Now whether you believe in this entity or not, it's quite interesting. In the literature there appears to be a debate that goes back and forth, mainly between two groups: one lead by Richard H. Sterns from University of Rochester School of Medicine and Dentistry, and the other from John K. Maesaka from Winthrop (supporting). The diagnosis appears to be heavily reliant on clinical hypovolemia. There have been several studies published indicating that clinicians (nephrologists, cardiologists, intensive care) are lousy at this determination, when compared to invasive or semi-invasive monitoring. Therefore, unless hypovolemia is obvious (hypotension, tachycardia, orthostasis), it is difficult to make this distinction from euvolemia.
To make this diagnosis, the patient should have substantial urine sodium excretion in the setting of hypovolemia. This is ofter suggested by having a negative sodium balance, more so than would normally be seen in "SIADH" which tends to be mild. The other absolute must in this diagnosis is that adrenal insufficiency (both glucocorticoid and mineralocorticoid) must be ruled out, since it presents similarly. CSW has been mostly implicated in patients that have subarachnoid hemorrages, but many have described this phenomenon without any neurological features. Proponents of this entity (Maesaka, et al) also describe a method to distinguish CSW from SIADH, and that involves looking at the FeUric Acid. This is high in both states, but the distinction comes with treatment (with FeUric Acid becoming normal in SIADH and remaining elevated in CSW after correction). Opponents feel the negative salt balance often reflects the high rate of Na infusion that is given to patients when they first present, and when seen days later by nephrologist, the physiologic excretion of this is then seen. They also propose that the water retention and catecholamine release result in a physiologic excretion rather than true "salt wasting".
I write about this due to a patient who presented similarly as described in the papers of CSW. I only recently discovered that CSW was described before SIADH, and that once SIADH had been described, CSW reports had virtually vanished, only to resurface decades later in the neurosurgical literature. I don't know if I believe it or not, but until this is absolutely proven or disproven, we need to keep our differential open. Whether you believe in CSW or not, optimal therapy in the setting of SAH is hypertonic saline, so it may not matter what you call it.. Ultimately it's a beast that probably will continue to be debated without definative answers.
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