eMedicine Specialties > Nephrology > Acid-Base, Fluid, and Electrolyte Disorders

Hypernatremia: Treatment & Medication

Author: Ivo Lukitsch, MD, Faculty, Department of Internal Medicine, Section of Nephrology, Tulane University School of Medicine
Coauthor(s): Trung Q Pham, MD, Consulting Staff, Department of Internal Medicine, Kayenta Health Center
Contributor Information and Disclosures

Updated: Apr 27, 2009

Treatment

Medical Care

The goals of management in hypernatremia are (1) recognition of the symptoms, when present; (2) identification of the underlying cause(s); (3) correction of volume disturbances; and (4) correction of hypertonicity.¹⁴

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 period of less than 48 hours, should be corrected rapidly. Chronic hypernatremia, however, should be corrected more slowly due to the risks of brain edema during treatment (see image below and Image 1). The brain adjusts to and mitigates chronic hypernatremia by increasing the intracellular content of organic osmolytes. If extracellular tonicity is rapidly decreased, water will move into the brain cells, producing cerebral edema (herniation, permanent neurologic deficits, myelinolysis).

• Correct the serum sodium at an initial rate of 1-2 mEq/L/hr
• Replace 50% of the calculated water deficit over the first 12-24 hours
• Replace the remaining deficit over the next 24 hours
• Perform measurements of 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/or a total of 10 mEq/d (eg, 160 mEq/L to 150 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

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 x premorbid weight x (1 - 140/Na⁺)

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
    • 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 (D₅ W): 0 mmol/L
• 0.2% sodium chloride in 5% dextrose in water (D₅ 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

And 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. The serum sodium concentration of a 70 kg man is 165 mmol/L. This man is found to have hypernatremia due to insensible water loss.

The man's TBW is calculated by the following:

(0.5 x 70) = 35 L

To reduce the man's serum sodium, D₅ W will be used. Thus, the retention of 1 L of D₅ W 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.

• Clinically important: In a study by Lindner and colleagues, the predictive potential of the above formulae (and others) were investigated.¹⁵ The investigators found that all formulae correlated significantly with measured changes in serum sodium in the patient cohort as a total. However the individual variations were extreme. Thus, the above formulae can only guide therapy, but serial measurements of serum sodiumare prudent. These data are no surprise considering that interindividual variables make it difficult to precisely estimate the individual TBW. For example, the degree to which interindividual differences in levels of body fatness affect TBW is very large.³

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.
• Hypernatremia in the setting of volume overload may require dialysis for correction.
• Although water can be replaced by oral and parenteral routes, an obtunded patient requires parenteral treatment. If the deficit is small and the is patient alert and oriented, oral correction may be substituted.
• 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.

Surgical Care

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

Consultations

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

Diet

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

Activity

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

Medication

Some patients with nephrogenic diabetes insipidus—particularly those in whom it is mild or incomplete—may benefit from diuretic therapy (ie, thiazides) in an effort to increase proximal tubular reabsorption and decrease delivery to diluting segments where water may be lost. Inhibition of cyclooxygenase by nonsteroidal anti-inflammatory drugs (NSAIDs) may attenuate the polyuria in these patients. In addition, any medications that may cause nephrogenic diabetes insipidus (such as lithium) may require discontinuation.

In patients with central diabetes insipidus, desmopressin administered orally or intranasally may be used. Pharmacologic agents can be used in partial central diabetes insipidus to increase circulating AVP. These drugs include chlorpropamide, clofibrate, and carbamazepine.

Diuretics

These drugs may be used to enhance sodium excretion.

Hydrochlorothiazide (Esidrix, HydroDIURIL, Microzide)

Inhibits the reabsorption of sodium in the distal tubules, causing increased excretion of sodium and water, as well as of potassium and hydrogen ions.

Vasopressin analogs

These agents may enhance sodium excretion.

Desmopressin (DDAVP)

Increases cellular permeability of collecting ducts, resulting in the reabsorption of water by the kidneys.

• Search for CME/CE on This Topic »

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