Pancreatic Injury and Glucose Dysregulation: Hyperglycemia, Ketosis, and Complications

Pancreatic injury disrupts endocrine (insulin/glucagon) and exocrine function, causing metabolic derangements:

1. Hyperglycemia

β-cell loss → insulin deficiency → ↓ glucose uptake (GLUT4), ↑ hepatic gluconeogenesis/glycogenolysis → fasting/postprandial hyperglycemia. Symptoms: polyuria, polydipsia, weight loss, fatigue.

2. Impaired Glucose Utilization

Peripheral insulin resistance (inflammatory cytokines, lipotoxicity) compounds deficiency → cellular energy crisis despite hyperglycemia.

3. Ketogenesis and Ketoacidosis

Low insulin/glucagon ratio → ↑ hormone-sensitive lipase → FFA flux to liver → ketogenesis (β-hydroxybutyrate, acetoacetate). Unchecked → DKA (pH <7.3, bicarbonate <15, anion gap ↑).

4. Glucosuria

Filtered glucose > renal threshold (~180 mg/dL) → osmotic diuresis → dehydration, electrolyte loss.

5. Hyperosmolar State

Extreme hyperglycemia (>600 mg/dL) + dehydration → hyperosmolar hyperglycemic state (HHS) — mental status change, no significant ketosis.

Management

• Insulin replacement (basal-bolus or pump).
• Fluid/electrolyte resuscitation.
• Exocrine replacement (pancrelipase) for malabsorption.
• Monitor: glucose, ketones, HbA1c, lipids, fat-soluble vitamins.

Multidisciplinary care (endocrine, surgery, nutrition) essential.