Reducing Acute Kidney Injury Due to Contrast … Acute Kidney Injury Due to Contrast Material: ... Nancy Roy, RN Brenda Homsted, RN, RNC Cindy Downs, RN, MSN Cathy S. Ross…

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www.ccnonline.org CriticalCareNurse Vol 37, No. 1, FEBRUARY 2017 13

©2017 American Association of Critical-Care Nurses doi: https://doi.org/10.4037/ccn2017178

CE 1.0 hour, CERP A

Peggy Lambert, RN, MBA, MS, CCRN

Kristine Chaisson, MS, CCRN

Susan Horton, DNP, APRN, CHFN

Carmen Petrin, APRN, MS

Emily Marshall, MPH

Sue Bowden, RN, BSN

Lynn Scott, APRN, MS

Sheila Conley, RN, BSN

Janette Stender, APRN

Reducing Acute Kidney Injury Due to Contrast Material: How Nurses Can Improve Patient Safety

BACKGROUND Acute kidney injury due to contrast material occurs in 3% to 15% of the 2 million cardiac catheterizations done in the United States each year. OBJECTIVE To reduce acute kidney injury due to contrast material after cardiovascular interventional procedures.METHODS Nurse leaders in the Northern New England Cardiovascular Disease Study Group, a 10-center quality improvement consortium in Maine, New Hampshire, and Vermont, formed a nursing task force to reduce acute kidney injury due to contrast material after cardiovascular interventional procedures. Data were prospectively collected January 1, 2007, through June 30, 2012, on consecutive nonemergent patients (n = 20 147) undergoing percutaneous coronary interventions. RESULTS Compared with baseline rates, adjusted rates of acute kidney injury among the 10 centers were significantly reduced by 21% and by 28% in patients with baseline estimated glomerular filtration rate less than 60 mL/min per 1.73 m2. Key qualitative system factors associated with improvement included use of multidisciplinary teams, standardized fluid orders, use of an intravenous fluid bolus, patient edu-cation about oral hydration, and limiting the volume of contrast material.CONCLUSIONS Standardization of evidence-based best practices in nursing care may reduce the incidence of acute kidney injury due to contrast material. (Critical Care Nurse. 2017;37[1]:13-26)

This article has been designated for CE contact hour(s). The evaluation tests your knowledge of the following objectives:1. Develop an understanding of contrast-induced acute kidney injury and adverse consequences to patient safety2. Identify key factors associated with the prevention of acute kidney injury in the context of a cardiac catheterization laboratory3. Apply a regional nurse-driven protocol to your local care setting

To complete evaluation for CE contact hour(s) for test #C1713, visit www.ccnonline.org and click the “CE Articles” button. No CE test fee for AACN members. This test expires on February 1, 2019.

The American Association of Critical-Care Nurses is an accredited provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation. AACN has been approved as a provider of continuing education in nursing by the State Boards of Registered Nursing of California (#01036) and Louisiana (#LSBN12).

Gertrude Kent, RN-BC, BSN

Ellen Hopkins, RN, BSN

Brian Smith, RN

Anita Nicholson, RN

Nancy Roy, RN

Brenda Homsted, RN, RNC

Cindy Downs, RN, MSN

Cathy S. Ross, MS

Jeremiah Brown, MS, PhD

For the Northern New England Cardiovascular Disease Study Group

14 CriticalCareNurse Vol 37, No. 1, FEBRUARY 2017 www.ccnonline.org

Acute kidney injury (AKI) is a frequent complica-tion associated with administration of intrave-nous contrast agents during diagnostic cardiac

catheterization and percutaneous coronary interven-tions (PCIs) and leads to increased morbidity and mortality.1 The Acute Kidney Injury Network defines AKI as an acute increase of 0.3 mg/dL or a 50% or greater increase in the serum level of creatinine within 48 hours from baseline.2 The incidence of contrast material–induced acute kidney injury (CI-AKI) varies because of differences in definitions, measurement of renal indi-cators, patient populations, and risk factors and depends on the severity of renal failure.3 Common definitions include the following3,4: the European Society of Uro-genital Radiology defines CI-AKI as an increase in the serum level of creatinine more than 0.5 mg/dL or more than 25% within 3 days of administration of contrast material; the Acute Kidney Injury Network defines CI-AKI as an increase of 0.3 mg/dL or more in the serum level of creatinine; and Kidney Disease: Improving Global Outcomes (KDIGO) defines AKI as a serum level of cre-atinine 1.5 times or greater than the baseline value or an increase of 0.3 mg/dL or greater.

CI-AKI is commonly underrecognized because of a lack of monitoring of renal function biomarkers after procedures that involve contrast material.5 The inci-dence of CI-AKI ranges from 3% to 15%, depending on

the definition used, and results in an additional cost of $15 900 per case compared with the cost of surgery in patients with no CI-AKI.6-10 In addition, CI-AKI patients and their families must cope with the emotional burden that comes along with unexpected complications after interventional procedures or surgery.

CI-AKI occurs in patients with chronic kidney disease (CKD) and in patients with normal kidney function. Patients with CKD have a reduced nephron capacity and are at greater risk for CI-AKI. Exposure to contrast mate-rial triggers a transient release of nitric oxide in the neph-ron, which induces endothelium-dependent vasodilatation. Within the renal vascular arcades, the vasodilatation results in transient renovascular dilatation and increased renal blood flow for a few minutes. After passing into the glomerulus through the fenestrated endothelium, the water-soluble contrast material enters Bowman’s capsule and the urinary space and provides rapid exposure of the contrast medium to the tubular epithelial cells. The contrast material is taken up by the epithelial cells and permeates gap junctions and the basal side of the tubule, with entry into the peritubular space. The subsequent response is tubuloglomerular feedback via adenosine release from the macula densa, release of endothelin, prostaglandin dysregulation, and subsequent decreased synthesis of nitric oxide. These mechanisms combine to cause sustained intrarenal vasoconstriction that persists

Authors

Peggy Lambert is executive director of critical care services, Sue Bowden is a nurse, and Carmen Petrin and Lynn Scott are nurse practitioners at Catholic Medical Center, Manchester, New Hampshire.

Kristine Chaisson is a nurse and executive director of the Central Maine Heart and Vascular Center, Central Maine Medical Center, Lewiston, Maine.

Susan Horton is a nurse and cardiac director and Nancy Roy is the nurse manager of the cardiac intensive care unit, Central Maine Medical Center.

Sheila Conley is a nurse database manager and Janette Stender is a cardiovascular medicine nurse practitioner at Dartmouth-Hitchcock Medical Center.

Ellen Hopkins and Gertrude Kent are ambulatory cardiac care nurses, Maine Medical Center, Portland, Maine.

Anita Nicholson is a cardiac catheterization nurse and Brian Smith is a cardiac catheterization technician, Wentworth Douglass Hospital, Dover, New Hampshire.

Cindy Downs and Brenda Homsted are nurses, Eastern Maine Medical Center, Bangor, Maine.

Cathy S. Ross is administrative director, Northern New England Cardiovascular Disease Study Group and manager of research projects at Dartmouth-Hitchcock Medical Center.

Jeremiah Brown is an associate professor and Emily Marshall is a research assistant, Dartmouth Institute for Health Policy and Clinical Practice, Geisel School of Medicine, the Department of Medicine, and the Department of Community and Family Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire. He is the principal investigator of the quality improvement project.Corresponding author: Dr Jeremiah R. Brown, HB 7505, One Medical Center Dr, Lebanon, NH 03756 (e-mail: [email protected]).

To purchase electronic or print reprints, contact the American Association of Critical-Care Nurses, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].


for approximately 2 hours. During this time, renal blood flow is markedly reduced, and contrast material accumulates in the renal medulla, causing further vaso-constriction, prolonged exposure of the renal tubular cells to contrast material, and direct chemotoxic cellular injury. This phenomenon has been described in numer-ous case reports of persistent nephrograms (prolonged renal cortical retention of contrast media), in which con-trast material has been trapped in the medulla for days and weeks.11 During this time, the prolonged exposure of the renal tubules to the contrast agent propagates direct cellular injury, inducing tubular apoptosis (Figure 1).12

Measures to prevent CI-AKI have been studied, includ-ing the use of physiological saline for volume expansion,13 intravenous versus oral volume expansion,14-19 physiological

saline versus sodium bicarbonate intravenous prophy-laxis,20 use of medications such as N-acetylcysteine21-23 and ascorbic acid,24 withholding nephrotoxic medica-tions before the procedure with contrast material and after the dose of contrast material is administered,3 type of contrast medium used,25 use of volumes of contrast material based on initial estimated glomerular filtration rate (eGFR),26-28 and postprocedure hydration. Such studies indicated the following: Use of physiological saline alone protected better against renal insufficiency than did physiological saline with mannitol or furose-mide.13 In 5 studies,14-17,19 oral volume expansion was not inferior to intravenous volume expansion; in 1 study,18 intravenous hydration was superior. Sodium bicarbonate was associated with a significantly lower risk for contrast

Figure 1 Pathophysiology of contrast-induced nephropathy and acute tubular necrosis. Reprinted from Brown and McCullough,12 with permission of Springer.

Catheter

Left maincoronary artery

Iodinatedcontrast

Normal tubularlumenCo

rtex

Oute

r med

ulla

Inne

r med

ulla

Acute tubularnecrosis

Acute ischemicinjury plus

chemotoxicity

Cell withoxidative stress

Cell attackedby free radicals

Free radicals

Kidney

Catheter

Necrosis

HeartIntra-arterial dye

Aortic arch

Cell swelling and blebbing

Formationof vacuoles


medium–induced renal failure than was sodium chlo-ride.20 Compared with physiological saline alone, N-acetylcysteine21-23 and ascorbic acid24 could reduce the risk for CI-AKI. Intra-arterial administration of iso-osmolar contrast medium, but not intravenous adminis-tration, was associated with lower risk for CI-AKI than was administration of low-osmolar contrast medium.25 Incremental increases in the volume of contrast medium exceeding the safe contrast limit were associated with a higher risk for contrast-induced nephropathy.26,27

These studies were performed primarily by physicians and researchers; the study by Solomon et al13 was the only investigation in which one of the authors was a nurse. Contrast-induced nephropathy prevention has been a topic of interest in nursing research, and reviews have published29,30; however, no treatment path has clearly reduced the risk for CI-AKI in all populations of patients. We report here the first development of a qual-ity improvement task force to reduce CI-AKI led and implemented by nursing professionals.

Little information is available on the role of nurses in quality improvement efforts to decrease the incidence of CI-AKI via an organized approach to patient care and monitoring of outcomes. Nurses in the Northern New England Cardiovascular Disease Study Group (NNECDSG) developed a multicentered collaborative task force to

develop a framework to identify best practices in nursing interventions to reduce CI-AKI and worked toward stan-dardizing these approaches across a region with 10 diverse centers with a 5-fold variation in rates of CI-AKI after PCIs31 (Table 1 and Figure 2).

In this article, we detail the elements we identified as essential to improving patient outcomes and illustrate the regional impact nurses in the collaborative had in standardizing care processes to reduce the incidence of CI-AKI in patients undergoing cardiac interventional procedures. Specifically, our aim was to reduce the occur-rence of CI-AKI after PCIs during a 3-year period by

Figure 2 Adjusted rates of acute kidney injury (AKI) by center are rank ordered with 95% confidence intervals. The regional rate of AKI was 6.28% (dashed line). Reprinted from Brown et al,31 with permission of BMJ Publishing Group Ltd.

Rate

, %

15

10

5

0A B C D

Center

Adjusted AKI Confidence limits

E F G H I J

Table 1 Process and procedural practices for each site by rate of AKIa

Center CI-AKI

Pre-PCI NPO IV NaCl IV NaHCO3 N-AC

Peri-PCI Contrast agent Osmolality

Post-PCI IV NaCl IV NaHCO3

Abbreviations: AKI, acute kidney injury; CI-AKI, adjusted rates (%) of contrast-induced nephropathy; iodixanol, Visipaque; iohexol, Omnipaque; iopamidol, Isovue; ioxaglate, Hexabrix; iso, iso-osmolal; IV, intravenous; mandated, a standardized and mandated institutional or cardiology practice protocol where the practice was routinely implemented; N-AC, N-acetylcysteine; NaCl, 0.9% normal saline; NaHCO3, sodium bicarbonate (1000 mL 5% dextrose in water mixed with 150 mEq NaHCO3) given at 3 mL/kg per hour for 1 h pre-PCI and 1 mL/kg per hour for 6 hours post-PCI; no, this option was not available or used at the center; NPO, nothing by mouth, preanesthesia orders (eating and drinking); PCI, percutaneous coronary intervention; yes, use of this practice as an optional selection for care, not mandated. a Reprinted from Brown et al,31 with permission of BMJ Publishing Group Ltd.

A 1.9

Mandated 4 hYes

Mandated1200 mg

Iopamidol

Low

NoMandated

B 3.6

Optional 2 hMandated

No1200 mg

Iopamidol

Low

MandatedNo

C 4.0

MidnightOptionalOptional600 mg

IohexolIodixanol

Low, iso

OptionalOptional

D 4.6


Iodixanol

Iso

OptionalOptional

E 5.5

MidnightOptional

No600 mg

Iodixanol

Iso

OptionalNo

F 7.0


IohexolIodixanol

Low, iso

OptionalOptional

G 7.1


Iodixanol

Iso

OptionalOptional

H 8.8

MidnightYes

Optional600 mg

Ioversol

Low

YesOptional

I 9.8

MidnightOptional

No1200 mg

IopromideIoxaglateIodixanolLow, iso

OptionalNo

J 10.1


IopamidolIodixanol

Low, iso

OptionalOptional


The commitment of nurses to implementing

proven strategies for the prevention of

AKI after PCI is a critical link to ensuring

optimal patient outcomes.

adopting best practices for CI-AKI prevention. We hypoth-esized that high-intensity quality improvement efforts focused on adopting best-practice approaches within the region could reduce the rate of CI-AKI after PCIs.

Material and MethodsThe project was funded by the Agency for Health-

care Research and Quality. None of the authors had any conflicts of interest. The project was conducted within a regional registry maintaining the highest degree of data security and protections. All measurements were con-ducted within the context of data elements submitted to the registry and provided no additional risk to patients participating in the registry.

The NNECDSG is a voluntary regional consortium of clinicians, hospital administrators, and health care research personnel who seek to continually improve the quality, safety, effectiveness, and cost of coronary revas-cularization. Of 10 member hospitals, 8 agreed to par-ticipate in the quality improvement effort. Data were prospectively collected on consecutive patients undergoing PCI January 1, 2007, through June 30, 2012 (n = 20 147). Patients were excluded if they had emergent conditions or a history of renal failure requiring renal replacement therapy. Information was collected on patients’ charac-teristics, medical and cardiac history, cardiac anatomy and function, procedural priority, indication for PCI, process, and outcomes by using standard data collection instruments (available online at www.nnecdsg.org).32

Planning the InterventionProvider Education and Behavior Change

The absolute commitment of nurses to implementing proven strategies for the prevention of AKI after PCI is a critical link to ensuring optimal patient outcomes. This commitment by nurses could not be accomplished without a carefully planned approach to provide educa-tion to effect changes in behavior and improve health care practice.

For the member institutions of the NNECDSG, the process of change began with a discussion of the incidence of CI-AKI and the comparison of health care practices and patient outcomes among the institutions. Everyone perceived that CI-AKI was a serious and potentially pre-ventable complication that demanded a well-crafted approach to solving the problem. A literature review indicated strategies to reduce the incidence of CI-AKI,

such as the critical importance of hydration, the appro-priate selection of type of contrast material, and the volume of contrast material infused during cardiac catheterization and PCI. During this time, the ACT study21 was published, which repudiated the efficacy of N-acetylcysteine (Mucomyst) for prevention of CI-AKI in patients with stage 3 CKD. Study results were discussed during a conference call and were also presented and discussed at a quarterly NNECDSG meeting. Thereafter, institutions sharply curtailed their use of N-acetylcysteine except for patients with stage 4 CKD. The desire to improve each institution’s standing relative to the incidence of CI-AKI was a powerful motivator for change. Because organizations have their own unique values and culture, champions were selected from within each institution to share information and recruit inter-ested and motivated staff to form multidisciplinary teams to develop and implement strategies to reduce CI-AKI. Teams met regularly within their institutions, and key members participated in monthly NNECDSG nursing task force conference calls, allowing for further sharing of information.

Hydration before PCI had been identified as the most critical factor on which nurses could have an important impact to reduce the incidence of CI-AKI. Institutions devised or revised standardized preprocedure orders to include hydration orders, presenting 1 primary option for hydration with 1 alternative option for patients with heart failure. Cardiologists, nurse practitioners, and phy-sician assistants responsible for ordering cardiac cathe-terization and PCIs and preprocedure hydration received education to ensure compliance with the agreed-upon hydration strategies. Nurses caring for cardiac catheter-ization and PCI patients in each institution were edu-cated by the nurse champions in the institution. Nurses were taught the importance of establishing intravenous access shortly after a patient was admitted and of start-ing intravenous hydration with physiological saline. Nurse leaders engaged their colleagues in meetings and at the bedside, organizational and regional data were shared with all nurses caring for patients who had car-diac catheterization and PCI to outline the problem and incidence of CI-AKI, and information was shared on


Recent evidence has suggested that oral

self-hydration by patients is not inferior

to intravenous volume expansion in the

prevention of CI-AKI.

harm and prevention of CI-AKI, generating enthusiasm to achieve active collaboration for improvement in prac-tice. Staff members in the catheterization laboratory participated by requesting information related to the patient’s hydration status. Nurses monitored compliance with agreed-upon measures.

Champion nurses periodically gathered statistical data within their own institutions, documenting fluid intake and serum creatinine levels before, during, and after the procedures and the type of contrast material used. All centers used low-osmolar contrast agents during the intervention period. Progress toward reduc-

ing the incidence of CI-AKI became readily

apparent over time, providing tangible evidence of the efficacy of implemented strategies and thus serving as a powerful motivator to strive for process standardization, consistent compliance, and further refinement of evidence-based strategies.

In the NNE region, we found that surveying clini-cians involved in each phase of cardiac catheterization (before, during, and after) was an important first step to determine if clinicians perceived CI-AKI as an important issue and to help clinicians understand which factors affect the incidence of CI-AKI. Oral hydration, appropri-ate administration of intravenous fluid, and withholding potentially nephrotoxic medications are paramount in caring for patients before catheterization. This process exemplifies the positive impact of collaboration within and among institutions and of a team approach to achieve a clearly identified goal.

Patient Education for Prevention of CI-AKI

Recent evidence14-19 has suggested that oral self- hydration by patients is not inferior to intravenous vol-ume expansion in the prevention of CI-AKI. On the basis of this evidence and the clinical success reported from our centers, we deemed it important to engage patients through education and instruction to help prevent CI-AKI. Benchmarking centers in our region accomplished CI-AKI prevention strategies via direct patient education, patient oral self-hydration before hospital admission, and agreement by anesthesiologists to limit the amount of time a patient takes nothing by

mouth (preferably for only 2 hours before the proce-dure). The importance of partnering with patients for shared responsibility in the prevention of CI-AKI cannot be overemphasized in patients without congestive heart failure. This partnering can be achieved by using a stan-dardized approach, institutional involvement, and care coordination before and after a patient’s arrival at the hospital. Hydration of congestive heart failure patients requires therapy individualized to the patient and obser-vation to prevent volume overload.

During the initial screening before cardiac catheter-ization, along with a thorough history and physical examination, a baseline serum level of creatinine was determined and eGFR was calculated to identify patients at risk for CI-AKI (eg, eGFR < 60 mL/min per 1.73 m2, diabetes, preexisting renal dysfunction, hypertension). Patients were educated according to a standardized pre-PCI approach about the critical importance of oral hydration with 8 glasses of water (8 oz [240 mL] each) starting the evening before and up to 2 hours before the scheduled procedure. Patients were told to come early the day of their procedure, and the need to have hydration continued with intravenous physiological saline was explained. Patients were instructed to with-hold any potentially nephrotoxic medication (eg, diuretics, angiotensin-converting enzyme inhibitors, angiotensin II receptor antagonists, nonsteroidal anti-inflammatory drugs). Patients with congestive heart fail-ure were instructed to comply with the fluid restrictions set by their clinician. The nurses monitored the efficacy of patient instructions and compliance.

Methods for educating patients varied across centers. Examples of the methods used include the following:

• Distribution of a standardized printed instruction sheet from the patient’s provider when the patient was scheduled for cardiac catheterization that pro-vided concise instructions outlining restrictions on fluid and food intake and individualized medication instructions (which medications to take the morning of the procedure and which medications to withhold)

• A telephone call from a nurse knowledgeable in cardiac care from the admitting hospital 1 to 3 days before the procedure to be sure the patient under-stood all instructions, stressing the importance of hydration, which medications to withhold, and assurance that all necessary laboratory testing has been completed


Current practice guidelines state that

patients who are having a procedure that

requires sedation are allowed clear liquids

until 2 hours before the procedure.

• Posting a detailed patient information pamphlet on the admitting hospital’s website, accessible to patients with internet access

Discharge planning is a critical component of patient education. The use of standardized discharge instructions helps decrease misunderstanding and improve patient compliance. Instructions should include stressing the importance of self-hydration after the procedure, identi-fying which medications and supplements to take and which to withhold or discontinue, scheduling outpatient laboratory evaluation approximately 48 to 72 hours after the procedure, and scheduling follow-up with the patient’s health care provider.

In order to effectively monitor the incidence of CI-AKI, patients were instructed to have laboratory tests as ordered, generally 48 to 72 hours after the procedure. In order to further decrease the chance of CI-AKI, they were told to not resume taking any potentially nephrotoxic medi-cations (unless instructed otherwise by their provider) until the follow-up laboratory work was completed. A telephone call 48 to 72 hours after the procedure by the cardiac catheterization laboratory personnel, unit nurse, or office nursing staff was valuable to assess for any poten-tial complications and provided an opportunity to ensure the patient understood all instructions.

Hydration

Although adequate hydration and volume expansion are key factors in decreasing the risk for CI-AKI, currently no standard is available for the quantity and timing of oral and intravenous fluids. Throughout the NNE region, many variations in practice exist.

Same Day Admission. Patients with an eGFR less than 30 mL/min per 1.73 m2 (CKD stage ≥ 4) should be considered for admission the night before the procedure for initiation of hydration with intravenous physiological saline at 1 mL/kg per hour overnight. If admission the night before is not possible, they should arrive 3 hours before the scheduled procedure to allow sufficient time for adequate hydration, and the procedure should not be scheduled for 7 AM. Same-day patients with an eGFR greater than 60 mL/min per 1.73 m2 (CKD stage < 2) may be scheduled for 7 AM, and then patients with an eGFR 30 to 59 mL/min per 1.73 m2 (CKD stage 3).

Before the Procedure. Patients (except those with symptomatic heart failure) are encouraged to drink 8 glasses of clear fluids (8 oz [240 mL] per glass) starting

the evening before their procedure until 2 hours before the procedure. Current practice guidelines33,34 for anes-thesiology state that patients who are having a procedure that requires sedation are allowed clear liquids until 2 hours before the procedure. Using these practice guidelines can be helpful to reach institutional consensus on orders for nothing by mouth before cardiac catheterization.

Intravenous Hydration. For outpatients, intravenous access is established when the patients arrive at the hos-pital. Intravenous physiological saline should be started as soon as possible after admission and should be infused at 500 mL/h for 1 hour or 200 mL/h for 2 hours and then decreased to 100 mL/h until the start of the proce-dure. The goal is to infuse a minimum of 500 mL before the patient is exposed to contrast material. For centers that use sodium bicarbonate and the Merten protocol, the recommendation is to infuse physiological saline until the intravenous infusion of sodium bicarbonate is initiated and then administer sodium bicarbonate solu-tion at 3 mL/kg per hour for 1 hour immedi-ately before the procedure and continue at 1 mL/kg per hour for 6 hours after the procedure.20 If the procedure is delayed, the intravenous infusion of sodium bicarbon-ate can be titrated back to 1 mL/kg per hour until the start of the procedure.

For inpatients with normal renal function at baseline, physiological saline should be started at 5 AM at a rate of 200 mL/h for 2 hours and then decreased to 100 mL/h until the start of the procedure. Patients with an eGFR less than 60 mL/min per 1.73 m2 (CKD stage ≥ 3) should have infusion of physiological saline started at 10 PM the night before the procedure at a rate of 1 mL/kg per hour until the start of the procedure.

Patients With Congestive Heart Failure. Oral and intravenous fluid strategies for volume expansion for patients with congestive heart failure should be deter-mined by the attending health care provider or, prefera-bly, the heart failure team, before the procedure. Patients whose status is well maintained with current therapies without any signs or symptoms of heart failure should have hydration according to the CI-AKI preven-tion protocols as described earlier. Patients with indica-tions of heart failure should be assessed on an individual


basis to first determine appropriate timing of the cathe-terization and PCI and to assess the patient’s tolerance of intravenous fluids. Patients undergoing right-sided heart catheterization for evaluation of right-sided heart hemodynamic status or pulmonary artery pressures should have individualized fluid orders; because contrast agents are not used during these procedures, the patients are not at risk for CI-AKI. Ejection fraction is also a predictor of CI-AKI.28 Both simple and complex risk scores can be calculated for patients before a proce-dure to estimate risk for CI-AKI.35,36

Hydration During the Procedure

The infusion rate of physiological saline should be increased to 200 mL/h at the start of the procedure.

Hydration After the Procedure

For outpatients with femoral artery access sites, infusion of physiological saline is continued at 200 mL/h, with a goal of a total of 1000 mL after the procedure before discharge. For outpatients with radial artery access sites, infusion of physiological saline is continued at 250 mL/h, with a goal of a total of 750 mL and an additional 500 mL of oral fluid intake after the procedure before discharge. Patients (except those with symptomatic congestive heart failure) should be encouraged to drink at least 1000 mL of fluid within 24 hours after discharge.

Inpatients should receive physiological saline at 200 mL/h or 1 mL/kg per hour or sodium bicarbonate for 6 hours after the procedure unless contraindicated. Patients with heart failure whose condition is well main-tained with their current therapies without any indica-tions of heart failure should have hydration according to the CI-AKI prevention protocols described earlier. Patients with heart failure who have signs or symptoms of heart failure should be assessed on an individual basis for hydration after the procedure.

Cardiac Catheterization Laboratory

As a patient is transported into the cardiac catheter-ization laboratory, the risk for CI-AKI remains a priority. Information about a patient deemed at risk for CI-AKI should be communicated to the entire laboratory team. The information can be communicated in the handoff report as well as in the electronic medical record. Docu-mentation includes acknowledgment of the risk and plan for preventing CI-AKI. Handoff communication

includes the patient’s history, maximum acceptable dose of contrast material (MACD, calculated as 5 mL contrast medium times body weight in kilograms divided by base-line level of serum creatinine) or the Gurm equation (calculated as 3 times the ratio of contrast volume to calculated creatinine clearance), eGFR, and hydration status.26,37,38 Most likely the MACD will be surpassed in some instances in patients with especially poor renal function, and the calculated MACD might be too low to complete the intervention. These key points must be communicated before the start of the procedure and acknowledged with the procedure time out.26,37,38 As shown in Figure 3, exceeding a safe dose of contrast material significantly increases the risk for CI-AKI.

Current intraprocedure strategies for preventing CI-AKI include selecting a nonionic iso-osmolar contrast agent that will be least toxic to the patient. The latest gen-eration of contrast media is nonionic and iso-osmolar. This type of agent has been associated with a lower inci-dence of CI-AKI in patients with high risk for the renal injury: patients who have a history of diabetes, CKD, or reduced eGFR.25 However, our top-performing centers use a low-osmolar contrast agent and maintain a low CI-AKI rate.

One center wrote the MACD value on a white board in the room for the procedural staff to see as a reminder.

Figure 3 Calculated ratios of contrast volume to the predicted maximum acceptable contrast dose (MACD) are plotted against the crude (bars) and risk-adjusted (line, diamonds) rates of acute kidney injury (AKI). Reprinted from Brown et al,26 with permission.

1.5-2 > 2< 0.50

30282624222018161412108642

0.5-0.75 0.75-1 1-1.5MACD ratio

Crud

e (b

ars)

and

adj

uste

d (li

ne) r

ate

of A

KI, %


Many cardiac catheterization laboratories have discon-tinued use of the manifold system for injecting contrast medium and are using an advanced injection device (Acist; Acist Medical Systems, Inc).39 The device contin-uously counts the amount of contrast medium delivered. Thus, the nursing staff can immediately communicate to physicians when the physicians are approaching the MACD to prevent inadvertent excess administration of contrast medium. The ability to measure accurate real-time volumes of contrast medium allows physicians to adjust the plan of care for the patient in whom the volume of contrast medium administered approaches the MACD.

Consideration may be given to staging an intervention or forgoing a ventriculogram in order to avoid exceeding the MACD. Nurses play a vital role in communicating information related to effective hydration during the cardiac catheterization, as well as blood pressure and use of contrast medium.

Strategies after cardiac catheterization also depend on communicating what transpired during the procedure. Clear handoff of a patient from nurse to nurse should include the type and amount of contrast material used in relation to the MACD, the intravenous volume of con-trast medium administered, and the patient’s hemody-namic status. One center uses a stamp that includes the MACD and the actual amount of contrast material administered (Table 2) to help strategize which labora-tory tests should be ordered and which interventions should be performed after the procedure. The plan for continued hydration and medication therapies must be ordered and documented to ensure that hydration is performed before, during, and after the procedure.

After the Procedure

Strategies for detecting CI-AKI include the develop-ment of a standardized approach to complete a thorough laboratory assessment of renal function on all post-PCI patients, not just patients at high risk for CI-AKI. Cur-rently, a controversy exists about the appropriate timing of postprocedural assessment of renal function and the determination of the person who should be responsible for tracking postprocedural serum levels of creatinine and the eGFR. For patients with CI-AKI, should the patient be evaluated by the interventional cardiologist, should a nephrology consultation be arranged, or is it sufficient to follow up with the patient’s primary care provider

only? Appropriate follow-up must be clearly delineated by each institution. Standardized laboratory slips or instructions with the fax number of the person or office responsible for tracking serum levels of creatinine and eGFR would help ensure that these data are collected. We recommend determining serum levels of creatinine and eGFR 48 to 72 hours after the PCI. Each institution should determine the course of action to implement if CI-AKI is detected, including the intervals for continued laboratory monitoring and the appropriateness of con-sultation with a nephrologist.

Planning the Study of the Intervention Identification of Benchmark and

Intervention Hospitals

According to data from January 1, 2007, through October 30, 2008, a total of 2 hospitals had significantly lower rates of CI-AKI than did the other 6 hospitals (2.3% vs 6.6%; P < .001). These 2 hospitals were identified as benchmark sites. Their experiences were used to inform the intervention, but these sites did not take part in the active intervention.31,32

Quality Improvement Intervention Phase

The intervention phase began on November 1, 2008, directly after a 2-day regional meeting focused on CI-AKI as an improvement target for NNECDSG hospitals, and continued through June 30, 2012. Participating hospitals agreed to do the following:

• Form multidisciplinary teams that included inter-ventional cardiologists, managers and technicians in cardiac catheterization laboratories, nurses rep-resenting the intensive care unit and/or holding areas, cardiology administration, and nephrologists

• Participate in monthly conference calls facilitated by a microsystems quality improvement coach

Table 2 Contrast stamp

Abbreviations: Contrast, contrast medium; eGFR, estimated glomerular filtra-tion rate; max, maximum.

Patient: __________________________Date: __________________________Baseline serum level of creatinine: _______(mg/dL)eGFR or creatinine clearance: _______(mL/min per m2)Contrast volume:creatinine clearance limit: _______(mL)Actual weight maximum dose contrast amount limit: _____(mL)Ideal weight max dose contrast amount limit: _______(mL)Actual contrast amount given: _______(mL)

Real-time data surveillance is important

to help clinicians understand the impact

of their collective actions on patients.


• Participate in a process of identifying best practices via a formal review of the literature and structured interviews with benchmark sites

• Participate in annual structured focus groups to acquire qualitative data on barriers and successes to improvement

• Have adjusted CI-AKI rates by hospital added to the NNECDSG biannual reports provided to all hospitals, administrators, and health professionals

In addition, hospitals were encouraged to have a member from each team undergo 6 months of quality improvement training in microsystems coaching. During the first year of the intervention, teams identified best practices by formal review of the literature as summarized by the primary investigator (J.B.) and by a series of structured interviews with benchmark sites. Sites were encouraged but not required to implement identified

best prac-tices. In addition to monthly

conference calls and annual focus groups, representa-tives from each hospital attended 3 regional NNECDSG meetings each year where trends of CI-AKI, implement-ing best practices, and novel approaches to minimize CI-AKI were presented and discussed.32

Determination of CI-AKI

The last measurement of the serum level of creati-nine before the procedure and the highest level after the procedure before discharge were used to determine the incidence of CI-AKI. Because data were collected in the routine process of care, nothing in the protocol man-dated measurement of the serum level of creatinine at a particular time. CI-AKI was defined by using the defi-nition in the KDIGO guidelines: serum level of creatinine 0.3 mg/dL or greater within 48 hours of the procedure or increased 50% or greater from baseline at any time during the hospitalization.40 Patients generally were hos-pitalized 2.7 (median, 2.0) days during the baseline period and 2.6 (median, 2.0) days during the follow-up period.32

Methods of Evaluation

Real-time data surveillance is important to help clini-cians understand the impact of their collective actions on patients. One way to convey this information is to post information on data walls.

Key metrics to monitor and analyze should include amount of fluid intake before admission, withholding of potentially nephrotoxic agents, baseline serum level of creatinine and eGFR, amount of intravenous physio-logical saline and/or sodium bicarbonate administered before the procedure, amount of intraprocedure physio-logical saline administered, volume and type of contrast medium administered during the procedure, amount of physiological saline or sodium bicarbonate adminis-tered in the initial hours after the procedure, and serum level of creatinine and eGFR after the procedure. Once centers analyze their own data and identify their own rates of CI-AKI, they can implement strategies to modify their practice of care to reduce the incidence of CI-AKI for all patients.31

Compliance can be measured by reviewing data on intake and output, determining the frequency and appro-priateness of oral and intravenous hydration orders, and reviewing a list of medications taken at home and hospi-tal administration records of medications administered during the admission.

Analysis

Patient, disease, and procedural characteristics at baseline were compared with those during the interven-tion period, overall and stratified by exposure: interven-tion and benchmark. We used 2 tests for categorical data and t tests for continuous data. Multilevel mixed-effects Poisson regression clustering to the patient and hospital level was used to calculate adjusted risk ratios with 95% CIs of CI-AKI between the intervention and baseline periods, with adjustments made for age, sex, body mass index, smoking history, diabetes, hyperten-sion, chronic obstructive pulmonary disease, peripheral vascular disease, heart failure, urgent priority for PCI, previous PCI, previous coronary artery bypass graft surgery, number of diseased vessels with more than 70% stenosis, number of vessels attempted, number of stents, radial access, and baseline eGFR calculated according to the National Kidney Foundation definition and using the Modification of Diet in Renal Disease equation.41-43 To show temporal trends in the rates of CI-AKI, we performed interrupted time-series analyses and plotted monthly rates of CI-AKI, with adjustments for covariates in the Poisson model. Because most improvement efforts and protocols were for high-risk patients with eGFR less than 60 mL/min per 1.73 m2,


analyses were repeated for patients who had that eGFR value at baseline.32 All statistical analyses were conducted by using Stata, version 11.2, software (StataCorp, LP).

Evaluation of Quality Improvement

Interventions

Annual structured focus groups of the multidisci-plinary clinical teams were conducted at all hospitals. Teams were asked guided open-ended questions about improvement efforts, barriers, successes, and quality improvement training. A research coordinator facili-tated and taped all meetings. Field notes were recorded. All notes and meeting transcriptions were systematically evaluated by using the grounded theory approach.44 We used open coding to develop initial themes and then axial and selective coding and aggregated across hospi-tals to find unifying themes. We aggregated key themes into domains.32

ResultsThe absolute commitment of nurses to implement

strategies for the prevention of CI-AKI is a critical link to ensuring optimal patient outcomes. Despite chal-lenges, the teams were successful in reducing the inci-dence of CI-AKI. The region followed 6983 consecutive patients undergoing PCI before the quality improvement interventions and 14 084 consecutive patients after the start of the interventions. Overall, the medical centers

using the quality improvement interventions reduced CI-AKI by 21% compared with the preintervention phase and by 28% among patients with preexisting CKD32 (Figure 4).

We leveraged the qualitative findings to help inform how teams (and medical centers) improved during the intervention period (Table 3). We discovered that high-functioning teams had interprofessional members with clinical champions. Teams reported struggling with key barriers to improvement efforts, including variation in physician ordering, changing orders for nothing by mouth, and the need to unlearn old protocols. However, the teams reported important improvement successes that included changing behavior with an increased aware-ness of CI-AKI prevention strategies, implementing hydra-tion protocols, standardizing order sets, minimizing the volume of contrast medium used by reducing test injections and eliminating ventriculography, mandating procedure delays to allow for intravenous boluses of fluid, and staging procedures. A full description of the qualita-tive findings and modeling has been previously described.32

DiscussionOverall, teams were successful in reducing the

occurrence of CI-AKI by more than 20%. Teams devel-oped innovative solutions for prevention. As previously discussed, educational materials were built into patient instructions to encourage patients to self-hydrate before

Figure 4 Adjusted rates of acute kidney injury (AKI) plotted by month for the Northern New England Cardiovascular Disease Study Group intervention hospitals by using interrupted time-series analysis. The vertical dashed line represents the start of the quality improvement intervention. Rates of AKI differed significantly between the baseline period and the intervention period (P = .04). Adapted from Brown et al,32 with permission.

8

6

4

2

03

Adju

sted

rate

of A

KI, %

6 9 12 15

Intervention period

Month

Baseline period

18 21 24 27 30 33 36 39 42 45 48 51 54 57 60 63 660


and after PCIs. Recent clinical trials14,45 have supported the use of oral fluids as an effective alternative to intrave-nous fluids. Teams were also innovative in developing hard stops in a patient’s process of care by delaying a procedure if the patient had not received an adequate fluid bolus until the ordered fluid bolus was delivered.32

Although many studies have been done on interven-tions to reduce the risk of CI-AKI, no previous investi-gations were focused on nurse-implemented quality improvement efforts to reduce CI-AKI. The most recent attempt of using a quality improvement initiative to reduce the incidence of CI-AKI was published in 2006 when the Michigan Cardiovascular Consortium reported on nephropathy due to contrast material and multiple quality indicators from a 1998 to 2002 intervention.46 Moscucci et al46 used techniques similar to ours and achieved significant improvement across multiple qual-ity indicators, including nephropathy due to contrast material. In our improvement effort, which was largely implemented by nurse champions, had a high-intensity quality improvement design, and took advantage of leveraging quality improvement coaching, we promoted change from within organizations to apply the best evidence-based medicine to prevent CI-AKI. We pro-moted this change by forming interprofessional teams that included nurses, provided a structure for protocol

transparency and sharing, had data feedback mecha-nisms, and made use of quality improvement training (microsystems coaching).32

Our project has several limitations. Although we did not conduct a randomized controlled trial, we did control for differences in patient risk factors between the base-line period and the intervention period. Second, patients were hospitalized for a mean of 48 hours, and this short time did not allow for the routine measurement of serum levels of creatinine commonly used in randomized trials.47 We were limited to our registry data, which included information on the serum level of creatinine before the procedure and the highest level after the procedure. Therefore we may have underestimated the true inci-dence of CI-AKI and the true benefit of our intervention. However, the mean length of stay was 2.7 days (median, 2 days) for the baseline period and 2.6 days (median, 2 days) for the follow-up period; therefore, most patients at least had 48 hours of follow-up before discharge from the hospital. Additionally, fluid protocols initially var-ied by center, and although we collected qualitative data on protocols over time, the study did not include fund-ing for data collectors at each site to measure fluid intake.

A recent meta-analysis48 has provided evidence that oral fluid protocols and intravenous fluid protocols do not differ significantly for prevention of CI-AKI. However,

Table 3 Domains and key themes in hospital AKI quality improvementa

Domain Teams

Intervention barriers

Patient and process interventions

Factors supporting success

Abbreviations: AKI, acute kidney injury; NPO, nothing by mouth.a Reprinted from Brown et al,32 with permission.

Key themes in AKI performance High-performance teams had multidisciplinary team members, clinical champions, empowered nurses,

multiple team champions, protected time for team meetings and improvement work, regular scheduled meetings, and quality improvement training (Lean, Six Sigma, microsystems)

Challenges included variation in physician ordering, variation in protocols, unlearning old protocols, NPO status of the patient, education, documentation, data collection, working with transferring facilities, phy-sician and patient noncompliance with orders, staffing, resources, time, staff buy-in, trade-offs with other quality targets

Hospitals adopted benchmark hospital protocols, standardized intravenous order sets, reduced NPO status to 2-4 hours prior to procedure, stop nephrotoxic drugs prior to procedure.

Hospitals also developed readiness checklists including volume status of the patient and fluid bolus, delayed procedures to allow for fluid bolus, limited contrast volume and exposure, eliminating left ventriculography, and conducted patient education about self-hydration using oral fluids (8 8-oz glasses of water 12 hours before and 12 hours after procedure)

Hospital changes in behavior during the intervention included increased awareness, standardized intrave-nous fluid order sets, reduced NPO status to 2-4 hours prior to procedure, staff and institutional buy-in, hydrating patients before and after the procedure, staff and patient education, limiting contrast volume, precalculated safe contrast dose per patient using the maximum acceptable contrast dose equation (5 mL x body weight in kg / baseline serum creatinine), staging procedures, delaying procedures to allow for fluid bolus, and quality improvement training


recent evidence49 indicates that sodium bicarbonate hydration is significantly more protective against CI-AKI than is hydration with physiological saline. Oral and intravenous fluid hydration should be paired to maxi-mize the fluid bolus before cardiac catheterization to allow patient-empowered self-hydration to help prevent CI-AKI if intravenous fluids are not administered before and after the procedure.50 A wise step for future imple-mentations of this intervention would be to measure and document the method used to administer fluids for hydration. Our data collection also did not include use of statins. However, we recommend that statin use be documented for future CI-AKI prevention studies because recent research51 has shown that statins can be significantly protective against CI-AKI.

Third, starting in 2010, our quality improvement effort competed in some centers with efforts to intro-duce radial access as a key quality factor to reduce length of stay and bleeding complications. Qualitative data from teams confirmed that radial access was a compet-ing quality target and might have diverted efforts of our improvement team to focusing on adoption radial access, leading to an underestimate of the true potential effect of our intervention in preventing CI-AKI. Addition-ally, an unmeasured mechanistic relationship may exist between reduced bleeding with radial access, shorter length of stay, and reduced incidence of CI-AKI.52,53 Last, responses to focus groups may be subject to recall bias. Teams who did not meet their goals or who perceived that they were underperforming because of barriers or attitudes toward improvement might be more likely than other teams to recall adverse aspects of their per-formance or institutional involvement. Teams who performed well might have found recall easier and been more willing to remember successes or not recall failures or barriers to improvement.32

Conclusions In summary, a regional collaborative took on the task

to reduce the incidence of CI-AKI through basic, team-based quality improvement methods. Interprofessional teams were formed and leveraged a culture of collabora-tion and transparency, implementing methods in quality improvement coaching to redesign systems of care to reduce CI-AKI. Each team worked within its own medi-cal center to encourage patient self-hydration, standard-ize intravenous fluid orders for volume expansion, delay

cases to ensure adequate volume expansion, reduce the time of nothing by mouth to 2 to 4 hours before the pro-cedure, influence the type of contrast material used, and limit the volume of contrast material used. Overall, the hospitals participating in the intervention significantly reduced CI-AKI by 21% by using simple team-based quality improvement and coaching.32 ��

AcknowledgmentsThe authors thank the NNECDSG hospitals and quality improvement teams participating in the CI-AKI quality improvement initiative.

Financial DisclosuresThis project was supported by grant HS018443 (Dr Brown) from the Agency for Healthcare Research and Quality and the Northern New England Cardio-vascular Disease Study Group participating medical centers.

Now that you’ve read the article, create or contribute to an online discussion about this topic using eLetters. Just visit www.ccnonline.org and select the article you want to comment on. In the full-text or PDF view of the article, click “Responses” in the middle column and then “Submit a response.”

See alsoTo learn more about diseases that affect the kidney, read “Long-Acting Insulin on the Road to Recovery With Diabetic Ketoacidosis” by Bunn and Halm in the American Journal of Critical Care, May 2016;25:277-280. Available at www.ajcconline.org.

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