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Hypernatremia Treatment & Management

  • Author: Ivo Lukitsch, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Jul 14, 2016
 

Medical Care

The goals of management in hypernatremia are as follows[29] :

  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. Chronic hypernatremia (>48 h), however, should be corrected 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. 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.

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 x premorbid weight x (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 (D 5 W): 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 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.

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.[30] 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.[31] 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.

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.

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Surgical Care

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

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Consultations

Consultations include the following:

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

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.

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Activity

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

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Contributor Information and Disclosures
Author

Ivo Lukitsch, MD Consulting Staff/Faculty, Department of Nephrology, Ochsner Medical Center

Ivo Lukitsch, MD is a member of the following medical societies: American Society of Nephrology, American Society of Transplantation

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Eleanor Lederer, MD, FASN Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD, FASN is a member of the following medical societies: American Association for the Advancement of Science, International Society of Nephrology, American Society for Biochemistry and Molecular Biology, American Federation for Medical Research, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, Kentucky Medical Association, National Kidney Foundation, Phi Beta Kappa

Disclosure: Received grant/research funds from Dept of Veterans Affairs for research; Received salary from American Society of Nephrology for asn council position; Received salary from University of Louisville for employment; Received salary from University of Louisville Physicians for employment; Received contract payment from American Physician Institute for Advanced Professional Studies, LLC for independent contractor; Received contract payment from Healthcare Quality Strategies, Inc for independent cont.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology

Disclosure: Nothing to disclose.

Additional Contributors

Anil Kumar Mandal, MD Clinical Professor, Department of Internal Medicine, Division of Nephrology, University of Florida College of Medicine

Anil Kumar Mandal, MD is a member of the following medical societies: American College of Clinical Pharmacology, American College of Physicians, American Society of Nephrology, Central Society for Clinical and Translational Research

Disclosure: Nothing to disclose.

Acknowledgements

Trung Q Pham, MD Consulting Staff, Department of Internal Medicine, Kayenta Health Center

Disclosure: Nothing to disclose.

References
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Figure A: Normal cell. Figure B: Cell initially responds to extracellular hypertonicity through passive osmosis of water extracellularly, resulting in cell shrinkage. Figure C: Cell actively responds to extracellular hypertonicity and cell shrinkage in order to limit water loss through transport of organic osmolytes across the cell membrane, as well as through intracellular production of these osmolytes. Figure D: Rapid correction of extracellular hypertonicity results in passive movement of water molecules into the relatively hypertonic intracellular space, causing cellular swelling, damage, and ultimately death.
Table 1. Characteristics and symptoms of hypernatremia
Characteristics of hypernatremia Symptoms related to the characteristics of hypernatremia
Cognitive dysfunction and symptoms associated with neuronal cell shrinkage Lethargy, obtundation, confusion, abnormal speech, irritability, seizures, nystagmus, myoclonic jerks
Dehydration or clinical signs of volume depletion Orthostatic blood pressure changes, tachycardia, oliguria, dry oral mucosa, abnormal skin turgor, dry axillae,
Other clinical findings Weight loss, generalized weakness
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