Why does necrotizing pancreatitis cause hyponatremia?

Why does necrotizing pancreatitis cause hyponatremia, and what are effective management strategies for patients with acute necrotizing pancreatitis who persistently exhibit low sodium and protein levels despite intravenous sodium supplementation and protein replacement? In patients with acute necrotizing pancreatitis, persistent hyponatremia and hypoalbuminemia can be challenging to correct. Hyponatremia in this setting often results from a combination of factors, including third-space fluid shifts due to systemic inflammation and capillary leakage, leading to extracellular volume expansion and dilutional hyponatremia. Additionally, non-osmotic vasopressin release, impaired renal function, and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) may contribute. Hypoalbuminemia is primarily caused by increased capillary permeability, resulting in significant protein loss into the interstitial space, along with reduced hepatic synthetic function and nutritional deficits. Effective management includes: 1. Addressing the underlying inflammatory process and ensuring adequate source control of pancreatic necrosis. 2. Careful fluid management—avoiding hypotonic fluids and favoring isotonic saline when appropriate, while closely monitoring serum sodium and volume status. 3. Nutritional support with early enteral nutrition to improve protein synthesis and reduce catabolism. 4. Albumin infusion may be considered in select cases with severe hypoalbuminemia and hemodynamic instability, although evidence remains limited. 5. Treating associated complications such as infections or organ failure that exacerbate metabolic imbalances. Close monitoring and individualized therapy guided by laboratory trends and clinical status are essential.