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Brain tissue oxygenation and cerebral metabolic patterns in focal and diffuse traumatic brain injury
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Neurokirurgi.
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Neurokirurgi.
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Neurokirurgi.
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap, Neurokirurgi.
Vise andre og tillknytning
2014 (engelsk)Inngår i: Frontiers in Neurology, ISSN 1664-2295, E-ISSN 1664-2295, Vol. 5, artikkel-id 64Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Introduction: Neurointensive care of traumatic brain injury (TBI) patients is currently based on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) targeted protocols. There are reasons to believe that knowledge of brain tissue oxygenation (BtipO2) would add information with the potential of improving patient outcome. The aim of this study was to examine BtipO2 and cerebral metabolism using the Neurovent-PTO probe and cerebral microdialysis (MD) in TBI patients.

Methods: Twenty-three severe TBI patients with monitoring of physiological parameters, ICP, CPP, BtipO2, and MD for biomarkers of energy metabolism (glucose, lactate, and pyruvate) and cellular distress (glutamate, glycerol) were included. Patients were grouped according to injury type (focal/diffuse) and placement of the Neurovent-PTO probe and MD catheter (injured/non-injured hemisphere).

Results: We observed different patterns in BtipO2 and MD biomarkers in diffuse and focal injury where placement of the probe also influenced the results (ipsilateral/contralateral). In all groups, despite fairly normal levels of ICP and CPP, increased MD levels of glutamate, glycerol, or the L/P ratio were observed at BtipO2 <5 mmHg, indicating increased vulnerability of the brain at this level.

Conclusion: Monitoring of BtipO2 adds important information in addition to traditional ICP and CPP surveillance. Because of the different metabolic responses to very low BtipO2 in the individual patient groups we submit that brain tissue oximetry is a complementary tool rather than an alternative to MD monitoring.

sted, utgiver, år, opplag, sider
2014. Vol. 5, artikkel-id 64
Emneord [en]
brain tissue oxygenation, cerebral metabolism, traumatic brain injury, cerebral ischemia, Neurovent-PTO
HSV kategori
Forskningsprogram
Neurokirurgi
Identifikatorer
URN: urn:nbn:se:uu:diva-194684DOI: 10.3389/fneur.2014.00064ISI: 000209629300064PubMedID: 24817863OAI: oai:DiVA.org:uu-194684DiVA, id: diva2:606159
Forskningsfinansiär
Swedish Research CouncilThe Swedish Brain FoundationTilgjengelig fra: 2013-02-18 Laget: 2013-02-18 Sist oppdatert: 2017-12-06bibliografisk kontrollert
Inngår i avhandling
1. Brain Tissue Oxygenation in Traumatic Brain Injury: Experimental and Clinical Studies
Åpne denne publikasjonen i ny fane eller vindu >>Brain Tissue Oxygenation in Traumatic Brain Injury: Experimental and Clinical Studies
2013 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
Abstract [en]

Traumatic brain injury (TBI) is a major cause of death and disability. TBI is frequently followed by cerebral ischemia which is a great contributor to secondary brain damage. The main causes of cerebral ischemia are pathophysiological changes in cerebral blood flow and metabolism. Treatment of TBI patients is currently based on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) targeted treatment protocols. However, ICP and CPP alone do not provide information of the oxygen availability in the brain. Monitoring of brain tissue oxygenation (BtipO2) may give additional and valuable information about the risk for development of ischemia in TBI patients.

The aims of this thesis were to study BtipO2 monitoring devices in-vitro regarding accuracy and stability, to detect threshold level of cerebral ischemia in-vivo and finally to examine the cerebral oxygen levels and cerebral metabolism in TBI patients.

The BtipO2 probes performed with high accuracy and stability at different clinically relevant oxygen concentrations.

A pig TBI model was developed by step-wise intracranial volume/pressure increase. Volume increase resulted in a gradual increased ICP, decreased CPP, intracranial compliance and BtipO2, respectively. Brain death (BD) was confirmed by negative CPP and negligible amount of previously injected microspheres in the brain tissue. The model simulated the clinical development of BD in humans with a classical pressure-volume response and systemic cardiovascular reactions. The model should be suitable for studies of brain injury mechanisms.

From the same in-vivo model it was also possible to detect the threshold level of cerebral ischemia in the pig, where BtipO2 below 10 mmHg and CPP below 30 mmHg was associated with an impaired cerebral metabolism (microdialysis lactate to pyruvate ratio >30).

BtipO2 together with cerebral microdialysis were studied in 23 severe TBI patients. We observed different patterns of changes in BtipO2 and cerebral microdialysis biomarkers in focal and diffuse TBI.  Increased cerebral microdialysis levels of glutamate, glycerol or the lactate/pyruvate ratio were observed at BtipO2 < 5 mmHg, indicating increased vulnerability of the brain at this critical level of tissue oxygenation in TBI patients.

sted, utgiver, år, opplag, sider
Uppsala: Acta Universitatis Upsaliensis, 2013. s. 74
Serie
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 869
Emneord
Brain tissue oxygenation, Cerebral metabolism, Traumatic brain injury, Cerebral ischemia, Threshold levels, Neurovent-PTO, Microdialysis
HSV kategori
Forskningsprogram
Neurokirurgi
Identifikatorer
urn:nbn:se:uu:diva-195867 (URN)978-91-554-8607-5 (ISBN)
Disputas
2013-04-19, Grönwallsalen, Akademiska sjukhuset, ingång 70, Uppsala, 09:00 (engelsk)
Opponent
Veileder
Tilgjengelig fra: 2013-03-27 Laget: 2013-02-28 Sist oppdatert: 2018-01-11bibliografisk kontrollert

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