Articles: brain-injuries.
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Mannitol has replaced other diuretics as the agent of first choice for control of raised intracranial pressure (ICP) after brain injury. Mannitol should be given as a bolus intravenous infusion, over 10 to 30 mins, in doses ranging from 0.25 to 1.0 g/kg body weight. It may be given when high ICP is suspected, prior to computed tomography scanning, e.g., in patients who develop a fixed, dilated pupil or neurologic deterioration. ⋯ A Foley catheter should always be inserted when mannitol is used. Serum osmolality should be measured frequently after mannitol and maintained < 320 mOsm to avoid renal failure. Its beneficial effects and the rationale for its use are also reviewed.
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Optimal trauma care, including that for head and spinal cord injury, requires system organization and adoption throughout the United States and the world. Neurosurgeons play an essential role in system design and development in addition to treating neurotrauma patients. Areas of neurosurgical involvement include defining prehospital triage and treatment guidelines, emergency department evaluation and therapy, operative management, and active involvement in the critical care and acute hospital settings. Collaboration among all members of the trauma team is essential to ensure the best possible outcome for patients with traumatic injuries.
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Head-injured patients require maintenance of systemic hemodynamics as well as attention to cerebral hemodynamics. Most head-injured patients have increased metabolic oxygen consumption, mild hypertension, and increased cardiac indices. Assessment of regional perfusion, difficult in many patients, includes monitoring of urinary output. In head-injured patients, especially those with multiple injuries, the two most important goals are preservation of cerebral perfusion pressure (mean arterial pressure minus intracranial pressure) and maintenance of systemic oxygen availability (cardiac index times arterial oxygen content).
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An important feature of traumatic brain injury is that much of the ultimate damage appears to occur in a delayed or secondary fashion. Although the exact timing of these secondary sequelae has yet to be elucidated, recent experimental evidence suggests that an extended window of opportunity exists during which various forms of therapy appear to be efficacious. Moreover, new therapies have been developed which can be targeted at distinct pathophysiologic aspects of brain trauma. This article summarizes recent efforts to define secondary mechanisms of brain trauma and review the development of therapeutic strategies for reversing these deleterious events.
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Mild to moderate traumatic brain injury (TBI) is associated with enduring impairments of cognitive function in both humans and animals. However, few experiments have investigated the role of post-injury pharmacologic strategies for attenuating the observed cognitive impairment after TBI. This investigation examined the effects of selective blockade of the presynaptic muscarinic M2 autoreceptor with BIBN 99 on cognitive recovery following rodent TBI. ⋯ Sham-injured animals injected (s.c.) with vehicle (n = 9) or 1.0 (n = 8) mg/kg of BIBN 99 were included for comparison. On days 11-15 after injury, cognitive performance was assessed with the MWM procedure. Results of the second experiment indicated that both doses of BIBN 99 were effective in attenuating cognitive deficits in the MWM as compared to the injured-vehicle treated animals (P < 0.05 for both comparisons).(ABSTRACT TRUNCATED AT 250 WORDS)