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Chapter 34 Vascular Thrombosis Due to Hypercoagulable States. Erika Lu August 22, 2005 Vascular Surgery Conference. Epidemiology. Thrombosis is the major cause of death in the world MI and stroke (arterial thrombosis) are the #1 and #2 killer worldwide

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chapter 34 vascular thrombosis due to hypercoagulable states

Chapter 34Vascular Thrombosis Due to Hypercoagulable States

Erika Lu

August 22, 2005

Vascular Surgery Conference

epidemiology
Epidemiology
  • Thrombosis is the major cause of death in the world
    • MI and stroke (arterial thrombosis) are the #1 and #2 killer worldwide
  • Molecular defects increase a patient’s risk for thrombosis in 18%-30% of all cases of venous thromboembolism
  • Arterial thrombosis more likely environmental/acquired cause rather than inherited disorder
biochemistry of thrombosis
Biochemistry of Thrombosis

PK Kallikrein Plasminogen

XII XIIa C4bBP PAI-1

XIa Protein S Plasmin

IXa APC Insol Fibrin FDP

VIIIa

VIIa-TF Xa FVL Sol Fibrin

Va AT

II G20210A Thrombin

HCII Fibrinogen

biochemistry of thrombosis1
Biochemistry of Thrombosis

PK Kallikrein Plasminogen

XII XIIa C4bBP PAI-1

XIa Protein S Plasmin

IXa APC Insol Fibrin FDP

VIIIa

VIIa-TF Xa FVL Sol Fibrin

Va AT

II G20210A Thrombin

HCII Fibrinogen

arterial thrombosis
Arterial Thrombosis
  • White clot – platelet rich
  • Rare to see arterial thrombus in a healthy vessel
  • Usually atherosclerotic change with…
    • Diabetes
    • Hyperlipidemia
    • Tobacco use
  • Acquired procoagulant states (i.e. HIT and antiphosholipid antibodies
arterial thrombosis1
Arterial Thrombosis
  • Manifests in large vessel occlusions
    • MI and stroke
    • Peripheral vascular occlusive disease
  • There are genetic polymorphisms that may increase your risk, but not really predictive of risk of thrombus when you look at large population studies
    • Elevated factor VII
    • Elevated fibrinogen
    • Hyperhomocysteinemia
    • Elevated lipoprotein a
venous thromboembolism
Venous Thromboembolism
  • Red clot – RBC’s trapped in fibrin strands
  • Virchow’s Triad: vessel wall change, hypercoagulability and stasis have a major role!
  • Classic Protein Deficiencies:
    • Antithrombin III deficiency
    • Protein C deficiency
    • Protein S deficiency
venous thromboembolism1
Venous Thromboembolism
  • Less common causes for thrombosis
    • Abnormal fibrinogen
    • Abnormal plasminogen
    • Elevated factors XI, IX, and VIII
  • Hematologic conditions that cause hypercoagulability
    • TTP
    • HUS
    • DIC
    • Polycythemia vera and essential thrombocythemia
venous thromboembolism2
Venous Thromboembolism
  • Acquired Risk Factors:
    • Immobility
    • Obesity
    • Chronic neurologic disease
    • Cardiac disease
    • Pregnancy, use of OCP’s
    • Surgery, particularly thoracoabdominal, ortho, GYN
    • Trauma
    • Malignancy
    • Nephrotic syndrome
venous thromboembolism3
Venous Thromboembolism
  • Interesting Factoids on Cancer and VTE
    • Occult cancer in 0.5 – 5% of VTE pts
    • 3x more likely to get cancer in next 3 yrs if idiopathic VTE
    • 19% of cancer pts have a VTE
    • Chemo increases risk of VTE because it increases tissue factor and expression of E-selectin, thereby increasing thrombus potential
what tests do we order
What tests do we order?
  • Antithrombin activity and antigen assay
  • Protein C activity and antigen assay
  • Free protein S antigen assau
  • APC resistance assay
  • Factor V Leiden by PCR
  • Homocysteine level
  • Prothromnin G20210A by PCR
  • Antiphospholipid or anticardiolipin Ab
  • Clottable fibrinogen and fibrinogen antigen
  • Dilute Russell viper venom time
  • Tissue thromboplastin inhibition time
  • Β2 glycoprotein I antibodies
  • PT/PTT
  • D-dimer
suggested treatment algorithm
Suggested Treatment Algorithm

3-6 months Aggessive ppx

anticoag for 2nd VTE

Yes

VTE Acute Identifiable

Therapy Risk/Etiology

No

Test for Hypercoag ? 6 months

State Neg Anticoagulation

+

Low risk recur

Hi-risk recurrence Life-long

anticoagulation

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