J Trauma
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The objective of this study was to determine the effects of recombinant human granulocyte colony-stimulating factor (rhG-CSF) administration in septic patients with neutropenia. ⋯ Administration of rhG-CSF attenuates inflammatory responses without inducing tissue injury in septic patients with neutropenia.
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Patients with closed head injury and expanding epidural (EDH) or subdural (SDH) hematoma require urgent craniotomy for decompression and control of hemorrhage. In remote areas where neurosurgeons are not available, trauma surgeons may occasionally need to intervene to avert progressive neurologic injury and death. In 1990, a young man with rapidly deteriorating neurologic signs underwent emergency burr hole decompression of a combined EDH/SDH at our hospital, with complete recovery. ⋯ One patient with a GCS score of 3 on arrival died. Seven survivors (mean follow-up, 3.9 years; range, 1-6.5 years), including the index case, function independently, although one survivor has moderate cognitive and motor impairment. We conclude that early craniotomy for expanding epidural and subdural hematomas by properly trained surgeons may save lives and reduce morbidity in properly selected cases when timely access to a neurosurgeon is not possible.
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Editorial Comment
Neurologic dysfunction in the multiple organ dysfunction syndrome.
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The coagulopathy noted in hypothermic trauma patients has been variously theorized to be caused by either enzyme inhibition, platelet alteration, or fibrinolytic processes, but no study has examined the possibility that all three processes may simultaneously contribute to coagulopathy, but are perhaps triggered at different levels of hypothermia. The purpose of this study was to determine whether, at clinically common levels of hypothermia (33.0-36.9 degrees C), there are specific temperature levels at which coagulopathic alterations are seen in each of these processes. ⋯ Patients whose temperature was > or =34.0 degrees C actually demonstrated a significant hypercoagulability. Enzyme activity slowing and decreased platelet function individually contributed to hypothermic coagulopathy in patients with core temperatures below 34.0 degrees C. All the coagulation measures affected are part of the polymerization process of platelets and fibrin, and this process may be the mechanism by which the alteration in coagulation occurs.