Deep Vein Thrombosis and Pulmonary Embolism Flashcards
How is DVT (deep vein thrombosis) presenteed? (signs and symptoms)
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!
How is DVT investigated?
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
What is the management of a DVT
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)
What is the presentation of a pulmonary thromboembolism?
Pleuritic chest pain, Dyspnoea Haemoptysis Tachycardia Pleural rub
severe: sudden severe dyspnoea collapse cyanosis low bp raised JVP
Sudden death
How are pulmonary thromboembolisms investigated?
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.
How are pulmonary thromboembolisms managed?
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)
WHat is a thrombus?
A blood clot where it’s not supposed to be, due to intravascular coagulation of blood. Comprised of fibrin, platelets and rbc
WHat is an embolism?
A thrombus on the move, has broken free and can now clog up somewhere else
What is the difference between haemostasis and thrombus
Haemostasis is there to stop a bleed, wheras a thrombus isn’t there for a good reason.
How is fibrin formed?
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
Virchows triad? wth eg
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
Arterial vs venous blood clots
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.
How deos a dvt lead to infarction and ischaemia?
Can lead to infarction and ischaemia if severe enough as can compress other vessels etc.
What is a thromboembolism?
A thrombus that has embolised and got stuck somewhere.
WHich tumour can especially lead to thromboembolims?
Renal cell tumous as they have a tendancy to grow up the IVC
men or women risk less of dvt
women slightly more risk
1/5 peeps with a dvt will have a pe t/f?
t
dvt 1/100000 t/f?
False, actually 1/1000
What is the leading cause of direct maternal death in the uk?
Venous Thromboembolism
Untreated PE death rate?
30%
Main risk factors for vte?
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)
Prevention of vte in hospital
Early mobilisation compression stockings or even ones which inflate to help return venous blood (mechanical thromboprophylaxis) Pharmalogical thromboprophylaxis (eg heparins!)
What is the Wells score for dvt?
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
What is D Dimer?
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)
What is alteplase?
A synthetic version of the body’s fibrinilytic agent
What is the sensitivity and specificty of d dimer in vte?
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)
How is PE diagnosed?
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)
Wells score PE
4.5+ = high risk
4 and below is low risk
What 2 negative tests do you need to discard pe/thromboembolisms
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
treatment length with and without known 1 off cause for dvt
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
How do we chekc for malignancy?
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.
VTE anticoagulation treatment options and acting places
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)
wHEN is a vasc surgeon involved and what do thye do?
Massive DVTs, can take them out/break them dwn with alteplase through catheters
Long term consequences of DVT
Post Thrombotic Syndrome
Damage to venous valves
Incidence of 20-60% within 2 years of DVT
Swelling
Discomfort
Pigmentation
Ulceration in severe form
Long term consequences of PE
Most recover fully
Pulmonary arterial hypertension
Serious outcome 4% patients (< 1/20)
If you can see varicose veins in the leg then is there a dvt?
No
