VTE Prevention and Management Flashcards

1
Q

Management of VTE

A
  1. primary prevention (various prophylactic strategy)
  2. Timely assessment of symptomatic patients (PTP, D-Dimer, CUS/CTPA, Assessment/ancillary of severity of PE)
  3. Instition of acute treatment (anticoagulation, thromboylysis (only if severe) embolectomy), IVC filter where appropriate)
  4. Assessment of recurrence risk
  5. Secondary prevention strategy – chronic anticoagulation, secondary prophylaxis at times of high risk
  6. Management of chronic complications
    - prothrombotic syndrome
    - chronic thromboembolic pulmonary hypertension
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2
Q

highest VTE risk

A

> 40 years and prior VTE or malignancy and major surgery, major elective orthopaedic surgery on lower extremities.

  • also in patients with no prior hx of VTE at times of high risk (ex/ major surgery) and in patients with prior VTE who have discontinued anticoagulation reaction (surgery, immobilization)–> there’s an increased risk if about to have surgery, should put them back onto anticoagulants
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3
Q

preventative VTE measures

A
  1. mechanical – compression stockings, early ambulation
  2. pharmacological: low dose UNFRACTIONATED or LMWHEP, warfarin, DOACs.

Mechanical methods for the prevention of VTE are primarily indicated in patients at high risk of bleeding or in whom anticoagulation is contraindicated. When used in these circumstances, transition to a pharmacologic agent should be considered as soon as the bleeding risk becomes
acceptably low or has been reversed.

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4
Q

3 main treatments for acute VTEW

A
  1. anticoagulation
  2. thrombolysis
  3. inferior vena cava filter
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5
Q

for acute treatment, anticoagulation medication should be initiated with:

A

an immediate acting agent at therapeutic doses:
LMWH, Unfractionated Hep
- DOACs like rivaroxaban, apixaban
-

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6
Q

T/F Cancer patients and pregnant patients can have apixaban

A

false. cancer and pregnant patients should be treated with LMWH or heparin

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7
Q

what is thrombolysis and when should you use it

A

TPA used to rapidly dissolve the clot to open blood vessels. there is a risk for bleeding out, and you should only do it if very serious.

Do it if the pt is hemodynamically unstable due to PE (cariogenic shock, hypotension), or if there’s a limb threatening DVT

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8
Q

what is the inferior vena cava filter

A

shunt used to strain out clots. captures embolism before it reaches Lungs. it doesn’t prevent the original DVT, just prevents the PE. you still need to do an anticoagulation therapy. IVC filter should be removed afterwards, minimum 3 months.

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9
Q

how long should anticoagulation treatment be for?

A
  • if the VTE risk factor is reversible like the person was on birth control, then it should be 3 month minimum and until the risk factor resolves

if vte risk is idiopathic, anticoagulation therapy should occur for 3 months. During the first event, consider a longer therapy but take into consideration pt preference and recurrence risk
if 2nd idiopathic event, consider long term therapy, but balance the risk and benefit (ex if on chronic anticoagulants, they have a higher bleeding risk doing basic activities)

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10
Q

how to predict the recurrence of VTE after first event

A

lots of prediction scores; DASH, VIENNA, HERDOO2. there are individuals who are at lower risk who can safely discontinue anticoagulation

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11
Q

DASH score

A

predicts the recurrence of VTE. takes into account the D-Dimer (if abnormal)= 2 points
age>5- years = 1 pt
male = 1 point
hormone-associated VTE (BC) = -2 points

recurrence risk is 2-20% for score ranging from -2 to 4

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12
Q

VTE treatment recommendations for:
first VTE provoked by TRANSIENT risk factors
first unprovoked episode of VTE
two provoked VTE
a second episode of unprovoked VTE
patients with active cancer and VTE
patients who have been recommended indefinite anticoagulant therapy;
for patients with unprovoked VTE and not continuing on indefinite anticoagulant therapy =

A

first VTE provoked by TRANSIENT risk factors= 3 months of anticoagulants, mitigate the temporary risk factor.

first unprovoked episode of VTE= 3 months of anticoagulants, predict the recurrence of VTE and consider longer term treatment

two provoked VTE= if both provoked by a transient risk factor which has been resolved, treat for 3 months ,followed by prophylaxis during high risk situations.

a second episode of unprovoked VTE= indefinite anticoagulation with routine check ups unless there is a very high bleeding risk.

patients with active cancer and VTE= indefinite anticoagulant therapy. Cancer patients with potentially curable disease and VTE should be treated for a minimum of 3 months but should continue if they are undergoing chemotherapy until this is completed.

patients who have been recommended indefinite anticoagulant therapy= should be reassessed periodically to re-estimate the VTE vs bleeding risk balance

for patients with unprovoked VTE and not continuing on indefinite anticoagulant therapy = consider long-term low dose aspirin prophylaxis if no contraindications (aspirin has been shown to be effective in reducing the recurrence VTE in patients with previous unprovoked VTE.

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13
Q

anticoagulation options

A

warfarin: vitamin K antagonist
Direct oral thrombin inhibitor = dabigatran
direct oral XA inhibitor = edoxaban and apixaban
Low molecular weight heparins
unfractionated heparins
fondaparinux.

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14
Q

the risk of bleeding from anticoagulant thromboprophyalxis is increased if:

A

The risk of bleeding is significantly
increased if the patient has an active gastrointestinal ulcer, previous bleeding (<3 months before hospitalization), known bleeding disorder, advanced age, severe renal failure, hepatic failure, active
cancer, or low platelet count (<50 × 109/L), recent surgery associated with a high bleeding risk.

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15
Q

patients at high risk for thrombosis

A

undergoing surgery, especially abdominal, pelvic
or orthopedic surgery. Medical patients at high thrombotic risk include those >70 years, previous
VTE, immobility ≥3 days, stroke, active cancer, known thrombophilia (essential thrombocythemia, polycythemia vera), acute inflammatory conditions,
acute infectious disease, recent surgery or trauma <1 month, obesity, pregnancy or hormone therapy.

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16
Q

UFHEP AND LMWH mechanism for anticoagulaiton

A

acts as an anticoagulant by increasing the activity of antithrombin. AT-LMWH complexes increases the inhibition’s of several activated blood coagulation factors (thrombin and Factor 10A) which reduces fibrin clot.

17
Q

Why does LMWH NOT prevent the initial formation of the blot?

A

The AT-UFH complex is unable to inactivate thrombin or factor Xa within a formed clot or clots that are bound to surfaces. Thus, UFH only prevents the growth and propagation of a formed thrombus and allows the patient’s endogenous anticoagulant systems to degrade the clot.

18
Q

which type of heparin has more predictable effects?

A

LMWH is smaller and have more predictable pharmacokinetic properties, which permits LMWHs to be administered subcutaneously in fixed doses, unlike UFH which need to be IV infused and monitored.

19
Q

what is fondaparinux.

A

a selective inhibitor of Factor Xa through the formation of AT-fondaparinux complexes. Neutralization of Factor Xa reduces the formation of thrombin and fibrin, but it does not inactivate thrombin.

Can cause bleeding.

20
Q

reversal agents for heparin and fondaparinux

A

protamine surface can be used to revers the anticoagulant effect of UFH, but is less effective at reversing LMWH.
there is no reversal agent for fondaparinux.

21
Q

which factors and protein does warfarin affect?

A

prevents the liver from synthesizing 5,7, 9, 10 and protein C, S by blocking vitamin K reductase.

22
Q

what must happen when you first start a pt on warfarin

A

therapy with warfarin should begin at the same time as heparin, and then heparin should be discontinued when the INR is between 2-3 on two consecutive measurements. patients need to be lab monitored.

this is because warfarin can actually cause MORE CLOTTING because it will cause protein C and S (anticoagulants) to run out first (they have shorter half life ) then the rest of the factors.

23
Q

how to reverse warfarin

A

vitamin K, or replacement of vitamin K deficient coagulation factors using plasma or prothrombin complex concentrates (should be done in times of emergencY (choosing wisely))

24
Q

Practical advantages of DOACs over warfarin:

A

fixed daily oral dosing without the need for lab monitoring. there is also less drug interactions and no known food interactions.

25
Q

when should doacs be avoided

A

during pregnancy, severe renal and hepatic dysfunction. patients with pregnancy, cancer, or renal dysfunction should go on heparin.