I recently saw a controversial tweet arguing against tx of chronic clot and restricting tx SOLEY to the CFV/iliac. While I agree (for the most part)- data is limited. At the end of the day we care about the pt, and not every pt is the same! Case➡️
It’s important to recognize the lesions that can form after a clot:
Spurs/Webs
Rokitansky/NIVL/fibrosis
Your pts CEAP >5 always consider for non thrombotic obstructions! Consider #IVUS if things don’t fit!
3/ Clot is in a constant state of evolution. #Fibrin—> #Collagen.
Unfortunately many patients present in the subacute or late phase of #clot development which hinders many of our treatment approaches.
7️⃣days- 20% collagen
1️⃣5️⃣ days- 50% collagen
2️⃣1️⃣days- 80% (!!) collagen
3/ When to tx?
In a rare subset of patients with CFV junction or deep femoral clot symptoms sometimes are not controlled with conservative management. I’ve noticed this more in my orthopedic patient that continue to suffer from limited mobility post event. SYMPTOMS MATTER
5/ Young
These Pts often are placed on OAC and due to limited mobility the amount of PTS I’ve seen is somewhat eye opening. What’s also worrisome is many of these patients are young with no other issues.
My patient: 2 months after DVT, compliant with xarelto
6/ Mobility
Limited mobility reduces their ability to wear/tolerate compression and also just getting them on. Also is the data with compression that good? 😔30-65% of patients will fail compression stockings
Raju S, Hollis K, Neglen P
Ann Vasc Surg. 2007 Nov; 21(6):790-5.
7/ Good study from JAMA on ASYMPTOMATIC patients with SVF/pop DVT post surgery. No difference in PTS if patients with Coumadin. So don’t treat right? jamanetwork.com/journals/jamai…
8/ You have to be able to separate patients in your mind CLINICALLY. The Doppler may be the same but there is a big difference between symptomatic and asymptomatic DVT patients. Does it have to do with reserve? Collateral flow? Developed saphenous system?
(Different case)
9/ Patient case
Young female with knee replacement, complicated by deep femoral (at junction) and significant pain/swelling. Tx conservatively. Pain continues. Doppler 3 months later with continued DVT (now chronic and occlusive). @RadialFirstBot@BotPci@CardioBot@EPeeps_Bot
10/ After discussion with patient and referring cardiologist/orthopedic surgeon we decided to proceed with invasive assessment. Popliteal access ➡️ venography/IVUS. Significant fibrosis/chronic clot deep femoral and down. Iliac and CFV appear under perfused #Clot#Thrombectomy
11/ We elected to use ClotTriever BOLD. This is different from the original in that it has a stiffer cage and can assist with chronic thrombus. This is the only device I’ve used that can actually remove chronic thrombus. @InariMedical@Thomas_TuMD@t_intheleadcoat@kabguy
15/ Next we take the BOLD once again, using #IVUS guidance to aim the mouth of the basket against the medial wall where the clot seemed adherent. You can also “spray paint” the clot to help see (video for education) #MechanicalThrombectomy#Thrombus
17/ Sheath was replaced and final IVUS/venography demonstrating improvement of flow. Patient has since followed up with near resolution of her infrapop swelling. Now we are working with PT to get her mobile! @IR_Doctor@LessneVIR@VIR_Li@_backtable@keithppereira@IRKhalsa
18/ No previous treatments
Now with catheter based devices we actually have the ability to safely/effectively tx pts we always elected to tx conservatively. The data is still limited, especially below the groin, but like everything in medicine, things evolve, but WE NEED DATA!
Thank you @InariMedical for the BOLD and @LindsayStearns_ for the support and Dr. Edwards for reaching out to collaborate and treat this patient and give her a new lease on life!
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1/ What features PRIOR to intervention are suggestive of adverse prognosis in acute PE?
Which marker do you suggest is the highest risk of poor outcome DURING intervention?
#Cardiotwitter #VTE #pe
2/ This is the list. I would suggest that a very large RV/LV ratio (>2) and presence of severe PH (PASP>60) yields significant risk during intervention
I know @AntoniousAttall has touched on this, but I would warn most operators extreme caution in this patient subset.
We don’t have a true list to assess during intervention!
I would argue we need to look at more markers prior to intervention to indicate treatment in the expanding role of intervention.
Markers such as RA/RV ratio, more echo criteria (60/60 rule), pulmonary artery obstruction index (PAOI), and The Hounsfield Unit Values of Acute and Chronic Pulmonary Emboli have been suggested
3/ Historically #EPeeps has taken the driver seat in this space (rightfully so) due to experience with the LA/transeptal. HOWEVER the new gen #IC/structuralist have become a vital part of the team.
2/ Middle age patient with hx of CAD and PCI to LAD presents with significant SOB and elevated Hs-Trop. No chest pain. No ECG changes. Echo with inferior hypokinesis.
Here’s the diagnostic with a JR4.
Notice the filling defect in the RCA. This is thrombus. How do we know?
The LAA is derived from the left wall of the primary atrium (embryo). Its diff from the true LA and its suited to function as a decompression chamber during left ventricular systole and during other periods when left atrial pressure is high
3/ the appendage is like your fingerprint. No two are the same.