Articles: brain-injuries.
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The goal of care of the traumatic brain-injured patient is to prevent secondary injury. Technology gives the caregivers information as to the cause and severity of injury and can guide appropriate management of the patient. Use of multimodality monitoring increases the complexity of care but may allow for better targeted therapy. This article will discuss the current state of technology, the physiology and pathophysiology that it assesses, the normal and abnormal values obtained, and how care will be impacted.
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Numerous differences exist between the pediatric and adult brain-injured patient. However, children with brain injuries are frequently cared for in adult Intensive Care Units (ICUs). ⋯ The article examines the care of the brain-injured child, including monitoring, psychosocial considerations, and supportive care with emphasis on avoiding secondary brain injury by decreasing and maintaining intracranial pressure. Differences between the pediatric patients and the adult patient are highlighted throughout.
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Journal of neurosurgery · Nov 2000
Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a preliminary report.
Recognition of pituitary hormonal insufficiencies after head injury and aneurysmal subarachnoid hemorrhage (SAH) may be important, especially given that hypopituitarism-related neurobehavioral problems are typically alleviated by hormone replacement. In this prospective study the authors sought to determine the rate and risk factors of pituitary dysfunction after head injury and SAH in patients at least 3 months after insult. ⋯ From this preliminary study, some degree of hypopituitarism appears to occur in approximately 40% of patients with moderate or severe head injury, with GH and gonadotroph deficiencies being most common. A high degree of injury severity and secondary cerebral insults are likely risk factors for hypopituitarism. Pituitary dysfunction also occurs in patients with poor-grade aneurysms. Postacute pituitary function testing may be warranted in most patients with moderate or severe head injury, particularly those with diffuse brain swelling and those sustaining hypotensive or hypoxic insults. The neurobehavioral effects of GH replacement in patients suffering from head injury or SAH warrant further study.
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Eur J Cardiothorac Surg · Nov 2000
Aortic arch repair using hypothermic circulatory arrest technique associated with pharmacological brain protection.
Hypothermic circulatory arrest is a standard procedure for the treatment of aortic arch. However, there is a time limit for this procedure. There is now an urgent need to develop prophylactic measures to extend the time limit. We have used a pharmacological mixture of thiopental, nicardipine and mannitol for all patients undergoing circulatory arrest since 1991 to extend the safe limit. The purpose of this study was to analyze the neurological complications demonstrated by these patients and to evaluate the brain-protective effects of our measure. ⋯ The findings of the present study suggest that our pharmacological brain protection appears to be effective for safely extending hypothermic circulatory arrest.
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Critical care medicine · Nov 2000
Effect of neutropenia and granulocyte colony stimulating factor-induced neutrophilia on blood-brain barrier permeability and brain edema after traumatic brain injury in rats.
Granulocyte colony stimulating factor (GCSF) has been used to increase systemic absolute neutrophil count (ANC) in patients with severe traumatic brain injury to reduce nosocomial infection risk. However, the effect of increasing systemic ANC on the pathogenesis of experimental traumatic brain injury has not been studied. Thus, we evaluated the effect of systemic ANC on blood-brain barrier (BBB) damage and brain edema after traumatic brain injury in rats. ⋯ Systemic ANC influences BBB damage after traumatic brain injury produced by CCI. Because BBB damage and brain edema are discordant, mechanisms other than BBB damage likely predominate in the pathogenesis of brain edema after contusion. The implications of increased BBB permeability with the administration of GCSF in our model remains to be determined. Increasing systemic ANC before CCI with GCSF administration does not increase posttraumatic brain neutrophil accumulation or brain edema after CCI in rats. The finding that neutrophil infiltration is not enhanced by systemic neutrophilia suggests that the ability of GCSF-stimulated neutrophils to migrate into injured tissue may be impaired. Further studies are needed to evaluate the effects of GCSF administration on secondary injury and functional outcome in experimental models of traumatic brain injury.