From my limited viewpoint (no youtube) this is an SVC thrombus widowmaker. Definitely do NOT replace with upper extremity permacath - likely to embolize the clot. DO admit for direct left IJ TPA for 24 hours then restudy, heparinize, anticoagulate. I have seen these disappear in 12 hours with TPA. Most likely will get a femoral permacath to pass the "unstable SVC clot" period. Likewise would not create fistula with potentially unstable clot in SVC - adding 1000cc of top flow could cause embolization.

I agree with Dr Webb. The degree of thrombus burden there is massive. Thrombolytics alone vs concomitant ultrasound lysis (such as with EKOS) may be a way to salvage the central veins. While embolization is possible during lysis, it could be substantially higher with a catheter exchange. At the very least, infusion of tPa through the dialysis catheter directly into the thrombus seems reasonable.

thanks for the comments..it looks like the thrombus has been there for a few weeks now atleast..how effective would be TPA at this stage?

The SVC thrombus is relatively fresh and hence, it will dissolve with thrombolytic infusion along with Heparin. The patient needs an inpatient management, preferably in the ICU or a ICU-step down ward with close monitoring while giving the thrombolytic and heparin infusion. The infusion can be given via the Right IJ temporary catheter.
At this point, you cannot change the temporary catheter into a tunneled catheter until the thrombus has been treated and cleared due to the high risk for PE.
After 24 to 48 hrs. of infusion, a venogram needs to be done or a CT Scan Venogram can be done in order to assess the therapeutic response. The venogram will also help to evaluate for an associated underlying Right Innominate Venous or SVC Stenosis.
After the complete resolution of the SVC thrombus, the temporary catheter can be changed to a tunneled catheter.
The risk for re-thrombosis is probably high in this patient following the insertion of another catheter and hence, one need to ponder about the need for a long term oral anticoagulation (as long the patient continues to have a catheter for hemodialysis).
At this point, surgical creation of an AV fistula need to deferred. This patient will need to be evaluated for the Thrombophilia Syndrome including assessment for an APS before venturing into the AV Fistula Surgery (it will be ideal if the blood can be drawn for the thrombophilia study before starting the anticoagulation treatment). If the patient is already getting the thrombolytic/heparin infusion, the blood sample for thrombophilia study can be drawn after stopping the infusion and before starting the patient on an Oral anticoagulant.

I agree with Suresh - this looks fairly fresh, and should respond to lytic therapy.
Having had a nightmare case with Factor V Leiden mutation thrombophilia, I echo the need to identify a coagulopathy as soon as an abnormal clot is seen,

thanks for the comments.. shall update the progress soon.

Any Ekos catheter may also work well with a slow tPA infusion. I just wonder how many times this occurs and none of us ever see it? Think about how many tunneled catheters have been removed once a functioning access is in place. Most of us do not do central imaging prior to removing a catheter that is no longer needed.

Marc,
Thank you and You are absolutely correct.
Thrombophilic confition are not uncommon in these patients . These needed to be considered and treated in order to prevent the pathetic loss of surgically created AV Access. I see them quite often and these patients keep bouncing back to the interventional center with thrombosis.

Wesley - do you happen to know if these posts are "discoverable", in other words liable to be used in a court of law? Are we free to share potentially actionable cases?

Very useful discussion.
Does anyone have a feel for how common this is?
I have always had concerns that some of the" cardiovascular deaths" that occur in renal failure patient's at home may be due to PE rather than MI.
Wonder if anyone has any views?

Dr. Inston
As an autopsy assistant before and during medical school, I was struck by the number of "heart attacks" ultimately caused by PE. As a dialysis access surgeon, we see frequent flyers, but rarely find a real documented coagulopathy - I don't know what the real rate is. I can tell you, though, I will never take a Factor V Leiden mutation lightly again -

I removed a tunneled catheter a few years ago in a patient with a functioning arm access. As mentioned above, no imaging is part of the standard routine. She showed up in the ED that evening complaining of chest pain and was diagnosed with a PE. Not clinically significant except for the pain. She was anticoagulated and did well. Probably a thrombus ball launched when the catheter was pulled out of the venotomy.

Even catheter removals aren't always benign.... Others probably have seen the same.

I totally agree with you Ryan.
In 20014, while I was the month's consult attending in the university for the nephrology service my fellow went and removed a tunneled catheter around 5.15PM as the patient had catheter related infection. The patient was stable except for a low grade fever and getting IV antibiotics. About 1.5 hr after the removal, the patient developed acute SOB, chest discomfort, dropped the saturation and deceased following a PEA arrest. The patient had a massive saddle PE. Since that time, this patient's event comes to my mind whenever a tunneled catheter gets removed.

I am really surprised about this condition and i have some questions.
1.- Do you recommend to make at least a fluoroscopy study before to remove a catheter? To prevent PE.
2.- I work at Health Public Hospital where use to non tunneled catheters are placing frecuently and staying for a long time and PE when they are removal are not usual. This situation should be considered also before to removal too?.

One could use TPA, or start long term anti coagulation, do no catheter procedures for now as long as catheter is working, and repeat angiogram in 4 weeks. Doing a low flow fístula may help flush the area and minimize clot extension.

Due to financial constraints and patient preference i had started him on oral anticoagulation after heparinisation maintaining an INR around 2-2.5. Planning to repeat imaging after 3-4 weeks. Shall update ..
thanks

As Dr. Margassery states it only takes one case of massive PE to demonstrate the problem.
I suspect that a lot of lines are used and a lot of lines don't get CLINICAL issues. Subclinical PEs may be a different story. I have always suspected that PE, especially on-going subclinical PEs may be a contributor to the poorer outcomes seen with lines over definitive access. (whilst most data shows increased mortality in CVCs vs AVF/AVG - it does not show the aetiological reasons).