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Updated: Aug 8, 2025
Veno-Venous Extracorporeal Membrane Oxygenation in a Mouse
Published on: October 24, 2018
Spinal Cord Infarction With Prolonged Femoral Venoarterial Extracorporeal Membrane Oxygenation
Chetan Pasrija1, Zachary N Kon2, Michael A Mazzeffi3
1Division of Cardiac Surgery, University of Maryland, School of Medicine, Baltimore, MD.
Objectives:
There have been sporadic reports of ischemic spinal cord injury (SCI) during venoarterial extracorporeal membrane oxygenation (VA-ECMO) support. The authors observed a troubling pattern of this catastrophic complication and evaluated the potential mechanisms of SCI related to ECMO.
Design:
This study was a case series.
Setting:
This study was performed at a single institution in a University setting.
Participants:
Patients requiring prolonged VA-ECMO were included.
Interventions:
No interventions were done. This was an observational study.
Measurements And Main Results:
Four hypotheses of etiology were considered: (1) hypercoagulable state/thromboembolism, (2) regional hypoxia/hypocarbia, (3) hyperperfusion and spinal cord edema, and (4) mechanical coverage of spinal arteries. The SCI involved the lower thoracic (T7-T12 level) spinal cord to the cauda equina in all patients. Seven out of 132 (5.3%) patients with prolonged VA-ECMO support developed SCI. The median time from ECMO cannulation to SCI was 7 (range: 6-17) days.There was no evidence of embolic SCI or extended regional hypoxia or hypocarbia. A unilateral, internal iliac artery was covered by the arterial cannula in 6/7 86%) patients, but flow into the internal iliac was demonstrated on imaging in all available patients. The median total flow (ECMO + intrinsic cardiac output) was 8.5 L/min (LPM), and indexed flow was 4.1 LPM/m2. The median central venous oxygen saturation was 88%, and intracranial pressure was measured at 30 mmHg in one patient, suggestive of hyperperfusion and spinal cord edema.
Conclusions:
An SCI is a serious complication of extended peripheral VA-ECMO support. Its etiology remains uncertain, but the authors' preliminary data suggested that spinal cord edema from hyperperfusion or venous congestion could contribute.
