Pathophysiology

Overview:

The pathophysiology of hyperglycemia in hospitalized patients is complex and often multifactorial. The condition may be categorized as either stress-induced hyperglycemia or uncontrolled diabetes mellitus. Both types are strongly influenced by a combination of increased hepatic glucose output and peripheral insulin resistance.

Stress-Induced Hyperglycemia:

In critically ill patients, stress-induced hyperglycemia is common. Stress triggers the release of counter-regulatory hormones such as cortisol, epinephrine, and glucagon, which increase hepatic glucose production and impair insulin sensitivity. This type of hyperglycemia is often transient and resolves as the acute illness improves.

Diabetes Mellitus:

In patients with a known history of diabetes, the etiology often involves a lack of insulin or insulin resistance. Type 1 diabetes results from autoimmune destruction of pancreatic beta cells, leading to an absolute insulin deficiency. On the other hand, Type 2 diabetes involves both insulin resistance and an insulin secretory defect.

Medication-Induced Hyperglycemia:

Certain medications like corticosteroids, antipsychotics, and diuretics can cause or exacerbate hyperglycemia. These medications may increase hepatic gluconeogenesis, decrease insulin sensitivity, or impair pancreatic insulin secretion.

Impact on the Body:

Hyperglycemia can have detrimental effects, including osmotic diuresis leading to dehydration, electrolyte imbalances, and a risk of acute complications like hyperglycemic hyperosmolar state (HHS) or diabetic ketoacidosis (DKA).