Renal Replacement Therapy

Quick Answer: Renal Replacement Therapy (RRT) in critical care encompasses continuous and intermittent modalities for acute kidney injury, electrolyte imbalance, volume overload, and intoxication. Continuous Veno-Venous Haemodiafiltration (CVVHDF) is the standard ICU modality at 20-25 mL/kg/h effluent flow rate. Regional citrate anticoagulation is first-line unless contraindicated. Access via double-lumen vascath (11-13 Fr). Major complications include citrate toxicity, membrane clotting, and hypophosphatemia.

CICM Second Part Exam Focus

High-Yield Areas:

RRT initiation criteria for AKI (KDIGO, renal recovery)
CRRT vs IRRT comparison (hemodynamics, clearance, outcomes)
CVVHDF vs CVVH vs CVVHD mechanisms (diffusion, convection, adsorption)
Dose prescription and delivery (20-25 mL/kg/h, pre- vs post-dilution)
Citrate anticoagulation mechanism and monitoring (ionised calcium gap, total Ca:ionised Ca ratio)
Complications: hypothermia, hypotension, citrate lock, filter life
Evidence: RENAL, ATN, BAXTER, IVOIRE, RRT dose meta-analyses

Common Viva Topics:

"You are called about a patient with AKI - discuss your approach to RRT decisions"
"Compare and contrast CRRT modalities available in ICU"
"Explain citrate anticoagulation for CRRT and how you troubleshoot problems"
"A patient on CVVHDF develops metabolic acidosis - what are your considerations?"

Key Clinical Pearls:

20-25 mL/kg/h effluent dose is optimal - higher doses increase complications without benefit
Citrate reduces bleeding 50% compared to heparin but requires ICU-level monitoring
CRRT preferred in hemodynamically unstable; IRRT acceptable in stable patients
Filter life averages 48-72 hours with citrate, 24-36 hours with heparin/no anticoagulation
Hypophosphatemia occurs in up to 80% on CRRT - requires aggressive repletion

Overview

Renal Replacement Therapy (RRT) refers to extracorporeal techniques that replace normal kidney function by removing solutes and fluid from the blood. In intensive care, RRT is most commonly indicated for acute kidney injury (AKI) but also serves critical roles in toxin removal, electrolyte management, and volume control. [1]

The choice between continuous (CRRT) and intermittent (IRRT) modalities, mode selection, anticoagulation strategy, and dose prescription all impact patient outcomes and resource utilisation. Current evidence supports CRRT as the default ICU modality for hemodynamically unstable patients, with regional citrate anticoagulation as the preferred approach when available. [2]

Critical care physicians must understand the mechanisms of each modality, appropriate anticoagulation strategies, common complications, and evidence base to optimise RRT delivery for critically ill patients.

Indications

Acute Kidney Injury

The decision to initiate RRT for AKI remains complex due to the absence of definitive evidence that early initiation improves outcomes. KDIGO guidelines suggest considering RRT for life-threatening changes in fluid, electrolyte, or acid-base balance, or when complications of uraemia occur. [3]

Absolute Indications:

Refractory hyperkalaemia (K+ greater than 6.5 mmol/L with ECG changes)
Severe metabolic acidosis (pH below 7.15 refractory to medical management)
Uraemic complications (pericarditis, encephalopathy, coagulopathy)
Fluid overload unresponsive to diuretics with pulmonary oedema
Certain intoxications (see below)

Relative Indications (clinical judgment required):

Progressive AKI with rising creatinine and oliguria
Severe oliguria (below 100 mL/12h) despite diuretics
Ongoing fluid accumulation compromising organ function
Difficulty administering nutrition/medications due to fluid restriction

Timing Studies:

ELAIN trial (early vs delayed CRRT in surgical ICU): Early group (KDIGO stage 2) had lower mortality at 90 days (39.3% vs 54.7%) and shorter ICU stay. However, trial methodology limited generalisability. [4]
AKIKI trial (early vs delayed RRT in mixed ICU): No difference in 60-day mortality (early 48.5% vs delayed 49.7%). Delayed group had 49% avoid RRT entirely. [5]
IDEAL-ICU trial (early vs delayed in septic shock): No mortality difference. Early group had more catheter-related complications. [6]

CICM Viva Key Point: No definitive evidence supports "early" RRT initiation. Base decisions on clinical need rather than arbitrary creatinine thresholds. Consider renal recovery potential, comorbidities, and trajectory.

Volume Overload

Positive fluid balance is independently associated with mortality in critically ill patients. CRRT provides precise ultrafiltration control when diuretics fail. [7]

Target negative fluid balance of 1-2% body weight/day in volume-overloaded AKI
CRRT allows 0-5 L/day ultrafiltration rates titrated to hemodynamics
SLED or IRRT may be suitable for stable patients requiring volume control

Evidence: Observational data from the BEST kidney study showed each litre of positive fluid balance increased mortality risk by 10% in CRRT patients. [8]

Uraemia

Uraemic complications warrant urgent RRT:

Pericarditis (friction rub, ECG changes)
Encephalopathy (asterixis, confusion, seizures)
Coagulopathy (platelet dysfunction, bleeding)
Uraemic pruritus, nausea/vomiting

BUN greater than 80-100 mg/dL or urea greater than 30-40 mmol/L alone is not an indication without clinical symptoms. [9]

Electrolyte Imbalance

Hyperkalaemia: RRT is definitive treatment when:

K+ greater than 6.5 mmol/L with ECG changes despite medical management
Refractory to standard therapy (calcium gluconate, insulin/dextrose, salbutamol)
Ongoing potassium release expected (tumour lysis, rhabdomyolysis)

CRRT removes potassium at 10-15 mmol/h depending on dialysate potassium concentration and effluent rate. High-dose CRRT may be required for severe hyperkalaemia. [10]

Other Electrolytes:

Refractory hyponatraemia (rare indication, risk of rapid correction)
Severe hypernatraemia with volume overload
Refractory metabolic acidosis (e.g., DKA/lactic acidosis)

Intoxication

RRT is indicated for dialysable toxins when:

Severe clinical toxicity (coma, arrhythmias, hemodynamic compromise)
Predicted lethal dose ingested
Lack of antidote or failure of antidote therapy
Ongoing absorption or endogenous production

Highly Dialysable (Extraction Ratio greater than 0.8):

Lithium (dialysable, preferred RRT modality)
Ethylene glycol, methanol (high dialysis clearance)
Theophylline, salicylates, valproate, carbamazepine
Metformin, metformin-associated lactic acidosis

Moderately Dialysable:

Phenytoin, phenobarbital (moderately protein-bound)
Aminoglycosides, vancomycin (adjunctive dosing)
Methotrexate (high-dose therapy)

Refer to EXTRIP guidelines for specific intoxication recommendations. CRRT provides continuous removal but lower clearance per hour compared to IRRT; IRRT preferred for life-threatening intoxications requiring rapid clearance. [11]

RRT Modalities

Continuous Renal Replacement Therapy (CRRT)

CRRT provides slow, continuous solute and fluid removal over 24 hours, mimicking native kidney function. Advantages include hemodynamic stability and better volume control.

CRRT Modes:

Continuous Veno-Venous Haemodiafiltration (CVVHDF)

Combines diffusion (haemodialysis) and convection (haemofiltration) in a single circuit. Dialysate and replacement fluid both used. [12]

Mechanisms:

Diffusion: Solute movement down concentration gradient across dialyser membrane. Effective for small molecules (urea, creatinine, electrolytes)
Convection: Solvent drag through ultrafiltration. Removes middle molecules (β2-microglobulin, cytokines, some drugs)
Adsorption: Solute binding to membrane surface (limited contribution)

Prescription:

Dialysate flow: 15-25 mL/kg/h
Replacement fluid flow: 15-25 mL/kg/h
Total effluent: 30-50 mL/kg/h (standard dose 20-25 mL/kg/h)
Common dialysate/replacement ratio: 1:1

Advantages: Combined small and middle molecule clearance, flexibility in adjusting diffusion vs convection components. Most commonly used ICU CRRT mode.

Continuous Veno-Venous Haemofiltration (CVVH)

Pure convective clearance using replacement fluid only.

Types:

Pre-dilution: Replacement fluid infused before filter. Reduces filter clotting (lower haematocrit at filter) but decreases solute clearance (dilutional effect)
Post-dilution: Replacement fluid infused after filter. Higher clearance but increased filter clotting risk

Prescription:

Replacement flow: 20-25 mL/kg/h (standard dose)
Pre-dilution ratio: 20-30% typically

Advantages: Superior middle molecule clearance, less hypotension than diffusion-dominant modes. No dialysate required.

Disadvantages: Higher anticoagulation requirements (post-dilution), more albumin loss.

Continuous Veno-Venous Haemodialysis (CVVHD)

Pure diffusive clearance using dialysate only.

Mechanism: Small molecule clearance via concentration gradient.

Prescription:

Dialysate flow: 20-25 mL/kg/h (standard dose)

Advantages: Efficient small molecule clearance, less anticoagulation needed than CVVH post-dilution. Useful when only urea/creatinine clearance needed.

Disadvantages: No middle molecule removal, slower cytokine clearance.

Slow Continuous Ultrafiltration (SCUF)

Ultrafiltration-only mode for volume removal without significant solute clearance.

Prescription:

Ultrafiltration rate: 100-500 mL/h (titrated to hemodynamics)
No replacement fluid or dialysate

Indications: Refractory volume overload in heart failure, when minimal solute removal needed.

Sustained Low-Efficiency Dialysis (SLED)

Hybrid technique using conventional haemodialysis machine at low flow rates for 6-12 hours.

Prescription:

Blood flow: 200 mL/min
Dialysate flow: 200-300 mL/min
Duration: 6-12 hours/session

Advantages: Provides rapid clearance for intermittent needs, better hemodynamic stability than IHD, uses standard dialysis equipment. Good compromise between CRRT and IRRT.

Disadvantages: Not truly continuous, cumulative clearance lower than CRRT 24-hour totals.

Intermittent Renal Replacement Therapy (IRRT)

Conventional haemodialysis delivered over 3-5 hours.

Prescription:

Blood flow: 250-400 mL/min
Dialysate flow: 500-800 mL/min
Duration: 3-5 hours, 4-7 sessions/week
SpKt/V ≥1.2 per session (equivalent to chronic dialysis adequacy)

Advantages: Higher urea clearance per hour, patient mobility between sessions, resource efficiency, catheter time reduced.

Disadvantages: Hemodynamic instability (hypotension common), slower middle molecule clearance, less precise volume control, inadequate for highly catabolic states.

Contraindications: Hemodynamic instability, cerebral oedema (rapid urea shifts increase ICP), severe organ failure requiring continuous support.

Dose Prescription

CRRT Dosing

Dose refers to effluent flow rate (dialysate + replacement + ultrafiltration). Standard dose is 20-25 mL/kg/h. [13]

Evidence for Dose:

RENAL Trial (2008): 1500 ICU AKI patients randomised to 25 vs 40 mL/kg/h. No difference in 90-day mortality (44.7% vs 41.8%). Higher dose group had more hypophosphatemia. [14]
ATN Trial (2008): 1124 ICU AKI patients, CVVHDF 20 vs 35 mL/kg/h. No mortality difference (52% vs 54%). Higher dose associated with more complications. [15]
IVOIRE Trial (2013): CVVHDF 25 vs 70 mL/kg/h. No difference in 28-day mortality or renal recovery. High-dose group had higher costs. [16]
Meta-analyses: High-dose CRRT does not improve survival or renal recovery. Standard dose 20-25 mL/kg/h is optimal balance of efficacy and safety. [17]

Prescribing CRRT Dose:

Calculate based on actual body weight (use adjusted body weight in obesity: IBW + 0.4(ABW-IBW))
Standard dose: 20-25 mL/kg/h total effluent
Pre-dilution: Increase prescribed dose by 20-30% to account for dilutional effect (prescribe 25-30 mL/kg/h to deliver 20-25 mL/kg/h)
Post-dilution: Prescribed dose = delivered dose
Monitor delivered dose via effluent collection (aim for ≥85% of prescribed dose)
Adjust for down-time (clotting, procedures, transport)

High-Dose CRRT Indications (rare):

Severe catabolism (burns, tumour lysis)
Life-threatening intoxication (temporary high-dose clearance)
Rhabdomyolysis (myoglobin removal - limited benefit despite theoretical rationale)

IRRT Dosing

Standard chronic dialysis adequacy targets:

spKt/V ≥1.2 per session
eKt/V ≥1.0 per session
Urea reduction ratio ≥65%

Frequency determined by clinical need and residual renal function (typically 3-5 sessions/week for anuric AKI).

Anticoagulation

Regional Citrate Anticoagulation (RCA)

Citrate is the preferred anticoagulant for CRRT, reducing bleeding complications by ~50% compared to heparin while extending filter life. [18]

Mechanism:

Citrate chelates ionised calcium in extracorporeal circuit, inhibiting coagulation cascade (calcium-dependent steps)
Citrate-calcium complex is metabolised in liver, muscle, and mitochondria via Krebs cycle
Calcium is infused systemically to maintain normal ionised calcium

Protocol:

Citrate solution (usually 4% trisodium citrate) infused pre-filter at blood flow rate × 1.2-1.5% (e.g., blood 150 mL/min → citrate 180-225 mL/h)
Target pre-filter ionised calcium: 0.25-0.35 mmol/L (anticoagulated zone)
Calcium chloride/gluconate infused systemically to maintain systemic ionised calcium: 1.1-1.2 mmol/L
Target total calcium:ionised calcium ratio below 2.5 (higher ratio indicates citrate accumulation)

Monitoring:

Ionised calcium: q4-6h (circuit and systemic)
Total calcium: q12h
pH, bicarbonate: q12-24h (citrate metabolism produces bicarbonate - metabolic alkalosis)
Citrate accumulation: Anion gap metabolic acidosis (unmetabolised citrate) or rising total Ca:iCa ratio

Advantages:

Reduced bleeding (no systemic anticoagulation)
Longer filter life (48-72 hours vs 24-36 hours with heparin)
Lower platelet consumption
Biocompatible (reduced complement activation)

Disadvantages:

Complex monitoring (ionised calcium, total Ca, pH)
Contraindicated in severe liver failure (impaired citrate metabolism)
Citrate toxicity risk (calcium overload, metabolic alkalosis, hypocalcaemia)
More expensive than heparin

Unfractionated Heparin

Systemic heparin remains an alternative when citrate unavailable or contraindicated.

Protocol:

Loading: 2000-5000 IU IV bolus
Infusion: 10-20 IU/kg/h adjusted to target APTT 1.5-2.5 × control
Alternatively, target anti-Xa 0.3-0.5 IU/mL

Advantages:

Familiar, inexpensive
No citrate toxicity risk
Easier monitoring (APTT/anti-Xa)

Disadvantages:

Systemic anticoagulation → bleeding risk
Heparin-induced thrombocytopenia (HIT) risk
Shorter filter life than citrate
Cannot be used in active bleeding or recent surgery

Regional Heparinisation

Heparin infused pre-filter, protamine infused post-filter to neutralise heparin systemically.

Protocol:

Heparin pre-filter: 500-1000 IU/h
Protamine post-filter: 0.5-1 mg per 100 U heparin

Advantages: Reduced bleeding compared to systemic heparin.

Disadvantages: Complex monitoring, protamine adverse effects (hypotension, anaphylaxis), rarely used in modern practice.

No Anticoagulation

Saline flushes every 30-60 minutes to maintain circuit patency.

Indications: Active bleeding, HIT, severe liver failure (citrate contraindicated).

Disadvantages: Very short filter life (often below 24 hours), frequent clotting, increased nursing workload, reduced delivered dose.

CICM Viva Key Point: Regional citrate is first-line CRRT anticoagulation unless contraindicated. Contraindications: severe liver failure (Child-Pugh C, lactate greater than 4 mmol/L), shock with liver dysfunction, citrate allergy.

Vascular Access

Catheter Selection

Type: Double-lumen, cuffed, tunnelled haemodialysis catheter (temporary non-cuffed also acceptable).

Size: 11-13.5 French diameter, length based on insertion site:

Right internal jugular: 12-15 cm
Left internal jugular: 15-20 cm
Femoral: 20-25 cm

Material: Polyurethane or silicone (biocompatible, reduced thrombogenicity).

Insertion Sites

First-line: Right internal jugular vein

Straight course to SVC/RA
Highest blood flow rates
Lowest complication rates
Comfortable for patient

Alternative: Left internal jugular

Tortuous course (risk of kinking)
Higher recirculation
Preferred if right IJ inaccessible

Alternative: Femoral vein

Easy insertion
Lower infection rates than IJ if below 5 days
Not ideal for mobilisation
Contraindicated in abdominal surgery, bowel injury

Last resort: Subclavian vein

Higher stenosis/thrombosis risk
Avoid if future AV fistula possible (preserves subclavian for vascular access)
Complication rate 20-40% for subclavian stenosis

Blood Flow Requirements

CRRT: 100-200 mL/min
IRRT: 250-400 mL/min

Complications

Immediate:

Arterial puncture (haemothorax, haemomediastinum)
Haematoma
Pneumothorax (IJ/Subclavian insertions: incidence ~2%)
Arrhythmia (atrial irritation)

Early (below 1 week):

Infection (CRBSI: 2-5 episodes/1000 catheter-days)
Thrombosis (5-10%)
Catheter malfunction (recirculation, positional)

Late (greater than 1 week):

Central vein stenosis (especially subclavian)
Catheter-related sepsis

CICM Practical Tip: Ultrasound-guided insertion is mandatory. Use aseptic technique (full barrier precautions). Prefer right IJ for CRRT. Consider antibiotic-coated or silver-impregnated catheters if prolonged use expected (greater than 7 days).

Complications

Hypothermia

CRRT circuits expose blood to extracorporeal environment, causing heat loss.

Incidence: Up to 50% develop temperature below 35°C without circuit warming.

Management:

Use in-line blood warmer (set 37-38°C)
Warm replacement/dialysate fluids
Cover exposed circuit tubing
Monitor core temperature q2-4h

Impact: Hypothermia increases vasoconstriction, coagulopathy, and shivering (increased oxygen consumption).

Citrate Toxicity

Occurs when citrate infusion exceeds metabolic capacity, leading to accumulation and systemic effects.

Mechanism: Unmetabolised citrate chelates ionised calcium, causes metabolic acidosis, and impairs coagulation.

Risk Factors:

Severe liver failure (Child-Pugh C)
Shock with hepatic hypoperfusion
High citrate infusion rates
Hypothermia (reduces metabolism)

Manifestations:

Rising total calcium:ionised calcium ratio (greater than 2.5)
Metabolic acidosis (unexplained anion gap)
Hypocalcaemia despite calcium infusion
Ionised calcium below 0.9 mmol/L

Management:

Reduce or stop citrate infusion
Switch to alternative anticoagulation
Monitor for hypocalcaemia (ECG changes, tetany, seizures)
Supportive: calcium supplementation if symptomatic

Membrane Clotting

Incidence: Filter life varies by anticoagulation:

Citrate: 48-72 hours
Systemic heparin: 24-36 hours
No anticoagulation: below 24 hours

Causes:

Inadequate anticoagulation
High haematocrit (greater than 35%)
High blood flow rates with catheter problems
Blood product administration
CRRT interruptions

Prevention:

Maintain adequate anticoagulation
Pre-filter citrate with appropriate target (pre-filter iCa 0.25-0.35 mmol/L)
Optimise blood flow (avoid catheter malfunction)
Minimise interruptions

CICM Practical Tip: Monitor transmembrane pressure (TMP) and filter pressure. Rising TMP predicts impending clotting. Pre-emptive circuit change may be planned for convenience.

Bleeding

Anticoagulation-related bleeding is the most common serious complication.

Incidence:

Citrate: 2-5% major bleeding
Heparin: 10-15% major bleeding

Risk Factors:

Systemic anticoagulation (heparin)
Recent surgery/trauma
Coagulopathy, thrombocytopenia
Concomitant antiplatelet therapy

Management:

Citrate: Stop citrate, continue CRRT without anticoagulation or switch to heparin (paradoxically less systemic effect)
Heparin: Stop heparin, consider protamine if life-threatening bleeding
Supportive: Blood products, local haemostatic measures

Hypophosphatemia

Incidence: Up to 80% on CRRT develop phosphate below 0.8 mmol/L. Risk increases with higher effluent rates.

Mechanism: Phosphate removed with effluent fluid. Replacement/dialysate fluids typically phosphate-free.

Management:

Phosphate 0.8-1.5 mmol/L target
IV phosphate replacement (30 mmol NaH2PO4 typically)
Phosphate-enriched replacement fluid (if available)
Monitor phosphate q6-12h initially

Consequences: Severe hypophosphatemia causes respiratory failure, diaphragmatic weakness, haemolysis, and cardiac dysfunction.

Nutrient Losses

CRRT removes amino acids, vitamins, water-soluble vitamins, and trace elements.

Losses:

Amino acids: 10-15 g/day
Thiamine, folate, vitamin C
Selenium, zinc

Management:

Increased protein intake (2.0-2.5 g/kg/day)
Multivitamin supplementation
Trace element replacement weekly

Electrolyte Abnormalities

CRRT can cause rapid shifts in sodium, potassium, magnesium, and calcium.

Prevention:

Customise dialysate/replacement fluid composition
Monitor electrolytes q4-6h initially
Adjust rates as needed

Equipment and Circuit

CRRT Machine Components

Blood Pump: Propels blood at 100-200 mL/min
Dialysate Pump: Delivers dialysate (CVVHD, CVVHDF)
Replacement Pump: Delivers replacement fluid (CVVH, CVVHDF)
Ultrafiltration Pump: Removes fluid
Access Pressure (Pre-filter): Monitors arterial (access) line pressure
Return Pressure (Post-filter): Monitors venous (return) line pressure
Effluent Pressure: Monitors fluid removal side
Transmembrane Pressure (TMP): Pressure gradient across filter
Air Detector: Prevents air embolism
Blood Leak Detector: Detects membrane rupture
Pressure Relief Valve: Prevents excessive pressure

Membrane Types

Synthetic High-Flux Membranes:

Polysulfone, polyacrylonitrile, polymethylmethacrylate
Larger pores (10-30 kDa cutoff)
Better middle molecule clearance
Higher biocompatibility

Cellulose-Based Membranes (rarely used now):

Lower biocompatibility (complement activation)
Smaller pores
Lower clearance

Solute Clearance by Size

Solute Size	Clearance Method	Examples
below 500 Da (small molecules)	Diffusion, convection	Urea, creatinine, electrolytes
500-15,000 Da (middle molecules)	Convection, adsorption	β2-microglobulin, cytokines, some drugs
greater than 15,000 Da (large molecules)	Adsorption limited	Myoglobin (17 kDa), some drugs

Evidence Summary

CRRT vs IRRT

RENAL Trial (2008): 1500 patients randomised to CVVHDF 25 vs 40 mL/kg/h. No mortality difference (44.7% vs 41.8%). Subgroup: Shock patients had trend to benefit from higher dose (not significant). [14]

ATN Trial (2008): 1124 patients in US academic ICUs, CVVHDF 20 vs 35 mL/kg/h or IHD spKt/V 1.2-1.4. No mortality difference (52% vs 54%). IRRT and CRRT had similar outcomes when matched to severity of illness. [15]

Meta-analyses (2020s): No clear mortality advantage of CRRT over IRRT. CRRT associated with better hemodynamic stability and renal recovery in hemodynamically unstable patients. IRRT more resource-efficient in stable patients. [19, 20]

CICM Viva Key Point: Choose modality based on hemodynamic status, not perceived survival advantage. CRRT for unstable; IRRT acceptable for stable.

Dosing Studies

RENAL, ATN, IVOIRE: Consistently show no benefit for doses greater than 25 mL/kg/h. Higher doses associated with more complications (hypophosphatemia, hypothermia, bleeding). [14-16]

Meta-analysis 2021: 30 RCTs, greater than 4000 patients. Standard dose 20-25 mL/kg/h is optimal. Doses greater than 30 mL/kg/h increase complications without benefit. [17]

Citrate vs Heparin

Regional Citrate Anticoagulation Trial (2015): Citrate reduced bleeding events (5% vs 15%) and increased filter life (70 hours vs 49 hours) compared to heparin. No mortality difference. [18]

Meta-analysis 2019: 9 RCTs, 800 patients. Citrate reduced major bleeding by 50%, extended filter life, had similar mortality to heparin. Citrate more expensive but cost-effective considering reduced complications. [21]

Complications and Outcomes

BEST Kidney Study (2008): Multinational observational study of 29,000 CRRT patients. Positive fluid balance independently associated with mortality. Each litre positive balance increased mortality 10%. [8]

VA/NIH Acute Renal Failure Trial Network (2008): IRRT vs CRRT mortality similar. However, CRRT patients had better renal recovery at 90 days if they survived to hospital discharge. [15]

Practical Management

Starting CRRT

Preparation:

Confirm indication (document decision)
Ensure vascular access (double-lumen 11-13 Fr)
Choose modality (CVVHDF default)
Choose anticoagulation (citrate first-line)
Prescribe dose: 20-25 mL/kg/h
Set fluid goals: ultrafiltration rate, net fluid balance target
Obtain baseline labs: CBC, electrolytes, calcium, Mg, Phos, ABG, coagulation

Circuit Priming:

Prime circuit with normal saline (or blood if patient anaemic)
Check for air bubbles
Connect patient lines
Initiate blood pump at 50-100 mL/min, titrate to target 150 mL/min

Initial Orders:

Mode: CVVHDF
Blood flow: 150 mL/min
Dialysate flow: 1000 mL/h (or 16 mL/kg/h)
Replacement flow: 1000 mL/h (or 16 mL/kg/h)
Net ultrafiltration: 100 mL/h (titrate to goals)
Effluent dose: ~32 mL/kg/h (total)
Anticoagulation: Regional citrate
  - "Citrate 4%: 200 mL/h"
  - "Calcium chloride 10%: 10 mL/h (titrate to iCa 1.1-1.2)"
  - "Target pre-filter iCa: 0.3 mmol/L"
Dialysate composition: Na 140, K 4, Cl 110, HCO3 35, Ca 1.5, Mg 0.5
Fluid source: 0.9% saline + sodium bicarbonate (or commercial bicarbonate-buffered solutions)

Troubleshooting

High Access Pressure:

Check catheter position (may have migrated)
Consider catheter thrombosis (may need alteplase)
Ensure no kinking in arterial line

High Return Pressure:

Check for venous line obstruction
Catheter tip may be against vein wall
Consider line malposition

Rising Transmembrane Pressure (TMP):

Filter clotting imminent
Check haematocrit (elevated increases viscosity)
Review anticoagulation adequacy
Plan circuit change

Blood Leak Alarm:

Membrane rupture
Stop CRRT immediately
Discard blood (risk of contaminated)
Replace circuit and filter

Air Detector Alarm:

Check for air in circuit (air ingress)
Stop CRRT
Remove air
Re-prime if needed
Check for catheter leak

Citrate Accumulation:

Total Ca:iCa ratio rising (greater than 2.5)
Metabolic acidosis
Reduce citrate infusion
Consider alternative anticoagulation

Metabolic Alkalosis:

Citrate metabolised to bicarbonate
Reduce dialysate/replacement bicarbonate
Reduce citrate dose
Consider acetate-buffered solution

Renal Recovery and CRRT Weaning

Predicting Renal Recovery

Favorable Prognostic Factors:

Baseline normal renal function
Non-oliguric AKI
Short duration of AKI (below 7 days)
Younger age, fewer comorbidities
Sepsis-related AKI (vs nephrotoxic or ischemic)

Unfavorable Factors:

CKD baseline (eGFR below 60)
Oliguria (below 100 mL/12h for greater than 48h)
Need for mechanical ventilation
Multiorgan failure
AKI greater than 14 days prior to CRRT

Weaning Criteria

Step 1: Trial off CRRT (stop circuit, monitor)

Assess urine output: greater than 0.5 mL/kg/h for 6-12 hours
Assess electrolytes, acid-base stable without support
Review volume status (tolerate fluid challenges)

Step 2: If stable for 24-48 hours off CRRT → successful wean

Remove catheter when stable greater than 48-72 hours
Monitor creatinine, electrolytes daily ×3 days

Re-initiation: If oliguria recurs, electrolytes/acidosis decompensate, or volume overload develops

Evidence: 30% of ICU AKI patients requiring CRRT progress to ESRD. 70% recover renal function, but 40% have residual CKD. [22]

Special Populations

Liver Failure

CRRT in ACLF (Acute-on-Chronic Liver Failure):

Citrate contraindicated (severe hepatic dysfunction impairs metabolism)
Use heparin or no anticoagulation
Monitor ammonia (CRRT removes ammonia but may rise during downtime)
Monitor lactate (reduced clearance)

CRRT for ALF (Acute Liver Failure):

Indicated for cerebral oedema (ammonia removal)
CRRT preferred over IRRT (slower ammonia removal prevents intracranial pressure spikes)
MARS (Molecular Adsorbent Recirculating System) for albumin-bound toxins (specialised CRRT variant)

Cardiac Failure

CRRT in Cardiogenic Shock:

SCUF for volume overload
CRRT for combined AKI and volume management
Ultrafiltration rate must balance cardiac output (avoid hypotension)
Consider peritoneal dialysis if CRRT not feasible

Sepsis-Associated AKI

CRRT Benefits in Sepsis:

Cytokine clearance (convection/adsorption)
Acidosis correction
Fluid optimisation
Temperature control

Evidence: High-volume CVVH (HVHF) 85 mL/kg/h for 8 hours in septic shock showed transient haemodynamic improvement but no mortality benefit in RCTs. Not recommended. [23]

Burns

CRRT Indications:

Rhabdomyolysis (myoglobin clearance limited benefit)
Severe hypermetabolism (fluid removal)
Sepsis from burn wound infections

Dosing: Higher protein requirements (3-4 g/kg/day) to compensate for CRRT losses

RRT for Specific Intoxications

Lithium:

Highly dialysable
CRRT or IRRT both effective
Indication: Level greater than 4.0 mmol/L, or greater than 2.5 mmol/L with symptoms
Monitor lithium q4-6h during RRT, then q12h post-RRT (rebound common)

Ethylene Glycol / Methanol:

CRRT effective for continuous removal
IRRT preferred for rapid clearance in life-threatening cases
Fomepizole essential (inhibit alcohol dehydrogenase)
Indication: Level greater than 50 mg/dL, or any level with visual symptoms (methanol), or anion gap metabolic acidosis with OG

Valproate:

Moderately protein-bound (90%)
CRRT less effective (protein-bound fraction not removed)
IRRT preferred
Indication: Level greater than 850 mcg/mL, or coma with respiratory failure

Salicylates:

CRRT effective for continuous removal
Alkalinisation essential first-line
Indication: Level greater than 100 mg/dL, or clinical toxicity with pulmonary oedema, altered mental status

Methotrexate:

High-dose therapy (greater than 1 g/m2)
CRRT or IRRT effective
Indication: Level greater than 10 µM, or greater than 1 µM with delayed renal excretion
Continue until level below 0.1 µM

Nursing and Technical Considerations

Monitoring Requirements

Hourly:

Blood pump speed, pressures (access, return, effluent, TMP)
Fluid balance (net UF, cumulative)
Alarm status

q4-6h:

Ionised calcium (circuit and systemic)
Potassium, sodium
Temperature

q12h:

CBC (platelets, haemoglobin)
Total calcium, magnesium, phosphate
ABG/VBG

q24h:

Creatinine, urea
Liver function tests (if on citrate)
PT/INR, APTT (if on heparin)

Safety Checks

Verify fluid connections (correct lines to correct bags)
Check for leaks (blood, dialysate)
Verify alarm settings (appropriate thresholds)
Confirm anticoagulation doses
Review net fluid balance targets

Cost and Resource Considerations

CRRT Costs

Equipment:

CRRT machine: $10,000-30,000 capital cost
Circuit + filter: $150-250 per set
Fluids: $50-100 per day

Personnel:

ICU nursing (1:1 or 1:2 nurse:patient ratio often required for CRRT monitoring)
Intensivist oversight

Total: $1000-2000 per day for CRRT (varies by region, contracts)

IRRT Costs

Equipment:

Dialysis machine: $20,000-40,000 capital cost
Dialyser: $20-50 per treatment
Fluids: $30-60 per treatment

Personnel:

Dialysis nurse (typically 1:1 for IRRT session)

Total: $300-600 per IRRT session (3-4 sessions/week = $900-1800/week)

Cost-Effectiveness

CRRT more expensive per day but may reduce overall costs if:

Fewer circuit changes
Reduced bleeding complications
Shorter ICU stay (controversial)
Better renal recovery (uncertain)

Cost-effectiveness analyses are heterogeneous. CRRT may be cost-effective in very unstable patients where IRRT is not feasible. [24]

Guidelines and Consensus Statements

KDIGO AKI Guidelines (2021)

RRT Initiation (Chapter 4.5):

Initiate emergently for life-threatening changes in fluid, electrolytes, acid-base balance
Consider RRT when complications of uraemia occur
No definitive evidence for "early" vs "delayed" initiation (Grade 2C)
Shared decision-making recommended considering patient values and preferences [3]

RRT Modality (Chapter 4.6):

Choose CRRT vs IRRT based on hemodynamic stability, availability, expertise (Grade 2B)
No modality proven superior for mortality
Consider hybrid therapies (SLED) as alternative

RRT Anticoagulation (Chapter 4.7):

Regional citrate recommended for CRRT (Grade 2B)
No anticoagulation acceptable for patients at high bleeding risk
Avoid heparin in patients with HIT

RRT Dose (Chapter 4.8):

Prescribe effluent dose 20-25 mL/kg/h (Grade 1A)
Higher doses not recommended (Grade 1A)

ADQI (Acute Disease Quality Initiative)

ADQI provides consensus statements on RRT topics:

CRRT anticoagulation (2019)
CRRT dose prescription (2016)
CRRT timing (2017)
RRT for intoxication (2015)

Summary

Renal Replacement Therapy is a cornerstone of critical care for AKI, electrolyte disturbances, volume overload, and intoxication. CRRT (particularly CVVHDF at 20-25 mL/kg/h) is the default ICU modality for hemodynamically unstable patients. Regional citrate anticoagulation is first-line, reducing bleeding by 50% compared to heparin while extending filter life. Evidence from RENAL, ATN, and IVOIRE trials demonstrates no mortality benefit for doses greater than 25 mL/kg/h. CRRT and IRRT have similar mortality outcomes; modality choice should be individualised based on hemodynamic status. Key complications include citrate toxicity, membrane clotting, bleeding, hypophosphatemia, and hypothermia. Careful monitoring and troubleshooting are essential for optimal CRRT delivery.

SAQ Practice Questions

SAQ 1: RRT Initiation and Modality Selection

Question (15 marks):

A 68-year-old man with septic shock is admitted to ICU. He has a history of type 2 diabetes and hypertension. On day 3, his creatinine rises from baseline 90 μmol/L to 280 μmol/L, with urine output 20 mL/h for the past 12 hours. His current vitals: BP 85/45 mmHg (on noradrenaline 0.3 mcg/kg/min), HR 110/min, SpO2 96% on 40% FiO2. His electrolytes: K+ 5.8 mmol/L, Na+ 140 mmol/L, HCO3- 18 mmol/L, pH 7.28. He has no evidence of volume overload.

Task: Discuss your approach to renal replacement therapy decisions in this patient. Include:

Indications for RRT initiation (5 marks)
Modality selection with justification (4 marks)
Anticoagulation strategy (3 marks)
Dose prescription and monitoring (3 marks)

Model Answer (15 marks):

Indications for RRT Initiation (5 marks):

The patient has KDIGO Stage 3 AKI (creatinine greater than 3× baseline or increase greater than 265 μmol/L, urine output below 0.3 mL/kg/h for 24 hours) [3]
However, absolute indications not yet met:
- Hyperkalaemia is borderline (K+ 5.8 mmol/L) without ECG changes [10]
- Acidosis is mild (pH 7.28, HCO3- 18) – may respond to treating underlying sepsis
- No evidence of volume overload or pulmonary oedema
- No uraemic complications (pericarditis, encephalopathy) [3]
Relative indications present: Progressive AKI with oliguria and rising creatinine
Current evidence (AKIKI, IDEAL-ICU) supports delaying RRT until clinical need emerges unless clear indications [5, 6]
Approach: Optimise haemodynamics (increase noradrenaline, consider fluid challenge), monitor closely (creatinine, electrolytes, urine output), avoid nephrotoxins, consider RRT if hyperkalaemia progresses, acidosis worsens, volume overload develops, or oliguria persists greater than 24-48 hours

Modality Selection (4 marks):

CRRT is preferred due to hemodynamic instability (BP 85/45 mmHg on noradrenaline) [2]
IRRT associated with hypotension due to rapid fluid/solute shifts, which may exacerbate shock [19]
Specific mode: CVVHDF (most commonly used ICU CRRT modality) [12]
- Combines diffusion (urea, electrolytes) and convection (middle molecules, cytokines)
- Flexible to adjust diffusion vs convection components
- Standard ICU practice with available equipment
Alternative considerations:
- CVVH if pure convective clearance preferred (better middle molecule clearance)
- SLED if machine availability limited (6-12 hours/day, uses standard dialysis machine)
- IRRT not appropriate initially due to hemodynamic instability
Indications for switching to IRRT: Patient becomes haemodynamically stable, mobilising, or if CRRT complications (e.g., repeated circuit clotting)

Anticoagulation Strategy (3 marks):

Regional citrate anticoagulation (RCA) is first-line for CRRT [18, 21]
- Reduces bleeding complications by ~50% compared to heparin
- Extends filter life (48-72 hours vs 24-36 hours with heparin)
- No systemic anticoagulation important in septic shock (risk of coagulopathy)
Citrate protocol:
- 4% trisodium citrate infused pre-filter (e.g., 200 mL/h)
- Target pre-filter ionised calcium 0.25-0.35 mmol/L (anticoagulated zone)
- Calcium chloride/gluconate infused systemically to maintain systemic iCa 1.1-1.2 mmol/L
- "Monitor total calcium:ionised calcium ratio (below 2.5 indicates no accumulation)"
Contraindications to citrate (check for): Severe liver failure (unlikely given patient history), shock with liver dysfunction (monitor lactate and liver enzymes)
If citrate contraindicated: Use no anticoagulation (accept shorter filter life) or regional heparinisation
Unfractionated heparin less preferred due to bleeding risk in septic shock

Dose Prescription and Monitoring (3 marks):

Standard CRRT dose: 20-25 mL/kg/h total effluent [13-17]
- Based on actual body weight (use adjusted body weight if obese)
- "For 70 kg patient: Prescribe ~1400-1750 mL/h effluent"
- "CVVHDF: Divide between dialysate and replacement (e.g., dialysate 1000 mL/h + replacement 500 mL/h)"
Evidence for dose: RENAL, ATN, IVOIRE trials show no mortality benefit for greater than 25 mL/kg/h; higher doses increase complications (hypophosphatemia, bleeding) [14-16, 17]
Monitoring:
- "Delivered dose: Collect effluent volume, aim for ≥85% of prescribed dose"
- Adjust for down-time (circuit changes, procedures, transport)
- Electrolytes q4-6h initially (especially K+, Ca, Phos)
- Ionised calcium (circuit and systemic) q4-6h (if on citrate)
- Phosphate q6-12h (high risk of hypophosphatemia on CRRT)
- ABG/VBG q12h (acid-base balance, citrate accumulation causes alkalosis)
- "Total calcium q12h (calculate Ca:iCa ratio)"
Nutritional support: Increased protein requirement (2.0-2.5 g/kg/day) to compensate for amino acid loss
Vitamin and trace element replacement (especially thiamine, folate, selenium, zinc)

Key Points: This patient with septic shock and progressive AKI requires close monitoring for RRT indications. CRRT with citrate anticoagulation at 20-25 mL/kg/h is appropriate if RRT becomes indicated. No urgent RRT required at present based on current electrolytes and volume status. Delayed RRT approach consistent with AKIKI/IDEAL-ICU evidence.

SAQ 2: Citrate Anticoagulation and CRRT Complications

Question (15 marks):

A 55-year-old woman with alcoholic cirrhosis develops septic shock and AKI. She is started on CVVHDF with regional citrate anticoagulation. On day 2, the nurse calls you because the patient has developed an anion gap metabolic acidosis: pH 7.25, HCO3- 15 mmol/L, lactate 4.0 mmol/L, anion gap 20 mmol/L. Total calcium 2.8 mmol/L, ionised calcium 0.95 mmol/L (ratio Ca:T/iCa = 2.95). The CRRT circuit pressures are: access pressure -10 mmHg, return pressure 180 mmHg, TMP 200 mmHg.

Task: Discuss the management of this patient, addressing:

Diagnosis of citrate toxicity (4 marks)
Management of citrate toxicity (5 marks)
Approach to circuit pressures (3 marks)
Prevention of future complications (3 marks)

Model Answer (15 marks):

Diagnosis of Citrate Toxicity (4 marks):

Citrate accumulation confirmed by total calcium:ionised calcium ratio of 2.95 (greater than 2.5 indicates citrate accumulation) [18, 21]
Pathophysiology: Citrate not metabolised (impaired liver function from cirrhosis + shock), accumulates, chelates ionised calcium, causes metabolic acidosis (unmetabolised citrate contributes to anion gap)
Risk factors in this patient:
- Alcoholic cirrhosis → impaired hepatic metabolism of citrate
- Septic shock → hepatic hypoperfusion
- Possible hypothermia
Manifestations:
- "Rising Ca:iCa ratio (greater than 2.5)"
- Metabolic acidosis (anion gap 20) despite CRRT (which typically corrects acidosis)
- Ionised calcium low (0.95 mmol/L) despite calcium supplementation
- Lactate elevation (4.0 mmol/L) may be due to impaired liver metabolism (some lactate converted to glucose in liver)
Differential diagnoses for metabolic acidosis:
- Lactic acidosis (type B due to liver failure)
- Sepsis-related lactic acidosis (type A due to tissue hypoperfusion)
- D-lactic acidosis (rare, usually short bowel)
- Pyroglutamic acidosis (paracetamol, malnutrition)
- "In this case, Ca:iCa ratio points strongly to citrate accumulation as contributor"

Management of Citrate Toxicity (5 marks):

Immediate action: Stop or reduce citrate infusion [18, 21]
- "Discontinue citrate completely if severe toxicity (Ca:iCa ratio greater than 3.0, symptomatic hypocalcaemia, severe acidosis)"
- "Reduce citrate infusion rate by 50% if moderate toxicity (Ca:iCa ratio 2.5-3.0)"
Switch anticoagulation strategy:
- "Option 1: No anticoagulation (may lead to short filter life, but safest in liver failure)"
- "Option 2: Regional heparinisation (some systemic effect, but less than full heparin)"
- "Option 3: Systemic heparin (higher bleeding risk, but citrate clearly contraindicated)"
- Avoid continuing citrate in severe liver failure (Child-Pugh C)
Correct hypocalcaemia:
- Check for symptoms (tetany, seizures, arrhythmias) - not mentioned but monitor
- "ECG: QT prolongation, T wave abnormalities"
- Calcium gluconate or chloride if symptomatic or iCa below 0.8 mmol/L (currently 0.95 mmol/L, may not need urgent replacement)
- "Over-correction: Excess calcium may cause tissue deposition with citrate complexes"
Address metabolic acidosis:
- CRRT will remove acid (bicarbonate-buffered dialysate)
- Consider bicarbonate infusion if severe (pH below 7.2)
- Treat underlying cause (sepsis, hypoperfusion)
Monitor liver function:
- Lactate clearance is impaired in liver failure
- Consider bilirubin, INR, transaminases
Circuit considerations:
- When citrate stopped, filter will likely clot quickly (12-24 hours)
- Plan for circuit change or switch anticoagulation promptly
- May need more frequent circuit changes with no anticoagulation or heparin

Circuit Pressures (3 marks):

Current pressures:
- "Access pressure -10 mmHg: Low/normal, indicates arterial (access) side functioning well"
- "Return pressure 180 mmHg: Elevated, suggests venous (return) side obstruction"
- "TMP 200 mmHg: Elevated (normal 100-150 mmHg), suggests filter clotting imminent"
Rising TMP causes:
- Filter clotting (protein/fibrin deposition)
- High haematocrit (greater than 35% increases viscosity)
- Blood flow rate too high for catheter
- Inadequate anticoagulation (now citrate stopped)
Management:
- Check blood flow rate (may need to reduce from 150 to 100 mL/min)
- Check haematocrit (transfuse if anaemic, but may be elevated due to hemoconcentration)
- Ensure adequate anticoagulation (switched to heparin or no anticoagulation)
- Prepare for circuit change (TMP greater than 250 mmHg typically requires change)
Access pressure low (-10 mmHg):
- Reassuring, no arterial line obstruction
- Catheter malposition unlikely
- Blood pump functioning adequately
Return pressure elevated (180 mmHg):
- Check venous line for kinking, obstruction
- Catheter tip may be against vein wall
- Consider catheter repositioning if pressures remain high

Prevention of Future Complications (3 marks):

Citrate toxicity prevention:
- Avoid citrate in severe liver failure (Child-Pugh C) or shock with liver dysfunction
- Consider citrate dose reduction in moderate liver dysfunction (Child-Pugh B)
- "Frequent monitoring: ionised calcium q4-6h, total calcium q12h, Ca:iCa ratio"
- "Early recognition: Rising Ca:iCa ratio greater than 2.5 → reduce citrate before full toxicity develops"
- Consider alternative anticoagulation from start in high-risk patients
Filter life extension (without citrate):
- Use pre-dilution CVVH (lower haematocrit at filter reduces clotting)
- Optimise blood flow (avoid low flows below 100 mL/min)
- Saline flushes every 30-60 minutes if no anticoagulation
- Avoid blood product administration through circuit
- Minimise CRRT interruptions (downtime promotes clotting on restart)
General complication prevention:
- "Hypophosphatemia: Monitor phosphate q6-12h, replace proactively (30 mmol phosphate daily)"
- "Hypothermia: Use in-line blood warmer, warm dialysate/replacement fluids"
- "Nutrient losses: Increased protein 2.0-2.5 g/kg/day, vitamin/trace element replacement"
- "Bleeding: Avoid systemic anticoagulation in high-risk patients"
Patient selection for CRRT modality:
- Consider SLED as alternative (uses standard dialysis machine, less citrate required)
- Consider IRRT if becomes stable (no continuous circuit concerns)
- Peritoneal dialysis as alternative if vascular access challenging

Key Points: Citrate toxicity in liver failure requires immediate discontinuation of citrate and switching anticoagulation. The Ca:iCa ratio is the key diagnostic marker (greater than 2.5 indicates accumulation). Elevated TMP suggests impending filter clotting, requiring proactive circuit management. Preventive strategies include avoiding citrate in severe liver dysfunction and frequent monitoring of calcium parameters. This patient may transition to no anticoagulation or heparin with expectation of shorter filter life.

Viva Scenarios

Viva 1: RRT Decision-Making and Modality Selection

Examiner: You are called to review a 72-year-old woman in the ICU. She is post-op day 2 following a Hartmann's procedure for perforated sigmoid diverticulitis. She has developed acute kidney injury. Let's discuss renal replacement therapy in this patient.

Examiner: What is your approach to deciding whether to initiate renal replacement therapy?

Candidate: My approach involves assessing for absolute and relative indications, while also considering the patient's overall prognosis and goals of care.

Absolute indications that would mandate RRT include:

Refractory hyperkalaemia with ECG changes (peaked T waves, widened QRS)
Severe metabolic acidosis (pH below 7.15) not responding to medical therapy
Uraemic complications such as pericarditis, pericardial effusion, encephalopathy, or coagulopathy
Volume overload causing respiratory compromise despite diuretic therapy
Specific intoxications where RRT is indicated [3]

Relative indications require clinical judgment:

Progressive AKI with rising creatinine and oliguria
Difficulty maintaining fluid balance for nutrition or medications
Severe electrolyte abnormalities that cannot be managed medically

In this patient, I would first review her current creatinine, urine output, electrolytes, acid-base status, and fluid balance. I would assess for any signs of volume overload on examination and imaging. I would also review her trajectory – is her renal function declining or improving? Is there a reversible cause?

The timing of RRT is controversial. Large RCTs like AKIKI and IDEAL-ICU showed that delayed initiation (waiting for absolute indications) was not associated with worse mortality, and many patients in the delayed arms recovered without ever needing RRT. [5, 6] However, the ELAIN trial in surgical ICU patients suggested earlier initiation at KDIGO stage 2 may improve outcomes. [4]

So, my decision would be to initiate RRT if there are absolute indications, or to monitor closely if there are only relative indications, with a low threshold to start if the patient deteriorates or shows no improvement after addressing reversible factors.

Examiner: The nurse notes the patient is oliguric, with urine output 15 mL/h for the past 12 hours. Her creatinine has risen from 80 μmol/L at admission to 320 μmol/L. Her current vitals are BP 95/55 on noradrenaline 0.15 mcg/kg/min, HR 100/min. Her electrolytes are K+ 6.2 mmol/L, Na+ 138 mmol/L, HCO3- 20 mmol/L, pH 7.32. Her chest X-ray shows pulmonary oedema. What is your management?

Candidate: This patient now has multiple indications for RRT:

Hyperkalaemia: K+ 6.2 mmol/L – this is elevated and may need treatment, though I would check for ECG changes (peaked T waves, PR prolongation). If ECG changes present, this becomes an absolute indication. Even without ECG changes, given the ongoing oliguria, hyperkalaemia is likely to worsen. [10]

Acidosis: pH 7.32 and HCO3- 20 mmol/L is mild acidosis, not severe enough to mandate RRT (which would be pH below 7.15). However, in the context of ongoing kidney dysfunction, this could progress.

Volume overload: Pulmonary oedema on CXR with oliguria indicates she is fluid overloaded and cannot mobilise this fluid. This is a clear indication for RRT for volume management. [7]

Oliguria and rising creatinine: She has KDIGO stage 3 AKI (creatinine greater than 3× baseline, urine output below 0.3 mL/kg/h). This, combined with the above factors, makes a strong case for RRT.

Hemodynamics: She is on noradrenaline 0.15 mcg/kg/min, indicating she is hemodynamically compromised, though not in severe shock.

Given these findings, I would initiate RRT now. The volume overload and oliguria with rising creatinine are sufficient indications, even before waiting for the hyperkalaemia to become more severe or acidosis to worsen.

Examiner: Which modality of RRT would you choose and why?

Candidate: Given her hemodynamic compromise (on noradrenaline 0.15 mcg/kg/min) and pulmonary oedema, I would choose continuous renal replacement therapy, specifically CVVHDF. [2, 12]

CRRT advantages:

Better hemodynamic tolerance – slow continuous removal avoids the rapid fluid and solute shifts that cause hypotension with IRRT
Better volume control – we can precisely manage her pulmonary oedema by titrating ultrafiltration
Continuous correction of electrolytes and acid-base balance
More gradual removal of urea, which is important if there's any concern about cerebral oedema (though less likely in this context)

Mode selection – CVVHDF:

This is the most commonly used ICU CRRT modality
Combines diffusion (haemodialysis) and convection (haemofiltration)
Diffusion provides excellent clearance of small molecules like urea, creatinine, and electrolytes
Convection provides middle molecule clearance (β2-microglobulin, cytokines)
Flexible – we can adjust the relative contributions of diffusion vs convection depending on clinical needs
Well-established in ICU practice with readily available equipment

Alternatives considered:

CVVH (pure convection) – could be considered if middle molecule clearance is particularly important (e.g., in sepsis), but I don't think this is a key concern here
CVVHD (pure diffusion) – would be sufficient for urea and electrolyte clearance but less middle molecule removal
SLED – a hybrid technique using a standard dialysis machine at low flow rates for 6-12 hours. This could provide efficient clearance but is less continuous than CRRT
IRRT – I would avoid due to her hemodynamic instability; the rapid fluid shifts could exacerbate hypotension

Examiner: How would you prescribe the CRRT?

Candidate: I would prescribe CVVHDF at a standard dose of 20-25 mL/kg/h total effluent. [13, 14, 15]

Dose calculation:

For a 70 kg patient, this would be approximately 1400-1750 mL/h total effluent
With CVVHDF, this is divided between dialysate and replacement fluids
A common approach is to use roughly equal amounts of each: e.g., dialysate 700 mL/h and replacement 700 mL/h (total 1400 mL/h)
Additional ultrafiltration for volume management: Start at 100 mL/h net fluid removal, titrated based on hemodynamics and pulmonary oedema

Fluid prescription:

Dialysate: Standard bicarbonate-buffered solution with composition tailored to her needs:
- Sodium 140 mmol/L (to avoid rapid shifts)
- Potassium 2-3 mmol/L (lower than physiological to help with hyperkalaemia, may increase once K+ normalises)
- Bicarbonate 35 mmol/L (to correct acidosis)
- Calcium 1.5 mmol/L (if not on citrate anticoagulation)
- Magnesium 0.5 mmol/L
Replacement fluid: Similar composition to dialysate
Net ultrafiltration: Start at 100 mL/h, aiming for negative fluid balance of 1-2% body weight per day to resolve pulmonary oedema

Blood flow: 150 mL/min (typical for CRRT; higher flows improve clearance but increase filter clotting risk)

Anticoagulation: Regional citrate anticoagulation (I'll come back to this in detail)

Monitoring:

Ionised calcium q4-6h (circuit and systemic)
Electrolytes q4-6h (K+, Na+, Ca, Mg, Phos)
ABG/VBG q12h
Daily creatinine and urea
Delivered dose: Collect effluent volume, aim for ≥85% of prescribed dose

Examiner: What anticoagulation would you use for this patient's CRRT?

Candidate: I would choose regional citrate anticoagulation (RCA) as first-line for CRRT. [18, 21]

Reasons for citrate:

Reduced bleeding complications – compared to heparin, citrate reduces major bleeding by approximately 50%
No systemic anticoagulation – important in this post-op patient who has had recent surgery
Longer filter life – citrate typically extends filter life to 48-72 hours compared to 24-36 hours with heparin
Better biocompatibility – reduced complement activation and platelet consumption

Citrate mechanism:

Citrate is infused pre-filter and chelates ionised calcium in the extracorporeal circuit
The coagulation cascade is calcium-dependent, so chelating calcium inhibits clotting locally
Citrate-calcium complex is metabolised in the liver, muscle, and mitochondria via the Krebs cycle
Calcium is infused systemically to maintain normal systemic ionised calcium

Citrate protocol:

4% trisodium citrate solution infused pre-filter at approximately blood flow rate × 1.2-1.5%
For blood flow 150 mL/min, citrate infusion would be approximately 180-225 mL/h
Target pre-filter ionised calcium: 0.25-0.35 mmol/L (this creates the anticoagulated zone)
Calcium chloride or gluconate infused systemically to maintain systemic ionised calcium at 1.1-1.2 mmol/L
Typical systemic calcium infusion: 10-15 mL/h of 10% calcium chloride, titrated to ionised calcium

Monitoring:

Ionised calcium (circuit and systemic): q4-6h
Total calcium: q12h
Calculate total calcium:ionised calcium ratio – should be below 2.5
If ratio greater than 2.5, indicates citrate accumulation
pH and bicarbonate: q12-24h (citrate metabolism produces bicarbonate – risk of metabolic alkalosis)

Contraindications to citrate:

Severe liver failure (Child-Pugh C) – impaired metabolism leads to citrate accumulation
Shock with significant liver dysfunction
Citrate allergy (rare)
This patient does not have obvious liver failure, so citrate is appropriate

Alternatives if citrate contraindicated:

Unfractionated heparin: Systemic anticoagulation, higher bleeding risk
No anticoagulation: Accept shorter filter life (below 24 hours), use saline flushes
Regional heparinisation: Heparin pre-filter, protamine post-filter – complex, rarely used

Given this patient's recent abdominal surgery, avoiding systemic anticoagulation is particularly important, making citrate the ideal choice.

Examiner: What complications would you monitor for during CRRT, and how would you manage them?

Candidate: I would monitor for several complications:

Hypothermia:

CRRT exposes blood to extracorporeal environment, causing heat loss
Incidence up to 50% develop temperature below 35°C without warming
Management: Use in-line blood warmer set to 37-38°C, warm dialysate and replacement fluids
Monitor core temperature q2-4h
Consequences: Hypothermia increases oxygen consumption (shivering) and can cause coagulopathy

Citrate toxicity:

If Ca:iCa ratio rises above 2.5
Manifestations: Metabolic acidosis, rising total calcium, hypocalcaemia despite supplementation
Management: Reduce or stop citrate, switch to alternative anticoagulation
This patient has no obvious liver failure, but sepsis can impair citrate metabolism

Membrane clotting:

Filter life with citrate typically 48-72 hours
Signs: Rising transmembrane pressure (TMP), rising filter pressures
Management: Optimise anticoagulation, consider pre-dilution, reduce blood flow, plan circuit change
Causes: Inadequate anticoagulation, high haematocrit, blood product administration

Bleeding:

Citrate reduces but doesn't eliminate bleeding risk
Monitor for signs of bleeding (surgical site, gastrointestinal, intracranial)
Management: Stop citrate, switch to no anticoagulation, transfuse blood products as needed

Hypophosphatemia:

Incidence up to 80% on CRRT
Phosphate removed with effluent fluid
Monitor q6-12h, replace aggressively (30 mmol phosphate daily as needed)
Consequences: Respiratory muscle weakness, haemolysis, cardiac dysfunction

Nutrient losses:

Amino acids: 10-15 g/day lost
Vitamins: Thiamine, folate, vitamin C
Trace elements: Selenium, zinc
Management: Increased protein intake 2.0-2.5 g/kg/day, multivitamin supplementation, trace element replacement weekly

Electrolyte abnormalities:

Customise dialysate and replacement fluid composition
Monitor electrolytes q4-6h initially
Adjust potassium (lower in hyperkalaemia, normalise when corrected)
Adjust sodium (avoid rapid shifts in chronic hyponatraemia)
Calcium and magnesium as needed

Circuit-related complications:

Air embolism – prevented by air detector alarms
Blood leak – stopped by detector, requires circuit change
Catheter-related complications: Infection, thrombosis, malposition

Examiner: How would you assess renal recovery and decide when to stop CRRT?

Candidate: Assessing renal recovery involves monitoring urine output, electrolyte stability, and fluid tolerance.

Favorable signs of recovery:

Increasing urine output (greater than 0.5 mL/kg/h sustained for 6-12 hours)
Stable or improving creatinine
Ability to maintain normal electrolytes without CRRT
Tolerating fluid challenges without pulmonary oedema

Weaning approach:

Trial off CRRT – stop the circuit but leave vascular access in place
Monitor urine output, creatinine, electrolytes, acid-base status, and fluid balance for 24-48 hours
If stable off CRRT for 24-48 hours → successful wean, can remove vascular access after another 24-48 hours
If oliguria recurs, electrolytes become abnormal, or volume overload develops → re-initiate CRRT

Predictive factors:

Baseline renal function (normal baseline predicts better recovery)
Non-oliguric AKI (better prognosis than oliguric)
Shorter duration of AKI (below 7 days) before CRRT
Fewer comorbidities, younger age
Cause of AKI (prerenal/ATN vs interstitial vs glomerular)

Long-term outcomes:

Approximately 70% of ICU patients requiring CRRT recover renal function
However, 40% have residual chronic kidney disease
30% progress to end-stage renal disease requiring dialysis

In this patient, I would assess recovery daily. Once she is more hemodynamically stable (off vasopressors), we could consider a trial off CRRT if urine output improves.

Examiner: Thank you. This has been a comprehensive discussion of renal replacement therapy.

Viva 2: CRRT Anticoagulation and Complication Management

Examiner: Let's discuss anticoagulation for continuous renal replacement therapy. You have started a 60-year-old man on CVVHDF for septic shock with AKI. He has no contraindications to anticoagulation. What is your preferred approach?

Candidate: My preferred anticoagulation strategy for CRRT is regional citrate anticoagulation (RCA), provided the patient has no contraindications. [18, 21]

Advantages of regional citrate:

Reduced bleeding: Major bleeding is reduced by approximately 50% compared to systemic heparin
Longer filter life: Citrate typically extends filter life to 48-72 hours, compared to 24-36 hours with heparin and below 24 hours without anticoagulation
No systemic anticoagulation: The anticoagulant effect is confined to the extracorporeal circuit, which is important in critically ill patients who are at increased bleeding risk
Biocompatibility: Citrate is biocompatible and may reduce complement activation and platelet consumption
Improved efficacy: Longer filter life means more continuous delivered dose and fewer interruptions

Mechanism of action:

Citrate is a calcium chelator
When infused into the CRRT circuit pre-filter, it binds ionised calcium, creating a localised anticoagulated zone
The coagulation cascade depends on calcium as a cofactor; by removing calcium from the circuit, clotting is inhibited
The citrate-calcium complex is metabolised in the liver (via the Krebs cycle), muscle, and mitochondria
To prevent systemic hypocalcaemia, calcium is infused into the patient systemically

Examiner: How do you prescribe and monitor regional citrate anticoagulation?

Candidate: Citrate prescription involves several components:

Citrate infusion:

Use 4% trisodium citrate solution (typically commercially available)
Infuse pre-filter at a rate proportional to blood flow: approximately 1.2-1.5% of blood flow rate
Example: Blood flow 150 mL/min → citrate infusion 180-225 mL/h (150 × 0.012 × 60 = 108 mL/h at 1.2%; 150 × 0.015 × 60 = 135 mL/h at 1.5%)
Alternatively, many ICU protocols use fixed citrate rates based on desired anticoagulation level

Target anticoagulation level:

Measure pre-filter ionised calcium: Aim for 0.25-0.35 mmol/L
This is the anticoagulated zone within the CRRT circuit
The systemic ionised calcium is maintained separately

Calcium supplementation:

Infuse calcium chloride or calcium gluconate systemically
Target systemic ionised calcium: 1.1-1.2 mmol/L
Typical infusion: 10% calcium chloride 10-15 mL/h, titrated to ionised calcium
Calcium gluconate may be used but has less bioavailability and different dosing

Monitoring schedule:

Ionised calcium (circuit and systemic): q4-6h, more frequently if unstable
Total calcium: q12h
Calculate Ca:iCa ratio: Total calcium ÷ ionised calcium (both mmol/L) – should be below 2.5
pH and bicarbonate: q12-24h (citrate metabolism produces bicarbonate)
Liver function: q24-48h if concern for liver dysfunction

Interpreting the Ca:iCa ratio:

Ratio below 2.5: No citrate accumulation
Ratio 2.5-3.0: Mild citrate accumulation – consider reducing citrate dose
Ratio greater than 3.0: Significant citrate accumulation – stop or significantly reduce citrate

Examiner: What are the contraindications to citrate anticoagulation?

Candidate: Contraindications to regional citrate include:

Absolute contraindications:

Severe liver failure (Child-Pugh C): Impaired metabolism of citrate leads to accumulation and toxicity
Citratespecific contraindications: Citrate allergy (very rare)

Relative contraindications / caution:

Moderate liver dysfunction (Child-Pugh B): May need reduced citrate dose or alternative anticoagulation
Shock with liver hypoperfusion: Even in absence of chronic liver disease, acute liver hypoperfusion (from sepsis, cardiac failure) can impair citrate metabolism
Severe hypothermia: Reduces citrate metabolism
Severe metabolic alkalosis: Citrate metabolism produces bicarbonate, exacerbating alkalosis

Contraindications to other anticoagulants:

If citrate is contraindicated and the patient has high bleeding risk, consider no anticoagulation
If citrate is contraindicated but the patient can tolerate systemic anticoagulation, use unfractionated heparin

Examiner: If citrate is contraindicated, what alternative anticoagulation strategies would you consider?

Candidate: If citrate is contraindicated, several alternatives exist:

No anticoagulation:

Suitable for patients with very high bleeding risk where any anticoagulation is unacceptable
Advantages: No bleeding risk from anticoagulation
Disadvantages: Very short filter life (often below 24 hours), frequent circuit changes, increased nursing workload, reduced delivered dose due to down-time
Enhancements: Saline flushes every 30-60 minutes, pre-dilution CVVH (lower haematocrit at filter), minimise blood product administration through circuit

Unfractionated heparin:

Standard systemic anticoagulation for CRRT
Prescription: Loading dose 2000-5000 IU IV, then infusion 10-20 IU/kg/h titrated to target APTT 1.5-2.5 × control or anti-Xa 0.3-0.5 IU/mL
Advantages: Familiar, inexpensive, no citrate toxicity risk, easier monitoring than citrate
Disadvantages: Systemic anticoagulation increases bleeding risk, Heparin-induced thrombocytopenia (HIT) risk, shorter filter life than citrate

Regional heparinisation:

Heparin infused pre-filter, protamine infused post-filter to neutralise heparin systemically
Prescription: Heparin 500-1000 IU/h pre-filter, protamine 0.5-1 mg per 100 U heparin post-filter
Advantages: Reduced systemic anticoagulation compared to full heparin
Disadvantages: Complex monitoring, protamine adverse effects (hypotension, bradycardia, anaphylaxis), rarely used in modern practice

Argatroban or bivalirudin (direct thrombin inhibitors):

Used in patients with HIT who need anticoagulation
More expensive, less experience in CRRT
Regional protocols available but complex

Selection approach:

For patients with severe liver failure and low bleeding risk: Heparin may be appropriate
For patients with severe liver failure and high bleeding risk: No anticoagulation (accept short filter life) or regional heparinisation
For patients with HIT: Direct thrombin inhibitor (argatroban, bivalirudin)

Examiner: A patient on citrate-anticoagulated CVVHDF develops a total calcium of 3.2 mmol/L, ionised calcium 0.9 mmol/L, with Ca:iCa ratio of 3.56. The pH is 7.30, HCO3- 18 mmol/L. What is your diagnosis and management?

Candidate: This is citrate accumulation with toxicity. The Ca:iCa ratio of 3.56 is markedly elevated (normal below 2.5), indicating significant citrate accumulation. [18, 21]

Pathophysiology:

Citrate is not being metabolised adequately
Unmetabolised citrate accumulates and continues to chelate ionised calcium
The ionised calcium is low (0.9 mmol/L) despite total calcium being elevated (3.2 mmol/L)
The total calcium is elevated because it includes both free ionised calcium and citrate-bound calcium
The citrate-calcium complex contributes to total calcium measurement but not to ionised calcium
This explains the high Ca:iCa ratio

Contributing factors (to investigate):

Liver dysfunction: Check liver function tests (bilirubin, transaminases, INR)
Hepatic hypoperfusion: Check lactate, haemodynamics
Hypothermia: Check temperature
High citrate infusion rate relative to metabolic capacity
Acidosis: May be multifactorial (citrate accumulation, sepsis, tissue hypoperfusion)

Immediate management:

Stop or reduce citrate infusion: I would stop citrate completely given the markedly elevated ratio (greater than 3.0)
Switch anticoagulation strategy:
- If the patient has high bleeding risk: No anticoagulation
- If the patient can tolerate systemic anticoagulation: Unfractionated heparin
Assess for hypocalcaemia:
- Ionised calcium 0.9 mmol/L is low-normal (normal 1.1-1.2 mmol/L)
- Check for symptoms: Tetany, seizures, ECG changes (QT prolongation)
- If symptomatic or iCa below 0.8 mmol/L: Administer calcium (10% calcium chloride 10 mL IV)
- However, be cautious about over-correcting – excess calcium can bind citrate and form tissue deposits
Address metabolic acidosis:
- pH 7.30, HCO3- 18 mmol/L is mild acidosis
- May be due to citrate accumulation (unmetabolised citrate contributes to anion gap)
- May also be due to underlying condition (sepsis, tissue hypoperfusion)
- CRRT will correct acidosis (bicarbonate-buffered dialysate)
- If severe acidosis (pH below 7.25), consider additional bicarbonate
Investigate underlying cause:
- Review liver function
- Assess haemodynamics
- Check temperature
- Consider reducing CRRT dose (lower citrate requirement)

Monitoring after changes:

Recheck ionised calcium and total calcium q2-4h
Monitor Ca:iCa ratio
Expect Ca:iCa ratio to normalise as citrate is metabolised (once infusion stopped)
Watch for hypocalcaemia (as citrate-calcium complex metabolises, releases calcium)
Monitor electrolytes, pH

Circuit considerations:

When citrate stopped, the circuit will likely clot quickly (within 12-24 hours)
Plan for circuit change or transition to alternative anticoagulation
With no anticoagulation, filter life may be below 24 hours
With heparin, filter life typically 24-36 hours

Prevention:

For patients with risk factors for citrate accumulation (liver dysfunction, shock, hypothermia):
- Use reduced citrate dose
- Monitor more frequently (ionised calcium q2-4h, total calcium q6h)
- Consider alternative anticoagulation from the start
- "Early recognition: Intervene when Ca:iCa ratio greater than 2.5, not wait for greater than 3.0"

Examiner: How do you differentiate citrate accumulation from other causes of metabolic acidosis in a patient on CRRT?

Candidate: Citrate accumulation has characteristic features that help differentiate it from other causes of acidosis:

Key distinguishing feature: Elevated total calcium:ionised calcium ratio

In citrate accumulation: Ratio greater than 2.5 (often 3.0-4.0 in severe cases)
In other causes of acidosis: Ratio typically below 2.5

Calcium pattern:

Citrate accumulation: Total calcium elevated (3.0-4.0 mmol/L) with ionised calcium low-normal or low (0.8-1.0 mmol/L)
Other causes: Total calcium and ionised calcium usually parallel each other

Acid-base pattern:

Citrate accumulation: Anion gap metabolic acidosis (unmetabolised citrate contributes to anion gap)
Lactic acidosis: Elevated lactate, Ca:iCa ratio normal
DKA/other ketoacidosis: Elevated ketones, Ca:iCa ratio normal
Renal tubular acidosis: Normal anion gap, hyperchloraemic

Associated features:

Citrate accumulation may also cause metabolic alkalosis (from citrate metabolism to bicarbonate), but this is typically seen earlier in the accumulation process; later, unmetabolised citrate causes acidosis
Lactic acidosis: Elevated lactate, often with tissue hypoperfusion signs
Uraemic acidosis: High urea, creatinine
Severe hyperchloraemia: Hyperchloraemic normal anion gap acidosis

Diagnostic approach:

Calculate Ca:iCa ratio (first-line diagnostic test for citrate toxicity)
Measure lactate
Check ketones (β-hydroxybutyrate) if DKA suspected
Review dialysate composition (excessive chloride can cause hyperchloraemic acidosis)
Consider mixed acid-base disorders (e.g., lactic acidosis + citrate accumulation)

Examples:

Citrate accumulation: Ca 3.2, iCa 0.9, ratio 3.56, anion gap 20, lactate 3 mmol/L
Pure lactic acidosis: Ca 2.3, iCa 1.15, ratio 2.0, anion gap 18, lactate 8 mmol/L
DKA: Ca 2.2, iCa 1.1, ratio 2.0, anion gap 25, glucose 30 mmol/L, ketones positive

Examiner: What are the strategies to prevent citrate accumulation and toxicity?

Candidate: Prevention of citrate accumulation involves patient selection, dose optimisation, and careful monitoring:

Patient selection:

Avoid citrate in patients with severe liver failure (Child-Pugh C)
Use caution in patients with moderate liver dysfunction (Child-Pugh B) – consider reduced citrate dose or alternative anticoagulation
Avoid citrate in shock with significant liver hypoperfusion (elevated lactate greater than 4-5 mmol/L may reflect impaired hepatic function)
Consider alternative anticoagulation in patients at high risk of accumulation

Dose optimisation:

Use the lowest effective citrate dose
Start at lower infusion rates in at-risk patients (e.g., 1.0-1.2% of blood flow rather than 1.5%)
Titrate to pre-filter ionised calcium target of 0.25-0.35 mmol/L (don't exceed lower end of range in at-risk patients)
Consider citrate dose reduction if total calcium rises or Ca:iCa ratio increases

Monitoring strategy:

Early monitoring: Ionised calcium (circuit and systemic) q2-4h in the first 24-48 hours of CRRT
Regular monitoring: Total calcium q12h, calculate Ca:iCa ratio at each measurement
Frequency adjustment: Reduce monitoring frequency once stable (q6h), but continue vigilance
Early intervention: Intervene when Ca:iCa ratio greater than 2.5 (not wait for greater than 3.0)

Recognition of early signs:

Rising total calcium without corresponding rise in ionised calcium
Rising Ca:iCa ratio (even if still below 2.5)
Metabolic alkalosis early in accumulation process (citrate metabolised to bicarbonate)
Later: Anion gap metabolic acidosis as unmetabolised citrate accumulates

Protocol adjustments:

Consider citrate dose reduction by 25-50% if Ca:iCa ratio 2.5-3.0
Stop citrate if Ca:iCa ratio greater than 3.0
Switch to alternative anticoagulation if persistent issues

Alternatives for high-risk patients:

No anticoagulation (accept short filter life)
Unfractionated heparin (if bleeding risk acceptable)
Regional heparinisation (reduces systemic anticoagulation compared to full heparin)

Education and communication:

Ensure nursing staff aware of citrate toxicity signs and when to call medical team
Establish clear protocols for citrate dose adjustment and switching anticoagulation
Regular review of CRRT parameters during rounds

Examiner: What other complications of CRRT are important, and how do you prevent them?

Candidate: Key complications of CRRT include:

Hypothermia:

Incidence: Up to 50% develop temperature below 35°C without warming
Mechanism: Extracorporeal circuit exposes blood to room temperature
Prevention: Use in-line blood warmer (set 37-38°C), warm dialysate and replacement fluids, cover exposed circuit tubing
Monitoring: Core temperature q2-4h
Management: Active warming if hypothermic
Consequences: Increased oxygen consumption (shivering), coagulopathy

Hypophosphatemia:

Incidence: Up to 80% on CRRT
Mechanism: Phosphate removed with effluent fluid; replacement/dialysate fluids typically phosphate-free
Prevention: Monitor phosphate q6-12h, replace proactively (30 mmol phosphate daily as needed)
Management: IV phosphate (NaH2PO4 30 mmol) when phosphate below 0.8 mmol/L
Consequences: Respiratory muscle weakness, haemolysis, cardiac dysfunction

Nutrient losses:

Amino acids: 10-15 g/day lost
Vitamins: Water-soluble vitamins (thiamine, folate, vitamin C)
Trace elements: Selenium, zinc
Prevention: Increased protein intake 2.0-2.5 g/kg/day, multivitamin supplementation, trace element replacement weekly

Membrane clotting:

Filter life: 48-72 hours with citrate, 24-36 hours with heparin, below 24 hours without anticoagulation
Signs: Rising transmembrane pressure (TMP), rising filter pressures
Prevention: Adequate anticoagulation, optimise blood flow, avoid blood product administration through circuit, use pre-dilution if appropriate
Management: Plan circuit change before complete clotting, optimise anticoagulation for next circuit

Bleeding:

Incidence: 2-5% with citrate, 10-15% with heparin
Prevention: Use citrate when possible (reduces bleeding by 50%), avoid systemic anticoagulation in high-risk patients
Management: Stop anticoagulant, consider no anticoagulation for subsequent circuits, transfuse blood products as needed

Infection:

Incidence: Catheter-related bloodstream infection 2-5 episodes/1000 catheter-days
Prevention: Aseptic technique during catheter insertion and handling, antibiotic-coated catheters for prolonged use, remove catheter when no longer needed
Management: Blood cultures, appropriate antibiotics, consider catheter removal if persistent

Electrolyte disturbances:

Prevention: Customise dialysate/replacement fluid composition, monitor electrolytes q4-6h initially, adjust as needed
Common issues: Hyperkalaemia or hypokalaemia, dysnatraemia, hypocalcaemia, hypomagnesaemia
Management: Adjust fluid composition, supplement as needed

Examiner: Thank you. This has been a comprehensive discussion of CRRT anticoagulation and complications.

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