The insulin infusion should never be discontinued until the acidosis is corrected. Rather, use additional sources of dextrose containing intravenous (IV) fluids if hypoglycemia develops.

DKA is the presenting symptom in approximately 40% of children and teenagers at the time of diagnosis and the most frequent diabetes-related cause of death in children, teenagers, and young adults. Most DKA-related morbidity and mortality can be avoided via early recognition and early intervention.

The underlying pathophysiologic cause of DKA is an absolute or relative deficiency of insulin. Declining insulin production lowers the ratio of insulin to glucagon, which leads to excess hepatic glucose production stimulating glycogenolysis and gluconeogenesis. When the serum glucose rises above 200 mg/dL, the renal threshold for glucose reabsorption is exceeded, causing osmotic diuresis with increased urine output. Physiologic stress from acidosis and progressive dehydration stimulates release of the counterregulatory hormones, cortisol, catecholamines (epinephrine and norepinephrine), and growth hormone. These hormones shift the metabolism of carbohydrate, protein, and lipids; and further increase hepatic glucose production, ketogenesis, and peripheral insulin resistance, thereby worsening acidosis and dehydration. The acidosis and dehydration in turn accelerate the development of DKA by further stimulating increase in the counterregulatory hormones. This cycle is responsible for the development of severe ketoaci- dosis.

The classic triad of DKA is hyperglycemia, ketosis, and acidosis. Presenting symptoms include polyuria polydipsia, weight loss, abdominal pain, nausea, vomiting, tachycardia, and hypoperfusion (cool extremities, decreased capillary refill, dry mucous membranes, poor skin turgor). The following lab criteria are used to diagnose DKA: blood glucose >250 to 300 mg/dL, pH <7.3, serum bicarbonate <15mEq/L, urinary ketones >3+, serum ketones positive. Furthermore, there is a high anion gap metabolic
acidosis due to the ketoacids. Severe DKA should be treated as a potentially life-threatening condition, thus frequent monitoring of patient status, and accurate intake and output, electrolytes, and blood pH is crucial.

The initial interventions should be