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Increased endothelial glycocalyx damage biomarkers in Emergency Department patients with infection, compared to trauma

Smart, L.ORCID: 0000-0003-4776-2849, Macdonald, S.P.J., Burrows, S., Bosio, E., Arendts, G. and Fatovich, D.M. (2016) Increased endothelial glycocalyx damage biomarkers in Emergency Department patients with infection, compared to trauma. In: 8th Congress of the International Federation of Shock Societies, 3 - 5 October 2016, Tokyo, Japan.

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Background: Endothelial glycocalyx damage (EGD) biomarkers are associated with poor outcomes in ICU patients with sepsis but there is little information on behaviour of these biomarkers in Emergency Department (ED) patients with infection.

Objectives: 1) To explore three biomarkers of EGD in ED patients with infection over the first 24 hours, 2) to compare these results to a trauma group, and 3) to explore associations with illness severity, comorbidities and clinical outcomes in patients with infection.

Methods: Banked serum samples were used from patients with simple infection (n = 22), sepsis (43), septic shock (45) and trauma (30) collected at: enrolment in the ED (T0), 1 hour (T1), 3 hours (T3) and 12–24 hours (T24) later. Healthy controls (n = 29) were included for T0 comparisons. Biomarkers syndecan-1 (SYN1), syndecan-4 (SYN4) and hyaluronan (HA) were measured via ELISA. Results were obtained using regression methods including random effects linear, logistic and truncated negative binomial methods. Significance was set at P < 0.05.

Results: SYN1 concentration at T0 was significantly higher in all groups compared to control (median 494pg/ml, [Q1-Q3 382–709]). Septic shock (3064pg/ml, [1645–7116]) and sepsis (2542, [1096–5263]) groups had significantly higher concentrations than simple infection (1207, [695–1647]) and trauma (1404, [1055–2265]). SYN1 increased between T0 and T24 in the simple infection and septic shock groups, which was significantly different to trauma.

SYN4 was not different among groups at T0. A decrease in SYN4 in the simple infection group at T3 was the only between-group difference.

HA concentration was significantly higher in the septic shock group at T0 (128 ng/ml, [62–425]) than simple infection (32, [13–89]), sepsis (62, [22–135]), trauma (45, [15–82]) and healthy control groups (41, [24–60]). HA increased between T0 and T3 in infection groups, whereas HA decreased between T0 and T3 in trauma.

Patients with liver disease or alcohol abuse had significantly higher SYN1 and HA over time, compared to others. Patients with vascular disease failed to show a peak in HA concentration at T3, compared to others. Higher SYN1 and HA at T0 significantly increased the odds of ICU admission and higher sequential organ failure assessment score.

Conclusions: ED patients with sepsis and septic shock had higher levels of EGD biomarkers compared to those with simple infection or trauma. Differing patterns of EGD occurred over the first 24 hours of hospitalisation for infection, compared to trauma. Increased SYN1 and HA was also related to key comorbidities, ICU admission and organ failure

Item Type: Conference Item
Other Information: Poster abstract
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