Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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The estimation of patients who are at risk for infection, sepsis, and organ dysfunction/failure is crucial not only for inclusion in treatment algorithms but also for entry into appropriate clinical trials of prophylaxis and therapy. Patients on the surgical service who have sustained major trauma or who have undergone transplantation are clearly at the greatest risk. Other immunosuppressed patients at risk for sepsis include those receiving myelosuppressive chemotherapy, those with overwhelming malignancy, and those who suffer from cirrhosis, diabetes mellitus, and severe malnutrition. ⋯ This score can identify patients within hours of hospitalization who are at risk of subsequently developing overt clinical infection and sepsis. Intervention then can be applied to such at-risk populations prior to the onset of sepsis and to evaluate the efficacy of prophylaxis. Patients in whom prophylaxis fails could be eligible for trials of therapeutic intervention as well.
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Burn injury results in a rapid loss of intravascular volume as wound edema forms, which reduces the circulating blood volume and generates the need for fluid therapy to combat hypovolemia. Fluid resuscitation of a burn patient is usually carried out with isotonic, sodium- and chloride-containing fluids, such as lactated Ringer's solution. The initial 24 h resuscitation volume is based on the burn size and body weight of the patient. ⋯ Care following resuscitation is focused on topical antimicrobial therapy, burn wound excision, and wound closure by grafting. Nutritional support and the prevention and control of infection are constant themes in burn patient management. A progressive improvement in general care of the acutely injured patient, prevention of shock, effective means of maintaining organ function, prevention and control of burn wound and other infections, and physiologically based metabolic support have significantly increased burn patient survival in recent decades.
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This study was designed to evaluate the effects of small-volume infusion of 7.5% hypertonic saline/6% dextran-70 (HSD) on the cardiovascular function of traumatic-hemorrhagic shock rats at simulated high altitude. 32 rats were randomly divided into four groups: 1) normal saline (NS)-treated group, 2) .9% NaCl/6% dextran-70 (Dex)-treated group, 3) 7.5% hypertonic saline (HS)-treated group, and 4) 7.5% hypertonic saline/6% dextran-70 (HSD)-treated group. The rats were exposed to a simulated high altitude of 4,000 m in a hypobaric hypoxic chamber, and traumatic-hemorrhagic shock was inflicted through fracture of the shaft of the left femur and bleeding from femoral vein to reduce mean arterial pressure (MAP) to 6.00 +/- .67 kPa within 5 min. ⋯ In the 5 h period after treatment, it was found that MAP, left ventricular systolic pressure, maximal rate of left ventricular pressure rise and drop (+/- dp/dtmax) were significantly higher in HSD group than in the NS, Dex and HS groups. It can be concluded that 1) HSD can improve the cardiovascular function and hemodynamics of traumatic-hemorrhagic shock rats at simulated high altitude and 2) HSD is more effective than HS.
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Patients with severe traumatic brain injury (TBI) show a profound acute-phase response. Because interleukin-6 (IL-6) is an important mediator of these pathophysiological changes, IL-6 levels were monitored in the cerebrospinal fluid (CSF) and serum of 20 patients with severe isolated TBI. All patients received indwelling ventricular catheters for intracranial pressure monitoring and for release of CSF when intracranial pressure exceeded 15 mmHg. ⋯ Thrombocytes decreased to a subnormal level during the first few days, but reached supranormal numbers by the end of the study period. Our results show that the increase of IL-6 levels in CSF and serum is followed by a profound acute-phase response in patients with TBI. Because cytokine concentrations are significantly lower in serum compared with CSF, we hypothesize that IL-6 produced in the central nervous system may play a role in initiating the acute-phase response.