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Identifying Risk for Acute Kidney Injury in Infants and Children Following Cardiac Arrest.

ABSTRACT: OBJECTIVES:Our goal was to identify risk factors for acute kidney injury in children surviving cardiac arrest. DESIGN:Retrospective analysis of a public access dataset. SETTING:Fifteen children's hospitals associated with the Pediatric Emergency Care Applied Research Network. PATIENTS:Two hundred ninety-six subjects between 1 day and 18 years old who experienced in-hospital or out-of-hospital cardiac arrest between July 1, 2003, and December 31, 2004. INTERVENTIONS:None. MEASUREMENTS AND MAIN RESULTS:Our primary outcome was development of acute kidney injury as defined by the Acute Kidney Injury Network criteria. An ordinal probit model was developed. We found six critical explanatory variables, including total number of epinephrine doses, postcardiac arrest blood pressure, arrest location, presence of a chronic lung condition, pH, and presence of an abnormal baseline creatinine. Total number of epinephrine doses received as well as rate of epinephrine dosing impacted acute kidney injury risk and severity of acute kidney injury. CONCLUSIONS:This study is the first to identify risk factors for acute kidney injury in children after cardiac arrest. Our findings regarding the impact of epinephrine dosing are of particular interest and suggest potential for epinephrine toxicity with regard to acute kidney injury. The ability to identify and potentially modify risk factors for acute kidney injury after cardiac arrest may lead to improved morbidity and mortality in this population.

SUBMITTER: Neumayr TM

PROVIDER: S-EPMC5628129 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature

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Identifying Risk for Acute Kidney Injury in Infants and Children Following Cardiac Arrest.

Neumayr Tara M TM Gill Jeff J Fitzgerald Julie C JC Gazit Avihu Z AZ Pineda Jose A JA Berg Robert A RA Dean J Michael JM Moler Frank W FW Doctor Allan A

Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies 20171001 10

<h4>Objectives</h4>Our goal was to identify risk factors for acute kidney injury in children surviving cardiac arrest.<h4>Design</h4>Retrospective analysis of a public access dataset.<h4>Setting</h4>Fifteen children's hospitals associated with the Pediatric Emergency Care Applied Research Network.<h4>Patients</h4>Two hundred ninety-six subjects between 1 day and 18 years old who experienced in-hospital or out-of-hospital cardiac arrest between July 1, 2003, and December 31, 2004.<h4>Intervention ...[more]

PMID: 28737594

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Project description:Acute kidney injury (AKI) after pediatric cardiac surgery is associated with high morbidity and mortality. Modifiable risk factors for postoperative AKI including perioperative anesthesia-related parameters were assessed. The authors conducted a single-center, retrospective cohort study of 220 patients (aged 10 days to 19 years) who underwent congenital cardiac surgery between January and December 2012. The incidence of AKI within 7 days postoperatively was determined using the Kidney Disease: Improving Global Outcomes (KDIGO) criteria. Ninety-two patients (41.8%) developed AKI and 18 (8.2%) required renal replacement therapy within the first postoperative week. Among patients who developed AKI, 57 patients (25.9%) were KDIGO stage 1, 27 patients (12.3%) were KDIGO stage 2, and eight patients (3.6%) were KDIGO stage 3. RACHS-1 (Risk-Adjusted classification for Congenital Heart Surgery) category, perioperative transfusion and fluid administration as well as fluid overload were compared between patients with and without AKI. Multivariable logistic regression analyses determined the risk factors for AKI. AKI was associated with longer hospital stay or ICU stay, and frequent sternal wound infections. Younger age (<12 months) [odds ratio (OR), 4.01; 95% confidence interval (CI), 1.77-9.06], longer cardiopulmonary bypass (CPB) time (OR, 2.45; 95% CI, 1.24-4.84), and low preoperative hemoglobin (OR, 2.40; 95% CI, 1.07-5.40) were independent risk factors for AKI. Fluid overload was not a significant predictor for AKI. When a variable of hemoglobin concentration increase (>3 g/dl) from preoperative level on POD1 was entered into the multivariable analysis, it was independently associated with postoperative AKI (OR, 6.51; 95% CI, 2.23-19.03 compared with no increase). This association was significant after adjustment with patient demographics, medication history and RACHS-1 category (hemoglobin increase >3g/dl vs. no increase: adjusted OR, 6.94; 95% CI, 2.33-20.69), regardless of different age groups and cyanotic or non-cyanotic heart disease. Prospective trials are required to evaluate whether correction of preoperative anemia and prevention of hemoconcentration may ameliorate postoperative AKI in patients who underwent congenital cardiac surgery.

Project description:Fluid resuscitation in the critically ill often results in a positive fluid balance, potentially diluting the serum creatinine concentration and delaying diagnosis of acute kidney injury (AKI).Dilution during AKI was quantified by combining creatinine and volume kinetics to account for fluid type, and rates of fluid infusion and urine output. The model was refined using simulated patients receiving crystalloids or colloids under four glomerular filtration rate (GFR) change scenarios and then applied to a cohort of critically ill patients following cardiac arrest.The creatinine concentration decreased during six hours of fluid infusion at 1 litre-per-hour in simulated patients, irrespective of fluid type or extent of change in GFR (from 0% to 67% reduction). This delayed diagnosis of AKI by 2 to 9 hours. Crystalloids reduced creatinine concentration by 11 to 19% whereas colloids reduced concentration by 36 to 43%. The greatest reduction was at the end of the infusion period. Fluid dilution alone could not explain the rapid reduction of plasma creatinine concentration observed in 39 of 49 patients after cardiac arrest. Additional loss of creatinine production could account for those changes. AKI was suggested in six patients demonstrating little change in creatinine, since a 52 ± 13% reduction in GFR was required after accounting for fluid dilution and reduced creatinine production. Increased injury biomarkers within a few hours of cardiac arrest, including urinary cystatin C and plasma and urinary Neutrophil-Gelatinase-Associated-Lipocalin (biomarker-positive, creatinine-negative patients) also indicated AKI in these patients.Creatinine and volume kinetics combined to quantify GFR loss, even in the absence of an increase in creatinine. The model improved disease severity estimation, and demonstrated that diagnostic delays due to dilution are minimally affected by fluid type. Creatinine sampling should be delayed at least one hour following a large fluid bolus to avoid dilution. Unchanged plasma creatinine post cardiac arrest signifies renal injury and loss of function.Australian and New Zealand Clinical Trials Registry ACTRN12610001012066.

Project description:ImportanceMany children with return of spontaneous circulation (ROSC) following cardiac arrest (CA) experience acute kidney injury (AKI). The impact of therapeutic hypothermia on the epidemiology of post-CA AKI in children has not been fully investigated.ObjectiveThe study aims were to: 1) describe the prevalence of severe AKI in comatose children following out-of-hospital CA (OHCA), 2) identify risk factors for severe AKI, 3) evaluate the impact of therapeutic hypothermia on the prevalence of severe AKI, and 4) evaluate the association of severe AKI with survival and functional outcomes.DesignA post hoc secondary analysis of data from the Therapeutic Hypothermia after Pediatric Cardiac Arrest Out-of-Hospital (THAPCA-OH) trial.SettingThirty-six pediatric intensive care units in the United States and Canada.ParticipantsOf 282 eligible subjects with an initial creatinine obtained within 24 h of randomization, 148 were randomized to therapeutic hypothermia and 134 were randomized to therapeutic normothermia.Main outcomes and measuresPrimary outcome was prevalence of severe AKI, as defined by stage 2 and 3 Kidney Disease Improving Global Outcomes (KDIGO) consensus definition; secondary outcome was survival with a favorable neurobehavioral outcome. For this study, risk factors and outcomes were compared between those with/without severe AKI.ResultsOf the 282 subjects enrolled, 180 (64%) developed AKI of which 117 (41% of all enrolled) developed severe AKI. Multivariable modeling found younger age, longer duration of chest compressions, higher lactate level at time of temperature intervention and higher number of vasoactive agents through day 1 of intervention associated with severe AKI. There was no difference in severe AKI between therapeutic hypothermia (39.9%) and therapeutic normothermia (43.3%) groups (p = 0.629). Survival was lower in those with severe AKI at 28 days (21% vs no severe AKI 49%, p < 0.001) and 12 months (21% vs no severe AKI 42%, p < 0.001). One year survival with favorable functional outcome was lower in those with severe AKI.Conclusions and relevanceSevere AKI occurs frequently in children with ROSC after OHCA, especially in younger children and those with higher initial lactates and hemodynamic support. Severe AKI was associated with worse survival and functional outcome. Therapeutic hypothermia did not reduce the incidence of severe AKI.

Dataset Information

Identifying Risk for Acute Kidney Injury in Infants and Children Following Cardiac Arrest.

Publications

Identifying Risk for Acute Kidney Injury in Infants and Children Following Cardiac Arrest.

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