Thrombosis & embolism

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Basic Science for Optometrists

Transcript of Thrombosis & embolism

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►1. Robbins pathologic Basis of Diseases 1. Robbins pathologic Basis of Diseases – 2000– 2000

►Pathology of Eye – GOH NaumannPathology of Eye – GOH Naumann►Ocular Pathology – 5Ocular Pathology – 5thth Edition Edition►Muir’s Textbook of PathologyMuir’s Textbook of Pathology► InternetInternet

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► 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

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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

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The 3 categories are: The 3 categories are: ( to make( to make the study easy)the study easy)

PrimaryPrimary hemostasis hemostasisSecondary hemostasisSecondary hemostasisTertiary HemostasisTertiary Hemostasis

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►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 , which

are released by endothelial cells, and bradykinin. are 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 AT binding to thrombin – enhanced by

heparin heparin

(Used to prevent thrombosis)(Used to prevent thrombosis)

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►TertiaryTertiary hemostasis: This is defined hemostasis: This is defined as the formation of plasmin for as the formation of plasmin for breakdown of the clot. breakdown of the clot. Drugs that inhibit fibrinolysis include Drugs that inhibit fibrinolysis include

epsilonaminocaproic acid and tranexamic epsilonaminocaproic acid and tranexamic acidacid

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Series of overlapping processes Series of overlapping processes after the damage of a blood after the damage of a blood

vessel: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 Formation of Prothrombin activator by extrinsic and

intrinsic pathwayintrinsic pathway

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Blood clotting factors:Blood clotting factors:I I Fibrinogen FibrinogenIIII Prothrombin ProthrombinIII Tissue factorIII Tissue factor

( Thromboplastin)( Thromboplastin)IV Calcium (CaIV Calcium (Ca++++))V Labile FactorV Labile FactorVII Stable factorVII Stable factorVIII 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 factorXI A.H. factor CXI A.H. factor CXII Hageman factorXII Hageman factorXIII Fibrin Stabilising FactorXIII Fibrin Stabilising Factor

► N.B.:N.B.: There is no factor There is no factor

VIVI Vit. K is essential Vit. K is essential

for the synthesis of for the synthesis of factors : ii vii ix & xfactors : ii vii ix & x

Their no.s Their no.s represent the order represent the order in which they were in which they were discovered.discovered.

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HemostasisHemostasis

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► 4. Fibrinolysis4. Fibrinolysis

Removing blood and healing damaged blood Removing blood and healing damaged blood vesselsvessels

ActivatorsActivators

Plasminogen Plasminogen Plasmin Plasmin

Fibrin Fibrin Breakdown products Breakdown products

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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 2. Presence of natural anticoagulants like HeparinHeparin

► 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.

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ThrombosisThrombosis► ThrombusThrombus: an : an

aggregation of blood aggregation of blood factors primarily platelets factors primarily platelets & fibrin with entrapment of & fibrin with entrapment of cellular elements, cellular elements, frequently causing frequently causing vascular obstruction at the vascular obstruction at the point of its formationpoint of its formation

► ThrombosisThrombosis : Formation : Formation of a solid or a semisolid of a solid or a semisolid mass from the constituents mass from the constituents of the blood within the of the blood within the vascular system within life.vascular system within life.

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ThrombosisThrombosis

► PathogenesisPathogenesis

Primary influences Primary influences predisposing to predisposing to thrombosisthrombosis

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Endothelial InjuryEndothelial Injury

► Dominant influenceDominant influence

► Any perturbation in Any perturbation in the dynamic the dynamic balance of the pro balance of the pro and antithrombotic and antithrombotic effects of the effects of the endothelium can endothelium can influence local influence local clotting effectsclotting effects

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► Endothelial dysfunction d/t hemodynamic Endothelial dysfunction d/t hemodynamic stresses of hypertension, turbulent flow over stresses of hypertension, turbulent flow over scarred valves, or bacterial endotoxinsscarred valves, or bacterial endotoxins

► Homocystinuria, Hypercholesterolemia, Homocystinuria, Hypercholesterolemia, radiation or products absorbed from cigarette radiation or products absorbed from cigarette smoke may initiate endothelial injury.smoke may initiate endothelial injury.

► Thrombosis in cardiac chambers, over Thrombosis in cardiac chambers, over ulcerated plaques in atherosclerotic arteries ulcerated plaques in atherosclerotic arteries or at traumatic or inflammatory vascular or at traumatic or inflammatory vascular injury - largely d/t endothelial injury.injury - largely d/t endothelial injury.

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Endothelial EnjuryEndothelial Enjury

► Exposure of subendothelial proteinsExposure of subendothelial proteins► Platelets adhesionPlatelets adhesion► Prevention from blood lossPrevention from blood loss

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Excessive adhesion of platelets - BlockageExcessive adhesion of platelets - Blockage

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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 Turbulence1.1. Disrupt laminar flow – Platelets into contact Disrupt laminar flow – Platelets into contact

with the endotheliumwith the endothelium

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

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Contribution of Turbulence & Stasis to Contribution of Turbulence & Stasis to Thrombosis in Clinical Settings:Thrombosis in Clinical Settings:

► Ulcerated atherosclerotic plaques – sources of Ulcerated atherosclerotic plaques – sources of turbulenceturbulence

► 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 and in sickle cell anemia deformed RBCs cause

vascular occlusionsvascular occlusions

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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

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Significances of inherited Significances of inherited disorders: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

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Acquired Thrombotic Acquired Thrombotic DiathesesDiatheses

►More complicated and multifactorialMore complicated and multifactorial

►Causes:Causes: Stasis or venous injuryStasis or venous injury Increased hepatic secretion of many Increased hepatic secretion of many

coagulation factors and reduced synthesis coagulation factors and reduced synthesis of antithrombin III of antithrombin III

Release of procoagulant tumourRelease of procoagulant tumour

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Hypercoagulability seen with Hypercoagulability seen with advancing age:advancing age:

►Due to Increased susceptibility to Due to Increased susceptibility to platelet aggregation platelet aggregation

►Smoking and obesity promote Smoking and obesity promote hypercoagulability by unknown hypercoagulability by unknown mechanisms.mechanisms.

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ThrombosisThrombosis► Basic Terms and Terminologies:Basic Terms and Terminologies:► Agonal Thrombus : Clot formed in the Heart during Agonal Thrombus : Clot formed in the Heart during

the process of dyingthe process 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

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Retinal branched vein Retinal branched vein ThrombosisThrombosis

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► Laminated Thrombus/ Laminated Thrombus/ mixed Thrombusmixed Thrombus

► Mural ThrombusMural ThrombusCoral ThrombusCoral Thrombus

Organized ThrombusOrganized Thrombus

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► Annular ThrombusAnnular Thrombus► Calcified Thrombus/ Calcified Thrombus/

PhlebolithPhlebolith

► White ThrombusWhite Thrombus

► Blood plate / Platelet Blood plate / Platelet ThrombusThrombus

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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 the leg veins, such as the femoral vein as the femoral vein or the popliteal vein or the popliteal vein or the deep veins of or the deep veins of the pelvis.the pelvis.

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Deep Vein ThrombosisDeep Vein Thrombosis

► SIGNS AND SIGNS AND SYMPTOMSSYMPTOMS 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 Anticoagulation is the

usual treatmentusual treatment

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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.

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►Causes Causes pancreatitis, cirrhosis, pancreatitis, cirrhosis,

►Treatments Treatments anticoagulants, shunts, bypass surgery, anticoagulants, shunts, bypass surgery,

and transplants.and transplants.

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HEPATIC VEIN THROMBOSISHEPATIC VEIN THROMBOSIS-Occlusion of hepatic vein-Occlusion of hepatic vein

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►Symptoms:Symptoms: progressive abdominal painprogressive abdominal pain hepatomegaly , and later the symptoms hepatomegaly , and later the symptoms

of hepatic dysfunctionof hepatic dysfunction

►Therapy:Therapy: anticoagulant medicationanticoagulant medication

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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

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General Morphology / Characteristics of General Morphology / Characteristics of

Arterial & venous ThrombiArterial & venous Thrombi CharacteristiCharacteristicscs

Arterial/ CardiacArterial/ Cardiac

ThrombusThrombusVenous/Red/Venous/Red/Stasis/Phlebo-Stasis/Phlebo-thrombusthrombus

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. Retrograde dir. From pt. of From pt. of attchmentattchment

In a directon of In a directon of blood flowblood flow

NatureNature Usually Occlusive Usually Occlusive Almost invariably Almost invariably occlusiveocclusive

Gray – Gray – white,Firmly white,Firmly adhered to arterial adhered to arterial wallwall

Red/stasis Red/stasis thrombusthrombus

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Composed Composed

of:of:

Tangled mesh Tangled mesh of platelets, of platelets, fibrin, fibrin, erythrocytes & erythrocytes & degenerating degenerating leucocytesleucocytes

More enmeshed More enmeshed erythrocyteserythrocytes

CommonCommon

sitessites

(In (In descending descending order)order)

Coronory Coronory ArteriesArteries

Cerebral Cerebral arteriesarteries

Femoral arteriesFemoral arteries

Veins ofVeins of

Lower extremitiesLower extremities

upper extremitiesupper extremities

Less commonLess common: :

Periprostatic plexusPeriprostatic plexus

Ovarian and Peri Ovarian and Peri uterine veinsuterine veins

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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 Clots Red ThrombiRed Thrombi

Gelatinous; red cells Gelatinous; red cells settled by gravitysettled by gravity

More enmeshed More enmeshed erythrocytes, under erythrocytes, under transection reveal transection reveal vague strands of pale vague strands of pale gray fibringray 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

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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

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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 effectiveness of oral anticoagulants like warfarinwarfarin

► Thrombin TimeThrombin Time► Fibrin Clot StabilityFibrin Clot Stability► Measurement of Fibrin degradation ProductsMeasurement of Fibrin degradation Products

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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 in considered – thrombotic in originorigin

► Results in partial or Results in partial or complete vascular complete vascular occlusionocclusion

► Potential consequence - Potential consequence - InfarctionInfarction

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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 Bland embolism – when thrombotic plug is composed

of non-septic materialof non-septic material► Bacillary embolism – By aggregation of bacilli.Bacillary embolism – By aggregation of bacilli.► Bone marrow embolism : By material from a Bone marrow embolism : By material from a

fractured bonefractured bone► Capillary Embolism – Blockage of capillaries with Capillary Embolism – Blockage of capillaries with

bacteriabacteria

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► Pulmonary Pulmonary embolismembolism

► Retinal Embolism – Retinal Embolism – Central artery of the Central artery of the retinaretina

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Cerebral embolism- Of a cerebral Cerebral embolism- Of a cerebral arteryartery

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ThromboembolismThromboembolism

► A)A) Pulmonary Pulmonary thromboembolismthromboembolism

Incidence : 20 – 25 / Incidence : 20 – 25 / 100,000 hospitalized 100,000 hospitalized patientspatients

►In 95 % instances, - In 95 % instances, - venous embolivenous emboli

Multiple Emboli : Pts. Who Multiple Emboli : Pts. Who had once – high risk of had once – high risk of having more.having more.

60 to 80 % pulmonary 60 to 80 % pulmonary emboli are silent – smallemboli are silent – small

When > 60 % pulmonary When > 60 % pulmonary circulation is obstructed with circulation is obstructed with emboli, - Right Heart Failureemboli, - Right Heart Failure

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# # Effects:Effects: Depends upon sizeDepends upon size May occlude main May occlude main

pulmonary artery, impact pulmonary artery, impact across the bifurcation across the bifurcation (Saddle embolus ) or (Saddle embolus ) or pass out into smaller pass out into smaller branching arteriolesbranching arterioles

Embolic Obstruction of :Embolic Obstruction of :► Medium sized arteryMedium sized artery::

Pulmonary haemorrhagePulmonary haemorrhage► Small End-arteriolar Small End-arteriolar

pulmonary branches:pulmonary branches: InfarctionInfarction

► Multiple EmboliMultiple Emboli : : Pulmonary hypertension Pulmonary hypertension

with right heart failurewith right heart failure

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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 Tissue’s vulnerability to ischemiaischemia

►Caliber of the vessel occluded.Caliber of the vessel occluded.► In GeneralIn General

►Infarction to tissues Infarction to tissues downstream of the obstructed downstream of the obstructed vesselvessel

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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, neurologic symptoms, anemia and anemia and thrombocytopeniathrombocytopenia

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

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Air EmbolismAir Embolism

► Can obstruct vascular Can obstruct vascular flow – Distal ischemic flow – Distal ischemic InjuryInjury

► EntranceEntrance During Obstetric During Obstetric

procedures procedures As a consequence of As a consequence of

chest wall injury ( Usu. In chest wall injury ( Usu. In excess of 100 cc – clinical excess of 100 cc – clinical effect)effect)

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► Decompression Decompression SicknessSickness 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.

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► 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 Haemorrhages and focal atelectasis or

emphysemaemphysema► 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 Persistence of gas emboli in the skeletal system

leads to multiple foci of ischemic necrosisleads to multiple foci of ischemic necrosis Common sites:Common sites:

► Heads of Femur, Tibia and HumeriHeads of Femur, Tibia and Humeri

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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 Infusion of amniotic fluid

or fetal tissue into or fetal tissue into maternal circulation maternal circulation through a tear in the through a tear in the placental membranes or placental membranes or rupture of uterine veinsrupture of uterine veins

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►Mortality rate 20 – 40%Mortality rate 20 – 40%►Not managed wellNot managed well

►Onset characterized by Onset characterized by sudden severe sudden severe dyspnea, cyanosis & dyspnea, cyanosis & hypotensive shock hypotensive shock followed by Seizures followed by Seizures and comaand coma

►Marked pulmonary Marked pulmonary edema edema

►Diffuse alveolar Diffuse alveolar damagedamage

►Systemic fibrin thrombiSystemic fibrin thrombi

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Thrombosis & EmbolismThrombosis & Embolism

►Most common causes of Occlusive Most common causes of Occlusive Disorders of RetinaDisorders of Retina

May arise from large vessels of neck or May arise from large vessels of neck or may be cardiac in originmay be cardiac in origin

Common in pt.s with Hypertension & Common in pt.s with Hypertension & other cardiovascular diseasesother cardiovascular diseases

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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

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Retinal Vein OcclusionRetinal Vein Occlusion► More common than artery occlusionMore common than artery occlusion► CRVOCRVO – – Non Ischemic ( Venous stasis Non Ischemic ( Venous stasis

retinopathy)-75%retinopathy)-75%►Mild to moderate vision lossMild to moderate vision loss

- Ischemic (Hemorrhagic retinopathy)- Ischemic (Hemorrhagic retinopathy)►Acute complete occlusion of central Acute complete occlusion of central

retinal vein; marked sudden visual lossretinal vein; marked sudden visual loss►Treatment : Panretinal PhotocoagulationTreatment : Panretinal Photocoagulation

► BRVOBRVO – – More Common Than CRVOMore Common Than CRVO Vision – affected only when macular area is Vision – affected only when macular area is

involvedinvolved►Treatment : Treatment : Grid retinal PhotocoagulationGrid retinal Photocoagulation

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► Retinal Vein Thrombosis - central retinal vein elderly; Retinal Vein Thrombosis - central retinal vein elderly; with Glaucoma, Diabetes Mellitus, and Hypertension. with Glaucoma, Diabetes Mellitus, and Hypertension.

► 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) Glaucoma can occur weeks after the secondary (neovascular) Glaucoma can occur weeks after the

occlusion. occlusion.

► Tests : fluorescein Angiography Tests : fluorescein Angiography

► Procedures (such as photocoagulation to remove new Procedures (such as photocoagulation to remove new vessels formed) can prevent secondary neovascular vessels formed) can prevent secondary neovascular Glaucoma.Glaucoma.

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Embolization In EyeEmbolization In Eye

► Microemboli are Microemboli are frequent causes of frequent causes of retinal arterial emboliretinal arterial emboli

► Sometimes Sometimes ophthalmoscopically ophthalmoscopically visible and may provide visible and may provide a clue to the diagnosis a clue to the diagnosis of the underlying of the underlying diseasedisease

► Types of EmboliTypes of Emboli 1. Calcium Emboli1. Calcium Emboli 2. Cholesterol Emboli2. Cholesterol Emboli ..........

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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 heart valves affected with rheumatic heart disease or derived from calcified atheromatous disease or derived from calcified atheromatous plaquesplaques

► Frequently seen after heart and vascular surgeryFrequently seen after heart and vascular surgery

► Can be recognized as white foci within the Can be recognized as white foci within the arterial channels most commonly in the major arterial channels most commonly in the major branches near the optic nervebranches near the optic nerve

► Calcific emboli within the central artery:Calcific emboli within the central artery: Not visible ophthalmoscopicallyNot visible ophthalmoscopically Visible histopathologicallyVisible histopathologically

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2. Cholesterol Emboli2. Cholesterol Emboli From atheromatous plaques From atheromatous plaques

of the carotid artery systemof the carotid artery system

In the ocular Fundus – Visible In the ocular Fundus – Visible ophthalmoscopically; ophthalmoscopically; multiple yellow shining multiple yellow shining flecks within retinal flecks within retinal arterioles, particularly arterioles, particularly concentrated at bifurcationsconcentrated at bifurcations

Dislodgement further into Dislodgement further into retinal periphery – Frequentretinal periphery – Frequent

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3. Fat Emboli3. Fat Emboli►Fat emboli usually occur after fracture Fat emboli usually occur after fracture

of long bones.of long bones.

► Indirect Traumatic RetinopathyIndirect Traumatic Retinopathy An episode of ischemic micro infarction of An episode of ischemic micro infarction of

the retina with cotton wool spots, retinal the retina with cotton wool spots, retinal edema and hemorrhagesedema and hemorrhages

d/t embolization of multiple fragments of d/t embolization of multiple fragments of bone marrow fat into the central and bone marrow fat into the central and peripheral branches of the central retinal peripheral branches of the central retinal arteryartery

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4. Thrombocyte – Fibrin 4. Thrombocyte – Fibrin emboliemboli

►GrayGray►Difficult to see ophthalmoscopicallyDifficult to see ophthalmoscopically►After myocardial infarction or open After myocardial infarction or open

heart surgical proceduresheart surgical procedures

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5. Myxoma Emboli5. Myxoma Emboli► Histopathologically :- Star Histopathologically :- Star

shaped tumor cells embedded shaped tumor cells embedded within the mucoid matrix within the mucoid matrix causing occlusion of the causing occlusion of the vascular lumenvascular lumen

► Should be suspected in young Should be suspected in young patients who suffer from patients who suffer from multiple retinal arterial multiple retinal arterial occlusionsocclusions

► In young patients; after In young patients; after myocarditis, it is the myocarditis, it is the commonest cause of multiple commonest cause of multiple ischemic infarctionischemic infarction

► Mistaken for retinal vasculitisMistaken for retinal vasculitis

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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 Histopathologically, the lesions consist of

perivascular accumulation of leucocytes with in perivascular accumulation of leucocytes with in surrounding areas of hemorrhagessurrounding areas of hemorrhages

► Mycotic – also rareMycotic – also rare Complication of long standing intravenous Complication of long standing intravenous

therapy and in immunocompromised patients.therapy and in immunocompromised patients.

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Experimental and Iatrogenic Experimental and Iatrogenic EmboliEmboli

► 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 By tiny metallic foreign bodies derived from

heart-lung machinesheart-lung machines Have been discovered in the retinal capillary treeHave been discovered in the retinal capillary tree Small particulate micro emboli have also been Small particulate micro emboli have also been

reported after injection of crystalline reported after injection of crystalline corticosteroids locallycorticosteroids locally

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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 hypotensive retinopathy (Venous stasis

retinopathy)retinopathy) narrowed retinal arterioles, narrowed retinal arterioles, neovascularization of the iris, optic disc or neural neovascularization of the iris, optic disc or neural

retinaretina & the ocular ischemic syndrome& the ocular ischemic syndrome