The causes of lowering of sodium in the blood (hyponatremia)

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

• Euvolemic hyponatremia (volume of circulating blood and plasma within normal limits, volume of extracellular fluid and total sodium content within the norm).
• Hypovolemic hyponatremia (deficiency of circulating blood volume, reduction of sodium and extracellular fluid, and sodium deficiency exceeds water deficit).
• Hypervolaemic hyponatremia (an increase in the volume of circulating blood, the total sodium content and the volume of extracellular fluid are increased, but the water is more than sodium).
• False (isoosmolar hyponatremia), or pseudohyponatremia (false results of laboratory tests).

With euvolemic hyponatremia, there are no signs of deficiency of extracellular fluid and circulating blood volume, as well as peripheral edema, that is, 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 form of disinatremia in hospitalized patients.

The main cause of euvolemic hyponatremia is the syndrome of inadequate secretion of antidiuretic hormone (ADH), that is, a condition characterized by a permanent autonomic release of antidiuretic hormone or enhanced kidney reaction to an antidiuretic hormone in the blood. Excess water in the body never arises as a result of its excessive use until the water balance is disturbed. Antidiuretic hormone belongs to the leading role in the regulation of sodium metabolism. Normally, the antidiuretic hormone is secreted with high plasma osmolality. Its secretion leads to an increase in tubular water reabsorption, resulting in decreased plasma osmolality and the secretion of antidiuretic hormone is inhibited. The secretion of antidiuretic hormone is considered inadequate when it does not cease despite the low osmolarity of the plasma (280 mOsm / L).

With euvolemic hyponatremia, the result of the action of the antidiuretic hormone on the cells of the collecting tubules increases the osmolality of the final urine and the concentration of sodium in it becomes greater than 20 mmol / l.

Hypothyroidism can be accompanied by hyponatraemia. As a result of a lack of thyroid hormones (T ₄, T ₃ ), cardiac output and glomerular filtration decrease. Reduction of cardiac output leads to a non-cosmos stimulation of the secretion of antidiuretic hormone and weakening of glomerular filtration. As a result, the excretion of free water falls and develops hyponatremia. The administration of drugs T ₄ leads to the elimination of hyponatremia.

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

The use of antidiuretic hormone analogues or drugs stimulating secretion or potentiating the action of vasopressin with therapeutic purposes can also lead to the development of hyponatremia.

Hypovolemic hyponatremia is possible in patients with a large loss of water and electrolytes or with the infusion of hypotonic solutions. Pathogenetic mechanisms of hypovolemic hyponatremia are associated with non-cosmetic stimulation of the secretion of antidiuretic hormone. Reduction of the volume of circulating blood due to water loss is perceived by the baroreceptor-mi of the aortic arch, carotid sinus and left atrium and maintains the secretion of antidiuretic hormone at a high level, despite the hypo-osmolar state of the blood plasma.

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

• Forced diuresis:
  • reception of diuretics;
  • osmotic diuresis;
  • diabetes mellitus with glucosuria;
  • hypercalciuria;
  • introduction of contrast agents in X-ray studies.
• Kidney diseases:
  • chronic renal failure;
  • acute and chronic pyelonephritis;
  • Obturation of the urinary tract;
  • polycystic kidney disease;
  • tubular acidosis;
  • use of antibiotics of the aminoglycoside group (gentamycin).
• Insufficiency of the adrenal cortex (Addison's disease).

The extrarenal loss of sodium is associated with gastrointestinal diseases (vomiting, fistula of the small intestine, ileostoma, biliary fistula, chronic diarrhea, etc.). Excess losses of sodium through the skin are possible abundant sweating, for example, when working in hot rooms, in hot climates, with delayed 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 having mineralocorticoid properties of cortisol due to decreased sodium reabsorption in nephrons, osmotic clearance increases and aqueous diuresis decreases. This leads to a decrease in the concentration of sodium in the body, thereby causing a shortage of volumes of interstitial fluid and circulating blood. Simultaneous drop of water diuresis causes hyponatraemia. Hypovolemia and a drop in the minute volume of blood circulation reduce GFR, which also leads to hyponatremia due to stimulation of the secretion of antidiuretic hormone.

With uncontrolled diabetes mellitus, the blood plasma osmolality increases (due to the increase in glucose concentration), which leads to the transfer of water from the cell fluid into 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).

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

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

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

Most patients with a serum sodium content above 135 mmol / l have no clinical symptoms. When the concentration of sodium is in the range of 125-130 mmol / l, the prevailing symptoms include apathy, loss of appetite, nausea, vomiting. Symptoms from the nervous system prevail when the sodium content falls below 125 mmol / l, mainly due to brain edema. They include headache, drowsiness, reversible ataxia, psychoses, convulsions, reflex reflexes, to whom. Thirst in these patients, as a rule, is not observed. When the concentration of sodium in the blood serum is 115 mmol / l and lower, the patient shows signs of confusion, he complains of fatigue, headache, nausea, vomiting, anorexia. At a concentration of 110 mmol / l, disturbances in consciousness increase and the patient falls into a coma. If this condition does not stop in time, then hypovolemic shock develops and death occurs.