| How is epidemiology of DVT? | • Venous thromboembolism (VTE) encompasses deep venous thrombosis (DVT) and pulmonary embolism (PE) and causes cardiovascular death and disability
• In the US 100.000 to 180.000 deaths annually from PE
• PE is the most common preventable cause of death among hospitalized patients |
| How is pathophysiology of DVT? | Virshow's triad (inflammation, hypercoagulability, endothelial injury), recruitments of platelets release microparticles, venous thrombi form and flourish in an environment of stasis, low oxygen tension, upregulation of proinflammatory genes.
Prothrombotic genes (factor V leiden [resistance to AG], prothrombin gene [increase prothrombin concentration], APS antibody most common cause of thrombophilia.
Embolization (when the thrombus detach they go to vena cava, RA, RV, pulmonary arterial circulation, cause acute PE, may embolize to arterial circulation by patent foramen ovale/septal defect. Many have no evidence of DVT clot already embolized to lung.)
Physiology (arterial hypoxemia, increased Aa gradient, increased anatomic dead space and physiologic dead space, vascular resistance, gas exchange impaired)
Pulmonary HTN (pulmonary artery obstruction, tension to right heart buldge to left heart impair filling and compress coronary artery |
| What are the classifications of PE? | PE (massive [5-10%, extensive thrombosis affecting at least half of pulmonary vasculature, dyspnea, syncope, cyanosis, cardiogenic shock]
Submassive [20-25%, RV dysfunction normal arterial pressure, right HF release of cardiac biomarkers may lead to deterioration]
low-risk PE [70-75%, excellent prognosis]) |
| What are the classifications of DVT? | Lower extremity (begins in calf propagates to popliteal vein, femoral vein, iliac vein, 10 times more common than upper)
Upper extremity (precipitated by placement of pace makers, internal cardiac fibrillators, indewlling central venous cath, as cath diameter increases risk increases)
Superficial venous thrombosis (erythema, tenderness, plapable cord, pt are at risk for DVT) |
| How is clinical aspect and dx of PE and DVT? | PE great masquerader, most common symptom is unexplained breathlessness, DVT common symptom is cramp/charley horse, Pulmonary infarct most painful since peripheral near to pleural nerves.
We have score of likelihood of PE and DVT accordingly we either r/o or undergo imaging.
Blood tests include (D-dimer [rules out DVT if normal], ECG [sinus tachycardia, S1Q3T3 lead III, T inversion V1-V4])
Imaging include (venous US [loss of vein compressibility due to passive distention] CXR [normal in PE, see Westmark's sign, Hampton's Hump, Palla's sign] CT [IV contrast, pelvic and proximal leg DVT] lung scan [pt not tolerating contrast] MRI [US equivocal , venography with gadolinium] TTE [normal echo, to R/O others], Pulmonary angiography [invasive]) |
| How is algorithm of DVT and PE dx? | . |
| How is the algorithm for dx imaging in cases of DVT and PE? | . |
| How is tx of DVT? | Primary therapy (low dose cath thrombolysis direct, reserved for pt with extensive femoral, iliofemoral or upper extremity)
Secondary prevention (AG, placement of inferior vena caval filter secondary prevention of VTE, below the knee stockings prescribed 30-40 mmHg for 2 years replaced every 3 months lose elasticity) |
| How is tx of PE? | Risk stratification (hemodynamic instability, RV dysfunction, RV enlargement on CT, elevated troponin)
IVC filter, fibrinolysis, embolectomy, mechanical cath |
| How is use of AGs in DVT and PE? | Conventional strategy of parenteral therapy bridged to warfarin/novel oral AGs, edoxaban, loading dose of monotherapy w/out PRL then oral AGs, heparin based [UFH, LMWH, fondaparinux, immediate]
Duration of AGs (DVT upper or calf provoked by surgery... 3 months sufficient, initial episode of proximal leg DVT 3-6 months, idiopathic VTE target INR 2-3 or alternative approach INR 1.5-2 in period 6 months |
| How is prevention of DVT? | . |
