Invited Commentary: Donald LaVan, MD

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We're discussing Felker et al, "Diuretic Strategies in Patients with Acute Decompensated Heart Failure," published in the New England Journal of Medicine March 3, 2011. The NHLBI-funded authors gave furosemide to 308 patients hospitalized for ADHF in an IV dose either equivalent to their home dose, or at 2.5 times their home dose, and either at q12-hour intervals or by continuous infusion (i.e., patients assigned to one of four groups in a 2x2 table). No one method was superior on the primary endpoint (a composite global assessment of symptoms). Higher doses of Lasix resulted in more fluid output, without significant renal failure. Continuous drips were not superior to bolus infusion in safety or efficacy. (n=308). Read the article / abstract 

Pulmonary Central: Dr. LaVan, what did you take away from this study by Felker et al?

Donald LaVan, MD: There are some worthwhile findings here. First, not surprisingly, a high-dose diuretic strategy worked better than a low-dose strategy. The high-dose group received about twice as much furosemide, and had greater fluid loss, less dyspnea, and were transitioned to oral diuretics earlier. Of course, this is something that we would all expect and I hope were doing already. The second finding was that a continuous infusion was no better than bolus dosing.

Pulmonary Central: What did you think about the trend toward worsened renal function in the high-dose diuretic group?

Dr. LaVan: I thought selecting a cutoff of a 0.3 mg/dL rise in creatinine to define worsening kidney function was awfully conservative. The high-dose patients’ creatinine only rose by a mean of 0.08. This was a clinical trial, but in the real world, that’s just not being aggressive enough; this is a dangerous condition and there’s no sense playing around. I would happily accept a much higher bump in creatinine, not uncommonly above 2 or greater, to reach fluid loss goals. There’s pretty good data that [the rise] is transient and longer term outcomes aren’t negatively affected.

PC: These were sick patients, admitted with decompensation of already severe baseline heart failure. The authors excluded those “requiring” IV vasodilators or inotropes from the study. Yet, after 72 hours, 85% were considered to remain congested and almost 40% were considered treatment failures; 60 days later, 43% had been re-hospitalized, visited the ED, or died. Does this paper send a wrong message, that as a rule we should treat this category of patients with diuretics and oral medications alone (and at their home dose of diuretic, at that)?

Dr. LaVan: Looking at their severity and acuity on paper, I would not treat these patients with diuretics and oral medicines alone. Inotropes and intravenous vasodilators would be at the front of my mind. You need to start out full-bore right away and use all the tools you have at hand.

I’m also not sure why they chose to use the patients’ global assessment of symptoms rather than more objective data as the primary endpoint. I think that limited a bit the conclusions we can draw.


PC: What can intensivists take away from this study, for when we see these patients in the ICU?

Dr. LaVan: Don’t fool around. Use high doses of diuretics, and use IV vasodilators and inotropes if necessary. In other words, be aggressive when your patient needs it. Judging by the net fluid losses in this study, many of these patients had more than three or four liters of urine output each day, and I would be delighted with that. Bolus dosing of diuretics is generally easier, and this supports the idea that a continuous infusion probably doesn’t add anything.

This was a well-done study, from a good place by good people, but in the end I didn’t find that much that was new here. It’s good to see validated some of the things most of us were already doing.


Donald LaVan, MD, a spokesperson for the American Heart Association, is a cardiologist and Clinical Associate Professor of Medicine at the University of Pennsylvania.

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