A normal platelet count may not be enough: the impact of admission platelet count on mortality and transfusion in severely injured trauma patients.

BACKGROUND: Platelets play a central role in hemostasis after trauma. However, the platelet count of most trauma patients does not fall below the normal range (100-450 × 10(9)/L), and as a result, admission platelet count has not been adequately investigated as a predictor of outcome. The purpose of this study was to examine the relationship between admission platelet count and outcomes after trauma. METHODS: A retrospective cohort study of 389 massively transfused trauma patients. Regression methods and the Kruskal-Wallis test were used to test the association between admission platelet count and 24-hour mortality and units of packed red blood cells (PRBCs) transfused. RESULTS: For every 50 × 10(9)/L increase in admission platelet count, the odds of death decreased 17% at 6 hours (p = 0.03; 95% confidence interval [CI], 0.70-0.99) and 14% at 24 hours (p = 0.02; 95% CI, 0.75-0.98). The probability of death at 24 hours decreased with increasing platelet count. For every 50 × 10(9)/L increase in platelet count, patients received 0.7 fewer units of blood within the first 6 hours (p = 0.01; 95% CI, -1.3 to -0.14) and one less unit of blood within the first 24 hours (p = 0.002; 95% CI, -1.6 to -0.36). The mean number of units of PRBCs transfused within the first 6 hours and 24 hours decreased with increasing platelet count. CONCLUSIONS: Admission platelet count was inversely correlated with 24-hour mortality and transfusion of PRBCs. A normal platelet count may be insufficient after severe trauma, and as a result, these patients may benefit from a lower platelet transfusion threshold. Future studies of platelet number and function after injury are needed.

Spinal cord injury: outcomes of ventilatory weaning and extubation.

BACKGROUND: Spinal cord injury (SCI) carries potentially devastating respiratory implications depending on injury level. Optimal strategies for mechanical ventilation in this setting remain poorly described. We reviewed our experience of ventilatory weaning and extubation outcomes in this patient population. METHODS: Eighty mechanically ventilated SCI patients over a 5-year period at a major Level I trauma center were assessed. Injury, clinical, and outcome data were extracted using our ICU database, chart, and registry data. RESULTS: We identified 80 patients with SCI, classified by anatomic injury and motor functional level. There were no differences in injury severity between patients who were successfully extubated and those who failed (all p = NS). Seventy-four percent were extubated at the time of discharge; successful extubation was associated with lower level of cord injury (p = 0.001) and higher arrival Glasgow Coma Scale score (13.7 ± 2.6 vs. 10.8 ± 5.0, p = 0.021). Of extubation failures, 80% were due to pulmonary mechanical insufficiency, 22% inadequate pulmonary toilet, and 5% sedation or neurologic issues. Patients with weaning or extubation failures had longer ICU (29.9 days ± 24.5 days vs. 8.5 days ± 9.3 days; p < 0.001) and hospital stays (45.8 days ± 45.8 days vs. 26.6 days ± 23.9 days; p = 0.009), and higher rates of ventilator-associated pneumonia (83% vs. 15%, p < 0.001). CONCLUSION: Higher level of SCI correlates strongly with failure to wean and extubate; despite this, a subset of patients with high cord injury who can be safely weaned and extubated exists. A multicenter study is warranted to specifically identify patients with high SCI who merit weaning and extubation trials.

Early release of soluble receptor for advanced glycation endproducts after severe trauma in humans.

BACKGROUND: The receptor for advanced glycation endproducts (RAGE) recognizes a variety of ligands that play an important role in the posttraumatic inflammatory response. However, whether soluble RAGE (sRAGE) is released early after trauma hemorrhage in humans and whether such a release is associated with the development of an inflammatory response and coagulopathy is not known and therefore constitutes the aim of this study. METHODS: One hundred sixty-eight patients were studied as part of a prospective cohort study of severe trauma patients admitted to a single Level I Trauma center. Blood was drawn within 10 minutes of arrival to the emergency department before the administration of any fluid resuscitation. sRAGE, tumor necrosis factor-alpha, interleukin-6, von Willebrand factor, angiopoietin-2, prothrombin time, prothrombin fragments 1 + 2, soluble thrombomodulin, protein C, plasminogen activator inhibitor-1, and d-dimers (fibrin degradation products) were measured using standard techniques. Base deficit was used as a measure of tissue hypoperfusion. Measurements were compared with outcome measures obtained from the electronic medical record and trauma registry. RESULTS: Plasma levels of sRAGE were increased within 30 minutes after severe trauma in humans and correlated with the severity of injury, early posttraumatic coagulopathy and hyperfibrinolysis, and endothelial cell activation (angiopoietin-1 and complement). Furthermore, we found that there was a significant relationship between plasma levels of sRAGE and the development of acute renal failure. This relationship was not quite significant for patients who developed acute lung injury (p = 0.11), although patients with <26 ventilator-free days had significantly higher plasma levels of sRAGE than those with >26 ventilator-free days. Finally, there was no relationship between plasma levels of sRAGE and mortality rate in trauma patients. CONCLUSION: The results of this study demonstrate that the release of sRAGE in the bloodstream of trauma patients requires severe injury and is associated with coagulation abnormalities and endothelial cell and complement activation.