Hyponatremia, causes of the disease. Hyponatremia symptoms Therapeutic approaches for a hypoosmotic state and hyponatremia in a patient

What is hyponatremia

Hyponatremia is a condition characterized by a decrease in serum sodium concentration to less than 135 mmol/l. Normally, a decrease in sodium intake into the body does not lead to the development of hyponatremia, since the excretion of water also decreases.

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.

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

Pathophysiology

Hyponatremia indicates that tissue fluids contain an excessive amount of water relative to the total amount of solute. Hyponatremia is a condition that is not identical to sodium deficiency. The latter is just one of the clinical conditions in which hyponatremia develops. In most cases, hyponatremia is due to insufficient diluting function of the kidneys. The body's normal reaction to dilution of the concentration of tissue fluids is manifested by water diuresis, which corrects the hypoosmotic state of liquid media.

For the normal process of water diuresis, three factors are necessary:
1) inhibition of ADH secretion;
2) sufficient supply of sodium and water to the areas of the nephron responsible for the dilution process [the ascending limb of the nephron loop (Henle) and the distal part of the convoluted tubule];
3) normal function of these areas of the nephron (sodium reabsorption and impermeability of the tubule wall to water).

Violation of one of the three listed mechanisms can cause weakening of water diuresis in patients with hyponatremia. For example, firstly, the secretion of ADH continues for an excessively long time, despite the hypotonicity of the extracellular fluid, which normally serves as a signal to stop its secretion. This occurs due to uncontrolled secretion of ADH in tumor formations or as a result of some non-osmotic secretion stimuli. The latter reason includes a reduction in the volume of tissue fluid, as well as factors associated with the nervous system (pain, emotions). Secondly, sodium enters the nephron segments responsible for the dilution process in insufficient quantities, resulting in the formation of a corresponding amount of unconcentrated urine. Inadequate supply of tubular fluid to the distal parts of the nephron occurs with a decrease in GFR and/or increased reabsorption in the proximal tubule. Even in the absence of ADH secretion, the distal portions of the renal tubules retain some permeability to water. A small amount of it constantly migrates from the hypertonic fluid of the lumen of the renal tubules into the interstitial fluid, which is isotonic in the renal cortex and slightly hypertonic in the medulla. The amount of water returned to the tubules in this way constitutes an increasingly large part of the volume of urine formed by dilution, since the dilution process itself is gradually limited due to a decrease in the flow of sodium and water into these segments of the nephron. Consequently, the osmotic concentration of urine gradually increases.

In some cases, this mechanism can even lead to the excretion of urine, the osmoticity of which is higher than that of plasma, despite the absence of ADH secretion. Thirdly, sodium passes through the wall of the tubule in the segments that are responsible for the dilution process in insufficient quantities or these segments are too permeable to water, despite the absence of ADH. One of the three mechanisms described above may cause hyponatremia.

Symptoms (manifestations) 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. A 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 the background of plasma hypoosmolality (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 into 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< 100 мОсм/кг и плотность < 1,003). Низкие уровни натрия и осмоляльности сыворотки крови, а также чрезмерно высокий уровень осмоляльности мочи (120-150 ммоль/л) по отношению к низкой осмоляльности сыворотки предполагают повышение или снижение объема жидкости либо синдром неадекватной продукции АДГ (СНСАДГ). Снижение и повышение объема жидкости дифференцируются клинически. Если данные состояния не подтверждаются, предполагается СНСАДГ. У пациентов с СНСАДГ обычно наблюдается нормоволемия или легкая гиперволемия. Уровни азота мочевины крови и креатинина обычно находятся в пределах нормы, уровень мочевой кислоты в сыворотке часто снижен. Уровень натрия в моче обычно более 30 ммоль/л, фракционная экскреция натрия более 1 %.

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.

What needs to be examined

What tests are needed

Sodium in the blood
Sodium in urine

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.

For 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< 109 мэкв/л, эффективная осмоляльность >238 mOsm/kg) in asymptomatic patients can be corrected by strict restriction of fluid intake. 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< 100 мл/ч в течение 4-6 часов в количестве, достаточном для повышения уровня Na сыворотки на 4-6 мэкв/л. Это количество может быть рассчитано по формуле:

(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.

Complications of hyponatremia

Central pontine myelinolysis was first observed in alcohol abusers and malnourished individuals. In the first descriptions, myelinolysis limited to the pons was accompanied by tetraplegia, and in some cases led to death. Subsequent observations established a connection between central pontine myelinolysis and treatment of hyponatremia. With aggressive therapy for hyponatremia aimed at eliminating cerebral edema, patients may develop mutism, dysphasia, spastic tetraparesis, pseudobulbar palsy and delirium. Patients who survive often have severe neurological impairment. CT and MRI have shown that myelinolysis extends beyond the pons, and in typical cases, brain areas at the border between gray and white matter are symmetrically affected.

Both animal experiments and observations in humans provide convincing evidence that this syndrome is associated with aggressive correction of hyponatremia. Given the lack of understanding about the pathogenesis of central myelinolysis, it is advisable to approach with caution the correction of chronic hyponatremia in patients with obvious changes in water content and distribution of solutes in the brain, increasing the level of Na + in the serum no faster than 0.5 mEq per hour. With acute hyponatremia (i.e., developing in less than 24 hours), the risk of redistribution of osmotically active substances is significantly less. A more aggressive approach may be used to address clinical signs of cerebral edema in such cases, although rates of correction of hyponatremia greater than 1 mEq/hour and maximum increases in serum Na+ levels of more than 12 mEq over the first 24 hours should be avoided whenever possible.

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 in children

As in adults, G. in children may reflect a general deficiency of sodium in the body (lack of salt intake, loss of salts) or be a consequence of sodium dilution when significant amounts of water are retained in the body. The first type of G. is more common in children with went.-kish. diseases with vomiting and diarrhea, diseases of the adrenal glands and kidneys, uncontrolled use of diuretics, significant losses of sodium through sweat, feeding young children with too diluted formulas or with a long-term salt-free diet in older children. G. in children may also be associated with a disorder of the nervous regulation of water-salt metabolism, especially with organic lesions of c. n. With.

The severity of the wedge, manifestations of G. depends on the pace of its development. Gradual development may be asymptomatic, since the body adapts to the disturbances that have arisen. This type of G. is often found in children with malnutrition. With the rapid development of G., the loss of salt is accompanied by the development of a severe symptom complex - circulatory disorders and climatic disorders. n. With. General weakness, lethargy, decreased muscle tone and muscle twitching are noted. Consciousness is depressed to the point of coma. Exicosis is clearly expressed: the skin is flabby, gray-earthy in color, turgor is reduced, weight loss reaches 10%. Blood pressure is reduced or undetectable, heart sounds are muffled, the pulse is weak and tense, frequent. Along with a decrease in the concentration of sodium in the blood serum, an increase in the content of residual nitrogen is often detected (a manifestation of renal failure and extrarenal hyperazotemia).

The condition of hyponatremia, in which the total amount of sodium in the body remains normal, is observed in cases of “water intoxication”; the development of the cut can be caused by the administration of excessive amounts of water or glucose solution, and in acute renal failure (oliguria or anuria) .

The symptoms of “water intoxication” are in many ways reminiscent of salt depletion: anxiety, general agitation, turning into stupor and coma, severe muscle hypotension, tremors and muscle twitching, tonic-clonic convulsions, collapse. In milder cases, nausea, dizziness, and vomiting are observed. Tissue turgor remains normal, the skin is moist and, unlike salt depletion, there are no signs of dehydration. The blood content of sodium, total protein, and hemoglobin is reduced; intravascular hemolysis is often noted; red blood cells, casts, and protein are found in the urine.

G. against the background of sodium retention in the body, hl is observed. arr. in edematous syndrome, it is caused by dilution of extracellular sodium and develops gradually. Most often, G. dilutions are found in patients with severe circulatory failure, with nephrotic syndrome. The immediate causes of G. in these patients are considered to be a disorder of osmoregulation, long-term treatment with a salt-free diet and diuretic drugs. With repeated abdominal punctures in patients with ascites, there is a risk of depletion of sodium reserves.

Treatment. With the rapid development of G. and significant severity of the general condition, immediate administration of saline solutions is required.
With yellowish intestines. diseases in early childhood, intravenous drip administration of isotonic sodium chloride solution is indicated, up to 100 ml per 1 kg of weight per day. Even with severe sodium deficiency, the total loss of sodium by an infant does not exceed 15 mEq per 1 kg of weight, i.e., the amount contained in 100 ml of isotonic sodium chloride solution.

If dehydration is mild or absent, 5% sodium chloride solution can be used to eliminate G.; it is advisable to calculate the dose based on data on sodium deficiency in the body (ionograms of serum or blood plasma). Elimination of salt depletion is facilitated by the additional introduction of 3-5 g of sodium chloride orally.

With asymptomatic G., forced administration of sodium salts is unacceptable. Restoring the salt balance should be achieved by gradually increasing salts in the diet or introducing an isotonic solution of sodium chloride parenterally from 20 to 50 ml per 1 kg of weight for 10-12 days. In case of “water intoxication”, careful administration of hypertonic solutions of sodium chloride and fluid restriction are indicated.

Attempts to eliminate G. dilution by introducing sodium chloride solution always lead to a deterioration in the general condition of patients, an increase in edema and other manifestations of circulatory failure. Temporary fluid restriction is recommended: the patient receives as much water and liquid food as he excreted in urine over the previous day. Potassium salts have a diuretic effect, so vegetables and fruits, especially those rich in potassium (carrots, potatoes, prunes, raisins), as well as potassium preparations are prescribed. Diuretics are discontinued for the period of G.'s treatment.

ICD-10 CODE

E87.1 Hypoosmolarity and hyponatremia

Which doctors should you contact if you have hyponatremia?

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.

Hyponatremia - sodium concentration< 135 ммоль/л. Это состояние достаточно часто наблюдают у госпитализированных больных. Показано, что примерно у 10-15% стационарных больных хотя бы на некоторое время концентрация натрия в крови падает ниже нормы. У пациентов, находящихся на амбулаторном лечении, гипонатриемия встречается гораздо реже и, как правило, связана с имеющейся хронической патологией.

Causes of hyponatremia

Hyponatremia with low plasma osmolality

Excessive secretion of ADH.

Ectopic ADH secretion, which occurs most commonly in small cell lung cancer, is also possible in many other tumors, including carcinoids, lymphoma, leukemia, and pancreatic cancer.
ADH hypersecretion syndrome, characterized by a decrease in the excretion of ingested fluid and a change in the mode of osmotic regulation (maintaining a stable sodium concentration in the blood serum, but at a lower level). There are many reasons for the development of this syndrome: it can be a consequence of major surgery, lung diseases (for example, pneumonia) and increased intracranial pressure. Idiopathic ADH hypersecretion syndrome often occurs against the background of an insidious malignant tumor, in particular small cell lung cancer.
Cytotoxic drugs prescribed to cancer patients, for example ifosfamide, vincristine, cyclophosphamide, administered intravenously in high doses, can stimulate the secretion of ADH.

Adrenal insufficiency, which develops, for example, after abrupt withdrawal of long-term glucocorticoids, is accompanied by an increase in potassium levels, and in some patients, metabolic acidosis.

Excessive fluid administration during fluid replacement therapy.

Hyponatremia with normal or excessive plasma osmolality (pseudohyponatremia)

This form of hyponatremia develops as a result of hyperglycemia or retention of mannitol administered as a hypertonic solution during chemotherapy. Mannitol causes an increase in plasma osmolality, which leads to the release of intracellular fluid into the vascular space and the development of hyponatremia. Unlike the hypoosmolality state, hyponatremia in this case does not increase the risk of developing cerebral edema, so treatment aimed at correcting serum sodium levels is not indicated.

Sodium loss:

Diuretics (initially).
Renal loss due to immaturity/tubular loss.
Renal tubular acidosis.

"Breeding":

Diuretics (later: due to hyponatremia, diuresis is reduced).
Excessive fluid intake.
Heart failure.
Muscle relaxants (pancuronium).
SIADH against the background of stress, pain, sepsis, pneumonia, meningitis, asphyxia, intracranial hemorrhage, increased intracranial pressure, opiates.
Hypertensive hyponatremia due to hyperglycemia.

Symptoms and signs of hyponatremia

Sodium loss: weight loss, oliguria, decreased tissue turgor, tachycardia.

Breeding: weight gain with development of edema (S1ADH without visible edema). Oliguria (relative to fluid intake), decreased urea and potassium levels.

It is often asymptomatic.

The clinical picture depends on the following factors:

degree of hyponatremia;
pace of development;
age and gender of the patient (the risk is highest in premenopausal women).

Neurological disorders predominate in the clinical picture:

nausea, malaise, weakness;
confusion, headache and drowsiness;
convulsions, coma and respiratory arrest.

Hyponatremia is the most common electrolyte imbalance observed in hospitalized patients. Subacute or chronic mild to moderate hyponatremia is often asymptomatic. However, severe hyponatremia (< 120 мэкв%), особенно развивающаяся быстро, может угрожать жизни больного.

There are hypo-, hyper- and normovolemic hyponatremia. Hypovolemic hyponatremia is associated with a decrease in circulating blood volume. When intravascular volume decreases by more than 9%, a non-osmotic stimulus to antidiuretic hormone (ADH) secretion occurs, reflecting the body's attempt to retain water and thereby maintain intravascular volume. This type of hyponatremia develops with prolonged vomiting and diarrhea or increased sweating, especially if fluid losses are replaced with water or hypotonic solutions. A decrease in circulating blood volume and hyponatremia may also be a consequence of renal sodium loss (with the administration of diuretics, mineralocorticoid deficiency, or other salt-wasting syndromes). The concentration of Na + in the urine in such cases is usually increased (> 20 mEq/L), while with a compensatory increase in ADH secretion, the reabsorption of Na + in all segments of the nephron increases, which leads to a decrease in the concentration of Na + in the urine.

Hypervolemic hyponatremia accompanies edematous conditions in which paradoxical water retention occurs, despite its general excess in the body. Specific causes of this type of hyponatremia are congestive heart failure, liver cirrhosis with ascites, and nephrotic syndrome. Hyponatremia in such cases is apparently due to the effect of reduced blood flow on the baroreceptors of the arterial bed. Information about this is transmitted along nerves to the hypothalamus, stimulating the secretion of ADH and water retention.

The most heterogeneous group is probably normovolemic hyponatremia, the pathogenesis of which is more difficult to explain. This group includes syndrome of inappropriate ADH secretion (SIADH), hypothyroidism, glucocorticoid deficiency (eg, secondary adrenal insufficiency), neural polydipsia, and hyponatremia developing after transurethral resection of the prostate.

Diagnosis of hyponatremia

Osmolality of blood plasma and urine (urine osmolality exceeds blood plasma osmolality).

Acute hyponatremia (onset in 24 hours or less) causes headache, nausea, vomiting, drowsiness, restlessness, seizures, and disturbances in perception of reality that may progress to stupor and coma. It is believed that the basis of these manifestations is cerebral edema, caused by the movement of hypotonic extracellular fluid into the cells of the cerebral cortex. This movement is initially counteracted by a decrease in the intracellular concentration of electrolytes and later by other solutes (eg, amino acids), which reduces the osmotic gradient and limits the flow of fluid into the brain. Over time, due to this mechanism, the water content in brain cells in chronic hyponatremia is restored to almost normal. Thus, the severity of the patient's condition depends on the rate and degree of decrease in the concentration of Na + in the serum. Severe consequences of cerebral edema are especially often observed in the postoperative period in young women with preserved menstrual function. Mortality and irreversible brain damage occur 25 times more often in this population than in postmenopausal women or men. Estrogen and progesterone appear to promote the accumulation of solutes in the cells of the central nervous system, which increases the osmotic gradient and the movement of water into the brain.
During diagnosis, it is first necessary to exclude pseudohyponatremia caused by high concentrations of triglycerides or osmotically active compounds (glucose or proteins) in plasma. Hypertriglyceridemia reduces sodium levels in the aqueous phase of plasma, although sodium levels in whole plasma may remain normal. This is easily detected by the milky appearance of the whey, and centrifugation of the sample before determining the Na + concentration in the aqueous phase avoids error. Osmotically active substances (for example, glucose) cause the movement of water from the intracellular space to the extracellular space, due to which the concentration of electrolytes (for example, Na +) in the serum may be temporarily reduced.

Having convinced of the truth of hyponatremia, we begin to find out its causes. Signs of congestive heart failure, liver cirrhosis, or nephrotic syndrome are usually detected upon examination of patients and are confirmed by the results of standard laboratory and imaging studies. With the help of routine studies, renal dysfunction is also excluded. A common cause of hyponatremia is the use of thiazide diuretics and this should be checked early. To exclude primary polydipsia, the patient is interviewed in detail and his fluid intake is measured. Hypothyroidism is excluded by determining serum levels of TSH and FT4, and glucocorticoid deficiency by using an ACTH stimulation test.

SIADH is characterized by non-osmotic and non-volume stimulation of ADH secretion. The diagnosis of this syndrome is made by exclusion in patients in the absence of hypovolemia, edema, renal or adrenal insufficiency, or hypothyroidism. Serum Na + levels and osmolality are reduced due to the excretion of concentrated urine. Urinary Na + levels are moderately elevated (> 20 mEq/L), reflecting activation of natriuresis in response to a general increase in body fluids. To confirm the diagnosis, you can use a water load test [with SIADH, patients excrete less than 90% of the ingested amount of water (20 ml/kg) within 4 hours or urine osmolality does not fall below 100 mOsm/kg]. SIADH develops in many diseases of the central nervous system (encephalitis, multiple sclerosis, meningitis, psychosis) and lungs (tuberculosis, pneumonia, aspergillosis), as well as in some solid tumors (small cell lung cancer, pancreatic, bladder or prostate cancer). This syndrome also occurs under the influence of certain medicinal compounds (cyclophosphamide, plant alkaloids, opiates, prostaglandin synthesis inhibitors, tricyclic antidepressants, carbamazepine, clofibrate and serotonin reuptake inhibitors).

Sometimes SIADH is difficult to distinguish from cerebral salt-wasting syndrome, which can also accompany central nervous system pathology, especially subarachnoid hemorrhage. It is believed that it is caused by a violation of the central mechanisms of regulation of sodium metabolism in the kidneys. Increased renal sodium loss leads to hypovolemia, stimulation of ADH secretion and hyponatremia. The main role in the mechanism of natriuresis in cerebral salt-losing syndrome is assigned to atrial or brain natriuretic peptide. SIADH and cerebral salt-wasting syndrome differ mainly in the volume of circulating blood. This is important to keep in mind because cerebral salt-wasting syndrome requires intravascular volume replacement, whereas SIADH therapy requires fluid restriction.

Treatment of hyponatremia

Weight loss: introduction of sodium (and fluid), reduction of losses.

Weight gain: limit fluid intake, sodium concentration should exceed 125 mmol/l.

Sodium Replacement Calculation: previous amount of sodium administered + absolute deficit relative to normal + ongoing losses.

If it is possible to determine the primary stimulus for increased water consumption (for example, nervous polydipsia) or for its retention in the body (for example, taking diuretics), then treatment is reduced to eliminating the original cause.

If the cause of hyponatremia remains unclear or unspecific (as in SIADH), then therapy is more general. For asymptomatic (mild or chronic) hyponatremia, simply limit water intake. In this case, it is necessary to calculate its daily consumption, including the water contained in dense foods. If the patient cannot or does not want to limit water intake, then the desired level of Na + in the serum can be maintained with the help of demeclocycline (600-1200 mg/day in fractional doses); this antibiotic interferes with the action of ADH on receptors. Restriction of water consumption during treatment with demeclocycline is not required. Moreover, it can even be dangerous. Such therapy requires careful monitoring of the patient to prevent dehydration and the development of renal failure. Another treatment approach may be to regularly take a loop diuretic (eg, furosemide), which eliminates the osmotic gradient that causes concentrated urine. Loop diuretics should be used concomitantly with NaCl supplements (2-3 g/day) to increase urinary solute excretion and thereby increase water loss.

For relatively mild symptoms of hyponatremia, the vasopressin receptor antagonist conivaptan (vaprizole) can be used. It is administered intravenously at a dose of 20 mg, then continuing the infusion at a rate of 20 mg/day for 1-3 days. If the serum sodium level does not rise sufficiently, the infusion rate can be increased to 40 mg/day. At the same time, moderate fluid restriction is recommended.

Treatment aimed at eliminating the causes of hyponatremia also requires caution. For example, rapid correction of hyponatremia by administration of glucocorticoids in adrenal insufficiency can cause central myelinolysis. If serum Na + levels rise too rapidly (> 1 mEq/hour), administration of a hypotonic solution or parenteral administration of 0.25-1 mcg of desmopressin acetate may be indicated.

It is often enough to limit fluid intake to 0.5-1 l/day, i.e. to a level below daily diuresis.

Suppression of the effect of ADH on the renal tubules, for example by prescribing demeclocycline, is advisable only in selected patients with severe persistent hyponatremia who are unable to limit fluid intake; monitoring of renal function is necessary.

Infusion of hypertonic (3%) sodium chloride solution is indicated only in cases where hyponatremia poses a threat to the patient's life. Such free individuals should be administered a hypertonic solution under the supervision of an experienced physician or specialist in the correction of metabolic disorders. Too rapid infusion is undesirable, especially in chronic hyponatremia. It is not recommended for most patients with a tumor, since the regulation of sodium content in ADH hypersecretion syndrome is not impaired, so the injected sodium will simply be excreted in the urine as long as the osmolarity of the injected solution exceeds the osmolality of the urine.

Complications of hyponatremia

Both animal experiments and observations in humans provide convincing evidence that this syndrome is associated with aggressive correction of hyponatremia. Given the lack of understanding about the pathogenesis of central myelinolysis, it is advisable to approach with caution the correction of chronic hyponatremia in patients with obvious changes in water content and distribution of solutes in the brain, increasing the level of Na + in the serum no faster than 0.5 mEq per hour. With acute hyponatremia (i.e., developing in less than 24 hours), the risk of redistribution of osmotically active substances is significantly less. A more aggressive approach may be used to address clinical signs of cerebral edema in such cases, although rates of correction of hyponatremia greater than 1 mEq/hour and maximum increases in serum Na+ levels of greater than 12 mEq in the first 24 hours should be avoided whenever possible.

General information

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.

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 polydipsia or 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), with cystic fibrosis, skin inflammation or burns, as a result of loss through sweat due to overheating, with massive bleeding, paracentesis (piercing the eardrum), sequestration blood in case of extensive injuries of the extremities, 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 a level of 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 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 the symptoms of hypovolemia are eliminated. 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.

liqmed.ru

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

Hypervolemic hyponatremia

Normovolemic hyponatremia

Hyponatremia in AIDS

ilive.com.ua
Do you know that:

In order to say even the shortest and simplest words, we use 72 muscles.

The highest body temperature was recorded in Willie Jones (USA), who was admitted to the hospital with a temperature of 46.5°C.

You are more likely to break your neck if you fall off a donkey than if you fall off a horse. Just don't try to refute this statement.

People who eat breakfast regularly are much less likely to be obese.

According to statistics, on Mondays the risk of back injuries increases by 25%, and the risk of a heart attack by 33%. Be careful.

Even if a person's heart does not beat, he can still live for a long period of time, as the Norwegian fisherman Jan Revsdal demonstrated to us. His “engine” stopped for 4 hours after a fisherman got lost and fell asleep in the snow.

Dentists appeared relatively recently. Back in the 19th century, pulling out diseased teeth was the responsibility of an ordinary hairdresser.

There are very interesting medical syndromes, for example, compulsive swallowing of objects. One patient suffering from this mania had 2,500 foreign objects in her stomach.

Four pieces of dark chocolate contain about two hundred calories. So if you don’t want to gain weight, it’s better not to eat more than two slices a day.

In an effort to get the patient out, doctors often go too far. For example, a certain Charles Jensen in the period from 1954 to 1994. survived more than 900 operations to remove tumors.

Most women are able to derive more pleasure from contemplating their beautiful body in the mirror than from sex. So, women, strive to be slim.

The human stomach copes well with foreign objects without medical intervention. It is known that gastric juice can even dissolve coins.

An educated person is less susceptible to brain diseases. Intellectual activity promotes the formation of additional tissue that compensates for the disease.

The liver is the heaviest organ in our body. Its average weight is 1.5 kg.

Human blood “runs” through the vessels under enormous pressure and, if their integrity is violated, it can shoot at a distance of up to 10 meters.

www.neboleeem.net

Hyponatremia - what is it? This is a condition in which the amount of sodium in the body decreases. Most often, this problem occurs when using diuretics, after receiving severe burns, or intestinal disorders. If you do not begin to eliminate this problem, you may experience severe headaches, visual hallucinations, and possible death. The body must receive enough sodium. Even if the deficiency of this element is quickly eliminated, there remains a high probability of developing neurological complications.

Causes and symptoms of the pathological condition

The causes of hyponatremia are associated with pathological processes that are accompanied by:

diluting the blood with plenty of water. This situation occurs when there is disproportionate production of antidiuretic hormone;
redistribution of the element between fluids inside and outside cells. This happens when hypoxia develops or if a person uses Digitalis for a long time;
loss of sodium by the kidneys and liver, when less sodium enters the body than is excreted.

The amount of sodium in the blood may decrease for the following reasons:

Extrarenal. If problems arise in the functioning of the gastrointestinal tract, which are accompanied by vomiting, diarrhea, as well as inflammatory processes on the skin and burns. Sodium deficiency can also occur with increased sweating, bleeding, or puncture of the eardrum.
Renal. In this case, increased excretion in the urine can reduce the content of this substance. When diagnosed with hyponatremia, its causes are nephropathies, neuritis, lack of mineralocorticoids, and use of diuretics.

The amount of sodium in the blood may decrease to a point where there is increased production of antidiuretic hormone. These include severe stress, pain, and use of opioids in the postoperative period. If sodium in the blood is low, the patient’s health worsens. Typically, a person experiences neurological signs of pathology due to a decrease in the tone of intracellular fluid and diffusion of water into brain cells. Because of this, the cells swell and the functioning of the central nervous system is disrupted.

Depending on the type, stage of development of the disease, condition and age of the patient, the following symptoms of hyponatremia occur:

Strong headache;
nausea;
disturbances of consciousness, fainting, high probability of developing a coma.

If there is a decrease in this substance inside the cells, cerebral edema may develop. If the amount of sodium in the blood is reduced, treatment must be started urgently, as the risk of developing serious, life-threatening complications increases.

If hyponatremia occurs in a chronic form, then muscle tone decreases, the skin becomes less elastic, the person suffers from neuropsychiatric disorders, and blood pressure decreases. With sodium deficiency, the heart rate increases and the patient quickly loses weight. When diagnosed with hyponatremia, some patients do not feel its symptoms at all.

Diagnosis and treatment of hyponatremia

Lack of sodium in the body is determined in the following ways:

Conduct an initial examination and study the patient's medical history.
Laboratory tests are prescribed to determine the content of electrolytes in the blood serum. If sodium is less than 135 mEq/L, hyponatremia is diagnosed.
Conduct a water load test.
To exclude adrenal insufficiency and hypothyroidism, the level of cortisol in the body is determined.
If brain disease is suspected, magnetic resonance imaging should be performed.

Low sodium in the blood must be treated. If it is possible to find out the cause of this phenomenon, then therapy is aimed at eliminating it. If it is not possible to find out why the disease occurred, general treatment is prescribed. It looks like this:

If there are no symptoms of illness, simply limit fluid intake. It is necessary not only to count how much water you drink per day, but also to take into account how much of it is contained in food. If it is not possible to limit water consumption, then try to maintain the required amount of sodium with the help of Demeclocycline. This is an antibacterial drug that reduces the effect of antidiuretic hormone. The patient should be closely monitored while using this drug, otherwise dehydration or kidney failure may occur.
If a person has hyponatremia, treatment can be done with loop diuretics. They reduce sodium excretion with water.
In critical situations, infusion of hypertonic sodium chloride solution is indicated. This should only be done by a doctor in a hospital setting.

Complications of the disease

If sodium is low and therapy is carried out too quickly, the following complications may develop:

Osmotic demyelination syndrome or pontine myelinolysis. The first complication leads to the development of lesions in other areas of the brain. This problem usually develops in alcoholics, during conscious (dieting) or forced fasting, as well as in the presence of chronic pathologies.
Peripheral paralysis may develop.
As the lesions spread, pseudocoma develops. This diagnosis is characterized by the fact that a person can only move his eyeballs.

Neurological symptoms may occur if sodium levels rise too quickly. If this happens, then you need to stop administering hypertonic solutions to prevent an increase in this element in the blood. If this is done in time, it will be possible to avoid possible neurological damage. To avoid the development of the disease, it is necessary to monitor your drinking ration and not drink more than the recommended amount of water per day. It is also necessary to eat properly; the body must receive sufficient quantities of all vitamins and microelements. It is also useful to play sports.

Hyponatremia is a fairly common pathology. This electrolyte disturbance occurs in approximately 20% of patients hospitalized in critical condition in intensive care. In patients treated on an outpatient basis, pathology occurs much less frequently - in only 5-7% of cases.

Sodium is the most important cation that ensures the functioning of body cells, including muscle and nerve cells. When sodium is low, the excitability of neurons and the rate of wave formation in the nervous system decreases. The tone of muscles, myocardium and blood vessels decreases.

With hyponatremia, the sodium concentration in the blood is below 135 mmol/l. Sodium is a macroelement on which the acid-base balance and stability of plasma osmotic pressure depend. Hyponatremia causes the plasma to become oversaturated with dissolved particles (hypoosmolarity). The fluid located in the intercellular space is directed into the cells. As a result, swelling appears. The cells swell and cannot function normally. The volume of circulating blood depends on the cause of the pathology.

Attention!

For the same disease, the presence of hyponatremia increases the likelihood of death from 10 to 30%.

Types and forms

Doctors classify hyponatremia according to several criteria. Depending on the mechanism of development of the pathology, its severity and other parameters, treatment is prescribed.

According to the mechanism of development, the following types of hyponatremia are distinguished:

Hypovolemic. Appears after loss of Na and water. This type of pathology occurs after diarrhea, vomiting and other conditions that cause sodium imbalance.
Hypervolemic. With this type of pathology, the content of Na and water in the body increases. Appears in conditions that cause swelling - liver cirrhosis, heart failure and others.
Isovolemic. It is characterized by a normal concentration of Na ions and an increased water content. It is observed in diseases and conditions that arise from stress and taking a number of medications.

There are three forms of hyponatremia based on severity:

Easy. Biochemical analysis of Na concentration shows 130-135 mmol/l.
Medium-heavy. The concentration level is 125-129 mmol/l.
Heavy. Na concentration – up to 125 mmol/l.

By duration:

acute – started 0-48 hours ago;
chronic – lasting more than 48 hours.

If it is impossible to determine the duration of the pathology, the case is classified as chronic.

According to symptoms:

moderately expressed;
heavy.

Etiology (causes)

A decrease in plasma sodium concentration can develop not only due to life-threatening painful conditions, but also for physiological reasons.

Physiological factors:

avoiding salt consumption and drinking plenty of water;
prolonged intense sweating - this situation is usually observed in athletes and people working in extreme heat.

Pathological factors:

Fluid retention. Occurs in renal failure - acute or chronic, as well as in liver cirrhosis. An imbalance can develop as a result of lung diseases, oncology and endocrine pathologies.
Large sodium losses. They occur with prolonged or chronic diarrhea, with prolonged vomiting and nephropathy, in which the process of sodium reabsorption is disrupted. This pathology is observed in nephritis and polycystic kidney disease.
Endocrine pathologies. Lack of hormones in adrenal insufficiency leads to impaired absorption of Na ions in the renal canals. This can occur with severe hyperglycemia, characteristic of decompensated diabetes mellitus.
Use of medications. Pathology can be caused by diuretics used in emergency situations. They are given to patients to relieve severe conditions. The use of hypoglycemic and psychotropic drugs can also provoke the problem.
Drink plenty of fluids. Drinking large amounts of regular (non-mineral) water. This situation is observed in diabetes – diabetes mellitus and diabetes insipidus.

Sodium losses can be:

Extrarenal. Associated with disruption of the gastrointestinal tract and its pathologies (pancreatitis, peritonitis, diarrhea, vomiting).
Renal. Sodium is excreted in the urine. Pathology occurs when using diuretics, renal failure, etc.

Attention!

An imbalance of sodium in the blood serum can provoke pancreatitis, peritonitis, massive burns, and surgical operations.

Symptoms

The symptoms are neurological in nature, since when Na concentration decreases, fluid penetrates into the brain cells. This situation leads to brain swelling and dysfunction of the central nervous system.

With hyponatremia, symptoms depend on the speed of development of the pathological process and its severity:

With a mild form of pathology, there are no serious damage to the central nervous system. Slight drowsiness and disturbances in the vestibular apparatus may occur.
In severe cases, the patient reacts poorly to external stimuli. An epileptiform seizure is possible.

Pathology may be accompanied by symptoms:

decreased vascular tone;
deterioration of myocardial contractile function;
muscle weakness;
signs of hypotension (rapid heartbeat, dizziness, fainting);
dry skin and mucous membranes;
headache.

Less commonly observed is a decrease in diuresis and gastrointestinal upset, expressed in nausea and lack of appetite. With acute hyponatremia, the patient may fall into a coma, the risk of death in this case is very high.

Diagnostics

Patients diagnosed with hyponatremia are jointly observed by a resuscitator and a specialized specialist - a nephrologist or endocrinologist.

Diagnostic procedure and features:

Study of anamnesis. The doctor finds out the probable cause of the pathological condition. Conclusions are drawn based on anamnestic data. To determine the type of pathology, signs of dehydration are identified - this could be dry skin, decreased diuresis, or hypotensive symptoms.
Identification of concomitant diseases. During the examination, the doctor pays attention to external signs - swelling in the face and legs, an enlarged and tense abdomen, dilated saphenous veins on the anterior wall of the abdomen.
Laboratory diagnostics. The concentration of electrolytes in the serum is determined.
Testing. A water load test is carried out, which determines their performance - the ability to excrete (remove) water.

The patient is prescribed laboratory tests:

determine the osmolarity of blood serum (the total concentration of all dissolved particles) and the concentration of electrolytes - calcium, potassium and magnesium;
carry out a biochemical blood test - determine the amount of glucose, enzymes, urea, creatinine;
determine the amount of thyroid and adrenal hormones;
the specific gravity and osmolarity of urine, the concentration of sodium, glucose and ketone particles in it are measured;
For hypothyroidism, cortisol levels are checked.

Instrumental studies are also prescribed:

CVP (central venous pressure) is measured - this is the most accurate way to determine the type of hyponatremia. Find out what type of pathology is present.
Chest X-ray. It is performed if there is a suspicion that the patient has pulmonary edema.
CT scan of the brain. It is carried out only if cerebral edema is suspected.

It is important to differentiate cerebral edema from hypernatremia, since the pathologies are accompanied by almost similar symptoms. It is important to distinguish cerebral edema that occurs during hyponatremia from edema caused by a hypertensive crisis, traumatic brain injury, or other etiology.

Treatment

In most cases, patients with hyponatremia are sent to the intensive care unit. The first step is to stop taking medications that could provoke the pathology. Also stop administering hypotonic solutions.

On a note!

When treating hyponatremia, patients may be prescribed the use of simple table salt. In mild forms of pathology, this measure alone may be sufficient to solve the problem.

Patients with moderate to severe forms are prescribed the following treatment:

Limit fluid intake. This is the main requirement in the treatment of hypervolemic pathology. Daily fluid intake should be limited to 1000 ml.
Saline solutions are administered. Infusion therapy is carried out using a 0.9% NaCl solution. This allows you to eliminate sodium deficiency. At the same time, they replenish the lack of other electrolytes. If neurological symptoms occur, 3% NaCl is administered.
Diuretics are prescribed. Excess fluid is removed from the body in the hypervolemic form of hyponatremia. Patients take diuretics. Diuretic thiazide drugs for hyponatremia are strictly prohibited, as they aggravate the pathology.
Arrange an ADH blockade. If increased secretion of antidiuretic hormone is observed, measures are taken to suppress its action. The use of inhibitors to block ADH is strictly contraindicated in patients with renal disease.

Since hypernatremia threatens the patient’s life, sodium concentration is first corrected. And only when the symptoms that threaten cerebral edema are eliminated, do they begin to treat the disease that caused the pathology.

Treatment of diseases that can provoke hypernatremia:

Chronic heart failure. ACE inhibitors, diuretics and other drugs necessary for CHF are prescribed.
Cirrhosis of the liver. Albumin is administered and fresh frozen plasma is transfused. There is a strict ban on alcoholic beverages.
Endocrine disorders. Hormone replacement therapy is prescribed. The recommended drug for adrenal insufficiency is hydrocortisone.
Chronic renal failure. Hemodialysis is performed.

Lack of sodium in the blood when treating a patient in a hospital is a reflection of the severity of the underlying disease. The appearance of hyponatremia indicates the severity of the patient's condition and a high probability of death.

Consequences and complications

The syndrome, in which Na concentration decreases, can be accompanied by a variety of complications. A greater number of consequences are caused by damage to the central nervous system.

Possible complications:

edema of the brain, less often of the lungs;
infarction of the pituitary gland or hypothalamus;
meningitis;
encephalitis;
thrombosis of cerebral vessels;
hernial protrusion of the brain stem.

Prevention and prognosis

Severe hyponatremia has a very poor prognosis. At a sodium concentration of 125 mmol/l, mortality reaches 25%, and at levels below 115 mmol/l – 50%. According to other statistics, the mortality rate of the pathology is 65%.

The main causes of death when sodium concentration decreases are cerebral edema and coma. With timely treatment, the prognosis is more favorable - it is possible to correct Na levels, eliminate life-threatening symptoms, and prevent complications.

Prevention:

timely treatment of diseases that can provoke hypernatremia;
regular monitoring of plasma sodium levels.

Attention!

To prevent the development of hypernatremia, it is unacceptable to exceed the daily water intake

A decrease in sodium levels in the blood is a dangerous condition that can quickly lead to death. To prescribe effective treatment, it is necessary to carry out an accurate diagnosis, which allows not only to differentiate the pathology from diseases with similar symptoms, but also to determine the type of hypernatremia.

Hyponatremia, causes of the disease. Hyponatremia symptoms Therapeutic approaches for a hypoosmotic state and hyponatremia in a patient

Causes

Kinds

Signs

Diagnostics

Treatment

Prevention

Consequences and complications

Causes of hyponatremia

Hyponatremia with low plasma osmolality

Hyponatremia with normal or excessive plasma osmolality (pseudohyponatremia)

Symptoms and signs of hyponatremia

Diagnosis of hyponatremia

Treatment of hyponatremia

Complications of hyponatremia

Hypovolemic hyponatremia

Hypervolemic hyponatremia

Normovolemic hyponatremia

Hyponatremia in AIDS

Types and forms

Etiology (causes)

Symptoms

Diagnostics

Treatment

Consequences and complications

Prevention and prognosis

We are in social networks

Categories