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Pediatric Hypernatremia Workup

  • Author: Ewa Elenberg, MD, MEd; Chief Editor: Timothy E Corden, MD  more...
Updated: Feb 13, 2014

Laboratory Studies

Studies indicated in patients with suspected hypernatremia are listed below.

Serum tests

Obtain levels of sodium, osmolality, BUN, and creatinine.

Other laboratory measurements include aldosterone, cortisol, antidiuretic hormone (ADH), and corticotropin (ACTH) levels

Urine sodium concentration and osmolality

In cases of hypovolemic hypernatremia, extrarenal losses show urine sodium levels of less than 20 mEq/L, and in cases of renal losses, urine sodium values are more than 20 mEq/L.

In euvolemic hypernatremia, urine sodium data vary.

In hypervolemic hypernatremia, the urine sodium level is more than 20 mEq/L.


Imaging Studies

Imaging studies of the head should be considered in alert patients with severe hypernatremia to rule out a hypothalamic lesion affecting the thirst center.

CT scans may help in diagnosing intracranial tumors, granulomatous diseases (eg, sarcoid, tuberculosis, histiocytosis), and other intracranial pathologies.

MRI further delineates the pathology.

Contributor Information and Disclosures

Ewa Elenberg, MD, MEd Associate Professor of Pediatrics, Renal Section, Texas Children's Hospital, Baylor College of Medicine

Ewa Elenberg, MD, MEd is a member of the following medical societies: American Society of Nephrology, American Society of Pediatric Nephrology

Disclosure: Nothing to disclose.


Muthukumar Vellaichamy, MD, FAAP Clinical Assistant Professor, Department of Pediatrics, Wesley Medical Center, University of Kansas School of Medicine-Wichita

Muthukumar Vellaichamy, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, Society of Critical Care Medicine

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.

Barry J Evans, MD Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center

Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society

Disclosure: Nothing to disclose.

Additional Contributors

G Patricia Cantwell, MD, FCCM Professor of Clinical Pediatrics, Chief, Division of Pediatric Critical Care Medicine, University of Miami Leonard M Miller School of Medicine/ Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Director, Palliative Care Team, Holtz Children's Hospital; Medical Manager, FEMA, South Florida Urban Search and Rescue, Task Force 2

G Patricia Cantwell, MD, FCCM is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, Wilderness Medical Society

Disclosure: Nothing to disclose.

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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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