Regarding sodium homeostasis in critically ill patients:
a) Outline the pathophysiological mechanisms responsible for the hyponatraemia commonly seen in hepatic and renal failure. (20% marks)
b) List the criteria essential for diagnosis of the syndrome of inappropriate antidiuresis (SIAD). (20% marks)
c) List 4 drugs from separate classes that may cause SIAD. (20% marks)
d) How would you distinguish SIAD from cerebral salt wasting syndrome (CSWS)? (20% marks)
e) List two drugs that may be useful in the management of SIAD. (20% marks)
2. Tolvaptan / Conivaptan
a) A more wordy answer as to why there is hyponatremia in hepatic and renal failure (which also works to explain CHF)
b) From the chapter on Syndrome of inappropriate ADH secretion (SIADH):
d) How to tell SIADH from CSW? The trick is demonstrating that the extracellular fluid 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 hydration.
In both conditions the ADH level is elevated, but only with euvolaemia is this "inappropriate" ADH seretion (and therefore it can then be called CSW). A heretical viewpoint (in which CSW does not exist) would call this SIADH with urinary sodium loss to compensate for daily maintenance intake, which gives the impression of salt wasting.
Drugs for management of SIADH include the following options:
An excellent 2012 article by Peter Gross ("Clinical management of SIADH") discusses these options with satisfying detail.
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Rosner, Mitchell H. "Lixivaptan: a vasopressin receptor antagonist for the treatment of hyponatremia." Kidney international 82.11 (2012): 1154-1156.
Erickson, Kevin F., Glenn M. Chertow, and Jeremy D. Goldhaber-Fiebert. "Cost-effectiveness of tolvaptan in autosomal dominant polycystic kidney disease." Annals of internal medicine 159.6 (2013): 382-389.