Cerebral salt-wasting syndrome (CSWS) is a medical entity that leads to hyponatremia and hypovolemia due to dehydration, as a result of an acute or chronic and persistent underlying CNS disorder, including trauma, tumors, and other pathologies.

Patients present with the clinical manifestations of hyponatremia and hypovolemia. In general, a case of very mild hyponatremia tends to produce no noticeable symptoms; however, it has been observed that even non-severe hyponatremia can lead to devastating clinical manifestations [1]. A serum sodium concentration lower than 135 mEq/L, but over 115 mEq/L usually leads to nausea and malaise. Values less than 135 mEq/L lead to profound neurological symptomatology due to cerebral edema, including a diminished level of consciousness and lethargy, cephalalgia, epileptic phenomena and, eventually, even a comatose state [2]. There is a positive correlation between the decrease in sodium levels and the aggravation of symptoms: as the concentration of sodium in the serum of the patient declines, symptoms are exacerbated.

Hypovolemia leads to symptoms that entail dried mucous membranes (oral or nasal cavity), dry skin that lacks elasticity, sunken anterior fontanelle, and tachycardia. Profound hypovolemia causes hypotension. A vital clinical characteristic of patients affected by cerebral salt-wasting syndrome is that the aforementioned manifestations tend to respond positively to volume and sodium replacement [3] [4]. Massive polyuria that can be reversed with the simultaneous administration of vasopressin and cortisone acetate, hypotension, the absence of cardiac symptoms and hypovolemia, constitute a potential clinical picture of a patient with central diabetes insipidus and CSWS, according to a recent study [5].

CSWS is a syndrome difficult to diagnose, due to the lack of a specific set of tests to detect any pathognomonic result. The primary difficulty is its differentiation from the syndrome of inappropriate antidiuretic hormone secretion (SIADH), due to a significant similarity between these two distinct entities. The workup involved in the diagnostic procedure encompasses:

Serum sodium concentration

Reveals hyponatremia, namely a serum sodium concentration < 135 mEq/L.

Urinary output

CSWS is expected to lead to increased urine flow and dilute urine, whereas SIADH leads to a low urine flow and concentrated urine.

Urinary sodium concentration

CSWS leads to a high urinary sodium concentration, that exceeds 40 mEq/L, followed by a negative net sodium balance.

Uric acid

Fractional excretion of uric acid (FEUA) is increased in patients with the cerebral salt-wasting syndrome and hyperuricemia is detected. These findings tend to remain, despite the reversion or hyponatremia. On the contrary, the same findings that are observed in SIADH tend to regress after the correction of serum sodium [6] [7].

Phosphate

Cerebral salt-wasting syndrome leads to an increase in the fractional excretion of phosphate (FEP), in contradistinction to SIADH [7].

The primary goal of CSWS treatment is to restore normal sodium levels and address dehydration. Treatment strategies include:

• Sodium Replacement: Administering sodium through oral supplements or intravenous saline solutions.
• Fluid Management: Ensuring adequate fluid intake to prevent dehydration while avoiding fluid overload.
• Monitoring: Regular monitoring of sodium levels and fluid balance to adjust treatment as needed.

In some cases, addressing the underlying neurological condition may also be necessary to manage CSWS effectively.

The prognosis for patients with CSWS largely depends on the underlying cause and the timeliness of treatment. With appropriate management, most patients can achieve normal sodium levels and recover from symptoms. However, if left untreated, severe hyponatremia can lead to serious complications, including neurological damage.

CSWS is often associated with conditions affecting the brain, such as:

• Traumatic brain injury
• Brain surgery
• Subarachnoid hemorrhage (bleeding in the space around the brain)
• Brain tumors or infections

The exact mechanism triggering sodium loss in these conditions is not fully understood, but it is believed to involve disruptions in the brain's regulation of sodium and water balance.

CSWS is considered a rare condition, and its exact prevalence is not well-documented. It is most commonly observed in patients with acute brain injuries or neurosurgical interventions. The condition can affect individuals of any age, but it is more frequently reported in adults.

The pathophysiology of CSWS involves an imbalance in the body's regulation of sodium and water. In CSWS, the kidneys excrete excessive amounts of sodium, leading to hyponatremia and dehydration. This process is thought to be triggered by factors related to brain injury or disease, which may alter the normal hormonal and neural signals that control sodium and water balance.

Preventing CSWS primarily involves managing the underlying neurological conditions that may trigger the syndrome. This includes:

• Prompt treatment of brain injuries or infections
• Careful monitoring of sodium levels in patients with known risk factors
• Early intervention to address any signs of hyponatremia or dehydration

Cerebral Salt-Wasting Syndrome is a rare but serious condition characterized by excessive sodium loss and hyponatremia, often associated with brain injuries or diseases. Accurate diagnosis and differentiation from similar conditions like SIADH are crucial for effective treatment. With timely intervention, most patients can recover, but untreated CSWS can lead to severe complications.

If you or a loved one has been diagnosed with Cerebral Salt-Wasting Syndrome, it's important to understand the condition and its management. CSWS involves losing too much sodium, which can cause symptoms like confusion, fatigue, and dizziness. Treatment focuses on replacing lost sodium and managing fluid levels. Regular monitoring and addressing any underlying brain conditions are key to recovery. Always follow your healthcare provider's advice and attend all follow-up appointments to ensure the best outcomes.

1. Grant P, Ayuk J, Bouloux PM, et al. The diagnosis and management of inpatient hyponatraemia and SIADH. Eur J Clin Invest. 2015 Aug; 45(8): 888–894.
2. Sherlock M, O'Sullivan E, Agha A, et al. Incidence and pathophysiology of severe hyponatraemia in neurosurgical patients. Postgrad Med J. 2009 Apr. 85(1002):171-5.
3. Cerdà-Esteve M, Cuadrado-Godia E, Chillaron JJ, et al. Cerebral salt wasting syndrome: review. Eur J Intern Med 2008; 19: 249–54
4. El-Amin Abdel-Latif M, Chan PWK, Yu-Teik Goh A, Chai-See Lum L. Cerebral salt wasting syndrome following atlantoaxial fracture dislocation in Down syndrome. BMJ Case Rep. 2009.
5. Wu X, Zhou X, Gao L, et al. Diagnosis and Management of Combined Central Diabetes Insipidus and Cerebral Salt Wasting Syndrome After Traumatic Brain Injury. World Neurosurg. 2016 Apr. 88:483-7.
6. Moritz ML. Syndrome of inappropriate antidiuresis and cerebral salt wasting syndrome: are they different and does it matter?. Pediatr Nephrol. 2012 May. 27(5):689-93. [Medline].
7. 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. 2007 Apr. 71(8):822-6.