Article first published online: 17 JAN 2012
© 2012 by the Society for Academic Emergency Medicine
Academic Emergency Medicine
Volume 19, Issue 1, pages 111–112, January 2012
How to Cite
Mitchell, A. M. and Kline, J. A. (2012), In Reply. Academic Emergency Medicine, 19: 111–112. doi: 10.1111/j.1553-2712.2011.01256.x
- Issue published online: 17 JAN 2012
- Article first published online: 17 JAN 2012
We appreciate the interest in our work. This letter primarily focuses on the important issue of contrast-induced nephropathy (CIN), which was the focus of a separate paper.1 The present article offers a preplanned subanalysis to measure the rate of complications from intravenous (IV) contrast that would manifest during the time of care in the emergency department (ED).2 We also appreciate the limitation in the use of serum creatinine (sCr) as a marker of acute kidney injury (AKI), but we point out that using estimated glomerular filtration rate (eGRF), an arithmetic formula that includes sCr, age, race, and sex, provided no improvement in prognostic accuracy for the outcome of CIN over the sCr alone.1
Despite its limitations, measured sCr remains the mainstay in estimating glomerular filtrate rate, particularly in the ED setting where methods to directly measure GFR, such as urinary creatinine or inulin elimination over 24 or more hours, are impractical at best. The diagnostic accuracy of other biomarkers for AKI remains uncertain and is the subject of a large body of ongoing clinical investigation. The most well-accepted, literature-based, contemporary definition of CIN is an interval rise in measured sCr of ≥0.5 mg/dL or ≥25% of baseline observed following exposure to intravascular iodinated contrast media.
We also agree that hydration remains key to preventing CIN, although much remains to be learned to define an optimal amount, rate, and route of administration. As shown in Figure 1, CIN tended to be uncommon in patients who received more than 2,000 mL of IV crystalloid while in the ED, recognizing that this figure does not reveal other predictors of CIN. Expert published guidelines clearly indicate hydration as the mainstay of prevention with the caveat that optimum timing, route, and duration of hydration are unknown, resulting in necessarily vague recommendations such as “… beginning [hydration] earlier and continuing longer is probably better.”3 Data guiding hydration strategies in the outpatient or acute care settings are also limited. Two small trials (<70 patients) demonstrated that bolus IV saline (approximately 300 mL) given immediately prior to cardiac catheterization, followed by 12 hours of a saline infusion, was inferior to a 24-hour infusion.4,5 The only trial involving oral hydration did conclude that 300 mL of bolus IV saline in combination with oral hydration (1000 mL) prior to catheterization, followed by a 6-hour saline infusion, was equivalent to a 24-hour infusion. However, this trial was very small (36 patients) and still does not account for the limited time available for hydration in the outpatient or acute care settings.4 Notably, no clinical trial of hydration to prevent CIN has been conducted in the ED setting or in populations receiving bolus IV contrast for CT imaging.
In summary, this letter underscores the need for more research into markers of CIN and to understand the role of hydration in the prevention of CIN.