Objective

Conventional clinical wisdom has often been nihilistic regarding the prevention and management of acute kidney injury (AKI), despite it being a frequent and morbid complication associated with both increased mortality and cost. Recent developments have shown that AKI is not inevitable, and that changes in patient management can reduce both the incidence and morbidity of perioperative AKI. The purpose of this narrative review is to review the epidemiology and outcomes of AKI in patients undergoing vascular surgery using current consensus definitions, discuss some of the novel emerging risk stratification and prevention techniques relevant to the vascular surgery patient, and describe a standardized perioperative pathway for the prevention of acute kidney injury after vascular surgery.

Methods

We performed a critical review of the literature on acute kidney injury in the vascular surgery patient using the PubMed and MEDLINE databases and Google Scholar through September 2017 using Web-based search engines. We also searched the guidelines and publications available online from the organizations Kidney Disease, Improving Global Outcomes (KDIGO) and the Acute Dialysis Quality Initiative (ADQI). The search terms used included acute kidney injury, AKI, epidemiology, outcomes, prevention, therapy and treatment.

Results

The reported epidemiology and outcomes associated with AKI have been evolving since the publication of consensus criteria that allow for accurate identification of mild and moderate AKI. The incidence of AKI following major vascular surgery using current criteria is as high as 49%, though there are significant differences depending on the type of procedure performed. Many tools have become available to assess and stratify the risk for AKI, and use that information to prevent AKI in the surgical patient. We describe a standardized clinical assessment and management pathway for vascular surgery patients, incorporating current risk assessment and preventive strategies to prevent AKI and decrease its complications. Patients without any risk factors can be managed in a perioperative fast-track pathway. Those patients with positive risk factors are tested for kidney stress using the urinary biomarker TIMP-2•IGFBP7, and care is then stratified according to the result. Management follows current Kidney Disease Improving Global Outcomes guidelines.

Conclusion

AKI is a common postoperative complication among vascular surgery patients and significantly impacts morbidity, mortality, and cost. Preoperative risk assessment and optimal perioperative management guided by that risk assessment can minimize the consequences associated with postoperative AKI. Adherence to a standardized perioperative pathway designed to reduce risk of AKI after major vascular surgery offers a promising clinical approach to mitigate the incidence and severity of this challenging clinical problem.

Keywords: Acute kidney injury, preoperative risk, postoperative complications, vascular surgery

Definitions and Epidemiology

Acute kidney injury is one of the most common yet underdiagnosed postoperative complications following any type of surgery. Historically there was wide variability in the reported incidence of postoperative AKI (pAKI) because of the widely variable definitions of AKI that were in use^9,10. Previous definitions focused on large increases in serum creatinine or the need for renal replacement therapy (RRT), which led to AKI being portrayed as a rare and fatal complication¹¹. In 2004, the Acute Dialysis Quality Initiative group introduced the Risk, Injury, Failure, Loss, and End-Stage Kidney (RIFLE) classification, a standardized definition for the diagnosis and staging of AKI using serum creatinine and urine output measurements¹². These consensus criteria were the first to recognize the less severe stages of AKI. The RIFLE criteria were further expanded in 2012 by the Kidney Disease: Improving Global Outcomes (KDIGO) clinical practice guidelines, which included even milder forms of AKI with serum creatinine increases as small as 0.3 mg/dL¹³. While the use of the consensus definition for AKI is now common in clinical studies, the definitions have not yet been incorporated into the common surgical registries. The American College of Surgeons National Surgical Quality Improvement Program database, the Society of Thoracic Surgeons National Database and The Society for Vascular Surgery Vascular Quality Initiative databases all use their own definitions for AKI, none of which corresponds to current consensus definitions (Table 1)^11,14,15.

The Vascular Quality Initiative (VQI) is a collaborative of regional quality groups collecting and analyzing perioperative and one-year follow-up data in an effort to improve patient care¹⁶. The VQI is governed by the SVS Patient Safety Organization which provides oversight of data sharing, outcome and quality measure analyses, and dissemination of information. Data collection for the VQI database is procedure-dependant. Data collected to assess renal dysfunction varies from none (for amputations, cava filter placements, hemodialysis access procedures and carotid procedures) to measurement of highest postoperative serum creatinine and recording of any dialysis (endovascular aortic procedures) to a staged measurement of any change in renal function (for open aortic procedures and peripheral bypass procedures). While it does not use the same staging as the consensus KDIGO guidelines, the Vascular Quality Initiative database does recognize the importance of even mild degrees of AKI, with any increase in serum creatinine of greater than 0.5 mg/dl recorded as a Stage 1 change of renal function.

The reported epidemiology and outcomes associated with pAKI have been evolving since the publication of these new consensus definitions. The incidence of AKI following major vascular surgery using the current criteria has been reported as high as 49% across a cohort of all vascular surgery patients, though there are significant differences depending on the type of procedure performed¹⁷. Peripheral vascular procedures have some of the lowest rates, from 4% for patients undergoing infrainguinal lower extremity bypass, up to 19% for endovascular revascularization of critical limb ischemia^18–21 (Figure 1).

Thoracic and abdominal aortic procedures generally have higher rates of pAKI than peripheral vascular operations. Elective endovascular aortic repair (EVAR) of infrarenal abdominal aortic aneurysms (AAA) have reported incidences of pAKI between 5.5% and 18%^22,23. One recent study reported a rate as low as 2.9%, however it is important to note that they defined AKI as an increase in serum creatinine of 0.5 mg/dL or a new dialysis requirement, differing from the more sensitive KDIGO consensus criteria²⁴. More complex AAA repairs have higher rates of AKI, up to 28% for those requiring branched or fenestrated devices, and as high as 32% for juxtarenal AAAs employing a snorkel or chimney approach^25,26. Similarly, the recently reported incidence of AKI after thoracic endovascular aortic repair (TEVAR) for thoracic aortic aneurysms (TAA) was 9.7%²⁷ and 30% after repair of Stanford Type B acute aortic dissections²⁸.

Open aortic procedures have significantly higher incidences of pAKI compared to endovascular approaches. Patients undergoing elective open aortic repairs of infrarenal AAAs have pAKI rates of up to 26%²². This risk increased for more proximal aneurysms, up to 47% for juxtarenal and 68% for suprarenal aneurysms²⁹. Emergent repair of a ruptured aneurysm has the highest risk with some series documenting rates of 75%^30,31. Open thoracic repairs had similarly elevated incidence of renal complications compared to their endovascular counterparts where pAKI rates can be 34% for elective TAA, 45% for Stanford Type A dissections, and 48% for aortic arch procedures^27,32,33.

Outcomes

Postoperative AKI has repeatedly been shown to be associated with increases in risk for other complications, in short and long term mortality, in hospital cost and in resource utilization among all surgical patients. Patients who develop AKI after major vascular surgery have higher rates of other postoperative complications such as infection, coagulopathy, anemia, need for mechanical ventilation, rates of tracheostomy, and cardiovascular events^{17,19,20,22,23,34,35}. Long term, pAKI patients are more likely to have subsequent episodes of AKI, develop CKD, have cardiovascular disease and have worse survival^{17,19,36–38}.

Both in-hospital and long term mortality is significantly elevated among vascular patients who develop pAKI compared to those who do not^18,19,34. Not only does this reduced survival risk persist for up to 10 years after the original episode, but it has been shown to exist even among patients who achieve full recovery of baseline renal function^39,40. For peripheral vascular procedures, patients who developed pAKI experienced higher rates of adverse cardiovascular events (odds ratio (OR) 2.50; 95% confidence interval (CI) 1.91–3.28), in-hospital mortality (OR 6.69; CI 3.94–12.31 ), and 5-year mortality (OR 2.09; CI 1.34–3.26)^18,19. Notably, cardiovascular-specific mortality is particularly elevated in this patient population⁴¹. In a cohort of all vascular surgery patients, for patients with normal preoperative renal function who developed AKI after surgery 5-year cardiovascular-specific mortality was 22%, compared to 10% for patients without AKI⁴². Even the least severe stage 1 AKI confers additional mortality risk, which increases with worsening AKI severity^34,40,43. Outcomes in the important prospective vascular surgery clinical trials, for both peripheral arterial disease and aortic disease, either don’t mention acute kidney injury⁴⁴ or provide minimal outcomes information such as a new need for dialysis⁴⁵ or a proscribed drop in eGFR^46–51.

The development of pAKI is associated with a substantial increase in hospital cost and resource utilization. These patients have longer ICU and overall hospital lengths of stay, as well a higher likelihood of being discharged to a skilled nursing facility or rehabilitation center^34,38,43. A large retrospective study of major surgery patients demonstrated a mean adjusted hospital cost of $42,600 for patients who developed pAKI compared to $26,700 for those who did not, a 59% increase³⁴. This cost differential increased incrementally with worsening RIFLE-AKI stage. A similar study of vascular surgery patients identified that either pre-existing CKD or pAKI results in additional adjusted incremental costs of $8,900 and $9,100 respectively, while the simultaneous presence of both of these conditions contributed to a $19,100 adjusted incremental cost increase¹⁷. The additional costs that these patients incur draws from across several different categories of care, including the ICU, medical supplies, laboratory, pharmacy, and respiratory services⁴³.

It is important to note that recent studies have shown that negative outcomes after AKI are not set in stone and in fact are modifiable with proactive prevention and management actions taken by the surgeon. Two recent prospective randomized trials of biomarker-guided prediction and management of pAKI in surgical patients, using the urinary biomarker TIMP-2•IGFBP7 to stratify patients into either a KDIGO care bundle or standard care, have shown that aggressive monitoring and management of pAKI in patients undergoing major surgery can lead to better outcomes^3,4. In both studies the overall incidence of pAKI, and the incidence of more severe stages of pAKI, was reduced in the study patients.

Risk Stratification and Prediction

An individual patient’s risk for developing pAKI is determined by a complex interaction of their preoperative kidney health, their physiologic reserve affecting their capacity to withstand surgical stress, and the type and course of the surgical procedure the patient undergoes. Moreover, this risk is unlikely to be a static value, but instead is actually a dynamic variable that changes in response to intraoperative and postoperative events that are difficult to predict in the preoperative setting. While attempts to stratify and predict AKI risk preoperatively are of primary importance, the ability to analyze and interpret the wealth of intraoperative clinical data and adjust risk for the events that can dramatically modify the risk, such as intraoperative hypotension or use of nephrotoxic drugs, will allow application of risk-targeted preventive strategies throughout the continuum of perioperative care.

There are many tools now available to evaluate preoperative risk for pAKI including clinical data, plasma and urine biomarkers and advanced imaging techniques. The large population of patients at low risk only need basic stratification using clinical evaluation of known risks for AKI such as CKD and albuminuria⁵². Patients at higher risk will need more complex, and thus more expensive, assessment of risk. Clinical risk scores were among the first strategies to predict patients who would develop AKI. Their utility is limited by their inability to incorporate dynamic intraoperative factors, and often they have been developed for a specific type of surgery and are not widely applicable. In a systematic review of several clinical risk scores for cardiac surgery patients, only moderate performance was observed with ROC-AUCs between 0.77 and 0.84⁵³. Many of these scores relied on easily abstracted preoperative variables and simple logistic regression analysis. A model designed for risk prediction in patients undergoing vascular surgery performed relatively poorly with ROC-AUC of 0.67 when using only preoperative variables, and only showed a modest improvement to 0.72 when incorporating some intraoperative variables⁵⁴. More recently, advanced computational approaches using techniques such as machine learning models that use electronic health record data have shown better performance. One such model developed for AKI prediction for patients undergoing any major surgery reported an AUC of 0.86 on internal validation⁵⁵. Models that are able to capture and process large volumes of data in real time, and process them automatically to create risk profiles, are likely to emerge as superior approaches to risk calculation compared to regression analyses⁵⁶. Until such tools are developed and validated, risk scores for pAKI cannot be recommended for routine clinical use.

Advanced imaging techniques are being developed and evaluated as a means to assess kidney function and AKI. The renal resistive index (RRI) uses Doppler ultrasound imaging to assess the resistance to blood flow in the kidney, and an elevated RRI has been associated with increased risk for AKI⁵⁷. An elevated RRI has been associated with increased risk and severity of AKI in sepsis and in patients who underwent cardiac and orthopedic surgery^58–62. It has also shown potential to predict the progression of postoperative AKI⁶³. Contrast enhanced ultrasound (CEUS) to assess renal perfusion has demonstrated promise as a predictor of risk and prognosis of surgical patients who develop AKI^64–66. Finally, blood oxygenation level dependent (BOLD) MRI uses deoxyhemoglobin as a contrast agent to study intrarenal oxygenation, and while promising in animal studies of AKI has not yet found a place in clinical practice^67–69. While none of these imaging techniques are in common clinical practice, and when they are used it is typically under the guidance of a nephrologist, they are evolving rapidly and likely will be seen more often.

Urine and plasma biomarkers for AKI are a significant focus of research efforts. Currently, serum creatinine (SCr) is the most widespread value used for diagnosing and monitoring AKI. Unfortunately, SCr is a measurement of renal function rather than renal injury, and degradation of function is not observed until tubular damage is already well underway. A suitable biomarker would detect tubular stress prior to the structural damage that results in functional impairment, and would have specificity for AKI as opposed to CKD or other disease processes⁷⁰. Two markers that showed some initial potential, but have been hampered by the previously described difficulties, are neutrophil gelatinase-associated lipocalin (NGAL) and Cystatin C (CyC)^71–75. More recently the combination of urinary tissue inhibitor of metalloproteinase-2 (TIMP-2) and insulin-like growth factor binding protein 7 (IGFBP7) has performed well in the prediction of moderate to severe AKI in critically ill patients in several multicenter studies, and has been approved by the Food and Drug Administration (FDA)^76–78. These markers are cell-cycle arrest proteins released by renal tubular cells in response to stress from toxins, inflammation, and hypoxia, and may indicate the risk of renal injury prior to any permanent tubular damage. Validation of these markers demonstrated sensitivity of 89% and negative predictive value of 97% for predicting AKI in critically ill patients within 12 hours⁷⁹. The TIMP-2·IGFBP7 test has been the most accurate biomarker developed to date, is FDA approved and commercially available, and has been shown to have clinical utility in surgery patients^4,80.

Prevention and Treatment

Optimal perioperative care of the vascular patient, using strategies evaluated in vascular surgery and in other major surgery, may prevent pAKI and/or limit the extent of injury if pAKI occurs (Table2). A protocol that emphasizes optimal hemodynamic function, along with avoidance of warm renal ischemic time and renal toxins (especially IV radiographic contrast), has been shown to be effective in preventing acute kidney injury in the vascular patient²². However many other approaches have been explored. Given that most patients undergoing vascular surgery will have numerous cardiovascular comorbidities, there has been significant interest in the pharmacological optimization of renal function, particularly in the preoperative setting. In general these interventions have been of little or no use in preventing pAKI. Antihypertensive therapies such as angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARB) have been proven beneficial for primary prevention and management of chronic kidney disease, however their use in the immediate perioperative setting is associated with postoperative hypotension^81–83. Several recent studies have demonstrated preoperative use of ACE inhibitors or ARBs is associated with higher rates of pAKI after noncardiac surgery^84–86. Similarly in a large prospective cohort of cardiac surgery patients, ACE inhibitor and ARB use was associated with higher rates of functional pAKI by serum creatinine values, however no evidence of structural kidney injury was observed by measurement of urinary biomarkers of structural damage such as NGAL, kidney injury molecule-1, IL-18, and liver-fatty acid-binding protein⁸⁷. While no prospective trials have yet been done, given these findings clinicians should consider holding ACE inhibitors and ARBs in the 24 hours immediately before surgery if possible. Other drugs that have been evaluated for their potential to prevent pAKI include n-acetyl cysteine, sodium bicarbonate, dopamine, fenoldapam (a selective D1 receptor partial agonist), theophylline, atrial naturetic peptide, clonidine and aspirin, and none have been shown to be clinically effective^88,89. Despite being commonly used during procedures requiring suprarenal aortic cross-clamping, mannitol has not been shown to significantly decrease rates of pAKI and may actually increase the risk among patients who receive intravenous contrast administration^90,91.

Initial trials of remote ischemic preconditioning as a technique to prevent pAKI were disappointing, however recent trials have demonstrated benefits in both cardiac and vascular patients^92–95. Remote ischemic preconditioning, which utilizes the concept of repeated cycles of transient ischemia in an extremity to enhance ischemic tolerance in visceral organs, has been shown to protect against many forms of AKI including contrast induced AKI prior to elective coronary angiography, and has been associated with decreased lengths of hospital and ICU stay in patients undergoing vascular surgery^93,96. In vascular surgery the technique can include intermittent clamping of the common iliac artery after access to the peritoneal cavity, or intermittent activation of a tourniquet on the thigh or arm⁹⁷. The mechanisms of remote ischemic preconditioning are poorly understood, however they are believed to include modification of mitochondrial function, metabolic down-regulation, and temporary cell-cycle arrest. Additionally, a recent study demonstrated elevated plasma vascular endothelial growth factor levels in animal model of remote ischemic preconditioning⁹⁸. While not in widespread practice, particularly in vascular surgery, studies continue to show improved outcomes in patients where the technique is used^92,99

Perioperative techniques that have been shown to minimize pAKI in cardiac and vascular surgery include cell salvage techniques, avoidance of anemia, avoidance of hypotension, enhancement of oxygen delivery, and minimization of allogenic blood product transfusion^100–104. The use of volatile anesthetics have been shown to provide renal protection in patients undergoing cardiovascular surgery¹⁰⁵. An early meta-analysis of goal-directed fluid management showed reduced complication rates in cardiac patients but no significant benefits in vascular patients, although rates of AKI were reduced¹⁰⁶. Utilization of bedside ultrasound in the intensive care unit to assess renal perfusion and renal resistive indices has demonstrated some promising results as an adjunct to resuscitation¹⁰⁷. However, further studies are warranted given the difficulty in determining optimal endpoints for both resuscitation and targeted MAP goals in the prevention of AKI.

Technical considerations relating to the duration and placement of vascular clamps may also impact the development and progression of renal ischemia. Extensive dissection with associated embolization of atheromatous material may precede the development of renal ischemia¹⁰⁸. Renal artery stenosis, if detected preoperatively, may be treated with angioplasty, stent or concurrently at the time of surgery. Several studies have demonstrated the feasibility of unilateral or bilateral renal artery endarterectomy with short term improvements in renal function and no significant difference on mortality^109–114. Duration of aortic cross clamp time with renal ischemia > 23 minutes was associated with renal dysfunction after juxtarenal AAA repair¹¹³. Hypothermic perfusion and maintenance of renal perfusion has been described in small cohorts of patients undergoing aortic surgery, with no long term elevations in serum creatinine upon hospital discharge¹¹⁵.

Timely referral and ongoing involvement with nephrology has been shown to minimize sequela related to AKI¹¹⁶. Delays in nephrology consultation are associated with increased mortality and dialysis dependence rates at hospital discharge, while early nephrology consultation has been shown to reduce the risk of worsening kidney function in diverse patient populations^116–118. Immediate nephrology consultation after AKI can influence outcomes both by insuring that care follows current AKI guidelines, and through appropriate initiation of renal replacement therapy when indicated¹¹⁹. When and how to initiate renal replacement therapy, and who makes that decision for the patient with AKI, is controversial. Later nephrology follow up, once a patient has been discharged from the hospital, has also been shown to impact all-cause mortality in survivors of severe kidney injury and to reduce subsequent deterioration of renal function^120,121. The 2012 KDIGO AKI guidelines, and recommendations from a recent ADQI consensus report on renal recovery after AKI, both suggest that close follow up after AKI can improve outcomes^122,123. This follow up care should be multidisciplinary and coordinated between a patient’s primary care practitioners, surgical providers and nephrology consultants.

A standardized perioperative pathway for prevention of acute kidney injury after vascular surgery

Routine assessment of the risk for acute kidney injury in the perioperative period is an essential part of high-quality care for the vascular surgery patient. An optimal and cost-effective strategy, combining both risk stratification and prevention, matches the complexity of interventions to the risk profile of the individual patient. Clinical risk stratification is applied to all patients, to identify the smaller population of patients with high clinical risk that warrant further assessment with biological and imaging markers. Preventive interventions are used throughout the continuum of perioperative care, with the timing and target patient population determined by the risk profile and expected benefit from each intervention. Considering the high prevalence of AKI, the high morbidity burden it imposes on other organ systems, and the associated long-term adverse outcomes, all phases of prevention should be included. Primary prevention of new episodes of AKI, secondary prevention after AKI (the mitigation of further injury as well as facilitation of renal recovery) and tertiary prevention (the treatment of complications of AKI that affect distant organs) are all essential components of the perioperative care of the vascular surgery patient.

Standardized clinical assessment and management pathways (SCAMPs) are used to standardize care in the perioperative period. They synthesize current medical knowledge with best clinical judgment and local practice experience in order to decrease practice variability and improve patient care¹²⁴. Using KDIGO clinical guidelines as a framework, and utilizing our institutional perioperative registry outcome data^38,39,125, we have developed a perioperative AKI SCAMP for vascular surgery patients: a multi-layered approach combining risk assessment with a set of preventive strategies to prevent AKI and decrease its complications among vascular surgical patients (Figure 2). This process incorporates routine preoperative and immediate postoperative assessment of the patient’s susceptibility to new injury, the degree of any renal insult, and the resulting distress or damage sustained by that insult. Based upon the results of this analysis, interventions for primary and secondary prevention of AKI are initiated, followed by frequent reassessment of kidney stress for 48 hours after surgery. Development of such a clinical pathway requires the surgeons, intensivists and specialty consultants to define the pathway for a specific institution.

For all vascular surgical patients we use a step-wise approach starting with clinical risk stratification to identify those patients who would benefit from more aggressive evaluation. Clinical risk stratification includes assessment of renal susceptibility to injury, general health factors and those operative factors and clinical exposures that can cause renal injury. Renal susceptibility to injury incorporates estimated GFR and CKD stage if any, previous episodes of AKI, and determination of albuminuria. A formal determination of functional renal reserve with a kidney stress test¹²⁶ rarely is indicated for more precise risk stratification among patients without apparent CKD, but with considerable risk due to age or other comorbidities such as heart failure, hypertension, COPD, diabetes or liver disease. General health factors of importance include the overall comorbidity burden and assessment of frailty and nutritional status^127–130. This assessment is one part of our overall preoperative patient assessment, and informs our decision-making on preoperative optimization and which procedure to offer the patient if any. Operative factors include specific technical details and emergent or prolonged surgery. Perioperative exposures include any hypotension, hypoxia, blood transfusion and any history of nephrotoxic medications or intravenous contrast.

Once the patient is out of surgery, the preoperative assessment and the operative course determines further management. Those patients with no risk factors are managed with standard postoperative care. Patients with any positive risk factors are evaluated for kidney stress using the urinary biomarker TIMP-2•IGFBP7 and care is then stratified according to the result. The TIMP-2•IGFBP7 score is calculated as the product of the measured concentrations of the two biomarkers, TIMP-2 and IGFBP-7, and is recorded as a value between 0.04 to 10.0^76,79. A TIMP-2•IGFBP7 score of < 0.3 indicates a patient at low risk for AKI that can be managed without specific AKI attention. A score of 0.3 – 2.0 indicates a patient at high risk for AKI and management according to our AKI bundle. A score of > 2.0 indicates a patient at critical risk for AKI and management according to our AKI bundle.

Our AKI bundle uses checklist implementation of simple preventive strategies including monitoring and optimizing hemodynamic status by goal directed fluid management and blood pressure control, strict avoidance of nephrotoxic medications, strict avoidance of glucose variability and careful monitoring of drug levels to adjust dosing in accordance with the GFR. The goal of this phase is to prevent the progression of tubular stress towards functional decline whenever possible, and to avoid the negative consequences of fluid overload and drug toxicity in patients with established tubular stress and thus prevent further decline in renal function. The bundle is repeated every 12 hours until resolution of the tubular stress or AKI. For patients at critical high risk of AKI (TIMP-2•IGFBP7 > 2.0) our AKI bundle incorporates all of the above, and adds a clinical action pathway directed by our nephrology consult service focused on identification of the cause of AKI using specialized clinical, laboratory and imaging tools and consideration for early renal replacement therapy (RRT). Early RRT may be appropriate for patients with large levels of tubular stress and rapid functional decline, where impaired handling of fluids may endanger other organs. Our preliminary experience with SCAMP implementation and compliance has been excellent, and recent studies have confirmed our preliminary findings that risk-stratification-guided implementation of prevention bundles translates into better renal outcomes after surgery.^3,4

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