CRRT IN AKI

RRT is frequently required in ptns with severe AKI. Acute RRTs may include IHDX, PD, CRRTs, as well as hybrid therapy

 

CRRT Prescription in AKI

 

 Abbreviations (read twice please):

o   A/V: Arteriovenous

o   AKI: acute kidney injury

o   ARDS: acute respiratory distress syndrome

o   AVFs: arteriovenous fistulas

o   AVGs: arteriovenous grafts

o   AB: antibiotic

o   BF: blood flow

o   BFR: blood flow rate

o   BUN: blood urea nitrogen

o   CO: cardiac output

o   CRRT: continuous renal replacement therapy

o   Ctr: citrates

o   CVVH: Continuous venovenous hemofiltration

o   CVVHDF: Continuous venovenous hemodiafiltration

o   DX: dialysis

o   Dzr: dialyzer

o   Dzt: dialysate

o   Dc Np: diabetic neuropathy

o   EF: ejection fraction

o   EFR: effluent flow rate

o   ESKD: end-stage kidney disease

o   FF: Filtration fraction

o   FRR: fluid removal rate

o   HCO³: bicarbonate

o   HDX: hemodialysis

o   Hf: hemofiltration

o   Hpt: Hypotension.

o   ICU: intensive care unit

o   ID: intermittent dialysis

o   IHDX: intermittent hemodialysis

o   IJ: internal jugular

o   IVC: inferior vena cava

o   IV: intravenous

o   KDIGO: kidney disease: Improving Global Outcomes guidelines

o   MAP: mean arterial pressure

o   MR: mortality

o   P⁺: phosphorus

o   PP: pulse pressure

o   PAES: Polyarylethersulfone

o   PD: peritoneal dialysis

o   PEI: Polycationic Saline solution

o   PES: Polyethersulfone

o   PIRRT: prolonged intermittent renal replacement therapy

o   RCA: regional citrate anticoagulation

o   RCT: randomized controlled trials

o   RF: replacement fluid

o   RRT: Renal replacement therapy

o   SCUF: Slow continuous ultrafiltration

o   ST: surface-treated

o   SF: substitution fluid

o   Sn (s): signs

o   TMP: transmembrane pressure

o   TPN: total parenteral nutrition

o   UF: ultrafiltration

o   WFR: water flow rate

 

RRT is frequently required in ptns with severe AKI. Acute RRTs may include IHDX, PD, CRRTs, as well as hybrid therapy, e.g., PIRRT. CRRT is commonly applied for acute RRT in ICU in developed centers. I will explain how to prescribe CRRT. CRRT is a complex procedure provided to the complicated ptns with critical illness. The CRRT should be provided with proper coordination between multiple specialties including critical care intensivists, nephrologists, nursery, pharmacy, and dietitians. It is believed that each institution should be compliant to specific protocol tailored by an expert panel within this institution. The designed protocol should include the key variables of the CRRT prescribing i.e., vascular access, anticoagulation, CRRT module, dosing, and CRRT fluids. Consequently, programmatic decisions can be implemented considering these items with fostered consistency and better service quality.

 

Whilst an entirely unlimited combination of modules (convective, diffusive, or combined), equipment, circuits, EFR, fluid removal plans, and vascular access’ device, with several approaches among CRRT providers leading to a wide variation in practice with increased possibility for error in medications’ dosing, anticoagulation protocols, machine setting-up, and nursing operators.

 

Moreover, each institution should be encouraged to design and monitor CRRT qualities indicating and tracking its outcome e.g., circuit longevity, small-solute clearance, hemorrhagic events, session interruption and down timing (i.e., time whilst CRRT is not provided to the ptn), catheter malfunction, fluid monitoring, and ptn MR. Whilst there’re no available data to track program that improving ptn outcome, there are data tracking protocols improving CRRT quality.

VASCULAR ACCESS: A perfectly-functioning vascular access is crucial to maintain CRRT circuit function as CRRT will not work properly with a malfunctioning access. A deep catheter (s) that could be inserted into a large central vein ending at the Rt. atrium or cavalatrial junction (i.e., IJ catheter) or an abdominal IVC (i.e., femoral catheter) will improve CRRT circuit adequacy and they are preferrable. Some experts utilize special triple-lumen DX catheter (s) for CRRT, despite others do not prefer this option for most ptns. Whilst the triple-lumen catheter may be efficacious in certain ptns, the 3^rd lumen may limit the inner diameter of the other 2 DX lumens, hence limiting the entire BF.

If a triple-lumen access is utilized, the 3^rd lumen should not be provided for lifesaving agents (e.g., antimicrobials) while CRRT is running. The 3^rd lumen should be dedicated for medications with no CRRT clearance (i.e., IV crystalloid or colloid infusion, systemic heparinization, blood products’ infusion, etc.). In theory, medications provided via the 3^rd lumen may be more fast cleared by DX than if given via another access. However, there’re no available data on the amount of 1^st pass clearance related to recirculation between the drug inflow lumen and the DX efflux lumen.

Moreover, Ca⁺ should not be infused via the 3^rd lumen in ptns on Ctr anticoagulation, as this may be complicated with recirculation, inaccurate Ca⁺ levels, and less efficacious RCA. For ESKD ptns, we do not utilize the AVF or AVG unless there’s lack of other access, despite there some data in those ptns have been provided. There’s a possible risk of vascular damage to the access with a rigid needle with possible blood losses if the needle dislodged, particularly with frequent re-positioning in the ICU. However, AVF & AVGs can be used with safety if PIRRT has been provided via either a CRRT machine or traditional DX facility.

HEMOFILTER: (also called hemo-Dzr) is the same device for all CRRT modules. Higher-permeability, high-flux biocompatible membranes are utilized for all modalities of CRRT. Typically, the membranes’ material used are polyacrylo-nitrile (AN69), PAES, & PES with no data available suggesting that one type of membrane is preferrable. In theory, owing to their negative charge, polyacrylo-nitrile membranes may provide more adsorption with elimination of the middle-molecule, e.g., cytokines. However, no difference in outcome has been reported.

The polyacrylonitrile membranes may induce bradykinin release. The untreated AN69 membrane should NOT be used in ptns with recent or current ACEi use, as this has been observed to induce anaphylaxis. However, AN69 ST membranes can be utilized safely with these agents. The AN69 ST membrane that is coated with a PEI can limit the surface electronegative charges avoiding bradykinin production. The AN69 ST membrane is not supplied in the US.

CRRT PRESCRIPTION: It includes choosing CRRT modality, anticoagulation (if applied), FF, BFR, dosing, CRRT replacement or DX solution, and the FRR.

CRRT modality: CRRT modalities include CVVH, CVVHD, and CVVHDF. The modalities can be differentiated by their current mechanism of solute elimination. CVVH applies convection, whereas CVVHD applies diffusion. CVVHDF applies combined convection and diffusion.  The application of CVVHD or CVVHDF rather than CVVH is preferred owing to their diffusive capabilities permitting the delivery of a higher RRT dosing with no driving up the FF value to an unacceptable higher level.

If the BF, Hct, and total EFR are kept constant, pure convective modality of therapy (e.g., CVVH) always showing a higher FF compared with diffusive modalities. The FF is the fraction of plasma water that’s eliminated from blood within UF. Greater FF value is currently complicated by a higher circuit clotting rate.

However, certain centers may apply CVVH, and this module is usually preferred according to the CRRT device available at certain institution. No studies available suggesting better outcome with certain modality. Meta-analysis: 19 RCT comp-aring Hf with HDX for ptns with AKI (with 16 studies of continuous modules), no difference in outcome, DX maintenance, organ failure, or vasopressor administration among studied survivors. In theory, purely convective modules (CVVH) and, to certain degree, combined convective/diffusive modules (CVVHDF) may eliminate large-sized solutes slightly better as compared with dialytic or diffusive modules (CVVHD), although the clinical value of this observation is not clear.

Anticoagulation: Common varieties of anticoagulation may include RCA and systemic unfractionated heparinization. Many physicians apply no anticoagulation, at least earlier in the management.

CRRT dose: Dosing is determined by the EFR. The effluent is the wasted fluid coming out of the outflow port of the Dzt/ultrafiltrate compartment outside the hemofilter. For CVVH, the effluent is consisting of UF volume (i.e., plasma water moving by convective power through the hemofilter membrane). For CVVHD, the effluent is mostly consisting of the spent Dzt and, to a little extent, UF volume given by convection. The prescribed EFR is usually 25 mL/kg/h in achieving (despite interruptions and CRRT downtime, that is often inevitable) a minimum effluent rate of 20 mL/kg/h. along 24-h. period. Excepted from this are the ptns showing severe metabolic alterations (e.g., hyper-K⁺ or acidemia) requiring more robust correction along 24-36 h. Here, we can provide a higher CRRT dosage, e.g., with intense metabolic acidemia (pH <7.1), we commence an EFR of 35-60 mL/kg/h., until acidosis is partially corrected. Once the intense metabolic error has been alleviated, we can decline the delivered dose of CRRT to mostly 25 mL/kg/h., this’s considered to be consistent with the 2012 KDIGO guidelines.

However, most clinical studies have not reported any benefit of higher CRRT dosing (>35-40 mL/kg/h) as compared with standard CRRT dosing (20-25 mL/kg/h) if considered over the whole timing of a ptn's CRRT program (i.e., days-weeks). Moreover, higher dosing of CRRT, especially if too long, may induce protein malnutrition, general hypovitaminosis and micronutrients with improper antimicrobial drug dosing. In ptns commencing higher CRRT dosing, it’s not easy to determine a strict threshold of lab alterations at which the CRRT dosage may be declined. Generally, deciding to lower the dose is primarily depending upon stability or improving lab profiles (i.e., K⁺ became stabilized within normal profile; pH and HCO³ are normalized or near normal and BUN is currently declining).

Filtration fraction (FF): The FF is the % of plasma water entering the Dzr and is moving by UF (convective power) across the DX membrane. In another words, it’s the fraction of water eliminated from blood. We usually keep the FF <20 %. Higher fraction (s) is complicated by higher circuit clotting, possibly related to hemoconcentration as well as blood protein-membrane interaction inside the hemofilter. FF is can be determined as follows:

Filtration fraction (FF) = UF flow rate / Plasma WFR

The UF flow rate = the rate at which plasma water is transferring across the membrane influenced by a pressure gradient between blood & Dzt / ultrafiltrate compartment (s).

Total UF volume = the overall UF volume attained during treatment and is the summation of the Rf volume and net UF volume eliminated from the ptn by the machine (i.e., FRR). For several CRRT machines, the total UF rate = the sum of RF rate + FRR. The definition of UF rate is varied from that applied in IHDX, where it is referring to the entire UF rate (i.e., rate of fluid elimination from the body). The plasma WFR is the rate of plasma water delivery to the Dzr or hemofilter. It equals:

The BFR x (1 - Hct) + The pre-filter Rf flow rate + Any other pre-pump infusion rate (e.g., Ctr).

Maintaining a relatively lowered FF can be achieved by:

o   Keep the UF flow (convective power) rate lowered.

o   Increase BFR (determining plasma WFR) (access should tolerate higher flow)

o   Utilizing a pre-filter Rf in CVVH or CVVHDF

To maintain the UF rate lowered may necessitate adding a diffusive element of clearance, particularly if a relatively higher EFR (i.e., >2 L/h) is decided according to ptn's weight or clinical status. In a purely convective treatment, like CVVH, solutes moving across the membrane is relying on the same force driving UF (i.e., TMP). To keep proper solute moving, TMP and, so, UF must be kept relatively higher. In diffusive treatment, solutes movement is greatly independent of the UF rates. This’s because it is driven by passive diffusion along concentration gradients and not by the TMP. The UF rate may be maintained relatively lower and still keeping solute movement.

As CVVHDF apply both combined diffusion and convection, the FF lies in between CVVH and CVVHD, according to the contributing share of convection and diffusion to the entire EFR. Generally, for a fixed effluent rate, the FF with CVVHDF is less than that with CVVH as a part of the dosing is given by diffusive power. The administration of a pre-filter RF in CVVH or CVVHDF will help to maintain a lowered FF as it augments the plasma WFR, at least in comparison with post-filter RF. However, this’s mostly not sufficient to halt hemoconcentration with filter clotting. Moreover, pre-filter replacement fluid will dilute the blood, so, it will limit the small-solute clearance as compared to post-filter RF.

CRRT BFR: For anticoagulated ptns, we may keep the BFR of 200 mL/min (although BFR of <200 mL/min are commonly used in RCA). Among ptns who’re not anticoagulated, a higher BFR (250-300 mL/min) may be warranted to assure catheter patency and CRRT circuit persistence. However, at least one RCT has shown there’s no difference in circuit lives between a BFR of 150 & 250 mL/min. FF is inversely proportional to the BF. So, a lowered BFR (<100-150 mL/min) can augment hemofilter/circuit loss owing to blood stasis with rising FF.

BFR > 250-300 mL/min may decline the circuit lifespan, as vascular access usually cannot accommodate this higher level of BFR along several hours or days in a critically ill ptn. Along this time an increased access and return pressure alarm, frequent blood pump stopping, blood stasis, and frequent circuit clotting could be obseved. Moreover, according to manufacturer’s guidelines, CRRT hemofilter life span can be limited both by timing pass and by the magnitude of blood processed. The maximum magnitude of the treated blood is reached earlier by higher BFR. BFR alterations between 100 & 300 mL/min usually does not impact solute clearance that can be limited by either BFR or the EFR. As the BFR is almost always much higher than EFR, solute clearance is mostly EFR limited. The exception is that the EFR is higher or equal to BFR.

Generally, for CVVHD, the BFR should be ≥2.5 times the Dzt flow rate. This allowing completely saturated Dzt and preserving the direct relationship between Dzt rate and small-solute clearance. With CVVH modality with post-filter Rf, the BFR should be ≥5 times the Rf rate to optimize the FF. If CVVH applied with pre-filter Rf, the BFR should be ≥6 times the Rf rate to optimize the solute clearance. Ptns anticoagulated with RCA, higher BFR also mandates rising the amount of required Ctr that increasing the cost (i.e., purchasing more Ctr) and the rate of complications, considering more Ctr will invade the ptn's systemic circulation. Lastly, the BFR does NOT impact the hemodynamic stability, as the amount of blood in the circuit at any time does not alter as BFR changes.

CRRT solution: Solutions provided for Rf/Dzt can either be customary compounded or purchased commercially. We prefer not to use customary CRRT solutions, in order to limit the risk of compounded solutions. There’re several commercial CRRT solutions with several levels of electrolytes & glucose:

{1} Sodium: The Na⁺ level in the commercially current solutions is ranging from 130-140 mEq/L. For many ptns, the Na⁺ level in CRRT solutions should be physiological (i.e., 135-140 mEq/L). A lowered Na⁺ (i.e., 130 mEq/L) may be used for ptns on RCA anticoagulation in order to avoid hypernatremia as the infused Ctr fluid could be hypertonic.  

{2} Potassium: The K⁺ level in a standard solution is ranging from 0-4 mEq/L. We use a 4 mEq/L K⁺ level for ALL ptns except those with intense hyper-K⁺ (>6 mEq/L with no ECG changes or increased to any level in ECG changes consistent with hyper-K⁺).

Either a 0 or 2 mEq K⁺ solution can be utilized to manage severe hyper-K⁺, according to solution availability (many stocks: 4 mEq/L K⁺ and either, but not both, a 0 or 2 mEq/L). Ptns on CVVHDF, a 2 mEq K⁺ solution may be utilized on the CRRT device via both 4 K + 0 K solutions provided on the same rate, e.g., if we use a 4 K pre-filter Rf at a rate of 1200 mL/h and a 0 K solution as Dzt at a rate of 1200 mL/h., then the final K⁺ level of the CRRT circuit will equal 2 mEq/L. However, we assure that IHDX rather than CRRT is indicated for the management of intense hyper-K⁺ (i.e., ECG alterations e.g., worsened peaked T-wave or prolonged QRS resistant to Ca⁺ supplements), even if the ptn requiring a vasopressor. Even with the highest effluent levels with the CRRT, the net eliminated K⁺ per minute is much higher with the standardized IHDX.

 

{3} Bicarbonate (HCO³): Most centers often use HCO³ rather than lactate-based CRRT fluids. Serum lactate values are usually greater if lactate-based fluids are utilized, especially among ptns with hepatic dysfunction that confusing the clinically interpreted blood lactate values. However, lactate-based fluids have been provided properly among ptns with a basal lactate value <4 mmol/L. The standard solution has a HCO³ level usually ranges from 22-35 mEq/L. We may use a "higher" HCO³ fluid (i.e., 32-35 mEq/L) in all ptns except those managed with RCA. With ptns on RCA, we provide "normal" HCO³ fluid (i.e., 22-25 mEq/L). Metabolic alkalosis is a commonly observed drawback of RCA as the provided Ctr is usually converted to HCO³.  

{4} Phosphate: Standard solution usually contains either no P⁺ or 1 mmol/L P⁺. P⁺ -containing solution is usually provided if serum P⁺ is <4.5 mg/dL and P⁺ free one for other ptns. Small reports observed that utilizing P⁺-containing CRRT solution may minimize the risk of severe hypophosphatemia evolution.

{5} Glucose: The standard solution is usually either glucose free or contains 100-110 mg/dL glucose. Many experts utilize a solution of 100 mg/dL of glucose. Other clinicians may suggest utilizing glucose-free solution to optimize glucose level among hyperglycemic ptns. However, this has not been assessed in a systematic manner, and at least theoretically, there’s a risk of hypoglycemia with providing glucose-free solution.

{6} Ca⁺: Standard fluid is Ca⁺ free or has 2.5-3.5 mEq/L Ca⁺. Ca⁺-free solution is used if RCA is provided. Ca⁺ level of 2.5 mEq/L is maximally provided if the solution containing P⁺.  

Ptn FRR: The targeted hourly fluid balance ranges from net even to net -ve 200-250 mL/h., with net result in a 24-h fluid balance of even to -ve 4-6 L. Sometimes, we halt ptn fluid removal entirely allowing an hourly net +ve fluid balance; this’s particularly seen in the setting where there’re higher ongoing sources of anuria, non-CRRT fluid loss e.g., surgical wounds/drains, intense burn, ongoing hemorrhage, etc. The net results and the rate of fluid elimination can be identified clinically. Almost all ptns in need for CRRT may show certain degree of volume overloading that may contribute to the total MR/morbidity. However, hemodynamic status is usually guiding the rate of fluid elimination, and our clinical behavior. It is believed that the most crucial for the collaborating team (i.e., nephrology + ICU teams) is to determine a target of hourly fluid balance, then the bedside ICU nurses could adjust the FRR as required to get the desired hourly fluid balance target.

As long as fluid is removing and a target negative fluid balance being achieved, the collaborating team should manage the ptn's hemodynamic stability and slowdown/halt fluid removing with any Sn of intolerance (i.e., declined CO, a progressively concerning rise in vasopressor requirements, etc.). In certain ptns, fluid removing may require prioritizing over mild rises in vasopressor administration or prolonged vasopressor exposure, e.g., intense ARDS with fluid overloading.  Additional tools (e.g., PP or stroke volume variations, bedside Echo, and IVC volume) may be added to evaluate volume settings if inquiries develop in regard to fluid removal.

LAB MONITORING: At the start, electrolytes & acid-base balance can be monitored every 6-12 hs. If the ptns remain stabilized with minimal alteration in electrolytes at 24-48 h, electrolytes monitoring can be diminished to every 12-24 hs. With RCA therapy, more frequent monitoring may be needed.  

COMPLICATIONS: may include electrolyte, minerals, and acid-base imbalance; Hpt; infectious episodes; bleedings; and hypothermia. Subtherapeutic AB dosing is frequently observed (usually unrecognized); so, careful revision of the antimicrobial dosage is required with CRRT therapy.

Electrolyte, mineral, and acid-base imbalance: Including hypo-PO⁴, hypo-K⁺, hypo-Mg⁺, and, less frequently, hypo-Ca⁺. Hypo-PO⁴, hypo-K⁺, and hypo-Mg⁺ are the most commonly observed lab abnormalities. Generally, if the electrolyte or mineral levels is not in physiological range in the CRRT fluid, lost electrolytes and/or minerals in the effluent will supervene requiring rapid repletion. The more physiological the electrolyte contents are in the CRRT fluids, the less likely repletion will be needed.

{1} Hypo-PO⁴: It is commonly and increasingly observed with the EFR. One RCT: hypo-PO⁴ observed in >50 %. Hypo-PO⁴ on CRRT can be complicated with prolonged respiratory failure.

Hypo-PO⁴ can be prevented via PO⁴-rich Dzt & Rf. If hypo-PO⁴ develops despite the administration of PO⁴-rich solution, parenteral P⁺ supplies may be given. Greater dosing of parenteral PO⁴ is usually needed compared with ptns who’re not on CRRT as PO⁴ is generally provided over 4-6 h.s and the current CRRT eliminates a significant amount of the administrated dose during the procedure.  

{2} Hypo-K⁺: Hypo-K⁺ is a commonly observed complication of CRRT. One RCT: Hypo-K⁺ reported in >23 % of ptns on CRRT. The risk is greater with the effluent rate rising and with contents of the CRRT fluid. In RCT: comparing intense (i.e., higher effluent rate) to less one (lowered effluent rate) RRT including continuous ones, hypo-K⁺ was reported in 7.5 & 4.5 % of intensive and less one RRT, resp.

The risk of hypo-K⁺ development also depending on ptn’s risk factors e.g., nutritional agents (i.e., composition of TPN and tube feedings, etc.) and the clinical settings. Hypo-K⁺ can be limited if CRRT replacing and/or Dzt fluids contain K⁺ 4 mEq/L. If hypo-K⁺ develops despite using of 4 mEq/L, we can replete with IV K⁺ as with any other case not on CRRT. Some experts may add K⁺ to the solution(s). Using the commercially current standard solution to prevent compounding error (s) is currently preferred.  

{3} Alkalosis: Ctr anticoagulation may induce either metabolic alkalosis or metabolic acidosis. Metabolic alkalosis may be seen in ptns with proper liver function and muscle perfusion, who’re able of metabolizing systemic Ctr into HCO³. Metabolic acidosis can occur in ptns with acute liver cell failure or severely shocked, who’re unable of metabolizing the accumulated systemic Ctr.  

{4} Hypo-Mg⁺: It is commonly seen among ptns on CRRT. It can be managed with IV Mg⁺ as in any other ptn not on CRRT. Some experts may add Mg⁺ to the CRRT fluids.

 {5} Hyper-Na⁺: may develop in ptns on RCA if the CRRT fluid contains standardized amount of Na⁺ (i.e., 140 mEq/L). Here, we can administer a solution with a lowered Na⁺ level of 130 mEq/L.

 {6} Hypo-Ca⁺: Hypo-Ca⁺ is uncommonly seen unless Ctr is being used for anticoagulation and DX or Rf do not contain Ca⁺. For ptns particularly on Ctr requiring Ca⁺ supplementations, Ca⁺ alterations can be corrected via adjusting the Ca⁺ infusion.  

Hypotension (Hpt): Generally, Hpt is less commonly seen with CRRT than with IHDX, despite, in one RCT: Hpt reported at similar incidence in ptns on CRRT vs HDX (35 vs 39 %, resp). The target UF rate is usually determining the risk magnitude of Hpt. Hpt observed if the FRR exceeding the rate at which the intravascular space could be refilled.

Ptns with Dc Np, low ventricular EF, diastolic malfunction, or sepsis are particularly prone to Hpt as refilling capacity (i.e., the rate of intravascular space refilling) is declining. The ptn's clinical status and hemodynamic stabilization must be closely monitored and the UF rate should be optimized in order to halt and/or diagnose Hpt. The rate of small-solute elimination could also affect in vivo fluid shifting regardless fluid elimination. The fast elimination of small solutes can induce a relative decline in the tonicity of the blood in comparison with the extravascular interstitial fluid leading to a transient shift of the intravascular water into the extravascular compartment.

Hypothermia: It may be observed due to extended blood circulation in the extracorporeal circuit. In RCT: hypothermia seen in 17 % of ptns on CRRT compared to 5 % of ptns on IHDX. Any finding of fever could be masked by the CRRT-induced hypothermia. A blood warmer or external warming device can be provided to halt extensive cooling.

Infection and bleeding:  well-proved sequalae of the vascular access.

CRRT in AKI

 

RRT is commonly provided in ptns developing severe AKI. Acute RRTs may include iHDX, PD, CRRTs, and hybrid modules e.g., PIRRTs that provide prolonged but still ID. I shall provide here an overview of several CRRT modules.

INDICATIONS

Indications to institute RRT therapy in AKI are similar in all modalities, but choosing the modality may be variable. Particular indications may include fluid overloading, hyper-K⁺, acidosis, and Sns of uremia.

In many centers, iHDX is the standard RRT module for ptns with hemodynamic stability. Considering the clinical practice pattern, the main indication for CRRT option over iHDX is the hemodynamic instability. Hpt is widely thought to be less commonly observed with CRRT (but still seen) considering the slower rates of fluid/solute removing compared with iHDX. However, RCT: No proved improving hemodynamic stability among ptns managed with CRRT compared with iHDX.

CRRT is particularly of benefits for ptns with hemodynamic instability requiring currently supplied large-volume fluids, e.g., multiple IV drugs, or TPN. As CRRT is a continuous provided therapy, the net solute elimination along 48 h.s is greater than with IHDX, despite its lowered rating. Frequently, CRRT is preferrable to IHDX for ptns with acute brain events or other disorders with elevated intracranial tension associated with AKI. As cerebral edema may be worsened with IHDX due to declined MAP (leading compensating cerebral vasodilation) and via a faster elimination of urea leading to shifting of water into the intracellular space.

Exception: IHDX rather than CRRT may be preferred for treating ptns with severe hyper-K⁺ (i.e., ECG changes, e.g., highly peaked T-wave or prolonged QRS, refractory to Ca⁺ supplies), even if the ptn requiring a vasopressor during the procedure. Even with applying the highest effluent rate available in the CRRT, bulk K⁺ elimination with standardized IHDX or PIRRT is much more beneficial on a minute-to-minute observation. Here, strict clinical monitoring is mandated and usually depending on many other variables e.g., available DX nurse staff.

MODALITY DEFINITIONS

There’re several CRRT modalities that’re differing from each other mainly relying upon the mechanism(s) of solute transport. In RRTs, solutes could be eliminated by diffusion and/or convection. Diffusion is the target mechanism underlying the standard HDX, despite little convection may occur. Whilst diffusion is urged by concentration gradient between blood and Dzt, convection is operated in Hf via the solutes’ moving across a hydrostatic pressure gradient.

No one CRRT modality has been reported to offer better outcome. Choosing of CRRT modality within an individual institution depends primarily on the current facilities and the clinician experience. In certain setting, the chosen technique is depending on the level at which solutes/fluid must be eliminated, e.g., slow continuous UF is used primarily to eliminate fluids but is not helpful for ptns requiring solute removing. All CRRT modalities today are utilizing venovenous circuits with blood flowing via the Dzr/hemofilter is driven by an extracorporeal blood pumps. All requiring placement of a dual-lumen IV HDX catheter.

A/V modalities, in which blood flowing was driven by the gradient between the MAP and venous pressure, are no longer utilized considering the risk associating with the arterial access (embolization, bleedings). The sole advantage of A/V modality was that they did not require the blood pump.

CVVH: CVVH applies hydrostatic pressure to produce plasma water filtration across the hemofilter membranes. Solutes being eliminated totally by convection. Dzt fluid is not provided. The UF flow rate is great (20-25 mL/kg/h). So, Rf must be readily provided to halt volume depletion. The magnitude of the provided Rf can be recognized by the desired net volume elimination.

Small- & middle-molecules (i.e., <5000 Daltons), e.g., urea and other electrolytes, are eliminated nearly the same % as plasma water. So, there’s no changes in the plasma concentration of these solutes by Hf. However, the provided SF declines via dilution the plasma concentration of solutes e.g., urea & Cr that’re usually not found in the SF. Removing urea (and other small, lipid-soluble solutes) may also be augmented by Rf administration before the hemofilter; this pre-dilution decreases the plasma urea concentrations, so permitting urea diffusion from within the RBCs to plasma water.

CVVHD: is mainly removing solute via diffusion. Dzt fluid is provided. As in IHDX, Dzt fluid is running in a countercurrent direction to that of blood flow at a rate of 1-2 L/h. In contrary to CVVH, the UF rate is usually limited to 2-8 mL/min. The Dzt flow rate is 20-25 mL/kg/h. In CVVHD, UF is limited to the rate of desired net fluid elimination, and no IV fluid replacing is provided.

CVVHDF: CVVHDF combined diffusion with convection modalities. CVVHDF needs infusion of both Rf and DX fluid. Similar to CVVH, the UF volume is variable, and Rf should be provided to optimize euvolemia. The magnitude of the provided Rf is recognized by the desired total volume elimination.

SCUF: utilized to manage isolated fluid overloading. SCUF is not beneficial in uremic or hyper-K⁺ ptns, considering solute elimination is minimized. SCUF can be safely removing up to 8 L of fluid/d. Here, neither Rf nor Dzt fluid is provided. Convective solute clearance is minimal as the UF rate is lowered as compared with CVVH. Also, there’s no diffusive solute clearance as Dzt fluid is not provided. The blood flow (QB) is usually 100-200 mL/min and the UF rate 2-8 mL/min.

VASCULAR ACCESS: CRRT needs properly patent vascular access capable of providing BFR of minimally 200-250 mL/min. The standardized is a double-lumen tunneled or non-tunneled DX catheter. For ESKD ptns having AVFs or AVGs to maintain HDX, the fistulas/grafts should not be utilized for CRRT unless there’s no other access, considering the risk of needle dislodgment with bleeding or damage to the AVF or AVG. The preferrable catheter access location is the Rt. IJ vein, despite the femoral vein can be utilized, if required. The subclavian vein should be avoided, if possible, as subclavian root could be complicated by stenosis of the subclavian vessel that may impede future AVFs or AVGs creation.

EQUIPMENTS: The basic constituents of the available CRRT programs are similar:

o   Blood flow & Dzt inflow and outflow can be managed via a roller pump.

o   Balance system providing UF control.

o   Dzt inflow & outflow are persistently recorded and the pump speed adjusted to optimize the desired flow rate. Via a microprocessor-driven control, UF rate can be optimized very precisely.

Several new machines can be utilized for all CRRT modalities, despite certain types cannot provide CVVHDF.

DRUG DOSAGES: The rate of the eliminated drugs via CRRT is affected by multiple ptn & drug-related factors and by CRRT modalities and their prescriptions.

LAB MONITORING: Lab profiles are common in ptns on CRRT, and lab values are properly monitored.  

CRRT WITHDRAWAL OR SHIFTIG TO IHDX: There’s no dedicated approach to hold CRRT. Ptns are usually shifted to HDX once they’re evidently hemodynamic stability and more mobility is desired. Alternative scenario, CRRT may be withheld if there’s sufficiently recovered renal function.  

COMPLICATIONS OF CRRT: Sequalae of CRRT are generally similar among CRRT modules. They include electrolytes, minerals, and acid-base imbalance; Hpt; infectious episodes; bleedings; and hypothermia.