The Experts below are selected from a list of 234 Experts worldwide ranked by ideXlab platform
Allan H. Ropper - One of the best experts on this subject based on the ideXlab platform.
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Management of raised Intracranial Pressure and hyperosmolar therapy
Practical Neurology, 2014Co-Authors: Allan H. RopperAbstract:The management of raised Intracranial Pressure is undergoing rapid change. The choice of medical treatments to reduce Intracranial Pressure varies between institutions and regions of the world. The mainstay of therapy, however, continues to be the infusion of a hyperosmolar solution to achieve an osmotic gradient to force the exit of water from the brain. This review introduces the basic concepts of raised Intracranial Pressure, summarises several recent studies that have challenged dogma in the field, and provides practical advice on hyperosmolar treatment, based on personal experience and a critical reading of the literature.
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Hyperosmolar Therapy for Raised Intracranial Pressure
New England Journal of Medicine, 2012Co-Authors: Allan H. RopperAbstract:A 49-year-old woman with traumatic brain injury after an automobile accident is found to have raised Intracranial Pressure, and hyperosmolar therapy is recommended. Hyperosmolar therapy with either hypertonic saline or mannitol reduces Intracranial Pressure by reducing brain volume.
Barry M. Jones - One of the best experts on this subject based on the ideXlab platform.
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Raised Intracranial Pressure in Apert syndrome.
Plastic and reconstructive surgery, 2008Co-Authors: Damian D. Marucci, David Dunaway, Barry M. Jones, Richard D. HaywardAbstract:Background:Raised Intracranial Pressure is a well-known complication of Apert syndrome. The current policy in the authors’ unit is to monitor these patients and only perform surgery when raised Intracranial Pressure has been diagnosed. The authors present their experience with this protocol, as it a
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Intracranial Pressure and Intracranial volume in children with craniosynostosis.
Plastic and reconstructive surgery, 1992Co-Authors: David T. Gault, Dominique Renier, Daniel Marchac, Barry M. JonesAbstract:Intracranial volume and Intracranial Pressure have been measured in 66 children with craniosynostosis, 48 boys and 18 girls. The premature fusion of skull sutures is assumed to restrict skull growth and predispose to elevated Intracranial Pressure. Thirteen children (20 percent) had raised Intracranial Pressure and demonstrated a significant restriction of skull growth. In this series, volume measurement alone, however, did not serve as a reliable predictor that the Intracranial Pressure was raised.
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Relationship between Intracranial Pressure and Intracranial volume in craniosynostosis.
British journal of plastic surgery, 1992Co-Authors: H. Fok, Barry M. Jones, D. G. Gault, U. Andar, Richard HaywardAbstract:Premature fusion of cranial sutures in craniosynostosis has been thought to lead to craniostenosis, which in turn may lead to increased Intracranial Pressures. In 41 consecutive patients with craniosynostosis, Intracranial Pressure and Intracranial volume were measured. Of the 41 patients, 38 (92.6%) had raised Intracranial Pressure but only 4 (9.7%) had a decreased skull volume. In the present study, there is no correlation between Intracranial volume and Intracranial Pressure. This study confirms that the measurement of Intracranial volume, a non invasive procedure, cannot be used to assess Intracranial Pressure and to avoid an invasive procedure.
Edwi N M. Nemoto - One of the best experts on this subject based on the ideXlab platform.
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Critical Cerebral Perfusion Pressure at High Intracranial Pressure Measured by Induced Cerebrovascular and Intracranial Pressure Reactivity
Critical Care Medicine, 2014Co-Authors: Denis E Bragin, Gloria Statom, Howard Yonas, Edwi N M. NemotoAbstract:Objectives: The lower limit of cerebral blood flow autoregulation is the critical cerebral perfusion Pressure at which cerebral blood flow begins to fall. It is important that cerebral perfusion Pressure be maintained above this level to ensure adequate cerebral blood flow, especially in patients with high Intracranial Pressure. However, the critical cerebral perfusion Pressure of 50 mm Hg, obtained by decreasing mean arterial Pressure, differs from the value of 30 mm Hg, obtained by increasing Intracranial Pressure, which we previously showed was due to microvascular shunt flow maintenance of a falsely high cerebral blood flow. The present study shows that the critical cerebral perfusion Pressure, measured by increasing Intracranial Pressure to decrease cerebral perfusion Pressure, is inaccurate but accurately determined by dopamine-induced dynamic Intracranial Pressure reactivity and cerebrovascular reactivity. Design: Cerebral perfusion Pressure was decreased either by increasing Intracranial Pressure or decreasing mean arterial Pressure and the critical cerebral perfusion Pressure by both methods compared. Cortical Doppler flux, Intracranial Pressure, and mean arterial Pressure were monitored throughout the study. At each cerebral perfusion Pressure, we measured microvascular RBC flow velocity, blood-brain barrier integrity (transcapillary dye extravasation), and tissue oxygenation (reduced nicotinamide adenine dinucleotide) in the cerebral cortex of rats using in vivo two-photon laser scanning microscopy. Setting: University laboratory. Subjects: Male Sprague-Dawley rats. Interventions: At each cerebral perfusion Pressure, dopamineinduced arterial Pressure transients (~10 mm Hg, ~45 s duration) were used to measure induced Intracranial Pressure reactivity (∆ Intracranial Pressure/∆ mean arterial Pressure) and induced cerebrovascular reactivity (∆ cerebral blood flow/∆ mean arterial Pressure). Measurements and Main Results: At a normal cerebral perfusion Pressure of 70 mm Hg, 10 mm Hg mean arterial Pressure pulses had no effect on Intracranial Pressure or cerebral blood flow (induced Intracranial Pressure reactivity = –0.03 ± 0.07 and induced cerebrovascular reactivity = –0.02 ± 0.09), reflecting intact autoregulation. Decreasing cerebral perfusion Pressure to 50 mm Hg by increasing Intracranial Pressure increased induced Intracranial Pressure reactivity and induced cerebrovascular reactivity to 0.24 ± 0.09 and 0.31 ± 0.13, respectively, reflecting impaired autoregulation (p < 0.05). By static cerebral blood flow, the first significant decrease in cerebral blood flow occurred at a cerebral perfusion Pressure of 30 mm Hg (0.71 ± 0.08, p < 0.05). Conclusions: Critical cerebral perfusion Pressure of 50 mm Hg was accurately determined by induced Intracranial Pressure reactivity and induced cerebrovascular reactivity, whereas the static method failed. (Crit Care Med 2014; XX:00–00)
Jose I. Suarez - One of the best experts on this subject based on the ideXlab platform.
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Raised Intracranial Pressure.
Current treatment options in neurology, 2005Co-Authors: Eliahu S. Feen, Jose I. SuarezAbstract:Raised Intracranial Pressure is a relatively common problem facing the clinician treating neurocritically ill patients. It is a leading cause of death in patients with Intracranial pathology. There is a lack of controlled clinical trials evaluating most of the therapies currently available for raised Intracranial Pressure. The basic pathophysiologic and clinical principles of raised Intracranial Pressure are discussed and the major treatment options are presented. Patients with raised Intracranial Pressure should be evaluated immediately with particular attention to airway and hemodynamic status. Controlled hyperventilation and hyperosmolality (using mannitol or hypertonic saline solutions) frequently are administered simultaneously. In patients with refractory elevation of Intracranial Pressure other therapies such as barbiturate coma and surgical interventions are available.
Denis E Bragin - One of the best experts on this subject based on the ideXlab platform.
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Critical Cerebral Perfusion Pressure at High Intracranial Pressure Measured by Induced Cerebrovascular and Intracranial Pressure Reactivity
Critical Care Medicine, 2014Co-Authors: Denis E Bragin, Gloria Statom, Howard Yonas, Edwi N M. NemotoAbstract:Objectives: The lower limit of cerebral blood flow autoregulation is the critical cerebral perfusion Pressure at which cerebral blood flow begins to fall. It is important that cerebral perfusion Pressure be maintained above this level to ensure adequate cerebral blood flow, especially in patients with high Intracranial Pressure. However, the critical cerebral perfusion Pressure of 50 mm Hg, obtained by decreasing mean arterial Pressure, differs from the value of 30 mm Hg, obtained by increasing Intracranial Pressure, which we previously showed was due to microvascular shunt flow maintenance of a falsely high cerebral blood flow. The present study shows that the critical cerebral perfusion Pressure, measured by increasing Intracranial Pressure to decrease cerebral perfusion Pressure, is inaccurate but accurately determined by dopamine-induced dynamic Intracranial Pressure reactivity and cerebrovascular reactivity. Design: Cerebral perfusion Pressure was decreased either by increasing Intracranial Pressure or decreasing mean arterial Pressure and the critical cerebral perfusion Pressure by both methods compared. Cortical Doppler flux, Intracranial Pressure, and mean arterial Pressure were monitored throughout the study. At each cerebral perfusion Pressure, we measured microvascular RBC flow velocity, blood-brain barrier integrity (transcapillary dye extravasation), and tissue oxygenation (reduced nicotinamide adenine dinucleotide) in the cerebral cortex of rats using in vivo two-photon laser scanning microscopy. Setting: University laboratory. Subjects: Male Sprague-Dawley rats. Interventions: At each cerebral perfusion Pressure, dopamineinduced arterial Pressure transients (~10 mm Hg, ~45 s duration) were used to measure induced Intracranial Pressure reactivity (∆ Intracranial Pressure/∆ mean arterial Pressure) and induced cerebrovascular reactivity (∆ cerebral blood flow/∆ mean arterial Pressure). Measurements and Main Results: At a normal cerebral perfusion Pressure of 70 mm Hg, 10 mm Hg mean arterial Pressure pulses had no effect on Intracranial Pressure or cerebral blood flow (induced Intracranial Pressure reactivity = –0.03 ± 0.07 and induced cerebrovascular reactivity = –0.02 ± 0.09), reflecting intact autoregulation. Decreasing cerebral perfusion Pressure to 50 mm Hg by increasing Intracranial Pressure increased induced Intracranial Pressure reactivity and induced cerebrovascular reactivity to 0.24 ± 0.09 and 0.31 ± 0.13, respectively, reflecting impaired autoregulation (p < 0.05). By static cerebral blood flow, the first significant decrease in cerebral blood flow occurred at a cerebral perfusion Pressure of 30 mm Hg (0.71 ± 0.08, p < 0.05). Conclusions: Critical cerebral perfusion Pressure of 50 mm Hg was accurately determined by induced Intracranial Pressure reactivity and induced cerebrovascular reactivity, whereas the static method failed. (Crit Care Med 2014; XX:00–00)