Diabetic patients tend to suffer from ketoacidosis less frequently after starting chronic dialysis than prior to it.The prolonged half life of insulin in advanced renal failure and frequent follow up of patients on chronic dilayis have been identified as reasons for the decreased frequency of ketoacidois in the dialysis population. The usual course leading to ketoacidosis is omission of one or more insulin doses, often due to an intercurrent illness. This is of prime importance as an underlying cause should always be looked for at presentation. The common ones being access related infections and myocardial ischemia.
The absence of osmotic diuresis distinguishes dialysis associated hyperglycemia from hyperglycemia observed in patients with normal renal function.The rise in plasma osmolality that is seen in diabetic ketoacidosis and non ketotic hyperosmolar coma is only in part due to the rise in serum glucose. The marked hyperosmolality is primarily due to the glucose osmotic diuresis that causes water loss in excess of sodium and potassium. The importance of effective plasma osmolality in the development of neurological symptoms are illustrated by observations in diabetic patients with end stage renal disease. These patients can develop severe hyperglycemia, with serum glucose concentrations that exceed 1000 to 1500 mg/dl . However because there is little or no osmotic diuresis, the rise in plasma osmolality is limited , hyponatremia is present, and there are few or no neurological symptoms.
Mainly because of the absence of the osmotic diuresis a dialysis patient in DKA may be less likley to be volume depleted and in most cases the extracellular volume is expanded from its baseline, and only if it is deemed clinically necessary should small aliquots of fluid be administered with continuous evaluation
Total body concentrations of potassium is unchanged, and they frequently have a high serum potassium level. Hyperglycemia has muliple effects on serum potassium: lack of insulin causes translocation of intracellular potassium to the extracellular compartment, a second hyperkalemic effect of hyperglycemia is the consequence of associated hypertonicity, which also leads to egress of potassium from the cells to the extracellular compartment
Insulin infusion is the only treatment required in majority of the patients. Emergency hemodialyis may be considered in severe pulmonary edema, profound metabolic acidosis and severe hyperkalemia with EKG mainfestations
I think if you dialyze pt's with DKA, hyperglycemia will resolve as long as the primary process which led to hyperglycemia is taken care of. Dialysate has glucose level of around 100.
ReplyDeleteNo, dear anonymus, being a staff nurse in a nephrology centre which caters to 200 dialysis sessions per week and about 20 acute admissions per week, we come across 67 anuric ESRD patients on dialysis who had DKA over the last 2 years. These patients had raised serum ketones, hyperglycemia, high anion gap metabolic acidosis. the AG met acidosis did not improve after dialysis. we treated these patients with continuous infusion of regular insulin with 1 hourly monitoring of blood sugar. Antibiotics were prescribed when patient was febrile, had obvious source of infection or raised WBC count. I/V fluid was never needed as patients were anuric. other friends may also share their experience.
ReplyDeleteMaria Chuhan
Staff Nurse, The National Institute of kidney Diseases,FPGMI,
Shaikh Zayyed Hospital, Lahore, Pakistan