Post on 02-Jun-2018
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Oleh :Berliana Kurniawati Nur Huda
102011101080
Pembimbing :dr. Dwikoryanto, Sp.BS
LAB/SMF ILMU BEDAHFAKULTAS KEDOKTERAN UNIVERSITAS JEMBER
RSUD. DR. SOEBANDI2014
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Traumatic brain injury (TBI) is a major cause of
death and disability in children and young adults
An important public health problem in the United
States and worldwideOver the past 15-20 years the reported incidence
of TBI resulting from mva in the United States
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Approximately 2 million persons suffer TBIin the US70,000 to 90,000 have
permanent long-term disability, creating a
significant socioeconomic and emotionalburden on the families and society.
Most commonly affected group is males
(15-24 years)
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TBI causes neural dysfunction and cell
death --> biomechanical load
Significant alterations of cerebral
metabolism and blood flow that result incellular dysfunction and vulnerability to
secondary injuries (such as hypoxia,
hypotension, seizures or repeated TBI).
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The biomechanics of traumatic brain injury
involve both linear and rotational forces
Biomechanical forces in the pediatric
different with the adults
In pediatric the forces of trauma can be
dampen with their structure that still less
developt
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TBI results in a significant increase of
glucose utilization (30 min post-
injury)lower about 5-10 days
Difficult to capture acute period of
hyperglycolysis in a critically ill TBI patient
Subacute phase, another study showed no
correlation between the level ofconsciousness as measured by GCS and
glucose metabolism
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Hyperglycolysisdisruption of ionic
gradients across the neuronal cell
membrane, activating energy-dependentionic pumps
Also increasing oxidative metabolism
brain trauma
As cerebral oxidative metabolism at
baseline already near or at maximum
levelsincreased energy demand
augmenting glycolysis Increased lactate levelsischemic and
concussive brain injuries
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Increased lactateneuronal dysfunction
acidosis, membrane damage, disruption
bbb and cerebral edema
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Cerebral hemodynamics change
significantly post injurydepends type of
injury and its severity
An ongoing debate as to whether these
low flow events are a contributing cause of
cell injury, a consequence of the injured
and dying tissue or a manifestation of anon-ischemic physiological perturbation
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Flow reductions were not associated with aconcomitant decrease of the cerebral
metabolic rate for oxygen (CMRO2)
beyond that induced by TBI itself
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Acute injurya rapid release of
glutamate
This indiscriminate release occurs as a
result of extensive triggering of action
potentials, synaptic neurotransmitter
release, and membrane disruption.
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