Hyponatremia: what is it, forms, causes, symptoms and treatment. Hyponatremia Hyponatremia dilution

Symptoms, risk factors

The change is easier to diagnose in acute forms. The chronic course proceeds with mild symptoms.
Without a clinical examination, the pathology can be diagnosed in doubt if the patient has signs of damage to the central nervous system. Dysfunction occurs due to edema, which occurs when the tone of the extracellular fluid falls, intracellular redistribution of water occurs. It has been practically determined that the presence of an element below the limit of 125 mEq/l leads to CNS failures in just a few hours. The patient appears lethargic, may develop epilepsy, even coma.
Important: Without treatment, this condition threatens lethal outcome.
A clinical urinalysis will confirm the decrease in the substance.
The main risk factors are: large, completely excessive for the body, water consumption, uncontrolled diets by specialists, kidney diseases.

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

Excess secretion of ADH.

• Ectopic secretion of ADH, most commonly seen 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 the fluid taken and a change in the osmotic regulation regime (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 the result of a major operation, lung diseases (for example, pneumonia) and increased intracranial pressure. The idiopathic syndrome of ADH hypersecretion often manifests itself against the background of an insidious malignant tumor, in particular small cell lung cancer.
• Cytotoxic drugs administered to cancer patients, such as ifosfamide, vincristine, and cyclophosphamide, administered intravenously in high doses, can stimulate the secretion of ADH.

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

Excessive administration of fluid during replacement infusion therapy.

Hyponatremia with normal or excessive plasma osmolality (pseudohyponatremia)

This form of hyponatremia develops as a result of hyperglycemia or a delay in 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. In contrast to the state of hypoosmolality, hyponatremia in this case does not increase the risk of developing cerebral edema, therefore, treatment aimed at correcting the content of sodium in the blood serum is not indicated.

Sodium loss:

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

"Breeding":

• Diuretics (later: against the background of hyponatremia, diuresis is reduced).
• Excess fluid intake.
• Heart failure.
• Muscle relaxants (pancuronium).
• SIADH on 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, reduced tissue turgor, tachycardia.

Breeding: weight gain with edema development (S1ADH without visible edema). Oliguria (relative to the intake of fluid), a decrease in the content of urea and potassium.

Often asymptomatic.

The clinical picture depends on the following factors:

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

Neurological disorders prevail in the clinical picture:

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

Hyponatremia is the most common electrolyte disturbance seen 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. With a decrease in intravascular volume by more than 9%, a non-osmotic stimulus to the secretion of antidiuretic hormone (ADH) occurs, reflecting the body's attempt to retain water and, thereby, maintain intravascular volume. Hyponatremia of this type develops with prolonged vomiting and diarrhea or increased sweating, especially if fluid loss is replenished with water or hypotonic solutions. A decrease in circulating blood volume and hyponatremia can also be a consequence of renal sodium loss (with the introduction of diuretics, mineralocorticoid deficiency, or other salt-wasting syndromes). The concentration of Na + in the urine in such cases, as a rule, is increased (> 20 mEq / l), while with a compensatory increase in secretion of ADH, 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 there is a paradoxical water retention, despite its general excess in the body. Specific causes of this type of hyponatremia are congestive heart failure, cirrhosis of the liver 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 sent along the 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 the syndrome of inappropriate secretion of ADH (SIADH), hypothyroidism, glucocorticoid deficiency (for example, in secondary adrenal insufficiency), nervous polydipsia, and hyponatremia that develops after transurethral resection of the prostate.

Diagnosis of hyponatremia

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

Acute hyponatremia (developing in 24 hours or less) presents with headache, nausea, vomiting, drowsiness, restlessness, seizures, and impaired perception of reality that may progress to stupor and coma. It is believed that these manifestations are based on cerebral edema due to the movement of hypotonic extracellular fluid into the cells of the cerebral cortex. Such a movement is initially counteracted by a decrease in the intracellular concentration of electrolytes, and later by other solutes (for example, 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 the brain cells in chronic hyponatremia is restored almost to normal. Thus, the severity of the patient's condition depends on the rate and degree of decrease in the concentration of Na + in 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 among this group of patients occur 25 times more often than in postmenopausal women or men. Apparently, estrogens and progesterone promote the accumulation of solutes in the cells of the CNS, which increases the osmotic gradient and the movement of water into the brain.
During the diagnosis, it is first of all necessary to exclude pseudohyponatremia due to a high concentration of triglycerides or osmotically active compounds (glucose or proteins) in plasma. Hypertriglyceridemia reduces the level of sodium in the aqueous phase of plasma, although its content in whole plasma may remain normal. This is easily detected by the milky appearance of whey, and centrifugation of the sample before determining the concentration of Na + 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.

Convinced of the truth of hyponatremia, proceed to clarify its causes. Signs of congestive heart failure, cirrhosis, or nephrotic syndrome are usually detected on examination and are confirmed by routine laboratory and imaging studies. With the help of conventional studies, impaired renal function is also excluded. Thiazide diuretics are a common cause of hyponatremia and should be checked early. To exclude primary polydipsia, the patient is interviewed in detail and his fluid intake is measured. Hypothyroidism is ruled out by determining the levels of TSH and fT 4 in serum, and glucocorticoid deficiency - using a stimulation test with ACTH.

SIADH is characterized by non-osmotic and non-volumetric stimulation of ADH secretion. The syndrome is diagnosed by exclusion in patients in the absence of hypovolemia, edema, renal or adrenal insufficiency, or hypothyroidism. The level of Na + in serum and its osmolality are reduced against the background of excretion of concentrated urine. Urinary Na + is moderately elevated (> 20 mEq/L), reflecting the activation of natriuresis in response to a general increase in body fluids. A water load test can be used to confirm the diagnosis [in SIADH, patients excrete less than 90% of the amount of water taken (20 ml/kg) in 4 hours or urine osmolality does not fall below 100 mosm/kg]. SSIADH develops in many diseases of the central nervous system (encephalitis, multiple sclerosis, meningitis, psychoses) and lungs (tuberculosis, pneumonia, aspergillosis), as well as in some solid tumors (small cell lung cancer, pancreatic cancer, 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 SSIADH is difficult to distinguish from cerebral salt wasting syndrome, which can also accompany CNS pathology, especially subarachnoid hemorrhage. It is believed that it is due to 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 the atrial or cerebral natriuretic peptide. SIADH and brain 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 replenishment, while SIADH therapy requires fluid restriction.

Treatment of hyponatremia

Weight loss: the introduction of sodium (and liquid), reducing losses.

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

Sodium reimbursement calculation: previous amount of sodium administered + absolute deficiency relative to normal + ongoing losses.

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

If the cause of hyponatremia remains unclear or non-specific (as in SIADH), then therapy is more general. With asymptomatic (mild or chronic) hyponatremia, water intake is simply limited. At the same time, it is necessary to calculate its daily consumption, including the water that is contained in solid foods. If the patient is unable or unwilling to restrict water intake, the desired serum Na + level can be maintained with demeclocycline (600-1200 mg/day in divided doses); this antibiotic interferes with the action of ADH on receptors. Restrictions on water intake during treatment with demeclocycline are not required. Moreover, it can even be dangerous. Such therapy requires careful monitoring of the patient in order to prevent dehydration and the development of renal failure. Another treatment approach may be regular loop diuretics (eg, furosemide), which reverse the osmotic gradient that produces concentrated urine. Loop diuretics should be used concomitantly with NaCl supplementation (2-3 g/day) to increase urinary excretion of solutes and thereby increase water loss.

For relatively mild symptoms of hyponatremia, the vasopressin receptor antagonist conivaptan (vaprizol) 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. With insufficient increase in serum sodium levels, 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 administering glucocorticoids in adrenal insufficiency can induce central myelinolysis. If the serum Na + level rises too rapidly (> 1 meq/hour), hypotonic saline or parenteral administration of 0.25-1 µg of desmopressin acetate may be indicated.

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

Suppression of the action of ADH on the renal tubules, for example, by the appointment of 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 administration of hypertonic saline should be done under the supervision of an experienced physician or a specialist in the correction of metabolic disorders. Too rapid infusion is undesirable, especially in chronic hyponatremia. It is not indicated for most patients with a tumor, since the regulation of the sodium content in the syndrome of hypersecretion of ADH is not impaired, therefore, 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

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. In subsequent observations, the association of central pontine myelinolysis with the treatment of hyponatremia was established. With aggressive therapy of hyponatremia, aimed at eliminating cerebral edema, patients may develop mutism, dysphasia, spastic tetraparesis, pseudobulbar palsy and delirium. Survivors often have severe neurologic deficits. Using CT and MRI, it has been shown that myelinolysis extends beyond the pons, and in typical cases, areas of the brain at the border between gray and white matter are symmetrically affected.

Both animal experiments and human observations strongly suggest an association of this syndrome with aggressive correction of hyponatremia. Given the lack of understanding of the pathogenesis of central myelinolysis, it is advisable to be cautious in correcting chronic hyponatremia in patients with a clear change in the water content and distribution of dissolved substances in the brain, increasing the level of Na + in serum no faster than 0.5 meq per hour. In acute hyponatremia (i.e., developed in less than 24 hours), the risk of redistribution of osmotically active substances is significantly less. A more aggressive approach can be used to address the clinical signs of cerebral edema in such cases, although in any case, hyponatremia correction rates greater than 1 mEq/hour and a maximum increase in serum Na+ levels greater than 12 mEq in the first 24 hours should be avoided whenever possible.

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Hyponatremia - a decrease in the blood of a very significant chemical element - which in the body is concentrated mainly outside the cells, and therefore is considered the main extracellular cation - Na +. Why is it called "basic" and why is there so much attention to sodium?

Anyone who had to “sit” on a salt-free diet for some time can tell about how difficult it is for us without salt, because in such cases the food becomes insipid and tasteless. However, salt (NaCl) does more than just improve the taste of food. The chemical elements (Na + and Cl-) supplied with food immediately begin their functional duties in a living organism. Sodium, which is part of table salt, provides many processes of its vital activity.

Every day a person consumes up to 10-12 grams of salt as part of his diet. Meanwhile, many physiologists are inclined to think that this amount is unnecessary, since it leads to the development of such a common disease as, which has become the scourge of our time. However, we must not forget the fact that sodium easily leaves the body with sweat and urine, therefore, under conditions of intense physical exertion or elevated ambient temperatures, there may be a loss of the element, which will cause hyponatremia.

Sodium drops - disaster?

Sodium is concentrated predominantly extracellularly, thanks to the Na/K-pump, which stabilizes the content of potassium (K+) inside the cell, keeping it (K+) at a high level. This occurs due to pumping out sodium cations from it and transferring them to the extracellular space, thereby creating a low concentration of Na + in the cell (less than 10%). The activity of the Na / K-pump, aimed at equalizing the concentrations of sodium and potassium: Na + (extracellular) \u003d K + (intracellular) - the reaction is complex and multi-stage, it makes no sense to dwell on its detailed description in this topic.

The norm of sodium in the body is from 130 to 150 mmol / l (in other sources it can be somewhat narrowed: from 135 to 145 mmol / l).

So what will happen if sodium suddenly becomes scarce and the body's needs are not satisfied? In a scientific way: hyponatremia will develop - a condition caused by a deficiency of this chemical element, but in a simple way: urine output will increase, along with which water will begin to leave the body. At the same time, it should be noted that the state of hyponatremia is by no means easy, it is dangerous not only because many functions of the body are largely impaired, this disorder can lead to death.

Causes of sodium deficiency

The reasons for the development of a pathological condition due to a decrease in the concentration of Na + - hyponatremia, are mainly associated with other problems, sometimes nutritional:

• Insufficient content of this chemical element in the diet, and, consequently, its low intake into the body - this happens with diseases of the gastrointestinal tract (gastrointestinal tract) or with the now fashionable syndrome with an eating disorder called anorexia;
• Large loss through the skin (frequent significant sweating, burn disease), as well as in the urine (with unreasonable intake);
• Enhanced excretion through the excretory system in case of kidney pathology or a violation (decrease) in the function of the adrenal cortex;
• Dehydration with simultaneous sodium loss with diarrhea and repeated vomiting, fluid withdrawal with hydrothorax (thoracic dropsy - accumulation of fluid in the pleural cavity) and ascites.

It should be noted that the intake and content of sodium is quite normal (or even somewhat elevated), but there are signs of hyponatremia. This occurs in cases of heart failure or damage to the liver parenchyma (cirrhosis), when the chemical element present in the body is diluted with water, that is, such hyponatremia occurs from dilution.

Will the symptoms tell?

Symptoms of this pathological condition may be absent, moreover, this happens more often than the manifestation of vivid clinical signs. In most cases, a person does not notice a decrease in sodium concentration in the blood to 130 mmol / l, unless the level drop was too rapid, and the body did not have time to adapt. Signs of the disease usually begin to bother if the sodium content crosses the border of 120 mmol / l, however, even with such indicators, the symptoms do not have specificity to attribute them to manifestations of hyponatremia. For example:

1. Frequent and rather intense headaches (characteristic of many diseases);
2. Lethargy, drowsiness, lethargy, apathy (as in slow motion);
3. (lowering blood pressure);
4. Cardiopalmus;
5. Periodically approaching feeling of nausea, which in other cases ends with vomiting (you can think of a functional disorder of the gastrointestinal tract - “I ate something wrong”);
6. Decreased skin elasticity, its dryness (also happens for various reasons);
7. Diuresis is usually reduced in hyponatremia.

Obviously, all of the listed signs are not a reflection of specific pathological events. Similar symptoms can accompany a wide variety of diseases and conditions (even physiological ones).

However, as plasma sodium continues to fall, other symptoms appear:

• Gastrointestinal disorders become more pronounced;
• Neurological symptoms appear;
• Possible convulsive syndrome;
• A coma is not ruled out.

And even the aggravation of the condition does not directly indicate a decrease in sodium levels. The symptoms of the second group may also be present in many diseases.

Diagnostics

Hyponatremia is a laboratory sign; it can be said that it does not create difficulties in the diagnosis. In order to find out the content of Na in the blood, it is enough to do a biochemical test that determines the concentration of its cations (and at the same time to establish the concentration of potassium and chlorine). But in order to find the cause and determine the form of hyponatremia, you will have to divide the diagnostic search into several stages, the first of which will be the most thorough collection of amnestic data (history of life and illness). The patient may be suffering from:

1. Congestive heart failure (CHF);
2. Diseases of the kidneys and liver that violate the functional abilities of these organs;
3. Oncology (has malignant neoplasms);
4. Pathology of the endocrine system (hypothyroidism - decreased thyroid function, Addison's disease - chronic insufficiency of the adrenal cortex);
5. Diseases of the gastrointestinal tract (then Na leaves the body through the gastrointestinal tract);
6. Mental disorders (inadequate eating behavior).

In addition, it is necessary to find out whether in the recent past the patient underwent surgical interventions and treatment associated with the introduction of a large amount of infusion solutions, or whether he was fond of medications that remove sodium from the body for a long time (a list of drugs that contribute to the development of hyponatremia will be given below ).

Based on the data obtained, the doctor examining the patient refers his condition to one of the forms of hyponatremia:

• Hyponatremia with, which is manifested by edema and is due to an increase in the content of Na and water reserves in the body, where, however, water prevails over the chemical element. This variant is formed due to severe diseases of the heart (CHF), kidneys (ARF and CRF), liver (cirrhosis);
• Normovolemic hyponatremia is established when the concentration of a chemical element approaches normal;
• a form that occurs against the background of a decrease in the volume of circulating blood - BCC. In this case, there is a drop in sodium levels and water reserves, but sodium is lost faster (disproportionate to the loss of H2O);

It should be noted that it is very difficult to distinguish between the normo- and hypovolemic variant of hyponatremia, especially if their characteristic signs (palpitations, orthostatic hypotension) do not manifest themselves very much. In such a situation, the diagnosis of these conditions is based on laboratory tests, which, by the way, also do not always change:

1. Ht - (usually increased with hypovolemia);
2. The ratio of urea / creat (/) - with hypovolemia more than 20.

If the tests performed do not clarify the picture, the patient is prescribed tests such as:

• (OSM);
• Study of sodium in urine.

During the diagnostic search, when the analysis was already obtained (sodium content is below 135 - 130 mmol / l), a detailed questioning was carried out, a form of hyponatremia was isolated on the basis of other laboratory tests, the doctor often suspects a specific disease (see above), which caused a decrease in sodium in the blood plasma. Then, to clarify the diagnosis, the doctor simultaneously uses instrumental (ECG, ultrasound, MRI, etc.) diagnostic methods.

Final diagnosis

Isolation of the forms of hyponatremia is very important, since the correction of sodium in the body and the therapy of the underlying disease that caused the decrease in Na cations depend on this. And, it should be noted, the last word in this division belongs to the two main laboratory indicators. It: blood osmolarity- it makes it possible to assign the patient to one category or another, and determination of sodium in urine, thanks to which the diagnosis will be established in patients with low blood osmolarity values. To make it clearer for the reader to understand the correspondence of these laboratory parameters to certain forms of hyponatremia, a table is presented below.

Table: combination of hyponatremia with blood osmolarity and sodium content in urine

It was mentioned in the text that the intake of certain pharmaceutical drugs can affect the decrease in sodium in the blood, so it would be useful to provide a list of them:

1. Diuretics and, of course, in the first place - siluretics (furosemide);
2. Indapamide, indapafon (antihypertensive drugs with a diuretic effect);
3. Antipsychotics: chlorpromazine (chlorpromazine), zeptol (carbamazepine);
4. Antidepressants - selective serotonin reuptake inhibitors (SSRIs - sertraline, citalopram);
5. Synthetic analogues of vasopressin (antidiuretic hormone - ADH);
6. Certain medicines used to treat respiratory problems (theophylline);
7. Separate antiarrhythmic drugs (amiodarone);
8. The psychoactive compound of amphetamine is Ecstasy.

It should be noted that antidepressants - SSRIs often cause the syndrome of inappropriate vasopressin production (SIADH), so their intake should be accompanied by periodic monitoring of Na + in the blood plasma. Correction of sodium levels in such situations is achieved quickly - by discontinuing the drug.

Parhon's syndrome

Parkhon's syndrome, syndrome of inadequate production of vasopressin, syndrome of inappropriate synthesis of antidiuretic hormone, SIADH cannot be ignored in the topic "Hyponatremia". SIADH arises on the basis of ADH production that does not meet the needs of the body (the hormone is synthesized “as it wants”), affecting water reserves, that is, replenishing them in the body, not allowing water to leave it.

The following laboratory and clinical signs of this pathology can be distinguished:

1. The content of Na in the blood plasma tends to decrease (less than 130 - 135 mmol / l);
2. OSM of blood plasma falls below 280 mosm/l;
3. The urine becomes quite concentrated with a relative gravity above 1.025;
4. The concentration of Na in the urine increases markedly (more than 30 mmol/l);
5. BCC is usually normal;
6. Functional disorders of the kidneys and the endocrine system (adrenals, "thyroid") are not observed.

Usually, the doctor suspects this syndrome in a patient in two cases:

• Decreased blood ORM does not fit in any way with increased (or normal) urine ORM;
• Decrease in uric acid (hypouricemia).
• The most common causes of the formation of SIADH are the following factors:
• The use of drugs intended for the treatment of mental disorders (SSRIs, chlorpromazine, zeptol), respiratory organs (theophylline), antiarrhythmic drugs (amiodarone);
• Brain damage (infections, neoplasms);
• Pathology of the respiratory system (pneumonia, empyema, tumors);
• Ectopic production of vasopressin (bronchogenic carcinoma is the most common source of ectopic synthesis of ADH);
• Less commonly, Parhon's syndrome is accompanied by diseases such as Guillain-Barré syndrome, multiple sclerosis, and acute intermittent porphyria.

Therapy for the syndrome of inappropriate synthesis of vasopressin is carried out taking into account clinical symptoms and laboratory parameters (to be described below).

Condition Correction

Therapy for hyponatremia should not be taken lightly, as it depends on many circumstances, for example, it is important to pay attention to:

1. Duration of the disease (acute - up to 2 days);
2. The severity of symptoms;
3. The degree of hyponatremia;
4. Patient's condition (if there is any hypotension, intensive care may be needed urgently).

Only after a thorough analysis of the above factors can one look for the best way to correct hyponatremia in order to proceed directly to the second step - the treatment of pathology.

Correction is carried out in accordance with the form of the disease (it should already be isolated before the start of therapy):

• In acute severe hyponatremia (Na - below 125 mmol / l), which, among the clinical manifestations, has neurological symptoms (accompanied by convulsions), there is a need for an urgent participation of physicians. The urgency is explained by the fact that in this case there is a high risk of developing encephalopathy due to a decrease in Na, and cerebral edema (GM). Urgent treatment involves the introduction of a hypertonic (10%) solution of sodium chloride (NaCl), where the initial rate of correction is from 1 to 2 mmol / hour, and does not allow hyper- or even normonatremia in the first 2 days;
• A rapid correction in patients with a chronic form of hyponatremia is also highly undesirable - it can provoke an often irreversible complication - a demyelinating process in the brain (myelinolysis of the brain bridge), which will give neurological symptoms within a week from the start of treatment;
• Correction of the chronic form of hyponatremia, poor in symptoms, is probably the simplest: it is worth eliminating the cause and the level of sodium in the blood plasma will recover (though if the cause is not a severe pathology);
• The main point in the treatment of SIADH (provided that its degree is mild or moderate) is the limitation of the amount of water drunk per day (no more than 1.5 liters). Correction of the sodium level in the chronic syndrome of inadequate vasopressin production is carried out by the simultaneous appointment of a diet (consumption of foods containing Na in abundance) and loop diuretics;
• If the patient is unable to endure a water-limiting regimen or with persistent hyponatremia occurring in severe form, the above methods of correction may not give the desired effect, then the doctor (and never the patient himself or his relatives!) Prescribes additional medication to regulate the water balance;
• Patients with a hypervolemic variant of the disease limit the intake of both water and a chemical element into the body, severe forms require the use of a loop diuretic, and renal failure requires hemodialysis;
• Recently developed synthetic ADH receptor antagonists offer considerable promise in terms of the treatment of chronic hyponatremia.

And in any case, be that as it may, people who have certain complaints, and laboratory testing revealed a low level of sodium, require close attention to their health, perhaps the cause of the development of such a condition was CHF or an unreasonable diuretic addiction. Other prerequisites for the occurrence of hyponatremia (for example, SIADH or diseases of the endocrine system) after in-depth diagnosis are treated according to the appropriate algorithms.

Hyponatremia is a fairly common pathology. This electrolyte disturbance occurs in about 20% of critically ill patients admitted to the intensive care unit. In patients who are treated on an outpatient basis, pathology is much less common - only 5-7% of cases.

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

With hyponatremia, the concentration of sodium in the blood is below 135 mmol / l. Sodium is a macroelement on which the acid-base balance and the stability of the osmotic pressure of plasma depend. Due to hyponatremia, there is a supersaturation of the plasma with dissolved particles (hypoosmolarity). The fluid in the intercellular space is sent to the cells. As a result, edema appears. Cells swell and cannot function normally. The volume of circulating blood depends on the cause that caused the pathology.

Attention!

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

Types and forms

Physicians 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:

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

There are three forms of hyponatremia according to severity:

1. Light. Biochemical analysis of Na concentration shows 130-135 mmol/l.
2. Medium-heavy. The concentration level is 125-129 mmol / l.
3. Heavy. The concentration of Na is 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 referred to as a chronic form.

According to symptoms:

• moderately pronounced;
• heavy.

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Etiology (causes)

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

Physiological factors:

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

Pathological factors:

1. Fluid retention. Occurs with renal failure - acute or chronic, as well as with cirrhosis of the liver. Imbalance can develop due to lung diseases, oncology and endocrine pathologies.
2. Large losses of sodium. They occur with prolonged or chronic diarrhea, with prolonged vomiting and nephropathies, in which the process of sodium reabsorption is disrupted. This pathology is observed in nephritis and polycystic kidney disease.
3. 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.
4. The use of medicines. Pathology can be caused by diuretics used in emergency situations. They are given to patients for the relief of severe conditions. The use of hypoglycemic and psychotropic drugs can also provoke a problem.
5. Plentiful drink. Drinking large amounts of ordinary (non-mineral) water. This situation is observed in diabetes - sugar and insipidus.

Sodium losses can be:

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

Attention!

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

Symptoms

Symptoms are neurological in nature, since with a decrease in the concentration of Na, fluid penetrates into the brain cells. This situation leads to cerebral edema and dysfunction of the central nervous system.

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

1. With a mild form of pathology, there are no serious lesions of the central nervous system. There may be slight drowsiness and failures in the vestibular apparatus.
2. In severe form, the patient reacts poorly to external stimuli. An epileptiform seizure is possible.

Pathology may be accompanied by symptoms:

• decreased vascular tone;
• deterioration of the contractile function of the myocardium;
• muscle weakness;
• signs of hypotension (palpitations, dizziness, fainting);
• dry skin and mucous membranes;
• headache.

Less commonly, there is a decrease in diuresis and gastrointestinal upset, expressed in nausea and lack of appetite. In 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.

The procedure and features of diagnostics:

1. The study of anamnesis. The doctor finds out the alleged cause of the pathological condition. Based on the anamnestic data, conclusions are drawn. To determine the type of pathology, signs of dehydration are revealed - it can be dry skin, decreased diuresis, or hypotensive symptoms.
2. Identification of comorbidities. During the examination, the doctor pays attention to external signs - swelling on the face and legs, an enlarged and tense abdomen, dilated saphenous veins on the anterior wall of the abdomen.
3. Laboratory diagnostics. Determine the concentration of electrolytes in the serum.
4. Testing. A test is carried out with a water load, which determines their performance - the possibility of excreting (removing) 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;
• conduct 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:

1. Measure CVP (central venous pressure) - this is the most accurate way to determine the type of hyponatremia. Find out what kind of pathology is present.
2. Chest x-ray. It is carried out if there is a suspicion that the patient has pulmonary edema.
3. 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 pathologies are accompanied by almost similar symptoms. At the same time, it is important to distinguish cerebral edema that occurs with hyponatremia from edema caused by a hypertensive crisis, traumatic brain injury, or other etiologies.

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 a pathology. Also stop introducing hypotonic solutions.

On a note!

In the treatment of hyponatremia, patients may be prescribed the use of plain table salt. In mild forms of pathology, this measure alone may be enough to solve the problem.

Patients with moderate and severe form are prescribed the following treatment:

1. Limit fluid intake. This is the main requirement in the treatment of pathology of the hypervolemic type. Daily fluid intake should be limited to 1000 ml.
2. Enter saline solutions. Infusion therapy is carried out using a solution of 0.9% NaCl. This eliminates sodium deficiency. At the same time, the lack of other electrolytes is replenished. If neurological symptoms occur, NaCl 3% is administered.
3. Diuretics are prescribed. They remove excess fluid from the body with a hypervolemic form of hyponatremia. Patients take diuretics. Diuretic thiazide drugs for hyponatremia are strictly prohibited, as they aggravate the pathology.
4. Arrange blockade of ADH. If there is an increased secretion of antidiuretic hormone, 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 life of the patient, sodium concentration is first corrected. And only when the symptoms that threaten brain edema are eliminated, they begin to treat the disease that caused the pathology.

Treatment of diseases that can provoke hypernatremia:

1. Chronic heart failure. ACE inhibitors, diuretics and other drugs are prescribed for CHF.
2. Cirrhosis of the liver. Albumin is administered, fresh frozen plasma is transfused. There is a strict ban on alcoholic beverages.
3. endocrine disorders. Hormone replacement therapy is prescribed. The recommended drug for adrenal insufficiency is hydrocortisone.
4. Chronic renal failure. Carry out hemodialysis.

The 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 the high probability of death.

Consequences and complications

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

Possible complications:

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

Prevention and forecasts

Severe hyponatremia has a very poor prognosis. At a sodium concentration of 125 mmol / l, mortality reaches 25%, with an indicator below 115 mmol / l - 50%. According to other statistics, the lethality of the pathology is 65%.

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

Prevention:

• timely treatment of diseases that can provoke hypernatremia;
• regular monitoring of sodium content in plasma.

Attention!

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

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