VTE Part 4 Flashcards
see slide 108
k
Low Dose ASA & Recurrent VTE
Unprovoked VTE, initial therapeutic anticoagulation completed 6-24 mos
• Randomized, double-blind trials of ASA 100 mg daily vs placebo
NEJM 2012;366:1959-67
Relative Risk Reduction of recurrent VTE vs placebo:
• 33% decrease with ASA
• ~80% decrease with DOAC
• ASA decreases risk of recurrent VTE by 1/3 vs placebo
What about ASA (CHEST 2016)?
“In patients with an unprovoked proximal DVT or PE who are stopping anticoagulant therapy and do not have a contraindication to aspirin, we suggest aspirin over no aspirin to prevent recurrent VTE (Grade 2C).
– Remark: Because aspirin is expected to be much less effective at preventing recurrent VTE than anticoagulants, we do not consider aspirin a reasonable alternative to anticoagulant therapy in patients who want extended therapy. However, if a patient has decided to stop anticoagulants, prevention of recurrent VTE is one of the benefits of aspirin that needs to be
balanced against aspirin’s risk of bleeding and inconvenience. Use of aspirin should also be reevaluated when patients stop anticoagulant therapy because aspirin may have been stopped with anticoagulants were started.
Mr. Smith is 60 years old and has been treated for 1
year with a DOAC following his unprovoked bilateral
segmental PE. You are seeing him in clinic today and
inform him:
- If he stops therapy, he is more likely to have a
recurrent DVT than a recurrent PE. - Given that he has been treated for a full year, he
should stop therapy as his likelihood of recurrent VTE
is low. - After a year of anticoagulant therapy he should
discontinue his anticoagulant and take ASA to
minimize bleeding yet have some protection against
recurrent VTE. - After taking either rivaroxaban 20mg daily OR
apixaban 5mg BID, he can step down to rivaroxaban
10mg daily OR apixban 2.5mg BID
would not give aspirin (only1/3 reduction compared to 80% with DOAC)
High Risk or Active Clot & Inability to Anticoagulate:
Inferior Vena Cava Filters
• Useful in patients with acute proximal DVT with a
contraindication to therapeutic anticoagulation due to high bleeding risk
• Reduce the risk of fatal PE in the short-term
• Increase the risk of DVT in the long term
• Presence of a permanent IVC filter may require long-term anticoagulation – foreign body in vasculature
• Retrievable Filters – removal rates poor (~20%)
– Remove within 3 months or may be permanent
only in ppt with active DVT
Post-Thrombotic Syndrome
• Occurs in nearly one-third of patients within
5 years after idiopathic DVT1
• PTS is characterized by: – Pain – Edema – Hyperpigmentation – Eczema – Varicose collateral veins – Venous ulceration • Severe PTS can lead to intractable, painful venous leg ulcers requiring on-going nursing and medical care
leg swelling, discolouration
Post-Thrombotic Syndrome vs.
DVT recurrence / extension
compare pain, swelling appearance
Pain ‘not as bad as when I had the clot’, ‘worse
after I’ve been on my feet’, ‘dull ache’
DVT: ‘just like the first time’,
‘worst it has ever been’
Swelling Usually will decrease after feet are
elevated (above level of the heart), gets
worse as leg is used / day evolves
DVT: Present at all times
Appearance Chronic changes
DVT: taut, Red, Warm
elevate them above heart
Post-Thrombotic Syndrome vs.
DVT recurrence / extension
leg symtpos
signs
Leg symptoms – Heaviness – Pain – Swelling – Itching – Cramps – Paresthesia – Burning pain • Aggravated by standing or walking
Signs – Edema – Telangiectasia – Varicose veins – Venous dilation – Hyperpigmentation – Eczema – Redness – Dependant cyanosis – Open/healed ulcers
Compression Stockings
• Designed to fit tight on affected leg, to assist in moving blood from the leg veins to circulation • Worn during waking hours • Avoid if: arterial insufficiency, intermittent claudication, uncontrolled heart failure, infection in area covered by stocking • Efficacy: Routine use found not to reduce PTS or have any important benefits* • Use: To reduce acute symptoms of DVT or chronic symptoms in those who have developed PTS • May start wearing within 1 month
Chronic Thromboembolic Pulmonary
Hypertension
(CTEPH)
- Serious complication of PE
- Up to 5% of patients with PE are reported to develop CTEPH1
- Thromboemboli may fail to resolve and organize into fibrotic deposits, permanently occluding pulmonary arteries → ↑flow patent vessels → augments shear stress → progressive pulmonary disease
- Initial phase of disease often asymptomatic and followed by progressive dyspnea and hypoxemia2
- Right heart failure can frequently occur
- Progressive condition associated with mortality rates of 4–20%2
need surgical tx
Venous Thromboembolism
Prevention is Key
Treatment –
Existing Clot
• DVT or PE
• PE can be lethal, DVT can
lead to PE
• Must treat with quick acting anticoagulant at full therapeutic dosing
• (Most effective strategy is to prevent VTE)
Prophylaxis –
At risk for Clot
• Risk stratification for patients at risk to develop clot (hospitalized)
• Orthopedic (hip/knee) replacement
• General Surgery
• Provide anticoagulant at prophylactic dose (=lower
than full therapeutic dose)
VTE Prophylaxis
when is it not indicated?
contra
see slide 119
• Very high risk with orthopedic (hip/knee) replacements
(40-80% will develop VTE)
• Medical / general surgery – 10-40% will develop VTE
• Consider for every hospitalized patient
not indicated if pt fully mobile, length of stay<72 hrs, minor surgery, <60 yrs old
contra: active bleeding, thrombocytopenia, severe HTN, bleeding disorder
drugs for VTE prophylaxis
slide 120
Which statement is correct?
- The signs and symptoms of PTS is very similar to
that of an acute DVT. - Post-thrombotic syndrome occurs more
commonly with larger DVTs that destroy venous
valves thereby promoting poor blood return. - Recurrent or large PEs in the pulmonary arteries
can lead to left ventricular dysfunction. - IVC filters should be inserted in patients with
evidence of PE that cannot be anticoagulated.
IVC filters should be inserted in patients with
evidence of PE that cannot be anticoagulated.?
COVID-19 & VTE
• General trend – saw higher VTE rates in hospitalized
patients earlier in the pandemic compared to later in the
pandemic
• Risk: ICU > non-ICU inpatient > ambulatory
– Hospitalized for COVID, prevalence of VTE 25% (95%CI 19-31%)
+/- thromboprophylaxis (double the rate reported in
hospitalized patients)
– ICU setting higher (17-31%) vs hospital ward (7-31%)
• Evidence evolving rapidly
Antithrombotic Therapy:
Balancing Risk
risk of thrombosis, bleeding
Risk of Thrombosis
• Clot event is indicationspecific
– Consequence is indication specific (eg., stroke, PE)
• May have good riskstratification tools (often we
don’t)
Risk Bleeding (Major vs Minor) • Is not indication specific but may be specific to a population • Concern with major bleeding (decline in Hgb 20g/L) – Intracranial hemorrhage (ICH) – Non-intracranial bleeding – Usually treatable (unless ICH)
• Should do a “Clot vs Bleed assessment” on all patients
– Clot risk almost always trumps bleed risk
– For those deemed long-term candidates for anticoagulant therapy, annual reassessment should occur (clot vs bleed risk, appropriateness of agent, renal function, INR control if on warfarin, etc…)
consequences of bleed usually worse
Foundational Patient Counseling
warfarin
DOAC
Warfarin:
– Benefit (indication), why they have to take
– Risk (bleeding, CBC)
– Need/rationale for routinecoagulation monitoring (INR)
– Factors affecting INR:
• Acute/ Chronic Diseases
• Drugs/Non-Rx, herbals
• Lifestyle factors (Vitamin K, ETOH, activity level)
– Miscellaneous:
• ID on Warfarin (bracelet, other)
• Procedures – Warfarin is delayed
DOAC – Benefit (indication) – Risk (bleeding, CBC) – No routine coagulation monitoring, CrCl – Factors: • Drugs/Non-Rx, herbals • Drug-Specific: – Riva 15 & 20 mg – food – Dabigatran – administration; “dyspepsia”10% – Miscellaneous: • ID on OAC (bracelet, other, emergency and cant speak) • Procedures – OAC needs to be with-held • Adherence, miss a day, not protected
Anticoagulants:
Areas you will see in practice
Anatomy of Heart Valves
which valve higher for thrombosis risk
• Mechanical heart valves
• Need for interruption of chronic therapy for
surgery / procedures
• Semilunar Valves:
– Aortic & Pulmonic
– 3 half-moons (aortic valve semilunar)
• Atrioventricular Valves – Mitral & Tricuspid – Structurally different: • Cusps (leaflets) • Chordae tendineae • Papillary muscles
operative risk high for mitral valve > aortic
mitral valve structure and pressure higher risk of thrombosis > aortic
Common Diagnoses for Valve
Replacement
• Stenosis – mechanical obstruction to blood flow, net
result of reduced valve orifice area
– Mitral, Aortic
• Regurgitation – backward flow of blood, ‘leaky’ valve,
may be called “insufficiency”
– Mitral, Aortic
• Prolapse – to fall or slip down
– Mitral
– Focus on Mitral & Aortic Valves
Types of Valves
2 types
Bioprosthetic (Tissue): • Heterograph (porcine) • Up to 30% failure rate at 10-15 years (may expose to anotehr open heart surgery) • Less thrombogenic Prosthetic (Mechanical): • 3 generations: Ball cage, single leaflet, double leaflet • More durable • More thrombogenic
Heart Valve Replacements
• Risks for thrombosis developing:
Presence of foreign body unable to combat clotting (not living tissue capable of releasing tPA, etc.)
Shear force of blood flow across the valve
Stasis of blood in the atria / ventricle (heart failure)
Tissue injury with implantation
• Ultimate risk of valve failure, stroke
Risk of
Thromboembolism wshich type of valve replacement
tissue valve has lowest risk
mecahnical higher risk
Mechanical:
Anticoagulant +/- Antiplatelet
Bioprosthetic Valves:
• Highest risk of thrombosis < 3 months post-surgery
• Long-term risk: 0.2-2.6% per year
• Anticoagulant for some, antiplatelet long-term
• Thrombotic risk = potential for valve failure, stroke
• Risk of thrombosis:
– Mitral»_space; Aortic
– Mechanical (prosthetic)»_space; Tissue (bioprosthetic)
– Presence of other factors increases risk (sluggish blood flow around valve): atrial fibrillation, heart failure, etc.
• Predominant role (based on thrombotic risk):
– Mechanical
• Anticoagulant (warfarin) for all mechanical
• Antiplatelet therapy (ASA 50-100 mg/day) often co-administered in North America for mechanical valves
– Tissue
• Antiplatelet alone vs. Warfarin for 3 months followed by Antiplatelet
recommended tx for bioprosthetic aortic valve bio mitral valve mechanical aortic valve mech mitral valve
ASA 50-100mg/day
Warfarin X 3 months (Target INR = 2.0-3.0), then ASA
Warfarin* (Target INR = 2.0-3.0)
Warfarin (Target INR = 2.5-3.5)
Mechanical Heart Valves: DOACs
SEE SLIDE 137
No DOAC use in mechanical heart valves
– PROACT Xa (warfarin vs apixaban in aortic OnX valves) is underway
- Major bleeding (all pericardial) in dabigatran (N=7; 4%) vs warfarin (N=2, 2%)
- Almost all events occurred in Group A (new valve implant) – thrombi arising from sewing rink of valve
Chronic Anticoagulant Therapy:
Need for Interruption
warfarin vs DOAC
• Reason: invasive procedure or surgery wherein bleeding will occur if anticoagulated
• Warfarin – delayed onset / offset
– Depending on risk of thrombosis may need to use LMWH (subcutaneously) given the delay with warfarin and hence time with sub-therapeutic anticoagulation
– Interruption with coverage with LMWH is referred to as “bridging”
– Must hold warfarin 5 days prior to procedure, then will take >/= 4 days following procedure to achieve therapeutic anticoagulation
• DOACs – short onset / offset
– No need for bridging with LMWH, simply hold / restart DOAC
• Post-procedure management
warfarin vs DOAC
Bleeding risk of procedure / surgery
– Does the patient need to stop anticoagulant therapy?
• Clotting risk of patient
– Warfarin – comfort being off anticoagulant therapy for
~ 10 days vs if clotting risk substantiates a need to
“bridge” with LMWH
– DOAC – timing of stopping
• Post-procedure management
– Hemostasis intact
– Initiation of anticoagulant(s) based on bleeding risk
associated with the procedure
• Quick acting (DOACs, LMWH) vs delayed (warfarin) acting anticoagulants
start and stop DOACs
VKA: Thromboembolic Risk Stratification
last inj of LMWH is at least 24 hours before procedure
High, moderate and low risk strata based on indirect evidence outside of perioperative setting
– High risk: > 10% annual risk for thromboembolism – “we suggest bridging anticoagulation
instead of no bridging”
– Moderate risk: 5-10% annual risk for thromboembolism – “the bridging or no-bridging
approach is based on an assessment of individual patient- and surgery-related factors”
– Low risk: < 5% annual risk of thromboembolism – “we suggest no bridging instead of
bridging”
Post-Procedural Management
restaring warfarin vs DOAC
• Restart anticoagulant once hemostasis is intact (this is
based on the procedure/surgery performed)
• Warfarin / LMWH:
– Prolonged time to achieve therapeutic INR if restart warfarin at previous maintenance dosing – local data estimates a median of 20.5 (14.3, 31.3) days
– Warfarin dose at 1.5 maintenance dose for 3 days then assess INR (given delay in onset)
– LMWH dosing as per pre-procedure, acknowledging quick onset, to stop once INR target achieved
• DOAC – start once hemostasis intact
• Restarting DOAC or LMWH → therapeutic anticoagulation
– Ensure hemostasis is intact
DOACs: Peri-procedural Management
see slide 144
know general principles
You are managing Mr. Hijab’s warfarin therapy and he has informed you he needs to have hernia surgery done and the surgeon wants him to have no anticoagulant on board during the procedure. He has good renal function and needs LMWH bridging. Which of the following is correct?
- He should hold warfarin for 5 days prior to
the procedure. - He should start injecting his LMWH on the
day that he starts to withhold his warfarin. - He should have his last dose of LMWH 48
hours before his surgery. - All of the statements are correct.
- He should hold warfarin for 5 days prior to
the procedure.
