34. Venous Thromboembolism Flashcards
How does a venous thrombi differ from an arterial thrombi?
List types of venous thromboembolism.
Where does most DVT occur and why?
Venous: “red clots” - red cells in fibrin mesh. Arterial: “white clots” - platelets and fibrin
DVT (distal - calf, proximal - popliteal vein and up), PE (most arise from DVT, 3rd most common cause of CDV death), venous thrombosis at other sites e.g. axillary vein, other causes e.g air, amniotic fluid
Calf venous sinuses, lack muscle wall and rely on external pressure for blood flow. May occlude vessel and cause symptoms or break off and travel up venous system -> pulmonary arteries.
What are the causes of VTE (i.e. why do blood clots occur)?
What are some risk factors for VTE?
Virchow’s triad: reduced blood flow (stasis), vessel wall disorder, hypercoagulability (sticky)
NB: VTE can be heritable
Strong RF: hip/pelvis fracture, hip/knee replacement, major surgery/trauma, SC injury, hospilisation
Moderate RF: previous VTE, cancer, CCF, pregnancy, pil/HRT, central venous line, IBD
Weak RF: bed rest >3 days, travel, obesity, varicose veins
What is this condition?
DVT
What is the presentation of DVT?
Why is objective diagnosis (measurable) of DVT important?
What are some differential diagnoses of DVT?
Pain, erythema, tenderness, swelling, palpable cord, warmth, ipsilateral oedema, superficial venous dilation
75% of suspected negative, and drugs used to treat cause serious/fatal SEs.
Ruptured Baker’s Cyst, cellulitis, lymphodema, musculo-tendinous - trauma etc. , CCF
How would you diagnose DVT?
1) clinical pre-test probability e.g Well’s score: >2: DVT likely. <1: DVT unlikey.
2) D-dimer: blood test for non-specific marker of fibrin formation (usually raised in VTE but also in cancer, inflammation, post op and pregnancy)
3) radiological assessment: usually compression ultrasound. Sometimes venography (gold std). Or CT, MR
What are some complications of DVT?
PE, clot extension, recurrent DVT, post-thrombotic syndrome: chronic or intermittant, recurrent pain and swelling in leg, may progress to local skin pigmentation and ulceration. Due to venous hypertension and abnormal microcirculation.
What is this condition?
Post-thrombotic syndrome
What does PE clinical presentation depend on?
What are the signs and symptoms of PE?
What preliminary investigations would you do?
Embolus size and cardiopulmonary reserve.
Signs: tachypnoea and tachycardia, crepitations, clinical signs of DVT.
Symptoms: breathlessness, pleuritic chest pain, hypotension, haemoptysis (cough blood)
ECG (may be normal or show tachycardia or pattern of R ventricle strain with T wave inversion), CXR (may be normal or small pleural effusion, focal oligaemia (reduction of blood vol)), arterial blood gases (often normal, hypoxia, low CO2)
PIC: T wave inversion in anterior leads, S1Q3T3 pattern:
What are some differential diagnoses for PE?
What are some diagnostic tests for PE?
What can you use to predict probability of PE?
Pneumonia, bronchitis, asthma, COPD exacerbation, anxiety, pneumothorax, aortic dissection, lung cancer, pericardial tamponade
CT pulmonary angiogram (CTPA) -24/7, isotope lung scan (V/Q scan) - inhale isotope - should be same on both sides, planar or SPECT, echocardiogram, pulmonary angiogram (gold std), leg ultrasound, D-dimer
Well’s score (>4 PE likely, <4 unlikely)
Pic: CTPA showing clot in L pulmonary artery
When is acute PE high risk?
What is the prognosis for PE?
If systolic BP <90mmHg; if shock/hypertension -> CT angiography immediately. If pt shocked = thrombolysis. If not high risk, assess clinical probability.
If treated, mortality <5%. Most deaths from associated comorbidities.
What is the management outline for VTE?
1) send of blood tests for DVT/PE suspects: FBC, clotting screen, D-dimer, Us and Es.
2) Check clotting normal, start heparin if DVT/PE likely (normally LMWH)
3) confirm diagnosis
4) continue heparin and start warfarin
5) Stop heparin after minimum 5d and when INR 2-3 for 2 consecutive days
6) Continue warfarin and ensure monitoring arrangements - reviewed at 3m
* NB: Anticoagulants prevent extension and recurrent - Not thrombolytic clot busters*
What are the 2 types of heparin (and 3rd v. similar type)?
1) unfractionated (UFH), IV or subcutaneous, immediate onset, short t1/2 (60-90mins), monitor by APTT, can reverse it with protamine
2) LMWH, agent of choice, safer than UFH, more predictable response, subcutaneous administration, longer t1/2 (4h), predominantly anti Xa effect, no monitoring, easier to use than UFH (but still used where reversal of effect imp, or hypotensive)
3) Fondaparinux. Synthetic pentasaccharide, t1/2 18h, fixed dose, suitable if renal impairment. Catalyses inhibition of Xa only.
How does heparin work?
What are the SEs of heparin?
Binds to enyme inhibitor antithrombin III, which inactivates thrombin and Xa and other proteases. Stabilises interaction between thrombin and AT III by 1000x to inhibit clotting.
Major bleeding (1-5% in 1st week), heparin-induced thrombocytopenia (HIT) - high risk of thrombosis, requires discontinuation of all heparin, osteoporosis, necrosis at skin injection site (pic)
What is warfarin and how does it work?
What are the SEs?
Vit k antagonist (prothrombin (FII), VII, IX, X, protein C and S), oral administration, long t1/2 (36h), delayed onset of action b/c affects sysntheis. Dose adjusted to maintain INR 2.0-3.0,
Multiple drug interactions, warfarin-induced skin necrosis, risk to foetus, major bleeding risk (then stop warfarin and consider oral vit k, or prothrombin concentrate if need rapid reversal).
What are the ‘new anticoagulants’?
Any disadvantages?
Work immediately, oral, less interaction with other drugs, easier to use, direct thrombin inhibitor e.g. dabigatran, ones with x in e.g. rivaroxiban inhibit Xa. Start oral e.g. rivaroxiban or apixaban with no heparin but with dabigatran and edoxaban give heparin for 5 days then direct switch.
Partly eliminated by kidneys so not good for pts with severe renal dysfunction.
