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PR3154 > DVT > Flashcards

DVT Flashcards

1
Q

DVT –> PE pathogenesis

A

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)

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2
Q

mechanism to control coagulation (hemostasis)

A
  • 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

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3
Q

mechanism in fibrinolytic system

A

tissue plasminogen activator (tPA) converts
plasminogen –> plasmin

degrades fibrin mesh
produced D-Dimer as by-pdt

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4
Q

Virchow’s triad for VTE

A

1) hypercoagulability (blood)
2) vascular damage (vessel)
3) circulatory stasis (flow)

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5
Q

hypercoagulability

A

BLOOD

major surgery
malignancy
preg (post partum)
thrombophilia
infection, sepsis
IBD
autoimmune conditions

estrogen therapy (COC, tamoxifen, HIT)
inflamm
dehydration

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6
Q

vascular damage

A

VESSEL

thrombophlebitis
cellulitis
atherosclerosis

catheter/ heart valve
venepuncture

physical trauma, strain, injury
microtrauma to vessel wall

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7
Q

thrombo-embolism process

A

calf source: unlikely to embolise

above knee source: more assoc w/ embolism –> Right Heart –> pul arteriole system

  • can lead to PE
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8
Q

criculatory stasis

A

FLOW

immobility
venous obstruction (obesity, tumor, preg)
varicose veins
Afib, LV dysfunciton

congenital abnormalities affect venous anatomy
bradycardia, low BP

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9
Q

DVT clinical presentation

A

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

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10
Q

wells score COPSBET3

A

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

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11
Q

wells scoring

A

=/>3 : high prob
1,2: mod prob
=/>0: low

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12
Q

wells score 0,1,2

A

1) D-dimer
2) positive –> imaging whole leg/ proximal CUS
3) neg –> rule out DVT

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13
Q

wells score >2 pt

A

1) imaging whole leg/ proximal CUS

2) distal DVT –> anticoag/ surveillance

2) proximal DVT –> initiate anticoag
- risk of embolism

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14
Q

D-dimer meaning

A

good negative predictive value
-ve rules out DVT

but +ve does not mean have DVT, plasmin just breaking down fibrin

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15
Q

distal DVT tx

A

high risk recurrence
- tx: 3mnths AC

low risk recurrence
- 4-6wk AC or venous US surveillance

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16
Q

proximal DVT tx

A

tc: at least 3mnths AC (DOAC if no CI)

3mnths: evaluation venous US

stop/ extended AC – yearly evaluation

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17
Q

AC for DVT (PO)

A

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

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18
Q

renal adj for DOAC

(D,R,A,E)

A

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)

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19
Q

prophylaxis with DOAC (riva)

A

TKR: 10mg OD x 2wk
THR: 5wk

medically ill for 31-39d

20
Q

switch AC for DVT (SC–>PO)

A

UFH, LMWH sc1mg/kg BD, (SC, 5d) –> dabigatran 150mg BD/ Edoxaban 60mg OD

21
Q

renal dose adj for DOAC (that requires sc doses first )

A

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)

22
Q

AC overlap for DVT tx

A

UFH, LMWH, (SC) + warfarin PO daily

(stop sc after =/>5d, INR >2)

23
Q

tx duration for DVT

A

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

24
Q

risk factor for VTE

A
  • to consider need for VTE prophylaxis
    age, prior VTE hist
    blood stasis
    vascular injury
    hypercoagulability
25
Q

VTE prophylaxis for specific grp of pts

A

1) medically ill – Padua risk score
2) surgical pt – Caprini risk score
3) cancer pt – Khorona risk score

26
Q

PE effect

A

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

27
Q

PE clinical presentation

A

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

28
Q

PE diagnosis modified wells criteria

HIPOD HM

HM
DO
100IP

A

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

29
Q

PE scoring modified wells criteria

A

> 6: high prob
2-6: mod prob
<2: low prob

30
Q

PE severity and risk assessment – determines drug choice

high, intermediate low parameters

A

high: haem instable, clinical parameters, RV dysfunction (TTE) , elevated troponin

intermediate:clinical parameters, TTE/ troponin lvls

low: all neg

31
Q

high risk PE tx

A

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

32
Q

thrombolytics used in PE

A

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

33
Q

CI for fibrinolysis

A

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

34
Q

alteplase

tenecteplase: AMI, IV bolus (BW)

A

dosed by BW, infusion

FU and monitor for bleed, BP –> intracranial haemorrhage

alteplase dose:
100mg over 2h/
0.6mg/kg over 15mins (max 50mg)

35
Q

thrombolysis protocol

A

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

36
Q

intermediate - low risk PE tx

A

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

37
Q

why LMWH > UFH

A

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)

38
Q

reperfusion in PE

A
  • rescue thrombolytic therapy recc in haem deterioration on anticaog tx
39
Q

duration of anticaog PE

A

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
40
Q

VTE in preg risk factors

A

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

41
Q

challenges of VTE in preg

A

D-Dimer rises in preg
differential diagnosis (oedema from preg)

42
Q

diagnosis of PE during preg

A

compression proximal US
chest x-ray

43
Q

tx of VTE in preg

A

LMWH, weight base dosing
sc enoxaparin 1mg/kg BD

APS +ve, switch to warfarin during breastfeeding

44
Q

fun facts of DOAC and LMWH

A

rivaroxaban 10mg (prophy) non-MAF

enoxaparin 60, 80mL is graduated at 10mL increments

45
Q

UFH VTE dose

A

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)

46
Q

why UFH is preferred in PE

A

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)
47
Q

enoxaparin VTE doses

A

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

PR3154 (11 decks)

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