Hypernatremia is an increase in plasma sodium (Na) concentrations greater than 145 mmol/L (mEq/L). The main reasons are lack of water in the body or excessive intake of sodium. Clinical manifestations include thirst, increased neuromuscular excitability, arterial hypertension. With a sudden onset of severe hypernatremia, convulsions and coma are possible. The condition is diagnosed by measuring Na levels and plasma osmolarity. Treatment includes oral or intravenous fluids, use of diuretics, and control of the underlying cause of the hypernatremia.
Sodium (Na) is the main extracellular electrolyte providing the osmotic pressure of the plasma. It determines the amount of almost all body fluids (circulating and deposited blood, cerebrospinal fluid, fluids of serous cavities, etc.), is a part of bicarbonate and phosphate buffers (regulation of ASC). Na is essential for nerve impulse transmission between neurons and neuromuscular junctions. All of the above causes the development of severe disorders in violation of the electrolyte balance. There are no exact statistics on the prevalence of hypernatremia.
This condition often has a multifactorial origin. A conditionally physiological cause (not associated with any disease) can be considered intense physical activity and dietary disorders - oversalting food, insufficient consumption of drinking water or prolonged intake of mineral water. Pathological causes of hypernatremia are:
An increase in plasma sodium leads to an increase in its osmolarity. Due to a change in the osmotic concentration gradient, fluid from the cells moves into the extracellular space (bloodstream and interstitium). Due to dehydration, the cells shrivel and collapse. Against the background of a violation of the ratio between the intra- and extracellular content of Na ions, the membrane potential changes in the direction of lowering the excitability threshold.
These mechanisms underlie the occurrence of neuropsychic and neuromuscular symptoms. Sodium is a sympathetic cation, that is, it increases the sensitivity of cells to catecholamines and other vasopressor mediators. Therefore, its accumulation in vascular smooth muscle cells causes an increase in vascular tone and an increase in blood pressure.
Conventionally, hypernatremia is divided into moderate and severe, focusing on clinical symptoms, since there are no clear numerical indicators for dividing this condition into degrees. Depending on the volume of circulating blood, the following variants of hypernatremia are distinguished:
According to the rate of development, hypernatremia can be:
The clinical picture directly depends on the rate of increase in sodium concentration. With slowly developing hypernatremia due to the inclusion of compensatory mechanisms (stimulation of the secretion of vasopressin and natriuretic peptides), an absolutely asymptomatic course can be observed. The most characteristic sign of rapidly advancing hypernatremia is thirst.
Other early symptoms are decreased appetite, nausea and vomiting. The central nervous system is particularly affected. There is excessive irritability, increased tendon reflexes, a violation of the sense of balance. Confusion and panic attacks are possible. Characterized by muscle rigidity, myoclonic twitches, painful spasms.
Due to high blood pressure, a patient with hypernatremia experiences heaviness in the back of the head, throbbing pain is possible. In the event of a significant loss of fluid (hypovolemic form), blood pressure decreases, which causes dizziness, darkening of the eyes, and sometimes loss of consciousness. In the hypervolemic form, edema of the lower extremities is often noted.
Hypernatremia has a very high frequency of adverse effects, including fatal ones. These include cerebral edema, thrombosis of cranial vessels, coma. Complications are also possible due to improper treatment, since in chronic hypernatremia, organic osmotically active substances (osmolytes) begin to accumulate in neurons as a compensatory mechanism.
If hypotonic solutions are administered too quickly, osmolytes do not have time to leave the neurons, as a result, water rushes into the cells, and brain edema develops. Sometimes with a long course, electrolyte-steroid cardiomyopathy with necrosis is observed. Arterial hypertension increases the risk of complications such as myocardial infarction, stroke. Isolated cases of rhabdomyolysis followed by acute renal failure in patients with hypernatremia have been described.
Patients with this condition are supervised by resuscitators together with specialized specialists (endocrinologist). On examination, attention is paid to hyperreflexia, muscle tone, clarity of consciousness. It is important to determine the type of hypernatremia, since the course of different types of pathology is different. They focus on such symptoms as signs of dehydration (dry skin and mucous membranes, reduced turgor) or peripheral edema and pressure indicators.
Until laboratory results are obtained, differentiation of hypernatremia is carried out primarily with hyponatremia due to very similar clinical symptoms. To confirm the diagnosis and establish the cause of the condition, the following methods are used:
All patients with an acute condition are transferred to the intensive care unit. Patients with a chronic form of hypernatremia can be treated in a general ward. The main condition for successful therapy is constant monitoring of water balance (taking into account the amount of fluid injected and excreted) and the concentration of blood electrolytes. Treatment includes the following main areas:
Hypernatremia is a severe electrolyte disorder with a poor prognosis. Death occurs in 50% of cases in the acute form and in 10-15% in the chronic form. In children, the death rate is much higher - about 65-70%. Approximately 2/3 of surviving patients have residual effects in the form of a neurological deficit to some extent.
Prevention consists in the competent treatment of diseases against which hypernatremia can develop (diabetes, diabetes insipidus, aldosteroma). The occurrence of this disorder in patients receiving hypotonic solutions or osmotic diuretics can be prevented by regular monitoring of sodium levels.