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  • Author or Editor: Nino Stocchetti x
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M. Ross Bullock

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Omer Doron, Ofer Barnea, Nino Stocchetti, Tal Or, Erez Nossek and Guy Rosenthal

OBJECTIVE

Previous studies have demonstrated the importance of intracranial elastance; however, methodological difficulties have limited widespread clinical use. Measuring elastance may offer potential benefit in helping to identify patients at risk for untoward intracranial pressure (ICP) elevation from small rises in intracranial volume. The authors sought to develop an easily used method that accounts for the changing ICP that occurs over a cardiac cycle and to assess this method in a large-animal model over a broad range of ICPs.

METHODS

The authors used their previously described cardiac-gated intracranial balloon pump and swine model of cerebral edema. In the present experiment they measured elastance at 4 points along the cardiac cycle—early systole, peak systole, mid-diastole, and end diastole—by using rapid balloon inflation to 1 ml over an ICP range of 10–30 mm Hg.

RESULTS

The authors studied 7 swine with increasing cerebral edema. Intracranial elastance rose progressively with increasing ICP. Peak-systolic and end-diastolic elastance demonstrated the most consistent rise in elastance as ICP increased. Cardiac-gated elastance measurements had markedly lower variance within swine compared with non–cardiac-gated measures. The slope of the ICP–elastance curve differed between swine. At ICP between 20 and 25 mm Hg, elastance varied between 8.7 and 15.8 mm Hg/ml, indicating that ICP alone cannot accurately predict intracranial elastance.

CONCLUSIONS

Measuring intracranial elastance in a cardiac-gated manner is feasible and may offer an improved precision of measure. The authors’ preliminary data suggest that because elastance values may vary at similar ICP levels, ICP alone may not necessarily best reflect the state of intracranial volume reserve capacity. Paired ICP–elastance measurements may offer benefit as an adjunct “early warning monitor” alerting to the risk of untoward ICP elevation in brain-injured patients that is induced by small increases in intracranial volume.

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Cristina Mattioli, Luigi Beretta, Simonetta Gerevini, Fabrizio Veglia, Giuseppe Citerio, Manuela Cormio and Nino Stocchetti

Object. The goal of this study was fourfold: 1) to determine the incidence of traumatic subarachnoid hemorrhage (tSAH) in patients with traumatic brain injury (TBI); 2) to verify agreement in the diagnosis of tSAH in a multicenter study; 3) to assess the incidence of tSAH on the outcome of the patient; and 4) to establish whether tSAH itself leads to an unfavorable outcome or whether it is a sign of major brain trauma associated with severe posttraumatic lesions.

Methods. Computerized tomography (CT) scans obtained in 169 head-injured patients on admission to 12 Italian intensive care units during a 3-month period were examined. The scans were collected for neuroradiological review and were used for the analysis together with data from a multicenter database (Neurolink).

A review committee found a high incidence of tSAH (61%) in patients with TBI and a moderate agreement among centers (K = 0.57). Significant associations were observed between the presence and grading of tSAH and patient outcomes, and between the presence of tSAH and the severity of the CT findings. Logistic regression analysis showed that the presence of tSAH and its grading alone do not assume statistical significance in the prediction of unfavorable outcome.

Conclusions. Traumatic SAH frequently occurs in patients with TBI, but it is difficult to detect and grade. Traumatic SAH is associated with more severe CT findings and a worse patient outcome.

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Sandra Magnoni, Laura Ghisoni, Marco Locatelli, Mariangela Caimi, Angelo Colombo, Valerio Valeriani and Nino Stocchetti

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.

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