Objective: To describe postoperative fluid overload patterns and correlate degree of fluid overload with intensive care morbidity and mortality in infants undergoing congenital heart surgery.
Design: Prospective, observational study. Fluid overload (%) was calculated by two methods: 1) (Total fluid in – Total fluid out)/(Preoperative weight) × 100; and 2) (Current weight – Preoperative weight)/(Preoperative weight) × 100. Composite poor outcome included: need for renal replacement therapy, upper quartile time to extubation or intensive care length of stay (> 6.5 and 9.9 days, respectively), or death ≤ 30 days after surgery.
Setting: University hospital pediatric cardiac ICU.
Patients: Forty-nine infants < 6 months of age undergoing congenital heart surgery with cardiopulmonary bypass during the period of July 2009 to July 2010.
Measurements and Main Results: Patients had a median age of 53 days (21 neonates) and mean weight of 4.5±1.3kg. Forty-two patients (86%) developed acute kidney injury by meeting at least Acute Kidney Injury Network and Kidney Disease Improving Global Outcomes stage 1 criteria (serum creatinine rise of 50% or ≥ 0.3mg/dL). The patients with adverse outcomes (n = 17, 35%) were younger (7 [5 – 10] vs. 98 [33 – 150] days, p = 0.001), had lower preoperative weight (3.7±0.7 vs. 4.9±1.4kg, p = 0.0002), higher postoperative mean peak serum creatinine (SCr) (0.9±0.3 vs. 0.6±0.3mg/dL, p = 0.005), and higher mean maximum fluid overload by both method 1 (12% ± 10% vs. 6% ± 4%, p = 0.03) and method 2 (24% ± 15% vs. 14% ± 8%, p = 0.02). Predictors of a poor outcome from multivariate analyses were cardiopulmonary bypass time, use of circulatory arrest, and increased vasoactive medication requirements postoperatively.
Conclusions: Early postoperative fluid overload is associated with suboptimal outcomes in infants following cardiac surgery. Because the majority of patients developed kidney injury without needing renal replacement therapy, fluid overload may be an important risk factor for adverse outcomes with all degrees of acute kidney injury.
1 Department of Pediatrics and Communicable Diseases, Division of Pediatric Cardiology, University of Michigan, Ann Arbor, MI.
2 Department of Pediatrics and Communicable Diseases, Division of Nephrology, University of Michigan, Ann Arbor, MI.
This work was supported by funds from the Division of Pediatric Cardiology and by a Child Health Research Center Career Development Award (National Institutes of Health, K12 HD 028820) to Dr. Blatt.
Dr. Blatt receives funding from the National Institutes of Health. The remaining authors have not disclosed any potential conflicts of interest.
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