Thromboelastography and rotational thromboelastometry for the surgical intensivist: A narrative review.

BACKGROUND: Viscoelastic tests (VETs), specifically thromboelastography (TEG) and rotational thromboelastometry (ROTEM), are gaining popularity in the management of critically ill surgical patients with hemorrhage or thrombosis due to their comprehensive characterization of the coagulation process and point-of-care availability in comparison to conventional coagulation tests (CCTs). We review current evidence for VET use in patients in the surgical intensive care unit (SICU). METHODS: We searched PUBMED, EMBASE and the Cochrane Library through May 30, 2018 for articles that evaluated the use of VETs in patient populations and clinical scenarios germane to the surgical intensivist. Individual articles were critically evaluated for relevance and appropriate methodology using a structured technique. Information on patient characteristics, timing and methods of CCTs/VETs, and outcomes was collected and summarized in narrative form. RESULTS: Of 2,589 identified articles, 36 were included. Five (14%) were interventional studies and 31 (86%) were observational. Twenty-five (69%) evaluated TEG, 11 (31%) ROTEM and 18 (50%) CCTs. Investigated outcomes included quantitative blood loss (13 (36%)), blood product transfusion (9 (25%)), thromboembolic events (9 (25%)) and mortality (6 (17%)). We identified 12 clinical scenarios with sufficient available evidence, much of which was of limited quantity and poor methodological quality. Nonetheless, research supports the use of VETs for guiding early blood product administration in severe traumatic hemorrhage and for the prediction of abstract excess bleeding following routine cardiac surgery. In contrast, evidence suggests VET-based heparin dosing strategies for venous thromboembolism prophylaxis are not superior to standard dosing in SICU patients. CONCLUSION: While VETs have the potential to impact the care of critically ill surgical patients in many ways, current evidence for their use is limited, mainly because of poor methodological quality of most available studies. Further high-quality research, including several ongoing randomized controlled trials, is needed to elucidate the role of TEG/ROTEM in the SICU population. LEVEL OF EVIDENCE: Systematic review, level IV.

The impact of hypothermia on outcomes in massively transfused patients.

BACKGROUND: Hypothermia is associated with poor outcomes after injury. The relationship between hypothermia during contemporary large volume resuscitation and blood product consumption is unknown. We evaluated this association, and the predictive value of hypothermia on mortality. METHODS: Patients predicted to receive massive transfusion at 12 level 1 trauma centers were randomized in the Pragmatic Randomized Optimal Platelet and Plasma Ratios (PROPPR) trial and were grouped into those who were hypothermic (<36°C) or normothermic (36-38.5°C) within the first 6 hours of emergency department arrival. The impact of hypothermia or normothermia on the volume of blood product required during the first 24 hours was determined via negative binomial regression, adjusting for treatment arm, injury severity score, mechanism, demographics, pre-emergency department fluid volume, blood administered before becoming hypothermic, pulse and systolic blood pressure on arrival, and the time exposed to hypothermic or normothermic temperatures. RESULTS: Of 680 patients, 590 had a temperature measured during the first 6 hours in hospital, and 399 experienced hypothermia. The mean number of red blood cell (RBC) units given to all patients in the first 24 hours of admission was 8.8 (95% confidence interval [CI], 7.9-9.6). In multivariable analysis, every 1°C decrease in temperature below 36.0°C was associated with a 10% increase (incidence rate ratio, 0.90; 95% CI, 0.89-0.92; p < 0.00) in consumption of RBCs during the first 24 hours of admission. There was no association between RBC administration and a temperature above 36°C. Hypothermia on arrival was an independent predictor of mortality, with an adjusted odds ratio of 2.7 (95% CI, 1.7-4.5; p < 0.00) for 24-hour mortality and 1.8 (95% CI, 1.3-2.4; p < 0.00) for 30-day mortality. CONCLUSION: Hypothermia is associated with increase in blood product consumption and mortality. These findings support the maintenance of normothermia in trauma patients and suggest that further investigation on the impact of cooling or rewarming during massive transfusion is warranted. LEVEL OF EVIDENCE: Prognostic, level III.

Harmful or Physiologic: Diagnosing Fibrinolysis Shutdown in a Trauma Cohort With Rotational Thromboelastometry.

BACKGROUND: Despite its central role in early trauma coagulopathy, abnormal fibrinolysis continues to be poorly understood. Excessive fibrinolysis is a known contributor to mortality. Recent studies with thromboelastography (TEG) suggest decreased fibrinolysis (or shutdown) may be just as harmful. Considering the broad use of 2 different viscoelastic assays, which are not interchangeable, we proposed for the first time to define and characterize fibrinolysis shutdown using rotational thromboelastometry (ROTEM). METHODS: Retrospective cohort study of severely injured patients with admission ROTEM. Shutdown was defined by the best Youden index value of the maximum lysis. Fibrinolysis phenotypes were physiologic, hyperfibrinolysis, and shutdown. Multivariable logistic regression evaluated association between Injury Severity Score and the fibrinolysis phenotypes, and the association among shutdown phenotype with mortality, blood transfusion, and thrombotic events. RESULTS: Five hundred fifty patients were included. Maximum lysis <3.5% was selected to define shutdown. Predominant phenotype was physiologic (70.7%), followed by shutdown (25.6%) and hyperfibrinolysis (3.6%). Shutdown patients had higher Injury Severity Score, lower base excess, and required more transfusions than physiologic group. Shutdown was associated with acidosis (base excess: odds ratio [OR] for a 1 mEq/L increase, 0.93; 95% confidence interval [CI], 0.88-0.98; P = .0094) and the combination of clotting derangements, higher clot firmness (maximum clot formation: OR for a 2 mm increase, 1.8; 95% CI, 1.5-2.27; P < .0001), lower fibrinogen (OR for a 0.5 g/dL decrease, 1.47; 95% CI, 1.18-1.84; P = .0006), and poor clot formation dynamics (clot formation time: OR for a 5 seconds increase, 1.25; 95% CI, 1.15-1.36; P < .0001). Fibrinolysis shutdown was not independently associated with mortality (OR, 0.61; 95% CI, 0.28-1.33; P = .21), massive transfusion (OR, 2.14; 95% CI, 0.79-5.74; P = .1308), or thrombotic events (OR, 1.08; 95% CI, 0.37-3.15; P = .874). Shutdown was associated with increased 24-hour transfusion (OR, 2.24; 95% CI, 1.24-4.04; P = .007). CONCLUSIONS: Despite higher injury burden, evidence of shock, and greater need for blood transfusions, early fibrinolysis shutdown was not associated with mortality, suggesting that it could represent an adaptive physiologic response to life-threatening trauma.

Catecholamines as outcome markers in isolated traumatic brain injury: the COMA-TBI study.

BACKGROUND: Elevated catecholamine levels might be associated with unfavorable outcome after traumatic brain injury (TBI). We investigated the association between catecholamine levels in the first 24 h post-trauma and functional outcome in patients with isolated moderate-to-severe TBI. METHODS: A cohort of 174 patients who sustained isolated blunt TBI was prospectively enrolled from three Level-1 Trauma Centers. Epinephrine (Epi) and norepinephrine (NE) concentrations were measured at admission (baseline), 6, 12 and 24 h post-injury. Outcome was assessed at 6 months by the extended Glasgow Outcome Scale (GOSE) score. Fractional polynomial plots and logistic regression models (fixed and random effects) were used to study the association between catecholamine levels and outcome. Effect size was reported as the odds ratio (OR) associated with one logarithmic change in catecholamine level. RESULTS: At 6 months, 109 patients (62.6%) had an unfavorable outcome (GOSE 5-8 vs. 1-4), including 51 deaths (29.3%). Higher admission levels of Epi were associated with a higher risk of unfavorable outcome (OR, 2.04, 95% CI: 1.31-3.18, p = 0.002) and mortality (OR, 2.86, 95% CI: 1.62-5.01, p = 0.001). Higher admission levels of NE were associated with higher risk of unfavorable outcome (OR, 1.59, 95% CI: 1.07-2.35, p = 0.022) but not mortality (OR, 1.45, 95% CI: 0.98-2.17, p = 0.07). There was no relationship between the changes in Epi levels over time and mortality or unfavorable outcome. Changes in NE levels with time were statistically associated with a higher risk of mortality, but the changes had no relation to unfavorable outcome. CONCLUSIONS: Elevated circulating catecholamines, especially Epi levels on hospital admission, are independently associated with functional outcome and mortality after isolated moderate-to-severe TBI.

Sympathoadrenal Activation is Associated with Acute Traumatic Coagulopathy and Endotheliopathy in Isolated Brain Injury.

BACKGROUND: Acute coagulopathy after traumatic brain injury (TBI) involves a complex multifactorial hemostatic response that is poorly characterized. OBJECTIVES: To examine early posttraumatic alterations in coagulofibrinolytic, endothelial, and inflammatory blood biomarkers in relation to sympathetic nervous system (SNS) activation and 6-month patient outcomes, using multivariate partial least-squares (PLS) analysis. PATIENTS AND METHODS: A multicenter observational study of 159 adult isolated TBI patients admitted to the emergency department at an urban level I trauma center, was performed. Plasma concentrations of 6 coagulofibrinolytic, 10 vascular endothelial, 19 inflammatory, and 2 catecholamine biomarkers were measured by immunoassay on admission and 24 h postinjury. Neurological outcome at 6 months was assessed using the Extended Glasgow Outcome Scale. PLS-discriminant analysis was used to identify salient biomarker contributions to unfavorable outcome, whereas PLS regression analysis was used to evaluate the covariance between SNS correlates (catecholamines) and biomarkers of coagulopathy, endotheliopathy, and inflammation. RESULTS: Biomarker profiles in patients with an unfavorable outcome displayed procoagulation, hyperfibrinolysis, glycocalyx and endothelial damage, vasculature activation, and inflammation. A strong covariant relationship was evident between catecholamines and biomarkers of coagulopathy, endotheliopathy, and inflammation at both admission and 24 h postinjury. CONCLUSIONS: Biomarkers of coagulopathy and endotheliopathy are associated with poor outcome after TBI. Catecholamine levels were highly correlated with endotheliopathy and coagulopathy markers within the first 24 h after injury. Further research is warranted to characterize the pathogenic role of SNS-mediated hemostatic alterations in isolated TBI.

Inflammatory cytokine and chemokine profiles are associated with patient outcome and the hyperadrenergic state following acute brain injury.

BACKGROUND: Traumatic brain injury (TBI) elicits intense sympathetic nervous system (SNS) activation with profuse catecholamine secretion. The resultant hyperadrenergic state is linked to immunomodulation both within the brain and systemically. Dysregulated inflammation post-TBI exacerbates secondary brain injury and contributes to unfavorable patient outcomes including death. The aim of this study was to characterize the early dynamic profile of circulating inflammatory cytokines/chemokines in patients admitted for moderate-to-severe TBI, to examine interrelationships between these mediators and catecholamines, as well as clinical indices of injury severity and neurological outcome. METHODS: Blood was sampled from 166 isolated TBI patients (aged 45 ± 20.3 years; 74.7 % male) on admission, 6-, 12-, and 24-h post-injury and from healthy controls (N = 21). Plasma cytokine [interleukin (IL)-1ß, -2, -4, -5, -10, -12p70, -13, tumor necrosis factor (TNF)-α, interferon (IFN)-γ] and chemokine [IL-8, eotaxin, eotaxin-3, IFN-γ-induced protein (IP)-10, monocyte chemoattractant protein (MCP)-1, -4, macrophage-derived chemokine (MDC), macrophage inflammatory protein (MIP)-1ß, thymus activation regulated chemokine (TARC)] concentrations were analyzed using high-sensitivity electrochemiluminescence multiplex immunoassays. Plasma catecholamines [epinephrine (Epi), norepinephrine (NE)] were measured by immunoassay. Neurological outcome at 6 months was assessed using the extended Glasgow outcome scale (GOSE) dichotomized as good (>4) or poor (≤4) outcomes. RESULTS: Patients showed altered levels of IL-10 and all chemokines assayed relative to controls. Significant differences in a number of markers were evident between moderate and severe TBI cohorts. Elevated IL-8, IL-10, and TNF-α, as well as alterations in 8 of 9 chemokines, were associated with poor outcome at 6 months. Notably, a positive association was found between Epi and IL-1ß, IL-10, Eotaxin, IL-8, and MCP-1. NE was positively associated with IL-1ß, IL-10, TNF-α, eotaxin, IL-8, IP-10, and MCP-1. CONCLUSIONS: Our results provide further evidence that exaggerated SNS activation acutely after isolated TBI in humans may contribute to harmful peripheral inflammatory cytokine/chemokine dysregulation. These findings are consistent with a potentially beneficial role for therapies aimed at modulating the inflammatory response and hyperadrenergic state acutely post-injury.

Fresh frozen plasma: red blood cells (1:2) coagulation effect is equivalent to 1:1 and whole blood.

BACKGROUND: Preemptive treatment of trauma-associated coagulopathy involves transfusion of fresh frozen plasma (FFP) at 1:1 ratio with red blood cells (RBCs), but the optimal ratio remains controversial. In combat theaters, fresh whole blood (FWB) is also an option. The objective of this study was to determine the effect of FFP:RBC ratios 1:1, 1:2, 1:3 and FWB on coagulation during resuscitation. MATERIALS AND METHODS: Thirty-six rats were randomized in the following six groups: Group 1: sham; Group 2: hemorrhage followed by sole lactated Ringer (LR) infusion; Group 3: FFP:RBC (1:1); Group 4: FFP:RBC (1:2); Group 5: FFP:RBC (1:3); Group 6: FWB transfusion. Another 25 animals were used for blood harvesting. Hemorrhage was induced by withdrawing 40% of total blood volume, mean arterial pressure (MAP) decreased to 45% of baseline, and laparotomy. Animals underwent LR infusion followed by blood product transfusion preset for each group. Blood samples were obtained at baseline and in the 105th minute for thromboelastometry and lactate. RESULTS: Hemorrhage caused a significant decrease in MAP and increase in lactate (P < 0.05). MAP was persistently low in group 2 despite fluid infusion (P < 0.05), but not in the other groups after 20 min of resuscitation. Mean clot formation time, alpha angle, and maximum clot firmness decreased significantly (P < 0.05) in group 2 (LR) and group 5 (1:3) compared with other groups. CONCLUSIONS: FFP:RBC in a 1:2 ratio optimally harnessed hemostatic resuscitation and prudent use of blood products compared with 1:1 and 1:3 ratios and to FWB transfusion.

Blood Biomarkers in Moderate-To-Severe Traumatic Brain Injury: Potential Utility of a Multi-Marker Approach in Characterizing Outcome.

BACKGROUND: Blood biomarkers are valuable tools for elucidating complex cellular and molecular mechanisms underlying traumatic brain injury (TBI). Profiling distinct classes of biomarkers could aid in the identification and characterization of initial injury and secondary pathological processes. This study characterized the prognostic performance of a recently developed multi-marker panel of circulating biomarkers that reflect specific pathogenic mechanisms including neuroinflammation, oxidative damage, and neuroregeneration, in moderate-to-severe TBI patients. MATERIALS AND METHODS: Peripheral blood was drawn from 85 isolated TBI patients (n = 60 severe, n = 25 moderate) at hospital admission, 6-, 12-, and 24-h post-injury. Mortality and neurological outcome were assessed using the extended Glasgow Outcome Scale. A multiplex platform was designed on MULTI-SPOT(®) plates to simultaneously analyze human plasma levels of s100 calcium binding protein beta (s100B), glial fibrillary acidic protein (GFAP), neuron specific enolase (NSE), brain-derived neurotrophic factor (BDNF), monocyte chemoattractant protein (MCP)-1, intercellular adhesion molecule (ICAM)-5, and peroxiredoxin (PRDX)-6. Multivariable logistic regression and area under the receiver-operating characteristic curve (AUC) were used to evaluate both individual and combined predictive abilities of these markers for 6-month neurological outcome and mortality after TBI. RESULTS: Unfavorable neurological outcome was associated with elevations in s100B, GFAP, and MCP-1. Mortality was related to differences in six of the seven markers analyzed. Combined admission concentrations of s100B, GFAP, and MCP-1 were able to discriminate favorable versus unfavorable outcome (AUC = 0.83), and survival versus death (AUC = 0.87), although not significantly better than s100B alone (AUC = 0.82 and 0.86, respectively). CONCLUSION: The multi-marker panel of TBI-related biomarkers performed well in discriminating unfavorable and favorable outcomes in the acute period after moderate-to-severe TBI. However, the combination of these biomarkers did not outperform s100B alone.

Multivariate analysis of traumatic brain injury: development of an assessment score.

Important challenges for the diagnosis and monitoring of mild traumatic brain injury (mTBI) include the development of plasma biomarkers for assessing neurologic injury, monitoring pathogenesis, and predicting vulnerability for the development of untoward neurologic outcomes. While several biomarker proteins have shown promise in this regard, used individually, these candidates lack adequate sensitivity and/or specificity for making a definitive diagnosis or identifying those at risk of subsequent pathology. The objective for this study was to evaluate a panel of six recognized and novel biomarker candidates for the assessment of TBI in adult patients. The biomarkers studied were selected on the basis of their relative brain-specificities and potentials to reflect distinct features of TBI mechanisms including (1) neuronal damage assessed by neuron-specific enolase (NSE) and brain derived neurotrophic factor (BDNF); (2) oxidative stress assessed by peroxiredoxin 6 (PRDX6); (3) glial damage and gliosis assessed by glial fibrillary acidic protein and S100 calcium binding protein beta (S100b); (4) immune activation assessed by monocyte chemoattractant protein 1/chemokine (C-C motif) ligand 2 (MCP1/CCL2); and (5) disruption of the intercellular adhesion apparatus assessed by intercellular adhesion protein-5 (ICAM-5). The combined fold-changes in plasma levels of PRDX6, S100b, MCP1, NSE, and BDNF resulted in the formulation of a TBI assessment score that identified mTBI with a receiver operating characteristic (ROC) area under the curve of 0.97, when compared to healthy controls. This research demonstrates that a profile of biomarker responses can be used to formulate a diagnostic score that is sensitive for the detection of mTBI. Ideally, this multivariate assessment strategy will be refined with additional biomarkers that can effectively assess the spectrum of TBI and identify those at particular risk for developing neuropathologies as consequence of a mTBI event.

Prehospital Resuscitation of Traumatic Hemorrhagic Shock with Hypertonic Solutions Worsens Hypocoagulation and Hyperfibrinolysis.

Impaired hemostasis frequently occurs after traumatic shock and resuscitation. The prehospital fluid administered can exacerbate subsequent bleeding and coagulopathy. Hypertonic solutions are recommended as first-line treatment of traumatic shock; however, their effects on coagulation are unclear. This study explores the impact of resuscitation with various hypertonic solutions on early coagulopathy after trauma. We conducted a prospective observational subgroup analysis of large clinical trial on out-of-hospital single-bolus (250 mL) hypertonic fluid resuscitation of hemorrhagic shock trauma patients (systolic blood pressure, ≤70 mmHg). Patients received 7.5% NaCl (HS), 7.5% NaCl/6% Dextran 70 (HSD), or 0.9% NaCl (normal saline [NS]) in the prehospital setting. Thirty-four patients were included: 9 HS, 8 HSD, 17 NS. Treatment with HS/HSD led to higher admission systolic blood pressure, sodium, chloride, and osmolarity, whereas lactate, base deficit, fluid requirement, and hemoglobin levels were similar in all groups. The HSD-resuscitated patients had higher admission international normalized ratio values and more hypocoagulable patients, 62% (vs. 55% HS, 47% NS; P < 0.05). Prothrombotic tissue factor was elevated in shock treated with NS but depressed in both HS and HSD groups. Fibrinolytic tissue plasminogen activator and anti-fibrinolytic plasminogen activator inhibitor type 1 were increased by shock but not thrombin-activatable fibrinolysis inhibitor. The HSD patients had the worst imbalance between procoagulation/anticoagulation and profibrinolysis/antifibrinolysis, resulting in more hypocoagulability and hyperfibrinolysis. We concluded that resuscitation with hypertonic solutions, particularly HSD, worsens hypocoagulability and hyperfibrinolysis after hemorrhagic shock in trauma through imbalances in both procoagulants and anticoagulants and both profibrinolytic and antifibrinolytic activities.

Detailed description of all deaths in both the shock and traumatic brain injury hypertonic saline trials of the Resuscitation Outcomes Consortium.

OBJECTIVE: To identify causes and timing of mortality in trauma patients to determine targets for future studies. BACKGROUND: In trials conducted by the Resuscitation Outcomes Consortium in patients with traumatic hypovolemic shock (shock) or traumatic brain injury (TBI), hypertonic saline failed to improve survival. Selecting appropriate candidates is challenging. METHODS: Retrospective review of patients enrolled in multicenter, randomized trials performed from 2006 to 2009. Inclusion criteria were as follows: injured patients, age 15 years or more with hypovolemic shock [systolic blood pressure (SBP) ≤ 70 mm Hg or SBP 71-90 mm Hg with heart rate ≥ 108) or severe TBI [Glasgow Coma Score (GCS) ≤ 8]. Initial fluid administered was 250 mL of either 7.5% saline with 6% dextran 70, 7.5% saline or 0.9% saline. RESULTS: A total of 2061 subjects were enrolled (809 shock, 1252 TBI) and 571 (27.7%) died. Survivors were younger than nonsurvivors [30 (interquartile range 23) vs 42 (34)] and had a higher GCS, though similar hemodynamics. Most deaths occurred despite ongoing resuscitation. Forty-six percent of deaths in the TBI cohort were within 24 hours, compared with 82% in the shock cohort and 72% in the cohort with both shock and TBI. Median time to death was 29 hours in the TBI cohort, 2 hours in the shock cohort, and 4 hours in patients with both. Sepsis and multiple organ dysfunction accounted for 2% of deaths. CONCLUSIONS: Most deaths from trauma with shock or TBI occur within 24 hours from hypovolemic shock or TBI. Novel resuscitation strategies should focus on early deaths, though prevention may have a greater impact.

Vagus nerve stimulation improves coagulopathy in hemorrhagic shock: a thromboelastometric animal model study.

INTRODUCTION: Inflammation plays a major role in the multifactorial process of trauma associated coagulopathy. The vagus nerve regulates the cholinergic anti-inflammatory pathway. We hypothesized that efferent vagus nerve stimulation (VNS) can improve coagulopathy by modulating the inflammatory response to hemorrhage. METHODS: Wistar rats (n = 24) were divided in 3 groups: Group (G1) Sham hemorrhagic shock (HS); (G2) HS w/o VNS; (G3) HS followed by division of the vagus nerves and VNS of the distal stumps. Hemorrhage (45% of baseline MAPx15 minutes) was followed by normotensive resuscitation with LR. Vagus nerves were stimulated (3.5 mA, 5 Hz) for 30 sec 7 times. Samples were obtained at baseline and at 60 minutes for thromboelastometry (Rotem®) and cytokine assays (IL-1 and IL-10). ANOVA was used for statistical analysis; significance was set at p < 0.05. RESULTS: Maximum clot firmness (MCF) significantly decreased in G2 after HS (71.5 ± 1.5 vs. 64 ± 1.6) (p < 0.05). MCF significantly increased in G3 compared to baseline (67.3 ± 2.7 vs. 71.5 ± 1.2) (p < 0.05). G3 also showed significant improvement in Alfa angle, and Clot Formation Time (CFT) compared to baseline. IL-1 increased significantly in group 2 and decrease in group 3, while IL-10 increased in group 3 (p < 0.05). CONCLUSIONS: Electrical stimulation of efferent vagus nerves, during resuscitation (G3), decreases inflammatory response to hemorrhage and improves coagulation.

Prehospital hypertonic saline resuscitation attenuates the activation and promotes apoptosis of neutrophils in patients with severe traumatic brain injury.

BACKGROUND: Activation of polymorphonuclear neutrophils (PMNs) is thought to contribute to traumatic brain injury (TBI). Since hypertonic fluids can inhibit PMN activation, we studied whether hypertonic fluid resuscitation can reduce excessive PMN activation in TBI patients. METHODS: Trauma patients with severe TBI were resuscitated with 250 mL of either 7.5% hypertonic saline (HS; n = 22), HS + 6% dextran-70 (HSD; n = 22), or 0.9% normal saline (NS; n = 39), and blood samples were collected on hospital admission and 12 and 24 h after resuscitation. Polymorphonuclear neutrophil activation (CD11b, CD62L, CD64) and degranulation (CD63, CD66b, CD35) markers and oxidative-burst activity, as well as spontaneous PMN apoptosis were measured by flow cytometry. RESULTS: Relative to healthy controls, TBI patients showed increased PMN activation and decreased apoptosis of PMNs. In the HS group, but not in the HSD group, markers of PMN adhesion (CD11b, CD64) and degranulation (CD35, CD66b) were significantly lower than those in the NS group. These effects were particularly pronounced 12 h after resuscitation. Treatment with HS and HSD inhibited PMN oxidative burst responses compared with NS-treated patients. Hypertonic saline alone partially restored delayed PMN apoptosis. Despite these differences, the groups did not differ in clinical outcome parameters such as mortality and Extended Glasgow Outcome Scale. CONCLUSIONS: This study demonstrates that prehospital resuscitation with HS can partially restore normal PMN activity and the apoptotic behavior of PMNs, whereas resuscitation with HSD was largely ineffective. Although the results are intriguing, additional research will be required to translate these effects of HS into treatment strategies that improve clinical outcome in TBI patients.

Physical rehabilitation of the critically ill trauma patient in the ICU.

OBJECTIVES: To 1) review the existing evidence for early mobilization of the critically ill patients in the ICU with polytrauma; 2) provide intensivists with an introduction to the biomechanics, physiology, and nomenclature of injuries; 3) summarize the evidence for early mobilization in each anatomic area; and 4) provide recommendations for the mobilization of these patients. DATA SOURCES: A literature search of the MEDLINE and EMBASE databases for articles published in English between 1980 and 2011. STUDY SELECTION: Studies pertaining to physical therapy and rehabilitation in trauma patients were selected. Articles were excluded if they dealt with pediatrics, geriatrics, burn injuries, isolated hand injuries, chronic (i.e., not acute) injuries, nontraumatic conditions, and pressure/decubitus ulcers, were in a language other than English, were published only in abstract form, were letters to the editor, were case reports, or were published prior to 1980. DATA EXTRACTION: Reviewers extracted data and summarized results according to anatomical areas. DATA SYNTHESIS: Of 1,411 titles and abstracts, 103 met inclusion criteria. We found no articles specifically addressing the rehabilitation of polytrauma patients in the ICU setting or patients with polytrauma in general. We summarized the articles addressing the role of mobilization for specific injuries and treatments. We used this evidence, in combination with biologic rationale and physician and surgeon experience and expertise, to summarize the important considerations when providing physical therapy to these patients in the ICU setting. CONCLUSIONS: There is a paucity of evidence addressing the role of early mobilization of ICU patients with polytrauma and patients with polytrauma in general. Evidence for the beneficial role of early mobilization of specific injuries exists. Important considerations when applying a strategy of early physical therapy and mobilization to this distinctive patient group are summarized.

Selective non-operative management of abdominal gunshot wounds: survey of practise.

BACKGROUND: There is a growing body of evidence attesting to the effectiveness and safety of selective non-operative management (SNOM) of abdominal gunshot wounds. However, much of the research which supports this conclusion has originated from a few centres, and the actual utilisation of SNOM by trauma surgeons is not known. We therefore conducted a survey to assess the acceptance of this strategy and evaluate variations in practise. METHODS: Electronic questionnaire survey of trauma surgeons in the United States of America, Canada, Brazil, and South Africa. Responses were compared using Chi(2) and Fisher's exact tests. RESULTS: 183 replies were received. 105 (57%) respondents practise SNOM of abdominal gunshot wounds, but there are marked regional variations in the acceptance of this strategy (p<0.01). Respondents who had completed trauma (p<0.01) or critical care (p<0.01) fellowships, and those who practise in a higher volume centre (defined as >50 penetrating abdominal injuries seen per year) (p<0.01) are more likely to practise SNOM of gunshot wounds. Most surgeons who practise SNOM regard peritonitis, omental and bowel evisceration, and being unable to evaluate a patient as a contraindication to attempting non-operative management. Almost all regard CT as essential. Respondents' preparedness to consider SNOM is related to injury extent. CONCLUSIONS: SNOM of abdominal gunshot wounds is practised by trauma surgeons in all four countries surveyed, but is not universally accepted, and there are variations in how it is practised.