Automated Contrast Injection and Targeted Renal Therapy: Strategies to Prevent Contrast-Induced Nephropathy (FULL TITLE BELOW)
- Volume 3 - Issue 3 - May/June 2006
- Posted on: 9/5/08
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David E. Allie, MD, Chris J. Herbert, RT, RCIS, and Craig M. Walker, MD
The role of CIN and perioperative ARF during vascular and cardiac surgical procedures likewise remains poorly defined. Strategies for contrast optimization and CIN prophylaxis will become increasingly important to the surgeon as increasing numbers of surgeons acquire catheter-based skills. Interestingly, contrast administration < 48 hours before coronary artery bypass (CABG) is a known, independent, preoperative predictor of worsening RI, but no guidelines exist for optimal renal protection in CABG performed within 72 hours of angiography.12,15 In fact, the association and incidence of CIN during cardiac surgery is unknown, and likely underestimated and a major contributing factor to a significant number of patients with worsening RI and ARF after cardiac surgery yearly. Loc et al. has shown that the 1-year mortalities after CABG are significantly higher (p < 0.0001) in patients with mild RI (11.1%) versus no RI (3.8%).15 The clinical implications become significant when considering that approximately 18% of the U.S. population (> 50 million) has some degree of RI and 14% of the approximately 750,000 patients undergoing cardiac surgical procedures have preoperative RI, and therefore are at risk for perioperative ARF.15–17
A heightened awareness of CIN and RI will become increasingly important in the treatment of aortic aneurysmal disease with endovascular aneurysm repair (EVAR) now available for thoracic (TAA) and abdominal aortic aneurysms (AAA). It is estimated that 10% of every male in the U.S. > 70 years old is harboring a AAA, and that there are approximately 1,000,000 AAAs that remain untreated.17,18 Approximately 30% of those 100,000 treated yearly undergo EVAR (30,000), and therefore will require contrast exposure.17,18 With the widespread acceptance of MDCTA, and AAA screening expected to be reimbursed in certain patient populations, it is anticipated that an increasing number of AAAs will be diagnosed yearly, and therefore treated with EVAR. Interestingly, the FDA has recently approved a novel, miniature implantable device capable of remote, radio-frequency monitoring of the AAA (or even TAA) sac pressure after EVAR. The EndoSure Wireless AAA Pressure Sensor (CardioMEMS, Inc., Atlanta, Georgia) would have the potential to significantly decrease the number of contrast studies currently recommended for EVAR follow up.
The incidence of RI after catheter-based AAA EVAR is also associated with preoperative RI and high post-procedure mortality.19,20 ARF is reported after 2–6% of infrarenal open AAA repairs, and is significantly higher in TAA.19–21 Worsening RI after EVAR is the third most commonly experienced morbidity and few reports exist implicating CIN as a prevalent etiology.19–21 Worsening RI post-EVAR has been reported from 6–39%.19–21 Carpenter et al. reported a 20% incidence of preop RI in 98 EVAR cases with an average volume of intraoperative contrast use of 152 cc (35–420 cc), underscoring the potential for intraoperative-induced CIN.22 Permanent RI was reported at 16% in this series, despite the liberal use of MRA and gadolinium. With the rapid adoption of MDCTA for the treatment of patients with TAA, AAA and PAD, the additional 75-mL to 125-mL of contrast volume required will further mandate the surgeon to develop strategies to minimize CIN.
Multiple strategies have been proposed for the prevention of CIN in PCI but few have strong supporting data. Randomized trials have demonstrated the importance of 0.9% saline infusions before and after contrast exposure in decreasing CIN.23,24 The infusion rates have varied between 1–3 mL/kg/hr for 6-12 hours after contrast exposure. Isotonic sodium bicarbonate solution started one hour before contrast exposure was recently associated with a 2% versus 17% incidence of CIN in a high-risk patient population when randomized to 0.9% saline.25 Further trials are being structured to validate the role of serum and urine alkalinization in the prevention of CIN. The role of N-acetylcysteine (NAC) in CIN prevention remains uncertain, with inconsistent results reported with regards to both the route and dose of administration.26 Interestingly, Barret and Parfay, recently reporting a review of strategies to reduce CIN, stated that NAC and IV sodium bicarbonate were “not generally recommended unless efficacy was confirmed by further trials.”26 Most cath lab protocols now incorporate some form or combination of 0.9% saline, sodium bicarbonate and NAC for CIN prevention, especially in the high-risk patient, despite a lack of validating data.
Intuitively, increasing renal blood flow and renal medullary vasodilatation would seem protective against CIN, since the proposed etiology of injury in CIN is an acute toxic injury induced by severe medullary vasoconstriction and critical cellular hypoxia. Fenoldopam (FEN) (Corlopam, Abbott Laboratories, Abbott Park, Illinois) is a short-acting, selective dopamine-1 agonist and vasodilator that is the only agent shown to increase both renal cortical and medullary blood flow.27 The initial favorable clinical reports of systemic IV-FEN administration in reducing CIN in PCI were not reduplicated in the randomized CONTRAST trial.28
Unfortunately, IV-FEN has a first-pass renal metabolism and can cause systemic hypotension at mild to moderate systemic doses. Therefore, it has been theorized that the CONTRAST trial results were secondary to an inability to deliver therapeutic doses directly to the renal medulla. Direct high-dose intrarenal (IR) infusion of FEN, in concept, has the potential to deliver selective high-dose renal vasodilatation and increased medullary blood flow without systemic hypotension, with the potential to reduce CIN in both the cath lab and surgical suites.
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