Cerebral salt wasting: is it all in the head?

I recently saw a patient in clinic who had sustained a head injury and developed hyponatremia that persisted after discharge. In his chart was a great deal of debate over the cause of his hyponatremia: SIADH or cerebral salt wasting? I decided this was a good time for a refresher on cerebral salt wasting (CSW), as I have seen far less of it than SIADH as a clinical fellow.


CSW is characterized by extracellular volume depletion and presence of hyponatremia due to renal salt wasting. It is most seen in patients with cerebral disease, suggesting a neurologic cause. Urine sodium is usually high, though low levels have been documented in patients on low Na diets, and the urine is concentrated. Hypouricemia is also usually present, due to an increase in FE urate. These findings suggest that the proximal nephron, where urate reabsorption and the bulk of Na reabsorption occur, is the main site of action in CSW. While the mechanism is still unclear, several theories predominate. One proposed hypothesis is that decreased sympathetic input to the kidney leads to alterations in salt and water reabsorption. Another is that cerebral damage causes an increase in circulating ANP or BNP, which leads to natriuresis. In either scenario, a decrease in circulating volume would cause an increase in arginine vasopressin, thus creating an “appropriate” increase in ADH.


Because the treatment for CSW is volume repletion with isotonic fluids, and the mainstay for SIADH therapy is water restriction, differentiation between the two conditions is desirable. The main distinguishing feature between SIADH and CSW is volume status, patients with SIADH being euvolemic and those with CSW, volume deplete. As many of us are aware, it is often extremely difficult to assess volume status, especially in the neurology intensive care units. Some other distinguishing tests have also been suggested. While serum uric acid tends to be low in both SIADH and CSW, some studies have shown that when hyponatremia is corrected in SIADH, uric acid levels rise, while they remain low in CSW despite normalization of serum Na. Another study has suggested that measuring the FE phosphate can be helpful—an FE phosphate >20% was a reliable indicator of CSW (presumably indicating additional effects on the proximal tubule).


One question that remains unanswered in the literature (and is important in the case of my patient) is how long these syndromes persist: is it likely that my patient will be able to come off his salt tablets and water restriction? For right now, he’s living a thirsty life.