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Absence of electroencephalographic seizure activity in patients treated for head injury with an intracranial pressure-targeted therapy.

https://arctichealth.org/en/permalink/ahliterature92263
Source
J Neurosurg. 2009 Feb;110(2):300-5
Publication Type
Article
Date
Feb-2009
Author
Olivecrona Magnus
Zetterlund Bo
Rodling-Wahlström Marie
Naredi Silvana
Koskinen Lars-Owe D
Author Affiliation
Department of Neurosurgery, University Hospital, Umeå, Sweden. magnus.olivecrona@vll.se
Source
J Neurosurg. 2009 Feb;110(2):300-5
Date
Feb-2009
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Child
Conscious Sedation
Drug Therapy, Combination
Electroencephalography - drug effects
Epilepsy, Post-Traumatic - physiopathology - prevention & control
Female
Fentanyl
Frontal Lobe - drug effects - physiopathology
Glasgow Coma Scale
Humans
Hypnotics and Sedatives
Intensive Care
Intracranial Pressure - drug effects - physiology
Male
Midazolam
Middle Aged
Parietal Lobe - drug effects - physiopathology
Propofol
Thiopental
Abstract
OBJECT: The authors prospectively studied the occurrence of clinical and nonclinical electroencephalographically verified seizures during treatment with an intracranial pressure (ICP)-targeted protocol in patients with traumatic brain injury (TBI). METHODS: All patients treated for TBI at the Department of Neurosurgery, University Hospital Umeå, Sweden, were eligible for the study. The inclusion was consecutive and based on the availability of the electroencephalographic (EEG) monitoring equipment. Patients were included irrespective of pupil size, pupil reaction, or level of consciousness as long as their first measured cerebral perfusion pressure was > 10 mm Hg. The patients were treated in a protocol-guided manner with an ICP-targeted treatment based on the Lund concept. The patients were continuously sedated with midazolam, fentanyl, propofol, or thiopental, or combinations thereof. Five-lead continuous EEG monitoring was performed with the electrodes at F3, F4, P3, P4, and a midline reference. Sensitivity was set at 100 muV per cm and filter settings 0.5-70 Hz. Amplitude-integrated EEG recording and relative band power trends were displayed. The trends were analyzed offline by trained clinical neurophysiologists. RESULTS: Forty-seven patients (mean age 40 years) were studied. Their median Glasgow Coma Scale score at the time of sedation and intubation was 6 (range 3-15). In 8.5% of the patients clinical seizures were observed before sedation and intubation. Continuous EEG monitoring was performed for a total of 7334 hours. During this time neither EEG nor clinical seizures were observed. CONCLUSIONS: Our protocol-guided ICP targeted treatment seems to protect patients with severe TBI from clinical and subclinical seizures and thus reduces the risk of secondary brain injury.
PubMed ID
18759609 View in PubMed
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Effective ICP reduction by decompressive craniectomy in patients with severe traumatic brain injury treated by an ICP-targeted therapy.

https://arctichealth.org/en/permalink/ahliterature77309
Source
J Neurotrauma. 2007 Jun;24(6):927-35
Publication Type
Article
Date
Jun-2007
Author
Olivecrona Magnus
Rodling-Wahlström Marie
Naredi Silvana
Koskinen Lars-Owe D
Author Affiliation
Department of Neurosurgery, University Hospital, Umeå, Sweden. magnus.olivecrona@vll.se
Source
J Neurotrauma. 2007 Jun;24(6):927-35
Date
Jun-2007
Language
English
Publication Type
Article
Abstract
Severe traumatic brain injury (TBI) is one of the major causes of death in younger age groups. In Umeå, Sweden, an intracranial pressure (ICP) targeted therapy protocol, the Lund concept, has been used in treatment of severe TBI since 1994. Decompressive craniectomy is used as a protocol-guided treatment step. The primary aim of the investigation was to study the effect of craniectomy on ICP changes over time in patients with severe TBI treated by an ICP-targeted protocol. In this retrospective study, all patients treated for severe TBI during 1998-2001 who fulfilled the following inclusion criteria were studied: GCS 10 mm Hg, arrival within 24 h of trauma, and need of intensive care for >72 h. Craniectomy was performed when the ICP could not be controlled by evacuation of hematomas, sedation, ventriculostomy, or low-dose pentothal infusion. Ninety-three patients met the inclusion criteria. Mean age was 37.6 years. Twenty-one patients underwent craniectomy as a treatment step. We found a significant reduction of the ICP directly after craniectomy, from 36.4 mm Hg (range, 18-80 mm Hg) to 12.6 mm Hg (range, 2-51 mm Hg). During the following 72 h, we observed an increase in ICP during the first 8-12 h after craniectomy, reaching approximately 20 mm Hg, and later levelling out at approximately 25 mm Hg. The reduction of ICP was statistically significant during the 72 h. The outcome as measured by Glasgow Outcome Scale (GOS) did not significantly differ between the craniectomized group (DC) and the non-craniectomized group (NDC). The outcome was favorable (GOS 5-4) in 71% in the craniectomized group, and in 61% in the non-craniectomized group. Craniectomy is a useful tool in achieving a significant reduction of ICP overtime in TBI patients with progressive intracranial hypertension refractory to medical therapy. The procedure seems to have a satisfactory effect on the outcome, as demonstrated by a high rate of favorable outcome and low mortality in the craniectomized group, which did not significantly differ compared with the non-craniectomized group.
PubMed ID
17600510 View in PubMed
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