Contents lists available at ScienceDirect Progress in Pediatric Cardiology journal homepage: www.elsevier.com/locate/ppedcard Pediatric ECMO after drowning: Neuroprotective strategies Jennifer S. Nelson a, ⁎ , Neha Longani b , Laufey Y. Sigurdardottir b , Timothy M. Maul a , Peter D. Wearden a , Constantinos Chrysostomou a a Department of Cardiovascular Services, Nemours Children's Hospital, 13535 Nemours Parkway, Orlando, FL, USA b Department of Pediatrics, Nemours Children's Hospital, 13535 Nemours Parkway, Orlando, FL, USA ARTICLE INFO Keywords: ECMO Hypothermia Neuroprotection Dexmedetomidine Erythropoietin Drowning ABSTRACT There are no established neuroprotective guidelines during pediatric extracorporeal membrane oxygenation (ECMO) after cardiac arrest. We report a case of unknown duration, out-of-hospital cardiac arrest after drowning in a toddler. The patient experienced severe cardiopulmonary failure shortly after return of spontaneous cir- culation and required veno-arterial ECMO. Clinical outcome was excellent. This report outlines a neuropro- tective strategy using high-dose erythropoietin, dexmedetomidine, and therapeutic hypothermia that was im- plemented during ECMO. Risk factors related to pediatric drowning with cardiac arrest are also discussed. 1. Introduction Neuroprotection including therapeutic hypothermia is a con- troversial topic after cardiac arrest in children. Recent clinical studies have shown no definitive benefit to therapeutic hypothermia compared to therapeutic normothermia after in-hospital or out-of-hospital cardiac arrest, including among pediatric drowning victims [1–3]. For infants receiving therapeutic hypothermia, there is a growing interest in using medications as adjunctive therapy [4]. For example, dexmedetomidine, an alpha-2 adrenoreceptor agonist, has been shown in animal studies to prevent neuroapoptosis and improve neurological outcomes [5]. Like- wise, recombinant human erythropoietin has shown promise as a neuroprotective agent in the context of neonatal brain injury [4,6]. 2. Case report A 22 month-old boy, previously neurodevelopmentally normal, and with no preexisting illness or disability, was discovered by family members floating face down near the edge of a retention pond. Immersion time and water temperature were unknown. By caregiver report, the boy was missing for 30–60 min. The water was tepid, and the air temperature was approximately 29 °C (85 °F). Bystander cardi- opulmonary resuscitation (CPR) was initiated and continued for 4 min until the arrival of emergency medical services (EMS). The initial rhythm was asystole. Advanced life support was continued en route to the hospital. After 14 total minutes of EMS-delivered CPR, return of spontaneous circulation (ROSC) was noted on arrival to the emergency department. Core temperature on admission was 31.8 °C. The patient's physical exam revealed weight of 13 kg, no external signs of trauma, copious frothy secretions in the airway, strong central pulses, a Glasgow Coma Scale (GSC) score of 3, and no clinical seizure activity. Initial pH and lactic acid were 6.63 and 17.7, respectively (Table 1). A head CT was obtained that demonstrated no bleed, trauma, cerebral edema or intracranial pathology. The patient was admitted to the pediatric intensive care unit (PICU) in critical condition requiring escalating cardiorespiratory support. On arrival to the PICU, the patient's initial core body temperature was 31.5 °C. His heart rate was 98 bpm and blood pressure was 80/ 52 mm Hg on a high-dose epinephrine infusion (0.3 μg/kg/min). Oxygen saturation was 60% on a conventional ventilator on 100% FiO 2 and PEEP of 12 cm H 2 O. Interval chest X-ray (CXR) showed diffuse bilateral interstitial and alveolar pulmonary opacities (Fig. 1A–B). Due to ongoing hypoxia and hypercarbia, high frequency oscillatory venti- lation was attempted, however it was unsuccessful due to severe, frank pulmonary edema. An echocardiogram showed a structurally normal heart with severely diminished biventricular systolic function (left ventricular ejection fraction (LVEF) < 20%). The patient's neurologic exam remained guarded with small and nonreactive pupils, but with intermittent positive cough and gag reflex. An electroencephalogram (EEG) placed 6 h after admission showed no evidence of seizures; al- though the background was abnormal, there was symmetrical brain activity (Fig. 2). Due to the patient's ongoing requirement for high dose inotropic and ventilatory support, ongoing severe acidosis (pH 7.16; PCO2 102; PaO2 43; HCO3 15) and impending cardiac arrest, the https://doi.org/10.1016/j.ppedcard.2018.05.004 Received 23 March 2018; Received in revised form 8 May 2018; Accepted 10 May 2018 ⁎ Corresponding author at: 6th Floor, Cardiac Surgery, Nemours Children's Hospital, 13535 Nemours Parkway, Orlando, FL 32827, USA. E-mail addresses: Jennifer.nelson@nemours.org (J.S. Nelson), Neha.longani@nemours.org (N. Longani), Laufey.sigurdardottir@nemours.org (L.Y. Sigurdardottir), Timothy.maul@nemours.org (T.M. Maul), Peter.wearden@nemours.org (P.D. Wearden), Constantinos.chrysostomou@nemours.org (C. Chrysostomou). Progress in Pediatric Cardiology xxx (xxxx) xxx–xxx 1058-9813/ © 2018 Published by Elsevier B.V. Please cite this article as: Nelson, J.S., Progress in Pediatric Cardiology (2018), https://doi.org/10.1016/j.ppedcard.2018.05.004