AKI, Acute kidney injury From Webb TN, Goldstein SL Congenital heart surgery and acute kidney injury Curr Opin Anaesthesiol 2017;30(1):105–112 Cardiac Surgery–Associated AKI and Outcomes This strong association between AKI after cardiac surgery in children and patient morbidity and mortality has been demonstrated repeatedly over the past decade Review of the largest studies, each comprising at least 400 surgeries (Table 78.5), reveals mortality rates ranging from 8.9% to 54% for patients who developed AKI versus 1.2% to 6% for patients who did not develop AKI (all P values < 0001) In addition, multiple studies demonstrate that increased fluid accumulation after surgery was associated with mortality, independent of serum creatinine based AKI status,11,17–19 and one showed that the association between AKI and outcomes was strengthened when serum creatinine concentration was corrected for the degree of fluid overload,17 suggesting that fluid accumulation may mask AKI severity by diluting the serum creatinine concentration; this is a phenomenon that has been described in critically ill adults.20 Most strikingly, the associations observed between AKI and/or fluid overload and mortality have been controlled for underlying heart disease and operative factors, and in some studies, the associated risk for mortality is higher with AKI development than single ventricular physiology.7,11 Both AKI development and excessive positive fluid accumulation have also been associated with prolonged mechanical ventilation/delayed extubation, increased need for inotropic support, and intensive care unit length of stay.11,21,22 Table 78.5 Outcome Comparisons for Patients With/Versus Acute Kidney Injury After Cardiac Surgery Study Author (Subjects) Blinder7 (n = 430) Mortality Rates for AKI OR (95% CI) for vs No AKI Mortality With AKI 11.6% vs 2.9% Stage 1 (1.3; 0.4–4.1)a Stage 2 (5.1; 1.7–15.2) Stage 3 (9.5; 2.5–30.7) Chiravuri13 (n = 54.4% vs 6% AKI-RI (6.7; 4.1– Ventilation Time (Median [IQR]) for AKI vs No AKI 5 [3–7] vs 3 [2–5] days NA 494) Toth12 (n = 1510) 10.8)b AKI-F (36.9; 20–67.9) 8.9% vs 1.2% NA 49 [26–112] vs 33 [15–76] hours aAcute Kidney Injury Network criteria used for AKI b Pediatric modified RIFLE (risk, injury, failure, loss, end-stage kidney disease)3 criteria used for AKI These criteria used decreases in estimated glomerular filtration rate (eGFR) to stratify AKI severity Risk: 25% decrease; injury: 50% decrease; failure: 75% decrease or an eGFR 3 months AKI, Acute kidney injury; CI, confidence interval; IQR, interquartile range; NA, not available; OR, odds ratio Interventions Given that nephrotoxic medication avoidance and fluid management represent the two modifiable risk factors for patients with, or at risk for AKI, systematic risk assessment to guide interventions is paramount Some recommend avoidance of greater than 10% fluid (in liters) accumulation based on body weight (in kilograms) using the following formula23: The 10% fluid overload threshold is based on numerous studies of critically ill children with AKI who received continuous renal replacement therapy (CRRT), which observed an association between >10% and 20% fluid overload at CRRT initiation and patient mortality, independent of patient severity of illness.24,25 Three recent studies in children after cardiac surgery show that avoidance of 10% fluid overload was associated with increased survival and/or decreased days of mechanical ventilation.11,21,22 The strategies to limit fluid overload in the setting of AKI are fluid restriction, administration of diuretics, and initiation of renal replacement therapy.26 While modified ultrafiltration during the CPB procedure is effective at minimizing fluid overload upon arrival to the cardiac intensive care unit, fluid restriction likely has little utility in the early postoperative period as patients develop capillary leak from the system inflammation caused by CPB and the surgery itself Furthermore, fluid restriction limits the ability to provide adequate nutrition for anabolism in patients who are highly catabolic and at risk for AKI for up to 72 hours due to the low cardiac output state associated with long bypass durations Therefore, fluid restriction alone, without escalation to diuretic administration or the initiation of renal replacement therapy, should only be considered in older pediatric patients (>1 year of age) with adequate nutritional reserves Diuretic, especially loop diuretic, administration is nearly ubiquitous and a “backbone” for patients with or at risk for AKI in the critical care setting with a goal of preventing or reversing fluid overload.27,28 Loop diuretics exhibit their effect by blocking sodium, potassium, and chloride resorption in the thick ascending limb of the loop of Henle Increased urinary excretion of sodium, potassium, and fluid are beneficial in the patient with AKI, and when effective, can allow for provision of adequate nutrition-associated volumes without the development of fluid overload Although some debate exists regarding the superiority of different loop diuretic medications (furosemide vs ethacrynic acid29), maximum dose and administration (intermittent bolus vs continuous infusion), a detailed discussion is beyond the scope of this chapter However, it is critical for the clinician to establish daily goals of diuretic therapy in terms of net fluid balance given the optimal fluid, nutrition, and blood product needs of the patient, and to be firm in their assessment of diuretic resistance Escalation of diuretic therapy to achieve these goals, including the addition of a thiazide diuretic30 should be made in a systematic and rational fashion, with a clear sense that diuretic resistance should not be defined by a particular urine flow rate in mL/kg per hour, but with an objective accounting of whether or not diuretics achieve the needed fluid balance In addition, potent and increased diuretic administration is not devoid of the consequences of ototoxicity, severe electrolyte derangement, including metabolic alkalosis,29 hyponatremia, hypokalemia, and worsening of functional AKI leading to decreased renal perfusion.31 Recently, the concept of the furosemide stress test (FST) has codified an objective metric for diuretic resistance in critically ill adults.32,33 The FST uses a standardized dose of intravenous furosemide (1 mg/kg in naive patients, 1.5 mg/kg in patients with chronic kidney disease [CKD] or who have received furosemide) and assesses urine output (UOP) in the 2 hours after administration Patients who did not have more than 200 mL/h of UOP progressed to worsening ... 8.9% vs 1.2% NA 49 [26–112] vs 33 [15–76] hours aAcute Kidney Injury Network criteria used for AKI b Pediatric modified RIFLE (risk, injury, failure, loss, end-stage kidney disease)3 criteria used for... administration or the initiation of renal replacement therapy, should only be considered in older pediatric patients (>1 year of age) with adequate nutritional reserves Diuretic, especially loop diuretic, administration is nearly ubiquitous and a