Thrombosis & embolism
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Basic Science for Optometrists

Basic Science for Optometrists

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Thrombosis & embolism Presentation Transcript

  • 1. Thrombosis & Embolism Himal Kandel Institute of Medicine [email_address]
  • 2.
    • 1. Robbins pathologic Basis of Diseases – 2000
    • Pathology of Eye – GOH Naumann
    • Ocular Pathology – 5 th Edition
    • Muir’s Textbook of Pathology
    • Internet
    Thrombosis Embolism References...
  • 3.
    • Hemostasis – Basic concepts
    • Thrombosis
      • Predisposing Factors
      • Basic terminologies
      • Morphology & Fate of Thrombi
    • Embolism
      • Introduction ; Terms & Terminologies
      • Major Types
    • Clinical Correlation to Eye
      • Retinal Vein Occlusion
      • Types of Embolization
    Thrombosis Embolism Presentation Layout
  • 4. Hemostasis
    • Hemostasis is a balance of two opposing forces: clot formation and dissolution
    • Major factors involved in Hemostasis:
      • Platelets, Vascular endothelium, Coagulation Process – Deposition of Fibrin
      • Plasmin / Fibrinolytic system – Digests Fibrin
    Thrombosis Embolism
  • 5. The 3 categories are: ( to make the study easy)
          • Primary hemostasis
          • Secondary hemostasis
          • Tertiary Hemostasis
    Thrombosis Embolism
  • 6.
    • Primary hemostasis : This is defined as the formation of the platelet plug.
      • Inhibitors
      • Natural prostacyclin and nitric oxide , which are released by endothelial cells, and bradykinin.
      • Acquired: Aspirin
    • Secondary hemostasis : formation of fibrin through the coagulation cascade.
      • Inhibitors: Natural : Antithrombin III
      • AT binding to thrombin – enhanced by heparin
      • (Used to prevent thrombosis)
    Thrombosis Embolism
  • 7.
    • Tertiary hemostasis: This is defined as the formation of plasmin for breakdown of the clot.
      • Drugs that inhibit fibrinolysis include epsilonaminocaproic acid and tranexamic acid
    Thrombosis Embolism
  • 8. Series of overlapping processes after the damage of a blood vessel:
    • 1. Vasoconstriction
      • Platelets adhere to the damaged wall.
      • Release Serotonin
      • Thromboxanes
    • 2.Platelet plug formation
      • Release of ADP
      • Positive feedback mechanism
      • Temporary seal
    • 3.Coagulation
      • Positive feedback mechanism
      • Mesh of fibrin – strong
      • Formation of Prothrombin activator by extrinsic and intrinsic pathway
    Thrombosis Embolism
  • 9. Blood clotting factors:
    • I Fibrinogen
    • II Prothrombin
    • III Tissue factor
    • ( Thromboplastin)
    • IV Calcium (Ca ++ )
    • V Labile Factor
    • VII Stable factor
    • VIII Antihaemophilic globulin
    • (A. H. factor A)
    • IX Christmas factor
    • (A.H. factor B)
    • X Stuart Power factor
    • XI A.H. factor C
    • XII Hageman factor
    • XIII Fibrin Stabilising Factor
    • N.B.:
      • There is no factor VI
      • Vit. K is essential for the synthesis of factors : ii vii ix & x
      • Their no.s represent the order in which they were discovered.
    Thrombosis Embolism
  • 10. Hemostasis Thrombosis Embolism Coagulation Casdcade
  • 11.
    • 4. Fibrinolysis
      • Removing blood and healing damaged blood vessels
      • Activators
      • Plasminogen Plasmin
      • Fibrin Breakdown products
    Thrombosis Embolism
  • 12. Control Of Coagulation:
    • 1. Perfect smoothness of blood vessel lining
    • 2. Presence of natural anticoagulants like Heparin
    • 3.Binding to Thrombin to a special thrombin receptor on the cells lining blood vessels.
    Thrombosis Embolism
  • 13. Thrombosis
    • Thrombus : an aggregation of blood factors primarily platelets & fibrin with entrapment of cellular elements, frequently causing vascular obstruction at the point of its formation
    • Thrombosis : Formation of a solid or a semisolid mass from the constituents of the blood within the vascular system within life.
    Thrombosis Embolism
  • 14. Thrombosis
    • Pathogenesis
      • Primary influences predisposing to thrombosis
    Thrombosis Embolism
  • 15. Endothelial Injury
    • Dominant influence
    • Any perturbation in the dynamic balance of the pro and antithrombotic effects of the endothelium can influence local clotting effects
    Thrombosis Embolism
  • 16.
    • Endothelial dysfunction d/t hemodynamic stresses of hypertension, turbulent flow over scarred valves, or bacterial endotoxins
    • Homocystinuria, Hypercholesterolemia, radiation or products absorbed from cigarette smoke may initiate endothelial injury.
    • Thrombosis in cardiac chambers, over ulcerated plaques in atherosclerotic arteries or at traumatic or inflammatory vascular injury - largely d/t endothelial injury.
    Thrombosis Embolism
  • 17. Endothelial Enjury
    • Exposure of subendothelial proteins
    • Platelets adhesion
    • Prevention from blood loss
    Thrombosis Embolism
  • 18. Excessive adhesion of platelets - Blockage Thrombosis Embolism
  • 19. Alterations in Normal Blood Flow ( Turbulence & Stasis)
    • Turbulence
      • Arterial & cardiac thrombosis
      • - endothelial injury or dysfunction
    • Stasis and Turbulence
      • Disrupt laminar flow – Platelets into contact with the endothelium
      • Prevent the dilution of activated clotting factors
      • Retard the inflow of clotting Factor inhibitors
      • Promote endothelial cell activation
    Thrombosis Embolism
  • 20. Contribution of Turbulence & Stasis to Thrombosis in Clinical Settings:
    • Ulcerated atherosclerotic plaques – sources of turbulence
    • Abnormal aortic and arterial dilations (Aneurysms) – Favored sites of Thrombosis
    • Myocardial Infarction - regions of non-contractile myocardium – stasis
    • : Mural Thrombi
    • Mitral valve stenosis – Left arterial dilation
    • Hyper-viscosity syndromes cause small vessel stasis
    • and in sickle cell anemia deformed RBCs cause vascular occlusions
    Thrombosis Embolism
  • 21. Hypercoagulability
    • Less contribution to thrombosis
    • Causes :
        • Primary (Genetic)
        • Secondary (Acquired)
    • Inherited causes of Hypercoagulability
      • Mutations in the factor v gene and Prothrombin
      • Polymorphisms
      • Inherited deficiency of anticoagulants such as Antithrombin III, Protein C or protein S
    Thrombosis Embolism
  • 22. Significances of inherited disorders:
    • Individually uncommon
    • 1. Mutations are usually co-inherited
        • ( a and b together ) > ( a + b)
    • 2.Higher risk of developing venous thrombosis
    Thrombosis Embolism
  • 23. Acquired Thrombotic Diatheses
    • More complicated and multifactorial
    • Causes:
      • Stasis or venous injury
      • Increased hepatic secretion of many coagulation factors and reduced synthesis of antithrombin III
      • Release of procoagulant tumour
    Thrombosis Embolism
  • 24. Hypercoagulability seen with advancing age:
    • Due to Increased susceptibility to platelet aggregation
    • Smoking and obesity promote hypercoagulability by unknown mechanisms.
    Thrombosis Embolism
  • 25. Thrombosis
    • Basic Terms and Terminologies:
    • Agonal Thrombus : Clot formed in the Heart during the process of dying
    • Antemortem Thrombus
    • Ball Thrombus
    • Milk Thrombus
    • Parietal Thrombus
    • Fibrin Thrombus
    • Hyaline Thrombus
    • Infective Thrombus
    • Primary Thrombus
    • Stratified Thrombus
    • Traumatic Thrombus
    Thrombosis Embolism
  • 26. Retinal branched vein Thrombosis Thrombosis Embolism
  • 27.
    • Laminated Thrombus/ mixed Thrombus
    • Mural Thrombus
    Coral Thrombus Organized Thrombus Thrombosis Embolism
  • 28.
    • Annular Thrombus
    • Calcified Thrombus/ Phlebolith
    • White Thrombus
    • Blood plate / Platelet Thrombus
    Thrombosis Embolism
  • 29. Deep Vein Thrombosis
    • formation of a blood clot in a deep vein.
    • It commonly affects the leg veins, such as the femoral vein or the popliteal vein or the deep veins of the pelvis.
    Thrombosis Embolism
  • 30. Deep Vein Thrombosis
    • SIGNS AND SYMPTOMS
      • pain,
      • swelling
      • redness of the leg and dilatation of the surface veins
    • THERAPY
      • Anticoagulation is the usual treatment
    Thrombosis Embolism
  • 31. PORTAL VEIN THROMBOSIS
    • a form of venous thrombosis affecting the portal vein, which can lead to portal hypertension and reduction in the blood supply to the liver.
    Thrombosis Embolism
  • 32.
    • Causes
      • pancreatitis, cirrhosis,
    • Treatments
      • anticoagulants, shunts, bypass surgery, and transplants.
    Thrombosis Embolism
  • 33. HEPATIC VEIN THROMBOSIS -Occlusion of hepatic vein Thrombosis Embolism
  • 34.
    • Symptoms:
      • progressive abdominal pain
      • hepatomegaly , and later the symptoms of hepatic dysfunction
    • Therapy:
      • anticoagulant medication
    Thrombosis Embolism
  • 35. RENAL VEIN THROMBOSIS
    • formation of a clot or thrombus obstructing the renal vein, leading to a reduction in drainage of the kidney.
    • can lead to imbalances in blood clotting factor
    • Symptoms
      • blood in urine
    Thrombosis Embolism
  • 36. General Morphology / Characteristics of Arterial & venous Thrombi Thrombosis Embolism
    • Characteristics
    • Arterial/ Cardiac
    • Thrombus
    Venous/Red/Stasis/Phlebo-thrombus
    • Location
    • At the site of endothelial injury or turbulence
    At the sites of Stasis
    • Direction
    • Retrograde dir. From pt. of attchment
    In a directon of blood flow
    • Nature
    • Usually Occlusive
    Almost invariably occlusive
    • Gray – white,Firmly adhered to arterial wall
    • Red/stasis thrombus
  • 37. Thrombosis Embolism
    • Composed
    • of:
    • Tangled mesh of platelets, fibrin, erythrocytes & degenerating leucocytes
    More enmeshed erythrocytes Common sites (In descending order) Coronory Arteries Cerebral arteries Femoral arteries Veins of Lower extremities upper extremities Less common : Periprostatic plexus Ovarian and Peri uterine veins
  • 38. At Autopsy, post mortem clots may be confused for venous thrombi: Thrombosis Embolism Post Mortem Clots Red Thrombi Gelatinous; red cells settled by gravity More enmeshed erythrocytes, under transection reveal vague strands of pale gray fibrin Not attached to the underlying wall Firmer, almost always have a point of attachment
  • 39. Fate of Thrombus :
    • 1. Propagation
    • – Accumulation of more platelets and fibrin; vessel obstruction
    • 2. Embolization
    • – Dislodge and travel to other sites
    • 3. Dissolution – Removed by fibrinolytic activity
    • 4. Organization and recanalization
    • - May induce inflammation and fibrosis
    • - Re-establish vascular flow
    Thrombosis Embolism
  • 40. Lab Tests to measure Coagulation and Thrombolysis
    • Platelet count
    • Bleeding time
    • APTT (Activated Partial Thromboplastin Time)
      • Measure of intrinsic pathway
      • Used to monitor Heparin Therapy
    • Prothrombin Time – Used to measure effectiveness of oral anticoagulants like warfarin
    • Thrombin Time
    • Fibrin Clot Stability
    • Measurement of Fibrin degradation Products
    Thrombosis Embolism
  • 41. Embolism
    • Embolus:
    • detached intravascular solid liquid or gaseous mass that is carried by the blood to a site distant from its point of origin
    • Unless otherwise considered – thrombotic in origin
    • Results in partial or complete vascular occlusion
    • Potential consequence - Infarction
    Thrombosis Embolism
  • 42. Thrombosis Embolism
  • 43. Terms and Terminologies
    • Thromboembolism
    • Pulmonary embolism
    • Air embolism – after trauma or surgical procedures
    • Amniotic Fluid Embolism
    • Fat / Oil embolism
    • Coronary embolism – of coronary arteries
    • Crossed / Paradoxical Embolism
    • Direct embolism – in the direction of the blood flow
    • Bland embolism – when thrombotic plug is composed of non-septic material
    • Bacillary embolism – By aggregation of bacilli.
    • Bone marrow embolism : By material from a fractured bone
    • Capillary Embolism – Blockage of capillaries with bacteria
    Thrombosis Embolism
  • 44.
    • Pulmonary embolism
    • Retinal Embolism – Central artery of the retina
    Thrombosis Embolism
  • 45. Cerebral embolism- Of a cerebral artery Thrombosis Embolism
  • 46. Thromboembolism
    • A) Pulmonary thromboembolism
      • Incidence : 20 – 25 / 100,000 hospitalized patients
        • In 95 % instances, - venous emboli
      • Multiple Emboli : Pts. Who had once – high risk of having more.
      • 60 to 80 % pulmonary emboli are silent – small
      • When > 60 % pulmonary circulation is obstructed with emboli, - Right Heart Failure
    Thrombosis Embolism
  • 47.
    • # Effects:
      • Depends upon size
      • May occlude main pulmonary artery, impact across the bifurcation (Saddle embolus ) or pass out into smaller branching arterioles
    • Embolic Obstruction of :
    • Medium sized artery :
      • Pulmonary haemorrhage
    • Small End-arteriolar pulmonary branches:
      • Infarction
    • Multiple Emboli :
      • Pulmonary hypertension with right heart failure
    Thrombosis Embolism
  • 48. Systemic Thromboembolism
    • = within the arterial circulation
    • 80% arise from intracardiac mural Thrombi
    • Major sites :
      • Lower extremities (75%)
      • Brain (10%)
    • Consequences:
      • Depends upon:
        • Extent of collatoral vascular supply in the affected tissue.
        • Tissue’s vulnerability to ischemia
        • Caliber of the vessel occluded.
    • In General
        • Infarction to tissues downstream of the obstructed vessel
    Thrombosis Embolism
  • 49. Fat Embolism
    • Fat released by marrow or adipose tissue injury
    • 90% with severe skeletal injuries
    • Fat Embiolism Syndrome:
      • Pulmonary insufficiency, neurologic symptoms, anemia and thrombocytopenia
      • Symptoms:
        • Tachycardia Dyspnea
        • Neurological Symptoms:
          • Irritaqbility & restlessness
          • Delirium to coma
    • Pathogenesis
      • Mechanical obstruction and biochemical injury
    Thrombosis Embolism
  • 50. Air Embolism
    • Can obstruct vascular flow – Distal ischemic Injury
    • Entrance
      • During Obstetric procedures
      • As a consequence of chest wall injury ( Usu. In excess of 100 cc – clinical effect)
    Thrombosis Embolism
  • 51.
    • Decompression Sickness
      • Exposition to sudden changes in atmospheric pressure
      • People at risk:
        • Deep sea divers, in unpressurized aircraft in rapid descent (??)
    • Bends
      • Rapid formation of gas bubbles with in the skeletal muscle & supporting tissues.
    Thrombosis Embolism
  • 52.
    • Effects:
      • May induce local ischemia in brain, Heart etc.
      • oedema in lungs leading to respiratory distress – Chokes
      • Haemorrhages and focal atelectasis or emphysema
    • Treatment:
      • Place the individual in compression chamber ( ??? )
    • Caisson Disease
      • More chronic form of decompression sickness
      • Persistence of gas emboli in the skeletal system leads to multiple foci of ischemic necrosis
      • Common sites:
        • Heads of Femur, Tibia and Humeri
    Thrombosis Embolism
  • 53. Amniotic Fluid Embolism
    • Grave but uncommon complication of labor & immediate postpartum period
    • Underlying Cause :
      • Infusion of amniotic fluid or fetal tissue into maternal circulation through a tear in the placental membranes or rupture of uterine veins
    Thrombosis Embolism
  • 54.
        • Mortality rate 20 – 40%
        • Not managed well
        • Onset characterized by sudden severe dyspnea, cyanosis & hypotensive shock followed by Seizures and coma
        • Marked pulmonary edema
        • Diffuse alveolar damage
        • Systemic fibrin thrombi
    Thrombosis Embolism
  • 55. Thrombosis Embolism Clinical Correlation to EYE
  • 56. Thrombosis & Embolism
    • Most common causes of Occlusive Disorders of Retina
      • May arise from large vessels of neck or may be cardiac in origin
      • Common in pt.s with Hypertension & other cardiovascular diseases
    Thrombosis Embolism
  • 57. Retinal Artery Occlusion
    • Usu. Unilateral
    • CRAO – Obstruction at Lamina Cribrosa
    • BRAO – Lodgement of embolus at bifurcation
    • Management
      • Rx : Unsatisfactory
      • Immediate lowering of IOP by IV mannitol & intermittent ocular massage
      • Anticoagulants
    Thrombosis Embolism
  • 58. Retinal Vein Occlusion
    • More common than artery occlusion
    • CRVO – Non Ischemic ( Venous stasis retinopathy)-75%
            • Mild to moderate vision loss
        • - Ischemic (Hemorrhagic retinopathy)
            • Acute complete occlusion of central retinal vein; marked sudden visual loss
        • Treatment : Panretinal Photocoagulation
    • BRVO – More Common Than CRVO
      • Vision – affected only when macular area is involved
        • Treatment : Grid retinal Photocoagulation
    Thrombosis Embolism
  • 59.
    • Retinal Vein Thrombosis - central retinal vein elderly; with Glaucoma , Diabetes Mellitus , and Hypertension .
    • Symptom: Painless visual loss
    • Examination:
      • the retinal veins appear distended and tortuous,
      • the fundus of the eye appears congested and swollen,
      • numerous hemorrhagic areas may be seen on the retina .
      • neo-vascularization
      • secondary (neovascular) Glaucoma can occur weeks after the occlusion.
    • Tests : fluorescein Angiography
    • Procedures (such as photocoagulation to remove new vessels formed) can prevent secondary neovascular Glaucoma .
    Thrombosis Embolism
  • 60. Embolization In Eye
    • Microemboli are frequent causes of retinal arterial emboli
    • Sometimes ophthalmoscopically visible and may provide a clue to the diagnosis of the underlying disease
    • Types of Emboli
      • 1. Calcium Emboli
      • 2. Cholesterol Emboli
      • .....
    Thrombosis Embolism
  • 61.
    • Calcium Emboli
    • Most commonly arise from the excrescences on heart valves affected with rheumatic heart disease or derived from calcified atheromatous plaques
    • Frequently seen after heart and vascular surgery
    • Can be recognized as white foci within the arterial channels most commonly in the major branches near the optic nerve
    • Calcific emboli within the central artery:
      • Not visible ophthalmoscopically
      • Visible histopathologically
    Thrombosis Embolism
  • 62. 2. Cholesterol Emboli
      • From atheromatous plaques of the carotid artery system
      • In the ocular Fundus – Visible ophthalmoscopically; multiple yellow shining flecks within retinal arterioles, particularly concentrated at bifurcations
      • Dislodgement further into retinal periphery – Frequent
    Thrombosis Embolism
  • 63. 3. Fat Emboli
    • Fat emboli usually occur after fracture of long bones.
    • Indirect Traumatic Retinopathy
      • An episode of ischemic micro infarction of the retina with cotton wool spots, retinal edema and hemorrhages
      • d/t embolization of multiple fragments of bone marrow fat into the central and peripheral branches of the central retinal artery
    Thrombosis Embolism
  • 64. 4. Thrombocyte – Fibrin emboli
    • Gray
    • Difficult to see ophthalmoscopically
    • After myocardial infarction or open heart surgical procedures
    Thrombosis Embolism
  • 65. 5. Myxoma Emboli
    • Histopathologically :- Star shaped tumor cells embedded within the mucoid matrix causing occlusion of the vascular lumen
    • Should be suspected in young patients who suffer from multiple retinal arterial occlusions
    • In young patients; after myocarditis, it is the commonest cause of multiple ischemic infarction
    • Mistaken for retinal vasculitis
    Thrombosis Embolism
  • 66. Bacterial & Mycotic Emboli:
    • Bacterial
      • Have become rare
      • Causes : Endocarditis, Septicemia
      • Pathognomic Sign : Roth Spot
      • Histopathologically, the lesions consist of perivascular accumulation of leucocytes with in surrounding areas of hemorrhages
    • Mycotic – also rare
      • Complication of long standing intravenous therapy and in immunocompromised patients.
    Thrombosis Embolism
  • 67. Experimental and Iatrogenic Emboli
    • Experimental
      • Using Latex or Glass spheres
      • Injection of air or fibrin
    • Iatrogenic
      • By tiny metallic foreign bodies derived from heart-lung machines
      • Have been discovered in the retinal capillary tree
      • Small particulate micro emboli have also been reported after injection of crystalline corticosteroids locally
    Thrombosis Embolism
  • 68. In brief…
    • Emboli in the visual system can cause
      • amaurosis fugax;
      • visual field defects,
      • cranial nerve palsies,
      • central or branched retinal vessel occlusion,
      • hypotensive retinopathy (Venous stasis retinopathy)
      • narrowed retinal arterioles,
      • neovascularization of the iris, optic disc or neural retina
      • & the ocular ischemic syndrome
    Thrombosis Embolism