jr neurosurgery

8/10/2019 JR Neurosurgery

1/12

Oleh :Berliana Kurniawati Nur Huda

102011101080

Pembimbing :dr. Dwikoryanto, Sp.BS

LAB/SMF ILMU BEDAHFAKULTAS KEDOKTERAN UNIVERSITAS JEMBER

RSUD. DR. SOEBANDI2014


2/12

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


3/12

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)


4/12

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).


5/12

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


6/12

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


7/12

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


8/12

Increased lactateneuronal dysfunction

acidosis, membrane damage, disruption

bbb and cerebral edema


9/12

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


10/12

Flow reductions were not associated with aconcomitant decrease of the cerebral

metabolic rate for oxygen (CMRO2)

beyond that induced by TBI itself


11/12

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.


12/12

jr neurosurgery

Documents