VTE Flashcards

1
Q

What is the mortality risk of PESI class 1 and 2?

A

30-day mortality of 0-1.6% and 1-3.6% respectively

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2
Q

What is the mortality risk of sPESI?

A

30-day mortality of 1.0% and 1.1% respectively for low risk and 9.6% for high risk

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3
Q

What is the sPESI?

A

Age >80 years
active Cancer/undergoing treatment
Chronic cardiopulmonary disease
Pulse ≥110 bpm
Systolic BP < 100 mmHg
oxygen saturation < 90%

‘High risk’ if you score 1 or more

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4
Q

What is the full PESI?

A

Age in years
Male sex +10
Cancer +30
Heart failure +10
Chronic lung disease +10
Pulse ≥ 110 bpm +20
Sys BP < 100 mm Hg +30
RR ≥ 30/min +20
Temp < 36°C +20
Altered mental status +60
oxygen sats < 90% +20

I: very low ≤65
II: low 66–85
III: intermediate 86–105
IV: high 106–125
V: very high ≥126

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5
Q

Hestia criteria?

A

haemodynamically unstable?
Is thrombolysis or embolectomy necessary?
Active bleeding or high risk?
>24 hours of oxygen to maintain saturation >90%?
PE diagnosed during anticoagulant treatment?
Needing intravenous pain medication for >24 hours?
Medical or social reason for treatment in hospital >24 hours?
Does the patient have a CrCl <30?
Does the patient have severe liver impairment?
pregnant?
documented history of HIT?

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6
Q

Do cancer patients need to be managed as IP?

A

Not if they do not forfil Hestia criteria

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7
Q

Wells score for DVT?

A

Active cancer 1
immobilisation of leg 1
bedridden for >3 days, or major surgery in 12 weeks 1
tenderness along deep venous system 1
Entire leg swollen 1
Calf swelling >3 cm larger 1
Pitting oedema to leg 1
Collateral veins 1
Previous DVT 1
alternative diagnosis likely -2

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8
Q

Wells score for PE?

A

signs and symptoms of DVT 3
alternative diagnosis is less likely than PE 3
Heart rate > 100 1.5
Immobilisation >3 days or surgery last 4 weeks 1.5
Previous DVT/PE 1.5
Haemoptysis 1
Malignancy 1

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9
Q

What anticoagulation can be used in a Patient with an eGFR of 15-50?

A

apixaban
rivaroxaban- caution if 13-29

LMWH for at least 5 days followed by:
edoxaban (dose adjust to 30mg OD - <60kg guidance)
dabigatran - >30

LMWH or UFH, with VKA for at least 5 days or until INR i>2.0 in 2 consecutive readings

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10
Q

What anticoagulation can be used in a Patient with an eGFR of <15?

A

LMWH or UFH, with VKA for at least 5 days or until INR i>2.0 in 2 consecutive readings

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11
Q

Which is the most cost effective DOAC?

A

Apixaban- lowest bleeding risk
2nd is rivaroxiban (slightly higher bleeding risk)

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12
Q

Is fondaparinex used?

A

No. increased bleeding risk

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13
Q

For high risk patients that do not want to take anticoag long term what can you offer?

A

Aspirin 75-150mg/day LT

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14
Q

When is Apixaban and rivaroxiban contraindicated?
HINT think foods

A

lactose allergy- contains cows milk

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15
Q

When do you offer IVC?

A

if anticoag is CI
VTE if already on treatment dose

NEED TO PLAN REMOVAL AT THE SAME TIME

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16
Q

what are the strong risk factors for VTE?

A

Fracture of lower limb
Hospitalization for HF or AF
(within 3 months)
Hip or knee replacement
Major trauma
MI (within 3 months)
Previous VTE
Spinal cord injury

17
Q

what are the moderate risk factors for VTE?

A

Arthroscopic knee surgery
Autoimmune diseases
Blood transfusion
Central venous lines, Intravenous catheters and leads
Chemotherapy
Congestive HF or resp failure
Epo-stimulating agents
HRT (depends on formulation)
IVF
Oral contraceptive therapy
Post-partum period
Infection (specifically pneumonia, urinary tract
infection, and HIV)
Inflammatory bowel disease
Cancer (highest in met disease)
Paralytic stroke
Superficial vein thrombosis
Thrombophilia

18
Q

what are the weak risk factors for VTE?

A

Bed rest >3 days
Diabetes mellitus
Arterial hypertension
Immobility due to sitting (e.g. car or air travel)
Increasing age
Laparoscopic surgery (e.g. cholecystectomy)
Obesity
Pregnancy
Varicose veins

19
Q

In acute PE, What percentage of the the arterial bed is occluded before you get raised PAP?

A

> 30-50% of the total cross-sectional
. area of the pulmonary arterial bed

20
Q

How does PE induce vasoconstriction?

A

release of thromboxane A2 and serotonin contributes to the initial increase in PVR after PE. Anatomical obstruction and hypoxic vasoconstriction in the affected lung area lead to an increase in PVR, and a proportional decrease in arterial compliance

21
Q

Why do patients arrest in PE?

A

abrupt increase in PVR results in RV dilation, which alters the contractile properties of the RV.
The increase in RV pressure and volume leads to an increase in wall tension and myocyte stretch. contraction time of RV is prolonged, while neurohumoral activation leads to inotropic and chronotropic stimulation.
Together with systemic vasoconstriction, these compensatory mechanisms increase PAP, improving flow through the obstructed pulmonary vascular bed and
thus temporarily stabilizing systemic BP.
However, the extent of immediate adaptation is limited, as a non-preconditioned, thin-walled RV is unable to generate a mean PAP>40 mmHg.

22
Q

What is the early mortality risk in a patient with an acute PE with no haem instability, sPESI >1 and high trop?

A

intermediate low

23
Q

What is the early mortality risk in a patient with an acute PE with no haem instability, sPESI >1, RVSD on echo and high trop?

A

intermediate high

24
Q

How does dabigatran work?

A

inhibits thrombin

25
Q

How does apixaban/rivaroxiban work?

A

inhibits factor Xa