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pr3154 > ic5 - management of acute and chronic VTE > Flashcards

ic5 - management of acute and chronic VTE Flashcards

1
Q

what plays an important role in regulating the initiation phase of coagulation

A

tissue factor pathway inhibitor

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2
Q

how do clots ensure they do not persist

A

clots formed should be able to cause fibrinolysis and degradation then leading to recanalisation and healing

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3
Q

when is D-dimer being produced

A

in the fibrinolytic system, when tissue plasminogen activator converts plasminogen into plasmin thus degrading the fibrin mesh, D-dimer is produced as a byproduct

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4
Q

what are the three main categories of risk factors that can lead to thromboembolism

A

hypercoagulability, vascular damage, circulatory stasis

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5
Q

what are the conditions that VTE encompass

A

DVT and PE

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6
Q

what are the risk factors of VTE

A

immobility, long haul flights, pregnancy, recent surgery, thrombophilia, polycythemia, SLE, malignancy

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7
Q

what is thrombophilia and what are the conditions that predisposes one to thrombophilia

A

thrombophilia refers to being prone to clots

conditions: antiphospholipid syndrome (APS), antithrombin resistance, protein C/S resistance, factor V leiden, activated protein C resistance, prothrombine gene variant

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8
Q

when might VTE prophylaxis be considered

A

if pt is scheduled for surgery and assess for risk of VTE when pt admitted into hospital

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9
Q

what should be given to pts for VTE prophylaxis

A

LMWH and antiembolic compression stockings unless c/i

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10
Q

what are the c/i for VTE prophylaxis

A

active bleeding and existing anticoagulation for LMWH

peripheral arterial disease for stockings

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11
Q

how does PE occur

A

when a thrombus develops, it can travel or embolise in the right side of the heart and into the lungs where it becomes lodged in the pulmonary arteries which blocks blood flow to areas of the lungs thus causing impaired gaseous exchange resulting in necrosis

this further causes impaired O2 delivery to other organs which can result in fatal circulatory collapse

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12
Q

what can small distal emboli cause

A

it can create small areas of alveolar hemorrhage which leads to hemoptysis, pleuritis and pleural effusion

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13
Q

what is the presentation (s/sx) of PE

A

sx: cough, chest pain, chest tightness, palpitations, sob, hemoptysis, dizziness/ lightheadedness

signs: tachypnea (rapid breathing), tachycardia, appear diaphoretic (sweating heavility), distended neck veins

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14
Q

what might the pt look like if he/she has massive PE

A

appear cyanotic (blue), becoming hypotensive and hypoxia and may go into cardiogenic shock and die within mins

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15
Q

how to diagnose PE

A

wells score, D-dimer, imaging like CTPA and V/Q (ventilation perfusion)

(draw the flow chart relating to all 3)

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16
Q

what are the clinical features and the respective scoring for well’s score and what scores relate to what probability

A

clinical sx of DVT (leg swelling, pain with palpitation) [3.0]

other diagnosis less likely than PE [3.0]

HR >100 [1.5]

prev hx of DVT/PE [1.5]

immobilisation (>3d) or surgery in last 4w [1.5]

hemoptysis [1.0]

malignancy [1.0]

high probability if score >6.0
moderate probability if score between 2.0-6.0
low probability if score <2.0

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17
Q

what does elevated cardiac troponin levels indicate

A

when heart muscles die or overworked

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18
Q

what are the indicators under PE severity and risk assessment

A

clinical parameters of PE severity and/or comorbidity

RV dysfunction on transthoracic echo (TTE) or computed tomography pulmonary angiogram (CTPA)

elevated cardiac troponin levels

19
Q

what are the tx approaches based on risk stratification for PE

A

high risk: give UFH or surgical pulmonary embolectomy

intermediate to low risk: [initiation] LMWH for parenteral, DOAC > VKA for OAC (LMWH preferred over DOAC bc administered by nurse), if given VKA overlap with parenteral until INR 2.0-3.0 **note DOACs not for severe renal impairment, pregnancy, lactation, APS Ab

[reperfusion] rescue thrombolytic tx recommended if hemodynamically deteriorate, if not UFH then when stable change to DOAC or LMWH **note UFH is short acting thus easily reversible, if not consider surgical embolectomy

20
Q

list examples of thrombolytics

A

rtPA, streptokinase, urokinase

21
Q

what are the c/i and relative cautions to fibrinolysis

A

c/i: hx of hemorrhagic stroke or stroke of unknown origin, ischemic stroke in prev 6m, surgery/ trauma/ head injury in prev 3w, bleeding diathesis, active bleeding, CNS neoplasm

caution: TIA in prev 6m, OAC, pregnancy or first week post partum, advanced liver disease, infective endocarditis, peptic ulcer, traumatic resuscitation, non compressible puncture sites, refractory HTN (systolic >180)

22
Q

what is the presentation (s/sx) of DVT

A

sx: unilateral, calf or leg swelling, pain or warmth

signs: dilated superficial veins (palpable cord which may be felt in affected leg), homan’s sign (pain in back of knee when examiner dorsiflexes foot of affected leg)

tenderness to the deep calf
edema in leg or ankle
colour changes to the leg

23
Q

what should you consider if there is bilateral presentation

A

HF, chronic venous insufficiency

24
Q

what should you consider if there is sob, chest pain, palpitations

A

check for potential PE

25
Q

how to diagnose DVT

A

well’s score, d-dimer, compression ultrasound (CUS) (relate using flowchart)

26
Q

what are the clinical features and their respective score for the wells-DVT scoring and relate the probabilities to the scoring

A

active cancer (ongoing tx, within prev 6m, palliative) [1]

paralysis, recent plaster immobilisation of lower extremities [1]

bedridden >3d or recent surgery within 4w [1]

localised tenderness along distribution of deep venous system [1]

calf swelling >3cm when comparing to asymptomatic leg (measured below tibial tuberosity) [1]

pitting edema (greater in symptomatic leg) [1]

collateral superficial veins [1]

other diagnosis as likely or more likely than that of DVT [-2]

high probability if score >2
moderate probability if score 1/2
low probability if 0 or less

27
Q

what is CDUS and how would you interpret it

A

compelx duplex ultrasound

a normal vein collapses under compression but if a thrombus is present it becomes incompressible

gold standard to identify where and how extensive the clots are (if more extensive means more proximal)

28
Q

compare the difference between proximal and distal DVT

A

distal DVT is anything below knee while proximal DVT is anything above the knee

29
Q

what is D-dimer a byproduct of

A

fibrinolysis

30
Q

draw out the decision algorithm for acute tx of VTE

A
31
Q

when tx for acute VTE what should you do at 3m (90d) mark

A

repeat US to see if clot still present, if clot present then continue AC but if not consider if the risk factors were provoked or transient, if transient consider stopping or stepping down

32
Q

when tx for acute VTE what should you do at 6m (180d) mark

A

step down DOAC to prophylaxis doses and maintain INR target of 2-3 if using VKA

33
Q

what are the doses of all possible tx regimens for acute tx of VTE

A

PO route: [option 1] apixaban 10mg BD x7d -> apixaban 5mg BD until 6m -> if need extend, apixaban 2.5mg BD
[option 2] rivaroxaban 15mg BD x21d -> rivaroxaban 20mg daily until 6m -> if need extend, rivaroxaban 10mg daily

switching route: UFH/ LMWH x5d -> dabigatran 150mg BD

overlapping route: UFH/ LMWH x5d with VKA until INR >2.0 then dose titrate to target 2.5 INR6

34
Q

how to select anticoagulant for VTE tx based on populations

A

general population: DOAC > VKA, VKA if renal impairment

CrCl <30: VKA overlapping with UFH or VKA overlapping with dose reduced enoxaparin (aka LMWH)

APS: indefinitely VKA with OAC

35
Q

why is monotx using UFH or LMWH not recommended for CrCl <30

A

LMWH is renally excreted thus will accumulate and though UFH have short half life and minimal renal excretion it is impractical for prolonged use

36
Q

what should you monitor if using enoxaparin for >5d

A

anti-Xa monitoring

37
Q

what are the risk factors for recurrence of VTE

A

proximal DVT location, old age, obesity, male sex, early post thrombotic syndrome (PTS) development, persistence of residual vein thrombosis at US, high D-dimer value, non O blood group, potentially inherited thrombophilia

38
Q

what is post thrombotic syndrome (PTS)

A

s/sx of chronic venous insufficiency that develop following DVT

39
Q

what is the choice of anticoagulant for tx of DVT or PE in pregnancy

A

LMWH (SC enoxaparin 1.0mg/kg q12h)

40
Q

what must you take note of when dosing enoxaparin for DVT or PE during pregnancy

A

dosage has to be adjusted according to incr BW

keep to usual tx dosing if >6m bc unclear data for dose reduction during prevention phase

examine for APS in young females with hx of thrombosis and spontaneous abortion

41
Q

what is the use of examining APS in young females with thrombosis and spontaneous abortion

A

to determine OAC for use post partum

if pos APS, use VKA during breastfeeding

if neg APS, use VKA/DOAC

42
Q

relate the different scorings for different types of patients when determining use of VTE prophylaxis

A

for medically ill patients, use padua scoring

for surgical patients, use caprini scoring

for cancer patients, use khorona scoring

43
Q

compare between UFH and enoxaparin for VTE tx, VTE prophylaxis, PCI and labs for monitoring

A

UFH: (mostly not used in SG except for PCI) [PCI] IV 2000-5000u to achieve ACT of 250-300sec and repeat bolus as needed to maintain ACT throughout PCI, if GPIIb/IIIai used, repeat bolus up to 7000u max as needed to maintain ACT throughout PCT, if prev LMWH/ heparin use, check ACT prior and do not initiate if >200sec [labs] aPTT, ACT measured for PCI

enoxaparin: [VTE tx] SQ 1mg/kg q12h, 1mg/kg QD if CrCl <30/ cancer/ pregnant [VTE p] SQ 40mg QD until ambulatory for 10-14d up to 35d, for CrCl 30-60 give SQ 30mg QD, for CrCl <30 give 20-30mg QD [labs] anti-Xa monitoring but only if renally impaired or pregnant

44
Q

compare between DOACs for tx and prevention of VTE (incl renal adjustments)

A

dabigatran: [VTE tx] parenteral for at least first 5d then give 150mg BD [renal adjust] avoid if CrCl <50 and concomitant PGPi [VTE p] when hemostasis achieved, start within 1-4h post op, 220mg QD for 10d (TKR) 28-35d (THR) if CrCl <30, 150mg OM for 10d or 28-35d

rivaroxaban: [VTE tx] 15mg BD for 21d -> 20mg QD up to 6m -> 10mg OM after [renal adjust] avoid if CrCl <30 [VTE p] when hemostasis achieved, start within 6-10h post op, 10mg QD for 14d (TKR ) or 35d (THR)

apixaban: [VTE tx] 10mg BD for 7d -> 5mg BD up to 6m -> 2.5mg BD after [renal adjust] caution if CrCl 15-29, avoid in HD [VTE p] when hemostasis achieved, start within 12-24h post op, 2.5mg BD 10-14d for TKR or 32-35d for THR

edoxaban: [VTE tx] parenteral for at least first 5d then give 60mg QD [renal adjust] if CrCl 30-60 or BW less than 60kg give 30mg QD, do not use if CrCl >95 [VTE p] 30mg QD

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