Guidelines Summary

The Society for Endrocrinology has issued guidelines for the inpatient management of cranial [central] diabetes insipidus (CDI) which include the following recommendations for the management of hypernatremia^[45]:

Patients with CDI and impaired consciousness or who are unable to manage own fluid intake should have fluid status assessed at least every 12 hours, with fluid input and urine output monitoring and measurement of serum sodium.
Patients with intercurrent illness or decompensated CDI should receive urgent clinical assessment of volume and hydration status and measurement of serum sodium and potassium and kidney function.Hypernatremia should be managed as a medical emergency. Serum sodium should be measured every 4 hours during fluid resuscitation, reducing to no less frequently than every 12 hours until the patient is clinically and biochemically stable. Patients with high urine output with low urine osmolality require desmopressin (DDAVP).
Fluid replacement optimization is the first priority, followed by need assessement for DDAVP.
The type and volume of fluid replacement should be a combination of the standard daily fluid and electrolyte requirement with a component of the estimated fluid deficit.
Avoid overcorrection of hypernatremia: For acute hypernatremia, serum sodium should be corrected at a rate of 5 mmol/L in the first hour (or until symptoms improve) and is limited to 10 mmol/L per 24 h. For asymptomatic or mild hypernatremia, serum sodium corrections should not exceed 0.5 mmol/Lhr and is limited to 10 mmol/L per 24 h

Medication

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Media Gallery

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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Author

Ivo Lukitsch, MD Consulting Staff/Faculty, Department of Nephrology, Ochsner Medical Center

Ivo Lukitsch, MD is a member of the following medical societies: American Society of Nephrology, American Society of Transplantation

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.

Eleanor Lederer, MD, FASN Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD, FASN is a member of the following medical societies: American Association for the Advancement of Science, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: American Society of Nephrology<br/>Received income in an amount equal to or greater than $250 from: Healthcare Quality Strategies, Inc.

Chief Editor

Vecihi Batuman, MD, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Interim Chair, Deming Department of Medicine, Tulane University School of Medicine

Vecihi Batuman, MD, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology, Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Additional Contributors

Anil Kumar Mandal, MD Clinical Professor, Department of Internal Medicine, Division of Nephrology, University of Florida College of Medicine

Anil Kumar Mandal, MD is a member of the following medical societies: American College of Clinical Pharmacology, American College of Physicians, American Society of Nephrology, Central Society for Clinical and Translational Research

Disclosure: Nothing to disclose.

Acknowledgements

Trung Q Pham, MD Consulting Staff, Department of Internal Medicine, Kayenta Health Center

Disclosure: Nothing to disclose.

Characteristics of hypernatremia	Symptoms related to the characteristics of hypernatremia
Cognitive dysfunction and symptoms associated with neuronal cell shrinkage	Lethargy, obtundation, confusion, abnormal speech, irritability, seizures, nystagmus, myoclonic jerks
Dehydration or clinical signs of volume depletion	Orthostatic blood pressure changes, tachycardia, oliguria, dry oral mucosa, abnormal skin turgor, dry axillae,
Other clinical findings	Weight loss, generalized weakness

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