Craig Futterman1, Joshua W Salvin2, Michael McManus3, Adam W Lowry4, Dimitar Baronov5, Melvin C Almodovar6, Jose A Pineda7, Vinay M Nadkarni8, Peter C Laussen9, Avihu Z Gazit10. 1. Division of Cardiac Critical Care Medicine, George Washington University, Children's National Medical Center, 111 Michigan Avenue, NW Washington DC, 200010 United States. Electronic address: cfutterm@cnmc.org. 2. Department of Cardiology, Division of Cardiovascular Critical Cares Medicine, Harvard Medical School, Boston Children's Hospital, 300 Longwood Avenue, Boston MA 02115 United States. Electronic address: joshua.salvin@cardio.chboston.org. 3. Etiometry, Inc 280 Summer St fl 4, Boston, MA 02210, United States. Electronic address: mmcmanus@etiometry.com. 4. Department of Cardiovascular Services, Division of Cardiac Critical Care, University of Central Florida, Nemours Cardiac Center, Nemours Children's Hospital, 13535 Nemours Parkway, Orlando, FL 32827, United States. Electronic address: adam.lowry@nemours.org. 5. Etiometry, Inc 280 Summer St fl 4, Boston, MA 02210, United States. Electronic address: baronov@etiometry.com. 6. Department of Pediatrics, Divisions of Cardiology and Critical Care Medicine, University of Miami Miller School of Medicine, Holtz Children's Hospital/Jackson Health System, 1611 NW 12th Avenue, North Wing, Suite 109 Miami, FL 33136 United States. Electronic address: melalmodovar@med.miami.edu. 7. Department of Pediatrics and Neurology, Washington University School of Medicine, Saint Louis Children's Hospital, 1 Children's Place, St. Louis, MO 63110, United States. Electronic address: pineda_j@wustl.edu. 8. Department of Anesthesiology, Critical Care, and Pediatrics, The Children's Hospital of Philadelphia, University of Pennsylvania Perelman School of Medicine, 3401 Civic Center Boulevard, Philadelphia, PA, 19104 United States. Electronic address: Nadkarni@email.chop.edu. 9. Department of Critical Care Medicine, The Hospital for Sick Children, 555 University Ave, Toronto, Ontario, M5G 1X8, Canada. Electronic address: Peter.laussen@sickkids.ca. 10. Department of Pediatrics, Divisions of Critical Care Medicine and Cardiology, Washington University School of Medicine, Saint Louis Children's Hospital, 1 Children's Place St. Louis MO 63110, United States. Electronic address: Gazit_a@wustl.edu.
Abstract
AIM: To evaluate the Inadequate oxygen delivery (IDO2) index dose as a predictor of cardiac arrest (CA) in neonates following congenital heart surgery. METHODS: Retrospective cohort study in 3 US pediatric cardiac intensive units (1/2011- 8/2016). Calculated IDO2 index values were blinded to bedside clinicians and generated from data collected up to 30 days postoperatively, or until death or ECMO initiation. Control event data was collected from patients who did not experience CA or require ECMO. IDO2 dose was computed over a 120-min window up to 30 min prior to the CA and control events. A multivariate logistic regression prediction model including the IDO2 dose and presence or absence of a single ventricle (SV) was used. Model performance metrics were the odds ratio for each regression coefficient and receiver operating characteristic area under the curve (ROC AUC). RESULTS: Of 897 patients monitored during the study period, 601 met inclusion criteria: 29 patients had CA (33 events) and 572 patients were used for control events. Seventeen (59%) CA and 125 (26%) control events occurred in SV patients. Median age/weight at surgery and level of monitoring were similar in both groups. Median postoperative event time was 0.73 days [0.05-22.39] in CA patients and 0.82 days [0.08 25.11] in control patients. Odds ratio of the IDO2 dose coefficient was 1.008 (95% CI: 1.006-1.012, p = 0.0445), and 2.952 (95% CI: 2.952-3.258, p = 0.0079) in SV. The ROC AUC using both coefficients was 0.74 (95% CI: 0.73-0.75). These associations of IDO2 dose with CA risk remained robust, even when censored periods prior to arrest were 10 and 20 min. CONCLUSION: In neonates post-CPB surgery, higher IDO2 index dose over a 120-min monitoring period is associated with increased risk of cardiac arrest, even when censoring data 10, 20 or 30 min prior to the CA event.
AIM: To evaluate the Inadequate oxygen delivery (IDO2) index dose as a predictor of cardiac arrest (CA) in neonates following congenital heart surgery. METHODS: Retrospective cohort study in 3 US pediatric cardiac intensive units (1/2011- 8/2016). Calculated IDO2 index values were blinded to bedside clinicians and generated from data collected up to 30 days postoperatively, or until death or ECMO initiation. Control event data was collected from patients who did not experience CA or require ECMO. IDO2 dose was computed over a 120-min window up to 30 min prior to the CA and control events. A multivariate logistic regression prediction model including the IDO2 dose and presence or absence of a single ventricle (SV) was used. Model performance metrics were the odds ratio for each regression coefficient and receiver operating characteristic area under the curve (ROC AUC). RESULTS: Of 897 patients monitored during the study period, 601 met inclusion criteria: 29 patients had CA (33 events) and 572 patients were used for control events. Seventeen (59%) CA and 125 (26%) control events occurred in SV patients. Median age/weight at surgery and level of monitoring were similar in both groups. Median postoperative event time was 0.73 days [0.05-22.39] in CA patients and 0.82 days [0.08 25.11] in control patients. Odds ratio of the IDO2 dose coefficient was 1.008 (95% CI: 1.006-1.012, p = 0.0445), and 2.952 (95% CI: 2.952-3.258, p = 0.0079) in SV. The ROC AUC using both coefficients was 0.74 (95% CI: 0.73-0.75). These associations of IDO2 dose with CA risk remained robust, even when censored periods prior to arrest were 10 and 20 min. CONCLUSION: In neonates post-CPB surgery, higher IDO2 index dose over a 120-min monitoring period is associated with increased risk of cardiac arrest, even when censoring data 10, 20 or 30 min prior to the CA event.
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