Search

Background: Randomized clinical trials (RCTs) support the use of prehospital plasma in traumatic hemorrhagic shock, especially in long transports. The citrate added to plasma binds with calcium, yet most prehospital trauma protocols have no guidelines for calcium replacement. We reviewed the experience of two recent prehospital plasma RCTs regarding admission ionized-calcium (i-Ca) blood levels and its impact on survival. We hypothesized that prehospital plasma is associated with hypocalcemia, which in turn is associated with lower survival., Methods: We studied patients enrolled in two institutions participating in prehospital plasma RCTs (control, standard of care; experimental, plasma), with i-Ca collected before calcium supplementation. Adults with traumatic hemorrhagic shock (systolic blood pressure ≤70 mm Hg or 71-90 mm Hg + heart rate ≥108 bpm) were eligible. We use generalized linear mixed models with random intercepts and Cox proportional hazards models with robust standard errors to account for clustered data by institution. Hypocalcemia was defined as i-Ca of 1.0 mmol/L or less., Results: Of 160 subjects (76% men), 48% received prehospital plasma (median age, 40 years [interquartile range, 28-53 years]) and 71% suffered blunt trauma (median Injury Severity Score [ISS], 22 [interquartile range, 17-34]). Prehospital plasma and control patients were similar regarding age, sex, ISS, blunt mechanism, and brain injury. Prehospital plasma recipients had significantly higher rates of hypocalcemia compared with controls (53% vs. 36%; adjusted relative risk, 1.48; 95% confidence interval [CI], 1.03-2.12; p = 0.03). Severe hypocalcemia was significantly associated with decreased survival (adjusted hazard ratio, 1.07; 95% CI, 1.02-1.13; p = 0.01) and massive transfusion (adjusted relative risk, 2.70; 95% CI, 1.13-6.46; p = 0.03), after adjustment for confounders (randomization group, age, ISS, and shock index)., Conclusion: Prehospital plasma in civilian trauma is associated with hypocalcemia, which in turn predicts lower survival and massive transfusion. These data underscore the need for explicit calcium supplementation guidelines in prehospital hemotherapy., Level of Evidence: Therapeutic, level II.

Background: During traumatic hemorrhage, the ability to identify shock and intervene before decompensation is paramount to survival. Lactate is extremely sensitive to shock, and its clearance has been demonstrated a useful gauge of shock and resuscitation status. Though lactate can be measured in the field, logistical constraints render it impractical in certain environments. The compensatory reserve represents a new clinical measurement reflecting the remaining capacity to compensate for hypoperfusion. We hypothesized the compensatory reserve index (CRI) would be an effective surrogate marker of shock and resuscitation compared to lactate., Methods: The CRI device was placed on consecutive patients meeting trauma center activation criteria and remained on the patient until discharge, admission, or transport to operating suite. All subjects had a lactate level measured as part of their routine admission metabolic analysis. Time-corresponding CRI and lactate values were matched in regards to initial and subsequent lactate levels. Mean time from lactate sample collection to data availability in the electronic medical record was calculated. Predictive capacity of CRI and lactate in predicting hemorrhage was determined by receiver-operator characteristic curve analysis. Correlation analysis was performed to determine if any association existed between changing CRI and lactate values., Results: Receiver-operator characteristic (ROC) curves were generated and area under the curve was 0.8052 and 0.8246 for CRI and lactate, respectively. There was no significant difference in each parameter's ability to predict hemorrhage (p = 0.8015). The mean duration from lactate sample collection to clinical availability was 44 minutes whereas CRI values were available immediately. Analysis of the concomitant change in serial CRI and lactate levels revealed a Spearman's correlation coefficient of -0.73 (p < 0.01)., Conclusion: CRI performed with equivalent predictive capacity to lactate with respect to identifying initial perfusion status associated with hemorrhage and subsequent resuscitation., Level of Evidence: Diagnostic, Level II.

Background: The initiation of coagulation in trauma is thought to originate from exposed tissue factor (TF); recent data have led to the alternative hypothesis that damage-associated molecular patterns may contribute to postinjury coagulation. In acute traumatic coagulopathy, aberrant coagulation is mediated via the activated protein C (aPC) pathway; the upstream regulators of this process and its relation to TF remain uncharacterized. To examine the role of the TF pathway in mediating acute traumatic coagulopathy, we used specific antibody blockades in an established murine model of traumatic hemorrhagic shock, hypothesizing that both coagulation activation after injury and aPC-mediated coagulopathy are driven by TF via thrombin., Methods: Mice underwent an established model of trauma and hemorrhage and were subjected to either sham (vascular cannulation) or trauma-hemorrhage (cannulation, laparotomy, shock to mean arterial pressure of 35 mm Hg); they were monitored for 60 minutes before sacrifice. Mice in each group were pretreated with either targeted anti-TF antibody to block the TF pathway or hirudin for specific blockade of thrombin. Plasma was assayed for thrombin-antithrombin (TAT) and aPC by enzyme-linked immunosorbent assay., Results: Compared with controls, trauma-hemorrhage mice treated with anti-TF antibody had significantly reduced levels of TAT (2.3 ng/mL vs. 5.7 ng/mL, p = 0.016) and corresponding decreases in aPC (16.3 ng/mL vs. 31.6 ng/mL, p = 0.034), with reductions to levels seen in sham mice. Direct inhibition of thrombin yielded similar results, with reduction in aPC to levels below those seen in sham mice., Conclusion: In this study, blockade of the TF pathway led to the attenuation of both thrombin production and aPC activation observed in traumatic shock. Specific thrombin inhibition achieved similar results, indicating that aPC-related coagulopathy is mediated via thrombin activated by the TF pathway. The near-complete blockade of TAT and aPC observed in this model argues for a dominant role of the TF-thrombin pathway in both coagulation activation after injury and traumatic coagulopathy.

Background: Trauma centers are increasingly advocating the replacement of arterial blood gas measurements with venous blood gas measurements for simplification of base deficit (BD) determination. These values have never been demonstrated to agree in important trauma populations, such as for patients in occult shock (OS) or the elderly. The goal of this study was to investigate the level of agreement between venous and arterial BDs from blood gases in critically ill or injured patients, specifically in OS and the elderly., Methods: This is a retrospective, consecutive, cohort study using matched pairs of venous and arterial blood gases from patients admitted to the Trauma and Neurosurgery Intensive Care Unit in a Level I trauma center in Toronto, Ontario, Canada. Agreement between near simultaneous arterial and venous BD was calculated using the Bland-Altman method. McNemar's test was used for differences in BDs in the presence or absence of OS and in elderly patients., Results: BDs for 466 arterial and venous samples from 72 patients were compared pairwise. There was no significant difference between samples (p = 0.88). Ninety-eight percent of samples were within 3.0 mmol/L of each other. No significant differences were detected between venous and arterial BD in the presence of OS or in the elderly (p = 0.72 and p = 0.25, respectively)., Conclusion: Arterial and venous BDs agree, including in the presence of OS and in the elderly. Consideration may be given to venous sampling both in the intensive care unit or in other areas of care, such as the trauma bay., Level of Evidence: Diagnostic study, level III.

Background: Normally, end-tidal CO(2) is within 2 mm Hg of arterial PO(2) (PaCO(2)). However, if dead space in the lungs increases owing to shock with poor lung perfusion, the arterial-end tidal PCO(2) difference [P(a-ET)CO(2)] increases. We have found that in severely injured patients, P(a-ET)CO(2) of less than 10 mm Hg is associated with survival and P(a-ET)CO(2) of greater than 16 mm Hg is usually fatal. Our initial studies suggested that intravenously administered bicarbonate increases P(a-ET)CO(2)., Methods: This retrospective therapeutic study evaluated the effects of intravenously administered bicarbonate in a cohort of 225 severely acidotic (arterial pH ≤ 7.10) trauma patients who underwent emergency surgery from 1989 through 2011. Patients were divided into groups: early deaths (<48 hours), deaths in the operating room, deaths within 48 hours, and survivors. Winter's formula was defined as PaCO(2) = (HCO(3)) (1.5) + 8 ± 4., Results: Of the 225 patients, the mean (SD) initial arterial pH was 6.92 (0.16) with HCO(3) of 11.0 (3.5) mEq/L. According to the Winter's formula, PaCO(2) should have been 24 (4) mm Hg but actually was 50 (14) mm Hg. In 73 patients, the effect of an average of two to eight vials of bicarbonate increased HCO(3) from 10.5 (3.1) mEq/L to 16.8 (4.0) mEq/L. In addition, PaCO(2) increased from 44 (9) mm Hg to 51 (11) mm Hg and end-tidal CO(2) stayed relatively constant (26 [6] to 25 [5]). This resulted in a increase in P(a-ET)CO(2) from 17 (9) mm Hg to 24 (13) mm Hg, affecting survival. In the final values after resuscitation, the P(a-ET)CO(2) in the 75 patients who survived was 10 (6) mm Hg, while the 103 patients who died in the operating room or within 48 hours of surgery had a P(a-ET)CO(2) of 23 (10) mm Hg (p < 0.001)., Conclusion: In severely acidotic, critically injured patients, reducing the PaCO(2) to less than 40 mm Hg and decreasing the P(a-ET)CO(2) to 10 (6) mm Hg should be attempted, using as little HCO(3) therapy as possible. Bicarbonate should be given only if severe acidosis persists despite resuscitation and if PaCO(2) levels near those which are appropriate can be obtained., Level of Evidence: Therapeutic study, level IV.

Background: After severe trauma and hemorrhage, it is generally assumed that the rate of fluid shift from the interstitial space into the vasculature is relatively slow and that initial hematocrit (Hct) does not reflect estimated blood loss. This study challenges that idea and tests the hypothesis that initial Hct correlates with signs of shock and hemorrhage in trauma patients., Methods: Data were retrospectively reviewed from 198 trauma patients requiring emergency surgery at a Level I center from July 2009 to April 2010. Patients were divided into quartiles based on the initial Hct measured within 10 minutes of arrival. Categorical data were compared using χ(2) test or Fisher's exact test, as appropriate. Normally distributed data were compared using Student's t test or analysis of variance. Nonparametric data were compared with a Mann-Whitney U test or Kruskal-Wallis test. Post hoc analysis was conducted using the Bonferroni correction or paired Mann-Whitney U tests., Results: The study population was 83% male, aged 35 ± 1 years (mean ± SE), with 71% penetrating injuries. Lower initial Hct correlated with hypotension (p < 0.001), acidosis (p = 0.003), altered mental status (p < 0.001), Injury Severity Score (p < 0.001), Revised Trauma Score (p < 0.001), estimated blood loss (p < 0.001), and usage of packed red blood cells (p < 0.001), fresh frozen plasma (p = 0.003), crystalloid (p = 0.021), and vasopressors (p < 0.001)., Conclusion: Admission Hct correlates with signs of shock and hemorrhage in trauma patients requiring emergency surgery because fluid shifts rapidly from the interstitial space into the vasculature. This finding of a rapid Hct change contradicts the current teaching in most trauma textbooks.