The College had never asked about this in any direct fashion. Rather, it appears in Question 20.1 from the first paper of 2013, which in this study resource has been classified as part of the Electrolytes and Fluids section. The examiners wanted two reasons as to why a head-injured patient might have hyponatremia and a high urinary sodium, with a urine osmolality higher than that of serum.
Cerebral salt wasting is only one of the differentials offered by the college. Broadly speaking, hypoosmolar hyponatremia is better explored in the Required Reading section dedicated to electrolyte disturbances, and so the other differentials will not be discussed here. Instead, the focus will be on cerebral salt wasting alone, mainly because it is a weird reason for being hyponatremic.
As far as references go, LITFL's quick comparison of SIADH and CSW is enough for the time-poor exam candidate. If the exam candidate is somehow time-rich, they can spend some minutes hovering over this 2015 review from Frontiers in Pediatrics, which covers essentially the same ground, but using about 2500 extra words. For a more precise focus on cerebral salt wasting, one is directed to this 2008 review from the European Journal of Internal Medicine, or this 2010 review from the Neurosurgery clinics of North America.
One of the major problems with making a diagnosis of CSW is the fact that nobody seems to agree on a set of diagnostic criteria. Whereas SIADH has some well-accepted criteria, CSW can only claim some vague definition (hypovolemic hyponatremia with diuresis and natriuresis).
So does it even exist as a discrete clinical entity? In 1999, Oh and Carrol reviewed the world literature on CSW and were forced to conclude that this disorder has never actually been demonstrated, in any of the case reports describing it. Each time either the hypovolemia or the severe renal salt loss has not been demonstrated unequivocally. More recently, Hannon et al published a prospective study where in a cohort of 100 subarachnoid haemorrhage patients the vast majority of hyponatremia was caused by SIADH, hypoadrenalism and unintelligent fluid management. Using even the flexible definition of CSW mentioned above, the authors were unable to identify even one episode (out of 42) which might have fit that description.
It has been pointed out that in SIADH, the urinary sodium is also high. This might give somebody the impression of "salt wasting" - the patient continues to irrationally excrete sodium in the face of serum hyponatremia, this must be some sort of sodium loss disorder! But, in actual fact, this all may be a normal phenomenon. In the presence of a chronically raised vasopressin level, the serum osmolality homeostasis has been set to a much lower point, and sodium is the main instrument of adjusting this homeostasis. In a steady state, the sodium losses therefore end up reflecting the sodium intake. The patient who appears to be "salt wasting" is in fact in a neutral sodium balance, trying to maintain a lower baseline sodium concentration with a normal sodium intake.
To add to the confusion, in both SIADH and in CSW the vasopressin levels are elevated. The trick is demonstrating that the volume is reduced. With a reduced volume, the elevated vasopressin level is a sensible response to dehydration, whereas with volume expansion the vasopressin level is "inappropriate". Thus, the most important diagnostic criterion discriminating between SIADH and CSW is really the assessment of extracellular fluid volume. Unfortunately, we clinicians suck at this, and the alternatives involve determining the volume of distribution of a (frequently noxious) tracer substance.
In summary, it is unclear whether the two conditions indeed overlap to the point of merging.
In response to a NEJM reader's letter about a certain hyponatremia case scenario, the author of the article responded that "some may choose to describe his condition as cerebral salt wasting, whereas others may prefer to call it SIADH with a physiologic natriuresis caused by iatrogenic hypervolemia" and that hypertonic saline "will increase the plasma sodium concentration, regardless of volume status or the terminology used". The pragmatic intensivist would applaud such a response.
Sceptical of the existence of this disorder, or at least aware that it's prevalence is miniscule, one is forced to admit the the diagnosis of CSW is one of exclusion, and thus it is a disorder defined by the absence of other more common and more physiologically sensible disorders. An article from 2002 which takes this viewpoint has offered some criteria for the diagnosis of cerebral salt wasting:
The following must be present:
The following must be absent:
Confronted by a confusing swamp of opinion, the pragmatic intensivist falls back on physiological certainties. Who cares what the diagnosis is. The correction of sodium is achieved by the administration of sodium. The correction of volume is achieved by the administration of volume. If one wants to get fancy, one could even deploy some sort of drug to stimulate the retention of both , eg. fludrocortisone.
Surprisingly, this KISS approach is precisely what is recommended by the authorities for the management of CSW. It seems much of the time these situations resolve completely with the administration of normal saline. Fludrocortisone is reserved for refractory cases, and can be viewed as a form of cheating, as it will produce water and sodium retention in virtually any situaton, and can be used without any knowledge of the actual diagnosis.