Sodium Excess (Hypernatremia)

SODIUM EXCESS (HYPERNATREMIA)

Hypernatremia is a higher-than-normal serum sodium level (ex-ceeding 145 mEq/L [145 mmol/L]) (Adrogue & Madias, 2000a). It can be caused by a gain of sodium in excess of water or by a loss of water in excess of sodium. It can occur in patients with normal fluid volume or in those with FVD or FVE. With a water loss, the patient loses more water than sodium; as a result, the serumsodium concentration increases and the increased concentration pulls fluid out of the cell. This is both an extracellular and intra-cellular FVD. In sodium excess, the patient ingests or retains more sodium than water.

Pathophysiology

A common cause of hypernatremia is fluid deprivation in uncon-scious patients who cannot perceive, respond to, or communicate their thirst (Adrogue & Madias, 2000a). Most often affected in this regard are very old, very young, and cognitively impaired patients. Administration of hypertonic enteral feedings without adequate water supplements leads to hypernatremia, as does wa-tery diarrhea and greatly increased insensible water loss (eg, hyper-ventilation, denuding effects of burns).

Diabetes insipidus, a deficiency of ADH from the posterior pituitary gland, leads to hypernatremia if the patient does not ex-perience, or cannot respond to, thirst or if fluids are excessively restricted. Less common causes are heat stroke, near-drowning in sea water (which contains a sodium concentration of approxi-mately 500 mEq/L), and malfunction of either hemodialysis or peritoneal dialysis proportioning systems. IV administration of hypertonic saline or excessive use of sodium bicarbonate also causes hypernatremia.

Clinical Manifestations

The clinical manifestations of hypernatremia are primarily neuro-logic and are presumably the consequence of cellular dehydration (Adrogue & Madias, 2000a). Hypernatremia results in a rela-tively concentrated ECF, causing water to be pulled from the cells (see Fig. 14-4). Clinically, these changes may be manifested by restlessness and weakness in moderate hypernatremia and by dis-orientation, delusions, and hallucinations in severe hypernatremia. Dehydration (resulting in hypernatremia) is often overlooked as the primary reason for behavioral changes in the elderly patient. If hypernatremia is severe, permanent brain damage can occur (especially in children). Brain damage is apparently due to sub-arachnoid hemorrhages that result from brain contraction.

A primary characteristic of hypernatremia is thirst. Thirst is so strong a defender of serum sodium levels in healthy people that hypernatremia never occurs unless the person is unconscious or is denied access to water. Unfortunately, ill people may have an impaired thirst mechanism. Other signs include a dry, swollen tongue and sticky mucous membranes. Flushed skin, peripheral and pulmonary edema, postural hypotension, and increased mus-cle tone and deep tendon reflexes are additional signs and symp-toms of hypernatremia. Body temperature may rise mildly but returns to normal when the hypernatremia is corrected.

Assessment and Diagnostic Findings

In hypernatremia, the serum sodium level exceeds 145 mEq/L (145 mmol/L) and the serum osmolality exceeds 295 mOsm/kg (295 mmol/L). The urine specific gravity and urine osmolality are increased as the kidneys attempt to conserve water (provided the water loss is from a route other than the kidneys) (Fall, 2000).

Medical Management

Hypernatremia treatment consists of a gradual lowering of the serum sodium level by the infusion of a hypotonic electrolyte so-lution (eg, 0.3% sodium chloride) or an isotonic nonsaline solution(eg, dextrose 5% in water [D₅W]). D₅W is indicated when water needs to be replaced without sodium. Many clinicians consider a hypotonic sodium solution to be safer than D₅W because it al-lows a gradual reduction in the serum sodium level and thereby decreases the risk of cerebral edema. It is the solution of choice in severe hyperglycemia with hypernatremia. A rapid reduction in the serum sodium level temporarily decreases the plasma osmo-lality below that of the fluid in the brain tissue, causing danger-ous cerebral edema. Diuretics also may be prescribed to treat the sodium gain.

There is no consensus about the exact rate at which serum sodium levels should be reduced. As a general rule, the serum sodium level is reduced at a rate no faster than 0.5 to 1 mEq/L to allow sufficient time for readjustment through diffusion across fluid compartments. Desmopressin acetate (DDAVP) may be prescribed to treat diabetes insipidus if it is the cause of hypernatremia.

Nursing Management

As in hyponatremia, fluid losses and gains are carefully monitored in patients at risk for hypernatremia. The nurse should assess for abnormal losses of water or low water intake and for large gains of sodium, as might occur with ingestion of over-the-counter medications with a high sodium content (such as Alka-Seltzer). Also, it is important to obtain a medication history because some prescription medications have a high sodium content. In addi-tion, the nurse notes the patient’s thirst or elevated body tem-perature and evaluates it in relation to other clinical signs. The nurse monitors for changes in behavior, such as restlessness, dis-orientation, and lethargy.

PREVENTING HYPERNATREMIA

The nurse attempts to prevent hypernatremia by offering fluids at regular intervals, particularly in debilitated patients unable to perceive or respond to thirst. If fluid intake remains inadequate, the nurse consults with the physician to plan an alternate route for intake, either by enteral feedings or by the parenteral route. If enteral feedings are used, sufficient water should be administered to keep the serum sodium and BUN within normal limits. As a rule, the higher the osmolality of the enteral feeding, the greater the need for water supplementation.

For patients with diabetes insipidus, adequate water intake must be ensured. If the patient is alert and has an intact thirst mechanism, merely providing access to water may be sufficient. If the patient has a decreased level of consciousness or other dis-ability interfering with adequate fluid intake, parenteral fluid re-placement may be prescribed. This therapy can be anticipated in patients with neurologic disorders, particularly in the early post-operative period.

CORRECTING HYPERNATREMIA

When parenteral fluids are necessary for managing hyperna-tremia, the nurse monitors the patient’s response to the fluids by reviewing serial serum sodium levels and by observing for changes in neurologic signs. With a gradual decrease in the serum sodium level, the neurologic signs should improve. As stated in the dis-cussion on management, too-rapid reduction in the serum sodium level renders the plasma temporarily hypo-osmotic to the fluid in the brain tissue, causing movement of fluid into brain cells and dangerous cerebral edema (Adrogue & Madias, 2000a).