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The clinical content and references are curated and reviewed by myself; however, AI was used to assist in organizing, paraphrasing, and formatting the information presented.

Bedside Topline (What to Remember First)

Fundamentals & Terminology

Continuous renal replacement therapy (CRRT) is any extracorporeal blood purification therapy applied continuously (~24 h/day) to replace impaired renal function in critically ill patients. It uses a hemofilter (artificial nephron) to remove water and solutes.

Key Solute Transport Mechanisms

  • Diffusion: solute movement down a concentration gradient across a semipermeable membrane (dialysate on the other side). Best for small solutes (urea, K⁺)
  • Convection: solvent drag – water is pulled across the membrane by transmembrane pressure and drags solutes with it. Better for middle molecules (e.g., some cytokines)
  • Adsorption: some solutes adhere to the membrane surface or matrix; limited capacity and saturates over time
Clinical Pearl: Think of diffusion like tea steeping (concentration gradient) and convection like water flowing through coffee grounds (solvent drag).
CRRT Modalities

Different CRRT modes use different combinations of diffusion and convection to achieve blood purification:

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Modality Main Mechanism Key Fluid Streams Typical Use Case
SCUF
(Slow continuous ultrafiltration)
Ultrafiltration only Ultrafiltrate (no dialysate or replacement) Pure fluid removal (refractory fluid overload with relatively preserved solutes)
CVVH
(Continuous veno-venous hemofiltration)
Convection Replacement fluid (pre/post-filter) + ultrafiltrate Solute + fluid removal using convective clearance; good for uremia and volume overload
CVVHD
(Continuous veno-venous hemodialysis)
Diffusion Dialysate + ultrafiltrate Primarily small-solute clearance (e.g., hyperkalemia, uremia) with some fluid control
CVVHDF
(Continuous veno-venous hemodiafiltration)
Diffusion + convection Dialysate + replacement + ultrafiltrate Most versatile; combines excellent small-solute removal with convective middle-molecule clearance
Bedside Tip: CVVHDF is the most commonly used mode in modern ICUs because it combines the benefits of both diffusion and convection.
CRRT vs Native Kidney & Intermittent HD

Compared with the Native Kidney

  • CRRT replaces only part of normal kidney function: water removal, small and some middle-solute clearance, and some acid–base control
  • It does NOT replace endocrine functions (erythropoietin, vitamin D activation, renin) or fine-tuned tubular transport
  • "24 h of CRRT ≈ 24 h of reduced kidney function" – it mitigates complications rather than fully normalizing physiology

CRRT vs Intermittent Hemodialysis (IHD)

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Feature CRRT IHD
Duration 24 h/day (or near-continuous) 2–5 h per session, several times per week
Fluid/solute removal rate Slow, steady Fast, high-volume shifts
Hemodynamic tolerance Better (less hypotension) More hypotension & osmotic shifts
ICU use Preferred in unstable, ventilated patients Often used when stable or in ESRD patients
Logistics Ties to machine continuously; nursing-intensive Short bursts; dialysis nurse-led
When to Choose CRRT: Hemodynamically unstable patients, severe volume overload requiring gentle removal, need for continuous control of uremia or electrolytes, or when patient cannot tolerate rapid fluid shifts.
Prescription – Dose, Flows & Fluid Balance

Dose of Dialysis (Small-Solute Clearance)

  • In practice, CRRT dose ≈ effluent rate (dialysate + ultrafiltrate + post-filter replacement)
  • Evidence suggests no mortality benefit above ~25–30 mL/kg/hr; many ICUs target 20–25 mL/kg/hr as delivered dose
  • To compensate for downtime (bag changes, clots), you often prescribe slightly higher (e.g., 25–30 mL/kg/hr) to deliver ≥20 mL/kg/hr
Quick Mental Math for Effluent Rate:
  • 70 kg patient × 25 mL/kg/hr ≈ 1750 mL/hr effluent
  • 100 kg patient × 25 mL/kg/hr ≈ 2500 mL/hr effluent
  • Remember: this is total effluent (dialysate + replacement + net fluid removal)

Fluid Balance Strategy

  • First stabilize hemodynamics (MAP, vasopressor dose, lactate) before aggressive net negative fluid balance
  • Net ultrafiltration (UFnet) = total effluent – (dialysate + replacement). Titrate UFnet to achieve desired daily balance (e.g., –500 to –2000 mL/day)
  • Start with low UFnet (e.g., 0–50 mL/hr) in unstable patients; gradually increase as tolerated
  • Use arterial line and echo to guide UF – watch for falling MAP, decreasing stroke volume, rising lactate, or poor organ perfusion
Warning: Aggressive fluid removal in a hemodynamically unstable patient can precipitate cardiovascular collapse. Always prioritize hemodynamic stability over diuresis.
Anticoagulation for CRRT Circuit

Filter life and circuit patency are major determinants of effective CRRT dose. Anticoagulation is usually needed unless contraindicated.

Regional Citrate Anticoagulation (RCA)

  • Mechanism: citrate chelates ionized calcium in the circuit, inhibiting coagulation; calcium is then infused systemically to normalize patient ionized Ca²⁺
  • Advantages: longer filter life, lower bleeding risk than systemic heparin, especially useful in coagulopathic or post-operative patients
  • Monitoring: systemic and post-filter ionized Ca²⁺, total Ca²⁺, Ca²⁺ ratio, bicarbonate/anion gap, and acid–base status
  • Citrate toxicity clues: rising total:ionized calcium ratio (>2.5), metabolic acidosis or alkalosis (depending on metabolism), high anion gap, refractory hypotension; risk increased in severe liver failure and shock with poor citrate metabolism
RCA Monitoring Pearl: Check ionized calcium every 4-6 hours. If total Ca/ionized Ca ratio > 2.5, suspect citrate accumulation.

Systemic Unfractionated Heparin

  • Mechanism: systemic anticoagulation via antithrombin III; monitored with aPTT or anti-Xa
  • Advantages: simple, familiar, useful when patient already requires systemic anticoagulation (e.g., PE, AF)
  • Disadvantages: higher bleeding risk, filter life often shorter than with citrate; problematic in HIT

No Anticoagulation / Alternatives

  • Reserved for very high bleeding risk or immediately peri-procedure; filter life is often short
  • Strategies to prolong circuit life: high blood flow rates, saline flushes, minimizing stasis (avoid frequent stops), optimizing catheter position
  • Alternatives like prostacyclin or regional heparin–protamine are niche and protocol-dependent
Common Alarms & Troubleshooting
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Alarm Physiology / Cause Quick Checks Interventions
Access pressure low (negative) Poor inflow from patient → catheter kinking, malposition, hypovolemia, or line occlusion Check catheter position (neck flexion, line kink, clamps, patient position), assess volume status and CVP Reposition patient/neck/line; flush catheter; consider volume bolus if truly hypovolemic; if persistent, consider catheter exchange
Return pressure high Resistance on blood return limb → kinked tubing, clot in filter or venous chamber, high central venous pressure Inspect line for kinks; check for visible clotting; review CVP and patient status Correct mechanical issues; if clotting suspected, change circuit and reassess anticoagulation
Filter pressure high / TMP rising Filter is clogging with clot or protein; transmembrane pressure (TMP) increases as membrane blocks Trend TMP; look for darkening of filter, shortened filter life, frequent pressure alarms Plan timely circuit change; optimize anticoagulation; avoid hemoconcentration (avoid aggressive UF with low blood flows)
Air-in-line / leak alarms Air in circuit or leak risk; may be from empty bags, loose connections, or cracked chambers Check all connections; ensure fluid bags not empty; inspect air detectors and drip chambers Stop pump, clamp lines as directed, clear air per protocol; do NOT override air alarms without resolving cause
Never Override Air Alarms: Air embolism is a potentially fatal complication. Always identify and resolve the source of air before resuming therapy.

Filter Life & P-Drop

The pressure drop (P-drop) is simply filter pressure minus return pressure. The blood pressure in the filter drops after the circuit, due to the resistance in the circuit, and from this one can estimate this resistance.

The P-drop is an important indicator of filter lifespan. An increasing P-drop signals an impending filter failure.

Filter Life Pearl: Typical filter life is 24-72 hours. If filters are clotting in < 12 hours, reassess anticoagulation strategy, blood flow rates, and catheter function.
Complications – What Can Go Wrong
  • Hemodynamic instability: excessive UF, rapid osmotic shifts, or underlying sepsis/cardiac dysfunction. Counter with slower UF, vasopressors, and careful titration
  • Electrolyte derangements: hypophosphatemia, hypokalemia, hypocalcemia (especially with citrate), and sometimes hypernatremia/hyponatremia depending on fluids used
  • Acid–base issues: metabolic acidosis (insufficient clearance, citrate accumulation) or metabolic alkalosis (citrate metabolism, high bicarbonate dialysate)
  • Hypothermia: continuous extracorporeal circuit cools blood; may worsen coagulopathy and arrhythmias
  • Bleeding: due to anticoagulation, platelet dysfunction, or line insertion; can be occult (GI, retroperitoneal)
  • Catheter-related complications: infection, thrombosis, air embolism, malposition, venous stenosis
  • Under-dialysis: frequent interruptions, clotted filters, low effluent prescription → inadequate solute removal and fluid burden
Electrolyte Monitoring: Check electrolytes (especially K⁺, PO₄³⁻, Mg²⁺, Ca²⁺) at least every 6-12 hours. Phosphate depletion is extremely common and often requires supplementation.
Temperature Management: Ensure circuit heater is functioning. Target patient temperature 36-37°C. Hypothermia increases filter clotting and bleeding risk.
Bedside & Transport Pearls
  • CRRT is a team sport: coordinate with nephrology/intensivist, bedside nurse, and RT when adjusting fluids, ventilator, or vasoactive drips
  • Never move the patient or bed without checking line routing; avoid pulling on the dialysis catheter or filter
  • During transport, strongly consider whether CRRT should run or be paused; if paused, flush lines as per protocol and document downtime
  • Keep accurate input/output and weight trends; CRRT makes fluid balance look deceptively "normal" unless meticulously tracked
  • Drug dosing: many critical meds (antibiotics, sedatives, anticonvulsants) are cleared by CRRT. Check local dosing guides or pharmacy for CRRT-specific doses
  • For the learner: always re-check which modality is running (CVVH vs CVVHD vs CVVHDF) before interpreting flows and prescription
Transport Checklist:
  1. Ensure battery is charged (minimum 30 min)
  2. Secure all lines and bags
  3. Brief transport team on CRRT alarms
  4. Have backup plan if circuit needs to be stopped
  5. Document downtime if CRRT paused
Common CRRT-Cleared Medications: Vancomycin, piperacillin-tazobactam, meropenem, levetiracetam, valproate. Always consult pharmacy for dosing adjustments.
Quick Teaching Script (5-Step Walk-Through)
  1. Start with the indication: Why does this patient need CRRT (volume, K⁺, acidosis, uremia)? Why continuous vs intermittent?
  2. Identify the modality: Is this CVVH, CVVHD, CVVHDF, or SCUF? Which bags are dialysate vs replacement vs simply UF?
  3. Check the prescription: What is the effluent rate (mL/kg/hr)? What is the net UF goal (mL/hr or per day)?
  4. Review anticoagulation: Citrate vs heparin vs none – what are the monitoring labs and what are we watching out for (e.g., citrate toxicity, bleeding)?
  5. Scan for complications: pressures and alarms, electrolytes, acid–base, temperature, and catheter issues – then tie it back to how the patient looks at the bedside
Bedside Teaching Tip: Use the "circuit walk-through" method: start at the patient's catheter, follow the blood path through pump → filter → return, then trace the dialysate/replacement fluids. This helps learners visualize the entire system.
Common Indications for CRRT
  • Volume overload: refractory to diuretics, especially with hemodynamic instability
  • Severe AKI/Uremia: BUN >100 mg/dL (or >35 mmol/L), symptoms of uremia (pericarditis, encephalopathy, bleeding)
  • Refractory hyperkalemia: K⁺ >6.5 mEq/L not responsive to medical management
  • Severe metabolic acidosis: pH <7.1 or bicarbonate <10 mEq/L
  • Toxin removal: certain drug overdoses (lithium, metformin, salicylates – though IHD may be better for some)
  • Severe electrolyte derangements: life-threatening hypernatremia, hypercalcemia, hypermagnesemia
Remember: CRRT is indicated when standard medical management fails AND the patient is hemodynamically unstable or cannot tolerate IHD.
Relative Contraindications & Cautions
  • Inability to secure vascular access: coagulopathy, anatomic issues, or vascular injury
  • Active uncontrolled bleeding: especially if systemic anticoagulation required
  • Hemodynamic collapse: may need to stabilize first (though CRRT can help achieve this)
  • Goals of care inconsistent with aggressive support: discuss with family and care team
  • Severe liver failure (for citrate anticoagulation): citrate metabolism impaired, risk of toxicity
Caution: CRRT is resource-intensive, requires specialized nursing, and commits the patient to continuous therapy. Always consider whether benefits outweigh risks and burdens.
References
  1. London Health Sciences Centre. (2024). Principles of CRRT. Critical Care Trauma Centre, LHSC.
  2. Yartsev, A. (2013–2025). Continuous renal replacement therapy (CRRT) and renal intensive care chapters. Deranged Physiology. derangedphysiology.com
  3. Yartsev, A. (2013–2025). Definitions of CRRT terminology. Deranged Physiology.
  4. Yartsev, A. (2015). Anatomy of the extracorporeal dialysis circuit. Deranged Physiology. Link
  5. Saunders, H., & Palevsky, P. M. (2024). Continuous renal replacement therapy. In StatPearls. StatPearls Publishing.
Additional Resources:
  • Prismaflex Operator's Manual (manufacturer documentation)
  • KDIGO Clinical Practice Guideline for Acute Kidney Injury
  • Local ICU CRRT protocols and nursing guidelines
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