Cerebral salt-wasting syndrome

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Cerebral salt-wasting syndrome
Classification and external resources
DiseasesDB 32234
eMedicine ped/354

Cerebral salt-wasting syndrome (CSWS) is a rare endocrine condition featuring hyponatremia (low blood sodium concentration) and dehydration in response to trauma/injury or the presence of tumors in or surrounding the brain. This form of hyponatraemia is due to excessive renal sodium excretion resulting from a centrally mediated process.

The condition was initially described in 1950.[1]


Primary symptoms include polyuria (at least 2.5 liters in the course of 24 hours, for adults) due to inadequate sodium retention in the body, polydipsia (excessive thirst) due to polyuria, extreme salt cravings (e.g. desire to drink pickle juice), dysautonomia, and dehydration. Patients often "self-medicate" by naturally gravitating toward a high-sodium diet and by dramatically increasing their water intake. Advanced symptoms include muscle cramps, lightheadedness, dizziness or vertigo, feelings of anxiety or panic (not mentally induced), tachycardia (rapid heart rate) or bradycardia (slow heart rate), hypotension and orthostatic hypotension sometimes resulting in syncope.[2] Other symptoms frequently associated with dysautonomia include: headaches, pallor, malaise, facial flushing, constipation or diarrhea, nausea, acid reflux, visual disturbances, numbness, nerve pain, trouble breathing, chest pains, loss of consciousness and seizures.[2]

Causes and Diagnosis[edit]

CSWS is usually caused by brain injury/trauma or cerebral lesion, tumor, or hematoma. CSWS is a diagnosis of exclusion and may be difficult to distinguish from the syndrome of inappropriate antidiuretic hormone (SIADH), which develops under similar circumstances and also presents with hyponatremia. The main clinical difference is that of total fluid status of the patient: CSWS leads to a relative or overt hypovolemia whereas SIADH is consistent with a normal to hypervolemic range. Random urine sodium concentrations tend to be lower than 100 mEq/L in CSWS and greater in SIADH . If blood-sodium levels increase when fluids are restricted, SIADH is more likely.[3]


While CSWS usually appears within the first week after brain injury and spontaneously resolves in 2–4 weeks, it can sometimes last for months or years. While fluid restriction is used to treat SIADH, CSWS requires aggressive hydration and correction of the low sodium levels using sodium chloride tablets. Sometimes, fludrocortisone (a mineralocorticoid) improves the hyponatremia.[4]


  1. ^ Peters JP, Welt LG, Sims EA, Orloff J, Needham J (1950). "A salt-wasting syndrome associated with cerebral disease". Trans. Assoc. Am. Physicians 63: 57–64. PMID 14855556. 
  2. ^ a b Tierney, Lawrence M.; McPhee, Stephen J.; Papadakis, Maxine A. (2006). Current Medical Diagnosis and Treatment 2007 (Current Medical Diagnosis and Treatment). McGraw-Hill Professional. p. 1010. ISBN 0-07-147247-9. 
  3. ^ Harrigan MR (1996). "Cerebral salt wasting syndrome: a review". Neurosurgery 38 (1): 152–60. doi:10.1097/00006123-199601000-00035. PMID 8747964. 
  4. ^ Betjes MG (2002). "Hyponatremia in acute brain disease: the cerebral salt wasting syndrome". Eur J Intern Med 13 (1): 9–14. doi:10.1016/S0953-6205(01)00192-3. PMID 11836078.