3. Objectives
RRT Indications
Modes and principles
Dosing
Replacement solutions
Anticoagulation
Special Circumstances
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4. AKI / CKD vs ARF / CRF
RIFLE
Renal failure - is the cessation
of renal function with or without
changes in urine volumes.
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6. Anaesthesia UK. Acute renal failure.
Renal replacement therapy on ITU
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7. “Renal tubular cell injury after a toxic or ischaemic insult results in
sloughing of tubular debris and cells into the tubular lumen with
eventual obstruction of tubular flow, increased intra-tubular
pressure and back leak of glomerular filtrate out of the tubule
1
and into the interstitium and renal venous blood”
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8. Renal:
Symptomatic Uraemia
Nephrogenic Pulmonary Oedema
Severe Hyperkalaemia
Severe metabolic acidemia
Relative Urea/Creatinine levels
Non Renal:
SIRS/sepsis
Fluid balance
Rhabdomyolsis *
Overdose/Drug accumulation
Renal protection pre/post contrast, CIN
Temperature control
Plasmapheresis/Exchange (immune complexes)
Severe acute liver failure with molecular adsorbent
re-circulating system (MARS, PROMETHEUS) as
bridge to transplant
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9. Early or late initiation of RRT (UO and Urea)
The answer to whether early initiation of RRT is
beneficial with regards to survival and/or renal
recovery is not clear. Why?
2
Getting et al 1999 . Urea 15.2 vs 33.7 conferred
survival benefit.
3 4
Ronco et al 2000 and Saudan et al 2006 both
dose/outcome studies suggested an early start.
5
Liu et al 2006 observational PICARD study (Urea
27) suggested an early start
6
Not all agree, Bouman et al 2002 RCT no benefit
in early initiation of RRT. CvvHF
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Recommendation?
10. Intermittent vs continuous
CRRT is an extracorporeal blood purification therapy intended to substitute for impaired
renal function over an extended period of time and applied for or aimed at being applied for
24 hours a day.
Patients with AKI as part of MODS are less likely to tolerate
Fluid shifts
CVS instabiltiy (hyovolaemia and hypotension)
Secondary renal insult
In MODS, CRRT is certainly better tolerated in terms of drop in CVP/CO/SVR/MAP 7-9.
Likely benefits in for CRRT in SIRS/SEPSIS & cytokine clearance over IHD10.
Many papers advocating the benefit of CRRT in patients with raised ICP 12-13.
In terms of survival and renal recovery the benefit of either is still to be demonstrated in all
AKI requiring RRT. Recent Cochrane Database review 2007 demonstrated important
haemodynamic effects but little survival benefits11.
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So is there a place for IRRT?
11. Ultrafiltration - movement of fluid across a pressure gradient,
via hydrostatic forces.
Convection - The movement of solutes with a water flow
or “Solvent drag”
Diffusion - Movement of solute from an area
of high concentration to an area of low concentration via
osmosis across a semi-permeable membrane
Adsorption -
Surface adsorption where the molecules are too large
to permeate and migrate through the membrane;
however can adhere to the membrane
Bulk adsorption within the whole membrane when
molecules can permeate it
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13. Intermittent RRT
HD most commonly
Peritoneal dialysis
CRRT
• SCUF - Slow Continuous Ultrafiltration
Ultrafiltration - fluid removal
• CVVHF - Continuous Veno-Venous Hemofiltration
Convection - Small, medium and some large size
molecules MW <30000 Daltons
• CVVHD - Continuous Veno-Venous Hemodialysis
Diffusion - Small molecules <500 Daltons
• CVVHDF - Continuous Veno-Venous
Hemodiafiltration
Diffusion and Convection- small and medium sized
molecules
Niche techniques
Plasmapheresis/exchange
Haemoperfusion
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14. Method
Peritoneal catheter
Instil 1-2 litres dialysis fluid
under gravity
Dialysis Fluid
Similar composition to ECF
Variable Tonicity
Variable K+ and glucose
content
Advantages
Technically simple
Safer than haemodialysis if:
high risk of systemic
bleeding
circulatory instability
vascular access difficult
Indicated in some cases of
pancreatitis
Disadvantages
Pain
Bowel perforation
Bleeding
Infection/Peritonitis/SP/SEP
Metabolic
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15. Requires AV shunt or Percutaneous catheter.
Removal of solutes by diffusion (mainly small
sized molecules) via conc gradient. Access
Ultrafiltration, via hydrostatic gradient. Very
effectively (1-2L/HR) Return
High blood flow rates required (350-400ml/min
+)
Semi permeable membrane is used for selected
diffusion. Dialysate is used to create a
concentration gradient across a semi permeable
membrane.
Need dialysate flow +/- countercurrent. The
counter-current flow increases solute removal by S
maintaining gradient along filter (flow rate 15-
45ml/min, 1-3L/Hr)
No replacement fluid
Minimal Adsorption Effluent
AKI without sepsis or CVS instability.
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16. Advantages to waste
Rapid correction of volume overload
Better solute clearance than
PD/CRRT Dialysate Out Blood In
Intermittent hence mobility (from patient)
Disadvantages
Specialist nurses, water tanks etc
Vascular access complications
Anticoagulation Dialysate In Blood Out
CVS instability
NO medium/large molecule (to patient)
clearance.
LOW CONC HIGH CONC
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17. Primary therapeutic goal:
Safe management of fluid
removal Blood In
UF rate ranges up to 2 L/Hr via (from patient)
hydrostatic forces.
No dialysate Fluid Volume
Reduction
No replacement fluids
Large fluid removal via
ultrafiltration Blood Out
Minimal solute clearance
to waste (to patient)
LOW PRESS HIGH PRESS
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18. Access
Primary therapeutic goal:
Convective solute removal Return
Management of intravascular
volume (pressure gradient)
Blood Flow rate = 10 - 180 ml/min,
newer machines 300ml/min.
UF rate ranges 6 - 50 L/24 h (> 500
Replacement
ml/h) GFR 10-20%.
Replacement solution can help to
drive convection
Removal of small and medium sized
molecules
No dialysate
Effluent
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19. Advantages
Better at removal of middle sized MW
molecules >500-1000 daltons
Use for Cytokine adsorption and CVS
instability in intractable septic shock10,16 to waste Blood In
Accurate control of ultrafiltered
volume (from patient)Repl.
CAVH self-regulating
CVVH requires no arterial access Solution
Disadvantages
Complex equipment
Worse clearance/diffusion of small MW Blood Out
solutes. NA/K/Ur/Creat
CAVH blood-pressure dependent
Access site complications (esp CAVH) (to patient)
LOW PRESS HIGH PRESS
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20. Primary therapeutic goal: Access
Solute removal by diffusion and
convection
Return
Management of intravascular Dialysate
volume
Blood Flow rate = 10 - 180ml/min, again
newer machines capable of 300ml/min
Combines CVVH and CVVHD therapies
UF rate ranges 12 - 24 L/24h (> 500
Replacement
ml/h)
Dialysate Flow rate = 15 - 45 ml/min (~1
- 3 L/h). Countercurrent flow
Uses both dialysate (1 L/h) and
replacement fluid (500 ml/h+)
Effluent
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21. to waste
Advantages Blood In
Better clearance of small solutes
(from patient)
over HF, K/Na/Ur/Creat
Less limited by poor access and Dialysate
hypotension Solution Repl.
Benefits in ARF & MOF4 Solution
Small/medium/large molecule
removal to a degree
Blood Out
Disadvantages
Not as efficient adsorption and (to patient)
middle molecular clearance
Solute and drug clearance less
LOW
predictable HIGH PRESS
Fluid balance complicated PRESS
Complicated equipment LOW HIGH CONC
Clotted filter may be disguised CONC
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22. Studies in patients with end stage kidney disease (ESKD) requiring IHD
have led to well defined targets for what constitutes adequate clearance17
In AKI the dosing/clearance/filtrations rates are not nearly so clear.
IHD fractional clearance Kt/V well used.
In post filter dilution CvvHF Ultrafiltration volume acts as a surrogate for
clearance in the critically ill16.
Ultrafiltration volume in ml/kg/hr represents the filtered fraction of
patient’s blood.
Remember that HDF incorporates diafiltration plus ultrafiltration to give
total filtration.
Recent studies have described dose of CRRT in terms of ml/kg/h of
ultrafiltrate production.
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23. Ronco et al 20003 used this approach (ml/kg/hr) to demonstrate survival
benefits of 35 over 20ml/kg/hr.
Kellum et al 200718 pooled 4 recent dose/outcome to demonstrate very large
effect on survival in favour of an augmented dose.
Landmark multicentre RCT in America (AKI study19) and Australasia (RENAL
study20) showed that a high renal dosing regime in RRT conferred no benefit.
The ideal dose for CRRT is not known or universally agreed upon; however 35
ml/kg/h of ultrafiltrate production is recommended as a minimum for CVVH
(post-dilution) and CVVHDF16.
Maybe room for Short term High volume isovolaemic haemofiltration (STHVH)
doses of up to 100ml/kg/min or ~8-9L/Hr exchange for severe SIRS/sepsis 10,18.
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24. Cellulose
Low flux
Poor at removing middle MW
molecules
Used in end ESRF.
Cause more complement and
leukocyte activation16
Leukocyte retention in the lungs,
renal parenchyma and other
organs, thus resulting in further
organ damage.
Not desirable in the critically ill
patient.
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25. Synthetic
Polysulphone (PS), Polyamide (PA), Polyacrylonitrile (PAN),
Polymethyl methacrylate (PMMA).
High flux membranes.
Flux being a measure of ultrafiltration capacity and based on the
membrane ultrafiltration coefficient.
High flux membranes are highly water permeable.
Allowing convective therapy and the removal of middle MW
molecules.
Better biocompatibility, less complement/leucocyte activation
and end organ disfunction16.
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26. Adjusted based on pt. clinical need
Help drive convective transport
Administered pre or post filter
Must contain:
Sodium
Calcium (except with citrate)
Base (bicarbonate, lactate or citrate)
May contain:
Potassium
Phosphate
Magnesium
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28. Patients with Liver dysfunction, profound hypoperfusion and pre-existing Lactic
acidaemia are at risk of lactate intolerance.
Some studies have suggested better control of acidaemia with bicarbonate
solutions14 this has not universal though16
Improved cardiovascular stability have also been reported14
To date though use of either base has not demonstrated any survival or renal
outcome benefits14-16
Conflicting views, as always! Bicarbonate in theory has some potential benefits
but currently no data to clearly advocate one or the other 16
Indications for bicarbonate buffer16
A rise of lactate of greater or equal to 5 mmol/L (from base-line) associated with a worsening
metabolic acidosis suggests lactate-intolerance.
Severe pre-existing lactic acidosis pH <7.2 with associated lactate of ≥ 8 mmol/L.
Severe liver dysfunction.
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29. Factors affecting filter life:
Access, Anticoagulation, Pre/Post dilution,
Hyperlipidemia, Sepsis
Pre-Dilution
Increases filter life
Increases convective transport
Reduced solute clearance
Some of delivered replacement fluid lost by
hemofiltration
Lower anticoagulation requirements
Higher UF required given loss of replacement fluid
through filter
Post-Dilution
No solute dilution, improved diffusion and solute
clearance
Increased hemoconcentration
Higher delivered dose of hemofiltration
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30. Heparin Prostacyclin (PGI2)
Intermittent bolus or continuous Inhibits platelet aggregation
infusion
Reduced risk of haemorrhage
Disadvantages Disadvantage
Haemorrhage vasodilation and hypotension
Anti-thrombin III deficiency
Thrombocytopaenia Citrate
Regional heparinisation Complexes ionised calcium
Ca infused in efferent limb
Low molecular weight heparin
Citrate metabolised Liver, renal and
Less effect on platelet function skeletal muscle.
Direct Thrombin Inhibitors Some evidence for prolonged filter life
and less bleeding events22.
r-Hirudin Disadvantages
Argatroban Low Ca++, Low Mg++
Hypotension and tetany
Acidaemia in renal/hepatic impairment
as a result of reduced citrate
metabolism.
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32. Principles
Same equipment as haemofiltration
Larger pores in filter
To remove pathogenic material (IgG/M, paraproteins etc) in plasma
Replace with equal volume of substitute
HAS, FFP
Often rebound antibody synthesis and may need immunosupression
Indications
Multiple Myeloma/Waldenström macroglobulinemia and hyperviscocity
syndrome (HVS)
Poisoning
SIRS in conjunction with HF, early days
Acute Guillian-Barre syndrome
TTP and HUS
Goodpastures
Meningococcal sepsis
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33. Techniques used for extracorporeal drug removal
Haemodialyis
Haemoperfusion
Continuous haemofiltration
Continuous haemodiafiltration
Factors effecting clearance
Molecular size (<500 daltons desirable)
Steric hindrance
Polarity
Volume of distribution, Water/lipid solubility
Protein binding, in particular in HD
Rate of Endogenous clearance
Rate of redistribution
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34. Substances for which haemodialysis may be used
Salicylates clearance doubled over UA
(seizures/coma/↓pH/AKI/absolute level/paeds)
Lithium
Alcohols:
- ethylene glycol, methanol, ethanol, isopropanol
Theophylline HP better
Metformin
(Bromide)
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35. HPF was first used in toxicology in the 1960s for barbiturate poisoning
Since these initial reports HPF has been attempted in the treatment of a number of other
poisonings
A standard haemofiltration / haemodialysis pump can be used
The only special equipment required is the perfusion column
Blood is pumped (150 - 250 mL/min) through a column containing an adsorbent, usually
activated charcoal, coated with a biocompatible ultrathin membrane
Characteristics of compound removed
Adsorbed by charcoal
Vd and endogenous clearance factors similar to previous
Protein binding, water solubility & molecular size are not such limiting factors
as with haemodialysis as blood in direct contact with adsorbent
NO prospective controlled studies looking at the effect of HPF on outcome in poisoned
patients
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36. Carbamazepine
Theophyllines
Causes significant and prolonged toxicity Both acute & chronic theophylline
(T1/2 19-32 hrs) poisoning can cause significant
Problem of enterohepatic recirculation morbidity and mortality
Binds activated charcoal Better clearance than MDAC
MDAC vs HP have similar ↑ clearance Applications in severe OD with
dysrrthmias and seizures
iIeus often limits MDAC/whole bowel
irrigation
Reserved for life threatening seizure, Phenobarbitone
cardiotoxicity, impaired gut motility or Both MDAC and HPF increase
phenobarbitone clearance, HP to a
deteriorating despite MDAC treatment.
greater extent
life-threatening toxicity &
deterioration despite full supportive
care
Others
TCA, Digoxin, Paraquat, Na valporate
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37. A common ‘non-renal’ indication for CRRT is in the management of severe sepsis.
It has been shown that many, if not all of the septic mediators can be removed by CVVHF16.
Cytokines (IL 1/6/8, TNF, complement, bradykinins, beta-2 microglobulin).
Due to the MW of inflammatory mediators it has been shown that CvvHF is particularly effective in
their clearance and adsorption16.
Due to high generation rate, studies have concentrated on the use of ‘high dose’ or ‘high volume’
haemofiltration.
High volume haemofiltration has also been used as ‘rescue therapy’ for patients with severe septic
shock unresponsive to other treatments, with encouraging results for cardiovascular
stability/outcomes3,10,21,23,24.
Ultrafiltration doses as high as 40-85ml/kg/Hr were shown to improve 28 day mortality in septic
shock23,24.
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39. Initiation of RRT should be started earlier rather than later particularly when -
AKI is unlikely to be reverse early
Patient had normal renal function prior to insult
CRRT
Appears to offers some benefits over IHD but no Grade A evidence.
Generally agreed that it is better tolerated in the critically ill.
Modality
No clear benefits for one modality over another when addressing the diverse
group that is AKI
However, there are encouraging results for the use of certain modalities in
specific subgroups (Septic shock ± AKI, ↑ICP, OD, Rhabdomyolysis, Pulmonary
oedema, Solute issues, Immunological conditions etc)
Correct modality for the correct patient
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40. Dose
No clear evidence on dosing and outcome benefit for all AKI
However 35 ml/kg/h of ultrafiltrate production is recommended as a minimum for CVVH
(post-dilution) and CVVHDF
Higher rates for Cytokine clearance and adsorption in unresponsive septic shock shows
some promise
Pre-dilution CRRT reduces solute clearance and an increase of 15% for ultrafiltration
rates of 2 L/h and up to 40% for rates of 4.5L/h should be considered.
Lactate-based replacement fluids are as effective as bicarbonate-based fluids except
in conditions where liver function is compromised but there is little evidence that
either kind of fluid has survival advantage.
Synthetic membranes for CRRT
UFH, LMWH and prostacylin are most commonly used, but Citrate may offer some
interest for the future.
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41. 1. Allen R. Nissenson (1998)Kidney International Vol. 53, Suppl. 66
2. Gettings LG et al. Outcome in post-traumatic acute renal failure when continuous therapy is
applied early vs late. Intensive Care Med 1999;25(8):805-813
3. Ronco C et al. Effects of different doses on continuous veno-venous haemofiltration on
outcomes of acute renal failure: a prospective randomised trial. Lancet 2000; 356(9223): 26-
30.
4. Saudan P et al. Adding dialysis dose to continuous haemofiltration increases survival in
patients with acute renal failure. Kidney Int 2006; 70(9): 1312-1317.
5. Liu KD et al. Timing of initiation of dialysis in critically ill patients with acute kidney injury.
Clin J Am Soc Nephrol 2006; 1(5): 915-919.
6. Bouman CS et al. Effects of early high volume continuous veno-venous haemofiltration on
survival and recovery of renal function in intensive care patients with acute renal failure:
prospective , randomised trial. Crit Care Med 2002: 30(10): 2205-2211.
7. Davenport A et al. Improved cardiovascular stability during continuous modes of renal
replacement therapy in critically ill patients with acute hepatic and renal failure. Crit Care Med
1993; 21(3): 328-338.
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42. 8. Augustine JJ et al. Randomised controlled trial comparing intermittent with continuous dialysis
in patients with ARF. Am J Kidney Dis 2004; 44(6): 1000-1007.
9. John S et al. Effects of continuous haemofiltration Vs intermittent haemodialysis on
haemodynamics and splanchnic regional perfusion in septic shock patients: A prospective
randomised clinical trial. Neprol Dial Transplant 2001; 16(2): 320-327
10. Patrick M et al. Prospective evaluation of short-term , high volume isovolemic hemofiltration on
the hemodynamic course and outcome in patients with intractable circulatory failure resulting
from septic shock. Crit Care Med 2000. Vol 28(11) 3581-3586
11. Cochrane Database Syst Rev. 2007 Jul 18;(3):CD003773
12. Davenport A et al. Changes in ICP during haemofiltration in oliguric patients with grade IV
hepatic encephalopathy. Nephron 1989; 53(2): 142-146
13. Ronco C et al. Brain density changes during renal replacement in critically ill patients with acute
renal failure: Continuous versus intermitent haemodialysis. J Nephrol 1999; 12(3): 173-178.
14. Barenbrock M et al. Effect of Bicarbonate and Lactate buffered replacement fluids on
cardiovascular outcome in CvvHF patients. Kidney Int 2000; 58 (4): 1751-1757.
Bringing excellence to life
43. 15. Thomas AN et al. Comparison of bicabonate or lactate buffered haemofiltration fluid; use in critically ill
patients. Nephrol Dial Transplant 1997; 12 (6): 1212-1217.
16. Standards and Recommendations for the provision of renal replacement therpy on intensive care units in the
UK. Intensive Care Society standards and Safety. 01/2009.
17. http://www.kidney.org/Professionals/kdoqi/
18. Kellum JA. Renal replacement therapy in critically ill patients with acute renal failure: does a greater dose
improve survival? Nature Clin Pract Nephrol 2007; 3(3):128-129.
19. VA/NIH Acute Renal Failure Trial Network. Intensity of renal support in critically ill patients with acute kidney
injury. N Engl J Med 2008; 359(1):7-20.
20. The RENAL Replacement Study Investigators. Intensity of Continuous Renal-Replacement Therapy in Critically
Ill Patients. N Engl J Med 2009; 361 (17): 1627-38.
21. Ratanarat et al. Pulse high-volume haemofiltration for treatment of severe sepsis: effects on hemodynamics
and survival. Critical Care 2005, 9:R294-R302
22. Monchi M et al. Citrate vs. heparin for anticoagulation in continuous venovenous haemofiltration: a prospective
randomised study. Intensive Care Med 2004; 30(2):260-265.
23. Honore PM et al. Prospective evaluation of short-term, high volume isovolemic haemofiltration on the
haemodynamic course and outcome in patients with intractable circulatory failure resulting from septic shock.
Crit Care Med 2000; 28(11): 3581-3587.
24. Ratanarat R et al. Pulse high-volume haemofiltration in critically ill patients: A new approach to patients with
septic shock. Seminar Dial 2006,19(1):69-74.
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Hinweis der Redaktion
ARF vs CRF CKD is of importance grade 1-4, Will concentrate mainly on AKI RIFLE risk, injury, failure, longterm damage, esrf, more itu orientated. 70%vs 30% oliguric/non oliguric . Non oliguric better outcomes
Not that simple though and not so pigeon holed and often multifactorial but a good start Pre-renal Hypovolaemia (Diuretic Induced) G.I. Losses Renal Artery Stenosis; Thrombus Anaphylaxis Dysrhythmias Myocardial Infarction Cardiac Tamponade Congestive Cardiac Failure Vena Cava Obstruction Hypovolaemic Shock Sepsis/Shock Dehydration Intrinsic as above Tubular, Vascular inflamatory vasculitic/IGE/pulmonary renal/thrombotic, Glomulerular, interstitial nephritis, IAH, hepatorenal Post renal Kidney stones and uteric obstruction, clots, tumours, crystals, atonic/neurogenic bladder
Acute tubular necrosis Severe ischaemia, with inadequate supply of oxygen and nutrients to the tubular epithelial cells Poisons, toxins or medications that destroy the tubular epithelial cells, including:
Very diverse list, and probably not exhaustive. OD HP carbomezapine/barbituates/theophylline/TCA CVVHDF aspirin/Benzodiazipnine/MgSO4/Lithium/ethanol/meth/ethylene/aminoglycoside
WHY? hypoten/SIRS/cytokine/renal rest/ATPase/ prior to irreversible tubular injury Ronco et al prospective rct 425 pts and 2 intensive cares, primary endpoint survival at 15 days! Secondary endpoint is recovery of renal function biochemistry and diuresesis. ARF defined by abnormal urea and uo less then 200ml/12 hrs. 20 35 and 45 ml/kg/hr. Not only recommend 35ml/kg /hr but also early starting seemed to confer a better outcome Liu et al clinical Am journal of nephrology 2006 observational study using a urea of 27 as the demarcation of early vs late showed benefit. However Bouman et al 2002 in the critical care medicine a RCT shoed no benefit again in all comers. Not a homogenous group, not one shoe fits all and use of different modalities may confer different survival and benefits. But certainly in ARF with no hx CKD and an unlikely quick recovery would all suggest early initiation would be wise. No negative outcomes demonstrated. Concurred by the recent recommendation by the ICS jan 2009.
IHD is the high filtrate intermittent dialysis Surivival benefits-Difficult randomising CVS unstable patients to IHD IHD not good for CVS unstable SIRS/SEPSIS and removing cytokines. better in terms of small solute clearance, fluid removal, no need for anticoagulation, freedom from machine
Adsorption Molecules that can be effectively adsorbed include:- B 2 Microglobulin- Cytokines- Coagulation factors- Anaphylatoxins
Medium sized molecules blood components cytokines IL1,6 and 8, TNF, bradykinins, endothelin, complement
Leave 30 mins, Drain under gravity over 20 mins or CAPD overnight SCP Sclerosising peritonitis and SEP Sclerosising encapsulating peritonitis.
Dialysate similar in composition to ECF once again
Patrick et al and ICS 10 Patrick et al 2000 crit care med. Prospective interventional 20 pts with intractacble septic shock looking at CI, ph, NA requirement, ScvO2. Using high ultrafiltration rates 85ml/kg/min!
Saudan et al 2006 kidney international Prospective RCT 371, 256 enrolled. AKI all comer group not just sepsis. 28 and 90 day survival significantly higher in CvvHDF group. Not as efficient as CvvHF for removal of medium and large molecules but better than HD. Saudan et al kidney int journal 2006 prospective 371 patients RCT all comer ARF CvvHF or CvvHDF 28 and 90 day survivals
In contrast to ESKD patients, critically ill patients are not in a metabolic steady state, are frequently catabolic and have labile, and often expanded fluid volumes.
Ronco et al Lancet 2000, 425 pts 2 centres, prospective RCT measuring survival at 15 days and renal recovery. ARF reduced UO and urea escalation. 20/35 and 45 ml/kg/hr. Significant survival benefit but no benefit in recovery of renal function biochemistry and diuresis STHVH in Severe sepsis both with either intractable shock and or renal injury Patrick et all 2000
CvvHDF/HF use synthetic
Dialsylate fluid contains elctrolytes at physiological level. It can be adjusted and is similar in some respects to replacement fluid except separated from patients circulation by semipermeable membrane to allow diffusion and equilibrium to be reached. As opposed to being directly added back to the patients circulating volume.
Remember pre dilution replacement will increase filtration rate 15% at 2L/HR and up to 40% 4L/hr
As a general rule, to prevent extracorporeal circuit clotting, clotting times are maintained at 1 ½ times the baseline. Heparin is most frequently used because it is widely available and the best understood anticoagulant. If heparin is contraindicated , tri-sodium citrate (commonly known as citrate) may be used. Citrate protocols anticoagulate the extracorporeal circuit by chelating (or binding with) calcium in the blood. Citrate anticoagulation is complicated by the fact that calcium chloride must be readministered to the patient to prevent tetany and other hypocalcemic effects. Special attention must be given to patient lab values. Literature has also reported the use of Prostacyclin and Nafamostat. At the 5th International Conference on CRRT in March, 2000, Dr. David Ward stated that “of the currently available regimens, citrate and synthetic heparinoids appear to have the greatest safety profile, in terms of reducing the risk of hemorrhage”. Regardless of the method of anticoagulation chosen, the nurse will administer the medication as ordered and will monitor parameters according to established protocol. The patient will be monitored for indications of bleeding and the CRRT system will be monitored and assessed for signs of clotting. If the CRRT extracorporeal circuit clots, it must be removed and replaced with a new circuit. It is important to maintain the vascular access according to established protocol.
MW <500 Higher the Vd the less available in the plasma for excretion Highly protein bound, less free substance available for excretion HD High rate of endogenous clearance eliminates need for extracorporeal circuit
IHD better and has more evidence but evolving for HDF and better for CVS instability Salicylates HD over HP as both have same clearance but HD clears the metabolic/electrolyte/fluid compenents!
Including -carbamazepine, theophylline, salicylates, meprobomate, phenytoin, sodium valproate, paraquat, thallium, dichlorvos, digoxin, tricyclic antidepressants etc Remember requires anticoagulation and can send patient profoundly hypotensive
Ronco et al Lancet RCT 2000, Honore et al crit care med 2000, Ratanarat et al 2006 crit care med. All mortality as primary outcomes! 40-85ml/kg/Hr is the next step and should be considered but is by no mean normal practice.
Early vs late more important in AKI rather than acute on CKD, but weak evidence So to summarize, let’s quickly compare and contrast the four basic CRRT therapies. SCUF is the most simple therapy, its purpose that of patient excess fluid removal. CVVH adds use of pumped replacement fluids, either pre or post filter, to enhance middle molecule clearance. CVVHD does not use replacement fluids, but incorporates use of pumped dialysate to enhance small molecule clearance. CVVHDF is the therapy that combines the benefits of CVVH and CVVHD with use of both replacement fluids and dialysate to achieve optimal benefits for the ARF patient.