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Philip Andrew eloquently explains the problems of referring to circulating plasma volume as “effective,” and we concur with his comments. Our reference to low effective circulating volume in heart failure1 implicitly suggests that cardiac failure and low cardiac output are the underlying problems leading to poor renal perfusion and, as Andrew states, to neurohormonal activation with elevation of natriuretic peptides.
Our article1 also refers to the other states of ECF volume overload (cirrhosis and nephrotic syndrome). In these situations, low effective circulating volume refers to low oncotic pressure, which is entirely different from the mechanisms seen in a state of low cardiac output. We agree that the term “low effective circulating volume” is used in our article to describe 2 different disease states and might lead to confusion.
While acknowledging the fact that “tonicity” and “osmolality” are frequently used interchangeably, Malvinder Parmar provides the correct definitions.
Parmar has concerns about the suggestion in our management algorithm1 that ECF volume be assessed after initial treatment of symptomatic acute or chronic hyponatremia and suggests that this assessment should be carried out before treatment is initiated. However, in clinical practice, in an emergent situation, assessment and treatment occur concurrently. Our algorithm is intended to suggest urgent treatment of a constellation of severe signs and symptoms of hyponatremia (confusion, ataxia, headache, seizures, obtundation); such urgent therapy will be essentially the same regardless of the ECF volume. We agree that headache in and of itself should not be an indication to pre-empt appropriate physical assessment before infusion of hypertonic or normal saline. Parmar also mentions that aggressive treatment of chronic hyponatremia in the setting of SIADH could lead to worsening of the hyponatremia. We agree and stated this in our article.1 However, seizures, obtundation and ataxia secondary to hyponatremia are all considered medical emergencies and thus require therapy. In the case of SIADH, infusion of normal (0.9%) saline may not improve sodium level and may in fact worsen it; hence, our recommendation for hypertonic (3%) saline in emergent situations. Unless the patient presents with a clear cause for the SIADH, it is impossible to know how to direct the therapy, especially if there is neurologic deterioration.
Parmar disagrees with our suggestion to use an alternative medication to treat the case patient's hypertension. We agree that the hyponatremia in this case was a direct result of ECF volume depletion due to gastroenteritis and replacement of that fluid loss with free water. Parmar's suggestion to reintroduce thiazide as the patient's diuretic would be a reasonable approach, if combined with appropriate close monitoring for hyponatremia soon after reinitiating the drug. An alternative choice would be an angiotensin II receptor blocker (ARB) or a long-acting dihydropyridine calcium channel blocker, both of which have been suggested as first-line therapy for patients with isolated systolic hypertension.2 If an ARB were initiated, the patient would have to receive instructions to stop the drug should ECF volume become contracted.
Guy Decaux and colleagues express concern about our suggestion that hyponatremia “be corrected at a rate similar to that over which it developed.” With this recommendation we were attempting to provide a very general rule for correction rates and intended to imply that if hyponatremia has been clearly documented to have developed over a 2- or 3-day period, than in most circumstances it can be corrected over 2 to 3 days, provided the patient does not have life-threatening signs or symptoms. Likewise, if hyponatremia has developed over several weeks, then it can be corrected much more slowly (although not necessarily over a 2- to 3-week period, since it may be adequately treated in a shorter period).
Karen E. Yeates Michael Singer A. Ross Morton Department of Medicine Division of Nephrology Queen's University Kingston, Ont.
Footnotes
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Competing interests: None declared.