FRCA Notes

Acute Kidney Injury After Cardiac Surgery

Resources

  • AKI is one of the commonest complications of adult cardiac surgery
  • Depending on the definitions used:
    • 10-36% of patients undergoing cardiac surgery develop AKI
    • Up to 50% of patients undergoing cardiopulmonary bypass develop AKI
    • Up to 2% of patients will require renal replacement therapy for their AKI
  • In reality, sub-clinical renal injury probably occurs in all patients undergoing cardiac surgery to some extent

Patient risk factors

  • Older age
  • Pre-existing renal dysfunction (prevalence ~20% of those presenting for cardiac surgery)
  • Raised BMI
  • Other comorbidities:
    • Vascular disease
    • COPD
    • Diabetes
  • Low pre-operative haematocrit or ferritin
  • Post-operative issues:
    • Hypotension ± need for IABP
    • AF
    • Sepsis

Surgical risk factors

  • Prior cardiac surgery
  • Long duration cardiopulmonary bypass; especially so once >180mins
  • Endocarditis
  • Greater urgency of surgery
  • Valve surgery (vs. CABG)
  • Long aortic cross-clamp time


Associations of AKI in cardiac surgery
↑ short-term morbidity e.g. higher likelihood of sepsis, GI bleeding, neurological complications or MI
↑ short-term mortality; if requiring dialysis mortality is 50-60%
Long-term reduction in kidney function
↑ length of ICU & hospital stay
↑ likelihood of discharge to an extended care facility
↑ long-term mortality
↑ economic cost


  • The pathophysiology of AKI following cardiac surgery is complex and polyfactorial
  • It is not merely due to periods of hypotension perioperatively, but involves:
Pathophysiology of AKI after cardiac surgery
Ischaemia-reperfusion injury
Impaired renal DO2
Exogenous nephrotoxins
Endogenous nephrotoxins
E.g. free Hb due to haemolysis
Oxidative stress
Inflammatory response/SIRS
Renal artery vasoconstriction or embolisation
Interstitial oedema
Medullary ischaemia
Tubular obstruction


Prevention

  • Acknowledge risk factors above and modify where possible
  • With further research it may be possible to measure biomarkers which could be predictive of post-operative AKI; NT-pro-BNP, TIMP-2, IGFBP7

  • 'Low dose' or 'renal dose' dopamine
    • Dopamine causes a dose-dependent increase in renal blood flow over the range 0.5-3mcg/kg/min
    • It therefore increases urine output
    • Not felt to actually afford any renal protection in patients undergoing cardiac surgery
    • May exacerbate renal tubular injury

  • Mannitol
    • Historically used as pharmacological prophylactic agent against AKI via its osmotic diuretic effect
    • Not robustly shown to prevent AKI

  • Furosemide
    • Used to reduce renal medullary oxygen consumption
    • Not demonstrated to be effective for preventing AKI

Management

  • Management is supportive and similar to AKI of any aetiology

  • Stop nephrotoxic agents
  • Ensure adequate hydration/volaemic status
  • Support haemodynamics perioperatively to maintain renal perfusion pressure
  • Consider RRT in those with refractory issues