A 26-year-old male, admitted to the ICU 7 days ago following a traumatic brain injury, now has the following blood and urine results:



Normal Adult Range


128 mmol/L

135 – 145


3.8 mmol/L

3.2 – 4.5


94 mmol/L

100 – 110


19 mmol/L

24 – 32


5.5 mmol/L

3.0 – 6.0


7.8 mmol/L

2.7 – 8.0


120 μmol/L

65 – 115

Measured Osmolality*

267 mosmol/Kg

275 – 290

Urine Sodium


Urine Potassium


Urine Chloride


Urine Osmolality

350 mosmol/Kg

50 – 1200

Give two possible diagnoses and the rationale for your answer.

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College Answer


Cerebral salt wasting.

The presence of features that indicate hypovolaemia - low bicarb, high Cr and low plasma osmo and high anion gap .

Plus those indicating an ADH response – low plasma and high urine osmo.

Urine Na inappropriately high.


Hyponatremia due to SIADH and CSW  is discussed in greated detail elsewhere.The combintion of traumatic brain injury and hyponatremia give rise to these two differentials almost involuntarily. This is a hypoosmolar hyponatremia with high urine osmolality and high urine sodium.

Urinary "osmo" (presumably, the examiner meant to finish typing "osmolality" but was called away to something very urgent) is relatively high, suggesting that there is a significant effect of ADH. This promotes SIADH as a differential. Consider that the serum osmolality is low, and the urine osmolality is high - obviously, the appropriate response to this situation would be to decreased ADH secretion and excrete buckets of dilute water-rich urine.

Urinary sodium sodium is also raised (i.e. over 40mmol/L), which suggests that for whatever reason, appropriate attempts to conserve sodium are not being made. This does not help to narrow the differentials very much, as it could be present in SIADH, cerebral salt wasting, hypoaldosteronism, hypoadrenalism, hypothyroidism, the polyuric phase of ATN, or with the use of thiazide diuretics. However, it excludes true hypovolemia (where efforts are made to conserve sodium).

Hypoaldosteronism and hypoadrenalism can be ruled out on the basis of a low serum potassium (it would normally be high in those situations). The polyuric phase of ATN normally has a more dilute urine, closer to 100mOsm/L. That leaves thiazides and hypothyroidism, which - though possible- have little relevance in the context of the history.

So, to discriminate between SIADH and cerebral salt wasting (both are a diagnosis of exclusion) one would have to examine the patient and decide whether they are underfilled (CSW) or euvolaemic (SIADH). This is the one situation in which the lazy man's approach to hyponatremia actually calls for a physical examination of the patient. The trick to discriminating between these two conditions lies in the ability to demonstrate that the body fluid volume is decreased. In both conditions the ADH level is elevated, but in cerebral salt wasting the ADH is elevated appropriately because the patient is hypovolemic, and so it cannot possibly be SIADH by definition.



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