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KEY POINTS
Diabetic ketoacidosis (DKA), hyperosmolar hyperglycemic state (HHS), and hypoglycemia represent the extremes of the glucose spectrum.
Hyperglycemia and ketoacidosis can occur in both type 1 and type 2 diabetes.
Dehydration and electrolyte abnormalities are common and are related to osmotic diuresis, reduced water intake, and acidemia.
Crystalloid resuscitation and exogenous insulin by continuous infusion are necessary to reverse DKA and HHS. A protocol-driven approach is ideal.
Premature cessation of insulin infusions may lead to recurrence of DKA.
Cerebral edema related to DKA or HHS is very rare in adults; however, it may be seen as a complication in children.
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Dysglycemia is frequently encountered in the critical care setting due to the high prevalence of diabetes mellitus (DM) and multiple effects of acute illnesses and their treatments on glucose homeostasis. Understanding the pathogenesis of dysglycemia and diabetes emergencies allows for targeted therapy and avoidance of the associated complications. We will review the pathophysiology, complications, and general approach to dysglycemia, including life-threatening diabetes emergencies, in the critical care setting.
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Pathophysiology of Dysglycemia in Acute Illness
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Serum glucose is a continuum and the pathogenesis of dysglycemia is complex with many factors contributing to altered glucose homeostasis (Table 105-1).1 Diabetic ketoacidosis (DKA), hyperosmolar hyperglycemic state (HHS), and hypoglycemia represent the extremes of the glucose spectrum and are commonly encountered in the critical care setting. While some elements of the clinical presentation and pathophysiology of DKA and HHS are distinct, the general principles of treatment are similar. Hypoglycemia, commonly seen in the acutely ill patient, is typically iatrogenic and requires prompt treatment. It is usually seen in patients with established DM on medications with the known side effect of hypoglycemia. Acute illness can alter the normal physiological response to falling serum glucose and results in hypoglycemia in those not taking glucose-lowering medications.
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In type 1 DM, autoimmune-mediated β-cell death leads to a dramatic fall, and eventually a complete cessation, of insulin production. This can lead to marked hyperglycemia over a very short period of time. Adult-onset type 1 DM may have a slower decline (sometimes termed latent autoimmune diabetes in adults). In type 2 DM, there is usually lowered insulin sensitivity, increased hepatic gluconeogenesis, and a more gradual reduction in insulin secretion over years. Heterogeneity in type 2 DM is increasingly recognized.2 Traditionally DKA was seen almost exclusively in patients with type 1 DM, while HHS was a rare complication of elderly patients with type ...