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Care for such patients must be coordinated between multiple specialties as the treatment of cerebral salt wasting may include additional fluid volume which can exacerbate issues including cerebral edema, pulmonary edema, heart failure, and renal dysfunction. Additional attention should be paid to the carrier fluids for the other medications and to avoid infusing too much free water to the patient. Ĭerebral salt wasting often occurs after significant CNS pathology such as aneurysmal subarachnoid hemorrhage. If the patient truly has cerebral salt wasting, they are hypovolemic, and the SIADH treatment modalities would be detrimental by exacerbating the hypovolemia. In cases of SIADH, the treatment is typically fluid restriction, hypertonic saline, demeclocycline, and/or furosemide.

The most important issue is to distinguish between cerebral salt wasting and syndrome of inappropriate secretion of antidiuretic of hormone (SIADH) as they are treated with opposite approaches. Most experts recommend correcting no more than 10 meq/L/24 hours or 1 meq/L every 2 hours. There is the risk of central pontine myelinolysis if the hyponatremia is corrected too quickly, especially for long-standing hyponatremia. Additionally, hyponatremia should not be corrected too quickly. Overcorrection of the serum sodium can lead to hypernatremia which can cause muscle twitching, lethargy, seizure, and death. When correcting the hyponatremia, the serum sodium should be monitored frequently. Some have advocated for the use of fludrocortisone as well for the treatment of cerebral salt wasting. For moderate to severe cases of hyponatremia, more aggressive sodium replenishment may be required with either hypertonic saline such as 3% hypertonic saline and/or salt tabs (1 to 2 grams up to three times daily) as well as limiting free water intake. The isotonic fluid provides the fluid for the hypovolemic patient as well as helps to restore the body's sodium stores.

Typically, the patient is started on isotonic saline for mild to moderate cases of hyponatremia of cerebral salt wasting. Secondly, the patient must be volume repleted while treating the hyponatremia. This treatment is covered in the StatPearls article on acute subarachnoid hemorrhage. The treatment of cerebral salt wasting (CSW) and syndrome of inappropriate secretion of antidiuretic of hormone (SIADH) is very different, so it is critical to have the correct diagnosis prior to initiating treatment.Īs cerebral salt wasting typically occurs after aneurysmal subarachnoid hemorrhage, the first treatment strategies are targeted at treating the underlying subarachnoid hemorrhage and aneurysm or another CNS insult. Many times cerebral salt wasting becomes a diagnosis of exclusion after labs reveal serum hyponatremia with increased urine sodium levels. Other potential causes of hyponatremia should also be sought including polydipsia, renal disease, use of diuretics, heart failure, hypothyroidism, heart failure, malignancies, hormone deficiency, and pseudohyponatremia. However, with SIADH, the patient is euvolemic to hypervolemic from the retained free water as compared to the hypovolemic picture of cerebral salt wasting. Syndrome of inappropriate secretion of antidiuretic of hormone (SIADH) will have a similar laboratory picture as cerebral salt wasting with hyponatremia and increased urine sodium.

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The patient must also have signs or symptoms of hypovolemia such as hypotension, decreased central venous pressure, lack of skin turgor, or elevated hematocrit. Urine osmolality is elevated above 100 mosmol/kg. Urine sodium is typically elevated above 40 meq/L. Urine studies are commonly checked for urine sodium and osmolality. Evaluation for cerebral salt wasting begins with a basic metabolic panel (BMP) to identify the hyponatremia (serum sodium less than 135 meq/L). It is critically important to distinguish cerebral salt wasting (CSW) from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) as the treatments are opposite.

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