DVT and PE Pharamcotherapy
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DVT and PE Pharamcotherapy TEACHING SLIDES. Olavo Fernandes Pharm.D. Pharmacy Practice Leader, University Health Network Assistant Professor, University of Toronto October 2002. UHN Residency Open House. Monday October 21 st , 2002 5:30 pm to 8:00 pm

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DVT and PE Pharamcotherapy TEACHING SLIDES

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Dvt and pe pharamcotherapy teaching slides

DVT and PE Pharamcotherapy

TEACHING SLIDES

Olavo Fernandes Pharm.D.

Pharmacy Practice Leader, University Health Network

Assistant Professor, University of Toronto

October 2002


Uhn residency open house

UHN Residency Open House

  • Monday October 21st, 2002 5:30 pm to 8:00 pm

  • Princess Margaret Hospital 610 University Ave 5th Floor Cafeteria

  • The evening will include:

  • An information session on our residency program

  • A question and answer period

  • Tours of the department and the hospitals

  • Food will be provided

  • Please RSVP to Tamar / Nancy at 416-340-3611

  • By October 18th, 2002


Defintions

DVT

thrombus material composed of cellular material (RBC, WBC, Plts) bound together with fibrin strands

forms in the venous portion of the vasculature

VTE= DVT + PE

PE

thrombus from from systemic circulation lodges in pulmonary artery or branches causing complete or partial obstruction of pulmonary blood flow

95% originate from DVT

Submassive

<50 % of pulmonary vascular bed occluded

Massive

<50 % of pulmonary vascular bed occluded

DEFINTIONS


Epidemiology

DVT

48 per 100, 000

PE

69 per 100, 000 (with our without associated DVT)

100, 000 deaths annually due to PE

Mortality (30% untreated; 8% with treatment )

EPIDEMIOLOGY


Pathophysiology

PATHOPHYSIOLOGY

  • Virchow’s Triangle

    • abnormalities in blood blow

      • (bed rest, tumour obstruction)

    • abnormalities in clotting function

      • (malignancy, pregnancy, deficiencies in Anti-thrombin III, Ptn S or C)

    • abnormal vascular surfaces

      • (catheters, vascular injury, trauma)

  • To form a clot: imbalance in triangle; activation of intrinsic and extrinsic pathway and cascade

  • Venous Thrombi (red)

  • Arterial Thrombi (white)


Risk factors for dvt

surgery or trauma

MI

stroke

increasing age

prior VTE

estrogen use

Factor V leiden

Anti-phospholipid syndrome

pregnancy

CHF

Cancer

obesity

prolonged immobilization

Smoking

Ptn C or S or antithrombin deficiency

HIT

RISK FACTORS for DVT


Clinical presentation

DVT

symptoms present when

obstruction of venous flow

inflammation of vein wall or perivascular space

embolization to lung

unilateral leg pain

leg tenderness

leg swelling

redness/ discolouration

palpable cord

venous distention

Homan sign (calf pain on dorsiflexion of the foot)

SILENT presentation

PE

*transient dyspnea (84%)

tachypnea (RR > 20) 85%

+pleuritic chest pain (74%)

*apprehension (63%)

tachycardia (HR > 100) (58%)

cough (50%)

+hemoptysis (28%)

*syncope (13%)

hypoxemia, hypotension, cardiogenic shock

*more often assoc with massive PE

+more often assoc with submassive PE

SILENT presentation

CLINICAL PRESENTATION


Endpoints outcome assessment

Endpoints: Outcome Assessment

  • VTE endpoints

    • Venography

    • Duplex compression ultrasonography

    • Impedance Plesmography

    • Fibrinogen Uptake

    • D-Dimer Testing

    • PE (lung scanning, angiography, autopsy)

  • Safety endpoints

    • Major and minor bleeds

    • Thrombocytopenia

  • Mortality


Management options

DVT

pharmacological agents

surgery (rarely indicated)

PE

pharmacological agents

thrombolytics

surgery (endarterectomy, can be life saving, specialized centres)

Greenfield Filters (px)

MANAGEMENT OPTIONS


Therapeutic options

THERAPEUTIC OPTIONS

  • Heparin

  • LMWH

  • Warfarin (oral)

  • Danaparoid

  • Hirudin/ Lepirudin

  • Ancrod

  • Thrombolytics (PE)

  • Pentasacharide Injection (phase 3)

  • Thrombin inhibitors (oral) (phase 3)


Pharmacologic agents

Pharmacologic Agents

  • MOA

  • Place in Therapy

  • Dosing

  • Monitoring

  • Adverse Effects/ Limitations

  • Reversal Agents


Heparin

MOA: binds to antithrombin III

Monitor: aPTT - heparin inhibition of thrombin (IIa) and factors Xa and IXa

platelets, bleeding

target: 1.5 -2.5 x control

onset: immediate

advantage: can stop if bleeding (t 1/2 short)

reversal: protamine effective

Unpredictable dose response requires monitoring

complications: HIT, long term osteoporosis

does not inactivate clot bound thrombin

HEPARIN


Dvt and pe pharamcotherapy teaching slides

MOA: preferentially inhibit factor Xa

Monitor: limited requirement ; anti-Xa for renal failure and obesity

platelets, bleeding

target: variable

onset: immediate

prolonged effect- more difficult to immediately reverse effect

reversal: difficult : protamine

OD vs. BID

as effective, same incidence of bleeds/ mortality

wt based dosing

LMWH


Ufh and lmwh

UFH and LMWH

  • Continue therapy for at least 5 days (Grade 1A)

  • longer duration of UFH or LMWH if massive PE

  • Should overlap with warfarin for at least 4-5 days.

    • D/C after 2 consecutive days of therapeutic INR


Favourable properties of a lmwh

Favourable properties of a LMWH

  • increased plasma half life- once daily/ bid dosing

  • reduced non-specific binding to plasma proteins (predictable anticoagulant response, predictable bioavialability)

  • reduced binding to platelets : (less HIT, potential for less bleeding)

  • less need for monitoring/ SC outpatient option

  • less daily injections

  • reduced binding to osteoblasts (less bone loss)


Favourable properties of a lmwh1

Favourable properties of a LMWH

  • less expensive

  • short acting- desirable in patients at high risk of bleeding - can quickly reverse anticoagulation


Warfarin

MOA: inhibits vit K dep coagn factors (II, VII, IX, X)

Monitor: INR , bleeding

target: 2-3 unless MVR

onset: delayed clotting factor half lives (factor II 72 hrs)

reversal: Vitamin K

Bleeding risk correlated to INR

inc with INR > 4

major bleeds < 3% INR 2-3

Drug Interactions

WARFARIN


Duration of warfarin therapy

Duration of Warfarin Therapy

  • Reversible or time limited RFs - first event (3-6 months)

  • Idiopathic VTE- first event (> 6 months)

  • 12 mos- lifetime

    • first event with: cancer until resolved; antithrombin deficiency; anticardiolipin Ab

    • recurrent event, idiopathic or with thrombophilia


Warfarin drug interactions increased inr

TMP/ SMX

inhibits hepatic metabolism of S-warfarin

increases response to warfarin (even 3 day course)

Amiodarone

dramatic increase

rough estimation - 50% decrease in therapeutic warfarin maintenance dose

Metronidazole

dramatic increase

Acetaminophen

interaction appears more likely at doses > 2000 mg/ day for a week or more

Ciprofloxacin

case reports - monitor INR

Fluconazole

inc INR especially with doses > 200 mg/ day

Phenytoin

can both increase or decrease INR

WARFARIN DRUG INTERACTIONS : Increased INR


Warfarin drug interactions pharmacodynamic and dec inr

Pharmacodynamic

ASA

NSAIDS

clopidogrel, ticlopidine

Decreased INR

carbamazepine

Binding resins

barbituates

WARFARIN DRUG INTERACTIONS : Pharmacodynamic and dec. INR


Warfarin counselling points

Indication

How it works-

prevents abnormal clots; stop existing clots from getting larger, decreases risk of clot breaking off

Blood Test Monitoring (INR)

Administration

Length of Therapy

Risks: bleeding (practical discussion)

advise dentist

Drug interactions

Rx and Herbal

Diet

Alcohol

Missed pills

WARFARIN COUNSELLING POINTS


Warfarin counselling points1

When to contact MD: blood in urine, stool, persistent nose bleed, increased swelling in extremity

When to go to ER:

SOB, Chest pain, coughing up blood, black tarry stools, severe HA of sudden onset, slurred speech

WARFARIN COUNSELLING POINTS


Thrombolytics for pe

Thrombolytics for PE

  • Indicated only if massive PE, submassive with hemodynamic compromise (or failure of heparin tx)

  • can start 7-14 days after PE dx

  • only when dx certain (V/Q scan, angiography)

  • only if no contraindications

    • absolute (active bleed; CVA or neurosurg in last 10 days)

    • relative (sx in last 10 days; severe HTN, pregnancy, GI bleed in last 3 months), arotic aneurysm, diabetic retinopathy, serious recent trauma

  • bleeding risks

  • expensive


Indications for exoxaparin

Indications for Exoxaparin

  • Non-ST segment elevation ACS

    • angina at rest lasting at least 10 min

    • evidence of underlying IHD - specific ECG changes

    • inpatients

  • Exclude:

    • chest pain NYD, persistent ST segment elevation; emergency intervention within 24 hrs


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