Lack of improvement in cerebral metabolism after hyperoxia in severe head injury: a microdialysis study

2003 ◽  
Vol 98 (5) ◽  
pp. 952-958 ◽  
Author(s):  
Sandra Magnoni ◽  
Laura Ghisoni ◽  
Marco Locatelli ◽  
Mariangela Caimi ◽  
Angelo Colombo ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brain Tissue ◽  
Cerebral Metabolism ◽  
Extracellular Fluid ◽  
Redox Status ◽  
Content Type ◽  
Lactate Levels ◽  
Microdialysis Study ◽  
Fine Print ◽  
Pyruvate Ratio

Object. The authors investigated the effects of hyperoxia on brain tissue PO2 and on glucose metabolism in cerebral and adipose tissue after traumatic brain injury (TBI). Methods. After 3 hours of ventilation with pure O2, 18 tests were performed on different days in eight comatose patients with TBI. Lactate, pyruvate, glucose, glutamate, and brain tissue PO2 were measured in the cerebral extracellular fluid (ECF) by using microdialysis. Analytes were also measured in the ECF of abdominal adipose tissue. After 3 hours of increase in the fraction of inspired O2, brain tissue PO2 rose from the baseline value of 32.7 ± 18 to 122.6 ± 45.2 mm Hg (p < 0.0001), whereas brain lactate dropped from its baseline (3.21 ± 2.77 mmol/L), reaching its lowest value (2.90 ± 2.58 mmol/L) after 3 hours of hyperoxia (p < 0.01). Pyruvate dropped as well, from 153 ± 56 to 141 ± 56 µmol/L (p < 0.05), so the lactate/pyruvate ratio did not change. No significant changes were observed in glucose and glutamate. The arteriovenous difference in O2 content dropped, although not significantly, from a baseline of 4.52 ± 1.22 to 4.15 ± 0.76 ml/100 ml. The mean concentration of lactate in adipose tissue fell significantly as well (p < 0.01), but the lactate/pyruvate ratio did not change. Conclusions. Hyperoxia slightly reduced lactate levels in brain tissue after TBI. The estimated redox status of the cells, however, did not change and cerebral O2 extraction seemed to be reduced. These data indicate that oxidation of glucose was not improved by hyperoxia in cerebral and adipose tissue, and might even be impaired.

Cerebral effects of hypocapnia plus nitroglycerin-induced hypotension in dogs

1986 ◽  
Vol 64 (6) ◽  
pp. 924-931 ◽  
Author(s):  
Alan A. Artru ◽  
Kim Wright ◽  
Peter S. Colley
Keyword(s):  
Sodium Nitroprusside ◽  
Brain Tissue ◽  
Cerebral Metabolism ◽  
Energy Charge ◽  
Metabolic Disturbances ◽  
Induced Hypotension ◽  
Content Type ◽  
Arterial Blood ◽  
Cerebral Metabolites ◽  
Fine Print

✓ This study examined the effect of hypocapnia (PaCO2 20 mm Hg) on cerebral metabolism and the electroencephalogram (EEG) findings in 12 dogs during nitroglycerin (NTG)-induced hypotension. Previous studies suggest that NTG is a more potent cerebral vasodilator than sodium nitroprusside or trimethaphan. It was speculated that combining hypocapnia with NTG-induced hypotension would cause less disturbance of cerebral metabolism and the EEG than the disturbances previously reported when hypocapnia was combined with hypotension induced by sodium nitroprusside or trimethaphan. All 12 dogs were examined at 1) normocapnia with normotension; 2) hypocapnia with normotension; and 3) hypocapnia combined with NTG-induced hypotension to mean arterial blood pressure (MABP) levels of 60, 50, and 40 mm Hg. In six dogs the cerebral metabolic rate of oxygen was determined, and the EEG was evaluated using compressed spectral analysis. Brain tissue metabolites were calculated in the other six dogs. During normotension, hypocapnia caused no deterioration of cerebral metabolism or of the EEG. Hypocapnia combined with NTG-induced hypotension caused a decrease of the power of the α and β2 spectra of the EEG at MABP's of 60 mm Hg or less. At an MABP of 40 mm Hg, brain tissue phosphocreatine and the cerebral energy charge decreased, while the brain tissue lactate:pyruvate ratio increased. Thirty minutes after restoration of normocapnia with normotension, cerebral metabolites returned to initial values, but the power of the EEG α and β2 spectra was decreased compared to baseline values. The cerebral metabolic disturbances and EEG alterations seen here with hypocapnia plus NTG-induced hypotension were similar to those previously reported with hypocapnia plus sodium nitroprusside-induced hypotension, and less than those previously reported with hypocapnia plus trimethaphan-induced hypotension. For hyperventilated patients, administration of NTG may be a better hypotensive treatment than trimethaphan, but similar in effect to sodium nitroprusside.

Influence of oxygen therapy on glucose—lactate metabolism after diffuse brain injury

2004 ◽  
Vol 101 (2) ◽  
pp. 323-329 ◽  
Author(s):  
Michael Reinert ◽  
Benoit Schaller ◽  
Hans Rudolf Widmer ◽  
Rolf Seiler ◽  
Ross Bullock
Keyword(s):  
Brain Injury ◽  
Brain Tissue ◽  
Brain Metabolism ◽  
Arterial Line ◽  
Content Type ◽  
Diffuse Brain Injury ◽  
Lactate Levels ◽  
The Brain ◽  
Fine Print ◽  
Diffuse Brain

Object. Severe traumatic brain injury (TBI) imposes a huge metabolic load on brain tissue, which can be summarized initially as a state of hypermetabolism and hyperglycolysis. In experiments O2 consumption has been shown to increase early after trauma, especially in the presence of high lactate levels and forced O2 availability. In recent clinical studies the effect of increasing O2 availability on brain metabolism has been analyzed. By their nature, however, clinical trauma models suffer from a heterogeneous injury distribution. The aim of this study was to analyze, in a standardized diffuse brain injury model, the effect of increasing the fraction of inspired O2 on brain glucose and lactate levels, and to compare this effect with the metabolism of the noninjured sham-operated brain. Methods. A diffuse severe TBI model developed by Foda and Maramarou, et al., in which a 420-g weight is dropped from a height of 2 m was used in this study. Forty-one male Wistar rats each weighing approximately 300 g were included. Anesthesized rats were monitored by placing a femoral arterial line for blood pressure and blood was drawn for a blood gas analysis. Two time periods were defined: Period A was defined as preinjury and Period B as postinjury. During Period B two levels of fraction of inspired oxygen (FiO2) were studied: air (FiO2 0.21) and oxygen (FiO2 1). Four groups were studied including sham-operated animals: air-air-sham (AAS); air-O2-sham (AOS); air-air-trauma (AAT); and air-O2-trauma (AOT). In six rats the effect of increasing the FiO2 on serum glucose and lactate was analyzed. During Period B lactate values in the brain determined using microdialysis were significantly lower (p < 0.05) in the AOT group than in the AAT group and glucose values in the brain determined using microdialysis were significantly higher (p < 0.04). No differences were demonstrated in the other groups. Increasing the FiO2 had no significant effect on the serum levels of glucose and lactate. Conclusions. Increasing the FiO2 influences dialysate glucose and lactate levels in injured brain tissue. Using an FiO2 of 1 influences brain metabolism in such a way that lactate is significantly reduced and glucose significantly increased. No changes in dialysate glucose and lactate values were found in the noninjured brain.

Increased inspired oxygen concentration as a factor in improved brain tissue oxygenation and tissue lactate levels after severe human head injury

1999 ◽  
Vol 91 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Matthias Menzel ◽  
Egon M. R. Doppenberg ◽  
Alois Zauner ◽  
Jens Soukup ◽  
Michael M. Reinert ◽  
...  
Keyword(s):  
Head Injury ◽  
Brain Tissue ◽  
Severe Head Injury ◽  
Control Cohort ◽  
Content Type ◽  
Glucose Levels ◽  
The Mean ◽  
Lactate Levels ◽  
Inspired Oxygen ◽  
Fine Print

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.

Cerebral metabolism after fluid-percussion injury and hypoxia in a feline model

2002 ◽  
Vol 97 (3) ◽  
pp. 643-649 ◽  
Author(s):  
Alois Zauner ◽  
Tobias Clausen ◽  
Oscar L. Alves ◽  
Ann Rice ◽  
Joseph Levasseur ◽  
...  
Keyword(s):  
Brain Injury ◽  
Brain Tissue ◽  
Cerebral Metabolism ◽  
Acid Base ◽  
Content Type ◽  
Hypoxic Injury ◽  
Fluid Percussion ◽  
Fluid Percussion Injury ◽  
Feline Model ◽  
Fine Print

Object. Currently, there are no good clinical tools to identify the onset of secondary brain injury and/or hypoxia after traumatic brain injury (TBI). The aim of this study was to evaluate simultaneously early changes of cerebral metabolism, acid—base homeostasis, and oxygenation, as well as their interrelationship after TBI and arterial hypoxia. Methods. Cerebral biochemistry and O2 supply were measured simultaneously in a feline model of fluid-percussion injury (FPI) and secondary hypoxic injury. After FPI, brain tissue PO2 decreased from 33 ± 5 mm Hg to 10 ± 4 mm Hg and brain tissue PCO2 increased from 55 ± 2 mm Hg to 81 ± 9 mm Hg, whereas cerebral pH fell from 7.1 ± 0.06 to 6.84 ± 0.14 (p < 0.05 for all three measures). After 40 minutes of hypoxia, brain tissue PO2 and pH decreased further to 0 mm Hg and 6.48 ± 0.28, respectively (p < 0.05), whereas brain tissue PCO2 remained high at 83 ± 13 mm Hg. Secondary hypoxic injury caused a drastic increase in cerebral lactate from 513 ± 69 µM/L to 3219 ± 490 µM/L (p < 0.05). The lactate/glucose ratio increased from 0.7 ± 0.1 to 9.1 ± 2 after hypoxia was introduced. The O2 consumption decreased significantly from 18.5 ± 1.1 µl/mg/hr to 13.2 ± 2.1 µl/mg/hr after hypoxia was induced. Conclusions. Cerebral metabolism, O2 supply, and acid—base balance were severely compromised ultra-early after TBI, and they declined further if arterial hypoxia was present. The complexity of pathophysiological changes and their interactions after TBI might explain why specific therapeutic attempts that are aimed at the normalization of only one component have failed to improve outcome in severely head injured patients.

Production and clearance of lactate from brain tissue, cerebrospinal fluid, and serum following experimental brain injury

1988 ◽  
Vol 69 (5) ◽  
pp. 736-744 ◽  
Author(s):  
Suguru Inao ◽  
Anthony Marmarou ◽  
Geoff D. Clarke ◽  
Bruce J. Andersen ◽  
Panos P. Fatouros ◽  
...  
Keyword(s):  
Brain Tissue ◽  
Severe Trauma ◽  
Serum Lactate ◽  
Content Type ◽  
Brain Ph ◽  
Csf Lactate ◽  
Lactate Levels ◽  
The Brain ◽  
Brain Lactate ◽  
Fine Print

✓ Lactate dynamics in the brain, cerebrospinal fluid (CSF), and serum were studied in 20 chloralose-anesthetized cats following fluid-percussion trauma. Brain lactate and brain tissue pH were measured by hydrogen-1 and phophorus-31 magnetic resonance spectroscopy. The CSF, arterial, and cerebrovenous serum lactate levels as well as serum glucose concentration were quantified. In the six sham-operated control animals, brain, CSF, cerebrovenous, and arterial lactate levels as well as brain pH remained at normal values. In the five animals in the mild-trauma group (1.6 atm), brain and CSF lactate levels were moderately elevated, although the brain pH and serum lactate content remained at control values. Severe trauma (3.1 atm) in nine cats produced an 82% increase in the brain lactate index and a reduction in brain tissue pH (7.02 ± 0.02 to 6.95 ± 0.02; mean ± standard error of the mean), indicating brain tissue acidosis caused by excessive lactate accumulation. Brain lactate levels reached a peak 1½ hours after severe trauma, then steadily decreased to normal levels by 8 hours posttrauma. Maximum increases of CSF and arterial lactate levels (from 1.4 ± 0.2 to 4.1 ± 0.4 and from 1.6 ± 0.2 to 4.1 to 0.6 mmol/liter, respectively) were observed 15 minutes after trauma, and the values decreased during the next 2 hours. The response was biphasic, with a secondary rise observed in both CSF and serum lactate levels during the remaining 4 hours of the experiment. The difference between the arterial and venous lactate levels (A-Vlact) gradually increased and reached a peak 2 hours postinjury (from −0.05 ± 0.10 to −0.41 ± 0.09 mmol/liter). The results of this study show that the production of lactate in brain tissue, CSF, and blood increased in proportion to the severity of the injury. The observation that lactate levels in blood and CSF are maximum immediately following impact while brain lactate and A-Vlact are gradually increasing suggests that the brain-tissue production of lactate fails to account for the rapid appearance of lactate in CSF and blood. It is speculated that the initial elevation of CSF lactate values reflects the systemic response of trauma, and the secondary rise of CSF lactate levels following severe trauma is due to slow seepage of lactate produced by brain tissue into the CSF space. These studies are the first to describe the temporal profile of brain lactate production and eventual clearance by CSF and blood in fluid-percussion injury. The results emphasize the need for caution in interpreting elevated CSF lactate levels following head injury.

Cerebral oxygen and microdialysis monitoring during aneurysm surgery: effects of blood pressure, cerebrospinal fluid drainage, and temporary clipping on infarction

2002 ◽  
Vol 96 (6) ◽  
pp. 1013-1019 ◽  
Author(s):  
Rupert Kett-White ◽  
Peter J. Hutchinson ◽  
Pippa G. Al-Rawi ◽  
Marek Czosnyka ◽  
Arun K. Gupta ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Brain Tissue ◽  
Total Duration ◽  
Wilcoxon Test ◽  
Fisher Exact Test ◽  
Content Type ◽  
The Impact ◽  
Temporary Clipping ◽  
Fine Print

Object. The aim of this study was to investigate potential episodes of cerebral ischemia during surgery for large and complicated aneurysms, by examining the effects of arterial temporary clipping and the impact of confounding variables such as blood pressure and cerebrospinal fluid (CSF) drainage. Methods. Brain tissue PO2, PCO2, and pH, as well as temperature and extracellular glucose, lactate, pyruvate, and glutamate were monitored in 46 patients by using multiparameter sensors and microdialysis. Baseline data showed that brain tissue PO2 decreased significantly, below a mean arterial pressure (MAP) threshold of 70 mm Hg. Further evidence of its relationship with cerebral perfusion pressure was shown by an increase in mean brain tissue PO2 after drainage of CSF from the basal cisterns (Wilcoxon test, p < 0.01). Temporary clipping was required in 31 patients, with a mean total duration of 14 minutes (range 3–52 minutes), causing brain tissue PO2 to decrease and brain tissue PCO2 to increase (Wilcoxon test, p < 0.01). In patients in whom no subsequent infarction developed in the monitored region, brain tissue PO2 fell to 11 mm Hg (95% confidence interval 8–14 mm Hg). A brain tissue PO2 level below 8 mm Hg for 30 minutes was associated with infarction in any region (p < 0.05 according to the Fisher exact test); other parameters were not predictive of infarction. Intermittent occlusions of less than 30 minutes in total had little effect on extracellular chemistry. Large glutamate increases were only seen in two patients, in both of whom brain tissue PO2 during occlusion was continuously lower than 8 mm Hg for longer than 38 minutes. Conclusions. The brain tissue PO2 decreases with hypotension, and, when it is below 8 mm Hg for longer than 30 minutes during temporary clipping, it is associated with increasing extracellular glutamate levels and cerebral infarction.

Persistent high lactate level as a sensitive MR spectroscopy indicator of completed infarction

1990 ◽  
Vol 72 (5) ◽  
pp. 763-766 ◽  
Author(s):  
Kiyohiro Houkin ◽  
Ingrid L. Kwee ◽  
Tsutomu Nakada
Keyword(s):  
Magnetic Resonance ◽  
Cerebral Infarction ◽  
Mr Spectroscopy ◽  
The Other ◽  
Proton Spectroscopy ◽  
Normal Pattern ◽  
Content Type ◽  
Lactate Levels ◽  
High Lactate ◽  
Fine Print

✓ Serial proton (1H) and phosphorus-31 (31P) magnetic resonance (MR) spectroscopy of cerebral infarction was performed in rats to assess the sensitivity of these techniques for use in clinical cerebral infarction. In this experimental chronic infarction model, 31P spectroscopy tended to return to a “normal” pattern within 24 hours after induction of infarction in spite of pathologically proven completed infarction and, therefore, appeared not to be sensitive enough for clinical application. On the other hand, proton spectroscopy invariably showed persistent high lactate levels and was capable of distinguishing completed infarction from reperfused recovered brain. Persistent high lactate levels appear to be a good MR spectroscopic indicator of completed infarction.

Role of hydrodynamic processes in the pathogenesis of peritumoral brain edema in meningiomas

2000 ◽  
Vol 93 (4) ◽  
pp. 594-604 ◽  
Author(s):  
Michael Bitzer ◽  
Thomas Nägele ◽  
Beverly Geist-Barth ◽  
Uwe Klose ◽  
Eckardt Grönewäller ◽  
...  
Keyword(s):  
Contrast Agent ◽  
Brain Edema ◽  
Brain Tissue ◽  
Magnetic Resonance Images ◽  
Content Type ◽  
Extracellular Contrast Agent ◽  
Peritumoral Brain Edema ◽  
Hydrodynamic Processes ◽  
Fine Print

Object. In a prospective study, 28 patients with 32 intracranial meningiomas were examined to determine the role of hydrodynamic interaction between tumor and surrounding brain tissue in the pathogenesis of peritumoral brain edema.Methods. Gadolinium—diethylenetriamine pentaacetic acid (Gd-DPTA), an extracellular contrast agent used for routine clinical imaging, remains strictly extracellular without crossing an intact blood—brain barrier. Therefore, it is well suited for investigations of hydrodynamic extracellular mechanisms in the development of brain edema. Spin-echo T1-weighted magnetic resonance images were acquired before and after intravenous administration of 0.2 mmol/kg Gd-DPTA. Additional T1-weighted imaging was performed 0.6, 3.5, and 6.5 hours later. No significant Gd-DPTA diffused from tumor into peritumoral brain tissue in 12 meningiomas without surrounding brain edema. In contrast, in 17 of 20 meningiomas with surrounding edema, contrast agent in peritumoral brain tissue was detectable after 3.5 hours and 6.5 hours. In three of 20 meningiomas with minimum surrounding edema (< 5 cm3), contrast agent effusion was absent. After 3.5 hours and 6.5 hours strong correlations of edema volume and the maximum distance of contrast spread from the tumor margin into adjacent brain parenchyma (r = 0.84 and r = 0.87, respectively, p < 0.0001) indicated faster effusion in larger areas of edema.Conclusions. The results of this study show that significant contrast agent effusion from the extracellular space of the tumor into the interstitium of the peritumoral brain tissue is only found in meningiomas with surrounding edema. This supports the hypothesis that hydrodynamic processes play an essential role in the pathogenesis of peritumoral brain edema in meningiomas.

Measurement of brain tissue oxygenation performed using positron emission tomography scanning to validate a novel monitoring method

2002 ◽  
Vol 96 (2) ◽  
pp. 263-268 ◽  
Author(s):  
Arun K. Gupta ◽  
Peter J. Hutchinson ◽  
Tim Fryer ◽  
Pippa G. Al-Rawi ◽  
Dot A. Parry ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Brain Injury ◽  
Brain Tissue ◽  
Tissue Oxygenation ◽  
Emission Tomography ◽  
Brain Tissue Oxygenation ◽  
Content Type ◽  
Positron Emission ◽  
Pet Scans ◽  
Fine Print

Object. The benefits of measuring cerebral oxygenation in patients with brain injury are well accepted; however, jugular bulb oximetry, which is currently the most popular monitoring technique used has several shortcomings. The goal of this study was to validate the use of a new multiparameter sensor that measures brain tissue oxygenation and metabolism (Neurotrend) by comparing it with positron emission tomography (PET) scanning. Methods. A Neurotrend sensor was inserted into the frontal region of the brain in 19 patients admitted to the neurointensive care unit. After a period of stabilization, the patients were transferred to the PET scanner suite where C15O, 15O2, and H215O PET scans were obtained to facilitate calculation of regional cerebral blood volume, O2 metabolism, blood flow, and O2 extraction fraction (OEF). Patients were given hyperventilation therapy to decrease arterial CO2 by approximately 1 kPa (7.5 mm Hg) and the same sequence of PET scans was repeated. For each scanning sequence, end-capillary O2 tension (PvO2) was calculated from the OEF and compared with the reading of brain tissue O2 pressure (PbO2) provided by the sensor. In three patients the sensor was inserted into areas of contusion and these patients were eliminated from the analysis. In the subset of 16 patients in whom the sensor was placed in healthy brain, no correlation was found between the absolute values of PbO2 and PvO2 (r = 0.2, p = 0.29); however a significant correlation was obtained between the change in PbO2 (ΔPbO2) and the change in PvO2 (ΔPvO2) produced by hyperventilation in a 20-mm region of interest around the sensor (ρ = 0.78, p = 0.0035). Conclusions. The lack of correlation between the absolute values of PbO2 and PvO2 indicates that PbO2 cannot be used as a substitute for PvO2. Nevertheless, the positive correlation between ΔPbO2 and ΔPvO2 when the sensor had been inserted into healthy brain suggests that tissue PO2 monitoring may provide a useful tool to assess the effect of therapeutic interventions in brain injury.

Delayed neurological deficits detected by an ischemic pattern in the extracellular cerebral metabolites in patients with aneurysmal subarachnoid hemorrhage

2004 ◽  
Vol 100 (1) ◽  
pp. 8-15 ◽  
Author(s):  
Jane Skjøth-Rasmussen ◽  
Mette Schulz ◽  
Soren Risom Kristensen ◽  
Per Bjerre
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Metabolism ◽  
Brain Infarction ◽  
Neurological Deficits ◽  
Parent Artery ◽  
Glycerol Concentration ◽  
Microdialysis Probe ◽  
Content Type ◽  
Fine Print

Object. In the treatment of patients with aneurysmal subarachnoid hemorrhage (SAH), early occlusion of the aneurysm is necessary as well as monitoring and treatment of complications following the primary bleeding episode. Monitoring with microdialysis has been studied for its ability to indicate and predict the occurrence of delayed ischemic neurological deficits (DINDs) in patients with SAH. Methods. In 42 patients with aneurysmal SAH microdialysis monitoring of metabolites was performed using a 0.3-µl/minute perfusion flow over several days, and the results were correlated to clinical events and to brain infarction observed on computerized tomography scans. The microdialysis probe was inserted into the territory of the parent artery of the aneurysm. The authors defined an ischemic pattern as increases in the lactate/glucose (L/G) and lactate/pyruvate (L/P) ratios that were greater than 20% followed by a 20% increase in glycerol concentration. This ischemic pattern was found in 17 of 18 patients who experienced a DIND and in three of 24 patients who did not experience a delayed clinical deterioration. The ischemic pattern preceded the occurrence of a DIND by a mean interval of 11 hours. Maximum L/G and L/P ratios did not correlate with the presence of DIND or outcome, and there was no association between the glycerol level and subsequent brain infarction. Conclusions. Microdialysis monitoring of the cerebral metabolism in patients with SAH may predict with high sensitivity and specificity the occurrence of a DIND. Whether an earlier diagnosis results in better treatment of DINDs and, therefore, in overall better outcomes remains to be proven, as it is linked to an efficacious treatment of cerebral vasospasm.

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