• Critical care medicine · Feb 2016

    Case Reports

    Spinal Cord Infarct During Concomitant Circulatory Support With Intra-Aortic Balloon Pump and Veno-Arterial Extracorporeal Membrane Oxygenation.

    • Behnoosh Samadi, Duy Nguyen, Sam Rudham, and Yael Barnett.
    • 1Intensive Care Unit, St Vincent's Hospital, Sydney, Australia. 2University of New South Wales, Sydney, Australia. 3Department of Radiology, St Vincent's Hospital, Sydney, Australia.
    • Crit. Care Med. 2016 Feb 1; 44 (2): e101-5.

    ObjectiveTo report a series of three patients who received simultaneous circulatory support with both veno-arterial extracorporeal membrane oxygenation and intra-aortic balloon pump and subsequently developed spinal cord infarction, and present a brief review of the relevant literature.Data SourcesHospital medical records and MEDLINE and PubMed databases.Study SelectionAny patient who developed lower limb neurologic symptoms during a period of concurrent venoarterial extracorporeal membrane oxygenation and intra-aortic balloon pump support, with subsequent MRI changes involving the spinal cord, from 2006 (the year of institution of venoarterial extracorporeal membrane oxygenation in our ICU) to 2014.Data ExtractionPatient records were retrospectively reviewed. Medical databases were searched for any literature linking intra-aortic balloon pump and/or venoarterial extracorporeal membrane oxygenation with neurologic injury of the lower limbs.Data SynthesisThree female patients presented in cardiogenic shock or arrest requiring circulatory support. Intra-aortic balloon pump was inserted, and peripheral veno-arterial extracorporeal membrane oxygenation was initiated with subsequent loss of native ejection in each case. Neurologic signs were noted clinically, and subsequent imaging demonstrated spinal cord infarction and small aortic size for all three patients.ConclusionsThe timeline of events suggests a causal relation between intra-aortic balloon pump, veno-arterial extracorporeal membrane oxygenation, and significant neurologic deficits. This is likely due to hypoperfusion of the spinal cord, which is multifactorial in origin, including small aortic calibre, low cardiac output states, high vasopressor requirements causing vasospasm of the artery of Adamkiewicz, occlusion of retrograde oxygenated blood flow from peripheral veno-arterial extracorporeal membrane oxygenation due to intra-aortic balloon pump being in situ, and possible thromboembolic phenomena. The thoracic spinal cord is intrinsically susceptible to ischemia due to the anatomy of the arterial supply, which is described here. We identify several risk factors and make several recommendations to avoid this rare but catastrophic complication in the future. We also suggest interventions should this challenging complication be identified.

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