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Guy Rosenthal, J. Claude Hemphill III, Marco Sorani, Christine Martin, Diane Morabito, Michele Meeker, Vincent Wang, and Geoffrey T. Manley

across all PaO 2 values, PbtO 2 is robustly related to PaO 2 (r = 0.70, p < 0.001), confirming the strong relationship between PaO 2 and PbtO 2 . As anticipated from the relationships between the PF ratio, PaO 2 , and PbtO 2 , we found a significant relationship between baseline PF ratio and challenge PbtO 2 (r = 0.41, p < 0.001). To further evaluate the effect of pulmonary status on brain tissue oxygenation, we compared baseline and challenge PbtO 2 in patients with a PF ratio > 250 with those patients with a PF ratio ≤ 250 ( Fig. 3 ). At baseline, no

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Andreas Jödicke, Felix Hübner, and Dieter-Karsten Böker

occlusion. 2, 5, 24, 30, 34–36, 38–40, 43, 46–48 Even without undergoing temporary arterial occlusion, patients are still at risk for secondary brain damage at surgery. Ferguson, et al., 13 coined the term “silent spasm” to refer to altered CBF despite good clinical grade in patients with SAH, which occurs together with a reduced CMRO 2 . 15 Moreover, anaerobic cerebral metabolism has been shown to occur in patients with SAH, 23, 41 indicating profound perturbation of cerebral metabolism early after SAH. Brain tissue oxygenation (PO 2 ) has been used in monitoring

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Arun K. Gupta, Peter J. Hutchinson, Tim Fryer, Pippa G. Al-Rawi, Dot A. Parry, Pawan S. Minhas, Rupert Kett-White, Peter J. Kirkpatrick, Julian C. Mathews, Steve Downey, Franklin Aigbirhio, John Clark, John D. Pickard, and David K. Menon

global cerebral oxygenation and metabolism, but it has significant limitations when used as a method of continuous monitoring in clinical practice. Most prominent among these are technical problems associated with maintenance of continuous monitoring and the inability of this technique to provide localized data (for example, data from sites of injury or healthy brain). 4 Direct continuous measurement of brain tissue oxygenation and metabolism has been attempted both intraoperatively and in an intensive care setting. 9, 15, 21, 23 Such studies have involved both

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Neurosurgical Forum: Letters to the Editor To The Editor Sandra Rossi , M.D. Nino Stocchetti , M.D. Ospedale Policlinico IRCCS Milan, Italy 1065 1067 We read with interest the paper by Menzel and coworkers (Menzel M, Doppenberg EMR, Zauner A, et al: Increased inspired oxygen concentration as a factor in improved brain tissue oxygenation and tissue lactate levels after severe human head injury. J Neurosurg 91: 1–10, July, 1999) and we would like to add some comments. The authors suggest that the increase in brain tissue oxygen tension (ptiO 2 ) obtained by

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Neurosurgical Forum: Letters to the Editor To The Editor Julio Cruz , M.D., Ph.D. The Comprehensive International Center for Neuroemergencies São Paulo, Brazil 736 737 This letter is in regard to a recently published paper (Menzel M, Doppenberg EMR, Zauner A, et al: Increased inspired oxygen concentration as a factor in improved brain tissue oxygenation and tissue lactate levels after severe human head injury. J Neurosurg 91: 1–10, July, 1999). As usual, the Richmond group overemphasized the occurrence of traumatic brain ischemia. It has long been known that

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Matthias Menzel, Egon M. R. Doppenberg, Alois Zauner, Jens Soukup, Michael M. Reinert, and Ross Bullock

arterial O 2 concentrations. 36, 40, 44, 53, 58 In these animal studies brain tissue oxygenation was monitored using different technical approaches in healthy noninjured brains. Van Santbrink, et al., 58 first described the effect of increasing brain tissue PO 2 in patients with severe head injury in response to normobaric hyperoxia induced by mechanical ventilation with 100% inspiratory O 2 over a period of approximately 30 minutes. This pilot study has shown that increasing the PaO 2 to levels higher than needed to fully saturate hemoglobin apparently can

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Anthony A. Figaji, Eugene Zwane, A. Graham Fieggen, Andrew C. Argent, Peter D. Le Roux, Peter Siesjo, and Jonathan C. Peter

tissue oxygenation study . Neurosurgery 63 : 83 – 91 , 2008 15 Fog M : The relationship between the blood pressure and the tonic regulation of the pial arteries . J Neurol Psychiatry 1 : 187 – 197 , 1938 16 Freeman SS , Udomphorn Y , Armstead WM , Fisk DM , Vavilala MS : Young age as a risk factor for impaired cerebral autoregulation after moderate to severe pediatric traumatic brain injury . Anesthesiology 108 : 588 – 595 , 2008 17 Hemphill JC III , Knudson MM , Derugin N , Morabito D , Manley GT : Carbon dioxide

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Matthias Menzel, Egon M. R. Doppenberg, Alois Zauner, Jens Soukup, Michael M. Reinert, and Ross Bullock

Object

Early impairment of cerebral blood flow in patients with severe head injury correlates with poor brain tissue O2 delivery and may be an important cause of ischemic brain damage. The purpose of this study was to measure cerebral tissue PO2, lactate, and glucose in patients after severe head injury to determine the effect of increased tissue O2 achieved by increasing the fraction of inspired oxygen (FiO2).

Methods

In addition to standard monitoring of intracranial pressure and cerebral perfusion pressure, the authors continuously measured brain tissue PO2, PCO2, pH, and temperature in 22 patients with severe head injury. Microdialysis was performed to analyze lactate and glucose levels. In one cohort of 12 patients, the PaO2) was increased to 441 ± 88 mm Hg over a period of 6 hours by raising the FiO2 from 35 ± 5% to 100% in two stages. The results were analyzed and compared with the findings in a control cohort of 12 patients who received standard respiratory therapy (mean PaO2 136.4 ± 22.1 mm Hg).

The mean brain PO2 levels increased in the O2-treated patients up to 359 ± 39% of the baseline level during the 6-hour FiO2 enhancement period, whereas the mean dialysate lactate levels decreased by 40% (p < 0.05). During this O2 enhancement period, glucose levels in brain tissue demonstrated a heterogeneous course. None of the monitored parameters in the control cohort showed significant variations during the entire observation period.

Conclusions

Markedly elevated lactate levels in brain tissue are common after severe head injury. Increasing PaO2 to higher levels than necessary to saturate hemoglobin, as performed in the O2-treated cohort, appears to improve the O2 supply in brain tissue. During the early period after severe head injury, increased lactate levels in brain tissue were reduced by increasing FiO2. This may imply a shift to aerobic metabolism.

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Roman Hlatky, Alex B. Valadka, Shankar P. Gopinath, and Claudia S. Robertson

. Hyperoxia influences PbtO 2 more than PjvO 2 or brain tissue oxygenation measured with near-infrared spectroscopy. 13 Using positron emission tomography studies to measure PvO 2 , Gupta et al. 5 showed that the absolute values for PbtO 2 and PvO 2 are not closely related, but changes in PbtO 2 and PvO 2 after therapeutic interventions are closely correlated. The purpose of this study was to examine the role of rCBF at the site of the PO 2 probe in determining the response of PbtO 2 to induced hyperoxia. Clinical Material and Methods Patient Selection

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Taek Hyun Kwon, Dong Sun, Wilson P. Daugherty, Bruce D. Spiess, and M. Ross Bullock

R ecent advances in brain monitoring techniques have provided new data on the time-dependent changes in brain tissue oxygenation after severe head injury in humans and revealed that low brain tissue PO 2 levels are a very common finding. 4, 13, 24, 25, 35, 54–56 Moreover, the lowest brain tissue PO 2 levels are reported to be associated with increased morbidity and mortality rates 53, 55 and correlate closely with reduced regional blood flow. 6, 15 It therefore seems logical to search for ways to improve brain tissue oxygenation in these circumstances. 5