Hyponatremia - forms, causes, symptoms and treatment. Hyponatremia: causes and development, forms, manifestations, diagnosis, principles of therapy Clinical manifestations of hyponatremia

E87.1 Hypoosmolarity and hyponatremia

Causes of hyponatremia

In pathology, the causes of hyponatremia are situations related to:

with renal and extrarenal losses of sodium, provided that the losses of the electrolyte exceed its total intake into the body;
with blood dilution (due to excess water intake in polydipsia or increased ADH production in the syndrome of disproportionate ADH production);
with the redistribution of sodium between the extracellular and intracellular sectors, which can occur with hypoxia, prolonged use of digitalis and excess ethanol consumption.

Pathological sodium losses are classified as extrarenal (extrarenal) and renal (renal).

The main extrarenal sources of sodium loss: gastrointestinal tract (with vomiting, diarrhea, fistulas, pancreatitis, peritonitis), skin (loss through sweat due to heat exposure, cystic fibrosis, skin damage due to burns, inflammation), massive bleeding, paracentesis, blood sequestration due to extensive limb injuries , dilatation of peripheral vessels. Sodium loss in urine can occur both with unchanged kidneys (use of osmotic diuretics, mineralocorticoid deficiency) and with renal pathology.

The main kidney diseases leading to sodium loss are chronic renal failure, non-oliguric acute renal failure, recovery period after oliguric acute renal failure, salt-wasting nephropathies: elimination of obstructive nephropathy, nephrocalcinosis, interstitial nephritis, cystic diseases of the renal medulla (nephronophthisis, spongiform medullary disease) , Bartter's syndrome. All of these conditions are characterized by the inability of the renal tubular epithelium to normally reabsorb sodium even under conditions of maximum hormonal stimulation of its reabsorption.

Since total body water content is closely related to ECF volume, hyponatremia should be considered in conjunction with the fluid status: hypovolemia, normovolemia, and hypervolemia.

Main causes of hyponatremia

Hyponatremia with hypovolemia (decreased TVO and Na, but sodium levels are relatively more reduced)

Extrarenal losses

Gastrointestinal: vomiting, diarrhea.
Sequestration in spaces: pancreatitis, peritonitis, small intestinal obstruction, rhabdomyolysis, burns.

Kidney losses

Taking diuretics.
Mineralocorticoid deficiency.
Osmotic diuresis (glucose, urea, mannitol).
Salt wasting nephropathy.

Hyponatremia with normovolemia (increased TVO, close to normal Na level)

Taking diuretics.
Glucocorticoid deficiency.
Hypothyroidism.
Primary polydipsia.

Conditions that increase ADH release (postoperative opioids, pain, emotional stress).

Syndrome of inappropriate ADH secretion.

Hyponatremia with hypervolemia (decrease in total Na content in the body, relatively greater increase in TVR).

Non-renal disorders.

Heart failure.
Kidney disorders.
Acute renal failure.
Chronic renal failure.
Nephrotic syndrome

Symptoms of hyponatremia

Symptoms of hyponatremia include the development of neurological symptoms (from nausea, headache, loss of consciousness to coma and death). The severity of symptoms depends on both the degree of hyponatremia and the rate at which it increases. The rapid decrease in intracellular sodium is complicated by the movement of water into the cell, which can lead to cerebral edema. Serum sodium concentrations below 110-115 mmol/l pose a risk to the patient's life and require intensive treatment.

The main symptoms include manifestations of central nervous system dysfunction. However, when hyponatremia is accompanied by disturbances in the total body sodium content, signs of changes in fluid volume may be observed. The severity of symptoms is determined by the degree of hyponatremia, the speed of its development, the cause, the age and general condition of the patient. In general, older patients with chronic diseases develop more symptoms than younger, otherwise healthy patients. Symptoms are more severe with rapidly developing hyponatremia. Symptoms usually begin to appear when the effective plasma osmolality decreases to less than 240 mOsm/kg.

Symptoms may be vague and consist primarily of changes in mental status, including personality disturbance, somnolence, and altered consciousness. When plasma sodium levels fall below 115 mEq/L, stupor, excessive neuromuscular excitability, seizures, coma, and death may occur. Premenopausal women with acute hyponatremia may develop severe cerebral edema, probably because estrogen and progesterone inhibit Na/K ATPase and reduce the clearance of solutes from brain cells. Possible consequences include infarction of the hypothalamus and posterior pituitary gland, and sometimes herniation of the brainstem.

Forms

The main mechanism for the development of hyponatremia - loss of sodium or impaired water excretion - determines the hemodynamic variant of hyponatremia: hypovolemic, hypervolemic or isovolemic.

Hypovolemic hyponatremia

Hypovolemic hyponatremia develops in patients with loss of sodium and water through the kidneys, gastrointestinal tract or due to bleeding or redistribution of blood volume (pancreatitis, burns, injuries). Clinical manifestations correspond to hypovolemia (hypotension, tachycardia, aggravated by standing; decreased skin turgor, thirst, low venous pressure). In this situation, hyponatremia develops due to excess fluid replacement.

There is a deficiency of BOO and total body sodium, although much more sodium is lost; Na deficiency causes hypovolemia. Hyponatremia is observed if fluid losses, in which salt is also lost, as with incessant vomiting, severe diarrhea, sequestration of fluid in spaces, are compensated by taking clean water or intravenous administration of hypotonic solutions. Significant losses of ECF can cause ADH release, causing renal water retention, which can maintain or worsen hyponatremia. For extrarenal causes of hypovolemia, since the normal response of the kidneys to fluid loss is sodium retention, the sodium concentration in the urine is usually less than 10 mEq/L.

Renal fluid loss leading to hypovolemic hyponatremia can occur with mineralocorticoid deficiency, diuretic therapy, osmotic diuresis, and salt-wasting nephropathy. Salt wasting nephropathy includes a broad group of kidney diseases with predominant dysfunction of the renal tubules. This group includes interstitial nephritis, juvenile nephrophthisis (Fanconi disease), partial urinary tract obstruction and sometimes polycystic kidney disease. Renal causes of hypovolemic hyponatremia can usually be differentiated from extrarenal causes by taking a history. It is also possible to distinguish patients with ongoing renal fluid loss from patients with extrarenal fluid loss by high urinary sodium concentrations (>20 mEq/L). An exception occurs in metabolic alkalosis (severe vomiting), when large amounts of HCO3 are excreted in the urine, requiring Na excretion to maintain neutrality. In metabolic alkalosis, the concentration of CI in the urine allows one to distinguish renal causes of fluid excretion from extrarenal ones.

Diuretics can also cause hypovolemic hyponatremia. Thiazide diuretics have the most pronounced effect on the excretory capacity of the kidneys, while simultaneously increasing sodium excretion. Following a decrease in ECF volume, ADH is released, leading to water retention and increasing hyponatremia. Concomitant hypokalemia leads to the movement of Na into the cells, stimulating the release of ADH, thereby reinforcing hyponatremia. This effect of thiazide diuretics can be observed for up to 2 weeks after discontinuation of therapy; but hyponatremia usually disappears when the deficiency of K and fluid is replaced and water intake is limited until the drug wears off. Hyponatremia caused by thiazide diuretics is more likely to occur in elderly patients, especially if there are impaired renal water excretion. Rarely, these patients develop severe, life-threatening hyponatremia within a few weeks of starting thiazide diuretics due to excessive natriuresis and impaired renal diluting capacity. Loop diuretics are less likely to cause hyponatremia.

Hypervolemic hyponatremia

Hypervolemic hyponatremia is characterized by an increase in total body sodium (and therefore ECF volume) and TVR, with a relatively large increase in TVR. Various disorders that cause edema, including heart failure and cirrhosis, lead to the development of hypervolemic hyponatremia. Rarely, hyponatremia occurs in nephrotic syndrome, although pseudohyponatremia may occur due to the influence of elevated lipid levels on sodium measurements. In all these conditions, a decrease in circulating blood volume leads to the release of ADH and angiotensin II. Hyponatremia occurs due to the antidiuretic effect of ADH on the kidneys and the direct impairment of renal water excretion by angiotensin II. A decrease in GFR and stimulation of thirst by angiotensin II also potentiate the development of hyponatremia. Urinary Na excretion is usually less than 10 mEq/L, and urine osmolality is high relative to plasma osmolality.

The main symptom of hypervolemic hyponatremia is edema. In such patients, renal blood flow is reduced, GFR is reduced, proximal sodium reabsorption is increased, and the excretion of osmotically free water is sharply reduced. This variant of water and electrolyte disturbances develops with congestive heart failure and severe liver damage. It is considered a poor prognostic sign. In nephrotic syndrome, hyponatremia is rarely detected.

Normovolemic hyponatremia

In normovolemic hyponatremia, the total body sodium content and ECF volume are within normal limits, but the amount of BVO is increased. Primary polydipsia can cause hyponatremia only if water intake exceeds the excretory capacity of the kidneys. Since the kidneys can normally excrete up to 25 liters of urine per day, hyponatremia due to polydipsia occurs when large amounts of water are ingested or when the excretory capacity of the kidneys is impaired. This condition is mainly observed in patients with psychosis or with a more moderate degree of polydipsia in combination with renal failure. Hyponatremia can also develop due to excess fluid intake without sodium retention in the presence of Addison's disease, myxedema, non-osmotic secretion of ADH (for example, stress; postoperative condition; taking drugs such as chlorpropamide or tolbutamide, opioids, barbiturates, vincristine, clofibrate, carbamazepine). Postoperative hyponatremia occurs due to a combination of non-osmotic ADH release and excessive administration of hypotonic solutions. Some drugs (eg, cyclophosphamide, NSAIDs, chlorpropamide) potentiate the renal effect of endogenous ADH, while others (eg, oxytocin) have a direct ADH-like effect on the kidney. In all these conditions, there is insufficient excretion of water.

Syndrome of inappropriate ADH secretion (SIADH) is characterized by excessive release of ADH. It is determined by the excretion of sufficiently concentrated urine against a background of hypoosmolality of plasma (hyponatremia) without a decrease or increase in fluid volume, emotional stress, pain, taking diuretics or other drugs that stimulate the secretion of ADH, with normal cardiac, hepatic, adrenal and thyroid function. SIADH is associated with a large number of different disorders.

Isovolemic hyponatremia develops when 3-5 liters of water are retained in the body, of which 2/3 is distributed into the cells, as a result of which edema does not occur. This option is observed in the syndrome of disproportionate secretion of ADH, as well as in chronic and acute renal failure.

Hyponatremia in AIDS

More than 50% of patients hospitalized with a diagnosis of AIDS were diagnosed with hyponatremia. Possible causative factors include the administration of hypotonic solutions, impaired renal function, ADH release due to decreased intravascular volume, and the use of drugs that impair renal fluid excretion. Also, in patients suffering from AIDS, adrenal insufficiency has recently been increasingly observed due to damage to the adrenal glands by cytomegalovirus infection, mycobacterial infection, and impaired synthesis of glucocorticoids and mineralocorticoids by ketoconazole. SIADH may be present due to concomitant pulmonary or CNS infections.

Diagnosis of hyponatremia

Diagnosis of hyponatremia involves determining serum electrolyte levels. However, Na levels can be artificially reduced if severe hyperglycemia increases osmolality. Water moves from the cells to the ECF. Serum sodium concentration decreases by 1.6 mEq/L for every 100 mg/dL (5.55 mmol/L) increase in plasma glucose above normal. This condition is called transfer hyponatremia, since there is no change in the amount of BOO or Na. Pseudohyponatremia with normal plasma osmolality can be observed in the case of hyperlipidemia or excessive hyperproteinemia, as lipids and proteins fill the plasma volume taken for analysis. New methods for measuring plasma electrolyte levels using ion-selective electrodes have overcome this problem.

Determining the cause of hyponatremia must be comprehensive. Sometimes the history suggests a specific cause (eg, significant fluid loss due to vomiting or diarrhea, kidney disease, excessive fluid intake, drugs that stimulate or enhance the release of ADH).

The condition of the patient's blood volume, especially the presence of a clear change in volume, also suggests certain causes. Patients with hypovolemia usually have an obvious source of fluid loss (with subsequent replacement with hypotonic solutions) or an easily identifiable condition (eg, heart failure, liver or kidney disease). In patients with normal fluid volume, more laboratory tests are needed to determine the cause.

The severity of the condition determines the urgency of treatment. The sudden onset of CNS abnormalities suggests acute onset of hyponatremia.

Laboratory tests should include determination of osmolality and electrolytes in blood and urine. In patients with normovolemia, it is also necessary to determine the function of the thyroid gland and adrenal glands. Hypoosmolality in normovolemic patients should result in the excretion of large amounts of dilute urine (eg, osmolality

In patients with volume depletion and normal renal function, sodium reabsorption results in urinary sodium levels of less than 20 mmol/L. Urinary sodium levels greater than 20 mmol/L in hypovolemic patients indicate mineralocorticoid deficiency or salt-wasting nephropathy. Hyperkalemia indicates adrenal insufficiency.

Treatment of hyponatremia

Successful treatment of hyponatremia depends on a preliminary assessment of the hemodynamic variant of the electrolyte imbalance.

When hypovolemic hyponatremia is detected, treatment is aimed at restoring fluid deficiency. A 0.9% sodium chloride solution is administered at a calculated rate until the symptoms of hypovolemia disappear. If the cause of hypovolemia is excessive and prolonged use of diuretic drugs, in addition to replenishing the fluid volume, 30 to 40 mmol/l potassium is administered.

In case of hyponatremia with normal BCC, treatment is carried out depending on the cause that caused the sodium imbalance. In case of kidney disease leading to loss of sodium, the amount of sodium administered should be increased. If large doses of diuretics are used, both sodium and potassium levels should be adjusted. If hyponatremia occurs as a result of the use of large quantities of hypoosmolar fluid, it is necessary to limit the introduction of water and correct the sodium content.

In case of hyponatremia with hyperhydration, the water intake is reduced to 500 ml/day, its excretion is stimulated with loop diuretics, but not with thiazide diuretics; in case of heart failure, ACE inhibitors are prescribed; it may be necessary to use peritoneal dialysis and hemodialysis. Treatment of hyponatremia with severe clinical symptoms must be carried out gradually and very carefully, since rapid administration of sodium can cause dangerous neurological disorders. The first stage of treatment is to increase the sodium content of blood serum to 125-130 mmol/l using hypertonic (3-5%) sodium chloride solutions; at the second stage, a slow correction of the sodium level is carried out with isotonic solutions.

Rapid correction of even mild hyponatremia is associated with a risk of neurological complications. Correction of sodium levels should occur no faster than 0.5 mEq/(LHC). The increase in sodium levels should not exceed 10 mEq/L during the first 24 hours. In parallel, the cause of hyponatremia should be treated.

Mild hyponatremia

Mild asymptomatic hyponatremia (ie, plasma sodium level > 120 mEq/L) should be prevented from progressing. For diuretic-induced hyponatremia, elimination of the diuretic may be sufficient; some patients require administration of sodium or potassium. Similarly, if mild hyponatremia is caused by inadequate parenteral fluid administration in a patient with impaired water excretion, discontinuation of hypotonic solutions may be sufficient.

In the presence of hypovolemia, if adrenal function is not impaired, administration of 0.9% saline usually corrects hyponatremia and hypovolemia. If plasma Na levels are less than 120 mEq/L, complete correction may not occur due to restoration of intravascular volume; It may be necessary to limit the intake of osmotically free water to 500-1000 ml per day.

In hypervolemic patients whose hyponatremia is associated with renal Na retention (eg, heart failure, cirrhosis, nephrotic syndrome), fluid restriction combined with treatment of the underlying cause is often effective. In patients with heart failure, correction of refractory hyponatremia can be achieved by combining an ACE inhibitor with a loop diuretic. If hyponatremia does not respond to fluid restriction, high-dose loop diuretics may be used, sometimes in combination with intravenous 0.9% saline. Replacement of K and other electrolytes lost in urine is necessary. If hyponatremia is severe and not corrected with diuretics, intermittent or continuous hemofiltration may be necessary to control ECF volume while hyponatremia is corrected by intravenous 0.9% saline.

With normovolemia, treatment is aimed at correcting the cause (for example, hypothyroidism, adrenal insufficiency, diuretics). In the presence of SIADH, strict fluid restriction is necessary (for example, 250-500 ml per day). In addition, a combination of a loop diuretic with intravenous 0.9% saline is possible, as for hypervolemic hyponatremia. Long-term correction depends on the success of treating the underlying cause. If the underlying cause is incurable (for example, metastatic lung cancer) and strict fluid restriction is not possible in this patient, demeclocycline (300-600 mg every 12 hours) may be used; however, use of demeclocycline may cause acute renal failure, which is usually reversible upon discontinuation of the drug. In studies, selective vasopressin receptor antagonists effectively induce diuresis without significant urinary electrolyte losses, which may be used in the future to treat resistant hyponatremia.

Severe hyponatremia

Severe hyponatremia (plasma sodium level 238 mOsm/kg) in asymptomatic patients can be corrected by strict fluid restriction. Treatment is more controversial in the presence of neurological symptoms (eg, confusion, somnolence, seizures, coma). Controversial points are the speed and extent of correction of hyponatremia. Many experts recommend increasing plasma sodium levels to no more than 1 mEq/(L h), but in patients with seizures, a rate of up to 2 mEq/(L h) is recommended for the first 2 to 3 hours. In general, the increase in Na levels should not exceed 10 mEq/L during the first 24 hours. More intensive correction increases the likelihood of developing demyelination of fibers of the central nervous system.

A hypertonic (3%) solution can be used, but subject to frequent (every 4 hours) determination of electrolyte levels. In patients with seizures or coma, it can be administered

(Desired change in Na level) / OBO, where OBO = 0.6 body weight in kg for men or 0.5 body weight in kg for women.

For example, the amount of Na required to raise the sodium level from 106 to 112 in a 70 kg man is calculated as follows:

(112 meq/l 106 meq/l) (0.6 l/kg 70 kg) = 252 meq.

Since hypertonic saline contains 513 mEq of Na/L, approximately 0.5 L of hypertonic saline is required to raise the sodium level from 106 to 112 mEq/L. Changes may be required, and therefore it is necessary to monitor plasma sodium levels from the first 2-3 hours from the start of therapy. Patients with seizures, coma, or impaired mental status require additional treatment, which may include mechanical ventilation and benzodiazepines (eg, lorazepam 1 to 2 mg IV every 5 to 10 minutes as needed) for seizures.

Osmotic demyelination syndrome

Osmotic demyelination syndrome (formerly called central pontine myelinolysis) may develop if hyponatremia is corrected too quickly. Demyelination can affect the pons and other areas of the brain. The lesion is more often observed in patients suffering from alcoholism, malnutrition or other chronic diseases. Peripheral paralysis, articulation disorders, and dysphagia may develop within days or weeks. The lesion can spread in the dorsal direction, involving the sensory pathways and lead to the development of pseudocoma (an “environment” syndrome in which the patient, due to generalized motor paralysis, can only make movements of the eyeballs). Often the damage is permanent. If sodium replacement occurs too quickly (eg, > 14 mEq/L/8 hours) and neurological symptoms begin to develop, it is necessary to prevent further increases in plasma sodium by stopping the administration of hypertonic solutions. In such cases, hyponatremia induced by the administration of hypotonic solutions may attenuate possible permanent neurological damage.

Hyponatremia is a condition that occurs in a wide range of pathologies and is quite often observed in clinical practice. It is detected in 15 - 20% of patients hospitalized due to emergency indications, and in 20% of patients hospitalized in critical condition.

This condition is more common in hospitalized patients than in outpatients (the prevalence of hyponatremia in outpatients is approximately 4–7%).

Hyponatremia in the hospital setting reflects the severity of the underlying disease and may be independently associated with mortality.

The case fatality rate in the presence of severe hyponatremia is higher than the case fatality rate in the absence of hyponatremia (approximately 29% versus 9%).

Death is more common in males, blacks, and older patients. Active smokers, hypertensive patients, people who take diuretics, or have a history of diabetes, cancer, chronic heart failure, or cirrhosis of the liver are also at significant risk.

Forms

There are different classifications of hyponatremia. Focusing on the mechanism of development of this condition, hyponatremia is distinguished:

Hypovolemic, which occurs when sodium and water are lost as a result of bleeding, persistent vomiting or severe diarrhea, during redistribution of blood volume (caused by trauma, burn, pancreatitis), as a result of diuretic therapy or osmotic diuresis, with mineralocorticoid deficiency and salt-wasting nephropathy. Hyponatremia in this case develops as a consequence of excessive fluid replenishment.
Hypervolemic, which is characterized by an increase in sodium content and a relatively greater increase in fluid in the body. Occurs with various disorders that cause edema (heart failure, cirrhosis, etc.). It develops as a result of the effect of antidiuretic hormone on the kidneys and the disruption of renal water excretion by angiotensin II.
Isovolemic (normovolemic), which develops with a normal concentration of sodium ions and an increased amount of fluid. Develops with Addison's disease, myxedema, conditions associated with non-osmotic secretion of antidiuretic hormone (stress, taking certain medications).

Taking into account the degree of severity, the following are distinguished:

mild form, in which the concentration of sodium in the blood serum detected by biochemical analysis is 130-135 mmol/l;
moderate-severe form, in which the sodium concentration in the blood serum is 125-129 mmol/l;
severe form, characterized by a sodium concentration of less than 125 mmol/l.

Based on the documented duration of this condition, hyponatremia is distinguished:

acute, the development of which began less than 48 hours ago;
chronic, developing over at least 48 hours.

Cases in which it is impossible to establish the duration of hyponatremia are classified as the chronic form of this condition.

There is also a classification that divides hyponatremia into the following conditions:

with moderately severe symptoms;
with severe symptoms.

Hyponatremia is also divided into:

True (hypotonic), which is characterized by an absolute decrease in sodium in the body. Observed when serum sodium concentration is less than 125 mEq/L and serum osmolarity is less than 250 mo/kg.
Pseudohyponatremia (isotonic hyponatremia), which develops in cases where water passes from intracellular fluid to extracellular fluid as a result of the influence of osmotically active particles of fluid in the extracellular space. In this case, there is no absolute decrease in sodium concentration, and the osmolarity of the extracellular fluid does not deviate from the norm or may exceed it.

Reasons for development

Hyponatremia develops in pathologies that are accompanied by:

renal and extrarenal loss of sodium in cases where electrolyte losses are higher than its total intake into the body;
blood dilution (decrease in osmolarity) associated with excess water intake (occurs with the syndrome of disproportionate production of antidiuretic hormone (ADH));
redistribution of sodium between extracellular and intracellular fluid (possibly with hypoxia or using digitalis for a long time).

Sodium loss may be:

Extrarenal (extrarenal). Occurs as a result of disturbances in the functioning of the gastrointestinal tract or its pathologies (vomiting, diarrhea, the presence of a fistula, pancreatitis, peritonitis), inflammation of the skin or burns, as a result of loss through sweat due to overheating, massive bleeding, paracentesis (piercing the eardrum), blood sequestration with extensive injuries of the limbs, dilatation of peripheral vessels.
Renal (renal). Sodium losses in urine occur when using osmotic diuretics and mineralocorticoid deficiency, chronic renal failure, non-oliguric acute renal failure, salt-wasting nephropathies (nephrocalcinosis, interstitial nephritis, Barter's syndrome, spongy medullary disease, etc.), in which the epithelium of the renal tubules is not able to reabsorb normally sodium.

Hypervolemic hyponatremia is detected in cirrhosis, heart failure, acute and chronic renal failure, and nephrotic syndrome.

Conditions that increase the release of ADH (emotional stress, pain, use of postoperative opioids) also cause hyponatremia.

Pathogenesis

Hyponatremia in most cases develops as a result of insufficient diluting function of the kidneys. Normally, the body’s reaction to dilution of the concentration of tissue fluids is water diuresis, which corrects the hypoosmotic state of fluid media.

The normal process of water diuresis occurs with a combination of three factors:

inhibition of ADH secretion;
sufficient supply of water and sodium to the ascending limb of the loop of Henle and the distal part of the convoluted tubule (areas of the nephron that are responsible for the dilution process);
normal sodium reabsorption and water impermeability of the tubule wall in these areas of the nephron.

Excessively long ADH secretion when the extracellular fluid is hypotonic (a signal to stop secretion) may be associated with non-osmotic secretion stimuli (pain, emotions, reduction in tissue fluid volume) or uncontrolled secretion of the hormone in tumor formations.

Sodium may enter the nephron segments in insufficient quantities, causing the formation of a corresponding amount of unconcentrated urine. Insufficient supply of tubular fluid to the distal parts of the nephron is observed with a low glomerular filtration rate (GFR) or increased reabsorption in the proximal tubule.

Even if ADH secretion is absent, the distal portions of the renal tubules remain somewhat permeable to water, which in small quantities constantly migrates into the interstitial fluid, which gradually increases the osmotic concentration of urine.

In areas responsible for the dilution process, sodium may pass through the tubule wall in insufficient quantities. In addition, these areas may be too permeable to water even in the absence of ADH.

Symptoms

Symptoms of hyponatremia are neurological symptoms, since with hyponatremia the tone of the extracellular fluid decreases and diffusion of water into brain cells along an osmotic gradient is observed. As a result of this diffusion, swelling of brain cells develops and dysfunction of the central nervous system is observed.

Depending on the degree of hyponatremia, the rate of its increase, the age and general condition of the patient, the severity of symptoms varies. Symptoms of acute hyponatremia include:

nausea;
headache;
loss of consciousness, coma (even death).

When intracellular sodium levels rapidly decrease, water moves into the cell and can cause cerebral edema. When the sodium concentration in the blood serum is less than 110-115 mmol/l, intensive treatment is necessary, since there is a risk to the patient's life.

With chronic hyponatremia, there is a tendency to arterial hypotension, dyspeptic disorders, a decrease in muscle tone and skin elasticity, and neuropsychiatric disorders occur.

With sodium loss, tachycardia and weight loss are often observed, and with a decrease in osmolarity, weight may increase due to the development of edema.

Hyponatremia may be asymptomatic.

Diagnostics

Diagnosis of hyponatremia includes:

Studying the medical history to suggest the cause of hyponatremia (fluid loss due to diarrhea, taking drugs that stimulate the release of ADH, etc.).
Laboratory diagnostics to help determine serum electrolyte levels. Hyponatremia is characterized by a decrease in sodium to less than 135 mEq/L. True hyponatremia is accompanied by an elevated serum potassium level (more than 5.0 mEq/L). Plasma hypotonicity is accompanied by urine osmolarity above 50-100 mol/kg. In syndrome of inappropriate ADH secretion (SIADH), the urinary sodium concentration is high when plasma volume increases, but may be low in the presence of edema. If the urine sodium concentration is less than 20 mEq/L, the diagnosis of SIADH is questionable.
A water load test to determine the ability of the kidneys to excrete water.

If true hyponatremia is suspected, cortisol and TSH levels are checked to rule out adrenal insufficiency and hypothyroidism.

Suspicions of SIADH or pituitary pathology require an MRI of the head.

Treatment

Treatment of hyponatremia depends on the hemodynamic variant of this disorder.

In case of hypovolemic hyponatremia, to restore fluid deficiency, a 0.9% sodium chloride solution is administered at a calculated rate until symptoms disappear. If hypovolemia has developed as a result of excessive long-term use of diuretics, an additional 30 - 40 mmol/l potassium is administered.

For hyponatremia with normal circulating blood volume, treatment depends on the cause that led to the sodium imbalance. If kidney function is impaired, the amount of sodium administered is increased, and when diuretics are used (large doses), correction of sodium and potassium levels is necessary. If the cause of hyponatremia is the use of hypoosmolar fluid in large quantities, the introduction of water is limited and the sodium content is corrected.

In case of overhydration, reduce the water intake to 500 ml/day. and stimulate its elimination with loop diuretics (thiazide diuretics are not used).

Hyponatremia in the presence of nephrotic syndrome, heart failure or cirrhosis requires the use of ACE inhibitors, and, if necessary, peritoneal dialysis and hemodialysis.

In severe hyponatremia, treatment is carried out with caution, since rapid administration of sodium often causes osmotic demyelination syndrome.

At the initial stage of treatment, the sodium level is increased to 125-130 mmol/l using hypertonic (3-5%) sodium chloride solutions, and then the sodium level is slowly adjusted using isotonic solutions.

Children with impaired consciousness and convulsive syndrome undergo rapid partial correction with a 3% sodium chloride solution.

Hyponatremia is a condition that occurs when the level of sodium in the blood is abnormally low.

Sodium is an electrolyte that helps regulate the amount of water in and around cells. With hyponatremia, under the influence of one or more factors, ranging from an underlying disease to an increase in thirst during prolonged physical activity, sodium dissolves in the blood. At the same time, the water content in the body increases and the cells begin to swell. This swelling causes many disorders of varying severity.

Treatment of hyponatremia is aimed primarily at eliminating the underlying disease. Depending on the cause of your hyponatremia, you may simply need to reduce your fluid intake. In other cases, hyponatremia may require intravenous fluids and medications.

The following are signs and symptoms of hyponatremia:

Nausea and vomiting
Confusion
Prostration
Fatigue
Anxiety and irritability
Muscle weakness, spasms or cramps
Convulsions
Loss of consciousness

Conditions under which you need to see a doctor

If you have a medical condition that increases your risk of developing hyponatremia, or if you have other risk factors for developing hyponatremia, such as high-intensity exercise, or signs and symptoms that indicate low blood sodium levels, you should consult your doctor.

Complications

With chronic hyponatremia, sodium levels gradually decrease over several days or weeks, and symptoms and complications are usually moderate in severity.

In severe hyponatremia, sodium levels drop sharply, which can cause potentially dangerous consequences, such as rapid development of cerebral edema, which can lead to coma and death.

Premenopausal women appear to be most at risk for developing brain disorders caused by hyponatremia. This may be due to the influence of female sex hormones on the body's ability to regulate sodium levels.

Symptoms of mild, moderate and severe hyponatremia

Mild hyponatremia, that is, a decrease in sodium levels in the range of 130 to 135 mmol/L, is often asymptomatic. Symptoms of moderate hyponatremia - (a decrease in sodium to 120-130 mmol / l) are also characteristic of other diseases, so they are difficult to diagnose without testing. Most often we feel weakness and nausea with accompanying vomiting. If sodium levels fall below 125 mmol/L, we experience severe hyponatremia, which can be life-threatening. Symptoms increase depending on the decrease in the concentration of the element in the blood and include:

orientation disorders,
headache,
convulsions,
breathing disorders,
cerebral edema,
heart failure.

Headache and disorientation are the first signs of hyponatremia.

If hyponatremia is suspected, the basis is a blood test, which is often supplemented by a urine test. The therapeutic procedure consists of leveling the level of sodium in the blood to the required value, which is carried out under the supervision of a specialist.

Delivering sodium too quickly can lead to life-threatening complications such as medial pontine myelinolysis. Then damage to the sheaths of myelin nerve fibers occurs in the brain, which very often ends in death. Therefore, the longer hyponatremia develops, the slower the sodium deficiency must be replenished.

When treating mild forms of hyponatremia, recommendations are often made to limit fluid intake (including water). Sodium can be consumed in food, but in quantities not exceeding 5 g/day (WHO recommendations - remember that sodium is usually found in food, so it is difficult to reduce its level through diet alone).

Supplementing too much with this element (taking medications containing sodium) also has its consequences. This can increase the risk of hypertension because sodium retains water in the blood, leading to increased blood pressure. In case of diagnosed hypertension, in the mildest cases of hyponatremia, ready-made electrolytic fluids available at the pharmacy are taken. In more severe cases, sodium preparations can be administered intravenously under medical supervision.

Causes of sodium deficiency

Hyponatremia usually occurs as a result of excessive dehydration—along with water loss, we lose other elements, including sodium. Dehydration may result from increased physical activity (for example, from strenuous exercise and excessive sweating), prolonged vomiting, diarrhea, or taking too many diuretics. Water loss may also occur due to extensive burns or the presence of osmotic substances in the urine (eg, glucose or urea, which can lead to excessive urine excretion).

Hyponatremia causes the following diseases: hypothyroidism, adrenal insufficiency, heart failure, liver cirrhosis or kidney disease, and syndrome of inappropriate antidiuretic hormone release (SIADH).

There are cases when the cause of low sodium levels in the body is conduction (water poisoning), including the so-called marathon runner's disease, which occurs as a result of drinking too much liquid with a small amount of sodium. It happens that in case of water poisoning, inpatient procedures are performed - washing the bladder or electrolyte-free or hypotonic infusions.

Hyponatremia due to drugs

Hyponatremia occurs when taking large amounts of diuretics. Most often it is mild in nature and resolves after limiting fluid intake, since most modern medications are adapted for long-term use and have limited side effects, even if we take them for many years.

Hyponatremia can be caused by a number of unfavorable factors, including: age, type of medications taken, high ambient temperature. The risk of developing hyponatremia is also higher in smokers and women. An overdose of drugs without the knowledge and control of a doctor can also lead to a more serious condition.

Prevention of the development of hyponatremia is based on regular monitoring of blood sodium levels (basic blood tests), especially in the case of people taking antipsychotics, antidepressants, carbamazepine or oxcarbazepine. It is also advisable to minimize factors that increase the risk of developing sodium disturbances.

What is it, ICD-10 code

This is a condition of the body having insufficient sodium. When the concentration of an element in the serum goes beyond the minimum limits of 135 mEq/l. From chemistry we know that sodium is a positively charged ion, denoted Na. The norm of presence in the blood is 135-145 meq/l (mg-eq/l) (135-145 mmol/liter (mmol/l). Hyponatremia as a pathology is recognized by the world medical community and is included in the International Classification of Diseases. Tenth version (ICD-10 ) includes two subspecies (adults and infants), located in different chapters, represented by two codes:

E87.1 Hypoosmolarity and hyponatremia.

Chapter IV. Diseases of the endocrine system, nutritional disorders and metabolic disorders, subsection Metabolic disorders (E70-E90)

P74.2: Sodium imbalance in the newborn.

Chapter XVI. Selected conditions arising in the perinatal period, subsection P70-P74: Transient endocrine and metabolic disorders specific to the fetus and newborn

Hyponatremia can be true - hypotonic and pseudohyponatremia - isotonic. The first type can occur when the amount of Na is reduced to the maximum. A clinical study shows the presence of a substance in the serum less than 125 mEq/L, osmolarity less than 250 mOsm/kg. The second type is determined when water from the cell flows into the extracellular space. There is no maximum decrease in Na. It is clinically determined that the osmolarity of the extracellular fluid may be normal or approximately. Changes in electrolyte metabolism are often complex, that is, simultaneously with a lack of sodium salts, hypokalemia, hypomagnesemia, and hypocalcemia occur. Hypokalemia and deficiency of other microelements are fraught with the development of diseases of the heart and other organs.

What is hyponatremia, symptoms

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Causes

Hyponatremia can occur for a variety of reasons. More often, as a consequence of certain painful conditions. For example, as a result of excessive vomiting caused by poisoning, gastrointestinal exacerbations (pyloric stenosis, etc.), abuse of diuretics. Sometimes this phenomenon manifests itself when renal perfusion is reduced (up to 10% of normal). A number of pathologies lead to this:

adrenal damage
hypothyroidism
chronic heart failure
cirrhosis of the liver
nephrotic syndrome

Also, a decrease in Na occurs when the supply of this element from the diet is limited. Diets poor in microelements, often mono-diets, also lead to problems.

Symptoms, risk factors

The change is easier to diagnose in acute forms. The chronic course occurs with mild symptoms. Without a clinical examination, the pathology can be diagnosed in doubt if the patient exhibits signs of damage to the central nervous system. Dysfunction occurs due to edema, which occurs when the tone of the extracellular fluid drops and intracellular redistribution of water occurs. It has been practically determined that the presence of an element less than the limit of 125 mEq/L already leads to central nervous system failure within a few hours. The patient looks inhibited, epilepsy and even coma may develop. Important: Without treatment, this condition can be fatal. A clinical urine test will confirm the decrease in the substance. The main risk factors are considered to be: large, completely unnecessary for the body, water consumption, uncontrolled dieting by specialists, and kidney diseases.

Read also: All about hemorrhagic diathesis

Details about all water and electrolyte disorders, including hyponatremia

The causes of the painful condition form the basis of various forms of this syndrome:

Hypovolemic. Na is washed out of the body with simultaneous dehydration. Water loss can be partially restored, but sodium is not automatically restored.

Another cause of hypovolemic hyponatremia is loss of Na through the kidneys. Contributes to: long-term use of diuretics, Addison's disease. A urine test shows the presence of a trace element of less than 20 mmol/l.

Hypervolemic (hyponatremia with dilution). The amount of water increases sharply (there is a delay in the removal of fluid), the volume of Na does not increase against the general background. Often occurs as a result of nephrotic syndrome, it is demonstrated by severe CHF, cirrhosis. Na content is less than 10 mmol/l.
Normovolemic. Otherwise, it is defined as the syndrome of inappropriate ADH secretion.

Here the trace element is excreted in the urine, although the kidneys are functioning normally. Common: exposure to the hormone vasopressin in a number of diseases. For example, some types of cancer, pneumonia, tuberculosis, meningitis, stroke, etc.

Disease in children

In childhood, the problem is also the result of insufficient intake of sodium salts or dilution of sodium due to water retention in the body. Stomach diseases, intestinal infections (accompanied by vomiting and diarrhea), kidney pathologies, and improper functioning of the adrenal glands lead to loss of the element. Uncontrolled use of diuretics also provokes the onset of this condition. Pediatricians confirm the fact that the problem can be caused by the use of infant formula in newborns, used in violation of the instructions (excessively diluted with water). In older children, a decrease in sodium salts can be caused by the use of a salt-free diet.

Children sometimes suffer from this disease almost asymptomatically, especially if the deficiency of the element develops gradually, the symptoms do not appear immediately, often the symptoms are similar to the characteristic manifestations of other diseases.

Rare cases of rapid loss of a microelement give rise to a very serious condition - imptomocomplex. There is a change in blood circulation, a disorder of the central nervous system. The baby becomes lethargic, inactive, and muscle twitching occurs. Possible coma. The symptoms are quite obvious: weight loss, skin becomes dull and sallow. The blood pressure drops sharply, the pulse is very weak and frequent, and the heart sounds are muffled. Clinical analysis shows a decrease in Na with a simultaneous increase in residual nitrogen. Exacerbations are relieved by the administration of medications, for example, prednisolone is often used.

Hyponatremia in patients with AIDS

This category is always at risk for the occurrence of this syndrome. Treating them is problematic. Half, according to some estimates 56%, of carriers of the disease exhibit a reduced content of this chemical element. A frequent consequence of a decrease in substance in these patients may be the use of various medications aimed at maintaining the body suffering from AIDS. In those suffering from this disease, natural damage to the adrenal glands, adrenal insufficiency. This disease has a destructive effect on many organs, as a result of which their work deteriorates and metabolism changes. Complex pathologies arise due to frequent exposure to viral infections (cytomegalovirus adrenalitis, mycobacterial infection, bacterial Pneumocystis carinii, etc.).

Long-term therapeutic effects and the use of strong medications cause disruption of the liver, kidneys, and adrenal glands, causing a decrease in sodium salts.

Diagnostics

At the first stage it is necessary to determine and then confirm the fact of a decrease in sodium salts. For this purpose, clinical tests of urine are carried out. The main indicators of the presence of a problem:

Serum Na exceeded the limit of 135 mEq/L downward
K more than 5.0 mEq/L (with true hyponatremia). A low potassium level indicates the presence of hypokalemia.
Urine osmolality is higher than 50–100 mOsm/kg in the presence of plasma hypotonicity.

Sometimes special testing is carried out - a person is given a large amount of water to check the ability of the kidneys to excrete it. Additional examinations are prescribed. To confirm true hyponatremia, the level of TSH and cortisol is checked to exclude hypothyroidism, adrenal insufficiency. At the second stage, the cause that provoked the syndrome is determined. If there is an increase in the amount of extracellular water, it is necessary to exclude or confirm pathologies such as cirrhosis of the liver, heart failure, nephrotic syndrome. Decrease in blood volume with a normal volume of extracellular fluid can provoke hypothyroidism and primary adrenal insufficiency. Sometimes a specialist may prescribe a head examination using magnetic resonance imaging. This effective method of examination will allow you to exclude pathology of the pituitary gland. Timely confirmation of the diagnosis will allow timely prescribing of the necessary treatment along with solving the problem.

Therapeutic actions are initially aimed at restoring the necessary balance of sodium salts in the patient’s body. Next - to treat the pathology leading to a change in this balance.

Correction of hyponatremia is very effective.

It is recommended to take Natrii chloridum in all cases.
If it is caused by heart failure, liver cirrhosis or nephrotic syndrome, captopril, a loop diuretic, is prescribed.
Excess water is treated by prescribing an infusion of a hypertonic solution of Natrii chloridum plus furosemide or bumetanide.
Patients with chronic renal failure are prescribed replacement treatment with prednisolone.
Severe cases of decompensation of Addison's disease require immediate administration of intravenous prednisolone or hydrocartisone. Prednisolone is not intended for long-term use. Being a synthetic drug, prednisolone has the property of intensely binding to proteins, receptors, and the ratio of various biological effects. However, prednisolone is actively used to relieve exacerbations. Prednisolone has different forms: tablets, injection solution, powder. Powdered prednisolone comes complete with ampoules to create a solution. To relieve acute forms, a prednisolone solution is used. Next, prednisolone tablets are prescribed. Patients are advised to limit fluid intake.

Read also: Necessary information about neutropenia

Treatment of organ diseases that cause this syndrome is prescribed by medical specialists of a specific profile after consultation.

Important: Particular attention is paid to the problem in those suffering from diabetes insipidus.

Diabetes insipidus is treated with thiazide diuretics, non-steroidal drugs, an overdose of some of them leads to fluid retention. Strict control of fluid intake in patients with diabetes insipidus is necessary. Acute conditions require immediate emergency care.

The main task: to quickly saturate the body with sodium chloride. The introduction of 50-60 ml of a ten percent Na salt solution into the blood is indicated. Subcutaneous injection of one liter of saline is also acceptable. It is usually used for sudden loss of fluid during diarrhea and vomiting.

If the patient experiences a strong decrease in blood pressure, 1 ml of cordiamine is injected subcutaneously. Plus to this therapy: 5 ml of carotene, 75 mg of hydrocortisone can also be administered subcutaneously.

Attention: If medical assistance is delayed, it is necessary to give the patient a glass of salt water. Calculation of the solution: 2-3 teaspoons of table salt, dissolved in 200-250 ml of water. Further hospitalization and inpatient treatment are required.

Complications

This pathology, like any disorder in the functioning of our body, if not diagnosed/treated in a timely manner is at risk of complications of varying degrees of severity.

Neurological complications are most often recorded: the central nervous system undergoes changes. Some patients have impaired gait and a tendency to fall for no reason. Epileptic seizures and coma are possible. Lack of medical support can be fatal.

Acute loss of a microelement is especially fraught with complex consequences. Complications affect the brain: brain herniation, cardiopulmonary arrest, cerebral edema (swelling of the brain). These diseases often end in coma and then death.

Elderly patients over 65 years of age are most susceptible to complications. Often the cause of death in such patients is not simply hyponatremia, but causes caused by it, for example, wounds from a fall or developed osteoporosis.

At risk are patients with diabetes insipidus, people leading an antisocial lifestyle, and those suffering from alcoholism. Timely diagnosis or constant monitoring of patients in any of the risk groups, adequate treatment, and adherence to a healthy lifestyle reduces possible complications and, for the most part, leads to recovery.

Causes of edema

The Ministry of Health and WH strictly warn: we can talk about a variety of pathologies of the body. So it is imperative to monitor swelling over time. Edema, for example, may hint at:

You sit at work all day long

Heart failure can also involve a combination of the two and means that fluids are not pushed by the body normally, allowing fluid to accumulate in the legs, ankles, chests, faces and other areas. If you have heart failure, it's important to follow your doctor's instructions about how much fluid you should drink each day, because drinking too much can worsen your condition, says the National Heart, Lung, and Blood Institute. There is no specific amount regarding fluid intake for all heart failure patients, as the amount will depend on your overall health, the severity of your heart failure, and other treatments you may receive.

kidney problems (if you feel that you are going to the toilet more often or less often, the color of your urine has changed, your back is stretching just above your lower back, run to the nephrologist with your heels sparkling);
heart failure (legs go numb, and by the evening they noticeably increase in size, the skin has acquired a bluish tint and feels cold to the touch, shortness of breath has appeared during previously habitual physical activity - you should see a cardiologist);
vascular diseases (swelling of the legs, accompanied by pain, and cramps are subtly hinted at. A more accurate diagnosis will be made by a phlebologist. Alas, the list of ailments is not limited to varicose veins);
dysfunction of the thyroid gland (swelling, looseness of the facial skin);
liver disease (the abdomen increases in volume due to free fluid (ascites);
allergies.

Measures against edema

The list of troubles could be continued, but it seems that the algorithm of actions is already clear:

if edema haunts you, despite a righteous lifestyle, and we are not talking about PMS, surrender to the hands of a doctor;

and (no magic again!) lead a healthy lifestyle.

I would like to talk about the last point in more detail. A healthy lifestyle for our body is not shocking fitness 3 times a week or even giving up bad habits. Everything is somewhat more complicated. Here's what we do to cause swelling:

We move little during the day;
having a tenderness for salty and spicy foods, no, no, and we abuse them;
we skip a glass or two right before bed (and we’re not just talking about alcohol);
We wear narrow shoes with high heels.

How to relieve swelling

If from time to time you commit the listed sins, first, promise yourself to do it less often. Secondly, follow our instructions.

You came home in the evening, so to speak, having abused it.

Take off your shoes, let the bath run (slightly above body temperature). While the water is collecting, lie down on the bed (for 10–15 minutes). Place a cushion under your feet or place your feet on the wall: let the blood drain from your limbs. Soak in the bath for 15 minutes, apply patches to the eye area or use a cooling face mask.

If you have 2-3 hours before bed, try not to drink or eat. Does hunger remind you that he is not an aunt? Unsweetened yogurt or a piece of boiled fish or poultry will help you. A cup of herbal tea (but not right before bed!) will calm an agitated nervous system and quench your thirst.

Read the label of your night cream (if you haven’t already done so): it’s better to choose a nourishing cream rather than a moisturizing one. Ideally, the product should not contain hyaluronic acid, which can attract moisture to the surface of the skin. You may have caused bags under your eyes to appear by using the wrong cream. It is better to leave the moisturizer for the morning.

You woke up and the problem was on your face.

Cotton pads soaked in tea may not look very beautiful on the face, but they effectively relieve swelling due to the effect of tannin on the skin. You can also wash your face with cold water (or a piece of ice) to improve blood microcirculation in the tissues. Impact fitness after a party is a bad idea, but 15-20 minutes of promenade at a fast pace will invigorate not only you, but also your skin.

You sit at work all day long.

Everything has already been written about pedometers and regular walks to the cooler (read). But there is another proposal. Place a ball under the table (preferably a massage ball covered with pimples) and, taking off your shoes, quietly roll it from time to time to make the blood flow more cheerfully through your veins.

Symptoms

Mild hyponatremia usually does not cause problems. When symptoms occur, they may include the following:

clouding of consciousness;
slowness and lethargy;
headache;
fatigue and low energy levels;
nausea;
anxiety.

As the disease progresses, it can cause more severe symptoms, especially in older people. These symptoms include the following:

vomit;
muscle spasms, weakness and twitching;
epileptic seizures;

In extreme cases, hyponatremia leads to death.

Sodium has an important effect on the functioning of the human body. It helps maintain normal blood pressure, ensures proper functioning of nerves and muscles, and regulates fluid balance.

Normal sodium levels are between 135 and 145 mEq/L. With hyponatremia, this value drops below 135 mEq/L.

Certain medical conditions, as well as some other factors, can lead to hyponatremia. In particular, potential causes of this disorder include the following.

Medicines. Some drugs, such as diuretics, antidepressants, and pain relievers, can interfere with hormones or interfere with normal kidney function. In both cases, sodium concentrations can drop to a critical level.
Problems with the heart, kidneys and liver. Acute heart failure, as well as some diseases affecting the kidneys and liver, can provoke the accumulation of fluids, which dilute calcium levels and lower its overall level in the body.
Syndrome of inappropriate vasopressin production (SIPV). In this condition, people produce high levels of the antidiuretic hormone vasopressin. This also causes the accumulation of water, which must be excreted from the body through urine.
Chronic, severe vomiting or diarrhea and other problems causing dehydration. This leads to a decrease in electrolyte levels and an increase in vasopressin concentrations.
Consuming too much water. When people drink a lot of water, low sodium levels can occur due to the kidneys' ability to eliminate water being suppressed. Because people lose sodium through sweat, drinking excessive fluids during intense physical activity, such as long-distance running, can dilute the sodium in the blood.
Hormonal changes. Adrenal insufficiency (Addison's disease) affects the adrenal glands' ability to produce hormones that maintain the balance of sodium, potassium and water in the body. Low thyroid hormone levels can also lead to low sodium levels in the blood.
Recreational drug ecstasy. This amphetamine increases the risk of severe and even fatal hyponatremia.

Risk factors

The following are factors that may increase your risk of developing hyponatremia.

Age. Older people are associated with a greater number of problems that can lead to hyponatremia. These problems include age-related changes, medications, and an increased risk of developing chronic diseases that affect the body's sodium balance.
Medicines. Medications may increase the risk of hyponatremia. These drugs include thiazide diuretics, some antidepressants and painkillers. In addition, as noted above, ecstasy can lead to fatal hyponatremia.
Conditions that impair the body's excretion of water. These conditions include kidney disease, syndrome of inappropriate vasopressin production (SIPV), and heart failure.
Intense physical activity. People who drink too much water during strenuous athletic training have an increased risk of developing hyponatremia.

Hyponatremia is a pathological condition of the body when the level of sodium in the blood decreases below 135 mmol/l.

Causes of hyponatremia

Often, the reasons for a decrease in sodium are its insufficient intake from food into the human body in conditions such as anorexia or during a salt-free diet. Also, diseases of the stomach and intestines can affect the absorption of sodium, which causes its decrease in the blood.

It is possible to reduce sodium levels if it is excreted excessively by the kidneys due to renal failure or when using diuretics. Prolonged vomiting, profuse sweating, constant diarrhea, and suction of fluid during ascites also provoke the development of hyponatremia by removing sodium along with natural body fluids.

There is also relative hyponatremia, when the amount of sodium in the blood decreases due to an increase in the total volume of water. This condition occurs in liver cirrhosis and chronic heart failure.

Clinical manifestations of hyponatremia

If less than 0.5 g of sodium enters the body per day, the following symptoms may occur:

dry skin,
decreased turgor and elasticity of the skin,
muscle cramps,
loss of appetite,
nausea, vomiting,
constant thirst,
confusion, drowsiness, apathy,
practically no urine is excreted,
Heart rate increases and blood pressure drops.

Treatment of hyponatremia

To correct conditions associated with a decrease in sodium levels in the blood, complex methods are used, aimed primarily at eliminating the disease that caused an imbalance of salts in the body.

If hyponatremia is associated with loss of fluid from the body, then replacement therapy is carried out through intravenous infusions of solutions containing sodium.

If sodium is lost through renal excretion, it is advisable to add potassium supplements to replacement therapy.

If the sodium level has increased while the circulating blood volume is normal or increased, then sodium correction must be carried out extremely carefully, as there is a risk of dangerous neurological disorders. This type of hyponatremia is corrected by administering hypertonic sodium solutions.

Complications of hyponatremia

In general, hyponatremia responds well to treatment, but correction should be carried out strictly in accordance with the severity of the disease, focusing on its degree. You should know that with intensive treatment of high-grade hyponatremia by quickly administering sodium-containing drugs to the patient, demyelination of the cerebral pons may develop, which often ends in death! Also, due to intensive correction of the amount of sodium, the development of paralysis and mental disorders is possible. If after the development of neurological complications the patient remains alive, then neurological disorders in the form of paralysis, mental disorders, and convulsive disorders remain for life.

Another complication of hyponatremia is the development of cerebral edema. This condition is extremely dangerous and threatens the death of the patient if the necessary treatment is not provided in a timely manner.

Hyponatremia is a pathological condition based on a decrease in the concentration of sodium ions in the blood to a level below 135 mEq/L.

Causes

Various conditions and diseases can lead to the development of hyponatremia:

Addison's disease;
taking diuretics (diuretics);
adrenal insufficiency;
inflammatory kidney diseases, in which increased salt excretion occurs;
metabolic alkalosis;
diabetes mellitus accompanied by ketonuria, glucosuria;
severe total hyperhidrosis;
uncontrollable vomiting;
severe diarrhea;
intestinal obstruction;
acute pancreatitis;
peritonitis;
hypothyroidism;
psychogenic polydipsia;
syndromes associated with impaired secretion of antidiuretic hormone (ADH);
taking certain medications;
nephrotic syndrome;
acute and chronic renal failure;
cachexia;
cirrhosis of the liver;
congestive heart failure;
hypoproteinemia.

Prevention of hyponatremia involves timely identification and active treatment of conditions and diseases that can lead to its development.

Kinds

Hyponatremia can be caused by both a lack of sodium in the body and an excess of water in the body. Depending on the sodium-water ratio, the following types of hyponatremia are distinguished:

Hypovolemic. It is caused by a large loss of extracellular fluid and with it sodium ions.
Hypervolemic. Caused by an increase in the volume of extracellular fluid.
Normovolemic or isovolemic. The total concentration of sodium ions in the body corresponds to the norm, but under the influence of certain factors there is a significant increase in fluid in the body. This form of hyponatremia usually occurs as a result of water poisoning (water intoxication).

The severity of hyponatremia is determined by the concentration of sodium ions in the blood serum:

mild – 130–135 mmol/l;
average – 125–129 mmol/l;
severe – less than 125 mmol/l.

There are acute and chronic forms of hyponatremia. The acute form is spoken of in cases where disturbances in water and electrolyte balance last no more than 48 hours.

Signs

The main sign of hyponatremia is the appearance of neurological symptoms of varying severity (from minor headache to deep coma), which is determined by the patient’s age, initial health status, as well as the degree of hyponatremia and the rate of loss of sodium ions.

When the sodium concentration in the blood decreases to a level of less than 115 mEq/L, the patient develops acute cerebral edema and coma.

Diagnostics

Diagnosis of hyponatremia presents certain difficulties, since the clinical manifestations of this pathology are nonspecific. Caution for acute hyponatremia is necessary in the following cases:

polydipsia (pathological thirst);
early postoperative period;
therapy with thiazide diuretics;
excessive physical activity;
initiation of vasopressin therapy;
taking amphetamine;
intravenous administration of cyclophosphamide;
preparation for colonoscopy;
the presence of signs of dehydration (decreased diuresis, tachycardia, constant or orthostatic hypotension, decreased skin turgor, dry mucous membranes).

To confirm hyponatremia, a number of laboratory tests are performed:

Determination of sodium concentration in blood. Normally, an adult contains 136–145 mEq/L of sodium ions in 1 liter of blood. Hyponatremia is indicated by a decrease in sodium concentration to a level below the physiological limit of normal.
Determination of plasma osmolarity. The results allow us to determine what type of hyponatremia is observed. Normal blood plasma osmolarity is 280–300 mOsm/kg.
Determination of urine osmolarity (normal range is 600–1200 mOsm/kg).
Determination of the level of total protein, triglycerides and cholesterol in the blood. The results of these studies allow us to exclude pseudohyponatremia.

Hyponatremia can be caused by both a lack of sodium in the body and an excess of water in the body.

Treatment

The treatment algorithm for hyponatremia depends on the severity of the electrolyte disturbance, its duration, and the characteristics of clinical manifestations (hypovolemia, hypervolemia, cerebral edema).

In case of hypovolemic variant, intravenous administration of isotonic sodium chloride solution is prescribed. The volume and rate of administration required for correction are calculated by the doctor in each specific case using special formulas.

If the cause of hyponatremia is too large a volume of infusion of hypoosmolar solutions, then it is necessary to limit further fluid intake into the body and correct the content of sodium ions.

Elimination of hyponatremia, especially with severe clinical manifestations, should be carried out with great caution and gradually. This approach reduces the risk of developing neurological disorders, including life-threatening ones.

Simultaneously with the correction of water and electrolyte balance, therapy is carried out for the diseases and conditions that caused its occurrence.

Prevention

Prevention of hyponatremia involves timely identification and active treatment of conditions and diseases that can lead to its development.

Consequences and complications

Complications of hyponatremia are associated with damage to the central nervous system. These include:

cerebral edema;
encephalitis;
meningitis;
thrombosis of cerebral arteries;
subarachnoid or subdural hematomas;
infarction of the hypothalamus and (or) posterior pituitary gland;
formation of hernial protrusion of the brain stem.