Abstract

Aims & Objectives: Hyperchloraemia and acute kidney injury (AKI) are common following cardiopulmonary bypass (CPB) in paediatric patients. It has not been established whether hyperchloraemia stems from chloride loading or defective chloride excretion. Our study sought to establish patterns of chloride and ammonia metabolism after CPB surgery. Methods: We examined 20 patients under two years, admitted to PICU following CBP surgery. Arterial blood gases, urine electrolytes, urinary strong ion difference, fluid and electrolyte administration, and fluid outputs were recorded pre CPB, on admission and at standardised intervals thereafter. AKI was defined using KDIGO criteria. Results: Urinary Cl (mmol/L;median,[IQR]) was 30[19–52] pre surgery, 15[15–65] on admission, 15[15-38], 20[15-67], 48[15-75] and 120[46-129] at 6,12,24, and 48hours. Serum chloride (mmol/L;median,[IQR]) was 105[98-107] pre surgery, 101[101–106] on admission, and 107[105-110], 109[106-110], 108[105-111] and 107[104-111] at 6,12,24 and 48hours. SIDurine increased from 49.8 to 122.7 at 6hours and dropped to 16 at 48hours. Median chloride administration was 67.7mmol/kg/day in first 24hours. Urinary Cl (mmol/L;median,[IQR]) was 30[19–52] pre surgery, 15[15–65] on admission, 15[15-38], 20[15-67], 48[15-75] and 120[46-129] at 6,12,24, and 48hours. Serum chloride (mmol/L;median,[IQR]) was 105[98-107] pre surgery, 101[101–106] on admission, and 107[105-110], 109[106-110], 108[105-111] and 107[104-111] at 6,12,24 and 48hours. SIDurine increased from 49.8 to 122.7 at 6hours and dropped to 16 at 48hours. Conclusions: Post CPB renal chloride excretion is impaired, despite chloride loading, and increased plasma chloride levels. The SIDUrine increase during the decrease in chloride excretion suggests renal ammonia metabolism is impaired following CPB. Our findings suggest NH4 is crucial in the development of renal impairment post CPB.

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