The labile glucose levels can be explained by several variables that influence glucose control in diabetes, including prandial state, exercise, stress, and nonphysiologic insulin delivery. The most dramatic expression of metabolic instability in IDDM is ketoacidosis. Ketoacidosis can be precipitated by interruption of insulin therapy or by a stress state, with elevated counterregulatory hormone levels, and inadequate insulin therapy. Insulin deficiency and glucagon enhance ketone production from free fatty acids supplied by lipolysis. Ketogenesis and unrestrained hepatic glucose output lead to hyperglycemia with consequent dehydration and ketoacidosis.
Hyperglycemia leads to dehydration and a hyperosmolar state.
As glucose levels rise in these patients, failure to replace free-water loss, often because of impaired thirst or mental status or denial of access to fluids, leads to increasing hyperglycemia and osmolarity, and, ultimately, to depressed mentation. Elevated postprandial glucose levels in patients who have impaired glucose tolerance result from decreased muscle uptake associated with insulin resistance.