Venous Thrombosis Flashcards
What are four severe consequences of VTE?
Sudden death
Cardiovascular collapse, cardiac arrest
Chronic thromboembolic pulmonary hypertension (due to recurring small PE’s)
Postphlebitic syndrome (DVT) = valves get damaged, so you can’t get fluid out of the legs –> edema, ulceration
Where can you get DVT?
Lower extremity: proximal are most important clincially
Upper extremity: 10%, catheter associated, Paget-Schroetter syndrome (large muscles in neck)
Pelvic and renal veins
What’s Virchow’s triad for VTE:
Stasis (hospitalization, travel, cast, pregnancy
Endothelial injury (trauma, catheter, surgery)
Hypercoagulable (malignancy, HF, oral contraceptives)
What are the 2 most inherited risk factors for VTE?
Factor V Leiden mutation
Prothrombin gene mutation
(Also: protein S deficiency, protein C deficiency, antithrombin deficiency)
What’s the acute presentation of DVT?
Pain, swelling, erythema in extremity
Asymmetry, warmth, edema, cords (thrombosed external veins)
Differential diagnosis: muscle strain, cellulitis, ruptured baker’s cyst, postphlebitic syndrome
Wells Score for DVT
What test is a good way to rule out DVT?
D-dimer, because it’s very sensitive: elevated in nearly all pt with DVT
If it’s negative, it’s probably not DVT
Which tests can you use to detect DVT?
Duplex ultrasonography: noninvasive test of choice
Contrast venography: gold standard
Also: magnetic resonance venography, CT with contrast
How can you treat DVT?
Anticoagulatns:
Unfractionated heparin
Complexes with antithrombin & inactivates thrombin, factor Xa, IXa, XIa
Narrow therapeutic window
Fully reversible with protamine
Does not cross placenta
LMWH
Complexes with antithrombin & inactivates thrombin, factor Xa, IXa, XIa
Subcutaneous injection
Reduces recurrent VTE & bleeding compared to UFH
Follow Xa in pregnant, obese, elderly, renal dz
Better bioavailability than Heparin so better prediction of how it will affect pt
Fondaparinux
Newer synthetic agent
Subcutaneous injection
Inactivates factor Xa directly
Equally effective as LMWH for VTE, similar precautions
When do you transition to oral anticoagulants?
i.e. warfarin
Should overlap with heparin 4-5 days, when all factors are sufficiently reduced
Treat for at least 3 months
What are your options for oral anticoagulatns?
- *Warfarin**: should overlap with heparin for 4-5 days, when all factors are sufficiently reduced, treat for 3 months at least, watch out for DDI, also it’s teratogenic
- inhibits vitamin K-dependent gamma-carboxylation of factors II, VII, IX, X
Dabigatran: direct thrombin inhibitor, the one in tv commercials, 2x/day, no monitoring
Rivaroxaban: also direct Xa inhibitor, takes effect immediately
All are equally effective
What are your other options for DVT therapy?
Catheter directed thrombolysis
IVC filter
What is a pulmonary embolism? What can cause it?
Obstruction of pulm artery or branches with material originating from elsewhere in the body (emboli from DVT, air, tumor, fat, foreign material)
What’s the pathophysiology of PE?
Thrombi lodge in main PA or smaller branches
Platelets release vasoactive & bronchoactive agents i.e. serotonin
Rarely pulm infarcation
How do you get hemodynamic compromise in acute PE?
Pulm Emboli –> increased pulm vasc resistance –> RV strain & reduced LV preloado –> reduced CO, RV ischemia, RV failure –> cardiovascular collapse/cardiac arrest due to R heart failure
What gas exchange abnormalities do patients with acute PE get?
Hypoxemia, hypocapnea, respiratory alkalosis (due to high RR) though not necessarily present always
V/Q mismatch: pulm blood flow redirected towards regions of low alveolar ventilation
Intrapulmonary shunting: observed & happens though unclear why
Clinical presentation of acute PE: Signs and Symptoms
Symptoms: dyspnea, pleuritic pain, leg pain/swelling, cough, wheezing, hemoptysis
Signs: tachypnea, DVT signs, tachycardia, abnormal breath sounds, signs of right heart failure
All are in order of most common to least common
Wells score to predict PE
Clinical symptoms of DVT = 3
Other diagnosis less likely than PE = 3
HR >100 = 1.5
Immobilization/surg within last 4 weeks = 1.5
Previous DVT/PE = 1.5
Hemoptysis = 1
Malignancy = 1
If >4 PE likely 37% chance
If <4, PE unlikely 12% chance
What diagnostic tests can you do for PE?
CT pulm angiography (CTA): most widely available, good diagnostic accuracy, requires IV contrast (nephrotoxic) & radiation exposure
V/Q scan: inject labeled albumin, inhale radioactive gas – assess V/Q mismatches
Duplex ultrasonography
Echocardiography: for risk stratification
Pulm angiography
MR angiography
Lab markers: D-dimer, cardiac troponins, BNP
- helpful in risk stratifying more than diagnosing
How do you treat acute PE
Stabilize the patient: supplement O2, hemodynamic support if needed
Assess probability of PE and bleeding risk
Obtain diagnostic tests
Treatments: anticoagulation (for almost all), thrombolysis (selected pt’s), IVC filter (if unable to receive anticoag or recurrent PE), emolectomy by catheter or surgery
How do anticoagulants work?
They prevent thrombus propagation & allows endogenous fibrinolytic activity to resolve clots
Variable rates of PE thrombus resolution - several days to months
Anticoagulants prevent recurrent PE & reduce mortality
Risk of bleeding is less than 3%
