RESUMEN
The aim of this study was to describe renal chloride metabolism following cardiopulmonary bypass (CPB) surgery in pediatric patients. A prospective observational trial in a tertiary pediatric intensive care unit (PICU) with 20 recruited patients younger than 2 years following CPB surgery was conducted. Urinary electrolytes, plasma urea, electrolytes, creatinine, and arterial blood gases were collected preoperatively, on admission to PICU and at standardized intervals thereafter. The urinary and plasma strong ion differences (SID) were calculated from these results at each time point. Fluid input and output and electrolyte and drug administration were also recorded. Median chloride administration was 67.7 mmol/kg over the first 24 hours. Urinary chloride (mmol/L; median interquartile range [IQR]) was 30 (19, 52) prior to surgery, 15 (15, 65) on admission, and remained below baseline until 24 hours. Plasma chloride (mmol/L; median [IQR]) was 105 (98, 107) prior to surgery and 101 (101, 106) on admission to PICU. It then increased from baseline, but remained within normal limits, for the remainder of the study. The urinary SID increased from 49.8 (19.1, 87.2) preoperatively to a maximum of 122.7 (92.5, 151.8) at 6 hours, and remained elevated until 48 hours. Plasma and urinary chloride concentrations were not associated with the development of acute kidney injury. Urinary chloride excretion is impaired after CPB. The urinary SID increase associated with the decrease in chloride excretion suggests impaired production and/or excretion of ammonium by the nephron following CPB, with gradual recovery postoperatively.
RESUMEN
Acute kidney injury (AKI) is common in intensive care patients. While creatinine definitions for AKI have been validated, oliguria criteria are less well evaluated in children. Our study compared the validity and agreement of creatinine and oliguria criteria for diagnosing AKI in a large mixed medical, surgical and cardiac paediatric intensive care unit (PICU), and assessed the significance of their independent and combined effects on predicted mortality relative to paediatric index of mortality (PIM risk of death) on admission. Creatinine measurements during PICU admissions in 2005 and 2015 were obtained from the electronic medical record. Urine output was reviewed to identify periods of oliguria of more than eight hours. We used the PIM3 model for predicted risk of death. AKI based on creatinine rise occurred in 23.6% of the total 2203 admissions (10.0%, 8.2% and 5.6% for mild, moderate and severe categories, respectively). Oliguria occurred in 11.4% (8.4%, 1.8% and 1.2% for mild, moderate and severe categories, respectively) and overlapped only partially with creatinine criteria. Mortality relative to predicted mortality increased with increasing creatinine and oliguria severity, but was lower than predicted where oliguria occurred without creatinine rise. AKI by creatinine criteria and/or oliguria are common in the PICU, but criteria overlap only partially. Increasing severity of creatinine rise and oliguria confers increasing risk-adjusted mortality, especially for admissions with low PIM3 risk of death. The mortality of patients with AKI defined by oliguria alone is low. Defining AKI by oliguria alone has less clinical utility and may not represent true AKI.
