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author:("Call, amariah")
1.  A Normal Platelet Count May Not Be Enough: The Impact of Admission Platelet Count on Mortality and Transfusion in Severely Injured Trauma Patients 
The Journal of trauma  2011;71(2 0 3):S337-S342.
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 ×109/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.
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 PRBCs transfused.
For every 50 × 109/L increase in admission platelet count, the odds of death decreased 17% at 6 hours (p=0.03, 95% 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 × 109/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- -0.14) and one less unit of blood within the first 24 hours (p=0.002, 95% CI -1.6 - -0.36). The mean number of units of PRBCs transfused within the first 6 and 24 hours decreased with increasing platelet count.
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.
PMCID: PMC4374734  PMID: 21814101
2.  Clinical and Mechanistic Drivers of Acute Traumatic Coagulopathy 
Acute Traumatic Coagulopathy (ATC) occurs after severe injury and shock and is associated with increased bleeding, morbidity and mortality. The effects of ATC and hemostatic resuscitation on outcome are not well-explored. The PRospective Observational Multicenter Major Trauma Transfusion (PROMMTT) study provided a unique opportunity to characterize coagulation and the effects of resuscitation on ATC after severe trauma.
Blood samples were collected upon arrival on a subset of PROMMTT patients. Plasma clotting factor levels were prospectively assayed for coagulation factors. These data were analyzed with comprehensive PROMMTT clinical data.
There were 1198 patients with laboratory results of whom 41.6% were coagulopathic. Using International Normalized Ratio (INR)≥1.3, 41.6% (448) of patients were coagulopathic while 20.5% (214) were coagulopathic using partial thromboplastin time (PTT)≥35. Coagulopathy was primarily associated with a combination of an ISS>15 and a BD<−6 (P<.05). Regression modeling for INR-based coagulopathy shows that pre-hospital crystalloid (odds ratio (OR)=1.05), Injury Severity Score (ISS, OR=1.03), Glasgow Coma Scale (OR=0.93), heart rate (OR=1.08), systolic blood pressure (OR=0.96), base deficit (BD, OR=0.92) and temperature (OR=0.84) were significant predictors of coagulopathy (all P<.03). A subset of 165 patients had blood samples collected and coagulation factor analysis performed. Elevated ISS and BD were associated with elevation of aPC and depletion of factors (all P<.05). Reductions in factors I, II, V, VIII and an increase in aPC drive ATC (all p<.04). Similar results were found for PTT-defined coagulopathy.
ATC is associated with depletion of factors I, II, V, VII, VIII, IX and X and is driven by the activation of the protein C system. These data provide additional mechanistic understanding of the drivers of coagulation abnormalities after injury. Further understanding of the drivers of ATC and the effects of resuscitation can guide factor guided resuscitation and correction of coagulopathy after injury.
PMCID: PMC3755603  PMID: 23778510
PROMMTT; Coagulation; Bleeding; Trauma; Injury
3.  Critical Role of Activated Protein C in Early Coagulopathy and Later Organ Failure, Infection and Death in Trauma Patients 
Annals of surgery  2012;255(2):379-385.
Recent studies have identified an acute traumatic coagulopathy that is present on admission to the hospital and is independent of iatrogenic causes. We have previously reported that this coagulopathy is due to the association of severe injury and shock and is characterized by a decrease in plasma protein C levels. Whether this early coagulopathy and later propensity to infection, MOF and mortality are associated with the activation of protein C pathway has not been demonstrated and constitutes the aim of this study.
Methods and Findings
This was a prospective cohort study of 203 major trauma patients. Serial blood samples were drawn on arrival in the ED, and at 6, 12, and 24 hours after admission to the hospital. PT, PTT, Va, VIIIa, PC aPC t-PA and D-Dimer levels were assayed. Comprehensive injury, resuscitation and outcome data were prospectively collected.
A total of 203 patients were enrolled. Patients with tissue hypoperfusion and severe traumatic injury showed a strong activation of the protein C which was associated with a coagulopathy characterized by inactivation of the coagulation factors V and VIII and a derepression of the fibrinolysis with high plasma levels of plasminogen activator and high D-dimers. Elevated plasma levels of activated protein C were significantly associated with increased mortality, organ injury, increased blood transfusion requirements, and reduced ICU ventilator-free days. Finally early depletion of protein C after trauma is associated with a propensity to post-traumatic ventilator-associated pneumonia.
Acute traumatic coagulopathy occurs in the presence of tissue hypoperfusion and severe traumatic injury and is mediated by activation of the protein C pathway. Higher plasma levels of aPC upon admission are predictive of poor clinical outcomes following major trauma. After activation, patients who fail to recover physiologic plasma values of protein C have an increased propensity to later nosocomial lung infection.
PMCID: PMC3549308  PMID: 22133894
4.  Early Release of soluble RAGE After Severe Trauma in Humans 
The Journal of trauma  2010;68(6):1273-1278.
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 the present study.
One hundred sixty eight patients were studied as part of a prospective cohort study of severe trauma patients admitted to a single Level 1 Trauma center. Blood was drawn within 10 minutes of arrival to the Emergency Department (ED) before the administration of any fluid resuscitation. sRAGE, TNF-a, IL-6, von Willebrand Factor (vWF), Angiopoietin-2 (Ang-2), Prothrombin time, (PT), prothrombin fragments 1+2 (PF1+2), soluble thrombomodulin (sTM), protein C (PC), plasminogen activator inhibitor-1 (PAI-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 to outcome measures obtained from the electronic medical record and trauma registry.
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 as well as with 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=.11), although patients with less than 26 ventilator-free days had significantly higher plasma levels of sRAGE than those with more than 26 ventilator-free days. Finally, there was no relationship between plasma levels of sRAGE and mortality rate in trauma patients.
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.
PMCID: PMC3531976  PMID: 20539169
sRAGE; Trauma; Coagulopathy; Protein C; Complement
5.  Active and Passive Cigarette Smoking and Acute Lung Injury after Severe Blunt Trauma 
Rationale: Cigarette smoking has been demonstrated in laboratory studies to have effects on lung epithelial and endothelial function similar to those observed in acute lung injury (ALI). However, the association between active and passive cigarette smoke exposure and susceptibility to ALI has not been prospectively studied.
Objectives: We hypothesized that both active and passive cigarette smoke exposure would be associated with increased susceptibility to ALI after severe blunt trauma.
Methods: We measured levels of cotinine, a metabolite of nicotine and validated biomarker of tobacco use, in plasma samples obtained immediately on arrival at the emergency department from 144 adult subjects after severe blunt trauma. Patients were then followed for the development of ALI.
Measurements and Main Results: Increasing quartiles of plasma cotinine were associated with the development of ALI (odds ratio [OR] for developing ALI in highest cotinine quartile, 3.25; 95% confidence interval [CI], 1.22–8.68; P = 0.017 for trend across quartiles). Moderate to heavy passive smoke exposure was associated with nearly the same odds of developing ALI as active smoking (OR for moderate to heavy passive smoking compared with no exposure or low level exposure, 3.03; 95% CI, 1.15–8.04; OR for active smoking, 2.77; 95% CI, 1.28–5.99). This association persisted after adjusting for other predictors of ALI, including Injury Severity Score and alcohol abuse.
Conclusions: Both moderate to heavy passive smoking and active smoking are independently associated with the development of ALI after severe blunt trauma. This finding has important implications both for public health and for understanding the pathogenesis of ALI.
PMCID: PMC3136993  PMID: 21471091
cigarette smoking; acute lung injury; acute respiratory distress syndrome; cotinine; secondhand smoke exposure

Results 1-5 (5)