Pediatric Hypernatremia Medication

  • Author: Ewa Elenberg, MD; Chief Editor: Timothy E Corden, MD   more...
 
Updated: Jan 10, 2012
 

Medication Summary

The medications described below are used in patients with diabetes insipidus who have hypernatremia.

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Vasopressin and vasopressin analogs

Class Summary

Desmopressin is a synthetic ADH with actions mimicking vasopressin. These agents are used to treat diabetes insipidus, which deprives the kidney of its capacity to produce concentrated urine. This effect results in large volumes of dilute urine (polyuria) and excessive thirst (polydipsia). Serum sodium concentrations may be elevated, but hypernatremia is most likely to be severe when fluid is restricted.

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Desmopressin acetate (DDAVP)

 

Structural analog of vasopressin (ADH), the endogenous posterior pituitary hormone that maintains serum osmolality in a physiologically acceptable range. Works in neurohypophysial (eg, central) diabetes insipidus. Exerts similar antidiuretic effects. Vasopressin increases resorption of water at level of renal collecting duct, reducing urinary flow and increasing urine osmolality.

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Vasopressin (Pitressin)

 

Exogenous, parenteral form of ADH. Antidiuretic and increases resorption of water at renal collecting ducts.

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Diuretics

Class Summary

These drugs promote the excretion of water and electrolytes by the kidneys. They are used in patients with nephrogenic diabetes insipidus.

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Hydrochlorothiazide (Esidrix, HydroDIURIL)

 

Works by increasing excretion of sodium, chloride, and water by inhibiting sodium ion transport across renal tubular epithelium. Resulting sodium depletion reduces glomerular filtration rate, enhancing reabsorption of fluid in proximal portion of nephron, decreasing delivery of sodium to ascending limb of loop of Henle and consequently reducing capacity to dilute urine.

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Contributor Information and Disclosures
Author

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

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

Disclosure: Nothing to disclose.

Coauthor(s)

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

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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; Medical Director, Palliative Care Team, Director, Pediatric Critical Care Transport, Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Manager, FEMA, Urban Search and Rescue, South Florida, Task Force 2; Pediatric Medical Director, Tilli Kids – Pediatric Initiative, Division of Hospice Care Southeast Florida, Inc

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, and Wilderness Medical Society

Disclosure: Nothing to disclose.

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, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Mary E Cataletto, MD  Director of Children's Sleep Services, Winthrop Sleep Disorders Center, Mineola, NY; Professor of Clinical Pediatrics, State University of New York at Stony Brook, Stony Brook, NY

Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians

Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

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, and Wisconsin Medical Society

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.
 
 
 
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