J Trauma
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Despite recent advances in the management of severe hepatic injuries, the operative mortality rate of grade V hepatic injuries still ranges from 67% to 80%. Grade V hepatic injuries involving the retrohepatic cava or main hepatic veins are almost always lethal, especially those from blunt trauma. The purpose of this study is to understand the risk factors determining operative mortality in grade V blunt hepatic trauma, and to try to improve the surgical management of these injuries. ⋯ Initial base deficit and total intraoperative blood loss were the significant factors that determined operative mortality after grade V blunt hepatic trauma. We suggest that prompt resuscitation and expeditious and appropriate surgical management, to control operative blood loss, is the only way to reduce operative mortality in patients with grade V blunt hepatic trauma.
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Restoration of oxygen delivery, especially to the splanchnic bed, is of critical importance during trauma resuscitation. Acute normovolemic hemodilution (ANH) has been used to reduce blood transfusion requirement during elective surgery. The effect of hemodilution on the splanchnic circulation during hemorrhagic shock (HS) is not well defined. ⋯ As long as an adequate intravascular volume is maintained, hemodilution is well tolerated by the gut after HS. Concern about the adequacy of gut perfusion should not be a transfusion trigger after HS.
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Edema of tissue not directly injured by heat is a common complication after resuscitation of burn shock. Hypertonic 7.5% NaCl 6% dextran (HSD) infusion reduces early fluid requirements in burn shock, but the effects of HSD on peripheral and visceral tissue edema are not well-defined. ⋯ There were no observed differences in edema in burn skin between the two treatment groups. The early volume-sparing effect of HSD and reduction in tissue edema are likely attributed to an increased extracellular osmolarity and a better maintenance of the plasma oncotic pressure.
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Although depression in hepatocellular function occurs early after trauma and severe hemorrhage and persists despite fluid resuscitation, it remains unknown whether reactive oxygen species (ROS) play any role in the initiation of hepatocellular depression and damage under those conditions. We hypothesized that administration of a ROS scavenger at the beginning of resuscitation will attenuate organ injury after severe shock. ⋯ Our data suggest that ROS play a role in producing the depression in organ functions after severe hemorrhagic shock. Thus, adjuncts that attenuate the detrimental effects of ROS may be useful for improving the depressed cardiac and hepatocellular functions after trauma hemorrhage and resuscitation.