What are the guidelines for Continuous Renal Replacement Therapy (CRRT) in patients with hepatic failure?

CRRT Guidelines for Hepatic Failure

CRRT is recommended for patients with acute liver failure who develop acute kidney injury, particularly when hemodynamically unstable, and should utilize bicarbonate-buffered solutions with cautious—but not prohibited—use of regional citrate anticoagulation. 1

Primary Indications for CRRT in Hepatic Failure

CRRT is the preferred renal replacement modality in liver failure patients with AKI, regardless of kidney injury type. 1 The specific indications include:

• Hemodynamic instability: CRRT provides superior hemodynamic stability compared to intermittent hemodialysis in critically ill liver failure patients, who frequently cannot tolerate the rapid fluid shifts of conventional dialysis. 1, 2
• Severe electrolyte or acid-base imbalances: Particularly when refractory to medical management, including severe hyponatremia requiring slower correction to avoid neurological complications. 1
• Volume overload: CRRT facilitates continuous fluid management in hemodynamically fragile patients. 1, 3
• Symptomatic azotemia: When uremic symptoms develop despite medical therapy. 1
• Cerebral edema or increased intracranial pressure: CRRT avoids the intracranial pressure spikes associated with intermittent hemodialysis (IHD can increase ICP by 45% during the first hour). 2

Technical Prescription and Dosing

Effluent Dose

• Target 20-25 mL/kg/hr of effluent generation as the standard CRRT dose in liver failure patients. 1, 4
• Frequently assess actual delivered dose and adjust prescription accordingly. 4

Modality Selection

• Continuous venovenous hemodiafiltration (CVVHDF) or continuous venovenous hemofiltration (CVVH) are the preferred modalities, as they combine convective and diffusive clearance. 1, 3
• Both CVVHDF and continuous arteriovenous hemodiafiltration (CAVHDF) demonstrate similar efficacy in reducing hyperbilirubinemia, uremia, and fluid overload in hepatic failure. 3

Buffer Selection

Use bicarbonate rather than lactate as the buffer in all dialysate and replacement fluids for liver failure patients. 5, 4 This is a strong recommendation (1B evidence) because:

• Patients with liver failure have impaired lactate metabolism. 5
• Lactate-buffered solutions risk worsening lactic acidosis. 4
• Bicarbonate provides safer acid-base correction in this population. 5

Anticoagulation Strategy in Liver Failure

Regional citrate anticoagulation can be used cautiously in liver failure but requires intensive monitoring—it is not an absolute contraindication. 5, 1

Key Considerations:

• Liver failure patients are often coagulopathic, making heparin-based anticoagulation potentially more hazardous than citrate. 5
• Monitor citrate accumulation by tracking systemic ionized calcium levels and the total calcium to ionized calcium (tCa/iCa) ratio—a ratio >2.4 suggests accumulation. 5, 6
• Extra-hepatic citrate metabolism exists: Studies show that even with severe liver dysfunction (mean ICG-PDR 9.8%), citrate accumulation occurred in only 23% of patients, and CRRT was never discontinued due to citrate-related complications. 6
• Alternative approach: If citrate is deemed too risky, consider CRRT with no anticoagulation or use intermittent modalities like sustained low-efficiency dialysis (SLED) where anticoagulation-free treatment is more feasible. 5
• For heparin-induced thrombocytopenia (HIT): Use direct thrombin inhibitors (argatroban) or Factor Xa inhibitors, but avoid argatroban in severe liver failure due to hepatic metabolism. 5

Vascular Access

Follow standard CRRT access guidelines with preferred vein selection order: 4

1. Right internal jugular vein (first choice)
2. Femoral vein (second choice)
3. Left internal jugular vein (third choice)
4. Subclavian vein (last choice—avoid due to thrombosis/stenosis risk)

• Use ultrasound guidance for all catheter insertions. 4
• Obtain chest radiograph after jugular/subclavian placement before first use. 4
• Use uncuffed nontunneled catheters for acute initiation. 4

Nutritional and Metabolic Monitoring

CRRT causes significant nutrient losses requiring aggressive replacement: 1

• Approximately 10-15g amino acids lost per day. 1
• Water-soluble vitamins are continuously removed. 1
• Electrolytes (particularly phosphate and magnesium) require frequent monitoring and replacement. 1

Clinical Outcomes and Prognosis

• Survival to liver transplant: 30-60% of liver failure patients receiving CRRT survive to transplantation. 7
• Overall survival: Approximately 30% in combined hepatic and renal failure. 3
• CRRT provides effective biochemical improvement: Significant reductions in blood urea, creatinine, and bilirubin are achievable despite hemodynamic fragility. 3
• Cardiovascular stability: During the first hour of treatment, CRRT shows no significant change in cardiac index, whereas intermittent hemodialysis causes a 15% reduction in cardiac output and 20% drop in mean arterial pressure. 2

Critical Pitfalls to Avoid

• Do not delay CRRT initiation in acute liver failure patients with AKI—early RRT may improve survival. 1
• Do not limit CRRT only to transplant candidates: Base decisions on individual severity of illness using prognostic scores, clinical judgment, and patient preferences. 1
• Do not use lactate-buffered solutions in liver failure patients. 5, 4
• Do not assume citrate is absolutely contraindicated: With proper monitoring (tCa/iCa ratio), citrate can be safely used even in severe liver dysfunction. 5, 6
• Do not rely solely on standard liver function tests to predict citrate accumulation—they show poor predictive capability. 6

Role as Bridge to Transplantation

Liver transplantation remains the definitive treatment for hepatorenal syndrome, and CRRT should be viewed as a bridge to transplantation or hepatic recovery. 1, 7 CRRT can be provided intraoperatively during liver transplant to control volume and electrolytes in patients presenting with renal failure. 7