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Hypernatremia in Emergency Medicine Treatment & Management

  • Author: Zina Semenovskaya, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
Updated: Jun 27, 2016

Prehospital Care

Standard supportive attention to the ABCs is appropriate. Hypovolemic patients with signs of hemodynamic compromise (eg, tachycardia, hypotension) should receive volume resuscitation with isotonic sodium chloride solution.

If a thirsty patient's mental status allows, he or she does not need to be kept in a nothing-by-mouth status. In the debilitated nursing home patient, hypodermoclysis (subcutaneous fluid administration) may be considered as an alternative to transport to a hospital.


Emergency Department Care

The emergency department management of hypernatremia revolves around 2 tasks: restoration of normal serum tonicity, and diagnosis and treatment of the underlying etiology. When possible, providing free water to a patient orally is preferred.

Hypernatremia should not be corrected at a rate greater than 1 mEq/L per hour.

Carefully monitor all patients' inputs and outputs during treatment.

Consider CNS imaging to exclude a central cause or to identify CNS bleeding from stretching of veins.

Using isotonic sodium chloride solution, stabilize hypovolemic patients who have unstable vital signs before correcting free water deficits because hypotonic fluids quickly leave the intravascular space and do not help to correct hemodynamics. Once stabilization has occurred, free water deficits can be replaced either orally or intravenously.

Euvolemic patients can be treated with hypotonic fluids, either orally or intravenously (ie, dextrose 5% in water solution [D5W], quarter or half isotonic sodium chloride solution), to correct free fluid deficits.

Hypervolemic patients require removal of excess sodium, which can be accomplished by a combination of diuretics and D5W infusion. Patients with acute renal failure may require dialysis.

Traditionally, correction of hypernatremia begins with a calculation of the fluid deficit as shown below. Predicted insensible and other ongoing losses are added to this number and the total is administered over 48 hours. Recheck serum electrolyte levels frequently during therapy. To avoid cerebral edema and associated complications, the serum sodium level should be lowered by no more than 1 mEq/L every hour. In patients with chronic hypernatremia, an even more gradual rate is preferred.

An alternative method to plan the correction of sodium imbalances has been proposed by Adrogue and Madias. They have devised a formula that can be used to calculate the change in serum sodium level after the administration of 1 L of a given infusate. This formula has the advantages of taking into consideration the tonicity of the infusate and encouraging reassessment of the treatment plan with each liter of solution or new set of electrolytes.

Free Water Deficit = Body Weight (kg) X Percentage of Total Body Water (TBW) X ([Serum Na / 140] - 1)

The percentage of TBW should be as follows:

  • Young men - 0.6%
  • Young women and elderly men - 0.5%
  • Elderly women - 0.4%

An example is as follows: A serum sodium level of 155 in a 60-kg young man represents a fluid deficit of 60 X 0.6 X ([155 / 140] - 1) or 3.9 L. With another 900 mL of insensible losses, the patient requires 4.8 L of fluid in the next 48 hours, resulting in an infusion rate of 100 mL/h.

The Adrogue and Madias formula is as follows: Change in Serum Sodium = ([Na] Infused - [Na] serum) / (TBW + 1)

The "1" in the denominator represents the extra liter of infusate added to TBW. When TBW is calculated as above, TBW = Body Weight (kg) X Percent Water

An example is as follows: For the patient above, the expected change can be calculated with D5W or D5 half isotonic sodium chloride solution.

For D5W, Change = (0 - 155) / ([60 X 0.6] + 1) = -4.18 mEq/L

For half isotonic sodium chloride solution, Change = (77 - 155) / ([60 X 0.6] + 1) = -2.1 mEq/L

If D5W is chosen to avoid fluid overload, an infusion rate of 250 mL/h results in a correction just over 1 mEq/h. (Note: This assumes the patient has no other losses during this time. Intrinsic losses make the correction slower [more conservative] than calculated.)



Patients with renal failure may require dialysis to help correct sodium and fluid balance.

Contributor Information and Disclosures

Zina Semenovskaya, MD Resident Physician, Department of Emergency Medicine, Kings County Hospital, State University of New York Downstate Medical Center College of Medicine

Disclosure: Nothing to disclose.


Richard H Sinert, DO Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Vice-Chair in Charge of Research, Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Steven L Stephanides, MD Attending Physician, Department of Emergency Medicine, Eisenhower Medical Center

Steven L Stephanides, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, Society for Academic Emergency Medicine, Wilderness Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Howard A Bessen, MD Professor of Medicine, Department of Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine; Program Director, Harbor-UCLA Medical Center

Howard A Bessen, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Chief Editor

Romesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School

Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society

Disclosure: Nothing to disclose.

Additional Contributors

Joseph J Sachter, MD, FACEP Consulting Staff, Department of Emergency Medicine, Muhlenberg Regional Medical Center

Joseph J Sachter, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Association for Physician Leadership, American Medical Association, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.


The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Richard Sinert, DO, to the development and writing of this article.

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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.
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