The Pathophysiology and Management of Hemorrhagic Shock in the Polytrauma Patient

Abstract

The recognition and management of life-threatening hemorrhage in the polytrauma patient poses several challenges to prehospital rescue personnel and hospital providers. First, identification of acute blood loss and the magnitude of lost volume after torso injury may not be readily apparent in the field. Because of the expression of highly effective physiological mechanisms that compensate for a sudden decrease in circulatory volume, a polytrauma patient with a significant blood loss may appear normal during examination by first responders. Consequently, for every polytrauma victim with a significant mechanism of injury we assume substantial blood loss has occurred and life-threatening hemorrhage is progressing until we can prove the contrary. Second, a decision to begin damage control resuscitation (DCR), a costly, highly complex, and potentially dangerous intervention must often be reached with little time and without sufficient clinical information about the intended recipient. Whether to begin DCR in the prehospital phase remains controversial. Furthermore, DCR executed imperfectly has the potential to worsen serious derangements including acidosis, coagulopathy, and profound homeostatic imbalances that DCR is designed to correct. Additionally, transfusion of large amounts of homologous blood during DCR potentially disrupts immune and inflammatory systems, which may induce severe systemic autoinflammatory disease in the aftermath of DCR. Third, controversy remains over the composition of components that are transfused during DCR. For practical reasons, unmatched liquid plasma or freeze-dried plasma is transfused now more commonly than ABO-matched fresh frozen plasma. Low-titer type O whole blood may prove safer than red cell components, although maintaining an inventory of whole blood for possible massive transfusion during DCR creates significant challenges for blood banks. Lastly, as the primary principle of management of life-threatening hemorrhage is surgical or angiographic control of bleeding, DCR must not eclipse these definitive interventions.

Update on Current Concepts in Management of Severe Hemorrhagic Shock and Optimal Individualized Fluid Therapy in Critically Ill Polytrauma Patients

“…After this threshold the O2ER reaches a plateau. If blood loss continues the compensatory mechanism will be overcome and VO2 will be dependent on flow [16][17][18][19]. Depending on the amount of blood lost, there are four stages of hemorrhagic shock and fluid resuscitation is based on these 4 stages.…”

Assessment of left ventricle myocardial deformation in a hemorrhagic shock swine model by two-dimensional speckle tracking echocardiography

“…1,2 Moreover, hemorrhagic shock (HS) is the most potentially preventable cause related to deaths after trauma, occurring early before arriving at the hospital, and associated with coagulopathy, microcirculation dysfunction, and prominent inflammatory response. 3,4 Several studies demonstrated the development of traumainduced secondary cardiac injury (TISCI) and dysfunction, independent of direct heart trauma, due to myocardial ischemia and ischemia-reperfusion injury, prompted by cardiomyocyte death and microvascular injury, and leading to increased morbidity and risk of death. 5,6 The analysis of myocardial deformation or strain by speckle tracking echocardiography (STE) is a novel noninvasive imaging tool to measure cardiac performance, and it has been shown to have superior sensitivity, reproducibility, accuracy, and predicted power to cardiovascular (CV) events when compared with established methods such as left ventricle (LV) ejection fraction.…”

Avaliação da disfunção miocárdica em modelo de choque hemorrágico controlado por meio de ecocardiografia 2D speckle tracking

“…1,2 O choque hemorrágico (CH), decorrente do trauma, é considerado uma causa de óbito evitável, ocorrendo precocemente antes da chegada ao hospital, e está associado à coagulopatia, disfunção da microcirculação e proeminente resposta inflamatória. 3,4 Vários estudos demonstraram o desenvolvimento de lesão e/ou disfunção secundária cardíaca relacionada ao trauma (ICRT) independente de traumatismo cardíaco direto, tendo como principais mecanismos fisiopatológicos isquemia miocárdica, lesão de isquemia-reperfusão e liberação de marcadores inflamatórios, ocasionando lesão microvascular e morte de cardiomiócitos, determinando um aumento da morbidade e mortalidade. [5][6][7][8] A presença da disfunção cardíaca está diretamente relacionada com a mortalidade, o que torna necessária melhor compreensão e determinação temporal das alterações na microestrutura miocárdica.…”

“…Uma hora após o estabelecimento do estado de choque hemorrágico grave, houve uma redução estatisticamente significativa no conteúdo de oxigênio no sangue venoso misto (6,2 [5,8, 7,2] vs. 1,8 [1,3,3,4] mL/dL), p = 0,018) e da oferta de oxigênio (48,1 [42,4,51,3] vs. 20,8 [17,8,26,5] mL/min, p = 0,018), com aumento possivelmente compensatório na extração de oxigênio (42,6 [39,8, 48,4] b A comparação entre os tempos de estudo experimental para cada variável foi feita por meio do teste de Wilcoxon. * P < 0,05 foi considerado significativo.…”

“…(e prime)(9,8 [8,0, 13,0] vs. 5,8[ 4,8,7,5] cm/s , p = 0,018); e houve aumento estatisticamente significativo na razão entre as velocidades de pico diastólico inicial de fluxo transmitral (E) e e…”