1130 Venous thrombosis Dr Denis O` Keeffe

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Transcript 1130 Venous thrombosis Dr Denis O` Keeffe

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1. Why does venous thrombosis happen ?
2. What are the risk factors ?
3. How do we prevent it ?
4. How do we treat it ?
5. Are there special considerations for cancer
patients ?
6. Scattered pointless NZ photos.
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10% of DVT
embolise to lungs
PE associated
with 5-10%
hospital deaths
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Age ( Over 70 -)
Sex , M:F 1.2:1
Hospitalization - Medical and surgical
Cancer ( x 20)
Immobilization
Drugs (OCP – 3,HRT-2)
Pregnancy (6-8)
Travel (2)
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Pregnancy x 6-8 1
postpartum period -20 2
HRT and OCP x 2 ( Depends on oestrogen
content <50ug low risk )3
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1.T&H 2010 Feb;103(2):306-11. Epub 2009 Nov
2.Obst Gynae . 2011 Mar;117(3):691-703
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3. J OBST GYN Can . 2010 Dec;32(12):1192-7
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Antithrombin deficiency
Protein C
Protein S
Factor V Leiden / APC resistance
Prothrombin 20210A mutation
Increased factor II, VIII, IX, XI
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9.7 fold
Marked in first year
MGUS x 3.5
Increased by IMIDs
Most hospitalized patients with cancer require
thromboprophylaxis throughout
hospitalization
 ● Thromboprophylaxis is not routinely
recommended for ambulatory patients with
cancer; it may be considered for very select
high-risk patients
 ● Assess using Khorana score but most
inpatient cancer patients need VTE
prophylaxis.
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Myeloma , immobilised patients
Myeloma on IMIDs
Lymphoma , large intra-abdominal mass
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A meta-analysis of 11 studies found an
increased risk of deep vein thrombosis for
PICCs (odds ratio [OR] 2.55, 95% CI 1.54-4.23);
there were no pulmonary embolism events
Risk factors for DVT associated with PICC
catheter placement include prior DVT, recent
surgery, and cancer
The rate of symptomatic venous thrombosis is
2-5%
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ACCP- Routine prophylactic systemic
anticoagulation is not recommended for
patients with indwelling central venous
catheters
It may be reasonable to administer
prophylactic anticoagulation in high–risk
patients when the perceived risk of
thrombosis outweighs the risk of bleeding
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Uncomplicated venous thrombosis anticoagulate
Line can be kept in
Duration depends on line remaining in place
Once line removed continue for 2-6 weeks.
Treat with LMWH
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LMWH and warfarin
Dabigatran
Rivaroxaban
Apixiban
Edoxaban
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Can initiate warfarin first day with LMWH
Adjust starting warfarin to patient
Ensure good communication to warfarin team
Ensure follow up
Target 2.5 INR
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Monitor
Narrow therapeutic index
High bleeding risk
Many drugs interact with it
Cumbersome to start and stop
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fractionation from UFH
MW 4,000-6,500 daltons
bioavailability 90%
t ½ 4-12 hours
function - accelerates inhibition of Xa > lla
Simple, safe and effective
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A meta-analyses (seven RCTs; 1908 patients with cancer),
reported that compared to VKAs, LMW heparin reduced the
rate of recurrent VTE (hazard ratio [HR], 0.47; 95% CI
0.32-0.71), a benefit that occurred without a survival
advantage.
The CLOT trial was a multicenter, international,
randomized trial of 672 cancer patients with acute VTE
that compared six months of treatment with warfarin with
the LMW heparin, dalteparin.
Dalteparin was associated with a significant reduction in
the rate of recurrent VTE at six months (9 versus 17
percent; HR, 0.48, 95% CI 0.30-0.77).
There were no significant differences in the rates of major
bleeding (6 versus 4 percent), any bleeding (14 versus 19
percent), or overall mortality (39 versus 41 percent).
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Six months of treatment with LMWH
Consider dose reduction to 75% after 4 weeks
Extend duration if persistent cancer
If recurrence on treatment consider 25% dose
increase
Avoid IVC filters if possible
And now into the
future and
beyond
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Direct thrombin inhibitor – Dabigatran
Direct Xa inhibitors – Rivaroxaban
- Apixiban
- Edoxaban
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Effective
As effective as enoxaparin for primary prevention of VTE in patients undergoing total hip or
knee replacement1
As effective at treating VTE as warfarin
As effective at preventing CVA in atrial fibrillation. Dabigatran is better at preventing stroke
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Safe
Reduced Cerebral bleeds by 60%
Reduced major bleeds by 30%
No liver toxicity observed2
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Fast onset and offset
of action
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Cmax achieved in 2 hours
Half-life: 12–17 hours4
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Predictable anticoagulant effect
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No routine coagulation monitoring required
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No clinically meaningful drug–food effects4
Low potential for cytochrome P450-related drug
interactions3
Cmax = maximum concentration; VTE = venous thromboembolism
1. Wolowacz SE et al. Thromb Haemost 2009;101:77–85; 2. Ezekowitz MD et al. Am Heart J 2009:157:
805–10.e2; 3. Stangier J. Clin Pharmacokinet 2008;47:285–95; 4. Pradaxa™ Product Monograph
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No accurate monitoring test
Compliance
Expensive
No reversing agent
Higher GI bleeding risk
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In one meta-analysis of six studies that
included 1132 patients with DVT and cancer,
compared with conventional therapy (heparin
plus warfarin) similar rates of VTE recurrence
(4 versus 6 percent; odds ratio [OR], 0.63;
95% CI, 0.37-1.10) and major bleeding (OR,
0.77; 95% CI, 0.41-1.44) were reported in
those taking DOACs [42].
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Not enough evidence with DOACs in cancer
Be pragmatic
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DVT nurse specialist
All VTE patients are seen by coagulation team
at outset
Reviewed at 3 months and decision on
duration made in thrombosis clinic
Standard of treatment is DOAC
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New VTE nurse specialist to investigate and
treat PE
Expand role of warfarin nurses in Nenagh and
Ennis to manage DVT to provide a regional
standard service
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1. Venous thrombosis is multifactorial
2. Cancer is a major risk factor for VTE
3. Routine prophylaxis is not recommended
outside of hospital but required in hospital
4. PICCs are associated with significant
thrombosis rates
5. Venous thrombosis in cancer should be
treated with LMWH at present but DOACs maybe
on the way
6. VTE in non- cancer patients should be treated
with DOACs
7. Hopefully the future lies with Nurse specialist
management of VTE