**4. Conclusion**

still occur due to a prolonged decrease in oral intake or increased insensible water losses re‐

The uremic environment can affect methods used to assess glycemic control. Changes in di‐ etary intake and exercise (ie, reduced intake due to anorexia prior to starting dialysis) can also affect the response to administered insulin). Renal inability to reabsorb/regenerate bi‐ carbonate and excrete hydrogen ions may lead to metabolic acidosis even in the absence of DKA; in addition, patients often suffer from anorexia, nausea, vomiting, infections, and even acute coronary events predisposing them to catabolic pattern of metabolism. In pa‐ tients treated with peritoneal dialysis, glucose contained in peritoneal dialysate will tend to

Therefore, the treatment of oliguric patient certainly differs from the wide accepted DKA treatment guidelines. [8]. First of all, end-stage-renal-disease patients with DKA may be less likely volume depleted; in most cases the extracellular volume is expanded from its baseline secondary to hyperglycemia. The volume expansion may cause dyspnea, nausea, vomiting, seizures and coma [54]. In oliguric patient, fluid hydration in amounts usually administered in the DKA treatment may precipitate severe pulmonary edema. Therefore, the need for flu‐ id resuscitation in these patients must be justified clinically or by laboratory testing and po‐ tential volume resuscitation should be performed carefully, using central venous access for continuous monitoring. [2]. When volume overload is apparent, immediate haemodialysis is

Metabolic control can be difficult to achieve. Insulin is normally metabolized by kidneys and in chronic renal failure insulin degradation is much slower. Furthermore, insulin is not ex‐ creted either by haemodialysis or peritoneal dialysis. Hyperinsulinemia resulting from ag‐ gressive glucose – lowering therapies may easily lead to severe and prolonged hypoglycemia. One cannot readily predict insulin requirements in this setting and careful

As already emphasized, kidneys in end-stage renal disease are not able to contribute to the overall acid-base balance. Therefore, DKA in these patients may be both profound and pro‐ longed. In addition, pulmonary dysfunction related to volume overload and sometimes un‐ derlying pulmonary infections can impair respiratory compensation to metabolic acidosis. Bicarbonate administration is rarely of value in DKA [55] and the associated volume, so‐ dium and osmotic overload may be particularly problematic for anuric patients. In this sit‐

Total body concentration of potassium is unchanged, and patients with DKA and end stage renal failure frequently have a high serum potassium level. Lack of insulin causes transloca‐ tion of intracellular potassium to the extracellular compartment. Hyperglycemia causes hy‐ pertonicity of extracellular fluids, which also leads to shift of potassium from the cells to the extracellular compartment. The important potassium – lowering effect of osmotic diuresis is missing. DKA aggravates hyperkalemia in more than 50% of cases [48]. Even when testing reveals hypokalemia, total body potassium stores may be high, and these patients are un‐ able to excrete a potassium load. Consequently, hypokalemia must be documented and

uation, significant metabolic acidosis will only be correctable by haemodialysis [53].

lated to tachypnea and fever.

324 Type 1 Diabetes

the therapy of choice.

individualized therapy is essential.

increase the need for hypoglycemic therapy.

Diabetic ketoacidosis is serious metabolic complication in diabetic patients with acute myo‐ cardial infarction, stroke and renal insufficiency. Conversely, severe diabetic ketoacidosis is an important risk factor for acute myocardial infarction, stroke and acute renal failure. The presence of DKA makes patients' management difficult and aggravates the outcome.

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Acidosis in these patients is usually deeper, prolonged and resistant to therapy. In all of the three conditions a fluid resuscitation in quantities commonly used in the treatment of DKA can not be performed. In addition, in many cases there is more or less marked insulin resist‐ ance. In chronic renal insufficiency, on the contrary, intensive insulin therapy usual for the treatment of ketoacidosis may carry a risk of hyperinsulinemia and prolonged hypoglyce‐ mia. Electrolyte imbalance, especially potassium deficiency or excess can have serious con‐ sequences, especially in patients with myocardial infarction, and special care should be given to electrolyte monitoring.

Finally, we believe that more attention should be paid to the possible acid-base disorders in diabetic patients suffering cerebrovascular insults. Clinical assesment in these cases is not sufficient because the significant overlapping of the signs and symptoms, therefore DKA symptoms may be attributed to cerebrovascular pathology. The conclusions based on blood glucose levels would not be appropriate, since glycemia tends to be high in distressed pa‐ tients. Acid-base status should be determined routinely, along with glycemia and HbA1c in all diabetics affected by stroke in order to prevent misdiagnosis.
