Deep Vein Thrombosis and Pulmonary Embolism

Question 1

How is DVT (deep vein thrombosis) presenteed? (signs and symptoms)

Answer 1

Often in leg, so often with a red (erythema) hot, swollen (unilateral pitting oedema), painful/tender leg. May also have prominent collateral veins and may be silent!

Question 2

How is DVT investigated?

Answer 2

Clinical assesment,

Well’’s score is used, if scores 2+ then much higher chance of DVT and skips straight to a doppler ultrasound scan, whereas with a score of only 1 then will have a D-Dimer test, which, if negative will rule out dvt for the minute.

If Ultrasound negative then D Dimer test is needed in which case if positive the ultrasound is repeated in another 7 days. If ultrasound and negative d dimer then rule out dvt for now

Question 3

What is the management of a DVT

Answer 3

Anticoagulation (and vascular surgical intervention/removal if bad enough)- can use thrombolytic agent such as alteplase.

Anticoagulation options:

Enteral:

• DOACs (factor 10A inhibitors: Rivaroxaban, Apixaban, edoxaban. Direct thrombin inhibitors dagigatran) -not as effective in some hypercoaguable states
• Warfrin - used less now, however, some sigificantly obese patients and patients with other comorbidities may require warfrin despite its pitfalls (close monitoring etc)

Parenteral (injected):

• Low molecular weight heparin (eg dalteparin, enoxaparin, tinzaparin 10a inhibitors, better than warfrin for patients with malignancy etc)
• unfractionated heparin - usually for thoser people with impaired renal function (GFR less than 30)

Question 4

What is the presentation of a pulmonary thromboembolism?

Answer 4

Pleuritic chest pain, 
Dyspnoea
Haemoptysis
Tachycardia
Pleural rub

severe:
sudden severe dyspnoea
collapse
cyanosis
low bp
raised JVP

Sudden death

Question 5

How are pulmonary thromboembolisms investigated?

Answer 5

Again, simelar to the DVT.

Wells score (different scoring tho, 4.5+ is much more likely to have a PE). If high risk then imaging is done (CT pulmonary angiogram/ventilation/perfusion scan) if low risk then D dimer is done. If D dimer is positive then scan, if scan is negative then d dimer.

Question 6

How are pulmonary thromboembolisms managed?

Answer 6

V simelar:

Anticoagulation (and vascular surgical intervention/removal if bad enough)- can use thrombolytic agent such as alteplase.

Anticoagulation:
** Given for 3 months if provoked cause of PE eg from thromboembolism due to broken leg, or considered life long in unprevoked due to high risk of recurrance **

Enteral:

• DOACs (factor 10A inhibitors: Rivaroxaban, Apixaban, edoxaban. Direct thrombin inhibitors dagigatran) -not as effective in some hypercoaguable states
• Warfrin - used less now, however, some sigificantly obese patients and patients with other comorbidities may require warfrin despite its pitfalls (close monitoring etc)

Parenteral (injected):

• Low molecular weight heparin (eg dalteparin, enoxaparin, tinzaparin 10a inhibitors, better than warfrin for patients with malignancy etc)
• unfractionated heparin - usually for thoser people with impaired renal function (GFR less than 30)

Question 7

WHat is a thrombus?

Answer 7

A blood clot where it’s not supposed to be, due to intravascular coagulation of blood. Comprised of fibrin, platelets and rbc

Question 8

WHat is an embolism?

Answer 8

A thrombus on the move, has broken free and can now clog up somewhere else

Question 9

What is the difference between haemostasis and thrombus

Answer 9

Haemostasis is there to stop a bleed, wheras a thrombus isn’t there for a good reason.

Question 10

How is fibrin formed?

Answer 10

Tissue factor X and Xa (produced directly eg damage to endothelium or indirectly though clotting cascade) causes prothrombin to change to thrombin, and thrombin causes fibrinogen to form fibrin

Question 11

Virchows triad? wth eg

Answer 11

Stasis, hypercoacgubility and endothelial damage are the three factors.

Stasis eg. long haul flight, immobility

Hypercoagubility eg pregnany, cancer, sepsis (inflammation, releases inflammatory markers etc)

Endothelial damage/dysfunction: damage eg catheters, trauma, surgery. Dysfunction eg hypertension, smoking, high cholesterol

Question 12

Arterial vs venous blood clots

Answer 12

Arrterial clot usually due to rupture of atherosclerotic plaque eg acute coronary artery syndrome, causes ischaemia and infarction, more white due to more platelets and fibrin.

, venous usually due to virchows triad, stasis and hypercoagulability, causes pack pressure. Usually more red due to more red blood cells.

Question 13

How deos a dvt lead to infarction and ischaemia?

Answer 13

Can lead to infarction and ischaemia if severe enough as can compress other vessels etc.

Question 14

What is a thromboembolism?

Answer 14

A thrombus that has embolised and got stuck somewhere.

Question 15

WHich tumour can especially lead to thromboembolims?

Answer 15

Renal cell tumous as they have a tendancy to grow up the IVC

Question 16

men or women risk less of dvt

Answer 16

women slightly more risk

Question 17

1/5 peeps with a dvt will have a pe t/f?

Answer 17

t

Question 18

dvt 1/100000 t/f?

Answer 18

False, actually 1/1000

Question 19

What is the leading cause of direct maternal death in the uk?

Answer 19

Venous Thromboembolism

Question 20

Untreated PE death rate?

Answer 20

30%

Question 21

Main risk factors for vte?

Answer 21

Surgery (any form of immobility inc. prolonged hospital stays)
Any form where will be hypercoaguable (eg cancer)
Lower limb issues eg fracture/varicose veins
Previous VTE
Obstresticks (late pregnanacy, c section, peureperium)

Question 22

Prevention of vte in hospital

Answer 22

Early mobilisation
compression stockings or even ones which inflate to help return venous blood (mechanical thromboprophylaxis)
Pharmalogical thromboprophylaxis (eg heparins!)

Question 23

What is the Wells score for dvt?

Answer 23

For DVT then 2 or more (high risk) and above means that a scan should be done (compression ultrasound), if 1 (low risk) then d-dimer

Question 24

What is D Dimer?

Answer 24

It is a product of the breakage down of a clot. If a clot is there the body is constantly trying to break it down, with the fibrinilytic agents in the blood, this produces products called D-dimers which can be measured and higher levels would therefore indicate a dvt/pe/clot.

Very sensitive but not specific, so a positive result does not necessarily mean a DVT/PE however, a negative result can be used to rule one out (for the moment)

Question 25

What is alteplase?

Answer 25

A synthetic version of the body’s fibrinilytic agent

Question 26

What is the sensitivity and specificty of d dimer in vte?

Answer 26

Highly sensitive but not specific (a positive result isn’t necesarrily a result of a DVT/PE as it could be due to other things eg inflammation/infection can cause activation of the clotting cascade, which can cause high d dimer result)

Question 27

How is PE diagnosed?

Answer 27

If patient high risk then (Wells 4.5+) then a scan is used eg CT pulmonary angiogram/ventilation-perfusion scan to look for a PE.

If patient is low risk then a D Dimer test is done

(need 2 negative tests to rule out (wells/D-dimer/scan)

Question 28

Wells score PE

Answer 28

4.5+ = high risk

4 and below is low risk

Question 29

What 2 negative tests do you need to discard pe/thromboembolisms

Answer 29

1st check is Wells.

If Wells is negative then you need a negative D DImer
If Wells is positive then you need a Negative Scan AND a negative D Dimer

Question 30

treatment length with and without known 1 off cause for dvt

Answer 30

If temporary cause eg following hip replacement then treatment is for 3 months and then checked and if D dimer is low enough can be taken off anticoagulation

If not knwon tempoary cause then life long anticoagulation is considered as there is a higher risk from a repeat thromboembolism then from the effects of the anticoagulation

Question 31

How do we chekc for malignancy?

Answer 31

Not routineely done, 1/10 to 1/5 people presenting with Thromboembolism willlikely be diagnosed with cancer in the following 12 months, however screening has shown to have little/no chnage in the outcome.

This being said, always dip urine to check for renal malignancy and do blood lft test and chest x ray.

Question 32

VTE anticoagulation treatment options and acting places

Answer 32

Enteral:

• DOACs (factor 10A inhibitors: Rivaroxaban, Apixaban, edoxaban. Direct thrombin inhibitors dagigatran) -not as effective in some hypercoaguable states
• Warfrin (vit K inhibitor)- used less now, however, some sigificantly obese patients and patients with other comorbidities may require warfrin despite its pitfalls (close monitoring etc)

Parenteral (injected):

• Low molecular weight heparin (eg dalteparin, enoxaparin, tinzaparin 10a inhibitors, better than warfrin for patients with malignancy etc)
• unfractionated heparin - usually for thoser people with impaired renal function (GFR less than 30)

Question 33

wHEN is a vasc surgeon involved and what do thye do?

Answer 33

Massive DVTs, can take them out/break them dwn with alteplase through catheters

Question 34

Long term consequences of DVT

Answer 34

Post Thrombotic Syndrome
Damage to venous valves
Incidence of 20-60% within 2 years of DVT

Swelling
Discomfort
Pigmentation
Ulceration in severe form

Question 35

Long term consequences of PE

Answer 35

Most recover fully
Pulmonary arterial hypertension
Serious outcome 4% patients (< 1/20)

Question 36

If you can see varicose veins in the leg then is there a dvt?

Answer 36

No