Causes of low blood sodium (hyponatremia)

Hyponatremia is a decrease in the concentration of sodium in the blood plasma to less than 135 mmol/l. There are four types of hyponatremia.

• Euvolemic hyponatremia (circulating blood and plasma volumes within normal limits, extracellular fluid volume and total sodium content within normal limits).
• Hypovolemic hyponatremia (deficit of circulating blood volume; decrease in sodium and extracellular fluid content, with the sodium deficit exceeding the water deficit).
• Hypervolemic hyponatremia (increased circulating blood volume; total sodium content and extracellular fluid volume are increased, but water to a greater extent than sodium).
• False (isosmolar hyponatremia), or pseudohyponatremia (false laboratory test results).

In euvolemic hyponatremia, patients do not have signs of extracellular fluid and circulating blood volume deficiency, nor do they have peripheral edema, i.e. signs of water retention in the interstitial space, but the total amount of water in the body is usually increased by 3-5 liters. This is the most common type of dysnatremia in hospitalized patients.

The main cause of euvolemic hyponatremia is the syndrome of inappropriate secretion of antidiuretic hormone (ADH), i.e. a condition characterized by constant autonomous release of antidiuretic hormone or an increased renal response to antidiuretic hormone in the blood. Excess water in the body never occurs as a result of its excessive consumption until the regulation of water balance is disturbed. Antidiuretic hormone plays a leading role in the regulation of sodium metabolism. Normally, antidiuretic hormone is secreted at high plasma osmolarity. Its secretion leads to an increase in tubular reabsorption of water, as a result of which plasma osmolarity decreases and the secretion of antidiuretic hormone is inhibited. Secretion of antidiuretic hormone is considered inadequate when it does not stop despite low plasma osmolarity (280 mosm/l).

In euvolemic hyponatremia, as a result of the action of antidiuretic hormone on the cells of the collecting ducts, the osmolarity of the final urine increases and the concentration of sodium in it becomes greater than 20 mmol/l.

Hypothyroidism may be accompanied by hyponatremia. As a result of the deficiency of thyroid hormones (T4 _, T3 ₎, cardiac output and glomerular filtration decrease. A decrease in cardiac output leads to non-osmotic stimulation of the secretion of antidiuretic hormone and weakening of glomerular filtration. As a result, the excretion of free water decreases and hyponatremia develops. The administration of T4 preparations _leads to the elimination of hyponatremia.

Similar mechanisms are involved in primary or secondary adrenal glucocorticoid insufficiency.

The use of antidiuretic hormone analogues or drugs that stimulate the secretion or potentiate the action of vasopressin for therapeutic purposes can also lead to the development of hyponatremia.

Hypovolemic hyponatremia may occur in patients with significant water and electrolyte loss or with infusion of hypotonic solutions. Pathogenetic mechanisms of hypovolemic hyponatremia are associated with non-osmotic stimulation of antidiuretic hormone secretion. A decrease in circulating blood volume due to water loss is perceived by baroreceptors of the aortic arch, carotid sinuses, and left atrium and maintains antidiuretic hormone secretion at a high level, despite the hypoosmolar state of blood plasma.

Hypovolemic hyponatremia can be divided into two types: with excess loss of sodium in urine and extrarenal loss of sodium. Among the main causes of hyponatremia of exhaustion associated with loss through the kidneys are the following.

• Forced diuresis:
  • taking diuretics;
  • osmotic diuresis;
  • diabetes mellitus with glucosuria;
  • hypercalciuria;
  • the introduction of contrast agents during X-ray examinations.
• Kidney diseases:
  • chronic renal failure;
  • acute and chronic pyelonephritis;
  • urinary tract obstruction;
  • polycystic kidney disease;
  • tubular acidosis;
  • use of antibiotics of the aminoglycoside group (gentamicin).
• Adrenal cortex insufficiency (Addison's disease).

Extrarenal sodium losses are associated with gastrointestinal diseases (vomiting, small intestinal fistula, ileostomy, biliary fistula, chronic diarrhea, etc.). Excessive sodium losses through the skin are possible with profuse sweating, for example, when working in hot rooms, in a hot climate, with slow healing of burns. Under such conditions, the concentration of sodium in the urine is less than 20 mmol/l.

With low secretion of aldosterone and cortisol, which has mineralocorticoid properties, due to decreased sodium reabsorption in the nephrons, osmotic clearance increases and water diuresis decreases. This leads to a decrease in the concentration of sodium in the body, thereby causing a deficit in the volume of interstitial fluid and circulating blood. The simultaneous decrease in water diuresis causes hyponatremia. Hypovolemia and a decrease in the minute volume of blood circulation reduce the SCF, which also leads to hyponatremia due to stimulation of the secretion of antidiuretic hormone.

In uncontrolled diabetes mellitus, the osmolarity of blood plasma increases (due to an increase in glucose concentration), which leads to the transition of water from the cellular fluid to the extracellular fluid (blood) and, accordingly, to hyponatremia. The sodium content in the blood decreases by 1.6 mmol/l with an increase in glucose concentration by 5.6 mmol/l (by 2 mmol/l in patients with hypovolemia).

Hypervolemic hyponatremia occurs as a result of pathological "flooding" of the interstitial space, which is caused by congestive heart failure, nephrotic syndrome, liver cirrhosis and other conditions. The total water content of the body increases to a greater extent than the sodium content. As a result, hypervolemic hyponatremia develops.

False or pseudohyponatremia is possible when the sodium concentration in plasma is not reduced, but an error was made during the study. This can occur with high hyperlipidemia, hyperproteinemia (total protein above 100 g/l) and hyperglycemia. In such situations, the non-aqueous, sodium-free fraction of plasma increases (normally 5-7% of its volume). Therefore, to correctly determine the sodium concentration in plasma, it is better to use ion-selective analyzers that more accurately reflect the real sodium concentration. Plasma osmolarity in pseudohyponatremia is within normal values. Such hyponatremia does not require correction.

The decrease in plasma sodium content due to hyperlipidemia and hyperproteinemia can be calculated as follows: decrease in Na (mmol/L) = plasma TG concentration (g/L) × 0.002; decrease in Na (mmol/L) = serum total protein above 80 g/L × 0.025.

Most patients with serum sodium levels above 135 mmol/L have no clinical symptoms. When the sodium concentration is in the range of 125-130 mmol/L, the predominant symptoms include apathy, loss of appetite, nausea, and vomiting. Nervous system symptoms predominate when the sodium concentration falls below 125 mmol/L, mainly due to cerebral edema. They include headache, drowsiness, reversible ataxia, psychosis, seizures, reflex disorders, and coma. Thirst is usually not observed in such patients. When the serum sodium concentration is 115 mmol/L and below, the patient shows signs of confusion, complains of fatigue, headache, nausea, vomiting, and anorexia. At a concentration of 110 mmol/L, impaired consciousness increases and the patient falls into a coma. If this condition is not stopped in time, hypovolemic shock develops and death occurs.