307 - Arterial Ischemic Stroke in Two Children Associated with Circuit Changes During Extracorporeal Membrane Oxygenation (ECMO).

Poster Number: 307
Publication Number: 307.205

Mauro Caffarelli, University of California, San Francisco, School of Medicine, San Francisco, CA, United States; Martina Steurer, UCSF Benioff Children's Hospital San Francisco, San Francisco, CA, United States; Edilberto Amorim, University of California, San Francisco, School of Medicine, San Francisco, CA, United States

Background: Arterial Ischemic Stroke (AIS) during ECMO is often diagnosed late due to absence of a reliable clinical exam, and high-risk periods associated with AIS are not clearly defined. Neuromonitoring methods are needed to allow early recognition of stroke by bedside providers. We previously described the Correlate Of Injury to the Nervous System (COIN) index, a real-time quantitative electroencephalographic (EEG) asymmetry index where values < -15 are associated with AIS. 

Objective: We present 2 cases of AIS in association with circuit change (CC) during ECMO.

Design/Methods: Clinical data including EEG and neuroimaging reports were collected from electronic health record. COIN was calculated from EEG using MATLAB.

Results: Patient 1 was a 4-month-old female with atrioventricular canal who required emergent ECMO cannulation during cardiac arrest 2 days post-Bidirectional Glenn. She had minimal pulsatility (pulse pressure < 6 mmHg) and was heparinized to maintain activated prothrombin time (aPTT) > 70. EEG on post-cannulation day 1 showed mild left voltage attenuation (COIN -30). CC occurred day 3 post-cannulation for increased transmembrane pressures with no apparent complications and onset of focal seizures 8 hours later. EEG showed new worsened left hemispheric voltage attenuation (COIN -71). Computed tomography (CT) 24 days after CC showed old ischemic injury to entire left hemisphere and right parieto-occipital region. Patient 2 was a 12-year-old female with sepsis following Orthotopic Heart Transplantation requiring ECMO on post-operative day 1. She had persistent hypotension (mean arterial pressure 16-23 mmHg) with absent pulsatility and was heparinized to maintain aPTT >60. CC occurred on day 1 post-cannulation to upsize the venous cannula and augment circuit flow. EEG was recorded during the 3-minute-long CC showing a progression from background symmetry to severe bilateral background suppression during CC followed by voltage attenuation and slowing in the left hemisphere (COIN -4 to -77). CT 6 hours later showed evidence of early ischemic injury to the left hemisphere.

Conclusion(s): CC represents a high-risk epoch for AIS in the pediatric ECMO population, potentially related to embolic events that occur during CC or transient cerebral hypoperfusion resulting in expansion of embolic stroke sustained prior to CC. Routine use of EEG during CC may allow early recognition of AIS, with implementation of COIN enhancing early detection by bedside providers. Prospective study is required to understand incidence and specific risk factors of AIS associated with CC on ECMO.