OBJECTIVE: The time course of circulating adhesion molecules was monitored in traumatized and sepsis patients. DESIGN: Prospective, descriptive. SETTING: A surgical intensive care unit of a university hospital. PATIENTS: A total of 30 consecutive critically ill patients suffering either from trauma (n = 15) or postoperative sepsis (n = 15). INTERVENTIONS: All patients were on continuous analgo-sedation and mechanical ventilation. MEASUREMENTS AND RESULTS: From arterial blood samples, plasma levels of soluble adhesion molecules [endothelial leukocyte adhesion molecules (sELAM-1), intercellular adhesion molecule-1 (sICAM-1)], and vascular cell adhesion molecule-1 (sVCAM-1) were measured on the day of admission (trauma patients) or on the day of diagnosis of sepsis (= baseline values), and during the following 5 days. In the trauma group, sELAM-1 (57.9 +/- 11.0 ng/ml) and sVCAM-1 (698 +/- 93 ng/ml) were within normal ranges at baseline, whereas they were markedly elevated in the sepsis group (sELAM-1: 340 +/- 95 ng/ml; sVCAM-1; 1,042 +/- 449 ng/ml). In the sepsis patients, sELAM-1 significantly decreased and sVCAM-1 increased, but remained almost unchanged in the trauma patients. Non-survivors showed markedly elevated plasma levels of sELAM-1 and sVCAM-1. sICAM-1 was elevated in both groups at baseline and was higher in the sepsis group (1,266 +/- 261 ng/ml) than in the trauma group. In the septic patients, sICAM-1 increased further (2,022 +/- 609 ng/ml) and remained unchanged in the trauma group. All non-survivors showed sICAM-1 plasma levels of > 800 ng/ml. CONCLUSIONS: Endothelial damage may result in multiple-organ dysfunction syndrome. Adhesion molecules are considered to be a cornerstone in this process. Trauma patients showed lower plasma levels of circulating adhesion molecules than did sepsis patients indicating more pronounced (inflammatory related) endothelial activation or damage in sepsis. Therapeutic modulation of circulating adhesion molecules may be of benefit to the patients outcome and therefore warrants further study.
OBJECTIVE: The time course of circulating adhesion molecules was monitored in traumatized and sepsispatients. DESIGN: Prospective, descriptive. SETTING: A surgical intensive care unit of a university hospital. PATIENTS: A total of 30 consecutive critically ill patients suffering either from trauma (n = 15) or postoperative sepsis (n = 15). INTERVENTIONS: All patients were on continuous analgo-sedation and mechanical ventilation. MEASUREMENTS AND RESULTS: From arterial blood samples, plasma levels of soluble adhesion molecules [endothelial leukocyte adhesion molecules (sELAM-1), intercellular adhesion molecule-1 (sICAM-1)], and vascular cell adhesion molecule-1 (sVCAM-1) were measured on the day of admission (traumapatients) or on the day of diagnosis of sepsis (= baseline values), and during the following 5 days. In the trauma group, sELAM-1 (57.9 +/- 11.0 ng/ml) and sVCAM-1 (698 +/- 93 ng/ml) were within normal ranges at baseline, whereas they were markedly elevated in the sepsis group (sELAM-1: 340 +/- 95 ng/ml; sVCAM-1; 1,042 +/- 449 ng/ml). In the sepsispatients, sELAM-1 significantly decreased and sVCAM-1 increased, but remained almost unchanged in the traumapatients. Non-survivors showed markedly elevated plasma levels of sELAM-1 and sVCAM-1. sICAM-1 was elevated in both groups at baseline and was higher in the sepsis group (1,266 +/- 261 ng/ml) than in the trauma group. In the septic patients, sICAM-1 increased further (2,022 +/- 609 ng/ml) and remained unchanged in the trauma group. All non-survivors showed sICAM-1 plasma levels of > 800 ng/ml. CONCLUSIONS: Endothelial damage may result in multiple-organ dysfunction syndrome. Adhesion molecules are considered to be a cornerstone in this process. Traumapatients showed lower plasma levels of circulating adhesion molecules than did sepsispatients indicating more pronounced (inflammatory related) endothelial activation or damage in sepsis. Therapeutic modulation of circulating adhesion molecules may be of benefit to the patients outcome and therefore warrants further study.
Authors: Wolfgang G Junger; Shawn G Rhind; Sandro B Rizoli; Joseph Cuschieri; Maria Y Shiu; Andrew J Baker; Linglin Li; Pang N Shek; David B Hoyt; Eileen M Bulger Journal: Shock Date: 2012-10 Impact factor: 3.454
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