Catherine E Ross1, Lisa A Asaro2, David Wypij3, Conor C Holland4, Michael W Donnino5, Monica E Kleinman6. 1. Division of Medicine Critical Care, Department of Medicine, Boston Children's Hospital and Harvard Medical School, 333 Longwood Avenue, Boston, MA, 02115, USA. Electronic address: Catherine.Ross@childrens.harvard.edu. 2. Department of Cardiology, Boston Children's Hospital and Harvard Medical School, 333 Longwood Avenue, Boston, MA, 02115, USA. 3. Department of Cardiology, Boston Children's Hospital and Harvard Medical School, 333 Longwood Avenue, Boston, MA, 02115, USA; Department of Biostatistics, Harvard T.H. Chan School of Public Health, 655 Huntington Avenue, Boston, MA, 02115, USA. 4. Etiometry Platform™, Etiometry Inc, 119 Braintree Street, Suite 210, Allston, MA, 02134, USA. 5. Department of Emergency Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 359 Brookline Avenue, Boston, MA, 02115, USA; Division of Pulmonary and Critical Care Medicine, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, 359 Brookline Avenue, Boston, MA, 02115, USA. 6. Division of Critical Care Medicine, Department of Anesthesiology, Perioperative and Pain Medicine, Boston Children's Hospital and Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA.
Abstract
AIM: To quantify the physiologic effects of pre-arrest bolus dilute epinephrine in the pediatric intensive care unit. METHODS: Patients <18 years old and ≥37 weeks gestation who received an intravenous bolus of dilute epinephrine (10 mcg/mL) in the pediatric intensive care units at our institution from January 2011 to March 2017 were retrospectively identified. Patients were excluded if doses exceeded 20 mcg/kg, or under the following circumstances: orders limiting resuscitation, extracorporeal membrane oxygenation, active chest compressions, simultaneous administration of other blood pressure-altering interventions or documented normotension prior to epinephrine. The primary outcome was change in systolic blood pressure within 5 min of epinephrine. Patients were categorized as non-responders if the change in systolic blood pressure was ≤10 mmHg. RESULTS: One hundred forty-four patients were analyzed. The median index dose was 0.7 mcg/kg (IQR, 0.3-2.0), and the mean increase in systolic blood pressure was 31 mmHg (95% CI, 25-36; P < 0.001). Thirty-nine (27%) patients were classified as non-responders. Compared to responders, non-responders had higher rates of cardiac arrest or extracorporeal membrane oxygenation within 6 h (26% vs 10%; relative risk, 2.69; 95% CI, 1.21-5.97; P = 0.03), and had higher in-hospital mortality (51% vs 21%; relative risk, 2.45; 95% CI, 1.51-3.96; P < 0.001). CONCLUSIONS: In the majority of pre-arrest pediatric patients, bolus dilute epinephrine resulted in an increase in systolic blood pressure, and lack of blood pressure response was associated with poor outcomes. Optimal dosing of dilute epinephrine remains unclear.
AIM: To quantify the physiologic effects of pre-arrest bolus dilute epinephrine in the pediatric intensive care unit. METHODS:Patients <18 years old and ≥37 weeks gestation who received an intravenous bolus of dilute epinephrine (10 mcg/mL) in the pediatric intensive care units at our institution from January 2011 to March 2017 were retrospectively identified. Patients were excluded if doses exceeded 20 mcg/kg, or under the following circumstances: orders limiting resuscitation, extracorporeal membrane oxygenation, active chest compressions, simultaneous administration of other blood pressure-altering interventions or documented normotension prior to epinephrine. The primary outcome was change in systolic blood pressure within 5 min of epinephrine. Patients were categorized as non-responders if the change in systolic blood pressure was ≤10 mmHg. RESULTS: One hundred forty-four patients were analyzed. The median index dose was 0.7 mcg/kg (IQR, 0.3-2.0), and the mean increase in systolic blood pressure was 31 mmHg (95% CI, 25-36; P < 0.001). Thirty-nine (27%) patients were classified as non-responders. Compared to responders, non-responders had higher rates of cardiac arrest or extracorporeal membrane oxygenation within 6 h (26% vs 10%; relative risk, 2.69; 95% CI, 1.21-5.97; P = 0.03), and had higher in-hospital mortality (51% vs 21%; relative risk, 2.45; 95% CI, 1.51-3.96; P < 0.001). CONCLUSIONS: In the majority of pre-arrest pediatric patients, bolus dilute epinephrine resulted in an increase in systolic blood pressure, and lack of blood pressure response was associated with poor outcomes. Optimal dosing of dilute epinephrine remains unclear.