DVT AND PTE Flashcards
Favorable environment for venous thrombi
- Stasis
- Low oxygen Tension
- Upregulated pro-inflammatory genes
is the most common preventable cause of death among hospitalizedpatients
Pulmonary thromboembolism or PE
Chronic thromboembolic pulmonary hypertension
causes breathlessness, especially with exertion
(also known as chronic venous insufficiency) damages the venous valves Of the leg and worsens the quality of life by causing ankle or calf swelling and leg aching, especially after prolonged standing
Post thrombotic syndrome
it’s-most severe form, postthrombotic syndrome causes
skin ulceration
Virchow’s triad
venous stasis,
hypercoagulability
endothelial injury
Prevention of VTE , most common in-hospital prophylaxis :
Low dose UFH OR LMWH
May possibly cure pulmonary hypertension and indicated mgt for chronic thromboembolic pulmonary hypertension
PULMONARY THROMBOENDARTERECTOMY
Approve clinical use of Fibrinolysis which is effective up to 14 days post PE
Massive PE
Additional indication for fibrinolysis:
Submissive PE
if with preserved BP
WITH MODERATE OR SEVERE RV DYSFUNCTION
Preferred fibrinolytic treatment
rtPA 100mg continuous 2 hour IV INFUSION
1st line inotropic agents for treatment of PE related shock
Dopamine, dobutamine
Principal indications of inferior vena cava IVC filters:
- Active bleeding precluding anticoagulation
2. Recurrent venous thrombosis despite intensive anticoagulation
Duration of anticoagulation: if DVT of upper extremity or calf provoked by surgery, trauma, estrogen exposure, in dwelling device/catheter:
3 months
Duration of anticoagulation:
provoked proximal leg DVT or PE
3-6 months
Duration of anticoagulation:
Cancer and VTE use
Use LMWH indefinitely until cancer free
Duration of anticoagulation: Idiopathic VTE (unprovoked, ex long haul flight) has high recurrence rate after stopping anticoagulants
Indefinite anticoagulation to INR 2-3
Duration of anticoagulation:
Moderate or high levels of antiphospholipids antibodies
Indefinite anticoagulation
Duration of anticoagulation:
Heterozygous factor V LEIDEN and prothrombin gene mutation
Not at increased risk of recurrent VTE
Most serious adverse effect of anticoagulation:
HEMORRHAGE
Treatment for anticoagulation hemorrhage sec to HEPARIN or LMWH
PROTAMINE SULFATE
Treatment for anticoagulation hemorrhage sec to dabigatran
IDARUCIZUMAB
Treatment for anticoagulation hemorrhage sec to APIXABAN, BETRIXABAN, RIVAROXABAN
Andexanet
Treatment for anticoagulation hemorrhage sec to warfarin and major bleeding
Prothrombin complex concentrate
Treatment for anticoagulation hemorrhage sec to WARFARIN and less serious bleeding
FFP or IV vitamin k
Treatment for anticoagulation hemorrhage sec to WARFARIN and minor bleeding
Oral vitamin k
Treatment for heparin induced thrombocytopenia or HIT for patients with renal insufficiency
Argatroban
Treatment for heparin induced thrombocytopenia or HIT for patients with hepatic failure
Lepirudin
Treatment for heparin induced thrombocytopenia or HIT for patients in the setting of PCI
BIVALIRUDIN
Resistance to activated protein c which inactivated factors 5 and 8
Factor 5 Leiden
Most common case of acquired thrombophilia
APAS
The usual cause of death from PTE
Progressive right Heart failure
10x more common than upper extremity DVT
Lower extremity DVT (from calf proximally to popliteal, femoral and iliac veins)
Most common symptom of the great masquerader / PE
Breathlessness
Presentation: erythema , tenderness and palpable cord
Superficial venous thrombosis
Most common symptom of DVT
Cramp or
Charley horse in the lower calf that persists and intensified over several days
Often present with marked THIGH swelling, tenderness and erythema
massive DVT
True or false
If leg is diffusely edematous, unlikely to be DVT
True
consists of clot dissolution with pharmacomechanical therapy that usually includes low-dose catheter-directed thrombolysis.
Primary therapy for DVT
secondary prevention of VTE
Anticoagulation or placement of an inferior vena caval (IVC) filter
For patients with swelling of the legs when acute DVT is diagnosed, below-knee graduated compression stockings may be prescribed, to lessen patient discomfort. Theyshould be replaced every 3 months because they lose their elasticity. What is the pressure needed?
usually 30–40 mmHg (secondary prevention)
Effective anticoagulation is the foundation for successful treatment ofDVT and PE. There are three major strategies:
1) the classical but waning strategy of parenteral anticoagulation with unfractionated heparin(UFH), low-molecular-weight heparin (LMWH), or fondaparinux“bridged” to warfarin, (2) parenteral therapy switched after 5 days to a novel oral anticoagulant such as dabigatran (a direct thrombininhibitor) or edoxaban (an anti-Xa agent), or (3) oral anticoagulation monotherapy with rivaroxaban or apixaban (both are anti-Xa agents)with a 3-week or 1-week loading dose, respectively, followed by a maintenance dose without parenteral anticoagulation
For patientswith VTE in the setting of suspected or proven heparin-induced thrombocytopenia, one can choose between two parenteral direct-thrombin inhibitors:
argatroban and bivalirudin
direct-thrombin inhibitors:
UFH anticoagulates by binding to and-accelerating the activity of antithrombin, thus preventing additional thrombus formation. The most popular nomogram uses an initial bolus of____, followed by an initial infusion rate of ____ in patients with normal liver function
80 U/kg
18 U/kg per h
UFH is dosed to achieve a target activated partial thromboplastin time (aPTT) of
60–80 seconds
These fragments of UFH exhibitless binding to plasma proteins and endothelial cells and consequently have greater bioavailability, a more predictable doseresponse, and a longer half-life than does UFH. No monitoring ordose adjustment is needed unless the patient is markedly obese orhas chronic kidney disease.
LMWH
An anti-Xa pentasaccharide, is administered as a weight-based once-daily subcutaneous injection in a prefilled syringe. It does not cause heparin-induced thrombocytopenia.
FONDAPARINUX
This vitamin K antagonist prevents carboxylation activation of coagulation factors II, VII, IX, and X.
WARFARIN
Increased d-dimER but low specificity
Pneumonia Pregnancy 2nd and 3rd trimester AMI Post surgery SEPSIS Cancer
Most frequently cited ECG abnormality
Sinus tachycardia
S1Q3T3
T wave in V1 to V4 (most common due to RV strain and ischemia)
True or false:
Wells Point Score criteria help estimate the clinical likelihood of DVTand PE. Patients with a low-to-moderate likelihood of DVT or PE should undergo initial diagnostic evaluation with d-dimer testing alone without obligatory imaging tests
True
True or false:
However, patients with a high clinical likelihood of VTEshould skip d-dimer testing and undergo imaging as the next step inthe diagnostic algorithm.
True
Second line diagnostic tests for PE
Lung scanning
equantitative plasma d-dimer enzyme-linked immunosorbent assay (ELISA)rises in the presence of DVT or PE because of the breakdown of fibrin by
plasmin
Chest X-ray PE abnormalities
focal oligemia (Westermark’s sign),
a peripheral wedged-shaped density usually located at the pleural base (Hampton’s hump),
and an enlarged Right descending pulmonary artery (Palla’s sign)
Primary therapy consists of clot dissolution with pharmacomechanicaltherapy that usually includes low-dose catheter-directed thrombolysis. This approach is reserved for patients with extensive
femoral
iliofemoral
upper extremity DVT
Risk stratification:
portend a high risk of an adverse clinical outcome despite anticoagulation.
Hemodynamic instability
RV dysfunction on echocardiography
RVenlargement on chest CT
or elevation of the troponin level due toRV microinfarction
