12: Venous Thromboembolism Flashcards
Venous thromboembolism overview
- Thrombi form in deep calf veins and propagate proximally
- Those involving popliteal vein and more proximal veins (femoral, iliac) are more likely to embolize
- Upper extremity veins in < 10% VTE
- Catheter associated
- More common in athletes
- Paget-Schroetter syndrome (effort-induced)
- Pelvic, renal veins: rare
- 79% of patients with pulmonary embolism (PE) have concurrent lower extremity DVT
Virchow’s Triad
- Theory of VTE pathogenesis:
- Altered blood flow (stasis): hospitalization, extended travel, casting of extremity, pregnancy
- Endothelial injury: trauma, central venous catheter, surgery
- Hypercoagulability (inherited vs. acquired): malignancy, heart failure, nephrotic syndrome, autoimmune dz, oral contraceptives
Inherited VTE risk factors
- Factor V Leiden mutation: slower inactivation of Va by Protein C
- Prothrombin gene mutation: increased prothrombin synthesis
- Protein S deficiency: reduced inactivation of Va
- Protein C deficiency: reduced inactivation of Va
- Antithrombin deficiency: reduced inactivation of IXa, XIa, Xa, thrombin
Acute DVT clinical presentation
- Sx: pain, swelling, erythema in extremity
- PEX: assymetry, warmth, edema, cords (thrombosed superficial veins); findings nonspecific and lack accuracy
- DDx: muscle strain, cellulitis, ruptured Baker’s cyst, post-thrombotic syndrome
Limb ischemia
- 2/2 massive proximal DVT
- Causes severely impaired venous return
- Venous gangrene
- Compartment syndrome
- Aterial compromise
- Rare, but requires immediate therapy
- Referred to as “phlegmasia cerulea dolens”
Wells Score for DVT
C3PO + R2D2
Cancer within 6 months
Calf swelling (3cm difference 10cm below)
Collateral superficial veins (non-varicose)
Pitting edema confined to symptomatic leg
Oedema of the entire leg
Tenderness along deep venous system
Recently bedredden for > 3 days
Recent immobilization of leg (cast, paralysis)
DVT in the past
Diagnosis other than DVT likely (2 points off)
D-dimer assay
- D-dimer: degradation product of cross-linked fibrin
- ↑in pts with VTE (very sensitive), but not specific
- DVT can be ruled out with low clinic suspicion (Wells score < 2) and a negative D-dimer
Diagnosis of DVT
-
Duplex ultrasonography
- Non-invasive test of choice; portable
- Dx made by:
- Abnormal compressibility of vein
- Abnormal Doppler color flow
- Presence of echogenic band
- Sensitivity and specificity > 95%
- Pts w/ high clinical suspicion but negative study should have test repeated in 5-7 days or undergo more testing
- Contrast venography
- Impedance plethysmography
- Magnetic resonance venography
- CT w/ contrast
May-Thurner Syndrome
Rare condition in which compression of the common venous outflow tract of the left lower extremity may cause DVT in the iliofemoral vein.
Initial therapy for DVT
-
Unfractionated heparin (UFH):
- Inactivates thrombin
- IV
- Narrow therapeutic window
- Reversible w/ protamine
- Does not cross placenta
-
Low molecular weight heparin (LMWH):
- Inactivates Xa
- SubQ injection
- ↓recurrent VTE and bleeding compared to UFH
- Caution in specific populations (pregnancy, elderly, renal dz, obese)
-
Fondaparinux
- Newer synthetic agent
- SubQ injection
- Inactivates Xa
- Equally effective as LWMH for VTE
- Similar precautions as LMWH
Transitional therapy for DVT
-
Warfarin
- Inhibits vitamin K-dependent gamma-carboxylation of II, VII, IX, X
- Highly effective at preventing recurrent VTE
- Overlap w/ heparin for 4-5 days
- Treat for at least 3 months
- Interactions with genetics, diet, drugs
- Teratogenic
- **Rivaroxaban **(factor Xa inhibitor)
- **Dabigatran **(direct thrombin inhibitor)
Other options for DVT therapy
-
Catheter directed thrombolysis
- For large clot w/ severe swelling or limb-threatening ischemia (not routine use)
- Improves complete clos lysis and reduced post-thrombotic syndrome, increased bleeding risk
-
IVC filter
- When anticoagulation contraindicated
- Prevent embolism in short-term
- Some brands removeable
- Does not protect against VTE long-term
**Pulmonary Embolism **overview
- Obstruction of pulmonary artery or branches with material originating from elsewhere in the body (mostly DVT, although rarely air, tumor, fat, foreign material)
- Recurrent PE is a common cause of death
Pulmonary embolism pathophysiology
- Thrombi lodge in main pulmonary artery or smaller branches
- Platelets release vasoactive and bronchoactive agents (e.g., serotonin)
- Pulmonary infarction occurs rarely (because dual blood supply of lung)
Hemodynamic compromise in acute pulmonary embolism
- Increased pulmonary vascular resistance
- RV strain and ↓LV preload
- ↓CO, RV ischemia and failure
- CV collapse