Page 102 - NNS 2014 Program & Abstract Book

Care Unit (ICU)] across 5 pediatric trauma centers. Overall, 140
(59%) patients had at-least one hypotension episode. Hypotension
occurred across treatment locations: OR (58/122;48%), ICU (101/
236;43%), PH (44/210;21%) & ED (29/224;13%). Hypotension
prevalence varied across centers for each location: PH (5–35%; p =
0.01), OR (16–74%; p < 0.001), and ICU (23–59%; p = 0.001). 65/236
(28%) had persistent ( > 1 location) hypotension, ranging from 13–
50% across centers (p < 0.001). Hypotension treatment varied across
centers: 1) 130/140 (93%; range 78–100%; p = 0.002) hypotensive
children received fluids; 2) 75/140 (54%; range 38–72%; p = 0.002)
received blood products and 3) 90/140 (64%; range 44–76%; p = 0.12)
received vasopressors. 52/90 (58%) hypotensive patients received one
and 38/90 (42%) received ‡ 2 vasopressors. Injury severity score
(ISS) was greater only in those patients who received combination vs.
single vasopressor therapy (mean ISS 34.2[SD15.4] vs. 30[SD11.3];
p = 0.04). The most commonly used single vasopressor was phenyl-
ephrine (22%), followed by epinephrine (13%), norepinephrine
(12%), dopamine (8%) and vasopressin (2%). Vasopressor use varied
by pediatric trauma center (p < 0.001). Overall, mortality rates ranged
from (2–23%; p = 0.02). In conclusion, single episode, persistent, and
refractory systemic hypotension are common after severe pediatric
TBI and may be associated with variation in outcomes. Reducing
variation in hypotension treatment, including vasopressor choice, may
be important to improving TBI outcomes.
Key words
hypotension, outcomes, persistent, traumatic brain injury, vasopressors
B4-31
POSTURAL ORTHOSTATIC TACHYCARDIA SYNDROME
AFTER MILD TBI
Choe, M.C., Fischer, J., Zeiger, M., Yudovin, S., Giza, C.C.
UCLA, Los Angeles, United States
The incidence of recreation-related concussions in the United States is
between 1.2–3.8 million per year. Post-concussive symptoms include
headache, dizziness, cognitive issues, and mood disturbances.
Symptoms typically resolve within 2 weeks, but may be prolonged,
causing extended absences from school/work and withdrawal from
normal activity. There are no standard treatments for concussion other
than cognitive/physical rest. Autonomic dysfunction after TBI ranges
from 8–33% of patients admitted to the ICU. While postural ortho-
static tachycardia syndrome (POTS), a type of dysautonomia, has
been described in case series in moderate/severe injuries, there is
limited data after mild TBI. Dysfunction may manifest as disturbances
in heart rate, blood pressure, and sweating/temperature. Symptoms
may include dizziness, fatigue, headache, and decreased concentra-
tion. In this study, we aim to determine the prevalence of autonomic
dysfunction after concussion, and characterize the relationship be-
tween POTS and post-concussive syndrome.
Data was prospectively collected from 52 individuals presenting to
our sports concussion/mild TBI clinic. Orthostatic vital signs were
obtained, and a threshold heart rate increase ‡ 30 signified identified
patients with POTS. Symptoms were ascertained using the Graded
Symptom Checklist portion of the Sport Concussion Assessment Tool
(SCAT2).
18/52 (34%) of our patients had heart rate change consistent with
POTS. The patients with POTS were less likely to have been injured
by a sport-related mechanism (55.6% vs 73.5%), and more likely to be
younger (average age 14.7 yrs vs 21.9 yrs).
A high proportion of symptomatic mTBI patients have concomitant
objective evidence of autonomic dysfunction. These problems may
potentially exacerbate headache, mood disturbances or other symp-
toms and may warrant a different treatment regimen. Careful risk
factor assessment may identify those patients who suffer from POTS
and manifest these post-concussive symptoms, enabling targeted
treatments and decreasing recovery time. Comprehensive evaluation
of symptomatic mTBI patients should include screening for auto-
nomic dysfunction.
Support: UCLA BIRC, HD061504, Morris A. Hazan Friends of
Semel Fellowship, NARSAD Young Investigator’s Grant, Child Neu-
rology Foundation/Winokur Family Foundation, Joseph Drown
Foundation, Today’s and Tomorrow’s Children Fund
Key words
autonomic dysfunction, mild TBI, post-concussive syndrome
B5-01
PROGRESSION OF MYELIN PATHOLOGY IN TBI WITH
TRAUMATIC AXONAL INJURY OF THE CORPUS CALLO-
SUM
Mierzwa, M.J., Marion, C.M., Sullivan, G.M., McDaniel, D.P.,
Armstrong, R.C.
CNRM/Uniformed Services University of the Health Sciences, Be-
thesda, MD
Traumatic brain injury (TBI) from impact-acceleration forces often
results in post-concussive symptoms that persist into a chronic disease
phase, even in patients diagnosed initially as mild TBI. To better
understand the progression to chronic disease, we examined acute
through chronic corpus callosum pathology in mice using a concus-
sive TBI model of traumatic axonal injury (Sullivan et al., 2013
JNEN). TBI was produced in adult male C57BL/6J mice by impact
onto the skull at bregma. Animals were perfused at multiple time
points between 3 d-6 wks post-TBI and tissues were processed for
either electron microscopy or immunohistochemistry. At all times
post-TBI, degenerating axons were evident in the corpus callosum,
particularly over the lateral ventricles. Degenerating axons were dis-
tributed among intact fibers – modeling the diffuse pattern of trau-
matic axonal injury in TBI. Axon diameters were reduced across the
overall population of remaining axons. Demyelination may contribute
to functional deficits and potentially leave denuded axons vulnerable
to further damage. After TBI, demyelination of intact axons signifi-
cantly increased at 3 d followed by remyelination evident at 1 wk.
Furthermore, abnormal myelin figures were prevalent at all post-TBI
times, yet rare after sham surgery. Myelin sheaths collapsed around
degenerating axons and also formed long outfoldings, with or without
an axon present. Due to this dispersed nature of demyelination and
axon degeneration, oligodendrocytes may increase myelin synthesis to
remyelinate intact axons or due to dysregulation in maintaining
multiple sheaths among a cohort including intact and degenerating
axons. Excessive myelin outfoldings may increase myelin debris,
which can stimulate microglial activation. Immunohistochemistry
demonstrated microglial activation and reactive astrogliosis that per-
sisted 6 wks post-TBI. Myelin outfoldings were increased over 10-
fold in comparison with cuprizone demyelination and remyelination.
Further studies will be important to determine the contribution of this
myelin pathology to persistent white matter neurodegeneration and
neuroinflammation after TBI. Supported by the DoD in the Center for
Neuroscience and Regenerative Medicine (CNRM).
Key words
corpus callosum, cuprizone, myelin, neuroinflammation
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