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:
|
Test |
Value |
Normal Adult Range |
|
Sodium* |
128 mmol/L |
135 – 145 |
|
Potassium |
3.8 mmol/L |
3.2 – 4.5 |
|
Chloride* |
94 mmol/L |
100 – 110 |
|
Bicarbonate* |
19 mmol/L |
24 – 32 |
|
Glucose |
5.5 mmol/L |
3.0 – 6.0 |
|
Urea |
7.8 mmol/L |
2.7 – 8.0 |
|
Creatinine* |
120 μmol/L |
65 – 115 |
|
Measured Osmolality* |
267 mosmol/Kg |
275 – 290 |
|
Urine Sodium |
76 |
|
|
Urine Potassium |
10 |
|
|
Urine Chloride |
96 |
|
|
Urine Osmolality |
350 mosmol/Kg |
50 – 1200 |
Give two possible diagnoses and the rationale for your answer.
SIADH
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.
Ashraf N, Locksley R, Arieff AI Thiazide-induced hyponatremia associated with death or neurologic damage in outpatients. Am J Med. 1981 Jun;70(6):1163-8.
Kyu Sig Hwang, M.D. and Gheun-Ho Kim, M.D. Published online 2010 June 30. Thiazide-Induced Hyponatremia Electrolyte Blood Press. 2010 June; 8(1): 51–57.
Kovesdy CP. Significance of hypo- and hypernatremia in chronic kidney disease. Nephrol Dial Transplant. 2012 Mar;27(3):891-8.
Ahmed AB, George BC, Gonzalez-Auvert C, Dingman JF. Increased plasma arginine vasopressin in clinical adrenocortical insufficeincy and its inhibition by glucosteroids. J Clin Invest. 1967 Jan;46(1):111-23.
Schmitz PH, de Meijer PH, Meinders AE.Hyponatremia due to hypothyroidism: a pure renal mechanism. Neth J Med. 2001 Mar;58(3):143-9.
Hanna FW, Scanlon MF. Hyponatraemia, hypothyroidism, and role of arginine-vasopressin. Lancet. 1997 Sep 13;350(9080):755-6.
Cerdà-Esteve M, Cuadrado-Godia E, Chillaron JJ, Pont-Sunyer C, Cucurella G, Fernández M, Goday A, Cano-Pérez JF, Rodríguez-Campello A, Roquer J Cerebral salt wasting syndrome: review. .Eur J Intern Med. 2008 Jun;19(4):249-54