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Welcome back to the tasty morsels of critical care podcast.
Usually the topics here follow the well trodden path of Oh’s manual, but we’re looking at something primarily because it is an ideal question for a fellowship exam. In this type of scenario you will almost be guaranteed to find that Deranged Physiology has already covered it comprehensively and in great detail. So as expected the DP post forms the bulk of the material for this short audio snippet.
First thing to consider is how long do you expect your filter to run for in the first place. This will likely vary between hospitals and more signfiicantly between different types and brands of filter. A common time to empirically take down the filter is around 72 hrs or so. At that point you’re at end of life as far as the manufacturer is concerned. All the microfibres are clogged with all the gunk your kidneys usually deal with and the filter isn’t going to work. Think about it like your vacuum cleaner bag getting full and needing a change.
I’m not sure a clear definition of recurrent clotting exists but I would usually consider it to be recurrent clotting when the nurses tell me it is, given that they spend all the time running the machines they, as always typically know best.
Once we know there’s a problem then it’s time to start thinking of some potential causes.
1) is the anticoagulation being done poorly?
There can be quite a lot to this really. Sometimes it can be as simple as just not following the citrate or the heprain protocols as you should. That’s a fairly simple “just read the instructions” type problem. However, particularly when it comes to heparin the tests we use to judge the level of anticoagulation are fairly blunt instruments in explaining the intricacies of the finely tuned coagulation system. Heparin resistance might be a problem or any number of other myriad of causes. I have linked to the excleent IBCC post looking at anticoagulation that I return to frequently. You might even be in the enviable position of being enlightened and use anti-Xa levels to monitor your anticoagulation.
Given all the issues with heparin I think the most appropriate answer to the question of “how to antioagulate your filter ciruit with heprain” is to use citrate instead.
2) Is your filter clotting because the flow rates are too poor?
There are a lot of reasons for poor flow rates, the catheter itself being a major contributor. That being said most units have only one type of catheter available so you usually don’t have much flexibility here. You will likely have different lengths of the same gauge of catheter available and remember that pouseille’s law might get the better of you with the flow being inversely proportional to the length of the catheter. In other words the longer the catheter the worse the flow rates.
You probably can optimise position. I don’t mean to pretend that these are definitively settled issues but RIJ is often favourable due to direct access to the central circulation and minimal impairment with mobilisation. However, it is interesting to note that the shiny, ivory tower of the Alfred in Melbourne have the femoral vein as their location of choice with some local obseravtional data supporting extended filter life.
Once you’ve decided on site you should consider tip placement. A brief review of a CXR of someone with a permacath, a tunnelled long term device, usually shows that the tip is probably in the RA. Typically I was taught that we shouldn’t have the tip in the RA and instead aim for that RA/SVC junction. The issue with the RA/SVC junction is that often one of the ports lies against the wall of the vessel and can obstruct and suck down and cause issues with flow. Again, hardly definitive but there is another small RCT of positioning in the RA that would suggest this is a safe and effective practice.
Finally, at least in this entirely non comprehensive list, we often worry about “filling” or “volume status” in inverted commas as an issue for flow rates. If the SVC is collapsing even with simple respiration then pulling off 150-200ml/min might be a challenge. Often a judicious fluid bolus can help. My issue with this is it can be fairly difficult to know if this is the problem without just giving it and seeing what happens
3) Is your patient in some kind of prothrombotic state?
The answer will usually be no. At least not in any more of a prothrombotic state than the usual ICU patients. But could this be a HIT, could there be something weird and wonderful underlying or is it just COVID like everyone else.
4) is viscosity an issue?
By viscosity I don’t really think they have waldenstrom’s macroglobulinaemia but you more like you not be diluting enough pre-filter . This should be taken care of by your protocols but the pre filter dilution is likely helpful in reducing clotting.
Fixing the clotting issue is obviously directed at the causes outlined above. But given the difficulty in diagnosing the problem in many of these cases I find myself addressing multiple different causes and switching anticoagulation and changing lines for a few days until either the patient gets better or the need for CRRT goes away. Honestly, it’s remarkable that they let me do this job at all.
References:
Intensive blog by Vui Kian Ho on mastering the vascath
Morgan D, Ho K, Murray C, Davies H, Louw J. A randomized trial of catheters of different lengths to achieve right atrium versus superior vena cava placement for continuous renal replacement therapy. Am J Kidney Dis. 2012 Aug;60(2):272-9. doi: 10.1053/j.ajkd.2012.01.021. Epub 2012 Apr 11. PMID: 22497790