Hypernatremia in Emergency Medicine Medication

  • Author: Zina Semenovskaya, MD; Chief Editor: Erik D Schraga, MD   more...
 
Updated: Aug 18, 2009
 

Medication Summary

Maintenance of adequate fluid intake is the most important therapy for all causes of DI that can result in hypernatremia. Hormonal and pharmacologic therapies must be tailored for the specific causes of DI (eg, central, nephrogenic). Central DI is treated with replacement therapy of ADH. The therapy for nephrogenic DI depends on reducing urine volume with combinations of salt restriction, thiazide diuretics, and prostaglandin synthetase inhibitors.

The other causes of hyponatremia do not require medications beyond hypotonic fluid for correction.

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ADH replacement therapy

Class Summary

This therapy reduces free water loss and concentrates the urine.

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Vasopressin (Pitressin)

 

Has vasopressor and ADH activity. Increases water resorption at the distal renal tubular epithelium (ADH effect) and promotes smooth muscle contraction throughout the vascular bed of the renal tubular epithelium (vasopressor effects). Vasoconstriction also is increased in splanchnic, portal, coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels. Decreases portal pressure in patients with portal hypertension. A notable undesirable effect is coronary artery constriction, which may dispose patients with coronary artery disease to cardiac ischemia. This can be prevented with concurrent use of nitrates. Duration of action is approximately 3-6 h. Short half-life lessens the risk of acute water intoxication and makes it the ideal treatment of central DI in emergent situations.

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Desmopressin acetate (DDAVP)

 

Increases cellular permeability of collecting ducts, resulting in reabsorption of water by the kidneys. Duration of action is approximately 12-24 h. Has become the long-term treatment of choice for central DI.

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Contributor Information and Disclosures
Author

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.

Coauthor(s)

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

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and 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, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

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 College of Physician Executives, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Howard A Bessen, MD  Professor of Medicine, Department of Emergency Medicine, UCLA 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.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Erik D Schraga, MD  Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

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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