Pediatric Diabetic Ketoacidosis Management in the Era of Standardization

Ildiko H Koves; Catherine Pihoker

Disclosures

Expert Rev Endocrinol Metab. 2012;7(4):433-443. 

In This Article

Pathophysiology

DKA occurs in absolute or relative insulinopenic states combined with increase in counter-regulatory hormones such as glucagon, epinephrine, cortisol and growth hormone.[11] States of absolute deficiency may be present at the initial presentation of diabetes mellitus, or if there is an interruption of insulin delivery, such as with continuous subcutaneous insulin infusion (insulin pump) failure or failure to administer insulin injections. Relative insulin deficiency occurs during stress, trauma, sepsis, surgery or common intercurrent illnesses such as gastroenteritis. The insulinopenia leads to an accelerated catabolic state (increased gluconeogenesis and glycogenolysis), resulting in hyperglycemia. Hyperglycemia leads to osmotic diuresis and dehydration. Impaired peripheral glucose utilization leads to the activation of an alternative pathway of lipolysis for an alternative fuel source, causing the production of free fatty acids and leading to ketogenesis and metabolic acidosis. The combination of these metabolic derangements, in particular the increasing degree of acidosis, leads to a diminished level of consciousness and coma without therapeutic interventions (Figure 1).

Figure 1.

Diabetic ketoacidosis pathogenesis. DKA: Diabetic ketoacidosis; FFA: Free fatty acids.Adapted from [3].

A case series suggests that consumption of large volumes of fluids with high carbohydrate and salt content (juices, salt and sugar containing soft drinks; Gatorade®)[12] may perpetuate hyperglycemia and hyperosmolarity, potentially leading to further detrimental consequences of hyperosmolar hypernatremic dehydration and further complications.

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