VTE Anticoagulation!

GUIDELINES! 

Key points from the 2016 CHEST guidelines for venous thromboembolism (VTE) antithrombotic therapy:

  • For patients with VTE who are HDS, the preferred initial treatment is either low-molecular weight heparin (LMWH; e.g. Lovenox/enoxaparin), DOAC, or fondaparinux
    • exception #1: unfractionated heparin (UFH) if unstable, ESRD, or need for quick discontinuation
    • exception #2: LMWH is generally the best initial therapy in pregnancy, coagulopathy, and active cancer (controversial with growing evidence for DOAC)
  • If unstable, give thrombolytics (unless bleeding risk) vs catheter removal
  • For patients without active cancer, the preferred long-term treatment for proximal DVT or PE is a DOAC for 3 months (best alternative is warfarin). 
  • Newer evidence from 2018 supporting DOACs as a reasonable option in patients with active cancer: SELECT-D, Hokusai cancer study

Key points from the 2018 ASH guidelines for VTE prophylaxis (ppx): 

  • Pharmacologic ppx > Mechanical ppx > No ppx

PEARLS!

  • Hospitalization and nursing home residency accounts for ~60% of all VTE events!
  • Efficacy of ppx in hospitalized medical pts is controversial 
  • There are MANY risk factors for VTE, but there is no consensus on how to predict a pt’s overall risk. One potential tool is the Padua Prediction Score (endorsed by the American College of Chest Physicians)
  • Always assess a patient’s bleeding risk before starting a heparin product. Use a tool like IMPROVE to estimate bleeding risk 
    • Key point: the HAS-BLED score assesses bleeding risk in pts with afib on anticoagulation (AC)
  • LMWH vs UFH: LMWH has fewer thrombotic complications, improved thrombus regression, decreased rates of major hemorrhage, and non-significant reduction in mortality (Cochrane review 2017)
  • Warfarin paradoxically leads to hypercoagulability initially because of its rapid effect in lowering protein C levels, which is one theoretical mechanism behind warfarin-induced skin necrosis.
  • MKSAP pearl: Factor 7 has the shortest half-life of the vitamin K-dependent coagulation factors (2, 5, 7, 8, 9, and 10). So, when starting warfarin, low levels of factor 7 lead to an elevated INR that does NOT reflect protective AC because the other coagulation factors are still active. Thus, for VTE, warfarin must be administered with parenteral AC generally for the first 5 days regardless of the INR. 
  • In some patients on warfarin with fluctuating INRs, daily supplementation with low-dose vitamin K can actually stabilize the INR!

COVID & CLOTS! 

There are reports of high incidence of VTE, particularly PE, in COVID pts with critical illness, in whom D-dimer tends to be very high. But D-dimer is tough to interpret because initial clinical findings from China showed elevated D-dimer >500 in 46% of pts overall (43% of non-severe pts and 59% of severe pts).

The International Society of Thrombosis and Hemostasis (ISTH) and JACC offer interim guidance on recognition and management of coagulopathy in COVID.

A hematologist at UVM discusses her hospital’s approach in an ACP interview.


QUESTIONS TO PONDER!

  • What’s the difference between subcutaneous and IV heparin?
  • For unprovoked VTE, how long should we continue AC?
  • Do we always need to give a loading dose when starting a heparin gtt? 
  • When, if ever, should we use an IVC filter?
  • What are indications for warfarin? What AC treatment should patients be on if they have APLS?
  • What labs should we check (and how often) when a patient is on a heparin gtt? 
  • When should we worry about HIT? Are we testing for it too much?
  • How does kidney disease impact our choice of VTE ppx? What about obesity?
  • Does antiplatelet therapy (e.g. ASA, clopidogrel) reduce risk of VTE?