Hypernatremia Treatment & Management

The goals of management in hypernatremia are as follows ^[39] :

1. Recognition of the symptoms, when present
2. Identification of the underlying cause(s)
3. Correction of volume disturbances
4. Correction of hypertonicity

Correcting the hypertonicity requires a careful decrease in serum sodium and plasma osmolality with the replacement of free water, either orally or parenterally. The rate of sodium correction depends on how acutely the hypernatremia developed and on the severity of symptoms.

Acute symptomatic hypernatremia, defined as hypernatremia occurring in a documented period of less than 24 hours, should be corrected rapidly. With chronic hypernatremia (> 48 h), established practice is to correct more slowly due to the risks of brain edema during treatment. The brain adjusts to and mitigates chronic hypernatremia by increasing the intracellular content of organic osmolytes. The concern is that if extracellular tonicity is rapidly decreased, water will move into the brain cells, producing cerebral edema, which may lead to herniation, permanent neurologic deficits, and myelinolysis.

However, a study by Chauhan et al found no evidence that rapid correction of hypernatremia is associated with a higher risk for mortality, seizure, alteration of consciousness, and/or cerebral edema in critically ill adult patients with hypernatremia. The study included 122 patients with serum sodium concentrations > 155 mEq/L on hospital admission and 327 patients whose serum sodium rose to > 155 mEq/L during hospitalization; 128 of the cases of hospital-acquired hypernatremia were considered chronic, because the disturbance developed over > 48 hours. ^[40]

In-hospital 30-day mortality rates were comparable with rapid (> 0.5 mmol/L per hour) and slower (≤0.5 mmol/L per hour) correction rates in patients with hypernatremia at admission (25% versus 28%, respectively; P=0.80) as well as in patients with hospital-acquired hypernatremia (44% versus 40%, respectively; P=0.50). The adjusted odds ratio (aOR) of mortality with rapid versus slow correction was the same (1.3) in both admission and hospital-acquired hypernatremia. Chart review did not reveal a single case of cerebral edema attributable to rapid hypernatremia correction. ^[40]

An accompanying editorial by Sterns points out that the recommendations for the slow correction of hypernatremia are derived from the pediatric literature, which contains reports of rehydration seizures due to cerebral edema infants with hypertonic dehydration. Those reports confirmed the safety of a correction rate ≤12 mEq/L per day for dehydrated infants, but never defined a precise harmful rate. ^[41]

Chauhan et al note that two previous studies of hypernatremia in adults reported a higher risk of mortality with excessively slow rates of sodium correction and lower mortality with a greater reduction rate. ^[40]

Treatment recommendations for symptomatic hypernatremia

Recommendations are as follows:

• Establish documented onset (acute, < 24 h; chronic, >24h)
• In acute hypernatremia, correct the serum sodium at an initial rate of 2-3 mEq/L/h (for 2-3 h) (maximum total, 12 mEq/L/d).
• Measure serum and urine electrolytes every 1-2 hours
• Perform serial neurologic examinations and decrease the rate of correction with improvement in symptoms
• Chronic hypernatremia with no or mild symptoms should be corrected at a rate not to exceed 0.5 mEq/L/h and a total of 8-10 mEq/d (eg, 160 mEq/L to 152 mEq/L in 24 h).
• If a volume deficit and hypernatremia are present, intravascular volume should be restored with isotonic sodium chloride prior to free-water administration.

Estimation of the replacement fluid

Total body water (TBW) refers to the lean body weight of the patient (percentage of TBW decreases in morbidly obese patients). The TBW deficit in the hyperosmolar patient that needs to be replaced can be roughly estimated using the formula following formula:

TBW deficit = correction factor × premorbid weight × (1 - 140/Na⁺)

Ongoing losses (insensible, renal) need to be added.

However, the formulae below, by Adrogué–Madias, are preferred over the conventional equation for water deficit, because the older equation underestimates the deficit in patients with hypotonic fluid loss and is not useful in situations in which sodium and potassium must be used in the infusate. Formulas used to manage hypernatremia are outlined below.

Equation 1: TBW = weight (kg) x correction factor

Correction factors are as follows:

• Children: 0.6
• Nonelderly men: 0.6
• Nonelderly women: 0.5
• Elderly men: 0.5
• Elderly women: 0.45

Equation 2: Change in serum Na⁺ = (infusate Na⁺ - serum Na⁺) ÷ (TBW + 1)

Equation 3: Change in serum Na⁺ = ([infusate Na⁺ + infusate K^+] – serum Na⁺) ÷ (TBW + 1)

Equation 2 allows for the estimation of 1 L of any infusate on serum Na⁺ concentration. Equation 3 allows for the estimation of 1 L of any infusate containing Na⁺ and K⁺ on serum Na⁺.

Common infusates and their Na⁺ contents include the following:

• 5% dextrose in water (D5W): 0 mmol/L
• 0.2% sodium chloride in 5% dextrose in water (D ₅ 2NS): 34 mmol/L
• 0.45% sodium chloride in water (0.45NS): 77 mmol/L
• Ringer's lactate solution: 130 mmol/L
• 0.9% sodium chloride in water (0.9NS): 154 mmol/L

An example of the use of the above calculations is as follows: An obtunded 80-year-old man is brought to the emergency room with dry mucous membranes, fever, tachypnea, and a blood pressure of 134/75 mm Hg. His serum sodium concentration is 165 mmol/L. He weighs 70 kg. This man is found to have hypernatremia due to insensible water loss.

The man's TBW is calculated by the following:

(0.5 × 70) = 35 L

To reduce the man's serum sodium, D5W will be used. Thus, the retention of 1 L of D5W will reduce his serum sodium by (0 - 165) ÷ (35 + 1) = -4.6 mmol. The goal is to reduce his serum sodium by no more than 10 mmol/L in a 24-hour period. Thus, (10 ÷ 4.6) = 2.17 L of solution is required. About 1-1.5 L will be added for obligatory water loss to make a total of up to 3.67 L of D₅ W over 24 hours, or 153 cc/h.

A clinically important study by Lindner and colleagues found that all the above formulae correlated significantly with measured changes in serum sodium in the patient cohort as a whole, but the individual variations were extreme. ^[42] Thus, although the above formulae can guide therapy, serial measurements of serum sodium are prudent. That finding is no surprise, considering that interindividual variables make it difficult to precisely estimate the individual TBW and its distribution in different body compartments. ^[43] For example, the degree to which interindividual differences in body fat percentage affect TBW is very large. ^[4]

Other treatment considerations

If hypernatremia is accompanied by hyperglycemia with diabetes, take care when using a glucose-containing replacement fluid. However, the appropriate use of insulin will help during correction.

In hypervolemic and hypernatremic patients in the ICU who have an impaired renal excretion of sodium and potassium (eg, after renal failure) an addition of a loop diuretic to free water boluses increases renal sodium excretion. Fluid loss during loop diuretic therapy must be restored with the administration of fluid that is hypotonic to the urine.

Use of thiazide diuretics to enhance sodium excretion has been suggested as a treatment for hypernatremia acquired in the ICU. However, a randomized, placebo-controlled trial in 50 ICU patients found that hydrochlorothiazide, 25 mg/day for up to 7 days, did not have a significant effect on serum or urinary sodium concentration. ^[44]

Hypernatremia in the setting of volume overload (eg, heart failure and pulmonary edema) may require dialysis for correction.

Although water can be replaced by oral and parenteral routes, an obtunded patient with a large free water deficit likely requires parenteral treatment. If the deficit is small and the patient is alert and oriented, oral correction may be preferred.

Once hypernatremia is corrected, efforts are directed at treating the underlying cause of the condition. Such efforts may include free access to water and better control of diabetes mellitus. In addition, correction of hypokalemia and hypercalcemia as etiologies for nephrogenic diabetes insipidus may be required. Vasopressin (AVP, DDAVP) should be used for the treatment of central diabetes insipidus. 

Inpatient care is appropriate only as it relates to the correction of underlying diseases that may lead to hypernatremia (diabetes mellitus). Transfer may only be necessary in the setting of severe head trauma with central diabetes insipidus.

Surgical treatment may be required in the setting of severe central nervous system trauma and associated central diabetes insipidus.

Consultations include the following:

• Neurosurgeon (head trauma)
• Endocrinologist (diabetes insipidus or diabetes mellitus)
• Nephrologist (nephrogenic etiologies for hypernatremia)

Diet should be altered as applicable to diabetes mellitus and need for increased water intake during increased insensible loss. A low-sodium diet will reduce oral solute intake and therefore diminish renal water loss.

Activity alterations are applicable only as related to free access to water.