Acute VTE therapy Flashcards
(44 cards)
General approach to acute VTE therapy
1) diagnosis of VTE: objective tests
2) how stable is the pt
3) do they need IVC filter
4) in vs out pt
5) selection of therapy
6) do they need stockings?
When would someone need to get an immediate removal of clot
PE: with RF for poor prognosis (hypotension, brady (low HR), shock —— could go into organ failure)
DVT with limb gangrene —- possible amputation
Methods of clot removal
1) pharmacological : thrombolysis (dissolve clot)
2) pulmonary embolectomy: indicated if CI to thrombolysis (active bleeding) OR failed thrombolysis therapy
What is an IVC filter
Filter that goes into IVC and blocks and parts of DVT that may fall off
- stops them from reaching lungs
When is an IVC filter indicated
1) pt with absolute CI to anticoagulation+ have DVT (ex// major active bleed, major bleeding disorder, platelets < 30 x 10^9)
2) pt survived major PE but wouldn’t survive 2nd
3) Pt has recurrent VTEs despite anticoag therapy
When would a pt with a VTE automatically be admitted to hospital ?
hypotension, hypoxemia or tachycardia (increased HR)
—- aka if unstable
What risk tool do we use to determine whether to treat VTE in or out pt
PESI score
- looks at age, sex, cancer, HR, T, RR, O2 levels
—-low risk < 66— can treat outpt
—— if older than 66— automatically high risk (treat in hospital)
What is defined as a rapid anticoagulant
something that becomes effective with 1 hour
— normally SC or IV (PO—- riva or apix)
How many days of overlap bw rapid and warfarin do we need to get adequate protection?
at least 5 days + 2 consecutive INR 24 hours apart that are > 2
- if using warfarin for long term therapy—- need to start when start Rapid+ have a 5 day overlap
What is a good duration for rapid therapy
5-7 days as long as being followed up with LT anticoag after for at least 3mths
What is the approximate bleed risk on UFH
2-5 %: increases if recent surgery, trauma, F, old, malignancy
T or F: About 30% of pt on UFH will experience thrombocytopenia
T: can be directly or indirectly caused
directly: heparin binds to platelets + causes clumps (common + little worry)
indirectly: immune mediated HIT (PF4 + heparin; body makes AB —- cause platelet aggregation + activation —- pro thrombosis state)
What are the main SEs of UFH
bleeding
HIT
osteoporosis: not common
—- heparin binds to blasts— activate clasts
—- only seen with LT > 6mths of use
How common is HIT with UFH use
< 5%
What to monitor when looking for HIT
sudden drop in platelets in first 5 days of UFH use
—- is happens: stop heparin + start fonda
Advantages of UFH
IV admin: if bleed, can suddenly stop
antidote: protamine sulphate (1mg/100 units of heparin; max 50mg)
How is IV UFH dosed
weight based initial dose + infusion rate
- initial bolus of 80-100units/kg + infusion rate of 17-20 units/kg/hour
—- check apTT in 4-6 hours to adjust dose if needed (if high——- lower dose)
Negatives of UFH
required monitoring — apTT
— need to be in pt (IV )
— requires blood draws
no SC dosing in Canada
What needs to be monitored with UFH
CBC + platelets at baseline + at 2 weeks
apTT at baseline + every so often based on protocol
What meds are LMWHs
dalt, tinza, enox
T or F: LMWH is better than UFH
F- there was a study that showed decreased risk of bleeds/mortality but HAD a lot of bias
—- therefore both considered equally effective
Dalt dosing
200 units/kg SC daily
if > 100kg: 100 units/kg SC BID
Tinzaparin dosing
175units/kg SC daily
Enoxaparin BID dosing
1.0mg/kg SC BID