Hypertonic Saline Resuscitation Modulates Neutrophil Adhesion Molecule Expression of Post-Traumatic Hemorrhagic Shock Patients

摘要

Fluid resuscitation for traumatic hemorrhagic shock remains controversial since current protocols using large-volume crystalloid may exacerbate post-traumatic inflammation and organ dysfunction. Experimental data suggests that hypertonic saline/dextran (HSD, 7.5% NaCl in 6% dextran-70) exerts antiinflammatory and immunomodulatory effects, reduces multiorgan dysfunction and improves outcome. First trial examining the immunomodulatory properties of HSD in humans. Based on experimental findings, this study proposes to determine whether a single bolus of HSD might modulate the inflammatory response to hemorrhagic shock. Randomized, double-blinded, placebo- controlled clinical trial. Patients - 27 adult patients, victims of blunt trauma and hypotension due to hemorrhage. 13 patients received HSD, 2 excluded for failing inclusion criteria and 1 for refusing participation. Upon arrival, eligible patients received a single 250-ml bolus of either HSD or placebo (0.9% NaCl) from unmarked bags. Blood samples were collected prior to infusion and over subsequent 24 hours. All patients underwent standard resuscitation. HSD markedly altered shock-induced changes in key adhesion molecules on circulating neutrophils compared to placebo. HSD abolished shock-induced upregulation of CD11b and caused extensive CD62L shedding. Leukocyte counts were similar, except for lymphocytes where HSD prevented the lymphopenia detected in the control group. HSD patients required less crystalloid and blood during the first 24 hours. HSD patients were liberated from mechanical ventilation 24 hours earlier than control. ICU stay, organ dysfunction, infections and mortality did not differ between groups. HSD modestly increased serum sodium and osmolarity. No complications were associated to HSD.