Deep venous thr:
mboembolism can be divided into 2 types (VTE)
1. Deep venous thrombosis (DVT)
2. Pulmonary embolism (PE)
DVT occurs due to coagulation of blood (formation of a thrombus) in one of the deep veins. DVT generally affects the veins in legs or arms. More common is lower extremity DVT. This results in pain and swelling in the affected limb.
If DVT is not treated, the throbs can get fragmented and can move up the arteries in the Lung. This can be potentially life threatening.
Diagnosis:
Gold standard is Venography
Alternatively Ultrasound examination may also be done.
Pathophysiology:
Virchow triad - venous stasis, activation of blood coagulation and vein damage. These 3 factors are responsible for development of DVT.
Venous stasis can be a result of any factor that slows or obstructs blood flow. This leads to increased viscosity of blood and microthrombi formation. Due to obstruction of blood , the microthrombi are not washed away and may increase in size.
Etiology
Can be due to acquired or congenital factors
Acquired factors can be those which result in prolonged immobilisation for e.g hospitalizations after surgery, bedridden patients, stroke, paraplegia or transcontinental flights.
Congenital factors such as enzyme deficiency or mutation, anatomic defects can lead to DVT.
Risk factors
1. History of previous VTE
2. Cancer
3. Age older than 75 years
4. Acute infectious disease
5. Obesity
6. Orthopedic surgery
7 . immobility for longer than 3 days
8. Pregnancy
9. Burns
10. Oral contraceptives
Treatment
Goal of therapy is to prevent PE and prevent post thrombotic syndrome.
I. Mainstay is anticoagulation. This therapy treats 90% of patients.
Agents used:
1. Heparin derivatives: unfractionated and low molecular weight heparin(LMWH). Act by inhibiting activated factor X. Bleeding complication is mainly attributed to higher molecular fragments and lower with LMWH
2. Factor Xa Inhibitors
A. Fondaparinux - direct inhibitor of factor X . administered as a once daily subcutaneous injection.
Monitoring of aPTT and PT not required.
3. Rivaroxaban - oral factor Xa inhibitor approved for treatment of DVT and PE
4. Apixaban - approved both for treatment as well as prophylaxis of DVT and PE.
5. Dabigatran - approved for treatment of DVT and PE and prevention of PE in stroke patients
Treatment for first episode should be for atleast 3 months and for recurrent episodes for a year.
Complications of therapy: hemorrhagic complications are yhe most common adverse events of anticoagulation therapy. Bleeding can occur in 3-10% people on 3-6 month anticoagulation therapy.
Emerging agents: razaxaban, idraparinux, bivalirudin, lepirudin, ximelagatran
II. Thrombolysis
III. Surgical thrombectomy
Prophylaxis of DVT
- Pneumatic compression
- aspirin
- warfarin
- heparins: unfractionated and LMWH( enoxaparin, deltaparin , nadroparin, tinzaparin, ardeparin)
- Rivaroxaban
-Apixaban
mboembolism can be divided into 2 types (VTE)
1. Deep venous thrombosis (DVT)
2. Pulmonary embolism (PE)
DVT occurs due to coagulation of blood (formation of a thrombus) in one of the deep veins. DVT generally affects the veins in legs or arms. More common is lower extremity DVT. This results in pain and swelling in the affected limb.
If DVT is not treated, the throbs can get fragmented and can move up the arteries in the Lung. This can be potentially life threatening.
Diagnosis:
Gold standard is Venography
Alternatively Ultrasound examination may also be done.
Pathophysiology:
Virchow triad - venous stasis, activation of blood coagulation and vein damage. These 3 factors are responsible for development of DVT.
Venous stasis can be a result of any factor that slows or obstructs blood flow. This leads to increased viscosity of blood and microthrombi formation. Due to obstruction of blood , the microthrombi are not washed away and may increase in size.
Etiology
Can be due to acquired or congenital factors
Acquired factors can be those which result in prolonged immobilisation for e.g hospitalizations after surgery, bedridden patients, stroke, paraplegia or transcontinental flights.
Congenital factors such as enzyme deficiency or mutation, anatomic defects can lead to DVT.
Risk factors
1. History of previous VTE
2. Cancer
3. Age older than 75 years
4. Acute infectious disease
5. Obesity
6. Orthopedic surgery
7 . immobility for longer than 3 days
8. Pregnancy
9. Burns
10. Oral contraceptives
Treatment
Goal of therapy is to prevent PE and prevent post thrombotic syndrome.
I. Mainstay is anticoagulation. This therapy treats 90% of patients.
Agents used:
1. Heparin derivatives: unfractionated and low molecular weight heparin(LMWH). Act by inhibiting activated factor X. Bleeding complication is mainly attributed to higher molecular fragments and lower with LMWH
2. Factor Xa Inhibitors
A. Fondaparinux - direct inhibitor of factor X . administered as a once daily subcutaneous injection.
Monitoring of aPTT and PT not required.
3. Rivaroxaban - oral factor Xa inhibitor approved for treatment of DVT and PE
4. Apixaban - approved both for treatment as well as prophylaxis of DVT and PE.
5. Dabigatran - approved for treatment of DVT and PE and prevention of PE in stroke patients
Treatment for first episode should be for atleast 3 months and for recurrent episodes for a year.
Complications of therapy: hemorrhagic complications are yhe most common adverse events of anticoagulation therapy. Bleeding can occur in 3-10% people on 3-6 month anticoagulation therapy.
Emerging agents: razaxaban, idraparinux, bivalirudin, lepirudin, ximelagatran
II. Thrombolysis
III. Surgical thrombectomy
Prophylaxis of DVT
- Pneumatic compression
- aspirin
- warfarin
- heparins: unfractionated and LMWH( enoxaparin, deltaparin , nadroparin, tinzaparin, ardeparin)
- Rivaroxaban
-Apixaban
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