Hyponatraemia

Etiological Factors of Sodium Deficiency

A decrease in body sodium levels occurs via three key mechanisms:

1. Inadequate intake (less than 6–8 g/day):
2. Complete starvation (voluntary or involuntary food restriction, weight loss).
3. Partial deficiency resulting from a strictly salt-free diet.

1. Enhanced sodium loss from the body:
2. Renal routes of excretion: aldosterone deficiency, diabetes mellitus, chronic forms of nephritis, renal failure, use of diuretics, as well as excessive production of atrial natriuretic peptide and prostaglandin $E$.
3. Sweat glands: profuse and prolonged sweating under high environmental temperatures.
4. Gastrointestinal losses: chronic diarrhea and repeated vomiting episodes. Combining these conditions causes the body to lose up to 10–15% of total sodium.

1. Hemodilution (plasma dilution):
2. Increased thirst (polydipsia), typical of diabetes mellitus, for example.
3. Excessive intravenous administration of sodium-free detoxification solutions.
4. Impaired renal excretory function against the background of renal failure or hypersecretion of antidiuretic hormone (ADH).
5. Fluid shift from the interstitial tissue into the vascular bed (during the correction of hypoproteinemia).

Pathogenesis and Clinical Presentation

The triggering mechanism for all manifestations is plasma and extracellular fluid hypo-osmolality. Osmotic disorders create a complex of symptoms:

• Water and electrolyte disturbances: Water rushes from the interstitial space into the cells along the osmotic pressure gradient. This causes cellular edema (cellular hyperhydration) against the background of extracellular dehydration. Extracellular deficit is manifested by dryness of mucous membranes and skin, and reduced skin elasticity and turgor.
• Neuromuscular disturbances: Low extracellular $Na^+$ levels raise the cell excitability threshold. Clinically, this manifests as muscle hypotonia and generalized decreased excitability.
• Cardiovascular syndrome: Arterial hypotension and compensatory tachycardia develop. The mechanism includes a drop in vascular smooth muscle tone, weakened myocardial contractility, and reduced cardiac output.
• Disorders of higher nervous activity: Result from ion imbalance, brain tissue hypoxia, and neuronal hydration. Manifestations range from psychoasthenia to central nervous system depression and altered consciousness.
• Dyspeptic symptoms: Nausea, vomiting, and loss of appetite are caused by edema of nerve center cells and metabolic disruption.
• General changes: Weight loss, and in prolonged pathology—delayed physical growth and development.

Adaptive Body Responses

To compensate for sodium deficit, the body engages the following endocrine and renal mechanisms:

• Activation of the aldosterone system: Aldosterone secretion increases, leading to enhanced tubular sodium reabsorption in the kidneys.
• Suppression of natriuretic factors: Production of and sensitivity to atriopeptin and renal prostaglandins, which normally block $Na^+$ reabsorption, are inhibited.
• Activation of ADH synthesis: In concurrent hypovolemia, vasopressin secretion is stimulated to retain water and preserve circulating blood volume.

Principles of Therapeutic Correction

Etiotropic therapy aimed at eliminating the underlying cause of hyponatremia is of primary importance.

To restore electrolyte balance, the following are used:

• Intravenous infusion: administration of a calculated volume of 1–2% sodium chloride solution.
• Parenteral administration of medications: infusions of blood plasma, plasma substitutes, and protein-containing solutions.