J Trauma
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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.
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Tension pneumoperitoneum is a known although rare complication of barotrauma, which can accompany blast injury. We report two patients who suffered from severe pulmonary blast injury, accompanied by tension pneumoperitoneum, and who were severely hypoxemic, hypercarbic, and in shock. ⋯ Several mechanisms to explain this improvement are suggested. In such cases the release of the tension pneumoperitoneum is mandatory, and laparotomy with delayed closure can be contemplated.
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Lactate production after hemorrhagic shock may be produced by aerobic glycolysis, which has been linked to activity of the Na+/K+ pump in smooth muscle and other tissues. We tested whether increased muscle Na+/K+ pump activity after shock was linked to increased lactate production. ⋯ Hypoxia is unlikely to account for increased muscle lactate production after resuscitated hemorrhagic shock, because high lactate production persists under well-oxygenated incubation conditions. Inhibition of shock-induced lactate production by ouabain indicates energetic coupling of glycolysis to the Na+, K+-ATPase.
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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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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.