258. Thrombotic Disorders - VTE

Question 1

Where is the most common location for VTE that progresses to PE?

What are factors found expressed near vein valves?

What is the difference between massive and submassive PE?

Answer 1

Proximal deep veins of lower extremity = highest rate of progression

Anticoagulant factors: Endothelial protein C receptors (EPCR), Thrombomodulin
vWF down regulated

Massive PE: hemodynamically unstable, shock (hypotension, tachycardia) with severe strain on heart

Submassive PE: associated RV strain without hemodynamic instability: Echo showing RV dilation/systolic dysfx; CT showing RV/LV ratio > 0.9 (high RV size) with septum flattening/bowing; elevated BNP/troponin (biomarkers of increased heart strain)

Question 2

Signs/Sx of DVT, PE

What is Well’s Scoring?

What is the screening tool for VTE?

What is the preferred imaging for DVT? PE?

Answer 2

DVT: pain, unilateral swelling, warmth, redness
PE: cough, dyspnea, fever, pleuritic chest pain (worse with deep breath), tachycardia, arrhythmia

Wells: progress straight to imaging if DVT >= 3 or PE > 6

Screening: if Well’s Criteria is low
- D-Dimer: measures degradation products of cross-linked fibrin (non-specific)

Imaging
DVT: compression duplex US (venography is gold standard but not done in practice), MRI if worry about pelvic veins
PE: CT-PA, V/Q Scan (Echo as adjunct if CT CI looking for RV strain)

Question 3

PE/DVT

• epidemiology
• causes
• RFs
• what is May Thurner Syndrome?

Answer 3

Epi: COMMON (900k/year), slightly M>F, increases with age, higher lifetime risk in black adults (higher mortality too)
Causes: Virchow's Triad
1. Abnormal blood flow (stasis)
2. Hypercoagulable state
3. Endothelial Cell Damage

RF
- increases with age
- unprotected orthopedic surgery
- air travel (>10k km)
- malignancy (tumor expresses tissue factor, releases procoagulants, compresses vessels more stasis)
- anatomy: May Thurner: chronic compression of L common iliac vein b/w overlying R common iliac artery and first vertebral artery; venous thoracic outlet syndrome
MAJOR
- surgery with gen anesthesia >30min
- confined to bed in hospital >3days
- Cesarean section
MINOR
- OCP use, pregnancy, postpartum
- surgery <30min, hospital <3days
- leg injury with reduced mobility for >3days

Question 4

VTE tx approach

• what is mainstay, how long?
• other tx not routinely used (2)

Answer 4

ANTICOAGULATION: mainstay (balance VTE with bleeding risks)

• Provoked by major RF = 3 mo tx
• Unprovoked by RF = consider indefinite

Other

• Thrombolytic Therapy: if systemic thrombolysis indicated (massive PE), catheter-thrombolysis (DVT or submassive PE)
• Thrombectomy (physical removal)
• IVC filter (when bleeding risk too high for anticoags) - may cause clot, obstruction, perforation, embolization

Question 5

What are the 4 complications of VTE?

Answer 5

1. Death (13% 1-year mortality is significant!)
2. Recurrence (30% in 10 years; highest incidence of recurrence is 2-4mo, why we tx for 3 mo; increased in M)
3. Post Thrombotic Syndrome (high venous pressure = incompetent valves and reflux = pain, paresthesia, heaviness, swelling, chronic venous insufficiency, discoloration, ulcers, permanent disability, no good tx besides increasing activity and compression stockings)
4. Pulm HTN (CTEPH)
   - Chronic Thromboembolic Pulm HTN
   - 4% PE pts
   - Pulm vasculature narrows due to wall thickening and lumen narrowing = pulm HTN
   - RF: younger age, previous PE, large perfusion defects, unprovoked/idiopathic CP
   - dx: dyspnea, fatigue, anorexia, hemoptysis
   - tx: chronic anticoag, thromboendarterectomy if severe (remove clot trees)