Geparatraemia

Hypernatraemia is characterized by a plasma sodium concentration of more than 145 meq / l, caused by a deficiency of water relative to the solute. The main symptom is thirst; other clinical manifestations are mainly neurological in nature (due to the osmotic transition of water from the cells), include impaired consciousness, excessive neuromuscular excitability, contractions and coma. 

Causes of the gyneperthemia

Hypernatraemia develops due to two main mechanisms - the lack of water in the body and excess sodium intake in the body.

The lack of water may be due to its inadequate intake into the body, but the main reason for the development of water deficiency is considered to be its increased loss. The loss of water may be accompanied by a simultaneous loss of sodium or be isolated.

Combined Water and sodium loss occurs when excessive sweating, as well as in the development of an osmotic diuresis ( diabetes  with glucosuria, chronic renal failure, poliuricheskaya stage of acute renal failure). An isolated water loss occurs during the development of enhanced water diuresis in diseases such as central diabetes insipidus, nephrogenic diabetes insipidus and diabetes insipidus developed under the influence of drugs.

Excess sodium intake with food, the introduction of hypertonic solutions and the state of hyper aldosteronism can also be the cause of hypernatremia. Hypernatraemia, which has developed under the conditions of normal sodium intake in the body, is associated with the release of sodium from the cells into the extracellular space, which is associated with the creation of a high osmotic gradient in it. According to the laws of osmotic balance, water begins to flow out of the cells and intracellular dehydration develops, which is a manifestation of all types of hypernatremia, while the volume of extracellular fluid may be different.

Hypernatremia in adults is characterized by a mortality rate of 40-60%. Hypernatraemia usually involves a violation of the mechanism of thirst or limited access to water. The high mortality rate is presumably due to the severity of the diseases, usually leading to inability to drink, and the effects of hyperosmolarity of the brain. Older people have a high predisposition, especially in warm weather, due to a decrease in thirst and the presence of various diseases.

Hypovolemic hypernatremia occurs with the loss of Na with the concomitant relatively large loss of water. The main extrarenal causes include the majority of those that cause hypovolemic hyponatremia. Hypernatraemia or hyponatremia can occur with significant fluid loss depending on the relative amount of water and Na lost, as well as the amount of water consumed before manifestation.

Renal causes of hypovolemic hypernatremia include diuretic administration. Loop diuretics inhibit Na reabsorption in the concentration section of the nephron and can enhance water purification. Osmotic diuresis can also impair the concentration function of the kidneys due to the presence of hypertonic substances in the lumen of the distal nephron tubes. Glycerol, mannitol and sometimes 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. Since glucose does not penetrate into cells in the absence of insulin, hyperglycemia causes further dehydration of the intracellular fluid. The degree of hyperosmolarity may be unclear due to the artificial reduction of plasma Na level as a result of the movement of water from the cells into the extracellular fluid (portable hyponatremia). Patients with kidney disease may also be predisposed to hypernatremia when it is impossible for the kidneys to concentrate urine as much as possible.

The 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, sweating.
• Kidney loss.
• Kidney disease.
• Loop diuretics.
• Osmotic diuresis (glucose, urea, mannitol).

Normovolemic hypernatremia (decrease in extracellular fluid; almost normal total body Na)

Extrarenal losses

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

Kidney loss

• central diabetes insipidus.
• Nephrogenic diabetes insipidus.

Other

• Lack of access to water.
• Primary hypodipsia.
• The phenomenon of osmoregulation adjustment “Reset osmostat”.
• Hypervolemic hypernatremia (increased Na; normal or increased extracellular fluid)
• Introduction of hypertonic solutions (hypertonic saline, NaHCO3, parenteral nutrition).
• An excess of mineralocorticoid
• tumors secreting deoxycorticosterone.
• Congenital adrenal hyperplasia (caused by a 11-hydrolase defect).
• Iatrogenic.

Normovolemic hypernatremia is usually characterized by a decrease in extracellular fluid with a normal content of Na in the body. Non-renal causes of fluid loss, such as increased sweating, lead to a slight loss of Na, however, due to the hypotonicity of sweat, hypernatremia can develop to significant hypovolemia. Deficit of practically pure water is also observed in case of central or nephrogenic diabetes insipidus.

Idiopathic hypernatraemia (primary hypodipsia) is sometimes observed in children with brain damage or in chronically ill elderly patients. It is characterized by a violation of the mechanism of thirst, a change in the osmotic stimulus to release ADH, or a combination thereof. With the neosmotic release of ADH in patients, normolemia is usually observed.

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

Hypernatremia is particularly common in the elderly. The reasons include insufficient water availability, impaired thirst mechanism, impaired kidney concentration ability (due to diuretic administration or loss of functioning nephrons with age or kidney disease), increased fluid loss. In older people, the release of ADH is increased in response to osmotic stimuli, but decreased in response to changes in volume and pressure. In some elderly patients, the production of angiotensin II may be impaired, which directly contributes to the violation of the mechanism of thirst, the release of ADH, the concentration function of the kidneys. Among elderly people, hypernatraemia is especially often observed in postoperative patients, as well as in patients receiving nutrition through a probe, parenterally or with the introduction of hypertonic solutions.

[1], [2], [3]

Options for hypernatraemia

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

Hypovolemic hypernatraemia develops due to the loss of hypotonic fluid through the kidneys, gastrointestinal and respiratory tract, or skin. The main reasons for the development of hypovolemic hypernatremia in nephrological practice are the 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 variant of electrolyte disturbances is observed with excessive production of mineralocorticoids, estrogens, Itsenko-Cushing's syndrome, and diabetes. The main reasons for the development of hypervolemic hypernatremia in nephrology practice are acute nephritic syndrome, acute renal failure in the oliguria stage, chronic renal failure in the oliguria stage, nephrotic syndrome. The positive sodium balance in these conditions is largely determined by a decrease in GFR.

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

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

Symptoms of the gyneperthemia

The main symptom is thirst. The absence of thirst in conscious patients with hypernatremia may indicate a violation of the mechanism of thirst. Patients with communication problems sometimes cannot express thirst or get the necessary water. The main signs of hypernatremia are caused by the disruption of the activity of the central nervous system due to shrinking of brain cells. Consciousness, excessive nerve irritability, seizures, or coma may develop; cerebrovascular disorders with subcortical or subarachnoid hemorrhages are often observed in patients dying from severe hyponatremia.

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

If hypernatremia develops in violation of the total sodium content in the body, there are typical symptoms of fluid volume disorders. Large amounts of hypotonic urine are usually excreted in patients with impaired concentration function of the kidneys. If the loss is extrarenal, the cause of water loss is often obvious (for example, vomiting, diarrhea, increased sweating), and the renal sodium level is low.

Symptoms of hypernatraemia are associated with damage to the central nervous system and are directly dependent on the level of sodium in the blood. With moderate hypernatremia (the concentration of sodium in the blood is less than 160 mmol / l), neurological manifestations such as irritability, drowsiness, and weakness are early signs of electrolyte imbalance. With increasing levels of sodium in the blood of more than 160 mmol / l develop convulsions, coma. While maintaining this concentration of sodium within 48 hours, the death 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 is usually devoid of certain neurological symptoms. This is due to the fact that in response to dehydration in the cells of the blood vessels of the brain, “idiogenic osmols” are synthesized, which prevent the brain cells from losing fluid. This circumstance must be taken into account, since with rapid rehydration of such patients, brain swelling may occur.

[10]

Diagnostics of the gyneperthemia

Diagnosis of hypernatraemia is based on the clinical manifestations and measurement of  sodium level. If the patient does not develop a response to normal rehydration or if hypernatremia recurs, despite adequate access to water, further diagnostic testing is necessary. Determining the original cause requires measuring urine volume and osmolality, especially after dehydration.

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

[11], [12]

Treatment of the gyneperthemia

The main goal of treatment is to replace osmotically free water. Oral hydration is effective in conscious patients without significant gastrointestinal dysfunction. In severe hypernatraemia or inability to drink due to continuing vomiting or mental disorder, intravenous hydration is preferred. If hypernatremia lasts less than 24 hours, correction should be made within 24 hours. But, if hypernatremia is chronic or the duration is unknown, the correction should be made within 48 hours, the plasma osmolality should decrease with a speed of no more than 2 mOsm / (lhch) in order to avoid cerebral edema caused by excessive hydration. The amount of water needed to compensate for the existing deficit can be calculated using the following formula:

Water deficit = extracellular fluid x [(plasma level / 140 / Na) 1], where extracellular fluid is in liters and is calculated by multiplying the mass in kg by 0.6; plasma sodium level in meq / l This formula takes into account the constant total sodium content in the body. In patients with hypernatremia and a decrease in the total sodium content in the body (for example, with a decrease in fluid volume), the deficiency of free water is greater than that calculated by the formula.

In patients with hypernatremia and hypervolemia (increased total Na content in the body), the deficiency of free water can be compensated for by a 5% dextrose solution, which can be supplemented with a loop diuretic. However, too fast administration of a 5% dextrose solution can lead to glucosuria, increasing the excretion of water without salt and hypertonicity, especially in diabetes mellitus. KCI should be administered depending on the concentration of K in the plasma.

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

Patients with hypovolemic hypernatremia, especially diabetic patients with a non-ketone hyperglycemic coma, can be given 0.45% saline solution as an alternative to a combination of 0.9% saline and 5% dextrose to restore the level of Na and water. In the presence of severe acidosis (pH> 7.10), a solution of NaHCO3 can be added to a 5% dextrose solution or a 0.45% saline solution, but the resulting solution should be hypotonic.

Treatment for hypernatremia is the administration of an adequate amount of water. To do this, calculate the current water shortage. Based on the position that normal water is 60% of body weight, the existing water deficit is calculated by the formula:

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

Where P _Na  - sodium concentration in serum.

In the conditions of acutely developed hypernatraemia, the replenishment of water deficit should be carried out quickly in order to prevent the risk of cerebral edema due to the accumulation of sodium and highly osmotic organic substances in it. In this situation, with the introduction of water, it is possible to quickly displace sodium into the extracellular space.

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

Methods for administering water to patients are different - from ingestion to administration through a nasogastric tube or intravenously. For intravenous administration, it is better to use a hypotonic solution of sodium chloride or 5% dextrose solution. Clean water cannot be injected because of the risk of hemolysis. When prescribing solutions containing glucose, the calculated dose of insulin is simultaneously used.