N-Acetylcysteine and Other Preventive Measures for Contrast-Induced Nephropathy in the Intensive Care Unit

Abstract

The increase in diagnostic imaging procedures that require infusion of intravenous radiographic contrast has led to a parallel increase in the incidence of contrast-induced nephropathy (CIN). Since CIN accounts for a significant increase of hospital-acquired renal failure, length of stay and mortality, several additive strategies to prevent CIN are presently advocated, including N-acetylcysteine (NAC), sodium bicarbonate, theophylline or fenoldopam, and peri-procedural hemofiltration/hemodialysis. As only one (non-randomized) study has been performed in the intensive care setting, at present it is hard to give firm recommendations on preventive measures for CIN in intensive care patients. Indeed, future studies are needed to determine the true role of the above-mentioned preventive measures in critically ill patients at risk for CIN. Since NAC has only few side-effects, we presently advise NAC as an additive preventive measure in the intensive care setting. Theophylline or sodium bicarbonate hydration are viable options, either in conjunction NAC or as alternatives.

Permanent and transient effects of locally delivered n-acetyl cysteine in a guinea pig model of cochlear implantation

“…Experimental studies have shown systemically delivered NAC reduces the permanent hearing loss associated with noise trauma, impulsive noise trauma and ototoxicity (summarized in ). The drug is currently used clinically, having been shown to reduce the incidence and severity of contrast-induced neuropathy (Sanaei-Ardekani et al, 2005;Schultz et al, 2006). It has also been used in clinical trials aimed at reducing reperfusion injury following knee surgery (Ege et al, 2006;Saricaoglu et al, 2005).…”

Low volume contrast CTPA in patients with renal dysfunction

“…CIN is an acute deterioration of renal function after administration of iodinated contrast media in the absence of another cause 6,7 . In clinical studies, it has been defined as an increase in 25% or more, or an absolute increase of 0.5 mg/dL (44.2 µmol/L) or more of serum creatinine from baseline 6–12 . The pathogenesis of CIN is incompletely understood but is thought to be because of a complex interaction of various mechanisms such as decreased renal blood flow as a result of vasoconstriction, direct tubular toxicity by oxidized free radicals and an osmotic effect 13 .…”

“…6,7 In clinical studies, it has been defined as an increase in 25% or more, or an absolute increase of 0.5 mg/dL (44.2 mmol/L) or more of serum creatinine from baseline. [6][7][8][9][10][11][12] The pathogenesis of CIN is incompletely understood but is thought to be because of a complex interaction of various mechanisms such as decreased renal blood flow as a result of vasoconstriction, direct tubular toxicity by oxidized free radicals and an osmotic effect. 13 CIN is a major health issue, and is the third most important cause of hospitalacquired renal failure.…”