eMedicine Specialties > Pediatrics: General Medicine > Endocrinology

Cerebral Salt-Wasting Syndrome

Author: James E Springate, MD, Associate Professor of Pediatrics, State University of New York at Buffalo; Attending Physician, Department of Pediatrics, Division of Pediatric Nephrology, Women & Children's Hospital of Buffalo
Contributor Information and Disclosures

Updated: Sep 23, 2009

Introduction

Background

First described by Peters et al in 1950, cerebral salt-wasting syndrome (CSWS) is defined by the development of excessive natriuresis and subsequent hyponatremic dehydration in patients with intracranial disease.1 Differentiation of this disorder from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), a common cause of hyponatremia in this setting, can be difficult but is important because treatment options may differ.

Possible mechanisms for cerebral salt-wasting syn...

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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Possible mechanisms for cerebral salt-wasting syn...

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.


Pathophysiology

The exact mechanism underlying renal salt wasting in this syndrome remains unclear. One hypothesis is that an exaggerated renal pressure–natriuresis response caused by increased activity of the sympathetic nervous system and dopamine release is responsible for urinary sodium loss. Another hypothesis involves release of natriuretic factors, possibly including brain natriuretic peptide (C-type natriuretic peptide or an ouabainlike peptide) by the injured brain. Kojima et al have described an animal model of cerebral salt-wasting syndrome that may allow better clarification of cerebral salt-wasting syndrome pathophysiology.2

Frequency

United States

Exact incidence data for this disorder are not available. Approximately 60% of children with brain injuries or tumors develop hyponatremia during their hospital course. Some experts suggest that cerebral salt-wasting syndrome is responsible for hyponatremia at least as often as SIADH, particularly in neurosurgical patients. Other studies indicate that cerebral salt-wasting syndrome explains the development of hyponatremia in no more than 6% of patients with acute brain injuries.3

Mortality/Morbidity

Cerebral salt-wasting syndrome usually appears in the first week after brain injury and spontaneously resolves in 2-4 weeks. Death and complication rates for this syndrome are not available. Failure to distinguish cerebral salt-wasting syndrome from SIADH as the cause of hyponatremia could lead to improper therapy (ie, fluid restriction), thereby exacerbating intravascular volume depletion and potentially jeopardizing cerebral perfusion.

Age

Cerebral salt-wasting syndrome can occur at any age. Published reports include patients aged 6 months to 65 years.

Clinical

History

  • Hyponatremia and cerebral salt-wasting syndrome (CSWS)
    • 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.
    • 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.

Physical

  • Physical signs 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.
  • 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 sunken anterior fontanel. These signs usually appear only when the degree of dehydration is moderate to severe.

Causes

Cerebral salt-wasting syndrome occurs in the setting of acute CNS disease. Conditions include the following:

  • Head injury
  • Brain tumor
  • Intracranial surgery
  • Stroke
  • Intracerebral hemorrhage
  • Tuberculous meningitis
  • Craniosynostosis repair

More on Cerebral Salt-Wasting Syndrome

Overview: Cerebral Salt-Wasting Syndrome
Differential Diagnoses & Workup: Cerebral Salt-Wasting Syndrome
Treatment & Medication: Cerebral Salt-Wasting Syndrome
Follow-up: Cerebral Salt-Wasting Syndrome
Multimedia: Cerebral Salt-Wasting Syndrome
References
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References

  1. Peters JP, Welt LG, Sims EA, et al. A salt-wasting syndrome associated with cerebral disease. Trans Assoc Am Physicians. 1950;63:57-64. [Medline].

  2. Kojima J, Katayama Y, Moro N, et al. Cerebral salt wasting in subarachnoid hemorrhage rats: model, mechanism, and tool. Life Sci. Apr 1 2005;76(20):2361-70. [Medline].

  3. Rivkees SA. Differentiating appropriate antidiuretic hormone secretion, inappropriate antidiuretic hormone secretion and cerebral salt wasting: the common, uncommon, and misnamed. Curr Opin Pediatr. Aug 2008;20(4):448-52. [Medline].

  4. Maesaka JK, Miyawaki N, Palaia T, Fishbane S, Durham JH. Renal salt wasting without cerebral disease: diagnostic value of urate determinations in hyponatremia. Kidney Int. Apr 2007;71(8):822-6. [Medline].

  5. Celik US, Alabaz D, Yildizdas D, et al. Cerebral salt wasting in tuberculous meningitis: treatment with fludrocortisone. Annals of Tropical Paediatrics. 2005;25:297-302. [Medline].

  6. Diringer MN, Zazulia AR. Hyponatremia in neurologic patients: consequences and approaches to treatment. The Neurologist. 2006;12:117-126. [Medline].

  7. Gutierrez OM, Lin HY. Refractory hyponatremia. Kidney Int. Jan 2007;71(1):79-82. [Medline].

  8. Harrigan MR. Cerebral salt wasting syndrome: a review. Neurosurgery. Jan 1996;38(1):152-60. [Medline].

  9. Kappy MS, Ganong CA. Cerebral salt wasting in children. Adv Pediatr. 1996;43:271-308. [Medline].

  10. Levine JP, Stelnicki E, Weiner HL, et al. Hyponatremia in the postoperative craniofacial pediatric patient population: a connection to cerebral salt wasting syndrome and management of the disorder. Plast Reconstr Surg. Nov 2001;108(6):1501-8. [Medline].

  11. Maesaka JK, Gupta S, Fishbane S. Cerebral salt-wasting syndrome: does it exist?. Nephron. Jun 1999;82(2):100-9. [Medline].

  12. McGirt MJ, Blessing R, Nimjee SM, et al. Correlation of serum brain natriuretic peptide with hyponatremia and delayed ischemic neurological deficits after subarachnoid hemorrhage. Neurosurgery. 2004;54:1369-1374. [Medline].

  13. [Guideline] Mentes JC. Hydration management. Iowa City (IA): University of Iowa Gerontological Nursing Interventions Research Center, Research Dissemination Core; 2004 Feb. [Full Text].

  14. Singh S, Bohn D, Carlotti AP, et al. Cerebral salt wasting: truths, fallacies, theories, and challenges. Crit Care Med. Nov 2002;30(11):2575-9. [Medline].

  15. Sterns RH, Silver SM. Cerebral salt wasting versus SIADH: what difference?. J Am Soc Nephrol. Feb 2008;19(2):194-6. [Medline].

  16. Taplin CE, Cowell CT, Silink M, Ambler GR. Fludrocortisone therapy in cerebral salt wasting. Pediatrics. Dec 2006;118(6):e1904-8. [Medline].

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Further Reading

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Keywords

cerebral salt-wasting syndrome, CSWS, intracranial disease, salt wasting, renal salt wasting, natriuresis, hyponatremic dehydration, syndrome of inappropriate secretion of antidiuretic hormone, SIADH, hyponatremia, cerebral edema

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Contributor Information and Disclosures

Author

James E Springate, MD, Associate Professor of Pediatrics, State University of New York at Buffalo; Attending Physician, Department of Pediatrics, Division of Pediatric Nephrology, Women & 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.

Medical Editor

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.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

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.

CME Editor

Merrily P M Poth, MD, Professor, Department of Pediatrics and Neuroscience, Uniformed Services University of the Health Sciences
Merrily P M Poth, MD is a member of the following medical societies: American Academy of Pediatrics, Endocrine Society, and Lawson-Wilkins Pediatric Endocrine Society
Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD, Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas and 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: Genentech, Inc. Honoraria Speaking and teaching; Pfizer, Inc. Honoraria Consulting

 
 
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