Thrombosis / coagulopathy Flashcards
Venous thromboembolism
Pathophys VTE:
- Virchow’s triad. A major theory delineating the pathogenesis of venous thromboembolism (VTE), often called Virchow’s triad [3,4], proposes that VTE occurs as a result of:
●Alterations in blood flow (ie, stasis)
●Vascular endothelial injury
●Alterations in the constituents of the blood (ie, inherited or acquired hypercoagulable state)
Superficial vein thrombosis:
- Superficial vein thrombosis (SVT), a less severe disorder than deep vein thrombosis (DVT), occurs in both inherited and acquired thrombophilic states and may progress to DVT and/or pulmonary embolism (PE)
Deep vein thrombosis:
- Proximal DVT is one that is located in the popliteal, femoral, or iliac veins. Anticoagulation is indicated for all patients with proximal DVT and select cases of distal DVT (below knee). anticoagulation is indicated in most patients with symptomatic isolated distal DVT, provided the risk of bleeding is low
Acquired “provoking” risk factors for VTE:
Transient risk factors:
● Immobilisation for >or=3days in the preceding month
● prolonged air travel (flight) >12hours duration
●Hospital admission in the past three months
●Major Surgery under GA >30mins in the preceding month
● pregnancy
● acute Infection in the past three months – 34% cases
● lower limb plaster cast
● exogenous oestrogen (OCP, HRT)
● direct leg trauma
Persistent risk factors:
● Malignancy in the past three months – 34% cases. Patients with cancer often have a hypercoagulable state due to the production of substances with procoagulant activity (eg, tissue factor and cancer procoagulant).
● Myeloproliferative disease
● Antiphospholipid syndrome
● Thrombophilia and inherited hypercoagulable states:
- Factor V Leiden mutation
- Prothrombin gene mutation
- Protein S deficiency
- Protein C deficiency
- Antithrombin deficiency
- Factor XII deficiency — Factor XII, Hageman factor
● Collagen vascular disease
Wells criteria for PE (refer to image):
- symptoms of DVT
- other diagnosis is LESS likely than PE
- HR >100
- immobilised >or=3days or surgery in prior 4wks
- phx VTE
- haemoptysis
- malignancy
Diagnostic algorithm:
- Pre-test probability
- D-Dimer
- CTPA (if haemodynamically stable)
- Whether or not patients with subsegmental PE should be anticoagulated is controversial, but anticoagulated if patient is symptomatic or infarct present
- beside TTE (if unstable): assess for right ventricle enlargement/hypokinesis, regional wall motion abnormalities that spare the right ventricular apex [McConnell’s sign], or visualization of clot
Management –> Anticoagulation
- initial stabilisation/management
- IVFT, oxygen (aim spO2 >90), inotropes (noradrenaline)
- Thrombolysis if signs of haemodynamic compromise inc: sBP <90mmHg for period of >15minutes or evidence of shock.
- Embolectomy if thrombolysis contraindicated or unsuccessful and there is ongoing haemodynamic compromise
- LMWH (clexane) or unfractionated heparin if haemodynamically stable
- Provoked PE:
- transient risk factors
- Treated for duration of 3months on maintenance warfarin or DOAC
- risk of recurrence is 1% in first year after ceasing anticoagulant, 0.5% per year after
- Unprovoked PE or persistent risk factors
- Up to 6 or 12months vs Indefinite anticoagulation due to higher risk of recurrence at 10% in the first year after stopping anticoagulant, and 5% per year thereafter
- If a patient with an unprovoked PE elects to discontinue anticoagulation, routine follow-up and serial D-dimer testing at 2-3 weeks and then again at 1-2 months after stopping treatment are recommended. If D-dimer elevated, should advise ongoing anticoagulation.
- If patients with unprovoked PE elect to discontinue anticoagulant treatment entirely, the use of aspirin 81 mg daily may be benefical in reducing major vascular events by about one-third compared with placebo, but aspirin does not reduce the recurrence of PE. Thus, it is important to counsel patients that the use of oral anticoagulants versus aspirin alone reduces the risk of recurrent VTE by approximately 81-92%.
- Absolute contra-indications for anticoagulation: recent surgery, hemorrhagic stroke, active bleeding
- IVC filter to be considered if anticoagulation contraindicaated
Risk assessment tools for recurrent VTE after stopping anticoagulation:
- HERDOO2 rule: points assigned for ongoing signs of DVT, high D-dimer levels whilst anticoagulated, BMI >or=30, age >or=65
- DASH prediction score: points assigned for high d-dimer 1month after stopping anticoagulant, age <or></or>
<p>- Vienna Prediction Mode: poinst assigned according to nomogram based score</p>
<p><strong>Risk factors for bleeding on anticoagulation:</strong></p>
<p>Low risk with 0 factors; mod risk 1 factor, high risk >or=2 factors:</p>
<p>- elderly</p>
<p>- history of bleeding</p>
<p>- cancer</p>
<p>- CKD</p>
<p>- liver disease</p>
<p>- thrombocytopenia</p>
<p>- previous stroke</p>
<p>- concurrent antiplatelet</p>
<p>- alcohol abuse</p>
<p> </p>
<p><strong><a>https://www.thanz.org.au/documents/item/414</a> guidelines from the Thrombosis and Haemostasis Society of Australia and New Zealand for the diagnosis and management of venous thromboembolism</strong></p>
<p>https://www.acc.org/latest-in-cardiology/articles/2019/03/22/07/45/duration-of-anticoagulation-post-pe#:~:text=Unprovoked%20or%20Persistent%20Risk%20Factors&text=As%20long%20as%20patients%20with,PE%20or%20persistent%20risk%20factors.</p>
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Disseminated intravascular coagulopathy
Thrombocytopenia is a common complication of severe infections, due to platelet consumption in disseminated intravascular coagulation (DIC) or bone marrow suppression from infection. Patients with DIC may also have bleeding (eg, oozing from catheter sites). Unlike most cases of HIT, DIC is associated with abnormal coagulation studies (eg, prolonged prothrombin time [PT] and activated partial thromboplastin time [aPTT], low fibrinogen, elevated D-dimer). Unlike HIT, infection-associated thrombocytopenia is often accompanied by other signs of bone marrow suppression (eg, anemia, leukopenia, decreased bone marrow megakaryocytes).
Tranexamic acid
Tranexamic acid is a synthetic derivative of the amino acid lysine and binds the 5 lysine binding sites on plasminogen. This inhibits plasmin formation and displaces plasminogen from the fibrin surface. It may also directly inhibit plasmin and partially inhibit fibrinogenolysis at higher concentrations.
