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  • Hyponatremia

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    Hyponatremia - a decrease in the concentration of sodium in the blood plasma is 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 normal limits).

    ■ Hypovolemic hyponatremia( deficiency of circulating blood volume, reduction of sodium and extracellular fluid, and sodium deficiency exceeds water deficit).

    ■ Hypervolaemic hyponatremia( increased volume of circulating blood, total sodium content and extracellular fluid volume increased, but water more than sodium).

    ■ False( isoosmolar hyponatremia), or pseudohyponatremia( false results from laboratory tests).

    In patients 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.

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

    With euvolemic hyponatremia, the effect of ADH on the cells of the collecting tubules increases the osmolarity of the final urine and the concentration of sodium in it becomes greater than 20 mmol / l.

    Hypothyroidism may be accompanied by hyponatraemia. As a result of a lack of thyroid hormones( T4, T3), cardiac output and glomerular filtration decrease. Reduction of cardiac output leads to non-ismotic stimulation of ADH secretion and weakening of glomerular filtration. As a result, the excretion of free water falls and develops hyponatriemia. The administration of T4 drugs leads to the elimination of hyponatremia.

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

    The use with therapeutic purposes of analogues of ADH or LS, stimulating secretion or potentiating the action of vasopressin, 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 neosmotic stimulation of ADH secretion. The decrease in the volume of circulating blood due to water loss is perceived by the baroreceptors of the aortic arch, the carotid sinus and the left atrium and maintains the secretion of ADH 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 sodium loss. Among the main causes of hyponatremia of depletion associated with loss through the kidneys, the following are distinguished.

    ■ Forced diuresis:

    □ taking diuretics;

    □ osmotic diuresis;

    □ diabetes mellitus with glucosuria;

    □ hypercalciuria;

    □ introduction of contrast agents in X-ray studies.

    ■ Kidney disease:

    □ CRF;

    □ acute and chronic pyelonephritis;

    □ obstruction of the urinary tract;

    □ polycystic kidney disease;

    □ tubular acidosis;

    □ use of antibiotics of the aminoglycoside group( gentamicin).

    ■ Insufficiency of the adrenal cortex( Addison's disease).

    Non-adrenal sodium loss 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 possessing the properties of the mineral-ralocorticoid cortisol due to decreased sodium reabsorption in nephrons, osmotic clearance increases and aqueous diuresis falls. 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 ADH secretion.

    With uncontrolled diabetes mellitus, the blood plasma osmolality increases( due to the increase in glucose concentration), which leads to a transition of water from the cellular fluid into 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 causes

    for congestive heart failure, nephrotic syndrome, 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 pseudo hyponotraemia is possible when the sodium concentration in the 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, 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 sodium in blood plasma due to hyperlipidemia and hyperproteinemia can be calculated as follows: decrease of Na( mmol / l) = plasma TG concentration( g / l) x0.002;decrease in Na( mmol / l) = amount of total protein in the serum above 80 g / l x 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.