Cerebral Salt-Wasting Syndrome Clinical Presentation

  • Author: Sudha Garimella-Krovi, MBBS; Chief Editor: Stephen Kemp, MD, PhD   more...
 
Updated: Mar 29, 2012
 

History

Hyponatremia and cerebral salt-wasting syndrome

As the decline in serum sodium concentration reduces serum osmolality, a tonicity gradient develops across the blood-brain barrier that causes cerebral edema. Symptoms include lethargy, agitation, headache, altered consciousness, seizures, and coma.[8]

The severity of symptoms typically reflects the magnitude and rapidity of the decrease in serum sodium concentration.

Intravascular volume depletion

Historical features suggesting hypovolemia include thirst, abrupt weight loss, decreasing urinary frequency, and negative fluid balance.

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Physical Examination

Physical signs of cerebral salt-wasting syndrome (renal salt wasting) include those associated with severe hyponatremia or intravascular volume depletion.

Hyponatremia can be indicated by acute CNS dysfunction such as altered mental status, seizures, and coma.

The differentiation of SIADH from cerebral salt-wasting syndrome depends on an accurate estimation of extracellular volume. Unfortunately, no single physical finding can accurately and reproducibly measure effective circulating volume. Commonly used signs of hypovolemia include orthostatic tachycardia or hypotension, increased capillary refill time, increased skin turgor, dry mucous membranes, and a sunken anterior fontanel. These signs usually appear only when the degree of dehydration is moderate to severe. Central venous pressure may be an unreliable determinant of extracellular volume.

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Contributor Information and Disclosures
Author

Sudha Garimella-Krovi, MBBS  Clinical Assistant Professor of Pediatrics, University of Buffalo, State University of New York School of Medicine and Biomedical Sciences

Sudha Garimella-Krovi, MBBS is a member of the following medical societies: American Society of Pediatric Nephrology

Disclosure: Nothing to disclose.

Coauthor(s)

James E Springate, MD  Associate Professor of Pediatrics, University of Buffalo, State University of New York School of Medicine and Biomedical Sciences; Attending Physician, Department of Pediatrics, Division of Pediatric Nephrology, Women and Children's Hospital of Buffalo

James E Springate, MD is a member of the following medical societies: American Academy of Pediatrics, American Physiological Society, American Society of Pediatric Nephrology, International Pediatric Transplant Association, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD  Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas for Medical Sciences College of Medicine, Arkansas Children's Hospital

Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Additional Contributors

Erawati V Bawle, MD, FAAP, FACMG Division of Genetic and Metabolic Disorders, Children's Hospital of Michigan; Professor (Clinician-Educator), Department of Pediatrics, Wayne State University School of Medicine

Erawati V Bawle, MD, FAAP, FACMG is a member of the following medical societies: American Academy of Pediatrics, American College of Medical Genetics, American Medical Association, and American Society of Human Genetics

Disclosure: Nothing to disclose.

Barry B Bercu, MD Professor, Departments of Pediatrics, Molecular Pharmacology and Physiology, University of South Florida College of Medicine, All Children's Hospital

Barry B Bercu, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Federation for Clinical Research, American Medical Association, American Pediatric Society, Association of Clinical Scientists, Endocrine Society, Florida Medical Association, Lawson-Wilkins Pediatric Endocrine Society, Pituitary Society, Society for Pediatric Research, Society for the Study of Reproduction, and Southern Society for Pediatric Research

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.

References

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Possible mechanisms for cerebral salt-wasting syndrome. The injured brain may release natriuretic proteins that act directly on the kidney. In addition, cerebral injury may increase sympathetic nervous system activity, elevating renal perfusion pressure and releasing dopamine.
 
 
 
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