOP by IV mannitol & Immediate lowering of IOP by IV mannitol &
intermittent ocular massageintermittent ocular massage
AnticoagulantsAnticoagulants

58. Thrombosis Embolism
Retinal Vein OcclusionRetinal Vein Occlusion
►More common than artery occlusionMore common than artery occlusion
►CRVOCRVO – – Non Ischemic ( Venous stasis retinopathy)-75%Non Ischemic ( Venous stasis retinopathy)-75%
►Mild to moderate vision lossMild to moderate vision loss
- Ischemic (Hemorrhagic retinopathy)- Ischemic (Hemorrhagic retinopathy)
►Acute complete occlusion of central retinal Acute complete occlusion of central retinal
vein; marked sudden visual lossvein; marked sudden visual loss
►Treatment : Panretinal PhotocoagulationTreatment : Panretinal Photocoagulation
►BRVOBRVO – – More Common Than CRVOMore Common Than CRVO
Vision – affected only when macular area is involvedVision – affected only when macular area is involved
►Treatment : Treatment : Grid retinal PhotocoagulationGrid retinal Photocoagulation

59. Thrombosis Embolism
►Retinal Vein ThrombosisRetinal Vein Thrombosis - central retinal vein elderly; with - central retinal vein elderly; with
GlaucomaGlaucoma, , Diabetes MellitusDiabetes Mellitus, and , and HypertensionHypertension. .
►Symptom: Painless visual lossSymptom: Painless visual loss
►Examination:Examination:
the retinal veins appear distended and tortuous,the retinal veins appear distended and tortuous,
 the fundus of the eye appears congested and swollen,the fundus of the eye appears congested and swollen,
 numerous hemorrhagic areas may be seen on the retina .numerous hemorrhagic areas may be seen on the retina .
neo-vascularizationneo-vascularization
 secondary (neovascular) secondary (neovascular) GlaucomaGlaucoma can occur weeks after the occlusion. can occur weeks after the occlusion.
►Tests : fluorescein Tests : fluorescein AngiographyAngiography
►Procedures (such as photocoagulation to remove new vessels Procedures (such as photocoagulation to remove new vessels
formed) can prevent secondary neovascular formed) can prevent secondary neovascular GlaucomaGlaucoma..

60. Thrombosis Embolism
Embolization In EyeEmbolization In Eye
►Microemboli are frequent Microemboli are frequent
causes of retinal arterial causes of retinal arterial
emboliemboli
►Sometimes Sometimes
ophthalmoscopically visible ophthalmoscopically visible
and may provide a clue to and may provide a clue to
the diagnosis of the the diagnosis of the
underlying diseaseunderlying disease
►Types of EmboliTypes of Emboli
1. Calcium Emboli1. Calcium Emboli
2. Cholesterol Emboli2. Cholesterol Emboli
..........

61. Thrombosis Embolism
1.1.Calcium EmboliCalcium Emboli
►Most commonly arise from the excrescences on Most commonly arise from the excrescences on
heart valves affected with rheumatic heart disease heart valves affected with rheumatic heart disease
or derived from calcified atheromatous plaquesor derived from calcified atheromatous plaques
►Frequently seen after heart and vascular surgeryFrequently seen after heart and vascular surgery
►Can be recognized as white foci within the arterial Can be recognized as white foci within the arterial
channels most commonly in the major branches channels most commonly in the major branches
near the optic nervenear the optic nerve
►Calcific emboli within the central artery:Calcific emboli within the central artery:
Not visible ophthalmoscopicallyNot visible ophthalmoscopically
Visible histopathologicallyVisible histopathologically

62. Thrombosis Embolism
2. Cholesterol Emboli2. Cholesterol Emboli
From atheromatous plaques of From atheromatous plaques of
the carotid artery systemthe carotid artery system
In the ocular Fundus – Visible In the ocular Fundus – Visible
ophthalmoscopically; multiple ophthalmoscopically; multiple
yellow shining flecks within yellow shining flecks within
retinal arterioles, particularly retinal arterioles, particularly
concentrated at bifurcationsconcentrated at bifurcations
Dislodgement further into retinal Dislodgement further into retinal
periphery – Frequentperiphery – Frequent

63. Thrombosis Embolism
3. Fat Emboli3. Fat Emboli
►Fat emboli usually occur after fracture of Fat emboli usually occur after fracture of
long bones.long bones.
►Indirect Traumatic RetinopathyIndirect Traumatic Retinopathy
An episode of ischemic micro infarction of the An episode of ischemic micro infarction of the
retina with cotton wool spots, retinal edema and retina with cotton wool spots, retinal edema and
hemorrhageshemorrhages
d/t embolization of multiple fragments of bone d/t embolization of multiple fragments of bone
marrow fat into the central and peripheral marrow fat into the central and peripheral
branches of the central retinal arterybranches of the central retinal artery

64. Thrombosis Embolism
4. Thrombocyte – Fibrin emboli4. Thrombocyte – Fibrin emboli
►GrayGray
►Difficult to see ophthalmoscopicallyDifficult to see ophthalmoscopically
►After myocardial infarction or open heart After myocardial infarction or open heart
surgical proceduressurgical procedures

65. Thrombosis Embolism
5. Myxoma Emboli5. Myxoma Emboli
►Histopathologically :- Star Histopathologically :- Star
shaped tumor cells embedded shaped tumor cells embedded
within the mucoid matrix causing within the mucoid matrix causing
occlusion of the vascular lumenocclusion of the vascular lumen
►Should be suspected in young Should be suspected in young
patients who suffer from multiple patients who suffer from multiple
retinal arterial occlusionsretinal arterial occlusions
►In young patients; after In young patients; after
myocarditis, it is the commonest myocarditis, it is the commonest
cause of multiple ischemic cause of multiple ischemic
infarctioninfarction
►Mistaken for retinal vasculitisMistaken for retinal vasculitis

66. Thrombosis Embolism
Bacterial & Mycotic Emboli:Bacterial & Mycotic Emboli:
►BacterialBacterial
Have become rareHave become rare
Causes : Endocarditis, SepticemiaCauses : Endocarditis, Septicemia
Pathognomic Sign : Roth SpotPathognomic Sign : Roth Spot
Histopathologically, the lesions consist of perivascular Histopathologically, the lesions consist of perivascular
accumulation of leucocytes with in surrounding areas of accumulation of leucocytes with in surrounding areas of
hemorrhageshemorrhages
►Mycotic – also rareMycotic – also rare
Complication of long standing intravenous therapy and Complication of long standing intravenous therapy and
in immunocompromised patients.in immunocompromised patients.

67. Thrombosis Embolism
Experimental and Iatrogenic EmboliExperimental and Iatrogenic Emboli
►ExperimentalExperimental
Using Latex or Glass spheresUsing Latex or Glass spheres
Injection of air or fibrinInjection of air or fibrin
►IatrogenicIatrogenic
By tiny metallic foreign bodies derived from heart-lung By tiny metallic foreign bodies derived from heart-lung
machinesmachines
Have been discovered in the retinal capillary treeHave been discovered in the retinal capillary tree
Small particulate micro emboli have also been reported Small particulate micro emboli have also been reported
after injection of crystalline corticosteroids locallyafter injection of crystalline corticosteroids locally

68. Thrombosis Embolism
In brief…In brief…
►Emboli in the visual system can cause Emboli in the visual system can cause
amaurosis fugax;amaurosis fugax;
visual field defects, visual field defects,
cranial nerve palsies, cranial nerve palsies,
central or branched retinal vessel occlusion, central or branched retinal vessel occlusion,
hypotensive retinopathy (Venous stasis retinopathy)hypotensive retinopathy (Venous stasis retinopathy)
 narrowed retinal arterioles, narrowed retinal arterioles,
neovascularization of the iris, optic disc or neural retinaneovascularization of the iris, optic disc or neural retina
& the ocular ischemic syndrome& the ocular ischemic syndrome