Renal replacement therapy

Surgical approach (when RRT requires a procedure)

  • RRT itself is not an operation; procedures relate to establishing access (vascular access or peritoneal access)
  • Temporary haemodialysis/CRRT access (vascath)
    • Ultrasound-guided cannulation: usually right internal jugular (preferred), femoral, or left IJV; subclavian generally avoided (stenosis risk for future AV fistula)
    • Large-bore double-lumen catheter inserted using Seldinger technique; tip position: SVC/RA junction (IJV) or IVC (femoral)
    • Asepsis, tunnelling optional (longer-term), securement and dressing; confirm position and exclude complications (CXR for IJV/subclavian)
  • Long-term haemodialysis access
    • AV fistula creation (radiocephalic, brachiocephalic, brachiobasilic transposition) or AV graft if vessels unsuitable
    • Avoid venepuncture/arterial lines/BP cuffs on fistula arm; protect access perioperatively
  • Peritoneal dialysis (PD) access
    • Surgical or laparoscopic placement of Tenckhoff catheter into peritoneal cavity; tunnelled subcutaneously with exit site
    • Potential adjuncts: omentopexy, adhesiolysis; test fill/drain intra-op

Anaesthetic management (procedures related to RRT access)

  • Temporary dialysis catheter (ICU/ED/theatre)
    • Type of anaesthesia: local anaesthetic infiltration ± light sedation; GA rarely required (uncooperative, severe agitation, paediatrics, complex access)
    • Airway: usually none; if deep sedation/GA then ETT; SGA possible but aspiration risk often higher in uraemia/critical illness
    • Duration: typically 15–45 min
    • Pain: mild–moderate (skin + deep tissue dilation); ensure adequate LA and analgesia
    • Key anaesthetic issues: haemodynamic instability, coagulopathy/anticoagulation, positioning, oxygenation/ventilation, sepsis, raised urea/platelet dysfunction
  • AV fistula/graft formation
    • Type of anaesthesia: regional (brachial plexus block) or GA; regional may improve fistula blood flow via sympathectomy and avoid GA in comorbid patients
    • Airway: if GA, usually ETT; SGA may be acceptable for short superficial surgery if aspiration risk low
    • Duration: ~1–2.5 h
    • Pain: usually mild–moderate; regional provides excellent analgesia
    • Key issues: preserve veins (avoid cannulation on planned fistula side), fluid balance, potassium/acid-base, BP targets to maintain fistula perfusion, anticoagulants/antiplatelets
  • Peritoneal dialysis catheter insertion
    • Type of anaesthesia: GA commonly (laparoscopic); open insertion may be possible under regional/LA with sedation in selected patients
    • Airway: ETT usually for laparoscopy; consider aspiration risk (uraemia, diabetes gastroparesis)
    • Duration: ~0.5–1.5 h
    • Pain: moderate (abdominal wall + peritoneal irritation); multimodal analgesia
    • Key issues: pneumoperitoneum effects, fluid restriction, electrolyte derangements, infection risk, postoperative nausea/vomiting

Definitions and aims

  • RRT = extracorporeal or peritoneal therapies replacing kidney functions: solute clearance, volume control, acid–base and electrolyte homeostasis
  • Aims in ICU: treat life-threatening complications (hyperkalaemia, pulmonary oedema), manage AKI with fluid overload, control uraemia, allow nutrition/drug dosing, manage severe acidosis
  • Core mechanisms: diffusion (dialysis), convection (haemofiltration), ultrafiltration (fluid removal), adsorption (some membranes/filters)

Indications for initiating RRT (AKI/critical care)

  • Common FRCA framework: AEIOU
    • A — Acidosis: severe metabolic acidosis refractory to medical therapy (e.g., pH ≤ 7.1–7.2 depending on context)
    • E — Electrolytes: refractory hyperkalaemia (esp. with ECG changes) ± severe hypermagnesaemia
    • I — Intoxications: dialysable toxins (e.g., lithium, salicylate, methanol, ethylene glycol, valproate in selected cases)
    • O — Overload: pulmonary oedema/volume overload refractory to diuretics; inability to achieve fluid balance
    • U — Uraemia: encephalopathy, pericarditis, bleeding, severe symptoms
  • Other ICU triggers: persistent oliguria/anuria with rising urea/creatinine, severe dysnatraemias in selected contexts, temperature control (rare), cytokine removal is not an established indication

Modalities of RRT

  • Intermittent haemodialysis (IHD)
    • Mechanism: mainly diffusion; high solute clearance over 3–5 h sessions
    • Pros: rapid K+ and toxin clearance; widely available; short treatment time
    • Cons: haemodynamic instability (rapid fluid/solute shifts), risk of dialysis disequilibrium, less suitable for raised ICP/unstable patients
  • Continuous RRT (CRRT): CVVH, CVVHD, CVVHDF
    • CVVH (haemofiltration): convection (solute drag) with replacement fluid
    • CVVHD (haemodialysis): diffusion with dialysate
    • CVVHDF: combined diffusion + convection
    • Pros: better haemodynamic tolerance, gradual fluid removal, better control of acid–base/electrolytes, preferred in cerebral oedema/raised ICP
    • Cons: anticoagulation issues, circuit clotting, hypothermia, electrolyte depletion (phosphate), nursing/technical burden
  • Sustained low-efficiency dialysis (SLED/SLEDD-f)
    • Hybrid: prolonged intermittent (6–12 h) with lower flow rates; improved haemodynamic tolerance vs IHD
    • Useful where CRRT resources limited; can be scheduled overnight
  • Peritoneal dialysis (PD)
    • Mechanism: diffusion across peritoneal membrane; ultrafiltration via osmotic gradient (glucose-based dialysate)
    • Pros: no extracorporeal circuit/anticoagulation; useful in children, difficult vascular access; gentler haemodynamics
    • Cons: peritonitis, lower clearance in hypercatabolic ICU patients, impaired ventilation with large volumes, contraindicated in recent major abdominal surgery/adhesions (relative)

Principles: diffusion, convection, ultrafiltration

  • Diffusion: solute movement down concentration gradient across semipermeable membrane; best for small molecules (urea, K+)
  • Convection: solvent drag with ultrafiltration; better for middle molecules; requires replacement fluid (pre- or post-filter)
    • Pre-dilution replacement: reduces haemoconcentration and clotting but lowers solute clearance
    • Post-dilution: higher clearance but higher filter clot risk
  • Ultrafiltration: fluid removal driven by transmembrane pressure; can be isolated (SCUF) for fluid overload

Vascular access for extracorporeal RRT

  • Sites: right IJV (first choice), femoral, left IJV; avoid subclavian if possible (central venous stenosis jeopardises future AVF)
  • Catheter characteristics: large bore, short and wide improves flow; double lumen; strict asepsis; ultrasound guidance reduces complications
  • Complications: bleeding/haematoma, arterial puncture, pneumothorax/haemothorax, air embolus, arrhythmias (wire), infection, thrombosis, catheter dysfunction/recirculation

Anticoagulation strategies (CRRT/IHD)

  • Why: blood–foreign surface contact activates coagulation; need to prevent circuit clotting while minimising bleeding
  • No anticoagulation
    • Consider if high bleeding risk; accept shorter filter life; optimise access, blood flow, pre-dilution, saline flushes
  • Unfractionated heparin (UFH)
    • Systemic anticoagulation; monitor APTT/anti-Xa; risks: bleeding, HIT, variable response in critical illness
    • Protamine reverses; consider in procedures/bleeding
  • Regional citrate anticoagulation (RCA) (common in CRRT)
    • Mechanism: citrate chelates ionised calcium in circuit → inhibits coagulation; calcium is replaced systemically (separate infusion)
    • Monitoring: systemic ionised Ca2+, post-filter ionised Ca2+ (target low), total Ca2+/ionised Ca2+ ratio (citrate accumulation if rising, e.g. >2.5)
    • Complications: hypocalcaemia, metabolic alkalosis (citrate metabolised to bicarbonate), metabolic acidosis if citrate accumulates, hypernatraemia (some solutions), hypomagnesaemia
    • Risk factors for citrate accumulation: severe liver failure, shock with poor perfusion, hypothermia (impaired metabolism)
  • Other anticoagulants (less common): LMWH, prostacyclin, direct thrombin inhibitors (argatroban) if HIT

Prescription variables (what you can change)

  • Blood flow rate (Qb): affects clearance and filter life; too low increases clotting/recirculation
  • Dialysate flow (Qd) (diffusion) and replacement flow (Qr) (convection): determine solute clearance
  • Net ultrafiltration rate: determines fluid removal; set according to haemodynamics and overall fluid balance goals
  • Effluent rate (CRRT dose surrogate): commonly prescribed ~20–25 mL/kg/h (delivered dose lower due to downtime); higher doses not shown to improve mortality routinely
  • Dialysate composition: K+, Ca2+, bicarbonate/lactate buffer; adjust to patient needs (avoid rapid shifts)

Physiological effects and complications relevant to anaesthesia/ICU

  • Haemodynamic instability
    • Causes: excessive ultrafiltration, vasodilation, myocardial stunning (IHD), sepsis, impaired autonomic responses
    • Management: reduce UF, fluid bolus if appropriate, vasopressors, consider CRRT/SLED instead of IHD
  • Electrolyte and acid–base disturbances
    • Hypokalaemia, hypophosphataemia (common in CRRT), hypomagnesaemia; monitor and replace proactively
    • Citrate: hypocalcaemia and alkalosis; accumulation causes acidosis and rising total:ionised Ca ratio
  • Temperature
    • Extracorporeal circuits can cool patient; use fluid warmers, warming blankets; hypothermia worsens coagulopathy and citrate metabolism
  • Bleeding risk
    • Uraemic platelet dysfunction + anticoagulation; consider DDAVP, tranexamic acid (case-dependent), correct anaemia, avoid unnecessary anticoagulation
  • Dialysis disequilibrium syndrome (DDS) (mainly IHD)
    • Mechanism: rapid urea removal → osmotic gradient → cerebral oedema; symptoms: headache, nausea, confusion, seizures, coma
    • Risk: first dialysis, very high urea, children, pre-existing CNS disease; prevention: slower/shorter dialysis, lower clearance, mannitol/hypertonic saline in selected cases
  • Drug dosing and removal
    • Removal depends on: molecular weight, protein binding, volume of distribution, water solubility, membrane type, modality and dose (effluent rate), adsorption
    • Antibiotics often need supplemental dosing (e.g., beta-lactams, vancomycin) guided by levels where possible

Anaesthetic considerations in patients receiving RRT (perioperative)

  • Preoperative assessment
    • Timing since last dialysis: aim for optimisation of volume status and K+; beware intradialytic hypotension and residual anticoagulation (heparin used during IHD)
    • Check: K+, bicarbonate/pH, Ca2+/phosphate, Hb, platelet count/function, coagulation, volume status, ECG, access sites (AVF/vascath/PD)
    • Comorbidities: IHD patients often have CAD, LVH, pulmonary oedema, autonomic neuropathy (diabetes), difficult airway (uraemic changes), gastroparesis
  • Intraoperative management
    • Monitoring: consider arterial line for major surgery/unstable patients; avoid lines/BP cuff on fistula arm; protect dialysis catheters
    • Induction/maintenance: reduce doses for some agents due to altered protein binding and sensitivity; titrate to effect; consider haemodynamic lability
    • Neuromuscular blockade: avoid/limit agents dependent on renal excretion (e.g., pancuronium); prefer atracurium/cisatracurium; sugammadex use in ESRD is possible but complex—follow local guidance and consider prolonged complexation/excretion
    • Fluids: avoid overload; balanced crystalloids often acceptable; consider potassium content (Hartmann’s contains ~5 mmol/L K+ but usually safe in small volumes—context dependent); use goal-directed therapy
    • Vasopressors: often required; dialysis patients may be vasoplegic/autonomic neuropathy
  • Postoperative considerations
    • Analgesia: avoid NSAIDs (AKI/bleeding); use opioids carefully (active metabolites accumulate: morphine, codeine); consider fentanyl/alfentanil/remifentanil intra-op; oxycodone/hydromorphone require caution; regional techniques useful
    • Plan for dialysis/CRRT restart: coordinate anticoagulation, haemostasis, and fluid balance; monitor K+ and acid–base closely

RRT and sepsis/critical illness: practical ICU points

  • CRRT is often chosen in septic shock due to haemodynamic tolerance; however, it can clear antibiotics—dose adjust and use TDM where possible
  • Common ICU problem: recurrent filter clotting—check access function, blood flow, filtration fraction (aim lower), anticoagulation adequacy, haematocrit, and interruptions
  • Nutrition/electrolytes: CRRT removes amino acids, water-soluble vitamins, phosphate; anticipate supplementation
Explain the principles of renal replacement therapy and compare diffusion with convection.

A common viva theme is demonstrating you understand mechanisms and can link them to modalities and what they remove.

  • Diffusion: solutes move down a concentration gradient across a semipermeable membrane; best for small molecules (urea, K+). Determined by gradient, membrane characteristics, surface area, and dialysate flow.
  • Convection: solutes are dragged with solvent flow (ultrafiltration) across the membrane; better for middle molecules; requires replacement fluid (pre- or post-filter).
  • Ultrafiltration: net water removal driven by transmembrane pressure; can be used alone for fluid overload (SCUF).
  • Link to modalities: IHD mainly diffusion; CVVH convection; CVVHD diffusion; CVVHDF combined.
List indications for initiating RRT in acute kidney injury.

Examiners often want a structured answer (AEIOU) plus ICU-specific triggers.

  • AEIOU: Acidosis (refractory), Electrolytes (refractory hyperkalaemia ± ECG changes), Intoxications (dialysable), Overload (pulmonary oedema/diuretic-resistant), Uraemia (encephalopathy, pericarditis, bleeding).
  • Pragmatic ICU triggers: inability to maintain fluid balance, progressive azotaemia with oliguria/anuria, severe metabolic derangements despite medical therapy.
Compare intermittent haemodialysis (IHD) with continuous renal replacement therapy (CRRT) in the critically ill.

This is a frequent written/viva comparison question.

  • IHD: 3–5 h, high solute clearance, rapid K+/toxin removal; more hypotension and rapid osmotic shifts; risk of dialysis disequilibrium; less suitable for unstable patients/raised ICP.
  • CRRT: 24 h (or prolonged), slower continuous clearance, better haemodynamic tolerance and fluid control; requires anticoagulation, more nursing/technical load; electrolyte depletion (phosphate), hypothermia.
  • SLED: hybrid (6–12 h), compromise between clearance and stability; useful when CRRT not available.
Describe regional citrate anticoagulation for CRRT: how it works, monitoring, and complications.

Common FRCA viva: mechanism + what can go wrong + how you detect it.

  • Mechanism: citrate infused pre-filter chelates ionised Ca2+ in circuit → anticoagulation; calcium is replaced systemically via separate infusion.
  • Monitoring: systemic ionised Ca2+ (avoid hypocalcaemia), post-filter ionised Ca2+ (ensure anticoagulation), total Ca2+:ionised Ca2+ ratio (rising suggests citrate accumulation).
  • Complications: hypocalcaemia, hypomagnesaemia; metabolic alkalosis (citrate → bicarbonate); citrate accumulation → metabolic acidosis + rising Ca ratio; possible hypernatraemia depending on solutions.
  • Risk factors for accumulation: severe liver failure, shock/poor perfusion, hypothermia.
A patient on CRRT develops a falling ionised calcium and rising total calcium. What is happening and what will you do?

This assesses recognition of citrate accumulation and safe response.

  • Interpretation: rising total Ca with falling ionised Ca suggests citrate accumulation (more Ca bound to citrate); check total:ionised Ca ratio (often >2.5).
  • Immediate actions: increase systemic calcium replacement to correct ionised Ca; reassess citrate rate and blood flow; consider reducing/pausing citrate and switching to alternative anticoagulation or no anticoagulation if bleeding risk.
  • Assess contributing factors: liver function, shock state, hypothermia; correct hypoperfusion and rewarm.
  • Check acid–base: citrate accumulation often causes metabolic acidosis (despite citrate usually generating bicarbonate when metabolised).
Explain dialysis disequilibrium syndrome: who is at risk, presentation, and prevention.

Classic exam topic linked to IHD initiation.

  • Mechanism: rapid reduction in plasma urea → osmotic gradient → water shifts into brain → cerebral oedema.
  • Risk: first dialysis, very high urea, children, pre-existing neurological disease, severe hyperosmolar states.
  • Presentation: headache, nausea/vomiting, agitation/confusion, seizures, reduced consciousness/coma.
  • Prevention: slower/shorter initial dialysis, lower clearance, consider CRRT/SLED, consider osmotherapy (mannitol/hypertonic saline) in selected cases.
How does RRT affect drug dosing? Give key determinants and examples relevant to anaesthesia/ICU.

Often asked in ICU pharmacology stations; focus on determinants rather than memorising every drug.

  • Determinants of removal: low molecular weight, low protein binding, low volume of distribution, water solubility, high dialysis/effluent dose, membrane characteristics and adsorption.
  • CRRT tends to remove drugs continuously; dosing often higher than in anuric non-dialysed patients; use therapeutic drug monitoring where possible (e.g., vancomycin, aminoglycosides).
  • Anaesthetic relevance: morphine metabolites accumulate in renal failure (not necessarily removed effectively acutely); remifentanil metabolism is non-specific esterases (independent of renal function); atracurium/cisatracurium organ-independent elimination.
A septic patient on CRRT has repeated filter clotting. What are the causes and how would you troubleshoot?

Practical ICU viva: show a systematic approach.

  • Access problems: malposition, kinking, thrombosis, poor blood flow, recirculation; check lines, aspirate/flush, ultrasound/CXR as appropriate.
  • Prescription factors: low blood flow, high filtration fraction (haemoconcentration), post-dilution only; consider increasing Qb, using pre-dilution, reducing net UF, changing modality.
  • Anticoagulation: inadequate UFH dosing/monitoring; citrate targets not achieved (post-filter iCa too high); consider switching strategy (RCA ↔ UFH) or adding anticoagulation if safe.
  • Patient factors: high haematocrit, hypercoagulability, sepsis inflammation, hypothermia; address temperature and underlying issues.
You are anaesthetising a patient with ESRD for emergency laparotomy. What are your key perioperative issues related to RRT and renal failure?

A common FRCA-style scenario integrating physiology, access, electrolytes, and drug choices.

  • Pre-op: assess volume status (may be overloaded), check K+/acid–base, Hb/coagulation (uraemic platelet dysfunction), timing of last dialysis and heparin exposure, ECG for hyperkalaemia changes.
  • Access: protect AV fistula arm; avoid BP cuff/venepuncture there; note presence of vascath/PD catheter and secure.
  • Induction/maintenance: titrate doses; anticipate haemodynamic instability; consider aspiration risk; use atracurium/cisatracurium; avoid long-acting renally excreted drugs where possible.
  • Fluids: avoid overload; use vasopressors early if needed; manage potassium-containing fluids in context; blood products as required.
  • Post-op: plan ICU and timing for dialysis/CRRT, manage analgesia (avoid NSAIDs; careful opioid selection), monitor K+/acid–base and bleeding.
Describe vascular access options for RRT and their complications. Which site is preferred and why?

Frequently examined as part of ICU lines and complications.

  • Preferred: right IJV (straight course to SVC/RA, lower pneumothorax risk than subclavian, easier ultrasound guidance).
  • Alternatives: femoral (easy in emergencies, higher infection/thrombosis risk, limits mobilisation), left IJV (more tortuous), subclavian generally avoided (central venous stenosis threatens future AVF).
  • Complications: arterial puncture, bleeding/haematoma, pneumothorax/haemothorax, air embolus, arrhythmias, infection, thrombosis, catheter dysfunction/recirculation.

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