Continuous Renal Replacement Therapy (CRRT)

Foundations: What CRRT Is and How It Works

1.1 Definition and rationale

Continuous renal replacement therapy (CRRT) is a family of extracorporeal blood-purification techniques delivered continuously (target ≥24 h/day) to replace kidney function in critically ill patients. By removing solutes and fluid slowly and continuously rather than in short intermittent sessions, CRRT achieves gradual, minute-to-minute control of volume, electrolytes, acid–base status, and uremic solutes with far less hemodynamic stress than intermittent hemodialysis (IHD).

The defining advantage is cardiovascular tolerability: slow ultrafiltration and low solute-clearance rates avoid the rapid osmotic and volume shifts that provoke intradialytic hypotension. This makes CRRT the preferred modality for hemodynamically unstable patients on vasopressors, and for patients in whom rapid solute shifts are dangerous (e.g., acute brain injury, cerebral edema, fulminant hepatic failure).

1.2 The three transport mechanisms

Every CRRT modality is built from combinations of physical processes acting across a semipermeable hollow-fiber membrane:

1.3 CRRT modalities

Modalities are named by the transport mechanism(s) used. "CVV" = continuous veno-venous (blood pumped from and returned to a vein through a double-lumen catheter — the standard access for all modern CRRT).

1.4 Circuit anatomy and key terms

Understanding the circuit makes prescription, documentation, and troubleshooting intuitive. Blood is drawn from the access limb, pumped through the hemofilter, and returned via the return limb.

Patient Selection, Indications & Timing

2.1 Indications for renal replacement therapy

The threshold to initiate RRT integrates the classic life-threatening indications with the overall trajectory and demand-versus-capacity balance of the kidney. The mnemonic AEIOU captures the emergent triggers:

2.2 Timing of initiation — what the trials show

Five landmark RCTs have tested "early/accelerated" versus "delayed/standard" initiation. The aggregate signal is clear: in the absence of a life-threatening indication, earlier initiation does not improve survival, and a watchful-waiting strategy lets a substantial minority of patients recover without ever needing RRT.

2.3 CRRT versus IHD versus SLED/PIRRT

Modality of RRT is chosen from the patient's hemodynamics, neurological status, and logistics. KDIGO recommends using CRRT and IHD as complementary therapies, with CRRT preferred for hemodynamically unstable patients and for acute brain injury / raised intracranial pressure.

2.4 Contraindications & cautions

• No absolute contraindication to CRRT itself when RRT is indicated; considerations are relative and logistical.
• Inability to obtain safe vascular access, or when goals of care make aggressive support inappropriate (integrate with palliative goals).
• Active uncontrolled bleeding complicates anticoagulation strategy — favors regional citrate or no-anticoagulation approaches rather than withholding therapy.
• Severe hepatic failure or shock with lactate accumulation raises citrate-accumulation risk — anticipate and monitor (see Anticoagulation).

Prescription & Dosing

3.1 The prescription checklist

A complete CRRT order specifies every element below. Standardizing the order set reduces error and downtime.

3.2 Effluent dose — the evidence and the math

Delivered effluent dose is the CRRT analog of Kt/V and is expressed in mL/kg/h. Two large RCTs — ATN (VA/NIH, higher- vs lower-intensity) and RENAL (40 vs 25 mL/kg/h) — showed no survival benefit from higher-intensity therapy. KDIGO therefore recommends delivering an effluent dose of 20–25 mL/kg/h for CRRT in AKI.

Worked example

3.3 Pre- versus post-dilution

3.4 Fluid management — the second prescription

Fluid balance is prescribed separately from clearance and is often the single most important daily decision. Distinguish three quantities:

• Ultrafiltration rate (gross): total fluid pulled across the membrane, mostly returned as replacement fluid.
• Net ultrafiltration (patient fluid removal): the actual fluid removed from the patient per hour — the number that changes the patient's volume status.
• Fluid balance: net UF minus all intake (infusions, nutrition, drugs, blood products, flushes). CRRT "creates space" for obligate intake.

3.5 Solutions: buffer and electrolytes

• Buffer: bicarbonate-buffered solutions are standard (lactate-buffered fluids are largely obsolete and problematic in lactic acidosis/hepatic failure).
• Potassium: select fluid K⁺ (commonly 0, 2, or 4 mmol/L) to the patient's needs; anticipate falling K⁺ once dialysis begins and adjust to avoid hypokalemia.
• Phosphate: hypophosphatemia is common and predictable on continuous therapy — use phosphate-containing solutions or supplement proactively.
• Calcium & magnesium: citrate anticoagulation removes calcium (chelated) and magnesium; replace per protocol (see Anticoagulation).

Vascular Access

Circuit performance begins at the catheter. A well-functioning, appropriately sited, non-tunneled double-lumen dialysis catheter is essential for adequate blood flow and long filter life.

4.1 Site selection

4.2 Catheter sizing and care

• Use a large-bore double-lumen catheter of adequate length for the site (femoral catheters must be long enough to reach the inferior vena cava for good flow).
• Confirm tip position and rule out complications before high-flow use (per site and institutional policy).
• Reserve the dialysis catheter for CRRT; avoid using it for routine infusions to preserve patency and reduce infection.
• Recirculation and poor flows are common with malpositioned or reversed lines — investigate persistent access alarms early (see Troubleshooting).

Anticoagulation

Blood contacting the extracorporeal circuit activates coagulation; without anticoagulation, filters clot prematurely, lowering delivered dose and wasting blood. The goal is to keep the circuit open while minimizing patient bleeding.

5.1 Options and the guideline position

5.2 Regional citrate anticoagulation (RCA) — mechanism

Citrate is infused into the blood as it leaves the patient (pre-filter). It chelates ionized calcium, and because calcium is an essential cofactor in the coagulation cascade, lowering ionized calcium inside the circuit (post-filter) halts clotting locally. Some calcium-citrate is removed in the effluent; the remainder returns to the patient, where citrate is rapidly metabolized (liver, muscle, kidney) to bicarbonate, releasing the chelated calcium. A separate systemic calcium infusion replaces the calcium lost in effluent and restores normal systemic ionized calcium — so the patient is not anticoagulated, only the circuit is.

5.3 Running and titrating RCA

• Citrate dose is set relative to blood flow (commonly ~2.5–3 mmol/L of blood flow) and titrated to the post-filter ionized calcium.
• Titrate citrate up if post-filter iCa is above target (circuit under-anticoagulated), down if below target.
• Titrate the systemic calcium infusion to the patient's systemic ionized calcium — up if the patient is hypocalcemic, down if hypercalcemic.
• Monitor per protocol: post-filter iCa and systemic iCa (e.g., q6h once stable, more often during titration), plus acid–base, sodium, and magnesium.

Regional citrate titration reference

Two independent knobs: post-filter ionized Ca (circuit) is controlled by the CITRATE rate; systemic ionized Ca (patient) is controlled by the CALCIUM infusion rate. Adjust each to its own target using its own lab.

Citrate → post-filter (circuit) ionized calcium [target ~0.25–0.35 mmol/L]

Calcium infusion → systemic (patient) ionized calcium [target ~1.0–1.2 mmol/L]

5.4 Citrate accumulation — recognize and manage

If citrate is metabolized too slowly (hepatic failure, severe shock/hypoperfusion with lactic acidosis), citrate–calcium complexes accumulate. Chelated calcium is measured by total calcium but not by ionized calcium, producing the characteristic signature:

5.5 Metabolic effects of citrate to watch

• Metabolic alkalosis: citrate → bicarbonate when metabolized normally; may need to reduce citrate or adjust buffer.
• Metabolic acidosis: when citrate is NOT metabolized (accumulation) — the opposite problem (see §5.4).
• Hypernatremia: some citrate solutions add a sodium load; monitor sodium.
• Hypomagnesemia: citrate also chelates magnesium; replace as needed.

Setup, Priming & Initiation

This operational section is written for the bedside team. Always follow your specific machine's guided setup; the sequence below is the common workflow and the safety checks that matter most.

6.1 Pre-initiation checklist

1. Confirm the order is complete: modality, Qb, effluent/dose, dialysate & replacement rates and split, net UF goal, anticoagulation, fluid electrolyte composition, temperature.
2. Confirm working vascular access: correct catheter, patency of both lumens, secure dressing, position verified.
3. Baseline labs drawn: electrolytes, calcium (ionized + total), magnesium, phosphate, acid–base, and (if citrate) baseline systemic ionized calcium.
4. Correct solutions at bedside and in date: bicarbonate-buffered dialysate/replacement with the ordered K⁺ and PO₄; citrate and calcium bags if RCA.
5. Machine, warmer, effluent bag, and anticoagulation lines ready; alarms and pressure limits set.
6. Patient consent/goals reconciled; hemodynamics and vasopressors noted for net-UF planning.

6.2 Priming and connection

1. Load the circuit/filter set per the machine's guided prompts; confirm no kinks and all connections Luer-locked.
2. Prime the circuit (typically saline ± heparin per protocol) to remove air and wet the membrane; run the automated air/pressure self-tests.
3. Attach and start anticoagulation (citrate pre-filter) before connecting the patient if using RCA, per protocol.
4. Connect access (red/arterial) then return (blue/venous) lines using aseptic technique; unclamp in the machine-directed order.
5. Start blood pump at a low rate and increase gradually while watching access and return pressures for stability.
6. Initiate dialysate/replacement flow and net UF; set temperature to counter circuit cooling.

6.3 First-hour verification

• Confirm pressures are stable and within limits (access, return, TMP, pre-filter).
• If RCA: draw post-filter and systemic ionized calcium at the protocol interval and titrate.
• Verify net fluid removal is tracking to goal and the fluid-balance ledger is started.
• Document baseline circuit pressures as the reference for later troubleshooting (a rising trend from baseline is more informative than any single value).

Documentation & Monitoring

Rigorous documentation is a patient-safety intervention: it detects clotting early, prevents fluid-balance error, and makes handoff reliable. This part provides a monitoring cadence, the required flowsheet fields, and a structured handoff.

7.1 Monitoring cadence

7.2 Required flowsheet fields

A CRRT flowsheet should capture, at minimum:

• Prescription in effect (modality, Qb, dialysate/replacement rates, dose, net UF goal, anticoagulation).
• Hourly circuit pressures: access, return, filter/TMP, pre-filter — recorded as a trend.
• Hourly fluid ledger: effluent volume, net UF removed, ALL intake (replacement returned, IV fluids, drips, nutrition, blood products, flushes), and cumulative balance.
• Anticoagulation: citrate rate, systemic calcium rate, post-filter iCa, systemic iCa (or heparin rate/aPTT).
• Labs with times; electrolyte/buffer additive changes.
• Events: alarms and interventions, circuit/filter changes with reason, downtime start/stop, transport off-therapy.
• Filter age (hours in service) and appearance.

7.3 Structured handoff (SBAR for CRRT)

Troubleshooting & Alarms

Most alarms are pressure alarms, and most pressure alarms are access or clotting problems. Work systematically: read which pressure is abnormal and in which direction, then act. Always treat the patient, not just the machine.

8.1 Pressure alarms — decode by signal

8.2 Circuit clotting — prevention and response

• Recognize early: rising TMP and pre-filter pressures, dark blood/streaking in the filter, blood in the bubble trap, poor solute clearance.
• Prevent: adequate anticoagulation (RCA preferred), maintain blood flow, keep filtration fraction < 25% (favor pre-dilution when clotting-prone), minimize interruptions and access alarms, avoid kinks.
• Respond: if clotting is advanced, return blood if still safe and possible, then change the circuit; if fully clotted or clot risk to patient, discard per protocol. Investigate the root cause (access? anticoagulation? downtime?) before restarting to avoid repeat loss.

8.3 Air-in-line and blood-leak alarms

• Air detector: stop and clear air from the venous/return chamber per machine guidance; check for loose connections and low chamber levels; never bypass an air detector.
• Blood-leak alarm: indicates blood crossing into the effluent (membrane rupture); stop therapy and change the circuit per protocol.

8.4 Metabolic & thermal complications

8.5 Step-by-step troubleshooting algorithms

The tables above tell you what to look for. The algorithms below tell you what to do, in order, with a checklist you can initial as you go. Work each one top to bottom; fix mechanical causes first, then physiologic, then circuit.

Special Populations & Drug Dosing

9.1 Special clinical situations

9.2 Drug dosing on CRRT — principles

CRRT provides continuous clearance roughly analogous to a modest, steady GFR, so most renally cleared drugs need more than anuric-patient dosing but less than normal-renal dosing. Underdosing antimicrobials is a real and dangerous error in sepsis.

• Drivers of removal: low protein binding, small volume of distribution, low molecular weight, and predominant renal clearance all increase CRRT removal.
• Dose scales with effluent (dose) rate: higher effluent flow → more drug removed; reassess when the CRRT dose changes.
• Loading doses are unchanged: base loading on volume of distribution (give a full load); adjust the maintenance dose/interval for clearance.
• Use levels where available: therapeutic drug monitoring (e.g., vancomycin, aminoglycosides, and where available beta-lactams) is the most reliable guide.
• Replace losses: water-soluble vitamins and trace elements are cleared — supplement, especially with prolonged therapy and in nutrition planning.

9.3 Nutrition on CRRT

• Continuous therapy causes ongoing amino-acid and micronutrient losses; protein needs are higher than in non-CRRT critical illness — coordinate with clinical nutrition.
• Account for non-nutritional calories/volume from citrate and glucose-containing solutions in the daily balance.
• Monitor and replace phosphate, magnesium, potassium, water-soluble vitamins, and trace elements (selenium, zinc, copper).

Weaning & Discontinuation

Stopping CRRT is a clinical judgment; there is no single validated threshold. The strongest practical predictor of successful liberation is recovering urine output (spontaneous or diuretic-assisted), reflecting returning kidney function.

10.1 Signals that recovery is underway

• Rising urine output (a common practical cue is increasing spontaneous urine output, e.g., trending well above minimal volumes), with or without diuretics.
• Improving fluid balance so that intake can be handled without continuous removal.
• Stabilizing/improving electrolytes and acid–base without escalating CRRT demand.
• Resolution of the acute illness that precipitated AKI (source control, off or weaning vasopressors).

10.2 How to discontinue

• Trial off therapy with close monitoring of potassium, bicarbonate, fluid balance, and urine output; restart if the patient cannot keep pace.
• Transition to IHD or SLED when hemodynamically stable but still needing RRT — this frees the patient, reduces anticoagulation exposure, and aids mobilization/rehab.
• Reassess drug dosing after stopping CRRT — clearance changes abruptly.

Quality, Safety & Program Metrics

A CRRT program's quality is measurable. Tracking a small set of metrics drives better delivered dose, longer filter life, and fewer complications.

Quick Reference — Starting CVVHDF Prescription Card

Conservative, commonly used starting points for an adult CVVHDF prescription with regional citrate — not fixed orders. Adjust to weight, labs, hemodynamics, and institutional policy.