DVT Flashcards
DVT –> PE pathogenesis
Blood clot (thrombi) developing in circulation.
Occurs 2nd to stagnation of blood and hyper-coagulable states.
* Thrombus develop in venous circ = DVT
* Thrombus –> emboli
* Right side, pul arteries = pulmonary embolism (PE)
mechanism to control coagulation (hemostasis)
- antithrombin (AT III)
- heparin
- thrombomodulin
- protein C, S
- tissue factor pathway inhibitor (regulates initiation phase
self-regulatory mechanisms intact so fibrin clot limited to vessel injury zone
mechanism in fibrinolytic system
tissue plasminogen activator (tPA) converts
plasminogen –> plasmin
degrades fibrin mesh
produced D-Dimer as by-pdt
Virchow’s triad for VTE
1) hypercoagulability (blood)
2) vascular damage (vessel)
3) circulatory stasis (flow)
hypercoagulability
BLOOD
major surgery
malignancy
preg (post partum)
thrombophilia
infection, sepsis
IBD
autoimmune conditions
estrogen therapy (COC, tamoxifen, HIT)
inflamm
dehydration
vascular damage
VESSEL
thrombophlebitis
cellulitis
atherosclerosis
catheter/ heart valve
venepuncture
physical trauma, strain, injury
microtrauma to vessel wall
thrombo-embolism process
calf source: unlikely to embolise
above knee source: more assoc w/ embolism –> Right Heart –> pul arteriole system
- can lead to PE
criculatory stasis
FLOW
immobility
venous obstruction (obesity, tumor, preg)
varicose veins
Afib, LV dysfunciton
congenital abnormalities affect venous anatomy
bradycardia, low BP
DVT clinical presentation
sx:
○ Leg swell, pain, warmth
○ Nonspecific. Obj test needed to establish diagnosis
○ unilateral
signs:
○ Superficial vein dilated
§ Palpable cord felt in affected leg
○ Homan’s sign: Pain in back of knee when dorsiflex leg of affected foot
wells score COPSBET3
1) active cancer (tx within 6mnths)
1) paralysis, immobilisation of lower extremities
1) bedridden >3days/ major surgery in 4wks
1) localised tenderness along distribution of deep venous system
1) entire leg swollen
1) calf swelling by more than 3cm, when compared to asx leg (below tibial tuberosity)
1) pitting oedema (in sx leg)
1) collateral superficial veins (nonvaricose)
-2) alt diagnosis more likely than DVT
wells scoring
=/>3 : high prob
1,2: mod prob
=/>0: low
wells score 0,1,2
1) D-dimer
2) positive –> imaging whole leg/ proximal CUS
3) neg –> rule out DVT
wells score >2 pt
1) imaging whole leg/ proximal CUS
2) distal DVT –> anticoag/ surveillance
2) proximal DVT –> initiate anticoag
- risk of embolism
D-dimer meaning
good negative predictive value
-ve rules out DVT
but +ve does not mean have DVT, plasmin just breaking down fibrin
distal DVT tx
high risk recurrence
- tx: 3mnths AC
low risk recurrence
- 4-6wk AC or venous US surveillance
proximal DVT tx
tc: at least 3mnths AC (DOAC if no CI)
3mnths: evaluation venous US
stop/ extended AC – yearly evaluation
AC for DVT (PO)
apixaban: 10mg BD 7d –> 5mg BD (day 8-90) –> 2.5mg BD (after 6mnths)
rivaroxaban: 15mg BD (21d) –> 20mg OD (day 22-90) –> 10mg OD (after 6mnths)
day 90 or up to 6mnths
renal adj for DOAC
(D,R,A,E)
D: <50ml/min + PGPi use (avoid)
R: CrCl < 30ml/min (avoid)
Apix: 15-29ml/min, caution. HD avoid
E: 30-50ml/min or BW <60kg (30mg/day)
avoid if >95ml/min (tx failure)
prophylaxis with DOAC (riva)
TKR: 10mg OD x 2wk
THR: 5wk
medically ill for 31-39d
switch AC for DVT (SC–>PO)
UFH, LMWH sc1mg/kg BD, (SC, 5d) –> dabigatran 150mg BD/ Edoxaban 60mg OD
renal dose adj for DOAC (that requires sc doses first )
Dabig: crcl <50ml/min + PGPi = VOID
edoxaban: 30mg/day (crcl 30-50ml/min or BW =/< 60kg)
dont use if crcl >95ml/min (tx failure cause renal too good)
AC overlap for DVT tx
UFH, LMWH, (SC) + warfarin PO daily
(stop sc after =/>5d, INR >2)
tx duration for DVT
90d, 3mnths (transient risk factor OR 1st unprovoked isolated distal DVT)
180d, 6mnths (1st unprovoked proximal DVT, PE)
- reduce to prophylaxis dose (riva, apix)
- INR 2-3 (warfarin)
extended duration
- yearly evaluation
** bleeding risk acceptable
risk factor for VTE
- to consider need for VTE prophylaxis
age, prior VTE hist
blood stasis
vascular injury
hypercoagulability
VTE prophylaxis for specific grp of pts
1) medically ill – Padua risk score
2) surgical pt – Caprini risk score
3) cancer pt – Khorona risk score
PE effect
RV failure
systemic congestion and low LV preload
reduced CO
overt RV failure
circulatory collapse + shock
occlude blood flow to lungs (alveolar haemorrhage)
less gas exchange
necrosis
impaired O2 delivery to organs
fatal circ collapse
PE clinical presentation
sx:
○ Cough, chest pain, chest tight, SOB, palpitation
§ Diff dx: myocardial infarction
○ Hemopytsis (cough blood)
○ Massive clot: dizzy, light headed
§ Poor perfusion
signs:
○ Tachypnea, tachycardia, diaphoretic (sweat, look unwell)
○ Neck vein distended
○ Massive clot: cyanotic, hypotensive
§ Hypoxic, cardiogenic shock. Die in mins
PE diagnosis modified wells criteria
HIPOD HM
HM
DO
100IP
3) clinical sx of DVT (leg swell, pain w/ palpation)
3) other diagnosis less likely than PE
1.5) HR > 100
1.5) immobilisation (=/>3days) or surgery in last 4wks
1.5) previous DVT/ PE
1) hemoptysis
1) malignancy
PE scoring modified wells criteria
> 6: high prob
2-6: mod prob
<2: low prob
PE severity and risk assessment – determines drug choice
high, intermediate low parameters
high: haem instable, clinical parameters, RV dysfunction (TTE) , elevated troponin
intermediate:clinical parameters, TTE/ troponin lvls
low: all neg
high risk PE tx
1) systemic thrombolytic therapy
- mortality > risk of bleeding
- followed by anticoag UFH, LMWH
2) anticaog + UFH (weight adj bolus)
- impt UFH is reversible esp for heam unstable
thrombolytics used in PE
1) rTPA 100mg over 2h/ 0.6mg/kg over 15mins max 50mg
2) streptokinase (not in SG)
3) urokinase (expensive, local catheter clot)
tenecteplase for MI, not for VTE
CI for fibrinolysis
absolute:
- hist of haemorrhagic stroke/ stroke of unknown origin
- ischaemic stroke previous 6mnths
- CNS tumour
- major trauma, surgery, head injury (past 3wks)
- bleeding diathesis (susp to bleed)
- active bleed
relative
- preg, post partum
- TIA in last 6mnths
- OAC
- liver disease
- PUD
- endocarditis
alteplase
tenecteplase: AMI, IV bolus (BW)
dosed by BW, infusion
FU and monitor for bleed, BP –> intracranial haemorrhage
alteplase dose:
100mg over 2h/
0.6mg/kg over 15mins (max 50mg)
thrombolysis protocol
inclusion
- acute ischemic stroke
- within 4.5hr of onset
- CT scan consistent with acute ischemic stroke
exclusion
hx of ICH, IS (3mnths), subarachnoid/ intracranial haemorrhage
- endocardities, aortic arch dissection
- active internal bleeds, GI haemorrhage
- major surgery/ serious trauma in last 14d
- Lumbar puncture in last 7d
- preg
BP > 185/110
counts: INR > 1.7, PLT <100,000, glucose < 2.7
use of DTI, Xa inhibitor in last 48hr
use of warfarin in last 48hr unless INR < 1.7
LMWH in last 24hr
intermediate - low risk PE tx
1) initiate anticoag
(if IV: LMWH > UFH)
(if PO: DOAC > VKA)
unless = VKA + LMWH (INR 2-3)
- renal impaired (<30ml.min)
- preg, lactation
- antiphospholipid Ab syndrome
why LMWH > UFH
less inhibitory activity against thrombin than UFH. both binds to antithrombin, cause conformational change to inactivate factor Xa
UFH has 18 saccharide units long, catalyse antithrombin-mediated inactivation of thrombin (antithrombin-thrombin complex)
LMWH: more specific for Xa
UFH: more specific to thrombin (PTT)
reperfusion in PE
- rescue thrombolytic therapy recc in haem deterioration on anticaog tx
duration of anticaog PE
therapeutic anticaog for =/> 3mnths for all pt with PE
- discontinue after 3mnth if reversible risk factors
- extension beyond 3mnths if APS, recurrent VTE (not transient risk factor)
consider: 1st PE no identifiable risk factor - FU: drug tolerance, adherence, hepatic, renal function, bleeding risk at regular intervals
VTE in preg risk factors
higher risk in preg > non-preg women
(incr during preg, peaks at post partum)
risk factors:
- prior VTE
- obesity
- medical comorbidities
- stillbirth
- pre-eclampsia
- post partum hemorrhage
- Caesarean section
challenges of VTE in preg
D-Dimer rises in preg
differential diagnosis (oedema from preg)
diagnosis of PE during preg
compression proximal US
chest x-ray
tx of VTE in preg
LMWH, weight base dosing
sc enoxaparin 1mg/kg BD
APS +ve, switch to warfarin during breastfeeding
fun facts of DOAC and LMWH
rivaroxaban 10mg (prophy) non-MAF
enoxaparin 60, 80mL is graduated at 10mL increments
UFH VTE dose
tx: 80 units/kg –> 18units/kg/hr infusion
prophylaxis: 5000units Q8-12h
PCI: 2000-5000 units for ACT of 250-300s (repeat bolus to maintain ACT)
monitor: aPTT, ACT (for PCI)
why UFH is preferred in PE
UFH is easily reversal when stopped
- Used in high risk pt for PE
- If pt starts to bleed, able to reverse easily (shorter half-life 1hr)
- To start on thrombolytics (if vv unstable, would have started this)
enoxaparin VTE doses
tx: 1mg/kg Q12H or 1.5mg/kg OD
renal <30ml/min, preg, cancer = 1mg/kg OD
prophy: 40mg OD until ambulatory or 30mg BD
PCI: 0.3mg/kg bolus
monitor: anti-Xa lvls when renally impaired, preg
