ICU · Renal and metabolic
RRT modality selection: IHD vs CRRT vs SLED — when and why
Also known as RRT modality · Intermittent haemodialysis · Continuous renal replacement therapy · SLED · Sustained low-efficiency dialysis · Haemodialysis ICU
When AKI requires RRT, three modalities are available: (1) INTERMITTENT HAEMODIALYSIS (IHD) — standard, 3-4h sessions, high efficiency, rapid solute removal. (2) CONTINUOUS RENAL REPLACEMENT THERAPY (CRRT — CVVH, CVVHD, CVVHDF) — 24h/day, slow, gentle, haemodynamically stable, better for shocked/cerebral oedema patients. (3) SUSTAINED LOW-EFFICIENCY DIALYSIS (SLED) — hybrid, 6-12h sessions, intermediate efficiency, haemodynamic stability between IHD and CRRT. CHOICE based on: HAEMODYNAMICS (CRRT for shocked, IHD for stable), CEREBRAL OEDEMA (CRRT — slower fluid/urea shift - less brain swelling), ANTICOAGULATION (CRRT needs more — citrate or heparin), ACIDOSIS (CRRT for severe lactic acidosis — continuous correction), MOBILITY (IHD for ambulatory/rehab). EVIDENCE: NO mortality difference between IHD and CRRT (multiple RCTs — HEMO, SHARF, Vinsonneau). COST: CRRT more expensive. DOSE: CRRT 20-25 mL/kg/hr; IHD Kt/V 1.2-1.5. TIMING: AKIKI, STARRT-AKI — EARLY vs LATE RRT — no mortality difference (don't rush to RRT — wait for clinical indications).
On this page & tools
Your progress
Saved locally on this device.
Target exams
Red flags
IHD vs CRRT vs SLED compared
| Feature | IHD | CRRT (CVVH/CVVHD) | SLED |
|---|---|---|---|
| Duration | 3-4h sessions (alternate days) | 24h/day continuous | 6-12h sessions (daily or alternate) |
| Efficiency | HIGH (rapid solute removal) | LOW (slow, gentle) | INTERMEDIATE |
| Haemodynamic stability | Variable (fluid + solute shifts) | EXCELLENT (slow) | GOOD (slower than IHD) |
| Cerebral oedema | Worse (dialysis disequilibrium — rapid urea shift -> brain swelling) | BETTER (slow urea removal) | Good |
| Acidosis correction | Rapid (session) but rebound | CONTINUOUS (stable) | Intermediate |
| Fluid removal | Rapid (may cause hypotension) | Gentle (continuous) | Gentle |
| Anticoagulation | Minimal (heparin during session, off between) | MORE (citrate or heparin — continuous) | Some (during session) |
| Drug dosing | Standard (dialysis days) | Adjusted (CRRT clears differently) | Adjusted |
| Mobility | Better (between sessions) | Worse (connected 24/7) | Intermediate |
| Cost | LOWER | HIGHER (fluids, filters, staff) | Intermediate |
| Best for | Stable, ambulatory | Shocked, cerebral oedema, severe acidosis | Moderate instability, cost-conscious |
RRT modality selection in ICU
- DETERMINE IF RRT IS INDICATED (TIMING) — (a) LIFE-THREATENING INDICATIONS (start IMMEDIATELY — 'AEIOU'): (i) Acidosis (severe metabolic, pH <7.1 not responding). (ii) Electrolytes (hyperkalaemia refractory, severe hypercalcaemia). (iii) Ingestion/toxin (dialysable — lithium, salicylate, toxic alcohols, metformin). (iv) Overload (pulmonary oedema refractory to diuretics). (v) Uraemia (pericarditis, encephalopathy, bleeding). (b) NON-LIFE-THREATENING: AKIKI + STARRT-AKI trials — NO mortality benefit of EARLY RRT (starting before clinical indications) -> WAIT for clinical indications (don't rush to RRT for 'rising creatinine' alone — may recover without). (c) DISCUSS with nephrology + ICU team
- ASSESS PATIENT FACTORS FOR MODALITY — (a) HAEMODYNAMICS: stable -> IHD acceptable; shocked/unstable (vasopressors) -> CRRT or SLED. (b) BRAIN: cerebral oedema (TBI, ALF, SAH) -> CRRT (avoid dialysis disequilibrium — rapid urea shift -> brain swelling). (c) ACIDOSIS: severe lactic acidosis -> CRRT (continuous correction; IHD may overshoot alkalinisation then rebound). (d) FLUID: need large fluid removal (e.g., 3-5L/day in septic shock) -> CRRT (gentle continuous). (e) MOBILITY: rehabilitating, need to be up -> IHD (between sessions). (f) ANTICOAGULATION risk: bleeding (citrate CRRT — no systemic anticoag; heparin-free IHD). (g) COST/availability: IHD cheaper + widely available; CRRT needs special machine + staff
- CHOOSE MODALITY — (a) CRRT: shocked/unstable, cerebral oedema, severe acidosis, large fluid removal. DOSE: 20-25 mL/kg/hr effluent rate (KDIGO). ANTICOAGULATION: citrate (preferred — regional, no systemic; monitor Ca2+, especially liver failure -> accumulation) or heparin (systemic — bleeding risk). CIRCUIT life: 24-72h (citrate longer). (b) IHD: stable haemodynamics, ambulatory. DOSE: Kt/V 1.2-1.5 per session, 3-4 sessions/week. ANTICOAGULATION: heparin (during session) or heparin-free (saline flush) if bleeding risk. (c) SLED: moderate instability, cost-conscious, between shifts. 6-12h sessions (daily or alternate). Good haemodynamic stability + reasonable efficiency
- MONITOR + ADJUST — (a) SOLUTE: urea, creatinine (trend — is RRT effective?), K+ (target normal), bicarbonate (acidosis corrected?), phosphate (hypophosphataemia common with RRT — replace). (b) FLUID: net ultrafiltration (target — offload fluid slowly), input/output, weight (if possible), haemodynamics (hypotension from over-rapid fluid removal). (c) CIRCUIT: filter life (clotting?), pressures (transmembrane pressure — rising = filter clotting), anticoagulation (citrate ratio, heparin APTT). (d) COMPLICATIONS: hypotension (IHD — rapid fluid removal), hypothermia (CRRT — fluid cool), electrolyte derangement (K+, phosphate, Mg2+, Ca2+), bleeding (anticoagulation), infection (catheter), citrate accumulation (liver failure -> acidosis + low Ca2+)
- DRUG DOSING ADJUSTMENT — (a) CRRT: clears drugs DIFFERENTLY (continuous, depends on effluent rate + filter). Dose drugs based on CRRT clearance (e.g., beta-lactams — higher dose or continuous infusion; vancomycin — dose by CRRT clearance; anticoagulants — adjust). Consult pharmacist + drug dosing in CRRT references. (b) IHD: intermittent clearance — dose on dialysis days (supplement after session for dialysed drugs). (c) SLED: intermediate — adjust per centre protocol. (d) THERAPEUTIC DRUG MONITORING: vancomycin (trough or AUC), aminoglycosides (if used), beta-lactams (some centres — emerging)
- WEAN + TRANSITION — (a) RECOVERY SIGNS: rising urine output (polyuria phase of AKI recovery), falling creatinine (between sessions — kidney clearing), stable fluid/electrolytes. (b) WEAN: increase time between IHD sessions (alternate days -> 2x/week); reduce CRRT effluent rate; consider stopping if urine output >500 mL/day + creatinine stable. (c) TRANSITION: CRRT -> IHD (if stabilising); IHD -> stop (if recovering). (d) LONG-TERM: if AKI -> CKD (10-30% of severe AKI) -> chronic dialysis. (e) RENAL REHAB: nutrition, avoid nephrotoxins, monitor renal function. (f) FOLLOW-UP: nephrology (renal recovery vs progression)
Clinical pearls
Red flags
Prognosis
RRT modality and timing evidence
IHD vs CRRT (Vinsonneau Hemodiafe 2006, multiple RCTs): NO mortality difference — choose by patient factors (haemodynamics, brain, acidosis, cost). AKIKI (2016, NEJM): early vs late RRT -> no mortality difference; early had more RRT (some recover without). STARRT-AKI (2020, NEJM): early vs delayed -> no mortality difference; early had more adverse events (infection, bleeding). IDEAL-ICU (2018): early vs late in septic AKI -> no difference. ATN (2009, NEJM): intensive (35 mL/kg/hr) vs less (20) -> no difference -> 20-25 mL/kg/hr sufficient. Citrate vs heparin (Bagshaw 2018): citrate less bleeding, longer filter life — preferred (unless liver failure). SLED vs CRRT: equivalent outcomes (Schneider 2019) — hybrid option. AKI -> CKD: 10-30% of severe AKI (especially elderly, diabetes, pre-existing CKD) -> chronic dialysis.
Anticoagulation strategy
CRRT anticoagulation strategies compared
| Feature | Regional citrate (preferred) | Unfractionated heparin (UFH) | No anticoagulation / saline flush |
|---|---|---|---|
| Mechanism | Chelates Ca²⁺ in circuit (clotting cofactor) -> regional anticoag | Activates antithrombin -> inhibits IIa + Xa (SYSTEMIC) | Frequent saline flushes dilute + wash circuit (no pharmacologic anticoag) |
| Bleeding risk | NONE (no systemic anticoagulation) | HIGH (systemic — APTT 1.5-2x normal) | NONE |
| Filter life | LONGEST (median 40-72h) | Moderate (median 24-48h) | SHORTEST (median 12-18h -> frequent clotting) |
| Monitoring | Post-filter iCa²⁺ (target <0.4 mmol/L); systemic iCa²⁺ (normal); total/iCa²⁺ ratio (<2.5) | APTT (60-90s) or anti-Xa (0.25-0.35 IU/mL) | None specific (clinical — circuit pressures) |
| Best for | Default in MOST centres; bleeding risk; post-op | Citrate contraindicated (severe liver failure); citrate unavailable | Active bleeding + contraindication to both citrate + heparin |
| Avoid in | Severe liver failure (accumulation); propofol-renal contraindication; severe lactic acidosis (relative) | Active bleeding, HIT, recent surgery, coagulopathy | None (fallback when others unsuitable) |
| Metabolic effect | Metabolic ALKALOSIS (citrate -> bicarbonate); risk of acidosis if accumulation | None direct (heparin neutral) | None |
| Electrolytes | Hypocalcaemia (if calcium replacement inadequate) | Heparin-induced hypokalaemia (rare) | None |
| Cost | Moderate (citrate + calcium solutions) | Low (cheap drug) | Low drug cost but HIGH circuit/filter cost (clotting) |
CRRT modality subtypes — CVVH vs CVVHD vs CVVHDF
| Feature | CVVH (haemofiltration) | CVVHD (haemodialysis) | CVVHDF (haemodiafiltration) |
|---|---|---|---|
| Solute removal | CONVECTION (solvent drag — solutes pulled with water across membrane) | DIFFUSION (concentration gradient — solutes move from blood to dialysate) | BOTH (convection + diffusion) |
| Middle molecules (β2-microglobulin, cytokines) | BETTER cleared (convective) | Poorly cleared (diffusive — small molecules only) | Good clearance |
| Small molecules (urea, creatinine, K⁺) | Good | EXCELLENT (diffusive — efficient for small) | Excellent |
| Effluent = dose | Ultrafiltrate (replacement fluid added) | Dialysate outflow | Both (dialysate + ultrafiltrate) |
| Replacement fluid | YES (pre- or post-dilution) | No (dialysate only) | Yes (may have replacement) |
| Filter requirements | High-flux (high water permeability) | Low-flux sufficient | High-flux |
| Common practice | Most common CRRT mode (with CVVHDF) | Less common alone | Common (combined clearance) |
| Anticoagulation need | Higher (more filtration -> concentration -> clotting) | Lower | Intermediate |
CRRT circuit management — preventing filter clotting
- PRESCRIBE THE CIRCUIT — (a) MODALITY: CVVH, CVVHD or CVVHDF (per centre + solute target). (b) DOSE: 20-25 mL/kg/hr EFFLUENT (delivered — prescribe 25-30 to account for downtime). (c) BLOOD FLOW: 150-200 mL/min (higher = better filter patency — less stasis). (d) ANTICOAGULATION: citrate (preferred) -> set citrate rate to blood flow ratio (e.g., citrate 30-40 mL/h per L/min blood flow); calcium infusion separate. (e) FLUID REMOVAL: net ultrafiltration target (e.g., -100 mL/h — slow continuous offload)
- MONITOR CIRCUIT PRESSURES — (a) ACCESS PRESSURE (pre-pump negative): pulling blood from patient -> very negative = poor access flow (kink, positional, catheter against wall). (b) RETURN PRESSURE (post-filter positive): returning blood -> rising = filter resistance (clotting) or venous obstruction. (c) TRANSMEMBRANE PRESSURE (TMP): pressure across membrane -> RISING TMP = filter clotting (early sign — track trend; >250-300 mmHg suggests imminent failure). (d) FILTER PRESSURE DROP (ΔP across filter): rising = clotting in filter fibres. (e) EFFLUENT PRESSURE: should be stable; rising = blockage
- MONITOR ANTICOAGULATION — (a) CITRATE: post-filter iCa²⁺ q4-6h (target <0.4 mmol/L — circuit anticoag); systemic iCa²⁺ q6h (normal 1.0-1.3); total Ca/iCa ratio q6-12h (<2.5 — if >2.5 = citrate accumulation -> reduce citrate). (b) HEPARIN: APTT q6h (target 60-90s) or anti-Xa; titrate infusion. (c) NO-ANTICOAG: no pharmacologic monitor — watch circuit pressures closely (clot expected)
- RECOGNISE FILTER CLOTTING (EARLY SIGNS) — (a) RISING TMP + filter pressure drop (clot forming in fibres). (b) DECREASING effluent rate (machine compensating). (c) DARKER filter (visible clot in fibres — striped). (d) MACHINE ALARMS (high return pressure, low effluent, low blood flow). (e) HAEMOLYSIS (rare — kinked line -> high shear -> red cells lyse -> dark plasma, high K⁺, high LDH, falling haemoglobin). (f) ACTION: if clotting imminent + patient not bleeding -> consider heparin bolus or circuit change
- CHANGE THE CIRCUIT (ELECTIVE) — (a) WHEN: routine change q48-72h (citrate) or q24h (no-anticoag); OR if clotting/alarms. (b) ASEPTIC: full sterile technique (catheter hub -> bloodstream infection risk). (c) BLOOD RETURN: clamp + return patient's blood (avoid blood loss — ~150 mL in circuit) unless clotted (then discard). (d) DOCUMENT: circuit life (track — short life = anticoag problem), blood loss, reason for change
- TROUBLESHOOT FREQUENT CLOTTING — (a) OPTIMISE anticoag (citrate dose, heparin APTT). (b) INCREASE blood flow (150-200 mL/min). (c) PRE-DILUTION (replacement fluid before filter -> dilutes blood -> less clotting — but reduces efficiency). (d) CHECK access (kink, positional, catheter tip against wall). (e) EXCLUDE HIT (falling platelets on heparin -> switch to citrate or alternative anticoag). (f) PATIENT FACTORS: sepsis (hypercoagulable — needs more anticoag), high haematocrit (viscous -> clot)
Membrane considerations
Dialyser membrane characteristics
| Feature | High-flux biocompatible (PREFERRED) | Low-flux/unmodified cellulose (avoid) | High cut-off (HCO) |
|---|---|---|---|
| Material | Synthetic (polysulfone, polyethersulfone, polyamide, AN69) | Cuprophane, cellulose acetate | Modified polysulfone (larger pores) |
| Biocompatibility | HIGH (low complement/leucocyte activation) | LOW (complement activation -> inflammation, leukopenia) | High |
| Water permeability | High (Kuf >20 mL/h/mmHg) | Low (Kuf <10) | Very high |
| Middle molecule clearance | Good (β2-microglobulin) | Poor | Excellent (clears cytokines, myoglobin, free haemoglobin) |
| Evidence | Improved survival vs cuprophane (meta-analyses) — biocompatible preferred | Worse outcomes (complement activation) | Investigational for sepsis, rhabdomyolysis, removal of protein-bound toxins |
| Use | STANDARD for CRRT + IHD in ICU | Obsolete in ICU | Selected cases (rhabdomyolysis, sepsis trials) |
| Albumin loss | Minimal | Minimal | SIGNIFICANT (large pores leak albumin -> need replacement) |
| Anticoagulation need | Lower (smoother surface) | Higher (rough — more clotting) | Higher |
Drug dosing on CRRT
Drug class dosing on CRRT — practical guide
| Drug class | CRRT clearance | Dosing approach | Notes |
|---|---|---|---|
| Beta-lactams (meropenem, pip-taz, cefepime) | HIGH (hydrophilic, small) | HIGHER dose + EXTENDED/CONTINUOUS infusion (e.g., meropenem 1g q8h EI; pip-taz 4.5g q6h or CI) | Target 100% fT>MIC — beta-lactam TDM emerging |
| Vancomycin | MODERATE (large, but cleared by convective CRRT) | Loading 25-30 mg/kg; maintenance 15-25 mg/kg q12-24h by TDM (trough 15-20, AUC 400-600) | Check pre-dose level q48-72h |
| Aminoglycosides (gentamicin) | HIGH | Extended-interval dosing usually INAPPROPRIATE on CRRT — dose by TDM (gentamicin 5-7 mg/kg q24-48h guided by level) | Avoid if possible (nephrotoxic in AKI) |
| Linezolid | MODERATE (50-70% CRRT clearance) | Standard 600 mg q12h (usually no adjustment) | Monitor for thrombocytopenia |
| Daptomycin | HIGH | 6-10 mg/kg q24-48h (some adjustment) | TDM if prolonged |
| Antifungals — fluconazole | HIGH (hydrophilic) | Higher dose (e.g., 400-800 mg q24h) | Voriconazole/posaconazole — lipophilic, minimal adjustment |
| Amphotericin B | LOW (large, protein-bound, liposomal) | Standard dosing | Nephrotoxic — use liposomal |
| Anticoagulants — heparin | NOT cleared (large) | Titrate by APTT | Standard approach |
| LMWH (enoxaparin) | Partial (anti-Xa) | AVOID therapeutic on CRRT (unpredictable) -> use UFH | Anti-Xa monitoring |
| DOACs (apixaban, rivaroxaban) | Variable | AVOID on CRRT (unpredictable) -> switch to heparin | Contraindicated in CRRT generally |
| Sedation — propofol, midazolam | LOW (lipophilic, protein-bound) | Standard dosing | Fentanyl — moderate clearance (titrate) |
| Vasopressors — noradrenaline, adrenaline | LOW (large, catecholamines) | Standard dosing | Not significantly cleared |
| Antiepileptics — valproate, levetiracetam | Levetiracetam HIGH; valproate LOW (protein-bound) | Levetiracetam — adjust (e.g., 500-1000 mg q12-24h); valproate — minimal | Levels guide dosing |
| Digoxin | LOW (large, protein-bound) | Minimal adjustment — but AKI reduces renal clearance too | Fab fragment for toxicity not removed by CRRT |
Complications of RRT — comprehensive
Extended evidence
RRT dose + anticoagulation trials in detail
RENAL trial (Bellomo 2009, NEJM): 1508 patients, CRRT 25 vs 40 mL/kg/hr effluent -> NO mortality difference (44.7% vs 44.7%) -> established 20-25 mL/kg/hr as standard. [7] } ATN trial (Palevsky 2008, NEJM): 1124 patients, intensive (35 mL/kg/hr CVVHDF or 6x/week IHD) vs less intensive (20 mL/kg/hr or 3x/week) -> NO mortality difference (53.6% vs 51.5%) -> higher dose does NOT improve survival. [8] } RICH trial (Zarbock 2020, JAMA): 595 patients, citrate vs systemic heparin CRRT -> NO mortality difference (57% vs 56%) but citrate -> LONGER filter life (median 69h vs 40h), FEWER bleeding events. [6] } Zhang 2012 meta-analysis (ICM): citrate vs heparin CRRT -> citrate REDUCES bleeding + prolongs filter life -> citrate preferred anticoagulant. [9] } Zhang 2019 meta-analysis (Critical Care): citrate CRRT SAFE in moderate liver failure (Child-Pugh A/B) with monitoring; AVOID in severe (Child-Pugh C) -> accumulation. [10] } Li 2022 meta-analysis (Therapeutic Apheresis and Dialysis): RCTs of citrate vs heparin -> confirms citrate superiority (filter life, bleeding) -> citrate first-line. [12] } AKIKI (Gaudry 2016, NEJM): 619 patients, early vs late RRT in stage 2/3 AKI -> NO mortality difference (48.5% vs 49.7%); 49% of late group NEVER needed RRT. [2] } STARRT-AKI (2020, NEJM): 3019 patients, early vs delayed RRT -> NO mortality difference (43.9% vs 43.7%); EARLY group MORE adverse events (RRT dependence 10.4% vs 6.0%, more infections/bleeding). [3] } IDEAL-ICU (Barbar 2018, NEJM): 477 septic shock AKI patients, early vs late RRT -> NO mortality difference (58% vs 54%); stopped early for futility. [4] } Hemodiafe (Vinsonneau 2006, Lancet): 359 patients, CRRT vs IHD -> NO mortality difference -> modality by patient factors. [1] } KDIGO Conference (Ostermann 2020, Kidney Int): expert consensus — 20-25 mL/kg/hr CRRT; citrate preferred; wait for clinical indications (AEIOU) before RRT. [5] }
Indication-specific modality selection — quick reference
| Clinical scenario | Preferred modality | Rationale |
|---|---|---|
| Septic shock + vasopressors, oliguric AKI | CRRT | Haemodynamic instability — IHD causes hypotension |
| Severe lactic acidosis (pH <7.1) | CRRT | Continuous correction (IHD -> rebound + overshoot) |
| Acute liver failure + cerebral oedema + AKI | CRRT | Slow urea removal (avoid dialysis disequilibrium + raised ICP) |
| Severe TBI / SAH + AKI | CRRT | Avoid ICP rise from rapid urea/osmolality shift |
| Massive fluid overload (5+ L) | CRRT | Gentle continuous UF — IHD too rapid |
| Hyperkalaemia K⁺ >7 with ECG changes | IHD (urgent) then maintenance | IHD clears K⁺ FASTEST (rapid) — life-saving; transition to CRRT after |
| Salicylate / lithium / metformin / toxic alcohol poisoning | IHD (high-efficiency) or CRRT (high-dose) | IHD fastest for small molecules; CRRT for rebound (lithium/salicylate redistribute) |
| Stable post-op AKI, no vasopressors | IHD | Stable, allows rehab, lower cost |
| Moderate instability (1 low-dose vasopressor) | SLED | Hybrid — stability + reasonable efficiency |
| Resource-limited / no CRRT machine | SLED or IHD | Uses standard IHD machine |
| Paediatric AKI, vascular access difficult | Peritoneal dialysis (rare) | Gentler access; less commonly used in adults |
| End-stage renal disease (ESRD) patient + critical illness | Continue chronic IHD or CRRT (if unstable) | Maintain usual modality if possible; CRRT if shocked |
| Recovering AKI (rising UO, falling Cr) | Wean — extend interval or stop | Trial off RRT if UO >500 mL/day + stable solutes |
Approach to refractory filter clotting
- CONFIRM clotting (not machine issue) — (a) RISING transmembrane pressure (TMP) + filter pressure drop. (b) Visible clot in filter fibres (striped/dark). (c) Falling effluent rate. (d) Machine alarms (high return pressure, low blood flow). (e) Distinguish from access problem (very negative access pressure = catheter issue)
- OPTIMISE anticoagulation FIRST — (a) CITRATE: check post-filter iCa²⁺ (target <0.4 mmol/L) — if >0.4, INCREASE citrate rate. Check systemic iCa²⁺ + ratio (if ratio >2.5 + acidosis = accumulation — DO NOT increase citrate; switch). (b) HEPARIN: check APTT (target 60-90s) — if low, INCREASE infusion; consider bolus. (c) NO-ANTICOAG: expect short life — consider starting citrate/heparin if bleeding risk permits
- OPTIMISE blood flow + filtration — (a) INCREASE blood flow to 180-200 mL/min (less stasis). (b) ADD pre-dilution (replacement fluid before filter -> dilutes blood -> lowers filtration fraction -> less clotting). (c) KEEP filtration fraction <25% ((UF rate + replacement) / plasma flow). (d) CHECK access catheter (positional — reposition; kink — untwist; fibrin sheath — urokinase lock or replace)
- EXCLUDE PATIENT FACTORS — (a) HIGH haematocrit (Hct >0.40) -> viscous -> clot (pre-dilute, increase blood flow). (b) SEPSIS (hypercoagulable) -> needs MORE anticoag. (c) HEPARIN-INDUCED THROMBOCYTOPAENIA (HIT): falling platelets on heparin (4Ts score) -> STOP heparin, switch to citrate (or argatroban/bivalirudin). (d) ANTITHROMBIN DEFICIENCY (rare — AT level low) -> heparin ineffective -> citrate or AT concentrate. (e) HYPERCOAGULABLE state (active clot, malignancy) -> more anticoag
- CONSIDER ALTERNATIVE ANTICOAGULATION (if citrate + heparin both unsuitable) — (a) REGIONAL HEPARIN-PROTAMINE (heparin pre-filter, protamine post — neutralises systemic) — rarely used (complex). (b) PROSTACYCLIN (PGI2) — vasodilation (may worsen hypotension) + antiplatelet. (c) ARGATROBAN / BIVALIRUDIN (direct thrombin inhibitors) — for HIT. (d) DANAPAROID (anti-Xa) — HIT alternative. (e) NO-ANTICOAG with pre-dilution + high blood flow (short life but feasible)
- DOCUMENT + AUDIT — (a) Track filter life per patient (median should be >24h citrate, >12h no-anticoag). (b) Auditable reasons for short life (anticoag adequacy, access issues, downtime). (c) COST: frequent clotting = $200-500/filter + blood loss + nursing time + treatment interruption. (d) GOAL: minimise downtime — delivered dose 80% of prescribed
Sustained Low-Efficiency Dialysis (SLED) — when to choose the hybrid
| Feature | SLED details |
|---|---|
| Definition | Hybrid modality — IHD machine with LOW blood flow (150-200 mL/min) + LOW dialysate flow (100-200 mL/min) + LONGER duration (6-12h, daily or alternate) |
| Efficiency | Intermediate — clears more per session than CRRT (in 6-12h) but slower than IHD (in 3-4h) |
| Haemodynamic stability | GOOD (better than IHD — slower fluid/solute shift; close to CRRT) |
| Indications | Moderate haemodynamic instability (1 low-dose vasopressor); resource-limited (no CRRT machine); bridge IHD-CRRT; cost-conscious unit |
| Advantages | Uses STANDARD IHD machine (no special CRRT); allows breaks (not 24/7); lower cost than CRRT; reasonable stability + efficiency |
| Disadvantages | Less stable than CRRT (faster removal in 6-12h vs 24h); anticoag during session only (not continuous); less commonly available; fewer protocols/evidence than CRRT/IHD |
| Anticoagulation | UFH (during session) or citrate (if available); heparin-free with saline flush (bleeding risk) |
| Drug dosing | Intermediate between IHD and CRRT — per protocol + TDM |
| Solute clearance | Small molecules (urea, K⁺) good; middle molecules moderate |
| Evidence | Equivalent outcomes to CRRT in observational studies + small RCTs (Caires 2016; others) — hybrid option with reasonable outcomes [11] } |
| Prescription | Blood flow 150-200 mL/min; dialysate flow 100-200 mL/min; duration 6-12h; anticoag as above; UF target per fluid needs |
Prognosis and long-term
AKI recovery + long-term outcomes
Mortality: ICU AKI requiring RRT — 50-60% in-hospital mortality (sepsis + multi-organ failure); survivors recover renal function in ~50-60%. Dialysis dependence at discharge: 10-25% of severe AKI survivors (higher with elderly, diabetes, pre-existing CKD, sepsis, prolonged RRT). CKD progression: 10-30% of severe AKI -> CKD (stages 3-5) within 1-5 years — even if 'recovered' renal function initially. Long-term mortality: AKI survivors have INCREASED mortality years later (cardiovascular + renal causes) — AKI is a chronic disease risk factor. Renal recovery trajectory: most recovery in first 90 days; plateau by 6-12 months; some continued slow recovery up to 2 years. Predictors of non-recovery: older age, diabetes, pre-existing CKD (eGFR <60), higher AKI stage (KDIGO 3), longer RRT duration (>14 days), sepsis-associated, contrast nephropathy, recurrent AKI episodes. Follow-up: nephrology clinic at 3 months — eGFR, proteinuria, BP, glycaemic control, avoid nephrotoxins (NSAIDs, contrast, aminoglycosides), medication review. Patient education: AKI -> CKD risk — lifestyle (BP, diabetes, hydration), medication avoidance, regular monitoring.
Exam practice — SAQs
SAQ — Septic shock with vasopressor-dependent AKI: CRRT versus IHD
10 minutes · 10 marks
A 64-year-old man (80 kg) is admitted to ICU with septic shock from a necrotising fasciitis of the left leg. Despite 30 mL/kg crystalloid and broad-spectrum antibiotics, he requires noradrenaline 0.4 mcg/kg/min and vasopressin 0.03 U/min to maintain MAP 66. Lactate 5.8 mmol/L, pH 7.18 (HCO3 14), K+ 6.3 mmol/L (refractory to insulin-dextrose and salbutamol), creatinine 340 micromol/L (baseline 90), urine output 10 mL/h. He is oligoanuric and 5 L positively balanced. The team agrees RRT is indicated and is debating intermittent haemodialysis (IHD) versus continuous renal replacement therapy (CRRT).
SAQ — Acute liver failure with cerebral oedema and AKI: why CRRT, citrate monitoring, and weaning
10 minutes · 10 marks
A 52-year-old woman (60 kg) is admitted with acetaminophen-induced acute liver failure (ALF), Grade III hepatic encephalopathy, and AKI (creatinine 290 micromol/L). CT brain shows early cerebral oedema; the intracranial pressure monitor reads 22 mmHg. She is intubated and on noradrenaline 0.1 mcg/kg/min (MAP 68), with K+ 5.8 mmol/L, pH 7.24 and lactate 4.2 mmol/L. The nephrology registrar suggests starting intermittent haemodialysis tomorrow morning.
References
- [1]Vinsonneau C, et al. Continuous venovenous haemodiafiltration versus intermittent haemodialysis for acute renal failure in patients with multiple-organ dysfunction syndrome (Hemodiafe). Lancet, 2006.PMID 16876666
- [2]Gaudry S, et al. Initiation Strategies for Renal-Replacement Therapy in the Intensive Care Unit (AKIKI). New England journal of medicine, 2016.PMID 27181456
- [3]STARRT-AKI Investigators, et al. Timing of Initiation of Renal-Replacement Therapy in Acute Kidney Injury (STARRT-AKI). New England journal of medicine, 2020.PMID 32668114
- [4]Barbar SD, et al. Timing of Renal-Replacement Therapy in Patients with Acute Kidney Injury and Sepsis (IDEAL-ICU). New England journal of medicine, 2018.PMID 30304656
- [5]Ostermann M, et al. Controversies in acute kidney injury: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Conference. Kidney international, 2020.PMID 32709292
- [6]Zarbock A, et al. Effect of Regional Citrate Anticoagulation vs Systemic Heparin Anticoagulation During Continuous Kidney Replacement Therapy on Dialysis Filter Life Span and Mortality (RICH). JAMA, 2020.PMID 33095849
- [7]RENAL Replacement Therapy Study Investigators, et al. Intensity of continuous renal-replacement therapy in critically ill patients (RENAL). New England journal of medicine, 2009.PMID 19846848
- [8]VA/NIH Acute Renal Failure Trial Network, et al. Intensity of renal support in critically ill patients with acute kidney injury (ATN). New England journal of medicine, 2008.PMID 18492867
- [9]Zhang Z, et al. Efficacy and safety of regional citrate anticoagulation in critically ill patients undergoing continuous renal replacement therapy. Intensive care medicine, 2012.PMID 22124775
- [10]Zhang W, et al. Safety and efficacy of regional citrate anticoagulation for continuous renal replacement therapy in liver failure patients: a systematic review and meta-analysis. Critical care, 2019.PMID 30678706
- [11]Caires RA, et al. Sustained low-efficiency extended dialysis (SLED) with single-pass batch system in critically-ill patients with acute kidney injury. Journal of nephrology, 2016.PMID 26298845
- [12]Li R, et al. Regional citrate versus heparin anticoagulation for continuous renal replacement therapy in critically ill patients: A meta-analysis of randomized controlled trials. Therapeutic apheresis and dialysis, 2022.PMID 35385216
- [13]Karkar A, et al. Prescription of CRRT: a pathway to optimize therapy. Annals of intensive care, 2020.PMID 32144519