This is an area of difficulty, confusion and controversy. Particularly as regards the logistics of RRT, it’s set-up and running etc. We have discussed this area before, but more from the evidence base side regarding modalities etc.
The evidence base is rather confusing, so we will try with these notes taken by Dr Dave Popple during a RRT workshop, to clear a few things up…and not just your patients’ renal function!
Formulae to get us started
- Dose = effluent flow rate
- Higher FF leads to more viscous blood and clots filter.
- Aim for FF <20% with no anticoagulant or on heparin
- Aim for FF <30% on citrate
- 2 important parameters in all RRT are FF (to avoid clotting) and dose (for rate of treatment)
- Total dose should range from 20-30ml/kg/hr (which should be sum of all from CVVH and DF)
- To reduce FF on a pt if >20
- Increase blood pump speed (up to limit of catheter access – if too high will cause access problems. Normally up to 200ml/min max).
- Once this has been optimised, reduce replacement fluid rates as this is the way of getting the filter to reduce the proportion of blood flow filtered (Fluid removal is adjusted independently).
- Need to reduce pre- and post-dilution to maintain ratios of 30:70 or 50:50 or whatever you want.
- Reducing this does however, reduce the efficiency of the filter so if this is a problem and you can’t achieve the desired dose then need to add dialysis.
- Useful to set blood pump speed lower if possible, whilst achieving desired prescription dose, as this causes less problems with access pressure.
- Can get replacement bags with phosphate in (more expensive) which reduce need for phosphate replacement when on RRT.
- Access pressure
- Problem with the line (not good enough for the blood flow speed)
- Return pressure
- Problem with the line (not good enough for the blood flow speed)
- Fix by checking line aspirates and flushes easily. If not, change the line (RIJ and fem best).
- If no problem check your blood pump speed is not too high.
- Problem with filter pores “clogging” with inflame mediators etc. (normal with filters and sign of it needing replacement.
- Use can be extended by reducing the filtation fraction, or increasing pre-dilution, but will reduce the efficiency at end of filter life.
- Pressure drop
- Problem with the fibres of the filter clotting off with blood.
- Need to reduce the filtration fraction again and consider more pre-dilution/improving anticoag.
- Space between channels carries effluent/dialysate
- Fibres through filter that carry blood
- If pores in sidewalls clog with inflam. mediators/cell debris etc. from effective function of filter you get a rise in TM pressure
- If fibre blocked with blood, you get pressure drop along length of filter
- Can get away with higher FF (>30), as much less likely to clot filter.
- In Prismaflex the Citrate is diluted in the pre-dilution bag.
- This eliminates the risk of hypernatraemia as less Na required to make solution.
- Means you can’t alter the pre-dilution rate, (this is always set high to give enough citrate to anticoagulate the circuit. Otherwise fluid similar to normal, but with no Ca2+ or K+.
- This pre-dilution happens at the pt end of the access line. Dialysate is also different (again with no Ca2+)
- Ca2+ added after the filter to chelate the citrate.
- Machine automatically adjusts the Ca2+ rate according to blood speed, dialysis prescription etc to ensure it matches the amount of citrate getting to the pt.
- Most citrate is removed by the filter, but that which is not is metabolised in the patient, mostly in the liver, but also in all other cells.
- Initial concerns about citrate use in liver failure may be unfounded as some liver units now starting to use it.
- Less circuit down time
- So more effective delivery of prescribed RRT dose
- Fewer set changes
- Which offsets the increased cost of the replacement fluid
- Less blood loss for pt
- With filter clots
- No systemic anticoagulation
- Although still recommend starting with no additional anticoag for pts with coagulopathy or on Rx dose anticoag
- Risks of citrate toxicity
- Manifests as hypocalcaemia due to reduced ionised Ca2+, and metabolic alkalosis).
- Also can’t run as CVVHD, (citrate used as pre-dilution for ultrafiltration) and riskier running as CVVH (most units only use it for CVVHDF).
- Target is Ionised Ca2+ of 0.25-0.5 in the circuit and normal ionised Ca2+ in pt.
- Frequent gases from circuit and pt. at set up to get it established and then only once/4-6hours.
- To monitor for signs of accumulation (infrequent), check total Ca2+:ionised Ca2+ ratio daily.
- If ratio >2.5 accumulation occurring.
- To reduce this you need to either:
- Reduce the blood flow (reducing the total dose of citrate administered)
- Increase the dialysate (which will increase the amount dialysed)
- Increase the post dilution (to increase the amount filtered)
- As a last resort you can reduce the dose of citrate administration, but this runs the risk of clotting the filter.
- If still a problem need to switch to other anticoag.
****Caution with pts with very poor global perfusion, as they may not metabolise citrate well and accumulate!****
- If pt has acidaemia, you need to reduce the dialysis rate, which is counterintuitive.
- This is because you don’t want to dialyse out your citrate which will be metabolised into bicarb and actually improve the acidosis.
- If you want to clear other small molecules, then increase dialysate as usual.
- Occasionally you may need to run a NaHCO3 infusion alongside to correct acidaemia if severe.
- Be wary that acidaemia is not caused by citrate toxicity, (check total:ionised Ca ratio).
RRT in special groups
- Tazocin – needs time above MIC to be effective.
- As dialysed, need to run an infusion to get maximal benefit, and indeed the benefit may be even greater in pts with mod AKI not on RRT (poss 18g/24hours to be sure you are maintained above MIC
- Other abx may also benefit from infusion depending on Vd and protein binding etc.
Patient with hyponatraemia and AKI
- Best option to avoid sudden changes and osmotic demyelination may be CVVH with replacement fluid diluted with sterile water.
- Normally replacement fluid has 140mmol Na.
- Can dilute a 5000ml bag with 1250ml sterile water to end up with Na conc 112mmol.
- This will also dilute the K and HCO3 though.
RRT in OD
- Mode depends on size of molecule, Vd and protein binding.
Location, Location, Location…
- Deeper insertion of RIJ cath into RA/SVC gives better performance
- Avoid LIJ, vein as has worse function
- Femoral veins 2nd line and similar infection rate to IJ for vascathsDown side is rehab mobility and increased risk of DVT with fem line.
- Comparable flow rates and performance to RIJ if length >25cm and tip in IVC (not iliac where recirculation increased too).
- Subclavian veins have lower infection and thrombosis rates, but not popular with nephrologists because they have highest rate of central venous stenosis which can preclude future AV fistulas.
- Step tip catheters (like we have) have lower clotting rates because of manufacturing techniques and better flow rates on access port (often the rate limit). However can’t switch lines over as this causes recirculation and reduced efficiency of RRT.
- Can get increased access pressures when starting up the filter due to vascular spasm so start slow and build up.
- If you can aspirate 20ml in 6 seconds this is equivalent to 200ml/min so should be adequate.
- Rewiring lines doesn’t increase colonisation rates of line tips, but does increase rate of catheter dysfunction 3x so probably not a good idea.
- Usual ones!
- Diuretic refractory fluid overload without AKI?
- If doing this, use max 200ml/hr removal as more doesn’t allow time for interstitial fluid to re-distribute into circulation.
Decompensated Heart Failure – CARRESS Study
NO difference in mortality and Furosemide arm had less requirement for RRT so prob not indicated.
Early Vs Late – ELAIN study
Early treatment had reduced mort and LOS. BUT limited statistical power and most pts post cardiac surgery with overload so may have already had a strong indication for RRT anyway.
Early Vs Late – AKIKI
No outcome difference (prim outcome 60 day mortality), and more RRT done in early group. But in post hoc analysis late group had 2 types of pt. ½ did well and had reduced mortality, other half had increased mortality. So late dialysis may benefit some but not all…wait and see not safe for all pts.
Intensity of RRT – RENAL
Increasing the intensity of continuous renal replacement therapy from 25ml/kg/hr to 40ml/kg/hr did not reduce mortality or the rate of dependence on dialysis among critically ill patients ***higher doses may be required in sepsic/catabolic pts.
Dose – ATN Study
A strategy of intensive renal support in critically ill patients with acute kidney injury does not decrease mortality, accelerate recovery of kidney function, or alter the rate of nonrenal organ failure as compared with a less-intensive regimen similar to usual-care practices
Cessation of RRT – Uchino
Urine output at the time of initial cessation of continuous renal replacement therapy was the most important predictor of successful discontinuation, especially if occurring without the administration of diuretics. UO >400ml/24hours – 80% success if RRT stopped
Furosemide stress test – Van Der Voort
Within 24 hours of discontinuation of RRT, a furosemide stress test was able to predict the development of renal damage stage III according to the Acute Kidney Injury Network classification in critically ill patients.
Continuous Vs Intermittent RRT – CONVINT
Our findings add to mounting data demonstrating that intermittent and continuous RRTs may be considered equivalent approaches for critically ill patients with dialysis-dependent acute renal failure. Intermittent can be beneficial for rehab and mobilisation.
Renal recovery post AKI
Dialysis-related factors may influence the outcomes. In our cohort, positive daily fluid balance during CRRT was associated with lower survival. Multicenter, randomized studies are needed to assess fluid balance as a primary outcome to define the best strategy in this patient population.
- If normal baseline renal function, 80% will recover.
- Risk factors for poor recovery include Age, comorbidities, nephrotoxic drugs and CVS instability.
The Role of good old Furosemide!?
- Diuretics don’t prevent AKI. This advice is based on studies in post cardiac surg, vascular and contrast neph pts.
- Theoretically, furosemide reduces the O2 consumption in the loop of Henle. I can only really find data on this in rats with a propensity to renal ischaemia though.
- Should be considered if fluid overloaded to treat this, but doesn’t resolve the AKI.
- Van der Voorts (2014) Furosemide stress test is also good for predicting the pts who need RRT (as above).
- If KIDGO stage 2 and no response to stress test, then one should start RRT. Better predictive power for need of RRT than biomarkers alone.
Bolus of infusion?
- If give boluses, you get increased Aldosterone release between doses with Na retention and reduced effectiveness.
- Possible better naturesis with IVI.
- Altenative is to give parallel Spironolactone to block Aldosterone +/- Acetazolamide for HCO3 +/- Aminophyline for naturesis
- See the brilliant article below from Craig Morris and James Plumb, as it adds context to the argument for multi-modal therapy to mobilise fluid
- Furosemide is bound to albumin and needs active transport to the effect site in the tubule.
- Giving combination of albumin and Furosemide for pts post early admission fluid resuscitation to patients with hypoalbuminaemia may be beneficial.
- We await the results of the FADE study.
- So far albumin and furosemide are proven to reduce FiO2 in ARDS pts.
- Judicious volume replacement is good, but if excessive, increases intracapsular pressure and reduces RBF and GFR.
- Therefore excess fluids are not only bad for the lungs, but also the kidneys.
- Avoid excess Cl- in fluids, as this is damaging to kidneys
NAC – studied extensively post surgery and in critical illness and no benefit
Contrast induced nephropathy!!!
- Most of the scares to do with this have been done to death on our site, and much was discussed at the ICS and iFAD regarding these issues!
- Mostly relates to older hypertonic contrast agents.
- Newer agents are hypo/iso tonic and probably much less harmful.
- 2017 observational study found no difference in AKI rates between contrast and non-contrast CTs, but these were not critically ill pts. There may still be a small risk for our pts.
- Normally expect the creatinine to peak at day 3-5 and then reduce.
- If eGFR <60 and intra arterial contrast procedure (higher risk) = preventive strategies
- If eGFR <45 and ANY contrast = preventive measures
- What are preventive measures though?
- AMACING trial 2017 compared hydration vs none and found no difference, but not sick pts and excluded those with eGFR <45 and ICU pts.
- Multiple studies have proven no superiority of NaHCO3 as bolus fluid/NaCl/NAC when compared with each other.
- Current KDIGO guideline recommends NaCl or NaHCO3 preloading, but guidance quite old.
- NAC – ACT trial found no difference.
- Administration of Rosuvastatin prior to intraarterial contrast in statin naive patients may reduce CIN.
What confounds some studies is that administering NAC can reduce creatinine production (surrogate end point), so if this is the outcome measure, then it looks like it helps but doesn’t actually reduce the rate of AKI or outcome.
So there we are! Food for thought, but to end:
Original scribblings by: Dr Dave Popple (Consultant Intensivist)
Edited by: Dr Jonny Wilkinson
Please also have a look at:
Ashley Miller’s section on RRT
Our other sections
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