Sodium Imbalances Sodium, the main cation of ECF, plays a major role in maintaining the concentration and volume of ECF and influencing water distribution between ECF and ICF. Sodium plays an important role in the generation and transmission of nerve impulses, muscle contractility, and the regulation of acid-base balance. Because sodium is the primary determinant of ECF osmolality, sodium imbalances are typically associated with parallel changes in osmolality. Serum sodium is measured in milliequivalents per liter (mEq/L) or millimoles per liter (mmol/L). The serum sodium level reflects the ratio of sodium to water, not necessarily the loss or gain of sodium. Changes in the serum sodium level may reflect a primary water imbalance, a primary sodium imbalance, or a combination of the two. Sodium imbalances are typically associated with imbalances in ECF volume Isotonic gains and losses affect mainly the extracellular fluid (ECF) compartment with little or no water movement into the cells. Hypertonic imbalances cause water to move from inside the cell into ECF to dilute the concentrated sodium, causing cell shrinkage. Hypotonic imbalances cause water to move into the cell, causing cell swelling. The GI tract absorbs sodium from foods. Typically, daily intake of sodium far exceeds the body’s daily requirements. Sodium leaves the body through urine, sweat, and feces. The kidneys are the primary regulator of sodium balance. The kidneys regulate the ECF concentration of sodium by excreting or retaining water under the influence of ADH. Aldosterone also plays a role in sodium regulation by promoting sodium reabsorption from the renal tubules. Hypernatremia Hypernatremia, an elevated serum sodium, may occur with water loss or sodium gain. Because sodium is the major determinant of the ECF osmolality, hypernatremia causes hyperosmolality. In turn, ECF hyperosmolality causes a shift of water out of the cells, which leads to cellular dehydration. As discussed earlier, the primary protection against the development of hyperosmolality is thirst. Hypernatremia is not a problem in an alert person who has access to water, can sense thirst, and is able to swallow. Hypernatremia secondary to water deficiency is often the result of an impaired level of consciousness or an inability to obtain fluids. Several clinical states can produce hypernatremia from water loss. A deficiency in the synthesis or release of ADH from the posterior pituitary gland (central diabetes insipidus) or a decrease in kidney responsiveness to ADH (nephrogenic diabetes insipidus) can result in profound diuresis, thus producing a water deficit and hypernatremia. Hyperosmolality with osmotic diuresis can result from administration of concentrated hyperosmolar tube feedings and hyperglycemia associated with uncontrolled diabetes mellitus. Other causes of hypernatremia include excessive sweating and increased sensible losses from high fever. TREATMENT of Hypernatremia The treatment of hypernatremia involves treating the underlying cause and correcting the water deficit. Determining volume status and calculating the total body water deficit are important. When correcting the total body water deficit, oral or enteral free water should be used whenever possible. When intravenous fluids are required, hypotonic solutions should be used. Rapid over-correction can result in cerebral edema; therefore, the least amount of fluid possible should be used. In patients with rapid development of hypernatremia, sodium can be corrected quickly with isotonic saline or water without increasing the risk of cerebral edema. A correction rate of 1 mEq per L per hour is considered safe in these patients. In patients with hypernatremia that developed over a longer period, the sodium level should be corrected at a rate of 0.5 mEq per L per hour, with no more than an 8 to 10 mEq per L decrease over 24 hours.The target sodium level should be 145 mEq per L. Diagnosis and management of Hyponatremia Source
