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Brain oxygen tension and outcome in patients with aneurysmal subarachnoid hemorrhage

Clinical article

Rohan Ramakrishna, Michael Stiefel, Joshua Udoteuk, Alejandro Spiotta, Joshua M. Levine, W. Andrew Kofke, Eric Zager, Wei Yang, and Peter LeRoux

arterial oxygen saturation) were recorded in all patients. Cerebral perfusion pressure was calculated for each patient using the formula CPP = MAP − ICP. All physiological variables were continuously recorded using a bedside monitor (Component Monitoring System M1046–9090C, Hewlett Packard). Intracranial monitoring was continued for at least 72 hours unless care was limited or the patient died first. Intracranial monitors were removed only when ICP had been normal for 24 hours without any treatment. General Patient Care Patients received treatment in the

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Somatosensory evoked potentials in intracranial hypertension: analysis of the effects of hypoxia

Paul R. Eldridge, D. Terence Hope, Patrick M. Yeoman, Iain K. Farquhar, Michael Mitchell, Sharon A. Clarke, and N. Jollyon Smith

for irreversible cellular damage, the somatosensory evoked response might be used as a marker of imminent brain damage, perhaps indicating when cerebral blood flow (CBF) has fallen to critical levels. In clinical practice, continuous measurement of CBF is not practical. Since CBF depends upon cerebral perfusion pressure (CPP), a similar logic applies to perfusion thresholds; however, CPP can be monitored continuously. In head injury, intracranial pressure (ICP) may rise due to diffuse brain swelling. Unless offset by a compensatory rise in mean systemic arterial

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Continuous monitoring of cerebrovascular pressure reactivity in patients with head injury

Christian Zweifel, Andrea Lavinio, Luzius A. Steiner, Danila Radolovich, Peter Smielewski, Ivan Timofeev, Magdalena Hiler, Marcella Balestreri, Peter J. Kirkpatrick, John D. Pickard, Peter Hutchinson, and Marek Czosnyka

intracranial pressure and cerebral perfusion pressure on severe disability and mortality after head injury . Neurocrit Care 4 : 8 – 13 , 2006 10.1385/NCC:4:1:008 5 Balestreri M , Czosnyka M , Steiner LA , Schmidt E , Smielewski P , Matta B , : Intracranial hypertension: what additional information can be derived from ICP waveform after head injury? . Acta Neurochir (Wien) 146 : 131 – 141 , 2004 10.1007/s00701-003-0187-y 6 Bouma GJ , Muizelaar JP , Choi SC , Newlon PG , Young HF : Cerebral circulation and metabolism after severe

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Brain tissue oxygen monitoring in pediatric patients with severe traumatic brain injury

Michael F. Stiefel, Joshua D. Udoetuk, Phillip B. Storm, Leslie N. Sutton, Heakyung Kim, Troy E. Dominguez, Mark A. Helfaer, and Jimmy W. Huh

follow-up head CT scans. All patients were monitored for at least 72 hours unless care was withdrawn or they died. Cerebral perfusion pressure was calculated from the measured parameters (CPP = MABP – ICP). Heart rate, blood pressure (measured via an arterial line), fraction of inspired oxygen, arterial oxygen saturation, partial pressure of arterial oxygen, end-tidal and arterial carbon dioxide, and arterial pH were measured in all patients. All physiological variables were continuously recorded using a bedside monitor (Solar 8000 M; GE Medical Systems Information

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Monitoring of cerebral oxygenation in patients with severe head injuries: brain tissue PO2 versus jugular vein oxygen saturation

Karl L. Kiening, Andreas W. Unterberg, Tillman F. Bardt, Gerd-Helge Schneider, and Wolfgang R. Lanksch

F ollowing severe head injury, patients run a high risk of developing secondary cerebral hypoxic and ischemic damage due to reduced cerebral perfusion pressure (CPP), either because of intracranial hypertension or arterial hypotension. 1, 3, 16, 21, 22 This may lead to a compromise in cerebral blood flow (CBF) and, thus, in oxygen supply, which in turn may negatively affect final outcome. 30 To minimize the risk of secondary cerebral hypoxia and ischemia following trauma, care should be taken to evacuate mass lesions as early as possible. As a follow

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Association between elevated brain tissue glycerol levels and poor outcome following severe traumatic brain injury

Tobias Clausen, Oscar Luis Alves, Michael Reinert, Egon Doppenberg, Alois Zauner, and Ross Bullock

: The Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Guidelines for cerebral perfusion pressure. J Neurotrauma 17 : 507 – 511 , 2000 Anonymous: The Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Guidelines for cerebral perfusion pressure. J Neurotrauma 17: 507–511, 2000 4. Asgeirsson B , Grande PO , Nordstrom CH : A new therapy of post-trauma brain oedema based

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Role of intracranial pressure monitoring in severely head-injured patients without signs of intracranial hypertension on initial computerized tomography

Michael G. O'Sullivan, Patrick F. Statham, Patricia A. Jones, J. Douglas Miller, N. Mark Dearden, Ian R. Piper, Shirley I. Anderson, Alma Housley, Peter J. Andrews, Susan Midgley, Jane Corrie, Janice I. Tocher, and Robin Sellar

physiological parameters digitized and transferred to a personal computer on a minute-to-minute basis so that detailed analysis may be performed. The purpose of this study was to determine whether comatose head-injured patients whose initial CT scan was normal or did not show a mass lesion, midline shift, or effaced cisterns developed elevated ICP, arterial hypotension, or reduced cerebral perfusion pressure (CPP) more frequently than has previously been considered. Clinical Material and Methods Patient Population Between January, 1989, and May, 1991, 170 severely

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Elevated jugular venous oxygen saturation after severe head injury

Manuela Cormio, Alex B. Valadka, and Claudia S. Robertson

normally less than 5%. 5 Cerebrovascular resistance (CVR) values were obtained by dividing cerebral perfusion pressure (CPP) by CBF. Classification of Groups High SjvO 2 (Group I) was defined as 75% or higher, normal SjvO 2 (Group II) as 56 to 74%, and low SjvO 2 (Group III) as 55% or lower. These categories refer to the mean SjvO 2 for the entire period of monitoring for each patient. Outcome at 6 months was assessed using the Glasgow Outcome Scale (GOS). 11 Outcomes were classified into three groups: 1) dead or persistent vegetative state; 2) severe disability

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Acute vasoconstriction: decrease and recovery of cerebral blood flow after various intensities of experimental subarachnoid hemorrhage in rats

Laboratory investigation

Thomas Westermaier, Alina Jauss, Jörg Eriskat, Ekkehard Kunze, and Klaus Roosen

differences between the SAH groups were not statistically significant. F ig . 1. Graphs showing the time course of ICP (A), MABP (B), and CPP (C). Secondary to a rapid elevation of ICP, MABP rose in the 3-0 and 4-0 groups. Thus, CPP was significantly elevated only 1 minute after SAH. *p < 0.05 versus the control group; §p < 0.05 versus the 4-0 and 5-0 groups. Cerebral perfusion pressure prior to SAH was 74 ± 15 mm Hg in the control group, 74 ± 14 mm Hg in the 3-0 group, 72 ± 14 mm Hg in the 4-0 group, and 72 ± 10 mm Hg in the 5-0 group. After SAH, CPP declined

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Experimental study on the pathogenesis of heat stroke

Chun-Jen Shih, Mao-Tsun Lin, and Shin-Han Tsai

. The values are expressed as the mean ± standard error of the mean. † Significantly different from corresponding control values (collected at T a = 24°C), at p < 0.05 (one-way analysis of variance). Table 2 contains a summary of the mean and the standard error values of mean arterial blood pressure (MABP), ICP, and cerebral perfusion pressure (CPP = MABP − ICP) in six rabbits both at the start of heat stress (T a = 40°C) and at the onset of heat stroke. It can be seen from the table that the CPP decreased significantly from an average value of 80