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Clinical Update

AKI Awareness: Variation in Contrast Usage Across ACC-NCDR CathPCI Operators

Cath Lab Digest talks with Amit P. Amin, MD, MSc, Cardiovascular Division, Washington University School of Medicine; Barnes-Jewish Hospital; Center for Value and Innovation, Washington University School of Medicine, St Louis, Missouri.

Tell us about acute kidney injury in percutaneous coronary intervention.
 
Acute kidney injury (AKI) is a severely adverse, morbid condition and is quite common after  percutaneous coronary intervention (PCI), because these patients already have so many comorbidities, such as diabetes and congestive heart failure. When we perform PCI or angioplasty, we give these patients contrast, and the contrast can adversely impact their kidneys. I view this almost as a tradeoff: on the one hand, you want their cardiac symptoms and function to improve; on the other, there is risk to the kidney, which can offset these benefits. Some studies have shown that when acute kidney injury occurs, some patients’ kidney function doesn’t return back to baseline and some degree of permanent damage occurs, and these patients are at risk for subsequent dialysis. They are also at risk for faster progression of atherosclerosis and cardiovascular disease. It is like a vicious cycle. Once the patient enters this cycle, they are at risk for progressive atherosclerosis and adverse complications such as heart attacks, strokes, and dialysis. Dialysis or end-stage renal disease, the ultimate sequelae of AKI, is truly a devastating complication; it is almost as bad as stroke. We see that the quality of life of these patients is reduced tremendously, and their ability to work and function goes down.
 
When patients come into the lab, how do we know that they are at high risk for AKI?
 
There are markers and conditions that help us understand risk better: for example, diabetes is a risk factor. Preexisting chronic kidney disease is another risk factor and so is congestive heart failure. The American College of Cardiology-National Cardiovascular Database (NCDR) CathPCI registry has published validated risk prediction models for AKI, so we are able to predict the patient’s exact risk for acute kidney injury.
 
What prompted you to do this study on AKI and contrast use?
 
Looking at the NCDR CathPCI data, we noticed that there were some hospitals and physicians who were using very little dye, and some who were completely focused on their angiographic success and not really aware of how much dye they were using. From this observation, we began our study on the variation in contrast usage across NCDR physicians. The CathPCI registry is a national registry that is representative of practice in the United States, involving hundreds of hospitals. It is contemporary data and generalizable to practice in the U.S. 
 
What did you find?
 
Our analysis is by physician across the CathPCI registry. We adjusted not only for patient factors, but also for the types of patients that present at certain hospitals. For example, at Barnes Jewish Hospital in St. Louis, where I practice, we see many patients with heart failure and diabetes. So patients’ risk profiles and practices vary across hospitals. We accounted not only for patient comorbidities and characteristics, but we also accounted for these site-level differences in a hierarchical or random effects model. After these adjustments, we found a large variation in the amount of contrast used, and of course, this translated into a large variation in acute kidney injury across physicians in the CathPCI registry. There were some physicians who were using less than 100 ccs of dye on average per case, while other physicians were using excessive contrast. A remarkable finding from our study was that physicians weren’t necessarily aware of the risk. We predicted patients’ risk of acute kidney injury, and then divided this risk into deciles, with 1 being the lowest risk patient and 10 being the highest risk patient. We examined the average amount of contrast use across these deciles of AKI risk. Only in decile 9 and 10 did we see a small reduction of 16 ccs of dye, on average, per case. Even in these extremely high-risk patients, the amount of contrast being used was excessive, which contributes to the high risk of AKI we see in the United States.
 
What have you learned thus far and how has it changed your practice?
 
One thing is the important correlation between AKI and dye. The more contrast  you use, the greater the risk of AKI. We have actually applied our findings at Barnes Jewish Hospital (BJH), where we predict in advance how much contrast a patient can safely tolerate. We are not only predicting risk, we are also predicting a safe contrast limit for the patient using a health IT solution, ePRISM (Health Outcomes Sciences). Once the physician performing the procedure is aware of the risk and the safe contrast limit, the procedure is planned accordingly. Should we fix all of the vessels at the same time? Should we stage some vessels? Staging procedures means you are limiting the amount of dye, and in our experience, it does not affect kidney function, even in high risk AKI patients. Obviously, the nature and severity of the coronary stenoses plays an important role in determining if and when staging should be done. AKI is really a multifactorial problem, however; it is not just the contrast, but a myriad of risk factors, the patient’s hemodynamic conditions, preexisting renal function, contrast use, and athero-embolism that occur during the case that together result in AKI. Creatinine is, at best, a very rough or inaccurate marker of what the kidneys are actually doing.  
 
Change is often physician-driven, but how can management work to help reduce AKI?
 
That is a great question. Change does come from the physician level, but the hospital administration obviously has to buy in as well. Acute kidney injury not only adversely impacts patients by increasing their risk of morbidity and mortality, and end-stage renal disease, but AKI also increases resource use. Patients stay in the hospital longer and are at greater risk for readmission. AKI costs about $10k per episode, and increases length of stay (LOS) by many days. When kidney injury is severe, leading to dialysis, LOS increases by almost a week or even longer. It is a resource-intense complication. The administration, especially in this era of value-based purchasing and bundled payments, needs to be aware of the adverse impact AKI has not only on patients, but on hospital efficiency and cost. At our hospital, we look very closely at these complications, not only for increasing patient safety, but to increase hospital efficiency. Our hospital administration is very much on board and we share these outcomes with our physicians on a monthly basis.  
 
How common is it that cath labs have protocols in place to reduce AKI?
 
Awareness is increasing, but many hospitals aren’t fully aware. Traditionally, AKI has been considered a non-preventable complication and because we see it in the sickest patients, we tend to rationalize that sicker patients develop it more. However when you take appropriate measures, AKI can be prevented. Most hospitals aren’t even aware, and this paper has done a tremendous job just in bringing awareness to our community that AKI is a big deal. As more and more physicians become increasingly aware, hopefully some of the changes that took place at BJH can be implemented across different systems. BJH is one hospital in the BJC HealthCare system. Our approach at BJH was successful; we were able to reduce our AKI rates from 8% to 3% over a year and other hospitals in the BJC system are also in the process of implementing these changes across the BJC HealthCare system, again, an example of strong leadership and an aware administration.  
 
What would you recommend?
 
First, be aware of risk, and by that, I mean specific, individual risk. In general, we are aware of patients being at high risk, but be aware of your patient’s risk, what their glomerular filtration rate (GFR) is, and how much dye they can safely tolerate. If risk is high and the ability to safely tolerate dye isn’t much, then we stage procedures, and use limited dye injections. We become careful with how much dye is being injected for certain aspects of the procedure such as wiring the vessel, or every time you do a balloon angioplasty it is not necessary to inject dye, for example. There are other adjunctive imaging modalities like intravascular ultrasound, which can substitute until dye is actually needed. It is important to be careful with the dye.
 
How do you track contrast volume during the procedure?
 
We look at the bottle, admittedly a crude way of measuring. I frequently ask the nurse or technologist in the room to let me know how much dye we have used. It helps me plan the rest of the procedure during the case. There are newer technologies available. I know of an upcoming Bluetooth technology that is able to gauge and measure very accurately how much dye is being used and also save dye.
 
Do you communicate with the team prior to the procedure as to how much dye you want to use?
 
Yes, we do a time-out procedure that involves the patient’s specific risks, and our time out might involve something like the following: “Mr. So-and-so is undergoing this procedure. His risk of AKI is x [number] and his safe contrast limit today is 127 ccs of dye.” It brings the whole team on the same page, and by doing so, we all track how much dye is being used during the procedure. It really helps us to complete the procedure with minimal dye. We have had some extreme cases. There was a patient who was in pending dialysis, but was not yet in dialysis. His creatinine was 6, which is an extremely high creatinine with very low kidney function. We used 20 ml of dye to complete the procedure. We have done many cases with less than 20 ml of dye. The average in the NCDR is about 200 to 220 ml. 
 
What do you think about some of the available technologies to reduce contrast use or the use of carbon dioxide, for example?
 
CO2 doesn’t really give the same resolution as contrast. There have been numerous studies on different types of dye and their impact on AKI; those studies have largely had conflicting results. Other treatments such as sodium bicarbonate (NaHCO3) and N-acetylcysteine (NAC), again, have shown disappointing results. So there is not one consistent technology or therapy that prevents AKI. A high dose cholesterol statin medication can sometimes reduce AKI, so making sure that these patients are on a high dose of cholesterol medication also helps. Some physicians in our cath lab use the ACIST injector. At BJH, we looked at dye usage between ACIST and non-ACIST-using physicians, and found that the amount was roughly the same. Another technology is the DyeVert system (Osprey Medical). When dye is injected, some of it goes down the coronary artery and some is wasted in the aorta. Through the use of a pressure gauge, the DyeVert is able to prevent waste with a 30-40% reduction in dye use. It also tracks the amount of dye being used during the case. 
 
So, to prevent AKI, there is only one sure way, and that is to limit as much dye as you can. Once we started implementing a risk-based approach, all of our physicians’ use of contrast use went down. So technology helps, but physicians being aware of the risk helps the most!
 
How can hospitals track their own AKI incidence?
 
All hospitals subscribing to the NCDR can look up the published reports provided by the CathPCI registry to look at AKI rates by physician. When we get these data, it is six months later, and by then, the patient has of course been discharged, and nothing can be done. We must challenge the notion that AKI is a non-preventable complication. At BJH, we have moved the whole process upstream. We know ahead of time that a patient is at high risk for AKI and how much dye we can safely use. We are able to do everything we can to proactively prevent AKI!  
 
Reference
  1. Amin AP, Bach RG, Caruso ML, Kennedy KF, Spertus JA. Association of variation in contrast volume with acute kidney injury in patients undergoing percutaneous coronary intervention. JAMA Cardiol. Published online July 05, 2017. doi:10.1001/jamacardio.2017.2156

Disclosure: Dr. Amin reports no conflicts of interest regarding the content herein.


Dr. Amit Amin can be contacted at aamin@wustl.edu.


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