Cardiac and Vascular Surgery–Associated Acute Kidney Injury: The 20th International Consensus Conference of the ADQI (Acute Disease Quality Initiative) Group

Figures

• 

  Figure 1. Major pathophysiological mechanisms for the development of cardiac and vascular surgery–associated acute kidney injury (CVS‐AKI). Many common factors contribute to the development of CVS‐AKI. Hemodynamic perturbations such as exposure to cardiopulmonary bypass (CPB), cross‐clamping of the aorta, high doses of exogenous vasopressors, and blood‐product transfusion all increase the risk of AKI. Similarly, the mechanical factors outlined may be associated with renal perfusion injury following episodes of ischemia, resulting in increased oxidative stress and associated inflammation as well as embolic disease including cholesterol emboli, all of which increase the pathological burden on the kidney. Other mechanisms such as neurohormonal activation are relevant, as is the generation of free hemoglobin and the liberation of free iron perioperatively, all potentiating AKI. Associated tissue damage is reflected in a systemic inflammatory response, and all these factors contribute to a significant inflammatory response. Immune activation, the generation of reactive oxygen species, and upregulation of proinflammatory transcription factors all play roles.

• 

  Figure 2. Risk assessment for acute kidney injury (AKI) following cardiac and vascular surgery (CVS). This figure provides a framework for the time course of risk assessment for AKI following CVS. Risk assessment should be a continual process that is repeatedly performed in the pre‐, peri‐, and early postoperative time course, and it should incorporate clinical factors and biomarkers if available. Patients deemed to be at high risk of AKI may benefit from the implementation of kidney‐focused care to improve patient outcomes. CHF indicates congestive heart failure; COPD, chronic obstructive pulmonary disease; CPB, cardiopulmonary bypass; EF, ejection fraction; IABP, intra‐aortic balloon pump; IGFBP7, insulin‐like growth factor binding protein 7; KDIGO, Kidney Disease Initiative Global Outcome; NGAL, neutrophil gelatinase–associated lipocalin; PVD, peripheral vascular disease; TIMP2, tissue inhibitor of metalloproteinases 2.

• 

  Figure 3. Classification of acute kidney injury (AKI) by changes in function and/or damage. Currently the diagnosis of AKI is made through changes in serum creatinine (sCr) or urine output (UO)—functional biomarkers. The 10th Acute Disease Quality Initiative consensus meeting delineated criteria for defining AKI in terms of changes in biomarkers of renal function (sCr/UO) and biomarkers of kidney damage. This paradigm allows for the combination of injury biomarkers with sCr and UO and has been useful in the discrimination of patients with AKI. The terms prerenal and intrinsic AKI are sometimes used to denote these relationships. The upper right box may be termed subclinical. The upper left box is yellow because we may still miss changes in function and damage in some patients; a role for additional diagnostics and/or stress tests is acknowledged.

• 

  Figure 4. A, Cardiorespiratory‐specific diagnostic approach. This diagnostic approach may be applied to a patient who has a cardiorespiratory cause of acute kidney injury (AKI). The level of intervention is governed by the degree and chronicity of cardiorespiratory dysfunction. Source: ADQI (Acute Disease Quality Initiative) 20th consensus meeting (http://www.adqi.org). Used with permission. B, Kidney‐specific diagnostic approach. This diagnostic approach may be applied to a patient who has a renal‐specific cause of AKI. The level of intervention is governed by the degree and duration of renal dysfunction. This is particularly relevant in the post–intensive care unit phase, in which a patient with persistent AKI (>2 or 3 days) or acute kidney disease should be monitored and followed up. BNP indicates brain natriuretic peptide; CI, cardiac index; CKD, chronic kidney disease; CO, cardiac output; CVP, central venous pressure; CXR, chest x‐ray; EVLW, extravascular lung water; HR, heart rate; MAP, mean arterial pressure; RR, respiratory rate; Scvo 2, central venous oxygen saturation; Spo 2, peripheral oxygen saturation; SVV, stroke volume variation; US, ultrasound.

• 

  Figure 5. Fluid management strategies in critical illness: the place of mechanical fluid removal. Once life‐threatening hypovolemia has been corrected (savage resuscitation), fluid overload (FO) needs to be avoided. Early mechanical fluid removal should be considered if specific indications exist. Note, the existence of an extracorporeal circuit for extracorporeal membrane oxygenation (ECMO) greatly reduces any added risk for renal replacement therapy (RRT), assuming this circuit is used rather than a separate line for RRT. However, some patients will respond well to diuretics, and thus an ECMO circuit in place is only a relative indication for early RRT initiation and only when fluid or solute management dictates. During therapy, hemodynamic and intravascular volume status should be monitored and fluid removal rate and fluid balance targets reassessed regularly, aiming for clinical stability and tolerance of fluid removal. Within this pathway, RRT should be considered at any point if additional solute clearance is necessary. FB indicates fluid balance; UF, ultrafiltration.