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 a low blood sodium concentration and dehydration in response to trauma/injury or the presence of tumors in or surrounding the brain. This form of low blood sodium is due to excessive sodium excretion from the normally functioning kidney due to a disorder of the cerebrum of the brain.[1] The condition was initially described in 1950.[2]

Signs and symptoms[edit]

Signs and symptoms of CSWS include large amounts of urination (at least 3 liters of urine output over a 24 hour period for adults) due to inadequate sodium retention in the body, high amounts of sodium in the urine,[1] low blood sodium concentration,[1] excessive thirst, extreme salt cravings, dysfunction of the autonomic nervous system, 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), increased heart rate or slowed heart rate, low blood pressure and orthostatic hypotension sometimes resulting in fainting.[3] 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.[3]

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.[1] The main clinical difference is that of total fluid status of the patient: CSWS leads to a relative or overt low blood volume whereas SIADH is consistent with a normal or high blood volume.[1] If blood-sodium levels increase when fluids are restricted, SIADH is more likely.[4]

Treatment[edit]

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. In contrast to the use of fluid restriction to treat SIADH, CSWS is treated by replacing the urinary losses of water and sodium with hydration and sodium replacement.[1] The mineralocorticoid medication fludrocortisone can also improve the low sodium level.[1][5]

References[edit]

  1. ^ a b c d e f g Yee AH, Burns JD, Wijdicks EF (April 2010). "Cerebral salt wasting: pathophysiology, diagnosis, and treatment". Neurosurg Clin N Am 21 (2): 339–52. doi:10.1016/j.nec.2009.10.011. PMID 20380974. 
  2. ^ 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. 
  3. ^ 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. 
  4. ^ Harrigan MR (1996). "Cerebral salt wasting syndrome: a review". Neurosurgery 38 (1): 152–60. doi:10.1097/00006123-199601000-00035. PMID 8747964. 
  5. ^ 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.