Cerebral salt-wasting syndrome

Overview

Cerebral salt-wasting syndrome (CSWS) is a rare but serious condition characterized by excessive renal loss of sodium, leading to hyponatremia (low blood sodium levels) and dehydration. It typically occurs in patients with intracranial disorders such as traumatic brain injury, subarachnoid hemorrhage, brain tumors, or neurosurgery. Unlike the more common syndrome of inappropriate antidiuretic hormone secretion (SIADH), CSWS involves true volume depletion and requires very different treatment. Prompt recognition is critical to avoid life-threatening complications.

Causes

CSWS is triggered by central nervous system (CNS) disturbances that affect the regulation of sodium and water balance. Common causes include:

• Subarachnoid hemorrhage (SAH): The most frequently associated condition

• Traumatic brain injury (TBI): Especially with damage to hypothalamic or brainstem regions

• Intracranial tumors: Particularly those involving the hypothalamus or pituitary gland

• Infections: Such as meningitis or encephalitis

• Neurosurgical procedures: Causing disruption of CNS sodium regulation

The pathophysiology involves increased secretion of natriuretic peptides and altered sympathetic nervous system activity, leading to enhanced renal sodium excretion and secondary water loss.

Symptoms

The symptoms of cerebral salt-wasting syndrome are primarily related to hyponatremia and dehydration. Common features include:

• Fatigue and weakness

• Confusion or altered mental status

• Nausea and vomiting

• Headache

• Seizures: In cases of severe hyponatremia

• Low blood pressure (hypotension)

• Decreased skin turgor and dry mucous membranes

• Polyuria (increased urination)

• Tachycardia (rapid heart rate): Due to volume depletion

Diagnosis

Diagnosis of CSWS requires careful differentiation from SIADH, as both present with hyponatremia but have opposite fluid balance profiles. Key diagnostic steps include:

• Serum sodium: Low levels (<135 mEq/L)

• Serum osmolality: Decreased, indicating true hyponatremia

• Urine sodium: Elevated (>40 mEq/L), showing inappropriate renal sodium loss

• Urine osmolality: Inappropriately high

• Volume status: Signs of hypovolemia (low blood pressure, dry mucosa, weight loss)

• Elevated hematocrit and BUN: Indicating dehydration

• Clinical context: CNS injury or neurosurgical history helps support the diagnosis

Treatment

The cornerstone of treatment for CSWS is volume and sodium replacement. Management strategies include:

• Isotonic or hypertonic saline: To correct hyponatremia and prevent further sodium loss

• Oral or IV sodium supplementation: In moderate to severe cases

• Fluid replacement: Using IV fluids to address dehydration and restore volume status

• Mineralocorticoids (e.g., fludrocortisone): May be used to promote sodium retention in persistent cases

• Frequent monitoring: Of serum sodium, electrolytes, and fluid balance to guide therapy and avoid overcorrection

Diuretics are contraindicated, and fluid restriction — used in SIADH — must be avoided in CSWS, as it worsens hypovolemia.

Prognosis

With timely and appropriate treatment, most patients with cerebral salt-wasting syndrome recover well. However, if left untreated or misdiagnosed as SIADH, it can lead to severe complications, including seizures, coma, and death due to progressive hyponatremia and dehydration. Prognosis is generally favorable when the underlying CNS condition is also managed effectively. Close monitoring and individualized fluid and sodium management are essential to prevent recurrence or long-term electrolyte imbalances.