Monitoring of Brain Tissue PO2 in Traumatic Brain Injury: Effect of Cerebral Hypoxia on Outcome

Bardt, Tillman; Unterberg, Andreas; Härtl, Roger; Kiening, Karl; Schneider, G.-H.; Lanksch, W.

doi:10.1007/978-3-7091-6475-4_45

Cited by 93 publications

(101 citation statements)

References 7 publications

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“…When CPP falls under a critical threshold (Ϸ50 to 60 mm Hg), PtO 2 drops to Ͻ10 mm Hg, which is known to be a threshold value for hypoxic tissue. 20 At this time point, a rise in the lactate-topyruvate ratio and hypoxanthine is detected, indicating a change from aerobic to anaerobic metabolism and increased breakdown of ATP under ischemic stress. Subsequently, concentrations of excitatory amino acids and GABA increase.…”

Section: Prediction Of Malignant Mca Infarction By Multimodal Neuromomentioning

confidence: 91%

Prediction of Malignant Course in MCA Infarction by PET and Microdialysis

Dohmen

Bosche

Graf

et al. 2003

Stroke

139

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Background and Purpose-To predict malignant course in patients with large middle cerebral artery (MCA) infarction, we combined PET imaging and neuromonitoring, including microdialysis. Methods-Thirty-four patients with stroke of Ͼ50% of the MCA territory in early cerebral CT scan were included. Probes for microdialysis and measurement of intracranial pressure and tissue oxygen pressure (PtO 2 ) were placed into the ipsilateral frontal lobe. PET was performed with 11 C-flumazenil to assess CBF and irreversible neuronal damage. Results-PET measurements within 24 hours after stroke showed larger volumes of ischemic core (mean, 144.5 versus 62.2 cm 3 ) and larger volumes of irreversible neuronal damage (157.9 versus 47.0 cm 3 ) in patients with malignant course (ie, edema formation with midline shift) than in patients with benign course. Mean cerebral blood flow values within the ischemic core were significantly lower and the volume of the ischemic penumbra was smaller in the malignant than in the benign group. In patients with malignant course, cerebral perfusion pressure dropped to Ͻ50 to 60 mm Hg 22 to 72 hours (mean, 52.0 hours) after onset of symptoms; subsequently, PtO 2 dropped and glutamate increased, indicating secondary ischemia. Maximal changes in the monitored variables reached significant levels for glutamate, aspartate, GABA, glycerol, lactate-to-pyruvate ratio, hypoxanthine, intracranial pressure, cerebral perfusion pressure, and PtO 2 . Conclusions-PET allowed prediction of malignant MCA infarction within the time window suggested for hemicraniectomy. Neuromonitoring helped to classify the clinical courses by characterizing pathophysiological sequelae of malignant edema formation. In contrast to PET, however, it did not predict fatal outcome early enough for successful implementation of invasive therapies.

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Section: Prediction Of Malignant Mca Infarction By Multimodal Neuromomentioning

confidence: 91%

Prediction of Malignant Course in MCA Infarction by PET and Microdialysis

Dohmen

Bosche

Graf

et al. 2003

Stroke

139

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“…MD has been studied more extensively in relation to ischemic stroke and traumatic brain injury [12,13], with one study of 34 patients with MCA infarction showing that a decrease in CPP to <50-60 mmHg, with a decrease in PbtO2 to <10 mmHg, and a significantly higher LPR occurred in 17 patients who experienced a malignant course and herniation [14]. A PbtO2 value of <10 mmHg has been previously shown to be threshold for significant tissue hypoxia as well [15]. There is increasing evidence for the relevance of high ICP and its relation to poor outcome in SAH [16].…”

Section: Discussionmentioning

confidence: 99%

Multimodality Neuromonitoring and Decompressive Hemicraniectomy After Subarachnoid Hemorrhage

et al. 2009

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“…van den Brink, in 2000, looked at 101 patients with severe TBI and found that hypoxia was an independent predictor of unfavorable outcome and death [17]. Barth et al, in 1998, reported that severe hypoxia for greater than 30 minutes resulted in substantially worse outcome than hypoxia limited to under 30 minutes [21]. Dings et al, in 1998, reported that patients with lower cerebral oxygenation showed lower Glasgow Outcome Scores (GOS) at 6 months [22].…”

Section: Discussionmentioning

confidence: 99%

Cerebral Oxygen Desaturation with Normal ICP and CPP in Severe TBI

Palmer¹,

Bader²

2008

TOCCMJ

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Abstract:Introduction: Standard monitoring of severe traumatic brain injury patients (TBI) by intracranial pressure (ICP) and cerebral perfusion pressure (CPP) monitoring fails to recognize episodes of cerebral oxygen desaturation. We found and characterized frequent episodes of desaturation of jugular venous oxygen (SjO2) in the face of normal ICP and CPP.Methods: Fifty six patients with severe TBI had SjO2 and ICP monitors placed. The charts were retrospectively reviewed and all episodes of desaturation were recorded and characterized.Results: Nineteen patients had episodes of desaturation with normal ICP and CPP. The average GCS score was 5.8. 63% of desaturations occurred in the first 24 hours, 17% of desaturations occurred in 24-48 hours, and 20% occurred in 48-72 hours. The depth of desaturation was 50-54% in 50% of instances, 45-49% in 37% of instances, and 40-44% in 13% of instances. The duration of the desaturation episodes was less than 10 minutes in 47%, 10-30 minutes in 17%, 30-60 minutes in 23%, and greater than 50 minutes in 13%. Treatment of the desaturation was elevation of FIO2 in all patients, elevation of pCO2 in 15 patients, volume expansion in 9 patients, pressors in 9 patients, and Propofol in 5 patients. Conclusions:The monitoring of severe TBI patients with ICP and CPP alone is insufficient to recognize cerebral oxygen desaturation episodes in 34% of patients. The monitoring of SjO2 facilitates the recognition and treatment of these episodes.

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Monitoring of Brain Tissue PO2 in Traumatic Brain Injury: Effect of Cerebral Hypoxia on Outcome

Cited by 93 publications

References 7 publications

Prediction of Malignant Course in MCA Infarction by PET and Microdialysis

Prediction of Malignant Course in MCA Infarction by PET and Microdialysis

Multimodality Neuromonitoring and Decompressive Hemicraniectomy After Subarachnoid Hemorrhage

Cerebral Oxygen Desaturation with Normal ICP and CPP in Severe TBI

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