Page 51 - NNS 2014 Program & Abstract Book

of each model to correctly assign patients to groups was evaluated by
calculating the area under the receiver operating characteristics curve
(AUC). The IMPACT models performed with increasing accuracy in
each more complex model. The ability to discriminate between mortality
and survival was 0.85 for the Core model, 0.87 for the Extended model,
and 0.87 for the Lab model in AUC analysis. The ability to discriminate
between unfavorable and favorable outcomes was 0.84 for the Core
model, 0.85 for the Extended model, and 0.87 for the Lab model in AUC
analysis. The models were able to discriminate well between patients
with mortality versus survival and unfavorable versus favorable outcome
in all three IMPACT models in this non-trial dataset.
Key words
outcome measures, prognosis, prognostic model, traumatic brain injury
A1-07
MODULATION OF INFLAMMATORY CYTOKINE BAL-
ANCE BY SYMPATHETIC NERVOUS SYSTEM ACTIVA-
TION AFTER TRAUMATIC BRAIN INJURY
Hassan, S.S.1, Di Battista, A.P.1, Baker, A.J.1,2, Topolovec-Vranic, J.2,
Capone-Neto, A.2, Rizoli, S.B.1,2, Rhind, S.G.3
1Institute of Medical Science, University of Toronto, Toronto, Canada
2Departments of Critical Care, Anesthesia and Surgery, University of
Toronto, Toronto, Canada
3Defence Research & Development Canada, Toronto, Canada
TBI elevates intracranial pressure and activates the sympathetic ner-
vous system (SNS) with massive catecholamine secretion and mod-
ulation of neuroimmune networks. Hyperadrenergic activity is
detrimental to the injured brain, amplifying secondary host inflam-
matory cascades. The extent to which the post-injury sympathetic
surge contributes to pro-/anti-inflammatory cytokine dysregulation
and impacts neurological outcome remains ill-defined. This study
evaluated temporal changes in circulating cytokines in association
with plasma epinephrine (E) and norepinephrine (NE) levels after TBI
and interrelationships with neurological outcome. Isolated head-injury
patients [N = 194; (mean – SD) age 37 – 18 y; 66% male] hospitalized
with moderate (27%) to severe (73%) TBI, defined as a Glasgow
Coma Scale (GCS) score of 8–10 or £ 8. Peripheral blood samples
were drawn from TBI patients on admission, 6, 12 and 24-h post-
injury; matching samples were collected from age-matched elec-
tive neurosurgical patients (N = 15) and healthy volunteers (N = 15).
Plasma levels (pg/mL) of interleukin (IL)-1b, IL-2, IL-4, IL-5, IL-8,
IL-10, IL-12, tumor necrosis factor (TNF)-a and interferon (IFN)-c
were quantified using high-density, ultra-sensitive MULTI-ARRAY
immunoassay; E and NE were measured by commercially available
immunoassay (CatCombi). Neurological outcome was assessed at
discharge and 6 months using Glasgow Outcome Scale. Mean
( – SEM) values of E (3.1 – 2.1) and NE (280 – 68) were within re-
ported normal ranges for healthy controls. Relative to healthy con-
trols, neurosurgical patients showed moderately elevated levels of E
(135 – 19) and NE (855 – 281). By comparison, severe TBI patients
exhibited highly elevated E values, which peaked on admission
(666 – 189) and gradually decreased over time. Similarly, NE was
markedly higher at all time-points, with max increases at 12 h
(10982.8 – 7310). TNF-a and IL-10 were differentially regulated in
moderate and severe TBI relative to controls. These results demon-
strate significant SNS activation after TBI, which correlates with in-
flammatory cytokine profiles and neurological outcome.
Key words
catecholamines, cytokines, IL-10, TNF
A1-08
MULTIMODALITY MONITORING OF PLATELET FUNC-
TION IN TRAUMATIC BRAIN INJURY PATIENTS WITH
TRAUMA INDUCED COAGULOPATHY
Brophy, G.M.1, Contaifer, D.1 , Mohammed, B.M.1, White, N.J.1,
Newton, J.C.1, Martin, E.J.1, Pusateri, A.E.3, Ward, K.R.4 , Brophy, D.F.1
1Virginia Commonwealth University, Richmond, USA
2Puget Sound Blood Center, Seattle, USA
3U.S. Army Medical Research and Materiel Command, Fort Detrick,
USA
4University of Michigan, Ann Arbor, USA
Coagulopathy occurs in 33% of traumatic brain injury (TBI) patients
during their hospital course. Platelet (PLT) function is a key mediator of
hemostasis; however, it remains poorly described in trauma induced
coagulopathy (TIC) in TBI patients. As part of a prospective observa-
tional polytrauma study, PLT function in TBI patients with TIC was
characterizes upon emergency department (ED) admission. A total of 99
trauma patients were enrolled between 2011 and 2013. Platelet function
was assessed by thromboelastography (TEG) with PLT mapping; He-
modyne (HAS); aggregometry; calibrated automated thrombography
(CAT); and flow cytometry. TIC was defined as INR ‡ 1.4. Patients were
divided into 2 groups based on presence or absence of TIC and compared
to a group of healthy volunteers. Of the 27 TBI patients identified, 41%
had TIC. TIC patients had significantly higher injury severity scores,
lower base excess and Hb consistent with hemorrhagic shock, and higher
inflammatory biomarker (IL-6) levels compared to those without TIC
(p < 0.01). TBI patients without coagulopathy showed a pro-coagulation
profile (higher platelet contractile force (PFC) and clot elastic
modulus (CEM), and shorter R-time versus controls (p < 0.05), while
TIC patients showed lower fibrinogen levels with a decrease in clot
strength (lower CEM and MA), and lower plasma peak thrombin
generation (C-max)(p < 0.05). Platelet mapping found patients with-
out coagulopathy presented with significant inhibition of PLT ADP-
mediated responsiveness compared to controls (83% vs 53%, p < 0.01),
while responsiveness was further reduced with TIC (96%, p < 0.01). TBI
polytrauma patients with TIC upon ED admit present with impaired
platelet function, lower fibrinogen, lower plasma peak thrombin gen-
eration, and elevated IL-6 which may increase the risk of uncontrollable
hemorrhage. Multimodality monitoring of coagulation, including plate-
let function, contributes to the understanding of hemostasis.
Key words
coagulation, platelet function
A1-09
TRENDS IN EMERGENCY DEPARTMENT TREATMENT OF
SPORT-RELATED TRAUMATIC BRAIN INJURY, 2006–2011
Haring, R.S.1–3, Canner, J.K.3, Selvarajah, S.3, Asemota, A.O.3,
George, B.P.3,4, Haider, A.H.1,3, Schneider, E.B.3
1Johns Hopkins Bloomberg School of Public Health, Baltimore, USA
2Lake Erie College of Osteopathic Medicine, Bradenton, USA
3Johns Hopkins School of Medicine, Baltimore, USA
4University of Rochester School of Medicine and Dentistry, Rochester,
USA
Traumatic brain injury (TBI) in sports has received substantial at-
tention in recent years, leading sport and government officials to
implement policies aimed at preventing such injuries or reducing their
severity. We sought to identify trends associated with sports-related
TBI in Emergency Departments (ED) nationwide from 2006–2011.
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