Treatment of DKA in End-Stage Renal Disease or on Maintenance Dialysis
Diabetic ketoacidosis in patients with end-stage renal disease or those receiving maintenance dialysis presents distinct management challenges. Several clinical considerations arise in this population that do not apply to DKA with preserved renal function.
When DKA does occur in end-stage renal disease, several issues need to be considered. The absence of functioning kidneys or dependence on dialysis substantially alters how fluid balance and electrolytes behave during the acute episode.
For people with end-stage renal failure or those on dialysis, insulin replacement is the mainstay of treatment. It is delivered intravenously, with adjustments guided by the glucose response.
Fluid replacement and potassium supplementation are managed quite differently from standard DKA protocols in this population. The clinical target for glucose reduction remains the same as for patients with preserved renal function.
Complete regimen details — infusion guidance, fluid indications, and electrolyte management — are available in the full protocol.References
When DKA does occur in end stage renal disease, several issues need to be considered.
For people with end stage renal failure or those on dialysis, insulin replacement is the mainstay of treatment. This should be given as a FRIII at an initial rate of 0.1 units/kg/hr, but may need to increase if the required rate of glucose fall is not achieved.
If the rate of fall is faster, or the glucose falls to <14.0 mmol/L strongly consider reducing the rate of intravenous insulin infusion to 0.05 units/kg/hr.
Therefore there may be no need for fluid replacement in those with end stage renal failure or those on dialysis.
However, for those who are deemed hypovolaemic, aliquots of 250 ml (0.9% sodium chloride or 10% dextrose) may be given with frequent clinical assessments.
Potassium supplementation is not usually required because the lack of the osmotic diuresis means that there is significantly less potassium loss that for those with preserved renal function.
However, the rate of glucose reduction is the same as for people with preserved renal function – i.e. 3.0 mmol/L/hour.
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