Neurodevelopmental delay is common in children who undergo surgery for Congenital Heart Disease (CHD) in infancy. Cardiac surgery associated acute kidney injury (CS-AKI) occurs frequently in the paediatric cardiac Intensive care unit (ICU). Cardiac surgery associated acute kidney injury (CS-AKI) is associated with worse neurodevelopmental scores and delay in cognitive, language, and motor domains in children with CHD. No known data exist regarding the association of CS-AKI and motor and language subscales. In this study, we explored the relationship between CS-AKI and receptive and expressive language, as well as gross and fine motor delay.

This was a single centre retrospective observational cohort study. Children who underwent surgery for CHD and developed recurrent CS-AKI in the first year of life who had follow-up neurodevelopmental testing using the Bayley Scale of Infant Development Version III were included. Neurodevelopmental delay subscales assessed included: receptive and expressive language, fine and motor skills.

The study cohort included 203 children. Recurrent CS-AKI was significantly associated with lower scores in receptive and expressive language, as well as fine and gross motor on unadjusted analyses. On adjusted analyses, recurrent CS-AKI was significantly associated with severe receptive language delay.

The independent association of recurrent CS-AKI with severe language delay in children who undergo surgery for CHD in infancy is novel. Our findings may contribute to the understanding of language impairment in this population. Further studies are required to better understand this relationship and any potentially modifiable factors.

Few data are available regarding the use of metolazone in infants in cardiac intensive care. Researchers need to carry out further evaluation to characterise the effects of this treatment in this population.

This is a descriptive, retrospective study carried out in patients less than a year old. These infants had received metolazone over a 2-year period in the paediatric cardiac intensive care unit at our institution. The primary goal was to measure the change in urine output from 24 hours before the start of metolazone therapy to 24 hours after. Patient demographic variables, laboratory data, and fluid-balance data were analysed.

The study identified 97 infants with a mean age of 0.32±0.25 years. Their mean weight was 4.9±1.5 kg, and 58% of the participants were male. An overall 63% of them had undergone cardiovascular surgery. The baseline estimated creatinine clearance was 93±37 ml/minute/1.73 m2. Initially, the participants had received a metolazone dose of 0.27±0.10 mg/kg/day, the maximum dose being 0.43 mg/kg/day. They had also received other diuretics during metolazone initiation, such as furosemide (87.6%), spironolactone (58.8%), acetazolamide (11.3%), bumetanide (7.2%), and ethacrynic acid (1%). The median change in urine output after metolazone was 0.9 ml/kg/hour (interquartile range 0.15–1.9). The study categorised a total of 66 patients (68.0%) as responders. Multivariable analysis identified acetazolamide use (p=0.002) and increased fluid input in the 24 hours after metolazone initiation (p<0.001) as being significant for increased urine output. Changes in urine output were not associated with the dose of metolazone (p>0.05).

Metolazone increased urine output in a select group of patients. Efficacy can be maximised by strategic selection of patients.

We evaluated the use of nesiritide in children with critical CHD, pulmonary congestion, and inadequate urine output despite undergoing conventional diuretic therapy.

We conducted a retrospective analysis of 11 patients with critical CHD, comprising 18 infusions, each of which occurred during separate hospitalisations. Haemodynamic parameters were assessed, and the stage of acute kidney injury was determined before and throughout the duration of therapy using a standardised definition of acute kidney injury – The Kidney Disease: Improving Global Outcomes criteria.

Children with critical CHD, pulmonary congestion, and inadequate urinary output despite undergoing diuretic therapy were included.

The use of nesiritide was associated with a significant decrease in the maximum and minimum heart rate values and with a trend towards a significant decrease in maximum systolic blood pressure and maximum and minimum central venous pressures. Urine output increased but was not significant. Serum creatinine levels decreased significantly during the course of therapy (−0.26 mg/dl [−0.50, 0.0], p=0.02), and the number of patients who experienced a decrease in the stage of acute kidney injury of 2 or more – where a change in the stage of acute kidney disease of 2 or more was possible, that is, baseline stage >1 – was highly significant (five of 12 patients, 42%, p<0.001).

Nesiritide had a favourable impact on haemodynamics, and its use was not associated with deterioration of renal function in patients with critical CHD.

Sequential nephron blockade using intravenous chlorothiazide is often used to enhance urine output in patients with inadequate response to loop diuretics. A few data exist to support this practice in critically ill infants.

We included 100 consecutive patients <1 year of age who were administered intravenous chlorothiazide while receiving furosemide therapy in the cardiac ICU in our study. The primary end point was change in urine output 24 hours after chlorothiazide administration, and patients were considered to be responders if an increase in urine output of 0.5 ml/kg/hour was documented. Data on demographic, clinical, fluid intake/output, and furosemide and chlorothiazide dosing were collected. Multivariable regression analyses were performed to determine variables significant for increase in urine output after chlorothiazide administration.

The study population was 48% male, with a mean weight of 4.9±1.8 kg, and 69% had undergone previous cardiovascular surgery. Intravenous chlorothiazide was initiated at 89 days (interquartile range 20–127 days) of life at a dose of 4.6±2.7 mg/kg/day (maximum 12 mg/kg/day). Baseline estimated creatinine clearance was 83±42 ml/minute/1.73 m2. Furosemide dose before chlorothiazide administration was 2.8±1.4 mg/kg/day and 3.3±1.5 mg/kg/day after administration. A total of 43% of patients were categorised as responders, and increase in furosemide dose was the only variable significant for increase in urine output on multivariable analysis (p<0.05). No graphical trends were noted for change in urine output and dose of chlorothiazide.

Sequential nephron blockade with intravenous chlorothiazide was not consistently associated with improved urine output in critically ill infants.