Heparin Induced Thrombocytopenia Flashcards

1
Q

What are the four valves of the heart?

A
  1. Pulmonary valve–>blood flows from right ventricle to the pulmonary artery
  2. Tricuspid valve–>blood flows from right atrium to right ventricle
  3. Mitral valve–>blood flowing from left atrium to left ventricle
  4. Aortic valve–>blood flowing from the left ventricle to the aorta
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2
Q

Which two valves are commonly associated with diseases?

A

Mitral and aortic

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3
Q

Two main types of valvular heart disease

A
  • Stenosis–>calcification and narrowing of the valve(a disease of aging)
  • Regurgitation–>Blood flow backwards through valve

Aortic stenosis is the most common valvular disease

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4
Q

Aortic stenosis

A

Decreases cardiac output causing chest pain, fatigue, shortness of breath, syncope

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5
Q

Mitral regurgitation

Most common mitral vlave disease

A

This is often due to heart failure(increase blood volume and pressure in the left ventricle pushes blood backwards from the left ventricle to the left atrium)

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6
Q

Types of valves (Aortic and Mitral)

A

* Mechanical valve
1. Lasts 20-30 years
2. Risk of thromboembolism is higher
3. Requires lifelong anticoagulation w/ warfarin( INR goal 2-3{aortic} and 2.5-3.5{mitral})
* Bioprosthetic valve
1. Lasts ~10years
2. Risk of thromboembolism is lower
3. Requires ~3months of anticoagulation or antiplatelet therapy

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7
Q

Which valve replace has more thrombogenicity associated with it?

A

Mitral valve(higher risk of clotting)

  • Mitral valve has mainly passive blood flow(low blood pressure)
  • Aortic valve has mainly high-pressure blood flow
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8
Q

Heparin induced thrombocytopenia(HIT)

A

Prothrombic disorder associated w/ unfractionated heparin(UFH) or low molecular weight heparin(LMWH)

URH:5% of patients
LMWH: 0.5-1% of patients

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9
Q

Types of HIT

A
  • Isolated HIT(HIT)–>labs are postive, but patient doesn’t have clot
  • HITT–> HIT complicated by thrombosis
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10
Q

Risk factors for HIT

A
  • Source of heparin–>Bovine is higher risk than porcine
  • Type of heparin product used–> UFH is higher risk than LMWH
  • Patient population–>Surgical patients are at higher risk than medical and obsetric patients
  • Duration of exposure–>Longer exposure=higher risk
  • Poute of adminsitration–>IV is higher risk than SQ
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11
Q

4T’s Pretest Score

A
  • </_ 3 points–> low probability
  • 4-5 points–>intermediate probability
  • 6-8points–> high probability
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12
Q

Diagnosis of HIT

A
  1. Platelet trend decreasing while patient recieving heparin or LMWH
  2. Determine pre-test probability score(4T/HEP)
  3. If score is NOT low, STOP heparin and consider alternative anticoagulants(non-heparin) and send testing
  4. Recommended tests
    * PF4IgG ELISA Immunoassay–> not diagnostic,detetcts heparin dependent IgG antibody, potential false positives
    * Serotonin Release Asssay(SRA)–>Validation test ,detects actual pathologic response
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13
Q

Treatments for HIT,HITT

A
  • 1st–> discontinue heparin and and initiate non-heparin coagulation
  • 2nd(conditional)–> Selection for non-heparin anticoagulants: argatroban,bivalirudin,fondaparinux, or a direct oral anticoagulant(DOAC)
  • 3rd(conditional)–>DOAC selection: rivoraxaban has the most evidence but any can be used
    ==>Dosing(rivoraxaban)
    HIT:15mg BID until platelet count recovery(>150K) then 20mg QD
    HITT: 15mg BIDx 3wks, then 20mgQD
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14
Q

Alternative IV coagulants

A

Argatroban and Bivalirudin

Similatrities:
* Direct thrombin inhibitor
* Continuous IV infusion
* Monitor hemoglobin,hematocrit,platelets
* Will elevate INR
Differences:
* Half-life–>Argatroban(39-51mins);Bivalirudin(10-24mins)
* Renal adjustments–>Argatroban(Not dialyzable);Bivalirudin(Dialyzable)
* Pearls–>Agratroban(~85% hepatobiliary elimination);Bivalirudin(~85% proteolytic elimination)

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15
Q

What happens if we are transitioning from DTI to Warfarin?

A

Transition after platelets >/-150,000; when using both adminster 5 doses of warfarin and recheck INR every 4hrs. If INR is > 4 stop argatroban, if INR is >3 stop bivalirudin
NB: if PTT baseline and INR are in range , leave drip off
if PTT baseline and INR below range restart drip

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16
Q

Transitioning from DTI to DOAC?

A

Stop DTI and start DOAC

17
Q

Duration of Therapy for HIT and HITT

A
  • HIT–>30 days
  • HITT–> 3months
18
Q

When do we reverse anticoagulation?

A

Life-threatning bleeds OR an urgent surgery/procedure that requires reversal

  • There is a preference to let the anticoagulants ‘wash-out’ for a few days(3-5 half lives)
  • Renally eliminated anticoagulants–> hold time maybe longer for those who have poor renal function
19
Q

Warfarin(reversal anticoagulant)

A
  • Specific–> Vitamin K(Phytonadione)
  • Non-specific–>Fresh frozen Plasma/Prothrombin Complex concentrate

Both 4-factor PCC and IV vitamin K should be administered

20
Q

Apixaban,Rivoraxaban,Edoxaban(reversal agents)

A
  • Specific–> Andexanet(Andexxa)
  • Non-specific–>Prothrombin Complex Concentrate
21
Q

Dabigatran(reversal agent)

A
  • Specific–>Idarucizumab(Praxbind)
  • Non-Specific–> Activated Prothrombin Complex concentrate
22
Q

Heparin and LMWH(reversal agent)

A

Specific–>Protamine

23
Q

Onset of actions for reversal agents of oral coagulants

A
  • Andexanet Alfa–> 2mins
  • 4-Factor PCC–>10mins
  • Idarucizumab–>5mins
  • Activated PCC–> 30mins
  • Vitamin K–>10-12hrs
24
Q

Duration of reversal agents for oral anticoagulants

A
  • Andexanet–>2hrs
  • 4-Factor PCC–>8hours
  • Idarucizumab–>12-24hrs
  • Activated PCC–> 12 hrs
  • Vitamin K–>24-48hrs
25
Q

Warfarin reversal

A
  • Oral Vitamin K–>takes 24-48 hours to normalize INR
  • IV vitamin K–>Starts to normalize INR ~12 hours, full effects seen at 24 hours
  • SQ vitmain K–> Avoid due to deleted and erratic absorption