Prehospital triage for mass casualty incidents using the META method for early surgical assessment: retrospective validation of a hospital trauma registry.

BACKGROUND: In mass casualty incidents (MCI), death usually occurs within the first few hours and thus early transfer to a trauma centre can be crucial in selected cases. However, most triage systems designed to prioritize the transfer to hospital of these patients do not assess the need for surgery, in part due to inconclusive evidence regarding the value of such an assessment. Therefore, the aim of the present study was to evaluate the capacity of a new triage system-the Prehospital Advanced Triage Method (META)-to identify victims who could benefit from urgent surgical assessment in case of MCI. METHODS: Retrospective, descriptive, observational study of a multipurpose cohort of patients included in the severe trauma registry of the Gregorio Marañón University General Hospital (Spain) between June 1993 and December 2011. All data were prospectively evaluated. All patients were evaluated with the META system to determine whether they met the criteria for urgent transfer. The META defines patients in need of urgent surgical assessment: (a) All penetrating injuries to head, neck, torso and extremities proximal to elbow or knee, (b) Open pelvic fracture, (c) Closed pelvic fracture with mechanical or haemodynamic instability and (d) Blunt torso trauma with haemodynamic instability. Patients who fulfilled these criteria were designated as "Urgent Evacuation for Surgical Assessment" (UESA) cases; all other cases were designated as non-UESA. The following variables were assessed: patient status at the scene; severity scales [RTS, Shock index, MGAP (Mechanism, Glasgow coma scale, Age, pressure), GCS]; need for surgery and/or interventional procedure to control bleeding (UESA); and mortality. The two groups (UESA vs. non-UESA) were then compared. RESULTS: A total of 1882 cases from the database were included in the study. Mean age was 39.2 years and most (77%) patients were male. UESA patients presented significantly worse on-scene hemodynamic parameters (systolic blood pressure and heart rate) and greater injury severity (RTS, shock index, and MGAP scales). No differences were observed for respiratory rate, need for orotracheal intubation, or GCS scores. The anatomical injuries of patients in the UESA group were less severe but these patients had a greater need for urgent surgery and higher mortality rates. CONCLUSION: These findings suggest that the META triage classification system could be beneficial to help identify patients with severe trauma and/or in need of urgent surgical assessment at the scene of injury in case of MCI. These findings demonstrate that, in this cohort, the META fulfils the purpose for which it was designed.

Endothelial glycocalyx shedding in patients with burns.

Shedding of syndecan-1 from the endothelial glycocalyx layer (EGL), referred to as endotheliopathy of trauma (EoT), is associated with poorer outcomes. This study aims to determine if EoT is also present in the burn population. We enrolled 458 burn and non-burn trauma patients at a Level 1 trauma center and defined EoT by a syndecan-1 level of ≥40 ng/mL. Sixty-eight of the enrolled patients had burns with a median TBSA of 19%, with 27.9% also suffering inhalational injury (II). Mortality was similar between the burn and non-burn group, also for patients with EoT. The incidence of II was significantly greater in the EoT+ burn group compared to the EoT- group (p = 0.038). Patients with II received significantly larger amounts of i.v. fluids (p = 0.001). The incidence of EoT was significantly different between the II-groups, as was mortality (pEoT = 0.038, pmortality < 0.001). EoT is attributed to the shock rather than the mechanism of trauma and may in burns be associated to II rather than TBSA. Patients with burns and II had worse outcomes and higher mortality compared to patients with burns alone. Burn injury induces EGL shedding similar to that in non-burn patients with EoT, and results in similar higher rate of mortality.

NF-κB mediates early blood-brain barrier disruption in a rat model of traumatic shock.

BACKGROUND: Blood-brain barrier (BBB) disruption is associated with a large number of central nervous system and systemic disorders. The aim of the present study was to investigate the dynamic change of BBB changes during traumatic shock and resuscitation as well as the mechanisms involved. METHODS: The experiments were performed on male Sprague-Dawley rats anesthetized with pentobarbital sodium. To produce traumatic shock, the rats were subjected to bilateral femoral traumatic fracture and blood withdrawal from the femoral artery to decrease mean arterial pressure (MAP) to 35 mm Hg. Hypovolemic status (at a MAP of 35 to 40 mm Hg) was sustained for 1 hour followed by fluid resuscitation with shed blood and 20 mL/kg of lactated Ringer's solution. RESULTS: The rats were sacrificed at 1 hour, 2 hours, or 6 hours after fluid resuscitation. Blood-brain barrier permeability studies showed that traumatic shock significantly increased brain water contents and sodium fluorescein leakage, which was aggravated by fluid resuscitation. Real-time reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analyses revealed that Na-K-Cl cotransporter-1 and vascular endothelial growth factor (VEGF) expression were upregulated in cortical brain tissue of traumatic shock rats, and this change was accompanied by downregulation of occludin and claudin-5. Traumatic shock also significantly increased the protein levels of NF-κB-p65 subunit. Of note, administration of NF-κB inhibitor PDTC effectively attenuated augmentation of the above changes. CONCLUSION: Our results suggest that traumatic shock is associated with early BBB disruption, and inhibition of NF-κB may be an effective therapeutic strategy in protecting the BBB under traumatic shock conditions.

Gender differences in trauma, shock and sepsis.

Despite efforts in prevention and intensive care, trauma and subsequent sepsis are still associated with a high mortality rate. Traumatic injury remains the main cause of death in people younger than 45 years and is thus a source of immense social and economic burden. In recent years, the knowledge concerning gender medicine has continuously increased. A number of studies have reported gender dimorphism in terms of response to trauma, shock and sepsis. However, the advantageous outcome following trauma-hemorrhage in females is not due only to sex. Rather, it is due to the prevailing hormonal milieu of the victim. In this respect, various experimental and clinical studies have demonstrated beneficial effects of estrogen for the central nervous system, the cardiopulmonary system, the liver, the kidneys, the immune system, and for the overall survival of the host. Nonetheless, there remains a gap between the bench and the bedside. This is most likely because clinical studies have not accounted for the estrus cycle. This review attempts to provide an overview of the current level of knowledge and highlights the most important organ systems responding to trauma, shock and sepsis. There continues to be a need for clinical studies on the prevailing hormonal milieu following trauma, shock and sepsis.

Poor microcirculatory flow dynamics are associated with endothelial cell damage and glycocalyx shedding after traumatic hemorrhagic shock.

BACKGROUND: Endothelial cell damage and glycocalyx shedding after trauma can increase the risk of inflammation, coagulopathy, vascular permeability, and death. Bedside sublingual video-microscopy may detect worse flow and perfusion associated with this endotheliopathy. We compared markers of endotheliopathy with physical flow dynamics after traumatic hemorrhagic shock. METHODS: Sublingual incident dark field video-microscopy was performed at three time points after injury (<10 hours, 10-30 hours, and 30-50 hours). Values for microcirculatory flow index (MFI), Point Of carE Microcirculation assessment (POEM) score, proportion of perfused vessels (PPV), microcirculatory heterogeneity index (MHI), perfused vessel density (PVD), and total vessel density (TVD) were obtained. ELISAs were performed to measure concentrations of thrombomodulin and syndecan-1 as biomarkers of endothelial cell damage and glycocalyx shedding respectively. Flow parameters were dichotomized to above and below average, and biomarkers compared between groups; below average MFI, POEM, PPV, PVD, and TVD, and above average MHI were considered poor microcirculatory flow dynamics. RESULTS: A total of 155 sublingual video-microscopy clips corresponding to 39 time points from 17 trauma patients were analyzed. Median age was 35 (IQR 25-52); 16/17 were men. Within 10 hours of injury, syndecan-1 concentrations were significantly higher compared to 17 age- and sex-matched healthy controls (30 [IQR 20-44] ng/mL) for worse TVD (78 [IQR 63-417] ng/mL), PVD (156 [IQR 63-590] ng/mL), PPV (249 [IQR 64-578] ng/mL), MFI (249 [IQR 64-578] ng/mL), MHI (45 [IQR] 38-68) ng/mL), and POEM scores (108 [IQR 44-462] ng/mL) (all p < 0.01). Thrombomodulin was also raised within 10 hours of injury when compared to healthy controls (2.9 [IQR 2.2-3.4] ng/mL) for worse PPV (4.1 [IQR 3.4-6.2] ng/mL) and MFI (4.1 [IQR 3.4-6.2] ng/mL) (both p < 0.05). CONCLUSIONS: Endothelial cell damage and glycocalyx shedding are associated with worse flow, density, and heterogeneity within microvessels after traumatic hemorrhagic shock. The clinical utility of these biomarkers and flow parameters at the bedside are yet to be elucidated. LEVEL OF EVIDENCE: Prognostic study, level III.

A retrospective analysis of the respiratory adjusted shock index to determine the presence of occult shock in trauma patients.

BACKGROUND: The shock index (SI), calculated as hear rate/systolic blood pressure, is a simple hemodynamic marker that may be used to assess for the presence of occult shock in trauma patients. The normal range for a healthy adult patient is 0.5 to 0.7. Recently, studies have demonstrated that tachypnea is the most important predictor of cardiac arrest in hospital wards and is an important indicator of derangements across multiple organ systems. As such, we have sought to determine whether the inclusion of the patient's respiratory rate (RR) to the already existing SI (called the Respiratory Adjusted Shock Index [RASI]), calculated as hear rate/systolic blood pressure*(RR/10), will improve the overall diagnostic accuracy of detecting patients in early occult shock. METHODS: A retrospective chart review over a 4-year period (2012-2016) at an urban, Level I trauma center was performed. All patients admitted to hospital for trauma were included in the study. Exclusion criteria were patients in traumatic arrest or in overt shock. Charts were reviewed for triage vital signs and point of care lactate drawn within 30 minutes of presentation. A lactate greater than 2 mmol/L was used to determine presence of hypoperfusion. The upper limit of normal for the RASI was calculated by multiplying the upper limit of the SI by 1.9 (RR of 19 divided by 10) and validated internally. RESULTS: A total of 3,093 patients were included in this study. There was no difference in SI for patients discharged versus patients admitted, 0.6 (95% CI, 0.5-0.7) versus 0.7 (95% CI, 0.5-0.8) and a significant difference between the same groups of patients (discharged vs. admitted) for the RASI, 1.1 (95% CI, 1.04-1.18) versus 1.46 (95% CI, 1.35-1.55), respectively. Area under the curve for SI was 0.58 and for the RASI score was 0.94. CONCLUSION: The RASI score improves diagnostic accuracy for detecting early occult shock in trauma patients when compared to the SI. LEVEL OF EVIDENCE: Diagnostic, level II.

Comparison of 3% and 7.5% Hypertonic Saline in Resuscitation After Traumatic Hypovolemic Shock.

Hypertonic saline solutions (HSSs) (7.5%) are useful in the resuscitation of patients with hypovolemic shock because they provide immediate intravascular volume expansion via the delivery of a small volume of fluid, improving cardiac function. However, the effects of using 3% HSS in hypovolemic shock resuscitation are not well known. This study was designed to compare the effects of and complications associated with 3% HSS, 7.5% HSS, and standard fluid in resuscitation. In total, 294 severe trauma patients were enrolled from December 2008 to February 2012 and subjected to a double-blind randomized clinical trial. Individual patients were treated with 3% HSS (250 mL), 7.5% HSS (250 mL), or lactated Ringer's solution (LRS) (250 mL). Mean arterial pressure, blood pressure, and heart rate were monitored and recorded before fluid infusion and at 10, 30, 45, and 60 min after infusion, and the incidence of complications and survival rate were analyzed. The results indicate that 3% and 7.5% HSSs rapidly restored mean arterial pressure and led to the requirement of an approximately 50% lower total fluid volume compared with the LRS group (P < 0.001). However, a single bolus of 7.5% HSS resulted in an increase in heart rate (mean of 127 beats/min) at 10 min after the start of resuscitation. Higher rates of arrhythmia and hypernatremia were noted in the 7.5% HSS group, whereas higher risks of renal failure (P< 0.001), coagulopathy (P < 0.001), and pulmonary edema (P < 0.001) were observed in the LRS group. Neither severe electrolyte disturbance nor anaphylaxis was observed in the HSS groups. It is notable that 3% HSS had similar effects on resuscitation because both the 7.5% HSS and LRS groups but resulted in a lower occurrence of complications. This study demonstrates the efficacy and safety of 3% HSS in the resuscitation of patients with hypovolemic shock.

Resuscitation strategies with different arterial pressure targets after surgical management of traumatic shock.

INTRODUCTION: Hypotensive fluid resuscitation has a better effect before and during surgical intervention for multiple trauma patients with haemorrhagic shock. However, it is questionable whether hypotensive fluid resuscitation is suitable after surgical intervention for these patients, and whether resuscitation with different mean arterial pressure (MAP) targets after surgical intervention can obtain different results. The aim of this study was to investigate these questions and to explore the underlying mechanisms. METHODS: A total of 30 anesthetized piglets were randomly divided into 3 groups (n = 10 per group): low MAP, middle MAP, and high MAP, which had MAP targets of 60, 80, and 100 mmHg, respectively. All animals underwent femur fracture, intestine and liver injury, haemorrhagic shock, early hypotensive resuscitation, and surgical intervention. Then, the animals received fluid resuscitation with different MAP targets as mentioned above for 24 hours. Hemodynamic parameters and vital organ functions were evaluated. RESULTS: Fluid resuscitation in the 80 mmHg MAP group maintained haemodynamic stability, tissue perfusion, and organ function better than that in the other groups. The 60 mmHg MAP group presented with profound metabolic acidosis and organ histopathologic damage. In addition, animals in the 100 mmHg MAP group exhibited severe tissue oedema, organ function failure, and histopathologic damage. CONCLUSIONS: In our porcine model of resuscitation, targeting high MAP by fluid administration alone resulted in a huge increase in the infusion volume, severe tissue oedema, and organ dysfunction. Meanwhile, targeting low MAP resulted in persistent tissue hypoperfusion and metabolic stress. Hence, a resuscitation strategy of targeting appropriate MAP might be compatible with maintaining haemodynamic stability, tissue perfusion, and organ function.

Local hemostasis, immunothrombosis, and systemic disseminated intravascular coagulation in trauma and traumatic shock.

Knowing the pathophysiology of trauma-induced coagulopathy is important for the management of severely injured trauma patients. The aims of this review are to provide a summary of the recent advances in our understanding of thrombosis and hemostasis following trauma and to discuss the pathogenesis of disseminated intravascular coagulation (DIC) at an early stage of trauma. Local hemostasis and thrombosis respectively act to induce physiological wound healing of injuries and innate immune responses to damaged-self following trauma. However, if overwhelmed by systemic inflammation caused by extensive tissue damage and tissue hypoperfusion, both of these processes foster systemic DIC associated with pathological fibrin(ogen)olysis. This is called DIC with the fibrinolytic phenotype, which is characterized by the activation of coagulation, consumption coagulopathy, insufficient control of coagulation, and increased fibrin(ogen)olysis. Irrespective of microvascular thrombosis, the condition shows systemic thrombin generation as well as its activation in the circulation and extensive damage to the microvasculature endothelium. DIC with the fibrinolytic phenotype gives rise to oozing-type non-surgical bleeding and greatly affects the prognosis of trauma patients. The coexistences of hypothermia, acidosis, and dilution aggravate DIC and lead to so-called trauma-induced coagulopathy. He that would know what shall be must consider what has been. The Analects of Confucius.

Beneficial effect of cyclosporine A on traumatic hemorrhagic shock.

BACKGROUND: Vascular hyporeactivity plays an important role in severe trauma and shock. We investigated the beneficial effect of cyclosporine A (CsA) on traumatic shock and its relationship to vascular reactivity improvement and mitochondrial permeability transition pore (MPTP). MATERIALS AND METHODS: Sodium pentobarbital-anesthetized rats were used to induce traumatic hemorrhagic shock by left femur fracture and hemorrhage, the beneficial effects of CsA (1, 5, and 10 mg/kg, intravenously) on animal survival, cardiovascular function, tissue blood perfusion, and mitochondrial function of vital organs were observed. In addition, hypoxia-treated vascular smooth muscle cells from normal rats were used to investigate the relationship of this beneficial effect of CsA to Rho-associated serine/threonine kinase (ROCK) and protein kinase C. RESULTS: CsA prolonged the survival time and increased the 24-h survival rate of traumatic hemorrhagic shock (31%, 56%, and 56% in 1, 5, and 10 mg/kg CsA group versus 25% in lactated Ringer solution group). Five milligrams per kilogram of CsA had the best effect, which stabilized and improved the hemodynamics, increased the tissue blood flow, and improved the liver and kidney function including its mitochondrial function in shock rats. CsA had no significant influences on the production of inflammatory mediators and cardiac output after traumatic hemorrhagic shock. Further results indicated that CsA significantly improved the vascular constriction and dilation reactivity of superior mesenteric artery to norepinephrine and acetylcholine, which was antagonized by ROCK inhibitor, Y27632, but not by protein kinase C inhibitor, staurosporine. Further studies showed that CsA restored hypoxia-induced decrease of ROCK activity and inhibited the opening of MPTP in hypoxia-treated vascular smooth muscle cells. CONCLUSIONS: CsA is beneficial for the treatment of traumatic hemorrhagic shock. The mechanism is mainly through improving the vascular reactivity, stabilizing the hemodynamics, and increasing tissue perfusion. This beneficial effect of CsA is related to the inhibitory effect of CsA on MPTP opening. ROCK is an important regulator molecule in this process.

Understanding traumatic shock: out-of-hospital hypotension with and without other physiologic compromise.

BACKGROUND: Among trauma patients with out-of-hospital hypotension, we evaluated the predictive value of systolic blood pressure (SBP) with and without other physiologic compromise for identifying trauma patients requiring early critical resources. METHODS: This was a secondary analysis of a prospective cohort of injured patients 13 years or older with out-of-hospital hypotension (SBP ≤ 90 mm Hg) who were transported by 114 emergency medical service agencies to 56 Level I and II trauma centers in 11 regions of the United States and Canada from January 1, 2010, through June 30, 2011. The primary outcome was early critical resource use, defined as blood transfusion of 6 U or greater, major nonorthopedic surgery, interventional radiology, or death within 24 hours. RESULTS: Of 3,337 injured patients with out-of-hospital hypotension, 1,094 (33%) required early critical resources and 1,334 (40%) had serious injury (Injury Severity Score [ISS] ≥ 16). Patients with isolated hypotension required less early critical resources (14% vs. 52%), had less serious injury (20% vs. 61%), and had lower mortality (24 hours, 1% vs. 26%; in-hospital, 3% vs. 34%). The standardized probability of requiring early critical resources was lowest among patients with blunt injury and isolated moderate hypotension (0.12; 95% confidence interval, 0.09-0.15) and steadily increased with additional physiologic compromise, more severe hypotension, and penetrating injury (0.94; 95% confidence interval, 0.90-0.98). CONCLUSION: A minority of trauma patients with isolated out-of-hospital hypotension require early critical resuscitation resources. However, hypotension accompanied by additional physiologic compromise or penetrating injury markedly increases the probability of requiring time-sensitive interventions. LEVEL OF EVIDENCE: Prognostic study, level II.

Pediatric specific shock index accurately identifies severely injured children.

INTRODUCTION: Shock index (SI) (heart rate/systolic blood pressure)>0.9 predicts mortality in adult trauma patients. We hypothesized that age adjusted SI could more accurately predict outcomes in children. METHODS: Retrospective review of children age 4-16 years admitted to two trauma centers between 1/07 and 6/13 following blunt trauma with an injury severity score (ISS)>15 was performed. We evaluated the ability of SI>0.9 at emergency department presentation and elevated shock index, pediatric age adjusted (SIPA) to predict outcomes. SIPA was defined by maximum normal HR and minimum normal SBP by age. Cutoffs included SI>1.22 (age 4-6), >1.0 (7-12), and >0.9 (13-16). RESULTS: Among 543 children, 50% of children had an SI>0.9 but this fell to 28% using age adjusted SI (SIPA). SIPA demonstrated improved discrimination of severe injury relative to SI: ISS>30: 37% vs 26%; blood transfusion within the first 24 hours: 27% vs 20%; Grade III liver/spleen laceration requiring blood transfusion: 41% vs 26%; and in-hospital mortality: 11% vs 7%. CONCLUSION: A pediatric specific shock index (SIPA) more accurately identifies children who are most severely injured, have intraabdominal injury requiring transfusion, and are at highest risk of death when compared to shock index unadjusted for age.

A 10-second fluid challenge guided by transthoracic echocardiography can predict fluid responsiveness.

INTRODUCTION: The accurate assessment of intravascular volume status for the therapy of severe hypovolemia and shock is difficult and critical to critically ill patients. Non-invasive evaluation of fluid responsiveness by the rapid infusion of a very limited amount of volume is an important clinical goal. This study aimed to test whether echocardiographic parameters could predict fluid responsiveness in critically ill patients following a low-volume (50-ml crystalloid solution) infusion over 10 seconds. METHODS: We prospectively studied 55 mechanically ventilated patients. Echocardiography was performed during a 50-ml infusion of crystalloid solution over 10 seconds and a further 450 ml over 15 minutes. Cardiac output (CO), stroke volume (SV), aortic velocity time index (VTI), and left ventricular ejection fraction (LVEF) were recorded. Patients were classified as responders (Rs) if CO increased by at least 15% following the 500-ml volume expansion or were classified as non-responders (NRs) if CO increased by less than 15%. Area under the receiver operating characteristic curves (AUC) compared CO variations after 50 ml over 10 seconds (∆CO50) and 500 ml over 15 minutes (∆CO500) and the variation of VTI after infusion of 50 ml of fluid over 10 seconds (∆VTI50). RESULTS: In total, 50 patients were enrolled, and 27 (54%) of them were Rs. General characteristics, LVEF, heart rate, and central venous pressure were similar between Rs and NRs. In the Rs group, the AUC for ∆CO50 was 0.95 ± 0.03 (P <0.01; best cutoff value, 6%; sensitivity, 93%; specificity, 91%). Moreover, ∆CO50 and ∆CO500 were strongly correlated (r = 0.87; P <0.01). The AUC for ∆VTI50 was 0.91 ± 0.04 (P <0.01; best cutoff value, 9%; sensitivity, 74%; specificity, 95%). ∆VTI50 and ∆CO500 were positively correlated (r = 0.72; P <0.01). CONCLUSION: In critically ill patients, the variation of CO and VTI after the administration of 50-ml crystalloid solution over 10 seconds (∆CO50 and ∆VTI50) can accurately predict fluid responsiveness. TRIAL REGISTRATION: Current Controlled Trials ISRCTN10524328. Registered 12 December 2013.

Hypertonic saline in the traumatic hypovolemic shock: meta-analysis.

BACKGROUND: A wealth of evidence from animal experiments has indicated that hypertonic saline (HS) maybe a better choice for fluid resuscitation in traumatic hypovolemic shock in comparison with conventional isotonic saline. However, the results of several clinical trials raised controversies on the superiority of fluid resuscitation with HS. This meta-analysis was performed to better understand the efficacy of HS in patients with traumatic hypovolemic shock comparing with isotonic saline. MATERIALS AND METHODS: According to the search strategy, we searched the PubMed, EMBASE, and the Cochrane Central Register of Controlled Trials, which was completed on October 2013. After literature searching, two investigators independently performed the literature screening, assessment of quality of the included trials, and data extraction. Disagreements were resolved by consensus or by a third investigator if needed. The outcomes included mortality, blood pressure, fluid requirement, and serum sodium. RESULTS: Six randomized controlled trials were included in the meta-analysis. The pooled risk ratio for mortality at discharge was 0.96 (95% confidence interval [CI], 0.82-1.14), whereas the pooled mean difference for the change in systolic blood pressure from baseline and the level of serum sodium after infusion was 6.47 (95% CI, 1.31-11.63) and 7.94 (95% CI, 7.38-8.51), respectively. Current data were insufficient to evaluate the effect of HS on the fluid requirement for the resuscitation. CONCLUSIONS: The present meta-analysis was unable to demonstrate a clinically important improvement in mortality after the HS administration. Moreover, we observed HS administration maybe accompanied with significant increase in blood pressure and serum sodium.

Anaerobic metabolism associated with traumatic hemorrhagic shock monitored by microdialysis of muscle tissue is dependent on the levels of hemoglobin and central venous oxygen saturation: a prospective, observational study.

BACKGROUND: Traumatic hemorrhagic shock resulting in tissue hypoxia is a significant cause of morbidity and mortality in polytraumatized patients. Early identification of tissue hypoxia is possible with microdialysis. The aim of this study was to determine the correlation between a marker of tissue hypoxia (L/P; lactate to pyruvate ratio) and selected parameters of systemic oxygen delivery (Hb; hemoglobin) and oxygen extraction (ScvO2; central venous oxygen saturation). We also investigated the severity of tissue hypoxia over the course of care. METHODS: Adult patients with traumatic hemorrhagic shock were enrolled in this prospective, observational study. Microdialysis of the peripheral muscle tissue was performed. Demographic data and timeline of care were collected. Tissue lactate, pyruvate, glycerol, glucose levels, hemoglobin, serum lactate and oxygen saturation of the central venous blood (ScvO2) levels were also measured. RESULTS: The L/P ratio trend may react to changes in systemic hemoglobin levels with a delay of 7 to 10 hours, particularly when systemic hemoglobin levels are increased by transfusion. Decrease in tissue L/P ratio may react to increase in ScvO2 with a delay of up to 10 hours, and such a decrease may signify elimination of tissue hypoxia after transfusion. We also observed changes in the L/P trend in the 13 hours preceding a change in the hemoglobin level. Fluid administration, which is routinely used as a first-line treatment of hypovolemic shock, can cause hemodilution and decreased hemoglobin. When ScvO2 decreases, increase in L/P ratio may precede the ScvO2 trend by 10 or 11 hours. An increase in the L/P ratio is an early warning sign of insufficient tissue oxygenation and should lead to intensive observation of hemoglobin levels, ScvO2 and other hemodynamic parameters. Patients who were treated more rapidly had lower maximal L/P values and a lower degree of tissue ischemia. CONCLUSION: The L/P ratio is useful to identify tissue ischemia and can estimate the effectiveness of fluid resuscitation. An increase in the L/P ratio is an early warning sign of inadequate tissue oxygenation and should lead to more detailed hemodynamic and laboratory monitoring. This information cannot usually be obtained from global markers.

[Surgical strategy in bullet wound of the thorax accompanied by shock].

The article analyzes the experience of treatment of bullet penetrating wounds of the thorax accompanied by shock in 131 armed forces personnel of internal army and officers of the Ministry of Home Affairs of Russia during contra-terrorist operations on the North Caucasus at the period from 2000 to 2011. The postoperative lethality was reduced from 22.7% to 10.8% due to usage of the strategy which was directed to decrease of surgical aggression in 65 patients.

Trauma-hemorrhagic shock induces a CD36-dependent RBC endothelial-adhesive phenotype.

OBJECTIVE: Microvascular dysfunction is a key element in the development of the multiple organ dysfunction syndrome. Although the mechanisms for this response are unclear, RBC adhesion to endothelium may initiate intravascular occlusion leading to ischemic tissue injury. Thus, we tested the hypothesis that trauma-hemorrhage induces RBC-endothelial cell adhesion. DESIGN: Prospective in vivo and in vitro animal study and analysis of patient blood samples. SETTING: University research laboratory and hospital emergency and trauma units. INTERVENTION: We initially assayed RBC adhesion to endothelial cells in vitro using RBCs obtained from rats subjected to trauma-hemorrhagic shock or sham shock as well as from severely injured trauma patients. Subsequently, we measured the role of putative RBCs and endothelial cell receptors in the increased RBC-endothelial cell adhesive response. MAIN RESULTS: In both rats and humans, trauma-hemorrhagic shock increased RBC adhesion to endothelium as well as increasing several putative RBC surface adhesion molecules including CD36. The critical factor leading to RBC-endothelial cell adhesion was increased surface RBC CD36 expression. Adhesion of trauma-hemorrhagic shock RBCs was mediated, at least in part, by the binding of RBC CD36 to its cognate endothelial receptors (αVß3 and VCAM-1). Gut-derived factors carried in the intestinal lymphatics triggered these trauma-hemorrhagic shock-induced RBC changes because 1) preventing trauma-hemorrhagic shock intestinal lymph from reaching the systemic circulation abrogated the RBC effects, 2) in vitro incubation of naïve whole blood with trauma-hemorrhagic shock lymph replicated the in vivo trauma-hemorrhagic shock-induced RBC changes while 3) injection of trauma-hemorrhagic shock lymph into naïve animals recreated the RBC changes observed after actual trauma-hemorrhagic shock. CONCLUSIONS: 1) Trauma-hemorrhagic shock induces rapid RBC adhesion to endothelial cells in patients and animals. 2) Increased RBC CD36 expression characterizes the RBC-adhesive phenotype. 3) The RBC phenotypic and functional changes were induced by gut-derived humoral factors. These novel findings may explain the microvascular dysfunction occurring after trauma-hemorrhagic shock, sepsis, and other stress states.

Tissue ischemia microdialysis assessments following severe traumatic haemorrhagic shock: lactate/pyruvate ratio as a new resuscitation end point?

BACKGROUND: Intensive care of severe trauma patients focuses on the treatment of haemorrhagic shock. Tissues should be perfused sufficiently with blood and with sufficient oxygen content to ensure adequate tissue oxygen delivery. Tissue metabolism can be monitored by microdialysis, and the lactate/pyruvate ratio (LPR) may be used as a tissue ischemia marker. The aim of this study was to determine the adequate cardiac output and haemoglobin levels that avoid tissue ischemia. METHODS: Adult patients with serious traumatic haemorrhagic shock were enrolled in this prospective observational study. The primary observed parameters included haemoglobin, cardiac output, central venous saturation, arterial lactate and the tissue lactate/pyruvate ratio. RESULTS: Forty-eight patients were analysed. The average age of the patients was 39.8 ± 16.7, and the average ISS was 43.4 ± 12.2. Hb < 70 g/l was associated with pathologic arterial lactate, ScvO2 and LPR. Tissue ischemia (i.e., LPR over 25) developed when CI ≤ 3.2 l/min/m(2) and Hb between 70 and 90 g/l were observed. Severe tissue ischemia events were recorded when the Hb dropped below 70 g/l and CI was 3.2-4.8 l/min/m(2). CI ≥ 4.8 l/min/m(2) was not found to be connected with tissue ischemia, even when Hb ≤ 70 g/l. CONCLUSION: LPR could be a useful marker to manage traumatic haemorrhagic shock therapies. In initial traumatic haemorrhagic shock treatments, it may be better to maintain CI ≥ 3.2 l/min/m(2) and Hb ≥ 70 g/l to avoid tissue ischemia. LPR could also be a useful transfusion trigger when it may demonstrate ischemia onset due to low local DO2 and early reveal low/no tissue perfusion.