Changes in “Inflammatory” Mediators and Total Body Water during Extra-Corporeal Membrane Oxygenation (ECMO). A Preliminary Study

Author:

Underwood M.J.1,Pearson J.A.2,Waggoner J.2,Lunec J.3,Firmin R.K.2,Elliot M.J.4

Affiliation:

1. Department of Cardiothoracic Surgery, Bristol Royal Infirmory, Bristol

2. Department of Cardiothoracic Surgery, Glenfield General Hospital, Leicester

3. Division of Chemical Pathology University of Leicester, Leicester

4. Department of Cardiothoracic Surgery, Great Ormond Street Hospital, London - UK

Abstract

We studied six patients (5 paediatric, 1 neonate) treated with ECMO to quantify changes in inflammatory mediators (neutrophil elastase (NE), free radical activity (FR), interleukin 8 (IL8)) and total body water (TBW). Blood samples were taken before instigation of ECMO, 4, 12, 24 hours post-ECMO and daily for six days. FR activity was quantified using the oxidised IgG FI/UV ration. NE and IL8 levels were measured by ELISA. TBW was assessed by electrical bioimpedance. Statistical analysis was made using repeated measures analysis of variance and modified t-test where appropriate. Results are presented as mean ± standard error of the mean. FR activity increased 4 hours after instigation of ECMO (IgG FI/UV 32.1 ± 3.2 from 24.1 ± 3.0 p=0.005) and remained elevated. NE also increased by 4 hours (94.8 μg/L ± 8.9 to 678 μg/L ± 153.4, p=0.005) but returned to pre-ECMO values by day 6. IL8 levels rose after ECMO (from 98 pg/ml ± 39, to 24 pg/ml ± 117.4) although no statistical difference was noted over time due to the large variation between subjects (p=0.009). TBW (% pre-ECMO body weight) fell by 24 hours (from 118.6 ± 12.6 to 96.5 ± 8.2 p=0.0004). This study demonstrated that ECMO stimulates an ‘inflammatory’ response to extracorporeal perfusion (increased FR, NE) but despite this, results in a reduction in total body water. The complex relationship between the inflammatory response to prolonged extracorporeal perfusion and its effect on tissue oedema merits further investigation.

Publisher

SAGE Publications

Subject

Biomedical Engineering,Biomaterials,General Medicine,Medicine (miscellaneous),Bioengineering

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