Group Title: Critical Care
Title: Brain biomarkers and brain tissue oxygenation: changes and correlations following severe head injury
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Permanent Link: http://ufdc.ufl.edu/UF00099889/00001
 Material Information
Title: Brain biomarkers and brain tissue oxygenation: changes and correlations following severe head injury
Series Title: Critical Care
Physical Description: Archival
Creator: Mondello,S.
Buki,A.
Bullock,R.
Robertson,C. S.
Czeiter,E.
Ezer,E.
Tortella,F. C.
Wang,K. K.
Hayes,R. L.
Publication Date: 2010
 Notes
General Note: Start pageP295
General Note: M3: 10.1186/cc8527
 Record Information
Bibliographic ID: UF00099889
Volume ID: VID00001
Source Institution: University of Florida
Holding Location: University of Florida
Rights Management: Open Access: http://www.biomedcentral.com/info/about/openaccess/
Resource Identifier: issn - 1364-8535
http://ccforum.com/content/14/S1/P295

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Critical Care 2010, Volume 14 Suppl 1
http://ccforum.com/supplements/14/S1


P292
Use of transcranial Doppler in patients with severe traumatic brain
injury
D Ziegler, G Cravens, G Angles, R Gandhi, P Cho
John Peter Smith Hospital, Fort Worth, TX, USA
Critical Care 2010, 14(Suppl 1):P292 (doi: 10.1186/cc8524)

Introduction Secondary ischemic insult after severe traumatic brain injury
(TBI) is correlated with poor outcome. Transcranial Doppler sonography
(TCD) permits a non-invasive measurement of cerebral blood flow. The
purpose of this study is to determine the usefulness of TCD in patients
with severe TBI.
Methods TCD was performed on 73 patients with severe TBI, defined
as a i, i Coma Scale of 8 or less on admission. All patients were
on mechanical ventilation. TCD was performed on hospital days 1, 2,
3 and 7. Hypoperfusion was defined by having two out of three of the
following: mean velocity of the middle cerebral artery less than 35 cm/
second, diastolic velocity of the middle cerebral artery less than 20 cm/
second and a pulsatility index greater than 1.4. Vasospasm was defined
by the following: mean velocity of the middle cerebral artery greater than
120 cm/second and/or Landegaard index greater than 3.
Results Thirty-four patients (64%) had normal measurements. Thirteen
were discharged home, 16 were discharged to a long-term care facility
and five died. Two of these patients were comatose and their families
requested withdrawal of care. The other three died from brain death.
Eighteen patients (25%) had hypoperfusion and all i I i1 I to brain
death. Twenty-one patients (29%) had vasospasm. Four of these patients
were discharged home, 11 to a long-term care facility and six died. The
vasospasm was detected on hospital day 1 in three patients, hospital
day 2 in seven patients, hospital day 3 in four patients and hospital day
7 in seven patients. Nimodipine was administered in six patients and all
six were discharged to a long-term care facility. However, in one patient,
nimodipine caused hemodynamic instability and was discontinued. In
15 patients, nimodipine was not given. Six of these patients expired from
brain death. Twelve of 21 patients (57%) with subarachnoid hemorrhage
on computed tomography had vasospasm.
Conclusions Most patients with normal measurements can be expected
to survive. Patients with hypoperfusion have a poor prognosis. In patients
with vasospasm, the use of nimodipine should be considered; however,
further studies are needed to determine safety and efficacy. TCD may be
useful in determining early prognosis. Further studies are also needed to
determine whether TCD can improve outcome in patients with severeTBI.


P293
Abstract withdrawn


P294
Effect of hyperbaric oxygen on cerebral oxygen saturation in
patients with sub-acute traumatic brain injury
L Liu, B Zhou, B Liu
Second Affiliated Hospital ofSoochow University, Suzhou, China
Critical Care 2010,14(Suppl 1):P294 (doi: 10.1186/cc8526)

Introduction How hyperbaric oxygen (HBO) affects injured brain tissue
is not yet confirmed. We suppose that HBO could make the oxygen stay
longer in the injured tissue, because of poor circulation or perfusion of
blood in the injured area.This mechanism may help to explain the longer
effect of HBO, after HBO treatment.That is the purpose of our study.
Methods Patients im i from sub-acute traumatic brain injury,
who would be treated with HBO, were enrolled in the study. They were
divided into two groups: frontal lobe lesion and nonfrontal lobe lesion


groups (n= 20) I i I,1, i on their iconography check (X-CT or MR). The
regional cerebral oxygen saturation (rSOl) was measured by a Somanetics
INVOS 5100 monitor before and after 90 minutes treatment with HBO
(15 minutes compression, 40 minutes breathing oxygen of FiO 99% by
mask, 10 minutes rest, 15 minutes decompression). Meanwhile, the arterial
blood was sampled to measure blood gas analysis and cytokine.
Results The parameter of rSO2 showed no i ,ii ...-i difference following
HBO treatment in two groups (t = 0.352, P >0.05); however, there were
inconceivable results in blood gas analysis. Partial pressure of oxygen
i .- was iii ,i... decreased after HBO treatment (P <0.05), although
these changes did not take effect on the clinical manifestation. Otherwise,
the measurement of cytokines (TNF, IL-1) before and after HBO has no
difference (P >0.05) in all groups.
Conclusions HBO has no effect on brain oxygen saturation, after HBO
treatment. But PaO2 was i, ii, ...i decreased following HBO. The
mechanism needs to be studied further.
Reference
1, Allen BW, et a/: Two faces of nitric oxide: implications for cellular
mechanisms of oxygen toxicity. JA106:


P295
Brain biomarkers and brain tissue oxygenation: changes and
correlations following severe head injury
S Mondello', A Buki2, R Bullock3, CS Robertson4, E Czeiter2, E Ezer2,
FCTortellas, i i,, n RL Hayes'
'Banyan Biomarkers and University of Florida, Alachua, FL, USA 2University of Pecs,
Hungary; 'University of Miami, FL, USA; 'BaylorCollege of Medicine, Houston, TX,
USA; Walter ReedArmy Institute of Research, Silver 4A
Critical Care 2010, 14(Suppl 1):P295 (doi: 10.1186/cc8527)

Introduction This study evaluated relationships between CSF levels of
brain biomarkers,, iii I fibrillary acidic protein (GFAP), ubiquitin C-terminal
hydrolase (UCH- L) and a -spectrin breakdown (SBDP145), partial pressure
of brain tissue oxygen (ptiO ) and brain temperature (Licox system) during
the first 24 hours and for up to 10 days following severe TBI.
Methods We studied 27 severe TBI patients having CSF drainage and
invasive monitoring of partial brain tissue oxygen tension (PbtO) and
brain temperature using the Licox (Integra Neurosciences, Plainsboro, NJ,
USA) probe. CSF SBDP145, UCH-L1 and GFAP levels were measured by
quantitative ELISA assay on admission and every 6 hours thereafter for a
maximum of 10 days. Using a double lumen bolt, ptiO2 and temperature
were measured with the Licox. This study focused on the recordings ofthe
first 24 hours following injury (27 patients), as well as preliminary data from
four patients for 10 days.
Results The total duration of monitoring was 1,512 hours. During the first
24 hours, biomarker levels decreased while levels of PbrO2 increased. All
three biomarkers correlated with PbrO2 (P <0.0001, P 0.016 and P= 0.023,
respectively). After the first 24 hours, there were statistically i iii i..
changes in levels of brain biomarkers (SBDP145, UCH-L1 and GFAP) as
well as in levels of ptiO2 (respectively, P = 0.025, P <0.0001, P = 0.033,
P<0.0001). However, the correlation between biomarkers and brain tissue
oxygenation was sustained, and for UCH L1 improved (P <0.0001). No
i iii .11 ... correlations between biomarker levels and brain temperature
were found. There were no complications from the monitoring.
Conclusions Our findings show that CFS levels of SBDP145, UCH-L1
and GFAP are related to brain tissue oxygenation in acute and possibly
the subacute (<10 days post injury) phases of severe TBI. Future studies
will more directly address relationships between changes in tissue
oxygenation and biochemical markers of injury following severe TBI. CSF
levels of biomarkers and brain tissue oxygenation could yield insights
into pathophysiological events following severe TBI and aid in clinical
assessments of severe TBI patients.


Table 1 (abstract P294)


Group Pre


PaO2 (mmHg)
Post Pre Post


PaCO2 (mmHg)
Pre Post




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