Acute kidney injury (AKI) occurs in a significant proportion of patients with severe sepsis, and is an important cause of mortality in such patients. Current concepts of pathogenesis of AKI are shifting from vasoconstriction-ischaemia induced injury to toxic and immune mediated injury and hyperaemic injury resulting in apoptosis of renal cells. Renal replacement therapy is the mainstay of management of AKI. Adequacy of dialysis is likely to be linked to better outcome, but there is still no clear consensus on the timing, modality, intensity or frequency of dialysis. Haemodynamically unstable patients usually require modes of continuous renal replacement therapy. Biocompatible dialyser membranes are likely to be safer than older cellulose membranes. Bicarbonate is preferred to acetate and lactate as dialysate buffer. Anticoagulation has to be undertaken with care to prevent excessive haemorrhage in the setting of already deranged haemostasis. Adequate volume resuscitation and maintenance of renal perfusion by the use of vasopressors is beneficial; norepinephrine is the vasopressor of choice. There is no place for the use of low- or renal-dose dopamine, mannitol or frusemide in the setting of sepsis-induced AKI, and in fact they may be detrimental. Prevention of kidney damage by nephrotoxic drugs and radio-contrast media is of vital importance. Careful dose management of nephrotoxic drugs will prevent renal injury. Hydration prior to administration of contrast media prevents nephrotoxicity, but the benefit of N-Acetylcysteine is unclear. Tight glycaemic control may have renoprotective effects, though its place in the management of severe sepsis is now controversial. No clear evidence of benefit is seen with other newer therapies.
How to Cite:
Rajapakse, S., Rodrigo, C. & Wijewickrema, E.S., (2009). Management of Sepsis-Induced Acute Kidney Injury. Sri Lanka Journal of Critical Care. 1(1), pp.3–14. DOI: http://doi.org/10.4038/sljcc.v1i1.937