J Trauma
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Patients who have an acute subdural hematoma with a thickness of 10 mm or less and with a shift of the midline structures of 5 mm or less often can be treated nonoperatively. We wonder whether the knowledge of the clinical status both in the prehospital determination and on admission to the neurosurgical center can predict the need for evacuation of subdural hematomas as well as the computed tomographic (CT) parameters. ⋯ Nonoperative management for selected cases of acute subdural hematomas is at least as safe as surgical management. GCS scoring at the scene and in the emergency room combined with early and subsequent CT scanning is crucial when making the decision for nonoperative management. This strategy requires that administration of long-lasting sedatives and paralytic medications be avoided before the patient arrives at the neurosurgical center.
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To determine the incidence and significance of free fluid on abdominal CT in blunt trauma. ⋯ The presence of more than trace amounts of free fluid without solid organ injury in patients with blunt trauma is a strong indication for exploratory laparotomy. Patients with isolated trace amounts of free fluid can be safely observed.
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Granulocyte colony-stimulating factor (G-CSF) increases production and release of neutrophil precursors and activates multiple functions of circulating polymorphonuclear neutrophils (PMNs). G-CSF has therapeutic effects in many experimental models of sepsis; its actions with superimposed reperfusion insults are unknown. In traumatic conditions, G-CSF could exacerbate unregulated, PMN-dependent injury to otherwise normal host tissue or, it could partially reverse trauma-induced immune suppression, which may improve long-term outcome. This study tested whether stimulating PMN proliferation and function with G-CSF during recovery from trauma+sepsis potentiated reperfusion injury or whether it improved host defense. ⋯ Our data show that G-CSF initiated at the time of resuscitation reduced the sequelae of posttrauma sepsis by increasing PMN proliferation and function without potentiating PMN-mediated lung reperfusion injury.