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Hypernatremia in Emergency Medicine Workup

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

Laboratory Studies

When hypernatremia is discovered in a patient, obtain urine osmolality and sodium levels. Check serum glucose level to ensure that osmotic diuresis has not occurred.

The kidneys' normal response to hypernatremia is excretion of a minimal amount of maximally concentrated urine. If urine osmolarity is high, suspect extrarenal hypotonic fluid losses (eg, vomiting, low sodium diarrhea, sweat, evaporation from burns, low sodium ostomy output). The urine also is concentrated in salt overload states, although the total volume should increase.

Isotonic urine osmolality can be observed with diuretics, osmotic diuresis (mannitol, glucose, urea), or salt wasting.

Hypotonic urine and polyuria are characteristic of DI. Note, however, that partial DI can occur in which some concentrating ability remains, especially in the absence of a water load.

Serum sodium levels of more than 190 mEq/L usually indicate long-term salt ingestion.

Serum sodium levels of more than 170 mEq/L usually indicate DI.

Serum sodium levels of 150-170 mEq/L usually indicate dehydration.


Imaging Studies

Head CT scan or MRI is suggested in all patients with severe hypernatremia.

Traction on dural bridging veins and sinuses caused by movement of water from the brain and brain shrinkage can lead to intracranial hemorrhage, most often in the subdural space.

Hemoconcentration from total body water loss may lead to dural sinus thrombosis.

Imaging studies may indicate a central cause for hypernatremia.


Other Tests

Water deprivation test

With DI, water deprivation induces serum hyperosmolality and hypernatremia, but urine osmolality does not increase appropriately.

ADH stimulation

With nephrogenic DI, urine osmolality does not increase after ADH or desmopressin acetate administration.

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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