Causes and Etiology
The development of hypernatraemia is associated with water-electrolyte balance disorders and endocrine system dysfunction. Key factors include:
- Endocrine disorders: hyperaldosteronism and increased angiotensin production.
- Insufficient water intake (restriction of fluid or food intake).
- Excessive fluid loss: vomiting, diarrhea, polyuria, and prolonged sweating.
- Hemoconcentration (blood thickening) due to fluid redistribution from vessels into tissues during hypoproteinemia or increased tissue oncotic pressure from proteolysis.
Pathogenesis and Clinical Manifestations
An excess of sodium ions triggers a cascade of pathological changes in the body's internal environment:
- Hyperosmolality of extracellular fluids due to the high osmotic activity of sodium.
- Cellular dehydration: water moves from cells into the interstitium along the pressure gradient, causing cellular shrinkage and destruction.
- Edema of the interstitial space.
- Hypertension due to sodium accumulation in vascular wall cells.
- Alkalosis (of exogenous or renal origin).
- Neuromuscular disturbances and higher nervous activity disorders, manifesting as anxiety, depression, and panic states.
Compensatory Mechanisms
The body deploys protective mechanisms to restore homeostasis:
- Activation of osmoreceptors and thirst center neurons stimulates the secretion of antidiuretic hormone (ADH), which ensures water retention to dilute the ions.
- Synthesis of natriuretic factors (e.g., atrial natriuretic peptide and renal prostaglandin $E_2$), which promote the excretion of excess salts.
Treatment Principles
Methods for correcting this pathology aim to address the water-electrolyte imbalance:
- Eliminating the root cause and restricting sodium intake.
- Stimulating sodium excretion using diuretics (loop, potassium-sparing) and aldosterone antagonists.
- Decreasing ion concentration through parenteral administration of fluids (5% dextrose/glucose solution or isotonic sodium chloride solution).