Continuous Renal Replacement

The contract between this chapter and the reader.

1. 1. Define CRRT and state when it is preferred over intermittent dialysis.
2. 2. Distinguish the CRRT modalities — SCUF, CVVH, CVVHD, CVVHDF — by transport mechanism.
3. 3. Explain diffusion versus convection and what each clears.
4. 4. Prescribe an effluent dose and explain why higher intensity does not improve survival.
5. 5. Manage regional citrate anticoagulation and recognise citrate accumulation.
6. 6. Set fluid-balance and electrolyte targets, anticipating hypophosphatemia.
7. 7. Recognise the indications and correct timing for starting CRRT.
8. 8. Troubleshoot circuit pressures and filter clotting.
9. 9. Anticipate the complications of CRRT.

A sixty-second reading. Each bullet stands alone.

• CRRT is slow, continuous extracorporeal therapy for critically ill acute kidney injury, tolerated when patients are hemodynamically unstable.
• It is preferred over intermittent haemodialysis in instability and in raised intracranial pressure, where rapid shifts are dangerous.
• The modalities differ by mechanism: SCUF removes fluid only; CVVH uses convection; CVVHD uses diffusion; CVVHDF uses both.
• Diffusion clears small solutes down a gradient; convection drags middle molecules with ultrafiltered water and needs replacement fluid.
• Effluent dose is the total effluent flow per kilogram per hour; deliver 20–25 mL/kg/h.
• Randomised trials show higher intensity — 35 to 40 mL/kg/h — gives no survival benefit over 20–25.
• Prescribe above target to offset the downtime lost to filter clotting and procedures.
• Regional citrate anticoagulation is first-line: it anticoagulates the circuit, not the patient, with less bleeding and longer filter life.
• Citrate accumulation — especially in liver failure — raises the total-to-ionised calcium ratio with metabolic acidosis; monitor ionised calcium.
• Net ultrafiltration is set to a fluid-balance goal; hypophosphatemia, hypokalemia, and hypomagnesemia are common and replaced.
• Start for an urgent indication — refractory acidosis, hyperkalemia, intoxication, fluid overload, or uremia — not preemptively.
• Randomised trials show no benefit to starting very early rather than waiting for a clear indication.
• Filter clotting shows as rising transmembrane and filter pressures; keep the filtration fraction below about 20–25%.
• Complications include hypothermia, hypophosphatemia, citrate toxicity, bleeding, and loss of drugs and nutrients.

The medical core. An expert should agree CRRT is fully covered here.

Why it matters at the bedside

The sickest patients with acute kidney injury are exactly the ones who cannot tolerate a fast intermittent run. CRRT trades speed for gentleness — removing fluid and solute slowly, around the clock — and that single trade is why it is the dialysis of the unstable. Master the mechanism, the dose, and the citrate, and the rest is troubleshooting.

What CRRT is, and when it is preferred

• CRRT is continuous (24-hour) veno-venous extracorporeal blood purification run in the intensive care unit through a double-lumen central catheter and a blood pump. Its slow, steady removal preserves haemodynamic stability and allows generous fluid intake for nutrition and drugs.
• It is preferred over intermittent haemodialysis when the patient is hemodynamically unstable or has cerebral oedema or raised intracranial pressure, where the rapid osmotic and volume shifts of intermittent dialysis are hazardous.

The modalities, by mechanism

• SCUF — slow continuous ultrafiltration: convection for fluid removal only, with no dialysate or replacement fluid; used for isolated volume overload.
• CVVH — continuous veno-venous haemofiltration: convection with replacement fluid, clearing middle molecules well.
• CVVHD — continuous veno-venous haemodialysis: diffusion against countercurrent dialysate, clearing small solutes.
• CVVHDF — continuous veno-venous haemodiafiltration: convection and diffusion together, with both replacement fluid and dialysate.

Diffusion versus convection

• Diffusion moves small solutes — urea, potassium — down their concentration gradient across the membrane into dialysate. Convection drags solutes along with ultrafiltered water (solvent drag) and clears larger middle molecules more effectively, but requires replacement fluid to make up the volume removed.

The prescription: dose and fluids

• Dose is the effluent dose — the sum of dialysate, replacement, and net ultrafiltration flow — expressed per kilogram per hour. Deliver 20–25 mL/kg/h, and prescribe somewhat higher because downtime from clotting and procedures erodes what is actually delivered.
• Replacement fluid given before the filter (pre-dilution) reduces clotting but dilutes the blood and lowers efficiency; given after the filter (post-dilution) it is more efficient but clots more. Keep the filtration fraction below about 20–25% to protect the filter.

Why more is not better

• It is tempting to equate a higher dose with better care, but randomised trials comparing intensive (35–40 mL/kg/h) with standard (20–25) effluent dose found no survival benefit from the higher intensity. The target is therefore delivery of 20–25, not escalation.

Anticoagulation: regional citrate

• Regional citrate anticoagulation is first-line. Citrate infused into the circuit chelates calcium, halting clotting within the circuit, while calcium is replaced systemically so the patient is not anticoagulated. Compared with heparin it gives longer filter life and less bleeding.
• Circuit ionised calcium is kept very low (below about 0.35 mmol/L) and systemic ionised calcium normal (about 1.0–1.2 mmol/L) by titrating the citrate and calcium infusions.

Citrate accumulation

• Citrate is metabolised to bicarbonate, mainly in the liver. When metabolism fails — classically in severe liver failure or shock — citrate accumulates, chelating systemic calcium: total calcium rises while ionised calcium falls, the total-to-ionised ratio climbs above about 2.5, and a metabolic acidosis develops. The response is to reduce or stop citrate, not to chase the rising total calcium.

Fluid balance and electrolytes

• Net ultrafiltration is set hourly to a fluid-balance goal. Continuous clearance steadily strips phosphate, potassium, and magnesium, so hypophosphatemia, hypokalemia, and hypomagnesemia are common and are replaced — often with phosphate-containing or potassium-supplemented fluids.

Indications and timing

• Start for an urgent indication — refractory metabolic acidosis, hyperkalemia, certain intoxications, diuretic-resistant fluid overload, or symptomatic uremia (the AEIOU list). Randomised trials show no benefit to starting very early over waiting for such an indication, so preemptive initiation is avoided.

Troubleshooting the circuit

• Read the pressures: a strongly negative access (arterial) pressure means the catheter is sucking against the vessel; a high return (venous) pressure means a clot or kink downstream; a rising transmembrane pressure means the membrane is clogging. Recurrent clotting points to inadequate anticoagulation, too high a filtration fraction, or access recirculation.

Complications

• Beyond citrate toxicity and clotting, watch for hypothermia from the extracorporeal circuit, hypophosphatemia and other electrolyte losses, bleeding (with heparin), and the unintended clearance of antibiotics and nutrients — which is why drug dosing is adjusted for CRRT.

Evidence base

• The 20–25 mL/kg/h target and the futility of higher intensity rest on large randomised trials. The preference for regional citrate over heparin rests on randomised filter-life and bleeding data. The lack of benefit from very early initiation rests on several timing trials. CRRT versus intermittent HD shows no clear survival difference, but CRRT is better tolerated in instability.

Five fully-built tables.

Table A — The CRRT modalities

Table B — Diffusion versus convection

Table C — Dose and fluids

Table D — Regional citrate monitoring

Table E — Circuit alarms and troubleshooting

Visualise & Map

Causal chains, each ending in a named action.

Chain 1 — Convection and middle molecules

Pressure gradient → ultrafiltration → solvent drag carries middle molecules → better middle-molecule clearance → ACTION: use CVVH or CVVHDF when middle-molecule clearance matters.

Chain 2 — Regional citrate

Citrate chelates calcium in the circuit → clotting stops in the circuit only → patient not anticoagulated → ACTION: replace systemic calcium and monitor ionised calcium.

Chain 3 — Citrate accumulation

Citrate is metabolised to bicarbonate in the liver → in liver failure it accumulates → it chelates systemic calcium (total up, ionised down) with acidosis → ACTION: reduce or stop citrate; do not chase the rising total calcium.

Chain 4 — Filtration fraction and clotting

High filtration fraction → haemoconcentration within the filter → clotting and short filter life → ACTION: use pre-dilution and keep the filtration fraction below ~20–25%.

Chain 5 — Continuous and gentle

Slow, continuous removal → minimal osmotic and volume shifts → haemodynamic stability → ACTION: choose CRRT for the unstable patient and for raised intracranial pressure.

Numbered rules. These numbers are the cross-reference handle for the cases and flowcharts.

Clinical Reasoning

Five cases. Each stops you at a decision before it answers it.

Every mechanism from Level 3 earns a bedside consequence and an action.

Exhaustive. Every threshold and rule in the chapter is here.

Safety & Evidence

Panel A — Red flags

Panel B — NEVER DO

Anti-patterns clinicians fall into. Each becomes a Level 22 distractor.

The grade reflects strength of evidence, not importance.

Patient Decisions

Outcomes as natural frequencies. Figures are representative; the direction of effect is given where precise numbers are uncertain.

Apply & Test

Copy-paste chart notes that map to the real decisions in this chapter.

Template 1 — CRRT prescription note

• Indication (AEIOU): ___; rationale for CRRT over IHD: ___.
• Modality: SCUF / CVVH / CVVHD / CVVHDF.
• Dose: delivered target 20–25 mL/kg/h; prescribed ___ mL/kg/h; weight ___ kg.
• Fluids: dialysate ___; replacement ___ (pre/post); filtration fraction target < ~20–25%.
• Anticoagulation: regional citrate / heparin / none; targets set.
• Net ultrafiltration goal: ___ mL/h; electrolyte additives: ___.

Template 2 — Daily CRRT / citrate review

• Delivered dose vs prescribed (downtime): ___.
• Citrate: circuit iCa ___; systemic iCa ___; total/ionised ratio ___; acid–base ___.
• Circuit: filter/TMP pressures ___; clotting events ___; access ___.
• Electrolytes: phosphate ___; potassium ___; magnesium ___; replacements given.
• Fluid balance achieved vs goal: ___; plan / drug-dose adjustments: ___.

Pre-rounds compression. Numbers and rules only.

Active recall. At least one card per objective.

Micro-teaching for rounds. Two scenarios, five steps each.

Metacognition anchored to this chapter's tensions. No answers provided.

1. 1. ‘Doing more’ feels safer in a dying patient; how do you hold to a standard dose when instinct and family pressure push toward intensity the evidence does not support?
2. 2. The prescribed dose and the delivered dose drift apart through downtime; how would you make that invisible gap visible on your unit?
3. 3. Citrate is elegant until the liver fails; how do you decide when its benefits no longer outweigh the risk of accumulation?
4. 4. Starting CRRT earlier feels proactive; what makes ‘waiting for an indication’ the harder but better discipline?
5. 5. When does the continuous clearance you rely on become a hidden source of harm — in drug levels, electrolytes, or temperature — and how do you stay ahead of it?

Nine items, each anchored in this chapter. At least one per objective.