A 55-year-old woman is brought to the emergency department by her husband with a 1 hour history of an unremitting headache. The headache started suddenly while she was eating dinner and she says it feels like the “worst headache of my life.” An emergent CT scan of the head without contrast confirms the diagnosis, and a CT angiogram identifies the source of bleeding. The patient undergoes surgical management of her condition. On hospital day 3, she is found to be disoriented to person, place, and time. She also develops nausea and vomiting. Her medical problems consist of heart failure for which she takes furosemide, spironolactone, and metoprolol, which were continued at admission. Her temperature is 99.6°F (37.6°C), blood pressure is 100/60 mmHg, pulse is 112/min, and respirations are 16/min. Physical examination shows poor skin turgor. Capillary refill time is 4 seconds. Serum laboratory results are shown below: Na+: 120 mEq/L Cl-: 92 mEq/L K+: 3.9 mEq/L HCO3-: 26 mEq/L BUN: 32 mg/dL Creatinine: 1.0 mg/dL Serum osmolality is 265 mEq/L and urine osmolality is 340 mEq/L. Urine sodium is 44 mEq/L. Which of the following is the most likely diagnosis?
Addison disease
Cerebral salt wasting
Diuretic overuse
Syndrome of inappropriate anti-diuretic hormone
Cerebral salt wasting
This patient presents with a subarachnoid hemorrhage (“worst headache of my life”) which is treated and then subsequently develops nausea, vomiting, and altered mental status with reduced serum sodium concentration, indicative of symptomatic hyponatremia. In the setting of serum hypo-osmolality, urine hyper-osmolality, urine sodium concentration > 20 mEq/L, and hypovolemia (low blood pressure, decreased skin turgor, and prolonged capillary refill), this is indicative of cerebral salt wasting.

The mechanism of cerebral salt wasting is unclear, although some hypotheses point to increased release of brain natriuretic peptide after injury leading to suppression of renal sodium reabsorption, or sympathetic nervous system injury resulting in an impaired renin response. Patients classically present several days after cerebral injury or neurosurgery with hypovolemic hyponatremia and hypochloremia. Water retention results in serum hypo-osmolality, hyponatremia, and hypochloremia with urine hyper-osmolality and increased urine sodium excretion. In patients with prolonged cerebral salt wasting, hypokalemia can also occur (potassium may be normal in acute states). Treatment in mild or moderate cases consists of normal saline infusion to correct both volume status and hyponatremia. Treatment in severe cases consists of hypertonic saline. During correction, serum sodium must be monitored closely to prevent central pontine myelinolysis.

Cui et al. describe the differences between syndrome of inappropriate anti-diuretic hormone (SIADH) and cerebral salt wasting. They discuss how volume status serves as the key differentiator between these conditions. They recommend paying closer attention to total body electrolyte balance in understanding these conditions.

Incorrect Answers:
Answer A: Addison disease, also known as primary adrenal insufficiency, results in salt wasting due to decreased mineralocorticoid activity. Because of reduced aldosterone release, patients also have hyperkalemia and metabolic acidosis. In contrast, this patient’s potassium and bicarbonate levels are normal. Treatment is with steroids.

Answer C: Diuretic overuse is occasionally observed in patients using loop diuretics. Overuse of loop diuretics can cause hyponatremia, hypokalemia, and hypochloremia. Metabolic alkalosis is commonly seen due to volume contraction. Cerebral salt wasting is more likely in this patient presenting after a recent cerebral injury. Treatment is the cessation of the causative medication.

Answer D: Primary polydipsia can cause symptomatic hyponatremia. The urine would be maximally diluted (urine osmolality < 100 mEq/L) due to an appropriate physiological response to hyponatremia and excess free water intake. Treatment is cessation of excessive water consumption.

Answer E: Syndrome of inappropriate anti-diuretic hormone (SIADH) presents with identical findings as cerebral salt wasting with the exception of euvolemia as opposed to hypovolemia. An assessment of volume status is essential to differentiate. This patient has clear signs of hypovolemia. Treatment of SIADH is fluid restriction followed by ADH inhibitors, if needed.

Bullet Summary:
Cerebral salt wasting presents with hyponatremia, hypochloremia, and hypovolemia in the setting of recent cerebral injury or neurosurgery.