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Critical Care |

Antithrombin III Deficiency in Patients Requiring Extracorporeal Membrane Oxygenation (ECMO) Support

Jonathan Sarik, MD; Shinya Unai, MD; Harrison Pitcher, MD; Qiong Yang, MD; Hitoshi Hirose, MD; Nicholas Cavarocchi, MD
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Thomas Jefferson University Hospital, Philadelphia, PA


Chest. 2013;144(4_MeetingAbstracts):319A. doi:10.1378/chest.1703464
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Abstract

SESSION TITLE: Cardiovascular Critical Care

SESSION TYPE: Medical Student/Resident Case Report

PRESENTED ON: Sunday, October 27, 2013 at 10:45 AM - 11:45 AM

INTRODUCTION: Formation of clots within the circuit of extracorporeal membrane oxygenation (ECMO) is a life-threatening emergency and requires emergent intervention. Decreased antithrombin III (ATIII) is associated with a hypercoagulable state, which can be a challenge for patients requiring mechanical circulatory support.

CASE PRESENTATION: A 56 year old male with known ischemic cardiomyopathy developed syncopal episodes associated with a ventricular arrhythmia. After initially presenting to an outside hospital the patient was transferred to our institution in cardiogenic shock requiring multiple inotropes and vasopressors; failure of medical management resulted in veno-arterial ECMO support. Cardiac catheterization with ECMO support showed complete occlusion of the left anterior descending artery; PCI was not appliable Heparin was initiated with a target PTT at 55-65 sec. On postoperative day (POD) 3, extensive clots formed in the oxygenator despite appropriate PTT with heparin infusion, which required circuit exchange. This problem recurred on POD 4 requiring a second oxygenator exchange. On POD 6, the ECMO oxygenator was again noted to contain extensive clots (Figure Top). The ATIII level was 52% (normal range 84-134%) and anti-factor Xa level was 0.10 IU/mL (normal range 0.3 IU/mL or above). ATIII replacement therapy was initiated and the clots in the oxygenator subsequently resolved (Figure Bottom). After ATIII replacement, the oxygenator remained clot free until the patient underwent coronary artery bypass graft and ECMO removal on POD 10.

DISCUSSION: Acquired ATIII deficiency is commonly seen in patients requiring mechanical circulatory support (Ref 1). The diagnosis of ATIII deficiency can be made by direct measurement of ATIII level although the ATIII assay may take several days to get results. Alternatively, rapid screening can be done measuring anti-factor Xa level. If the anti-factor Xa level is low and the patient clinically appears to be in a hypercoagulable state, ATIII deficiency is strongly suspected. ATIII replacement therapy is simple and effective for treating the clots formed in the ECMO device in these patients, preserving hospital resources in a situation where the circuit would otherwise need to be exchanged.

CONCLUSIONS: In patients on ECMO developing unexplained clots despite adequate anticoagulation therapy, ATIII deficiency should be considered. Prompt recognition of the ATIII deficiency and ATIII replacement can prevent clot burden complications in patients requiring ECMO and can avoid unnecessary ECMO circuit exchange.

Reference #1: Bembea MM, Annich G, Rycus P, Oldenburg G, Berkowitz I, Pronovost P. Variability in Anticoagulation Management of Patients on Extracorporeal Membrane Oxygenation: An International Survey. Pediatr Crit Care Med 2013;14:e77-e84.

DISCLOSURE: The following authors have nothing to disclose: Jonathan Sarik, Shinya Unai, Harrison Pitcher, Qiong Yang, Hitoshi Hirose, Nicholas Cavarocchi

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