Cardiopulmonary Bypass Is Associated With Hemolysis And Acute Kidney Injury In Infants And Children

Mamikonian, Lara S.; Mamo, Lisa B.; Smith, Patricia B.; Koo, Jeannie; Bartle, Bronwyn H.; Hiller, Christine E.; Miller, Coleen E; Turi, Jennifer L.

doi:10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1834

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“…Hyperchloremia is an established phenomenon following cardiopulmonary bypass (CPB) in both children and adults and has been observed both in the presence and absence of AKI. 3 5 6 9 11 It is unclear whether hyperchloremia is a result of increased chloride loading, impaired renal chloride excretion, or a combination of these processes. It is also unclear whether hyperchloremia is a primary consequence of AKI, or if it contributes to its development.…”

Section: Introductionmentioning

confidence: 99%

Urinary Chloride Excretion Postcardiopulmonary Bypass in Pediatric Patients—A Pilot Study

Fincher

Gibbons

Johnson

et al. 2021

J Pediatr Intensive Care

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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.

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