J Trauma
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Although the use of computed tomographic (CT) scanning in severe head trauma is an accepted practice, the indications for its use in minor injury remain ill defined and subjective. We sought to define the incidence and identify risk factors for intracranial injury (ICI) after minor head trauma in children who did not have suspicious neurologic symptoms in the field or on presentation. ⋯ A normal neurologic exam and maintenance of consciousness does not preclude significant rates of intracranial injury in pediatric trauma patients. Contrary to convention, neither LOC nor mild altered mentation is a sensitive indicator with which to select patients for CT scanning. Skull fractures and superficial craniofacial injury are similarly unreliable. Identification of these patients is important for the occasional case requiring intervention and for the tracking of complications. A liberal policy of CT scanning is warranted for pediatric patients with a high-risk mechanism of injury despite maintenance of normal neurologic status in the field and at hospital screening.
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Two series of experiments were performed in swine who received severe blunt chest trauma. The goals were to determine the time course of constitutive and inducible cyclooxygenase (COX) isozyme expression in pulmonary macrophages (Mphis), and to determine whether COX expression and cardiopulmonary dysfunction were altered when neutrophils (PMNs) were pharmacologically depleted with cyclophosphamide (CYC). ⋯ After unilateral chest trauma, Mphi COX-1, not COX-2, is induced bilaterally and before fluid resuscitation; CYC prevented PMN infiltration and attenuated structural and functional changes after resuscitation, which suggests that PMNs have a role in the pathogenic mechanism of secondary lung injury; Mphi COX expression and other injury markers were not altered by CYC; and since Mphis continued to express proinflammatory COX protein even after pretreatment with a powerful nonspecific immunosuppressant, and since there is residual alveolar capillary damage even in the absence of PMNs, it is logical to conclude that no single cell type or mediator is a practical therapeutic target and that novel resuscitation strategies must address multiple elements in the inflammatory cascade.
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Changes in flow to the gut and the kidney during hemorrhage and resuscitation contribute to organ dysfunction and outcome. We evaluated regional and splanchnic oxygen (O2) flow distribution and calculated oxygen supply distribution during hemorrhage and reperfusion and compared them with global measures. ⋯ During hemorrhage, the gut is more prone than other regions to O2 consumption supply dependency. After resuscitation, standard clinical parameters do not detect residual O2 debt. Lactate, arterial pH, base excess, and intramucosal gut pH are all markers of residual tissue hypoperfusion.