Effect of SAM junctional tourniquet on respiration when applied in the axilla: A swine model / 中华创伤杂志(英文版)

PURPOSE@#SAM junctional tourniquet (SJT) has been applied to control junctional hemorrhage. However, there is limited information about its safety and efficacy when applied in the axilla. This study aims to investigate the effect of SJT on respiration when used in the axilla in a swine model.@*METHODS@#Eighteen male Yorkshire swines, aged 6-month-old and weighing 55 - 72 kg, were randomized into 3 groups, with 6 in each. An axillary hemorrhage model was established by cutting a 2 mm transverse incision in the axillary artery. Hemorrhagic shock was induced by exsanguinating through the left carotid artery to achieve a controlled volume reduction of 30% of total blood volume. Vascular blocking bands were used to temporarily control axillary hemorrhage before SJT was applied. In Group I, the swine spontaneously breathed, while SJT was applied for 2 h with a pressure of 210 mmHg. In Group II, the swine were mechanically ventilated, and SJT was applied for the same duration and pressure as Group I. In Group III, the swine spontaneously breathed, but the axillary hemorrhage was controlled using vascular blocking bands without SJT compression. The amount of free blood loss was calculated in the axillary wound during the 2 h of hemostasis by SJT application or vascular blocking bands. After then, a temporary vascular shunt was performed in the 3 groups to achieve resuscitation. Pathophysiologic state of each swine was monitored for 1 h with an infusion of 400 mL of autologous whole blood and 500 mL of lactated ringer solution. Tb and T0 represent the time points before and immediate after the 30% volume-controlled hemorrhagic shock, respectively. T30, T60, T90 and T120, denote 30, 60, 90, and 120 min after T0 (hemostasis period), while T150, and T180 denote 150 and 180 min after T0 (resuscitation period). The mean arterial pressure and heart rate were monitored through the right carotid artery catheter. Blood samples were collected at each time point for the analysis of blood gas, complete cell count, serum chemistry, standard coagulation tests, etc., and thromboelastography was conducted subsequently. Movement of the left hemidiaphragm was measured by ultrasonography at Tb and T0 to assess respiration. Data were presented as mean ± standard deviation and analyzed using repeated measures of two-way analysis of variance with pairwise comparisons adjusted using the Bonferroni method. All statistical analyses were processed using GraphPad Prism software.@*RESULTS@#Compared to Tb, a statistically significant increase in the left hemidiaphragm movement at T0 was observed in Groups I and II (both p < 0.001). In Group III, the left hemidiaphragm movement remained unchanged (p = 0.660). Compared to Group I, mechanical ventilation in Group II significantly alleviated the effect of SJT application on the left hemidiaphragm movement (p < 0.001). Blood pressure and heart rate rapidly increased at T0 in all three groups. Respiratory arrest suddenly occurred in Group I after T120, which required immediate manual respiratory assistance. PaO2 in Group I decreased significantly at T120, accompanied by an increase in PaCO2 (both p < 0.001 vs. Groups II and III). Other biochemical metabolic changes were similar among groups. However, in all 3 groups, lactate and potassium increased immediately after 1 min of resuscitation concurrent with a drop in pH. The swine in Group I exhibited the most severe hyperkalemia and metabolic acidosis. The coagulation function test did not show statistically significant differences among three groups at any time point. However, D-dimer levels showed a more than 16-fold increase from T120 to T180 in all groups.@*CONCLUSION@#In the swine model, SJT is effective in controlling axillary hemorrhage during both spontaneous breathing and mechanical ventilation. Mechanical ventilation is found to alleviate the restrictive effect of SJT on thoracic movement without affecting hemostatic efficiency. Therefore, mechanical ventilation could be necessary before SJT removal.

Fatores solúveis de células-tronco mesenquimais (FS-CTM) como uma ferramenta potencial para reduzir a inflamação nos pulmões de doadores após choque hipovolêmico / Soluble factors of mesenchimal stem cells (FS-MSC) as a potential tool to reduce inflammation in donor's lungs after hypovolemic shock

RESUMO Objetivo A escassez de pulmões viáveis ainda é um grande obstáculo para o transplante. As vítimas de trauma, que constituem potenciais doadores de pulmão, comumente apresentam choque hipovolêmico que acarreta inflamação e deterioração pulmonar e rejeição após o transplante. Buscando melhorar o enxerto pulmonar, testaram-se novas abordagens ao tratamento do doador. Este estudo foca o tratamento com células-tronco mesenquimais (CTMs) ou fatores solúveis produzidos pelas CTMs (FS-CTMs), usando um modelo com ratos para doadores de pulmão após choque hemorrágico. Métodos Quarenta e oito ratos foram divididos em quatro grupos: Controle (n=12), animais sem indução de choque hipovolêmico; Choque (n=12), animais submetidos a choque hipovolêmico (pressão arterial média de 40 mmHg); CTM (n=12), animais submetidos a choque hipovolêmico e tratados com CTMs; e FS (n=12), animais submetidos a choque hipovolêmico e tratados com FS-CTMs. Os animais foram submetidos a um procedimento de choque hipovolêmico (40 mmHg) com 50 minutos de duração. Os animais tratados foram monitorados por 115 minutos. Realizamos análise histopatológica do tecido pulmonar e quantificação dos marcadores inflamatórios (TNF-α, IL-1β, IL-6, IL-10, iCAM e vCAM) no tecido pulmonar e leucócitos no sangue periférico (LSPs). Resultados O choque hemorrágico resultou em taxas mais altas de LSPs e infiltrado de neutrófilos nos pulmões. Os animais do grupo FS apresentaram menor densidade de neutrófilos em comparação com os animais dos grupos Choque e CTM (p<0,001). Não foram observadas diferenças entre os grupos quanto aos níveis de citocinas no tecido pulmonar. Conclusão Os pulmões dos ratos submetidos a choque hemorrágico e tratados com FS-CTM apresentaram inflamação reduzida indicada por uma diminuição do infiltrado de neutrófilos nos pulmões.

ABSTRACT Objective The shortage of viable lungs is still a major obstacle for transplantation. Trauma victims who represent potential lung donors commonly present hypovolemic shock leading to pulmonary inflammation and deterioration and rejection after transplantation. Seeking to improve lung graft, new approaches to donor treatment have been tested. This study focuses on treatment with mesenchymal stem cells (MSCs) or soluble factors produced by MSCs (FS-MSC) using a rat model for lung donors after hemorrhagic shock. Methods Forty-eight rats were divided into four groups: Sham (n=12), animals without induction of hypovolemic shock; Shock (n=12), animals submitted to hypovolemic shock (mean arterial pressure 40 mmHg); MSC (n=12), animals submitted to hypovolemic shock and treated with MSCs, and FS (n=12), animals submitted to hypovolemic shock and treated with FS-MSC. The animals were subjected to a 50-minute hypovolemic shock (40 mmHg) procedure. The treated animals were monitored for 115 minutes. We performed histopathology of lung tissue and quantification of inflammatory markers (TNF-α, IL-1β, IL-6, IL-10, iCAM and vCAM) in lung tissue and peripheral blood leukocytes (PBLs). Results Hemorrhagic shock resulted in higher PBLs and neutrophil infiltrate in the lungs. FS animals had lower neutrophil density comparing with Shock and MSC animals (p<0.001). No differences in the cytokine levels in lung tissue were observed between the groups. Conclusions The lungs of rats submitted to hemorrhagic shock and treated with FS-MSC showed reduced inflammation indicated in a decrease in lung neutrophil infiltrate.

Whole blood for blood loss: hemostatic resuscitation in damage control / Sangre total: la nueva alternativa en la resucitación hemostática

Abstract Hemorrhagic shock and its complications are a major cause of death among trauma patients. The management of hemorrhagic shock using a damage control resuscitation strategy has been shown to decrease mortality and improve patient outcomes. One of the components of damage control resuscitation is hemostatic resuscitation, which involves the replacement of lost blood volume with components such as packed red blood cells, fresh frozen plasma, cryoprecipitate, and platelets in a 1:1:1:1 ratio. However, this is a strategy that is not applicable in many parts of Latin America and other low-and-middle-income countries throughout the world, where there is a lack of well-equipped blood banks and an insufficient availability of blood products. To overcome these barriers, we propose the use of cold fresh whole blood for hemostatic resuscitation in exsanguinating patients. Over 6 years of experience in Ecuador has shown that resuscitation with cold fresh whole blood has similar outcomes and a similar safety profile compared to resuscitation with hemocomponents. Whole blood confers many advantages over component therapy including, but not limited to the transfusion of blood with a physiologic ratio of components, ease of transport and transfusion, less volume of anticoagulants and additives transfused to the patient, and exposure to fewer donors. Whole blood is a tool with reemerging potential that can be implemented in civilian trauma centers with optimal results and less technical demand.

Resumen El choque hemorrágico y sus complicaciones son la principal causa de muerte en los pacientes con trauma. La resucitación en control de daños ha demostrado una disminución en la mortalidad y mejoría en el manejo del paciente. La resucitación hemostática consiste en la recuperación del volumen con hemoderivados como glóbulos rojos, plasma, crioprecipitado y plaquetas, en proporciones de 1:1:1:1. Sin embargo, esta demanda de hemo componentes podría no aplicarse para toda Latinoamérica u otros países de medianos y bajos ingresos. Las principales barreras para la implementación de esta estrategia serían la escasa disponibilidad de bancos de sangre y de hemoderivados insuficientes para contar con un protocolo de transfusión masiva. Una propuesta para superar estas barreras es el uso de sangre total fresca fría para la resucitación hemostática de los pacientes exsanguinados. Ecuador ha sido pionero en la implementación de esta estrategia con una experiencia ya de seis años, en que han demostrado que la sangre total tiene ventajas sobre la terapia de hemo componentes incluyendo, pero no limitando, la trasfusión de sangre con una razón fisiológica de componentes, fácil transporte y transfusión, menor volumen de anticoagulantes y aditivos trasfundidos al paciente, y menor exposición a donantes. La sangre total es una herramienta con un potencial reemergente que puede ser implementado en centros de trauma civil con óptimos resultados y menor demanda técnica.

Bleeding management after implementation of the Hemorrhage Code (Code H) at the Hospital Israelita Albert Einstein, São Paulo, Brazil / Manejo de sangramento após implantação do Código Hemorrágico (Código H) no Hospital Israelita Albert Einstein, São Paulo, Brasil

ABSTRACT Objective To describe the implementation of a care protocol based on rapid response teams, for management and resolution of bleeding. Methods A hospital protocol called Hemorrhage Code (Code H) was devised and developed. In a flow line, a multidisciplinary team provides comprehensive, fast and effective care to the patient with a severe hemorrhagic condition. In another flow line, professionals based at the hospital pharmacy focus on identifying patients at risk of bleeding, to avoid this event. Several hospital professionals and sectors were trained, each with specific roles, ensuring full support to the medical and nursing staffs. Results After implementing this protocol, we were able to significantly reduce the number of catastrophic events related to failure in bleeding management. Conclusion Code H is an example of a value-based medicine and precision medicine project by delivering comprehensive and multidisciplinary care, in addition to point-of-care testing introduced in clinical practice, optimizing patient safety and care practices at the hospital. Furthermore, it will be possible to minimize the risk of lawsuits for the hospital and physicians, as well as rationalizing resources with benefits for administrators and payers.

RESUMO Objetivo Descrever a implantação de um protocolo de atendimento nos moldes de times de resposta rápida, para manejo e resolução do sangramento. Métodos Foi idealizado e desenvolvido um protocolo institucional, chamado Código Hemorrágico, ou Código H, no qual, em um fluxo, um time multiprofissional e multidisciplinar foi constituído para atendimento integral, rápido e eficaz do paciente com doença hemorrágica grave. Em um outro fluxo, os profissionais, centralizados na farmácia do hospital, focavam na identificação do paciente com risco de hemorragia, no sentido de evitar o evento. Vários profissionais e setores do hospital foram treinados, e cada um, com funções específicas, deveria oferecer garantia total de apoio e suporte às equipes médica e de enfermagem. Resultados Após a implementação do protocolo, o número de eventos catastróficos relacionados à falha no manejo do sangramento reduziu significativamente. Conclusão O Código H é um exemplo de projeto de medicina baseada em valor e de medicina de precisão, por meio de atendimento integral e multidisciplinar, além de testes point of care introduzidos na prática clínica, com otimização da segurança do paciente e da prática assistencial na instituição. Ainda, por meio dele, deve ser possível minimizar o risco de ações judiciais para o hospital e os médicos, além de racionalizar recursos, com benefícios para administradores e fontes pagadoras.

Resucitación hemostática en el paciente con choque hipovolémico hemorrágico. Reporte de un caso / Case report: Hemostatic resuscitation in the patient with hemorrhagic hypovolemic shock

In the world, traumatic pathology continues to be a problem of great magnitude, from the point of view of public health. Today, the volumemic resuscitation in hypovolemic hemorrhagic shock is still controversial; a new alternative in volemic resuscitation is the hemostatic resuscitation that consists of the rapid use of whole blood or of the administration of the concentrate of erythrocytes (CE), fresh frozen plasma (PFC) and platelet concentrate (CP), with a fixed ratio between the products. OBJECTIVE: Clinical case presentation, as well as review of the published literature on hemostatic resuscitation in patients with hemorrhagic hypovolemic shock. MATERIAL AND METHODS: We present the case of a female patient of 16 years of age with penetrating injuries in the neck, thorax and abdomen; management and evolution in the operating room, intensive care unit until discharge. RESULTS: The adequate initial resuscitation in the patient with hemorrhagic hypovolemic shock has been shown to improve their survival, so that nowadays the application of new alternatives in resuscitation; As is the hemostatic resuscitation, they have yielded better results in the patient's prognosis. CONCLUSIONS: Trauma remains one of the main causes of admission to hospital units, with the young population being the most vulnerable due to car accidents. Strategies in improving the time of transfer from the accident site to the hospital unit, its definitive management in the operating room (if required) and the use of new alternatives in the management of hemorrhagic hypovolemic shock; such as hemostatic resuscitation, and the administration of pro-hemostatic drugs, are of great importance in the evolution and prognosis of the patient.

En el mundo, la patología traumática continúa siendo un problema de gran magnitud, desde el punto de vista de salud pública. Hoy en día la resucitación volémica en el choque hemorrágico hipovolémico todavía es controversial; una nueva alternativa en la resucitación volemica es la resucitación hemostática que consiste en el uso rápido de sangre total o de la administración del concentrado de Eritrocitos (CE), Plasma Fresco Congelado (PFC) y Concentrado de Plaquetas (CP), con una razón fija entre los productos. OBJETIVO: Presentación de caso clínico, así como revisión de la literatura publicada sobre resucitación hemostática en el paciente con choque hipovolémico hemorrágico. MATERIAL Y MÉTODOS: Se presenta el caso de paciente femenino de 16 años de edad con lesiones penetrantes en cuello, tórax y abdomen; manejo y evolución en sala de operaciones, unidad de cuidados intensivos hasta su egreso. RESULTADOS: La adecuada resucitación inicial en el paciente con choque hipovolémico hemorrágico ha demostrado mejorar su sobrevida, por lo que hoy en día la aplicación de nuevas alternativas en la reanimación; como es la resucitación hemostática, han arrojado mejores resultados en el pronóstico del paciente. CONCLUSIONES: El trauma sigue siendo una de las principales causas de ingreso a las unidades hospitalarias, siendo la población joven la más vulnerable por accidentes automovilísticos. Las estrategias en la mejora del tiempo de traslado del lugar del accidente hasta la unidad hospitalaria, su manejo definitivo en sala de quirófano (si así lo requiere) y el uso de nuevas alternativas en manejo del choque hipovolémico hemorrágico; como es la resucitación hemostática, y la ministración de fármacos pro hemostáticos, resultan de gran importancia en la evolución y pronóstico del paciente.

A fatal and metabolic experimental hemorrhagic shock in immature swine

Abstract Purpose: To use blood lactate (BL) as an end-point metabolic marker for the begin resuscitation of volume replacement in experimental hemorrhagic shock. Methods: Group I (n=7) was not bled (Control). Animals in Group II (n=7) were bled to a MAP of 30mmHg in thirty minutes. Hemodynamic and metabolic data were recorded at Baseline, at 30, 60 and 120 minutes after Baseline. The animals were intubated in spontaneous breathing (FIO2=0.21) with halothane. Results: Group I all survived. In Group II all died; no mortality occurred before a BL<10mM/L. Beyond the end-point all animals exhibited severe acidemia, hyperventilation and clinical signs of shock. Without treatment all animals died within 70.43±24.51 min of hypotension shortly after reaching an average level of BL 17.01±3.20mM/L. Conclusions: Swine's breathing room air spontaneously in hemorrhagic shock not treated a blood lactate over 10mM/L results fatal. The predictable outcome of this shock model is expected to produce consistent information based on possible different metabolic and hemodynamic patterns as far as the type of fluid and the timing of resuscitation in near fatal hemorrhagic shock.

Cardiovascular Effects of Shock and Trauma in Experimental Models. A Review

Abstract Experimental models of human pathology are useful guides to new approaches towards improving clinical and surgical treatments. A systematic search through PubMed using the syntax (shock) AND (trauma) AND (animal model) AND (cardiovascular) AND ("2010/01/01"[PDat]: "2015/12/31"[PDat]) found 88 articles, which were reduced by manual inspection to 43 entries. These were divided into themes and each theme is subsequently narrated and discussed conjointly. Taken together, these articles indicate that valuable information has been developed over the past 5 years concerning endothelial stability, mesenteric lymph, vascular reactivity, traumatic injuries, burn and sepsis. A surviving interest in hypertonic saline resuscitation still exists.

Effect of volume replacement during combined experimental hemorrhagic shock and traumatic brain injury in prostanoids, brain pathology and pupil status / Efeito da reposição volêmica durante o choque hemorrágico combinado com traumatismo craniencefálico sobre prostanóides, patologia cerebral e status pupilar

Traumatic brain injury (TBI) is the main cause of trauma-related deaths. Systemic hypotension and intracranial hypertension causes cerebral ischemia by altering metabolism of prostanoids. We describe prostanoid, pupilar and pathological response during resuscitation with hypertonic saline solution (HSS) in TBI. Method Fifteen dogs were randomized in three groups according to resuscitation after TBI (control group; lactated Ringer’s (LR) group and HSS group), with measurement of thromboxane, prostaglandin, macroscopic and microscopic pathological evaluation and pupil evaluation.Result Concentration of prostaglandin is greater in the cerebral venous blood than in plasma and the opposite happens with concentration of thromboxane. Pathology revealed edema in groups with the exception of group treated with HSS.Discussion and conclusion There is a balance between the concentrations of prostaglandin and thromboxane. HSS prevented the formation of cerebral edema macroscopically detectable. Pupillary reversal occurred earlier in HSS group than in LR group.

O traumatismo cranioencefálico (TCE) é a principal causa de morte relacionada ao trauma. O choque hemorrágico e hipertensão intracraniana causam isquemia cerebral alterando o metabolismo de prostanóides. Neste estudo, relatamos o comportamento dos prostanóides, resposta pupilar e patologia durante a reposição volêmica com solução salina hipertônica (SSH) no TCE. Método Quinze cachorros foram randomizados em três grupos (controle, grupo de Ringer lactato e grupo de SSH) e foram avaliados tromboxane, prostaglandina, avaliação patológica macroscópica e microscópica e status pupilar.Resultado A concentração de prostaglandina é maior no sangue cerebral em comparação ao plasma, e o inverso ocorre com o tromboxane. A patologia revelou edema em todos os grupos, com exceção do grupo tratado com SSH.Discussão e conclusão Existe um equilíbrio entre concentrações cerebrais e plasmáticas de prostaglandina e tromboxane. A SSH protegeu o cérebro da formação de edema pós traumático.

ROC trials update on prehospital hypertonic saline resuscitation in the aftermath of the US-Canadian trials

The objectives of this review are to assess the current state of hypertonic saline as a prehospital resuscitation fluid in hypotensive trauma patients, particularly after the 3 major Resuscitation Outcomes Consortium trauma trials in the US and Canada were halted due to futility. Hemorrhage and traumatic brain injury are the leading causes of death in both military and civilian populations. Prehospital fluid resuscitation remains controversial in civilian trauma, but small-volume resuscitation with hypertonic fluids is of utility in military scenarios with prolonged or delayed evacuation times. A large body of pre-clinical and clinical literature has accumulated over the past 30 years on the hemodynamic and, most recently, the anti-inflammatory properties of hypertonic saline, alone or with dextran-70. This review assesses the current state of hypertonic fluid resuscitation in the aftermath of the failed Resuscitation Outcomes Consortium trials.

Ressuscitação hemostática no choque hemorrágico traumático: relato de caso / Hemostatic resuscitation in traumatic hemorrhagic shock: case report / Resucitación hemostática en el choque hemorrágico traumático: relato de caso

JUSTIFICATIVA E OBJETIVOS: O objetivo deste artigo é relatar um caso em que a estratégia damage control (RDC) com ressuscitação hemostática foi usada com sucesso em paciente politraumatizada com choque hemorrágico grave. RELATO DE CASO: Paciente de 32 anos com choque hemorrágico grave por politraumatismo com fratura de bacia, que evoluiu com acidose, coagulopatia e hipotermia. Durante a ressuscitação volêmica, a paciente recebeu transfusão de hemocomponentes - plasma fresco congelado/concentrado de plaquetas/concentrado de hemácias, na razão de 1:1:1. Evoluiu no período intraoperatório, com melhora dos parâmetros perfusionais, e prescindiu de drogas vasoativas. No fim da operação a paciente foi levada para unidade de terapia intensiva e teve alta no sétimo dia de pós-operatório. CONCLUSÃO: A terapêutica ideal do choque hemorrágico traumático ainda não está estabelecida, porém a rapidez no controle da hemorragia e do resgate perfusional e protocolos terapêuticos bem definidos são as bases para se evitar a progressão da coagulopatia e a refratariedade do choque.

BACKGROUND AND OBJECTIVES: The aim of this paper is to report a case in which the damage control resuscitation (DCR) approach was successfully used to promote hemostatic resuscitation in a polytraumatized patient with severe hemorrhagic shock. CASE REPORT: Female patient, 32 years of age, with severe hemorrhagic shock due to polytrauma with hip fracture, who developed acidosis, coagulopathy, and hypothermia. During fluid resuscitation, the patient received blood products transfusion of fresh frozen plasma/packed red blood cells/platelet concentrate at a ratio of 1:1:1 and evolved intraoperatively with improvement in perfusion parameters without requiring vasoactive drugs. At the end of the operation, the patient was taken to the intensive care unit and discharged on the seventh postoperative day. CONCLUSION: The ideal management of traumatic hemorrhagic shock is not yet established, but the rapid control of bleeding and perfusion recovery and well-defined therapeutic protocols are fundamental to prevent progression of coagulopathy and refractory shock.

JUSTIFICATIVA Y OBJETIVOS: El objetivo de este artículo es relatar un caso en que la estrategia damage control (control de daños [RDC]) con resucitación hemostática, fue usada con éxito en paciente politraumatizada con choque hemorrágico grave. RELATO DE CASO: Paciente de 32 años, con choque hemorrágico grave por politraumatismo con fractura de cadera, que evolucionó con acidosis, coagulopatía e hipotermia. Durante la resucitación volémica, la paciente recibió transfusión de hemocomponentes a una razón de PFC/CP/CH de 1:1:1. Evolucionó en el período intraoperatorio, con una mejoría de los parámetros perfusionales y no necesitó fármacos vasoactivos. Al término de la operación, la paciente fue derivada a la unidad de cuidados intensivos y tuvo su alta al séptimo día del postoperatorio. CONCLUSIONES: La terapéutica ideal del choque hemorrágico traumático todavía no ha quedado establecida, pero la rapidez en el control de la hemorragia y del rescate perfusional, junto con protocolos terapéuticos bien definidos, sientan las bases para evitar la progresión de la coagulopatía y la refractariedad del choque.

Terapia de transfusion en trauma, ¿hora de cambiar nuestro enfoque? / Transfusion therapy in trauma: time to change our approach?

En la actualidad, el trauma constituye, por su alta frecuencia de presentación un problema no solo en su manejo sino que también de salud pública. La mejoría en los diferentes sistemas de rescate permite la recepción de pacientes más graves cuyo requerimiento de transfusiones es mayor y si bien son en grupo minoritario dentro del total de trauma aportan con una alta mortalidad especialmente en las primeras horas siendo la hemorragia y la coagulopatía la causa de ésta. Los recientes conflictos bélicos han planteado un cambio en el manejo transfusional de estos pacientes orientando hacia prácticas que incrementan la relación de GR, plasma fresco congelado (PFC)y plaquetas aportadas, tratando de simular el aporte de sangre total en las primeras horas de ocurrido el accidente.

Trauma is a very important public health problem and also a practice management. The aim of prehospital care of bleeding patient is to deliver the patient to a facility for definitive care. Trauma associated bleeding and coagulopaty is the principal cause of preventible death. Recent military experience suggest that FFP and platelets should be given early and more often to injured patient.

Reanimación y manejo de la coagulopatía en el trauma / Resuscitation and management of coagulopathy in trauma

La coagulopatía inducida por el shock hemorrágico se encuentra presente en casi un 25 por ciento de los pacientes ingresados por esta causa. Una vez que la coagulopatía se ha instalado aumenta drásticamente la morbimortalidad. Los paradigmas en la reanimación en el paciente traumatizado han variado dramáticamente en los últimos años, cambiando el uso de grandes volúmenes de cristaloides con el uso precoz de los hemoderivados y otros productos para tratar de revertir la coagulopatía y la "triada de la muerte". El objetivo de este trabajo es revisar la fisiopatologia de la coagulopatía en el trauma y las tendencias terapéuticas para revertiría.

Coagulopathy induced by hemorrhagic shock is present in almost 25 percent of patients admitted for this reason. Once the coagulopathy develops patients morbidity and mortality dramatically increases. The paradigms in trauma patients resuscitation have changed considerably in the last years by changing the use of large volumes of crystalloid with the early use of blood products and other products to try to reverse the coagulopathy and the "triad of death." The aim of this paper is to review the pathophysiology of coagulopathy in trauma and therapy trends to reverse it.

Shock hemorrágico / Hemorrhagic shock

El shock hemorrágico es la principal causa de muerte en el trauma, la principal causa de muertes potencialmente prevenible y una de las principales causas de muerte en la población menor de 44 años. La hemorragia masiva puede producir inestabilidad hemodinámica, disminución de la perfusión tisular, daño de órganos y muerte. Los principales objetivos de la resucitación son restaurar el volumen sanguíneo circulante y detener la hemorragia, mientras se activan los protocolos de manejo de la hemorragia masiva. Si bien el método óptimo de resucitación no ha sido claramente establecido, el uso de fluidos intravenosos y productos sanguíneos son elementos esenciales del manejo. Los defectos hemostáticos son frecuentes en la hemorragia masiva y evolucionan rápidamente. Se recomienda el uso precoz de plasma fresco congelado y plaquetas para prevenir el mecanismo dilucional de la coagulopatía, y el manejo agresivo de ésta una vez establecida. Finalmente, el manejo posterior a la emergencia incluye los cuidados intensivos para una monitorización estricta y el manejo de las eventuales complicaciones sistémicas, como la falla multiorgánica.

Hemorrhagic shock is the leading cause of death after injury, the major cause of potentially preventable deaths and one of the leading cause of death in young people. Massive hemorrhage may lead to hemodynamic instability, decreased tissue perfusion, organ damage, and death. The main goals of resuscitation are to restore circulating blood volume and to stop the source of hemorrhage, while the major hemorrhage protocols must be immediately declare. Although the optimal method of resuscitation has not been clearly established, the use of intravenous fluids and blood products are the key aspects of the management. The haemostatic defects are common in massive hemorrhage and trauma, and are likely to evolve rapidly. The early use of fresh frozen plasma and platelets is recommended to prevent the dilutional mechanism, and if the haemosthatic defect is established, it should be aggressively treated. Finally, further management includes intensive therapy to closely monitoring and management of any systemic complications, as multiorganic organ damage.

Rabbit model of uncontrolled hemorrhagic shock and hypotensive resuscitation

Clinically relevant animal models capable of simulating traumatic hemorrhagic shock are needed. We developed a hemorrhagic shock model with male New Zealand rabbits (2200-2800 g, 60-70 days old) that simulates the pre-hospital and acute care of a penetrating trauma victim in an urban scenario using current resuscitation strategies. A laparotomy was performed to reproduce tissue trauma and an aortic injury was created using a standardized single puncture to the left side of the infrarenal aorta to induce hemorrhagic shock similar to a penetrating mechanism. A 15-min interval was used to simulate the arrival of pre-hospital care. Fluid resuscitation was then applied using two regimens: normotensive resuscitation to achieve baseline mean arterial blood pressure (MAP, 10 animals) and hypotensive resuscitation at 60 percent of baseline MAP (10 animals). Another 10 animals were sham operated. The total time of the experiment was 85 min, reproducing scene, transport and emergency room times. Intra-abdominal blood loss was significantly greater in animals that underwent normotensive resuscitation compared to hypotensive resuscitation (17.1 ± 2.0 vs 8.0 ± 1.5 mL/kg). Antithrombin levels decreased significantly in normotensive resuscitated animals compared to baseline (102 ± 2.0 vs 59 ± 4.1 percent), sham (95 ± 2.8 vs 59 ± 4.1 percent), and hypotensive resuscitated animals (98 ± 7.8 vs 59 ± 4.1 percent). Evidence of re-bleeding was also noted in the normotensive resuscitation group. A hypotensive resuscitation regimen resulted in decreased blood loss in a clinically relevant small animal model capable of reproducing hemorrhagic shock caused by a penetrating mechanism.

A novel fluid resuscitation strategy modulates pulmonary transcription factor activation in a murine model of hemorrhagic shock

INTRODUCTION: Combining the hemodynamic and immune benefits of hypertonic saline with the anti-inflammatory effects of the phosphodiesterase inhibitor pentoxifylline (HSPTX) as a hemorrhagic shock resuscitation strategy reduces lung injury when compared with the effects of Ringer's lactate (RL). We hypothesized that HSPTX exerts its anti-inflammatory effects by interfering with nuclear factor kappa B/cAMP response element-binding protein (NF-êB-CREB) competition for the coactivator CREB-binding protein (CBP) in lung tissue, thus affecting pro-inflammatory mediator production. METHODS: Male Sprague-Dawley rats underwent 60 minutes of hemorrhagic shock to reach a mean arterial blood pressure of 35 mmHg followed by resuscitation with either RL or HSPTX (7.5 percent HS + 25 mg/kg PTX). After four hours, lung samples were collected. NF-êB activation was assessed by measuring the levels of phosphorylated cytoplasmic inhibitor of kappa B (I-êB) and nuclear NF-êB p65 by western blot. NF-êB and CREB DNA-binding activity were measured by electrophoretic mobility shift assay (EMSA). Competition between NF-êB and CREB for the coactivator CBP was determined by immunoprecipitation. Interleukin-8 (IL-8) levels in the lung were measured by ELISA. RESULTS: RL resuscitation produced significantly higher levels of lung IL-8 levels, I-êB phosphorylation, p65 phosphorylation, and NF-êB DNA binding compared with HSPTX. NF-êB-CBP-binding activity was similar in both groups, whereas CREB-CBP-binding activity was significantly increased with HSPTX. CREB-DNA binding-activity increased to a greater level with HSPTX compared with RL. DISCUSSION: HSPTX decreases lung inflammation following hemorrhagic shock compared with conventional resuscitation using RL through attenuation of NF-êB signaling and increased CREB-DNA binding activity. HSPTX may have therapeutic potential in the attenuation of ischemia-reperfusion...

Hyperkalemia accompanies hemorrhagic shock and correlates with mortality

OBJECTIVE: This study was designed to evaluate the effects of terlipressin versus fluid resuscitation with normal saline, hypertonic saline or hypertonic-hyperoncotic hydroxyethyl starch, on hemodynamics, metabolics, blood loss and short-term survival in hemorrhagic shock. METHOD: Twenty-nine pigs were subjected to severe liver injury and treated 30 min later with either: (1) 2 mg terlipressin in a bolus, (2) placebo-treated controls, (3) 4 mL/kg 7.5% hypertonic NaCl, (4) 4 mL/kg 7.2% hypertonic-hyperoncotic hydroxyethyl starch 200/0.5, or (5) normal saline at three times lost blood volume. RESULTS: The overall mortality rate was 69%. Blood loss was significantly higher in the hypertonic-hyperoncotic hydroxyethyl starch and normal saline groups than in the terlipressin, hypertonic NaCl and placebo-treated controls groups (p<0.005). Hyperkalemia (K>5 mmol/L) before any treatment occurred in 66% of the patients (80% among non-survivors vs. 22% among survivors, p=0.019). Post-resuscitation hyperkalemia occurred in 86.66% of non-survivors vs. 0% of survivors (p<0.001). Hyperkalemia was the first sign of an unsuccessful outcome for the usual resuscitative procedure and was not related to arterial acidemia. Successfully resuscitated animals showed a significant decrease in serum potassium levels relative to the baseline value. CONCLUSION: Hyperkalemia accompanies hemorrhagic shock and, in addition to providing an early sign of the acute ischemic insult severity, may be responsible for cardiac arrest related to hemorrhagic shock.

In vitro and in vivo resuscitation with adenosine retains cardiomyocyte structure and function following hemorrhagic shock in rats

Successful treatment of hemorrhage requires restoration of normal cardiac function following resuscitation. However, many interventions used to attempt to restore cardiac function may cause additional myocardial injury, cardiac dysfunction and failure. The purpose of this study was to examine the ability of therapeutic intervention using adenosine to protect the heart from contractile dysfunction and post-resuscitation injury following hemorrhagic shock. Male Spargue-Dawley rats were divided into 3 groups: 1] In vivo hemorrhagic shock [1hour] followed by in vitro treatment with adenosine and ex vivo resuscitation using the Langendorff apparatus [60 minutes], 2] In vivo hemorrhagic shock [1 hour] followed by in vivo treatment with 20 microM adenosine and resuscitation [30 minutes] then ex vivo perfusion [60 minutes] and 3] In vivo hemorrhagic shock [2 hours] followed by in vivo treatment with 20 microM adenosine and resuscitation [30 minutes] then ex vivo perfusion [60 minutes]. Arterial blood samples were collected for measurements of TNF-alpha. Treatment with adenosine before resuscitation from hemorrhagic shock significantly improved left ventricular contractile function compared to the untreated resuscitated group. Treatment with adenosine also decreased the inflammatory response to shock by lowering the levels of TNF. In conclusion, treatment with adenosine before resuscitation of hemorrhagic shock protected the heart from post-resuscitation myocardial dysfunction and injury in rats

Resuscitation with adenosine retains cardiomyocyte structure following hemorrhagic shock in rats

Despite the improvement in resuscitation strategies, the incidence of post-resuscitation myocardial injury and failure remains high. Hemorrhagic shock activates an inflammatory response that can lead to myocardial cellular injury. Adenosine has been shown to protect the heart against ischemia reperfusion injury. However, the cardioprotective effects of adenosine following hemorrhagic shock may reduce myocardial injury by decreasing the inflammatory response to shock in rats. After 60 min on hemorrhage, 10 rats were randomized in vivo resuscitation with [n=8] microM adenosine for 30 min. heart Biopsies were collected from histological and electron microscopy examination. Light microscopy demonstrated decreased neutrophil infiltration, absence of contraction band necrosis and hydropic degeneration in the adenosine treated group compared to the hemorrhage untreated. Electron microscopy showed relative preservation of myocardial structure with absence of mitochondrial swelling in the hemorrhage treated group. These findings suggest that treatment with adenosine before in vivo resuscitation of hemorrhagic shock protected the heart from post-resuscitation myocardial injury in rats and the mechanism could be mediated by lowering the inflammatory response to shock

Does the type of resuscitative fluid affect healing of colonic anastomosis in experimentally induced hemorrhagic shock in rats?

The aim of the study was to investigate the effects of different resuscitative fluids on the healing of intestinal anastomosis in a hemorrhagic-shock rat model. Closed-colony Wistar male rats [n = 40; 8 rats per group] were subjected to volume-controlled hemorrhagic shock, followed by a 30-min shock phase. The animals were then resuscitated with one of the following fluids [which also corresponds to their respective groups]: lactated Ringer's solution [LR], hydroxyethyl starch [HES], 7.5% hypertonic saline [HS] and autologous blood [AB]. There was also a control group [CL], which did not experience hemorrhagic shock or receive any resuscitative fluids. All rats underwent laparotomy, segmental resection and anastomosis of the left colon. Five days later, a 2nd laparotomy was performed and the anastomotic bursting pressure was measured in vivo. Thereafter, the anastomosed segment was resected to measure the tissue hydroxyproline level and the grade of anastomotic fibrosis. All experimental groups [LR, HES, HS and AB] exhibited lower anastomotic bursting pressures than the CL group; however, nointergroup differences achieved statistical significance. The mean tissue hydroxyproline level and fibrosis grade also were similar across all 5 groups. In traumatic hemorrhagic shock, anastomosis safety does not appear to be affected by the type of fluid used for resuscitation. Moreover, LR, HES and HS all seemed to reinforce healing as effectively as transfused blood

Resuscitation with adenosine retains cardiomyocyte structure following hemorrhagic shock in rats

Successful treatment of hemorrhage patients requires restoration of normal cardiac function following resuscitation. However, many interventions used to attempt to restore cardiac function may cause additional myocardial injury, cardiac dysfunction and failure. The purpose of this study was to examine the ability of therapeutic intervention using adenosine to protect the heart from contractile dysfunction and post-resuscitation injury following hemorrhagic shock. Male Sprague- Dawley rats were divided into 3 groups: 1] in vivo hemorrhagic shock [1 hour] followed by in vitro treatment with adenosine and ex vivo resuscitation using the Langendorff apparatus [60 minutes], 2] in vivo hemorrhagic shock [1 hour] followed by in vivo treatment with 20 mirco M adenosine and resuscitation [30 minutes] and then ex vivo perfusion [60 minutes] and 3] in vivo hemorrhagic shock [2 hours] followed by in vivo treatment with 20 mircoM adenosine and resuscitation [30 minutes] and then ex vivo perfusion [60 minutes]. Arterial. The results showed that blood samples were collected for measurements of TNF- treatment with adenosine before resuscitation from hemorrhagic shock significantly improved left ventricular contractile function compared to the untreated resuscitated group. Treatment with adenosine also decreased the inflammatory response to shock by lowering the levels of TNF. In conclusion, treatment with adenosine before resuscitation of hemorrhagic shock protected the heart from post-resuscitation myocardial dysfunction and injury in rats