venous thromboembolism Flashcards
virchows triad
stasis
hypercoagulabilty
vascular injury
risk factors for venous thromboembolism
age
obesity
varicose veinse
previous vte
thrombophilia
cancer
other thrombotic states
hormone therapy
pregnancy, puerperium
immobility
immobility during travel
hospitalisation
anaesthesia
central venous catheters
types of venous thrombosis
deep vein thrombosis
pulmonary embolism
cerebral, mesenteric, axillary, splanchnic, splenic
lower limb dvt clinical features
pain, swelling, increased temp of limb, dilation of superficial veins
usually unilateral
- may be bilateral if thrombosis sited in inferior vena cava
- differential diagnosis - calf haematoma, ruptured baker’s cyst, cellulitis
clinical probability - well’s score
dvt investigations
use of d-dimer as negative predictor of VTE
gold standard - contrast venography
venous ultrasonography
- non compressibility of common femoral vein or popliteal vein are diagnostic of dvt
- sensitivity 95%, specificity 96% for diagnosis of symptomatic proximal dvt
- sensitivity and specificity only 60-70% for isolated calf vein thrombosis
PE clinical features
depends on number, size and distribution of emboli
collapse, faintness, crushing central chest pain
pleuritic chest pain
difficulty breathing
haemoptysis
exertional dyspnoea
diagnosis of PE
chest xray
ECG
ABG
d-dimer
ventilation perfusion (V/Q) scan
ct-pulmonary angiogram
echocardiogram
rapid initial anticoagulation
parenteral anticoagulant - heparin, low molecular weight heparin, fondaparinux
OR
direct oral anticoagulant
aim - to reduce risk of thrombus extension and fatal PE
extended therapy
orally active anticoagulant - vit K antagonist
OR
direct oral anticoagulant
aim - to prevent recurrent thrombosis and chronic complications such and post-phlebitic syndrome
direct oral anticoagulants
dabigatran, rivaroxaban, edoxaban and apixaban in UK - treatment for acute DVT
enables rapid initial anticoagulation orally
continue maintenance dose for 6 months or longer for secondary prevention of VTE
apixaban and rivaroxaban dont need overlap with heparin
investigation of a procoagulant tendency
full blood count
antithrombin
protein c
free protein s
antiphospholipid antibodies and lupus anticoagulant
thrombin time/reptilase time to investigate fibrinogen function
factor 5 leiden, prothrombin 20210A genetic tests
jak-2 mutation to investigate myeloproliferative conditions
PNH screen - if patient has cytopenia, for splanchnic bed thrombosis
who to test for thrombophilia
venous thrombosis < 45 years
recurrent venous thrombosis
family history of unprovoked thrombosis
combined arterial and venous thrombosis
venous thrombosis at unusual site
what does dabigatran act on
factor 2a
what do rivaroxaban, apixaban, edoxaban and batrixaban act on
factor 10a
heparins
unfractioned
low molecular weight
unfractioned heparin
heterogenous group of molecules with a range in MW from 3000 to 30,000D
unpredictable anticoagulant response due to binding plasma proteins
monitoring required by activated partial thromboplastin time
unfractioned heparin properties
binds to plasma proteins so requires monitoring
monitor using APTT
continuous iv infusion or twice daily sc administration
risk of osteoporosis, heparin induced thrombocytopenia
reverse by d/c infusion, protamine
low molecular weight heparin properties
nearly 100% bioavailability mean reliable dose dependent anticoagulant effect
no monitoring required unless renal impairment or extremes of body weight
once daily dosing
reduced risk of osteoporosis and HIT
cannot be reversed
coumarins - e.g. warfarin
inhibit vit K dependent carboxylation of factor 2, 7, 9 and 10 in liver
causes relative deficiency of those coagulation factors
many drug interactions
required monitoring at least monthly or more
most common side effect - bleeding
reversal of warfarin
is patient bleeding?
vit K - oral or IV
can reverse by administering deficient clotting factors
tendency to use factor concentrate in place of fresh frozen plasma
DOAC indications
treatment of DVT and PE
prevention of cardioembolic events in patients with AF
benefits of DOACs over warfarin
more predictable anticoagulant profile
fewer drug and food interactions
wider therapeutic window compared to warfarin
oral administration
no need for monitoring
simple dosing
idarucizumab
humaised fab fragment
high binding affinity to thrombin
prevention of venous thrombosis
mechanical - foot pumps, graduated compression stocking
pharmacological - LMWH, UFH, fondaparinux, dabigatran, rivaroxaban, warfarin
