Hypernatremia

Hypernatremia is characterized by a plasma sodium concentration greater than 145 mEq/L, caused by a deficit of water relative to the solute. The main symptom is thirst; other clinical manifestations are primarily neurological (due to osmotic movement of water out of cells) and include altered consciousness, excessive neuromuscular excitability, seizures, and coma.

Causes hypernatremia

Hypernatremia develops as a result of two main mechanisms: water deficiency in the body and excess sodium intake.

Water deficiency may be associated with insufficient water intake, but the main reason for the development of water deficiency is considered to be its increased loss. Water loss may be accompanied by a simultaneous loss of sodium or be isolated.

Combined loss of water and sodium occurs with excessive sweating, as well as with the development of osmotic diuresis ( diabetes mellitus with glucosuria, chronic renal failure, polyuric stage of acute renal failure). Isolated loss of water occurs with the development of increased water diuresis in diseases such as central diabetes insipidus, nephrogenic diabetes insipidus, and diabetes insipidus developed under the influence of drugs.

Excessive sodium intake with food, administration of hypertonic solutions and hyperaldosteronism may also cause hypernatremia. Hypernatremia that develops under conditions of normal sodium intake is associated with the release of sodium from cells into the extracellular space, which is associated with the creation of a high osmotic gradient in it. According to the laws of maintaining osmotic balance, water begins to leave the cells and intracellular dehydration develops, which serves as a manifestation of all types of hypernatremia, while the volume of extracellular fluid may vary.

Hypernatremia in adults has a mortality rate of 40-60%. Hypernatremia usually involves a disordered thirst mechanism or limited access to water. The high mortality rate is thought to be due to the severity of the diseases that typically cause inability to drink and the effects of brain hyperosmolality. Older people are at high risk, especially in warm weather, due to decreased thirst and the presence of various diseases.

Hypovolemic hypernatremia occurs when Na is lost with a relatively greater loss of water. The major extrarenal causes include most of those that cause hypovolemic hyponatremia. Hypernatremia or hyponatremia may occur with significant fluid loss, depending on the relative amounts of water and Na lost and the amount of water consumed before the onset.

Renal causes of hypovolemic hypernatremia include diuretic therapy. Loop diuretics inhibit Na reabsorption in the concentrating compartment of the nephron and may enhance water clearance. Osmotic diuresis may also impair renal concentrating function because of the presence of hypertonic substances in the lumen of the distal nephron tubules. Glycerol, mannitol, and occasionally urea can cause osmotic diuresis, leading to hypernatremia. Probably the most common cause of hypernatremia due to osmotic diuresis is hyperglycemia in patients with diabetes mellitus. Because glucose does not enter cells in the absence of insulin, hyperglycemia causes further dehydration of the intracellular fluid. The degree of hyperosmolality may be obscured by an artificial decrease in plasma Na levels resulting from water movement out of cells into the extracellular fluid (transfer hyponatremia). Patients with kidney disease may also be predisposed to hypernatremia when the kidneys are unable to concentrate urine as efficiently as possible.

Main causes of hypernatremia

Hypovolemic hypernatremia (decrease in extracellular fluid and Na; relatively greater decrease in extracellular fluid)

Extrarenal losses

• Gastrointestinal: vomiting, diarrhea.
• Skin: burns, increased sweating.
• Renal losses.
• Kidney disease.
• Loop diuretics.
• Osmotic diuresis (glucose, urea, mannitol).

Normovolemic hypernatremia (decreased extracellular fluid; virtually normal total body Na content)

Extrarenal losses

• Respiratory: tachypnea. Skin: fever, increased sweating.

Renal losses

• Central diabetes insipidus.
• Nephrogenic diabetes insipidus.

Other

• Lack of access to water.
• Primary hypodipsia.
• The phenomenon of restructuring of osmoregulation "Reset osmostat".
• Hypervolemic hypernatremia (increased Na; normal or increased extracellular fluid)
• Administration of hypertonic solutions (hypertonic saline, NaHCO3, parenteral nutrition).
• Excess mineralocorticoids
• Adrenal tumors secreting deoxycorticosterone.
• Congenital adrenal hyperplasia (caused by a defect in 11-hydrolase).
• Iatrogenic.

Normovolemic hypernatremia is usually characterized by a decrease in extracellular fluid with normal Na content in the body. Extrarenal causes of fluid loss, such as increased sweating, lead to a small loss of Na, but due to the hypotonicity of sweat, hypernatremia can develop into significant hypovolemia. A deficit of almost pure water is also observed in central or nephrogenic diabetes insipidus.

Idiopathic hypernatremia (primary hypodipsia) is sometimes seen in children with brain damage or in chronically ill elderly patients. It is characterized by a disturbance of the thirst mechanism, a change in the osmotic stimulus for ADH release, or a combination of both. With nonosmotic ADH release, patients are usually normovolemic.

Rarely, hypernatremia is associated with hypervolemia. In this case, hypernatremia is caused by a significant increase in Na intake with limited access to water. An example would be excessive administration of hypertonic NaHCO3 during cardiopulmonary resuscitation or in the treatment of lactic acidosis. Hypernatremia can also be caused by the administration of hypertonic saline or excessive dietary intake.

Hypernatremia is especially common in the elderly. Causes include inadequate water availability, impaired thirst mechanism, impaired renal concentrating ability (due to diuretic use or loss of functioning nephrons with aging or kidney disease), and increased fluid loss. In the elderly, ADH release is increased in response to osmotic stimuli but decreased in response to volume and pressure changes. Some elderly patients may have impaired angiotensin II production, which directly contributes to impaired thirst mechanism, ADH release, and renal concentrating function. Among the elderly, hypernatremia is especially common in postoperative patients and in patients receiving tube feeding, parenteral nutrition, or hypertonic solutions.

[ 1 ], [ 2 ], [ 3 ]

Variants of hypernatremia

The hemodynamic variant of hypernatremia depends on the distribution of sodium in the intravascular and interstitial spaces. In the clinic, several variants of hypernatremia are distinguished - hypovolemic, hypervolemic and isovolemic.

Hypovolemic hypernatremia develops due to the loss of hypotonic fluid through the kidneys, gastrointestinal and respiratory tract or skin. The main causes of hypovolemic hypernatremia in nephrological practice are long-term use of osmotic diuretics, acute renal failure in the polyuria stage, chronic renal failure in the polyuria phase, post-obstructive nephropathy, and treatment with peritoneal dialysis.

The cause of hypervolemic hypernatremia is most often iatrogenic factors - the introduction of hypertonic solutions, drugs. In pathology, this type of electrolyte disorders is observed in excess production of mineralocorticoids, estrogens, Itsenko-Cushing syndrome, diabetes mellitus. The main causes of hypervolemic hypernatremia in nephrological practice are acute nephritic syndrome, acute renal failure in the oliguria stage, chronic renal failure in the oliguria stage, nephrotic syndrome. A positive sodium balance in these conditions is largely determined by a decrease in SCF.

The main cause of isovolemic hypernatremia is diabetes insipidus. Due to the lack of ADH production (diabetes insipidus of central genesis) or renal insensitivity to ADH (renal diabetes insipidus), hypotonic urine is excreted in large quantities. In response to fluid loss, the thirst center is stimulated, and the fluid loss is replenished. Hypernatremia in these conditions is usually low.

[ 4 ], [ 5 ], [ 6 ], [ 7 ], [ 8 ], [ 9 ]

Symptoms hypernatremia

The cardinal symptom is thirst. Absence of thirst in conscious patients with hypernatremia may indicate a disorder of the thirst mechanism. Patients with communication problems may be unable to express thirst or obtain the water they need. The cardinal signs of hypernatremia are caused by CNS dysfunction due to shrinkage of brain cells. Impaired consciousness, excessive neuromuscular excitability, seizures, or coma may develop; patients dying from severe hyponatremia often have cerebrovascular accidents with subcortical or subarachnoid hemorrhage.

In chronic hypernatremia, osmotically active substances appear in the CNS cells and increase intracellular osmolality. Consequently, the degree of dehydration of brain cells, as well as symptoms from the CNS, are less severe in chronic hypernatremia compared to acute hypernatremia.

If hypernatremia occurs with total body sodium depletion, typical symptoms of volume depletion are present. Large amounts of hypotonic urine are usually excreted in patients with impaired renal concentrating function. If losses are extrarenal, the cause of water loss is often obvious (eg, vomiting, diarrhea, increased sweating), and renal sodium levels are low.

Symptoms of hypernatremia are associated with damage to the central nervous system and are directly dependent on the sodium level in the blood. With moderate hypernatremia (sodium concentration in the blood is less than 160 mmol/l), early signs of electrolyte imbalance are neurological manifestations: irritability, drowsiness, weakness. With an increase in the sodium level in the blood above 160 mmol/l, convulsions and coma develop. If this sodium concentration is maintained for 48 hours, the mortality rate of patients is more than 60%. The immediate cause of death in this situation is intracellular dehydration, leading to irreversible changes in the vascular system of the brain. At the same time, long-term (chronic) moderate hypernatremia, as a rule, is devoid of certain neurological symptoms. This is due to the fact that in response to dehydration, "idiogenic osmoles" are synthesized in the cells of the brain vessels, which prevent the loss of fluid by the cells of the brain. This circumstance must be taken into account, since rapid rehydration of such patients may cause cerebral edema.

[ 10 ]

Diagnostics hypernatremia

The diagnosis of hypernatremia is based on clinical presentation and sodium measurement. If the patient fails to respond to routine rehydration or if hypernatremia recurs despite adequate access to water, further diagnostic testing is necessary. Determining the underlying cause requires measurement of urine volume and osmolality, particularly after dehydration.

A dehydration study is sometimes used to differentiate between several conditions characterized by polyuria (eg, central and nephrogenic diabetes insipidus).

[ 11 ], [ 12 ]

Treatment hypernatremia

The primary goal of treatment is replacement of solute-free water. Oral hydration is effective in conscious patients without significant gastrointestinal dysfunction. In severe hypernatremia or inability to drink due to ongoing vomiting or altered mental status, intravenous hydration is preferred. If hypernatremia has been present for less than 24 hours, correction should be made within 24 hours. However, if hypernatremia is chronic or the duration is unknown, correction should be made within 48 hours, and plasma osmolality should be reduced at a rate of no more than 2 mOsm/(lh) to avoid cerebral edema caused by overhydration. The amount of water needed to replace the existing deficit can be calculated using the following formula:

Water deficit = extracellular fluid x [(plasma Na level/140)1], where extracellular fluid is in liters and is calculated by multiplying weight in kg by 0.6; plasma sodium level is in mEq/L. This formula assumes constant total body sodium content. In patients with hypernatremia and decreased total body sodium content (eg, due to volume depletion), the free water deficit is greater than that calculated by this formula.

In patients with hypernatremia and hypervolemia (increased total body Na), the free water deficit can be replaced with 5% dextrose, which can be supplemented with a loop diuretic. However, too rapid administration of 5% dextrose can lead to glucosuria, increasing salt-free water excretion and hypertonicity, especially in diabetes mellitus. KCI should be administered depending on the plasma K concentration.

In patients with normovolemic hypernatremia, administration of 5% dextrose solution or 0.45% saline solution is used.

In patients with hypovolemic hypernatremia, especially in diabetic patients with nonketotic hyperglycemic coma, 0.45% saline can be administered as an alternative to the combination of 0.9% saline and 5% dextrose to restore Na and water levels. In the presence of severe acidosis (pH> 7.10), NaHCO3 solution can be added to 5% dextrose or 0.45% saline, but the resulting solution must be hypotonic.

Treatment of hypernatremia involves administering adequate amounts of water. To do this, it is necessary to calculate the existing water deficit. Based on the assumption that water normally makes up 60% of body weight, the existing water deficit is calculated using the formula:

Water deficiency=0.6 x body weight (kg) x (1-140/P _Na ),

Where P _Na is the concentration of sodium in the blood serum.

In conditions of acute hypernatremia, water deficiency should be replenished quickly to prevent the risk of cerebral edema due to the accumulation of sodium and highly osmotic organic substances in the brain. In this situation, the introduction of water allows sodium to be quickly displaced into the extracellular space.

At the same time, in conditions of chronic hypernatremia, rapid fluid administration is dangerous and can lead to cerebral edema. This is due to the fact that organic substances and electrolytes have already accumulated in the brain and their removal requires 24 to 48 hours. In the presence of clinical symptoms of chronic hypernatremia, the doctor's tactics consist of an initial rapid administration of such a volume of fluid that the sodium concentration decreases by no more than 1-2 mmol / (lh). After the disappearance of clinical symptoms of hypernatremia, the remaining water deficit is replenished within 24-48 hours. Treatment of hypernatremia must be combined with constant and careful monitoring of the patient's neurological status. Deterioration of the condition after a period of acute fluid administration may indicate the development of cerebral edema, which requires immediate termination of the procedure.

Methods of administering water to patients vary, from oral administration to administration through a nasogastric tube or intravenously. For intravenous administration, it is better to use a hypotonic solution of sodium chloride or a 5% dextrose solution. Pure water should not be administered due to the risk of hemolysis. When prescribing solutions containing glucose, a calculated dose of insulin is used simultaneously.