J Trauma
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Complete resuscitation from shock is one of the primary concerns of the surgeon taking care of injured patients. Traditionally, the return to normalcy of blood pressure, heart rate, and urine output has been the end point of resuscitation. ⋯ We believe that the current data support the use of lactate, base deficit, and/or gastric intramucosal pH as the appropriate end points of resuscitation of trauma patients. The goal should be to correct one or all of three of these markers of tissue perfusion to normal within the initial 24 hours after injury.
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Comparative Study
Cytokines and adhesion molecules in elective and accidental trauma-related ischemia/reperfusion.
The major pathophysiologic role of cytokines such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-1, and IL-6, as well as of the (soluble) adhesion molecules ICAM-1 and E-selectin, has been identified using different experimental models of ischemia/reperfusion injury. Moreover, in intensive care management, evaluation of these agents as diagnostic or prognostic tools is of great interest in ischemia/reperfusion injury caused by surgical or accidental trauma. For this reason, inflammatory mediators including those mentioned above were investigated in three different groups of surgical patients. ⋯ The release of cytokines and soluble adhesion molecules into the circulation correlates well with the degree of trauma (elective surgery vs. accidental multiple trauma), depending on the extent of the associated ischemia/reperfusion injury. Both groups of mediators are also clearly related to the development of MOD in patients with multiple injuries with generalized ischemia/reperfusion injury caused by hemorrhagic shock. They may be predictive of patients at risk for MOD when measured early in the posttraumatic period.
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Comparative Study
Trauma mortality patterns in three nations at different economic levels: implications for global trauma system development.
Whereas organized trauma care systems have decreased trauma mortality in the United States, trauma system design has not been well addressed in developing nations. We sought to determine areas in greatest need of improvement in the trauma systems of developing nations. ⋯ The majority of deaths occur in the prehospital setting, indicating the importance of injury prevention in nations at all economic levels. Additional efforts for trauma care improvement in both low-income and middle-income developing nations should focus on prehospital and emergency room care. Improved emergency room care is especially important in middle-income nations which have already established a basic EMS.
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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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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.