Check out our ICEM poster on this.
So, I see this old chestnut is under discussion again. A couple of us from the EmergINg team brought a poster to ICEM on this very topic. Sure you’ll all degree it’s another thorny VTE question well worthy of discussion.
In keeping with Rick and Simons previous posts, this is a decision very much about risk. I have a young fit man with a clinical thrombophlebitis to the Long Saphenous Vein (LSV). It’s a bit sore, but he is well and has no overt risk factors for VTE. Do I bash out some NSAIDS and tell him that we’ve been ignoring these for ages, it will probably go away? Or do I try and maximise information through USS then go through the risks and benefits of differing treatment strategies?
The initial step to scan is an important one in my opinion. A lot of these will be associated with distally propagating calf DVT. Once you are in the axial deep calf veins then there is an increasing risk that at least warrants serial USS. These calf DVTs can be silent if the Superficial Venous Thrombosis (SVT) is distractingly sore. Secondly, a scan can delineate the extension of the SVT and help you assess risk further. Is it >5cm for example, in which case the new American guidelines would recommend 45 days prophylactic dose Fonda/LMWH . Is it tiny and chronic? Does it go all the way up to the Sapheno Femoral Junction (SFJ), in which case a vascular surgeon may be interested in acutely tying off the vessel. The scan really helps and reassures the patient that you are taking their symptoms seriously.
Next comes the discussion regarding risk. Both of conservative and aggressive management. In the CALISTO study 1500 patients were treated conservatively for SVT and had a composite endpoint event rate of 5.9%. The Number Needed to Treat (NNT) with Fondaparinux would therefore be 20. Pretty good. But what actually made up the composite outcome?
Only 5 patients out of 1500 in the conservative group developed a PE (0.2%). Only 18 patients developed a DVT (1.2%). The majority of outcome events were made up of propagation within the superficial veins or recurrence. So you may not be doing quite as much good as you think you are with treatment. Also, any anticoagulant treatment of course carries a risk of bleeding. 1% in the Fonda group for any bleeding in this trial, which is likely to be more aggressively monitored than in the real world on more compliant patients (volunteering for research) and therefore reduced as a consequence. There has also been criticism of the study due to the lack of prescribed NSAIDS/monitoring. Many VTE clinicians wanted to see Fonda/LMWH vs naproxen, not Fonda vs placebo.
The Cochrane review on the topic has been updated to reflect the CALISTO trial results and provides a nice overview of the evidence . But we are left in the realms of uncertainty still. And we haven’t even started talking about cost effectiveness yet… though there is a nice article on this in the jounral CHEST here
“If we don’t treat your disease, the risk of serious clot related illness if probably about 1-2%. It will probably be sore for a while also. If we treat it the risks and symptoms are reduced, but about 1% patients may bleed or have a reaction to the drug. Also, you have to stick yourself daily with a needle for 45 days.”
What do you think? What would you want for your relative? What would you want for yourself? Low levels of risk but with emotive consequences like this are clinical situations where we as EPs need to stop and think carefully. We are often in a rush and used to making quick critical decisions. But in a situation like this one we need to understand the evidence and relay that in understandable terms to the person in front of us.
We are good at this overall. It is a particular skill set of Emergency Medicine. We just need to recognise when to use it and to force ourselves to take the time to do so.
Very interested to know what the world is doing about these where you are. Let us know and shout out if you feel strongly one way or the other.
1 thought on “Superficial Venous Thrombosis: watch and wait or anticoagulate?”
I guess the question we are asking ourselves is do we want to take on board the risk of CAUSING bleeding in 1% of patients by prescribing the low molecular weight heparin that does the harm and doesnt give much benefit, as appose toaccepting the more passive 1-2% complication rate which we’re not really in control over when treating more conservatively.
A potentially catastrophic bleed which we “caused” vs the uninterrupted natural history of the disease process which we didnt cause…..I’