Contrast-induced nephropathy

Surgical approach (procedural context)

• Not an operation; occurs after iodinated contrast exposure during procedures (often radiology/cardiology). Typical procedural pathways:
  • CT with IV contrast (ED/acute medicine; oncology staging; trauma imaging).
  • Coronary angiography ± PCI (radial/femoral access; heparin; stents; potential haemodynamic instability).
  • Endovascular procedures: EVAR/TEVAR, peripheral angioplasty, carotid stenting (often high contrast volumes).
  • Interventional radiology: embolisation, biliary/renal interventions, TIPS, complex CT-guided procedures.
• Key procedural determinants of renal risk:
  • Contrast volume and repeated doses within 48–72 h.
  • Intra-procedural hypotension, bleeding, atheroembolism (esp. vascular/cardiac catheter work).
  • Choice of contrast (low/iso-osmolar non-ionic preferred in high-risk patients).

Anaesthetic management (for contrast-requiring procedures)

• Type of anaesthesia: depends on procedure and patient.
  • CT/short IR: often no anaesthesia or minimal sedation; GA occasionally (paediatrics, severe agitation, inability to lie flat).
  • Coronary angiography/PCI: usually LA ± sedation; GA uncommon (unstable, airway risk, inability to cooperate).
  • EVAR/complex IR: GA or regional (spinal/epidural) ± sedation depending on centre and patient factors.
• Airway: if GA, ETT often preferred for longer/complex cases; SGA may be acceptable for short, low aspiration risk cases.
• Duration: highly variable.
  • CT: minutes; diagnostic angiography: ~30–60 min; PCI: 1–2 h; EVAR/complex IR: 2–4+ h.
• Pain: usually mild–moderate (access site, immobility); EVAR/complex vascular can be moderate–severe post-op.
• Renal-protective anaesthetic priorities:
  • Avoid hypotension; maintain perfusion pressure (treat promptly with vasopressors + appropriate fluids).
  • Optimise volume status (avoid dehydration; avoid fluid overload in HF).
  • Avoid/withhold nephrotoxins where possible (NSAIDs; consider ACEi/ARB/diuretics case-by-case).
  • Monitor urine output in longer cases/high risk; consider arterial line for major vascular/unstable patients.

Definitions and terminology

• Traditional definition (CIN): rise in serum creatinine ≥25% or ≥44 µmol/L (0.5 mg/dL) within 48–72 h after iodinated contrast, without alternative cause.
• Modern terminology: Contrast-associated AKI (CA-AKI) acknowledges many cases are multifactorial (sepsis, hypotension, atheroembolism). Contrast-induced AKI implies causality (harder to prove).
• Timing: creatinine typically peaks at 3–5 days and returns towards baseline within 1–3 weeks if uncomplicated.

Epidemiology and clinical impact

• Risk is low in patients with normal renal function, but increases with CKD and haemodynamic instability.
• Associated with increased length of stay, need for RRT (rare), and mortality (often reflecting comorbidity/illness severity).

Pathophysiology (what to say in a viva)

• Renal haemodynamics: contrast can cause biphasic flow changes with net medullary hypoperfusion (vasoconstriction via endothelin, adenosine; reduced NO/prostaglandins).
• Direct tubular toxicity: contrast can injure tubular epithelial cells; increased viscosity may worsen tubular obstruction and oxygen demand.
• Oxidative stress: reactive oxygen species contribute to endothelial and tubular injury.
• Why the medulla is vulnerable: already low PO2, high metabolic demand (thick ascending limb), sensitive to reduced perfusion.

Risk factors (patient, procedure, and peri-procedural)

• Patient factors:
  • CKD (especially eGFR <30 mL/min/1.73 m²); prior AKI; proteinuria.
  • Diabetes (particularly with CKD).
  • Age, frailty, dehydration, hypotension, sepsis, anaemia.
  • Heart failure/low cardiac output; cirrhosis; nephrotic syndrome.
  • Concomitant nephrotoxins: NSAIDs, aminoglycosides, amphotericin, calcineurin inhibitors; recent chemotherapy.
• Procedure/contrast factors:
  • High contrast volume; intra-arterial administration (esp. supra-renal) generally higher risk than IV.
  • High-osmolar agents (less used); repeated contrast within 48–72 h.
  • Concomitant haemodynamic insults: bleeding, shock, prolonged procedure time.

Clinical features and diagnosis

• Often asymptomatic; detected by rising creatinine / falling eGFR; may have oliguria in severe cases.
• Diagnosis is one of exclusion: consider sepsis, hypovolaemia, obstruction, atheroembolism (livedo, eosinophilia), drug-induced AKI, rhabdomyolysis.
• Monitoring: baseline creatinine/eGFR pre-contrast in at-risk patients; repeat creatinine at ~48–72 h (local policy varies).

Prevention (core FRCA content)

• General principles:
  • Use contrast only if it will change management; consider non-contrast imaging or alternatives (US/MRI where appropriate).
  • Use lowest feasible contrast dose and avoid repeat exposure within 48–72 h if possible.
  • Prefer low- or iso-osmolar non-ionic contrast in high-risk patients.
• Volume expansion (most evidence-supported intervention):
  • IV isotonic crystalloid (e.g., 0.9% saline) peri-procedurally for high-risk patients, tailored to cardiac status.
  • Typical regimens in practice: start several hours pre and continue post (exact rate/duration varies by guideline and HF risk). Aim euvolaemia; avoid overload.
• Medication management (pragmatic):
  • Avoid NSAIDs around contrast exposure in at-risk patients.
  • ACEi/ARB/diuretics: consider withholding in selected high-risk patients prone to hypotension/volume depletion; individualise (HF/HTN control vs AKI risk).
  • Metformin: not nephrotoxic but risk of lactic acidosis if AKI occurs; follow local policy (often withhold if eGFR low or if AKI develops).
• Pharmacological prophylaxis (what to say):
  • N-acetylcysteine: evidence inconsistent; not routinely recommended in many guidelines; may be used locally due to low cost/low harm.
  • Sodium bicarbonate infusion: mixed evidence; not clearly superior to saline; may be used in some protocols.
  • Statins (peri-PCI): some evidence of benefit in coronary angiography/PCI populations, but practice varies; not a universal anaesthetic intervention.
  • Diuretics (mannitol/furosemide) and dopamine/fenoldopam: not recommended for prevention; may worsen outcomes via hypovolaemia/arrhythmia.
• Renal replacement therapy (RRT) prophylaxis:
  • Prophylactic haemodialysis/haemofiltration solely to remove contrast is not routinely recommended; consider nephrology input for complex cases (advanced CKD, fluid balance issues).

Anaesthetic implications and peri-procedural plan

• Pre-procedure assessment:
  • Identify high-risk patients (CKD, prior AKI, HF, sepsis, hypotension, anaemia). Check baseline creatinine/eGFR and trend.
  • Review nephrotoxins and volume status; consider pre-hydration plan and monitoring strategy.
  • Discuss contrast volume minimisation with operator for high-risk cases (esp. complex IR/PCI/EVAR).
• Intra-procedure:
  • Maintain MAP/perfusion: avoid prolonged hypotension; use vasopressors early if needed (noradrenaline/metaraminol depending on setting).
  • Fluids: aim euvolaemia; balanced crystalloid vs saline—saline is commonly used in CIN protocols; avoid chloride load in large volumes if alternative strategy available and patient-specific factors favour balanced solutions.
  • Avoid additional renal insults: hypoxia, hypercapnia (if severe), nephrotoxic drugs, rhabdomyolysis (positioning), excessive haemodilution/anaemia.
  • Monitoring: consider arterial line for major vascular/unstable; urine output for longer cases (recognise oliguria is late and non-specific).
• Post-procedure:
  • Continue hydration plan if indicated; monitor UO and creatinine at 48–72 h in high-risk patients.
  • Manage AKI early: stop nephrotoxins, optimise haemodynamics, treat sepsis/obstruction, early renal referral if severe or worsening.

Differential diagnoses after angiography (high-yield viva list)

• Pre-renal: hypovolaemia, bleeding, sepsis, heart failure/low output, over-diuresis.
• Intrinsic: ATN (ischaemic/toxic), atheroembolic renal disease (livedo reticularis, eosinophilia), interstitial nephritis (drug-related), rhabdomyolysis.
• Post-renal: obstruction (catheter issues, stones, prostate).