Ketones, in particular beta hydroxybutyrate , induce nausea and vomiting that consequently aggravate fluid and electrolyte loss already existing in DKA.
Acetone produces the characteristic fruity breath odour of ketotic patients.
Hyperglycemia usually exceeds the renal threshold of glucose absorption Significant glycosuria Osmotic diuresis Water is lost in urine resulting in Severe dehydration, thirst, tissue hypoperfusion, and, possibly,lactic acidosis.
-to halt movement of fatty acids from periphery to liver
However,an initial insulin BOLUS does NOT speed recovery,and may increase the risk of hypoglycemia and hypokalemia. Therefore,insulin INFUSION is started (WITHOUT A BOLUS) at the rate of 0.1 U/kg/hour.
Clinically apparent cerebral edema occurs in approximately 1% of childhood DKA and is associated with high mortality and neurological morbidity.
The pathogenesis of the cerebral edema is not understood; Some studies have attributed it to cellular swelling as a result of rapid osmolar changes occurring during intravenous infusions.
Several studies, however, have shown no relationship to the volume or sodium content of the infusion nor any association with the rate of change in serum glucose concentration. This suggests that other factors may be important in the pathophysiology of DKA-related cerebral edema.
Clinical signs are variable
Gradual deterioration and worsening of conscious level, or
More commonly a gradual general improvement followed by sudden neurological deterioration