Syndrome of inappropriate ADH secretion is a situation where the ADH hypersecretion is... inapropriate... in contrast to all the other situations where it might be elevated "appropriately". Now, one must acknowledge that a raised ADH level is a perfectly reasonable response to hypovolemia, but it is difficult to use the word "appropriate" to describe ADH elevation in states of apparent volume depletion such as cirrhosis, congestive cardiac failure or myxoedema. The name "syndrome of inconvenient ADH secretion" might have been better, and we can still keep the acronym.
As one might imagine, elevated vasopressin levels tend to result in water retention, and a dilutional hyponatremia develops. These patients have no way of increasing their water excretion in response to an increased water intake.The urinary mechanisms of solute excretion remain intact, hence the high urinary sodium.
The college loves SIADH. Among causes of hyponatremia, it is over-represented in the SAQs:
Unfortunately, Oh's Manual only devotes one paragraph to this condition. Its wedged in between an expansive treatise on TURP syndrome and an even shorter paragraph on cerebral salt wasting.
Ectopic ADH production
The key feature if hypovolemia. These patients are dry and they produce a high urine output; in contrast SIADH patients are normovolemic, and have low urine output. 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.
Now, this statement is not to be taken as an endorsement of CSW as a genuine disease state; many smarter people with serious endocrinology cred argue that it may not exist. The controversy is discussed in greater detail in the Required Reading chapter on cerebral salt wasting from the Neurology and Neurosurgery section.
Mitchell H Rosner (2012), in his homage to a novel vaptan agent, has an excellent table of the different therapeutic options, which I have shamelessly plagiarised below:
|Fluid restriction||Simple, easily implemented
Can be useful in patients with urine osmolality <400–600 mosmol/kg
|Minimally effective and requires several days to achieve correction
Hard for patients to remain compliant
|Demeclocycline||Effective in raising serum sodium||Slow response
|Loop diuretics with or without salt supplementation||May allow relaxation of fluid restriction and decreases urine-concentrating ability||Requires careful titration and monitoring
Risk for other electrolyte abnormalities
|Urea||Effective and inexpensive||Palatability
|Hypertonic (3%) saline||Effective for severe acute and symptomatic chronic hyponatremia||Risk of overly rapid correction
Requires careful, intensive monitoring
|Vasopressin receptor antagonists||Targets excessive arginine vasopressin
Safe and effective
Predictable rise in sodium values
No risk for concomitant electrolyte disorders
Requires close monitoring of serum sodium at initiation with inpatient admission
Usually, fluid restriction is enough - but it is distasteful: people are thirsty, and want to drink; it seems cruel to forbid nanna her extra cup of tea. Moreover, sometimes you just can't fluid restrict somebody (see the SAH section below). Ergo, one resorts to pharmacological measures. Question 29 from the first paper of 2015 asked for specific drug options. These may include:
Gross (2012) discusses these options in more detail in his article.
Question 30 from the first paper of 2022 asked the candidates what they were planning to do with a patient whose sodium was trivially depressed (126 mmol/L) and who had a high grade subarachnoid haemorrhage. The problem is, whereas normally you would fluid-restrict these patients, in this scenario you wouldn't want to do that, because hypovolemia promotes vasospasm. Also, you can't just leave it and monitor them, as for these people hyponatremia is associated with a poor outcome. Thus, you're forced to replace the sodium intravenously, while maintaining a high or normal fluid balance.
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