Traumatic Brain Injury

Usually c other injuries

Types of TBI according to visual:
o open:
Lacerated or open na yung meninges
esp. Dura
o closed
o penetrating:
Could be under open, but c penetration of
foreign object;
post traumatic epilepsy is common
MC: MOI
1. GSW
2. Stab Wound
3. Missile Wound (like in Blast Injury; e.g.
sharpnels)
Epidemiology:
M; young adults
Mild TBI is Most common
o Hindi lang siya nadodocument ng maayos
o Concussion (din a sinusugod sa hospital)
o Clinical setting: more Severe TBI pt.
MOI:
o Direct causes:
1. Falls MC now
2. MVA considered MC before
3. Disaster events
4. Assaults (Violence Related)
o Indirect causes: Alcohol Abuse
Pathophysio:
Types according to resulting injury:
1. Contact Injury
o Usually c pasa around area of blow
o Usually, damage to brain is where the blow had
contact in
o Could have:
Coup Injury
damage to brain is where the blow had
contact in
usually in acceleration forces: you are
still, biglang may force
Contre(Counter)coup: 1 word
damage to brain is opp. to blow(recoil)
LARGER, and worse
Usually in deceleration forces:
gumagalaw ka, may force na tumigil
sayo; brain shake
Usually c whiplash injury: ito yung
punta muna sa harap yung head,
tas likod ulit.
*Hindi isolated ang coup sa contrecoup
injury vice versa
o Could be (+) Fx in skull (along sa ibang parts of
body)
Depressed Fx
May lumubog if na press
Be careful in Dx: Hematoma (bukol)
lumulubog din): mas lubog ang Fx
X-ray to be sure
Concomitant Fx: c existing Fx sa ibang parts
Pond Fx: sa children; lubog lang talaga, s
cracks (not yet completely ossified)
Assault Fx: if, 1-3 y.o. Shaken Baby
Syndrome

Damages in brain:
1 Injury
o Diffused Axonal Injury
Initial LOC is related here
(+) Shearing of axons (fray like rope)
Difficult to detect; MRI for detection
Usually in: Subcortical white matter, corpus
callosum, midbrain, pons
o Contusion:
bruises in brain
may occur anywhere, but MC @ inf parts of
brain (d/t sharp edges of cranial vault):
Inf. Frontal
Ant. Temporal
o Petechial Hemorrhage:
Like DAI; but blood vessels are the ones
affected
If Capillaries = small hemorrhages
o CN Lesion
Usually CN 1,3,7 (no matter which site)
Ant. Fossa Fx
CN 1 (cribriform plate)
Most: Frontal Lobe
Orbital & Nasal Cavity
Orbital Cavity:
Periorbital Hematoma
Raccoon Sign
Panda Bear Sign
Not to be confused c Black Eye,
kasi bruise lang yun
Doesnt appear until 2-3 days
(wiki)/ several hrs(magee)
Nasal Cavity:
Rhinorrhea: CSF leaks out of nose
Differentiate from sipon:
-May crystals
-Chromatograph: orange tinge
Petrous Fx
Battle Sign:@Mastoid Process
Otorrhea:CSF sa ear
CN 7,8 (Internal Auditory Meatus)
Connected sa Temporal Fx
CN 9,10,11 usually unaffected
2 Injury
o Intracranial hemorrhage
Long time before seen; accumulation
Related areas: Epidural & Subdural spaces
Epidural:
MOI: Lateral Pterion Fx
Meningeal (superficial) vessels
ruptures
Subdural:
c Shift of brain
Sup. Cerebral veins might be
sheared
A-P Force (naalog)
o Cerebral Edema/Swelling
Check ICP
Has many causes(like HTN,
hydrocephalus)
If inc:

 Brain Herniation
Cerebral perfusion pressure (60-160
mmhg) cant be overcome
o Hypoxia: Blood vessels ruptured/are
compromised
o Excitotoxicity
Inc excitatory neurotransmitters
If stimulated, channels open
Ca rushes inside
Swell, then apoptosis of neurons
Sumabog, kumalat=toxic
d/t injury kasi
Sympathetic nervous system is active
E.g. glutamate
Assessment:
Coma:
o LOC: compressed Dien & Brainstem
o DAI usually
o Could be d/t secondary injuries
o Happenings in coma
1. Eye opening
2. Sleep/wake cycle:c time frame na
3. Follows command:basta may response
4. Speaking:ungol/groaning is very good
prognosis na
Vegetative State
o (+) eye opening and sleep/wake
o (-)follows command and speaking
Minimally conscious state
o Voluntary activities, but minimal
o Do not confuse it c REFLEX (check consistency)
If @ the scene of TBI:
Call ambulance first
Keep pt awake
o if ayaw, PHYSIOLOGIC DETERIORATION OF
STATUS
ER:
o CT(for hematoma) and acute stage; fast; check
swelling
o MRI for small lesions, DAI, petechial hemorrhage
*Kung may Brain Injury kahit anong bet magising ay
matutulog at matutulog yan
*TBI plus SCI so may position na need iwasan

PEDIATRIC GCS
o For children and babies
o Has 2 subsets for 2 age ranges
Glasgow-Liege Scale
o GCS + Brainstem reflexes(should be intact)
Frontoorbicular reflex
-glabellar tap=close eyes
Vertical oculocephalic/oculovestibular
reflex
-Doll eyes
Horizontal oculocephalic/oculovestibular
reflex
-levelled gaze
Pupillary light reflex
-light:constrict; dark:dilate
Oculocardiac reflex Aschner Dagnini
Reflex
-pressure on eyeballs=bradycardia
GOAT (Galveston Orientation And Amnesia Test)
o 0-100; (N) >75 for 2 consecutive days)
o For PTA (Posttraumatic Amnesia)
GOS Glasgow Outcome Scale
o A bit vague
o Outcomes ang chinecheck
o Check 6 mos. After tx/ @ d/c
6 mos: greatest recovery of TBI
1 Death
2 Persistent Vegetative
State (if TBI >1yr; if
Anoxic >3mos)
3 Severe Disability
(Dependent)
4 Moderate
DisabilityIndependent
but disabled
5 Good recovery

RLA or LCFS
o Better than GOS

7 and 8: needs OT; cant easily discern eh

RDRS (Rappaport Disability Rating Scale)

FIM: you may use 6-MWT; is slow, mataas kasi

chance to fall

Severity prognosis
GCS:7 below poor; good na pataas
PTS: >2wks=poor; <2wks=better
(+) CT findings=poor
Motor: can localize=good
Brain stem testing: intact = good

Meds:
Neurotrophin neuroprotective, also contributes in
promoting long-term recovery
NEUROSTIMULANTS
- dopamine dysfunction
dopamine systems are key pathways involved in
attention, task salience, and cognition.
methylphenidate (dopamine transporter inhibitor,
more effect pronounced in males), amantadine
(dopamine enhancer), bromocriptine (D2 receptor
agonist)
- norepinephrine dysfunction
Noradrenergic systems affect arousal, sleepwake
cycles, vigilance, and cognition, also interact with
dopamine systems. NE is critical for governing cortical
plasticity and facilitating recovery post-TBI.
local NE infusions (given early, neuroprotective),
amphetamine (adrenergic stimulation, also
neurotrophin production), L-theodihydroxyphenylserine (L-DOPS, precursor for NE),
atomoxetine (NE transporter inhibitor)
- cholinergic dysfunction
Cholinergic systems are important for memory and
cognition (esp. in hippocampus)
cytidine diphosphate(CDP)-choline (intermediary in
biosynthesis of phosphatidylcholine, also Ach levels),
rivastigmine (Ach inhibitor), NE agonists
Acute Medical Mx: Moderate to Severe TBI
Begins in the field
Guidelines for Prehospital Mx of TBI:
Facilities should provide CT scanning, 24-hour
neurosurgical care, intensive care treatment and ICP
monitors
Recommendation: complete and rapid resuscitation,
correction of hypoxia (also intubation) if apt, sedation &
neuromuscular blockade may be necessary to optimize
transport
ICP Monitoring
Ventriculostomy is preferred because it also allows
CSF drainage
Indicated for: GCS <8 after resuscitation, head CT
showing contusions or edema, or SBP <90 mmHg
To consider for px with severe TBI with (-) CT scan if
>40 y/o, posturing, and/or SBP <90 mmHg
Elevated ICP is defined as 20 to 25 mmHg
Mx: HOB elevation 30, tx of hyperthermia, mannitol
administration, sedation, and brief hyperventilation
prolonged hyperventilation negatively affect CBF
CPP
worse clinical outcomes if with episodes of low CPP
should be maintained >60 mmHg in adults
Tissue oxygenation monitors
measures oxygen tension
directly placed in brain tissue via an external
ventricular drain (EVD) can detect focal ischemic
changes that can go undetected with global or indirect
measures (e.g. CPP or ICP)

Surgical Treatment
indicated when there is a significant mass effect
gauged by degree of midline shift on neuroimaging
depressed skull fractures should be elevated if greater
than the thickness of the skull esp. if there is dural
laceration
decompressive craniectomy to ICP
Nutrition
metabolic rates can 40% during early stages
delaying nutrition replacement is assoc with
mortality
recommendation: replacement of 140% of resting
metabolism expenditure (ref. to paralyzed pxs),
preferred to use GIT route. Goal is to maintain nitrogen
balance, measured by metabolic cart study, prealbumin
levels and liver functions
Secondary complications in ICU
glucose levels is assoc with mortality (attributed
to lactic acid)
sodium imbalance is assoc with seizures, and worsen
levels of consciousness (rel. volume status)
hyponatremia d/t excessive us of IV fluids
hyperthermia
Poor Prognosis:
ICP > 20 mmHg, CPP < 70 mmHg, CBR < 18
mL/100g
Surgical Intervention
focal evacuation of hematoma
debridement of parenchymal contusion
focal skull flaps swelling
bifrontal craniectomies intractable ICP
Complications:
Neuromuscular
Motor recovery 2-3 months
Heterotrophic ossification
After 1-3 mo, shoulder, (if (-) x-ray, proceed with bone
scan), (+) alkaline phosphatase, meds:
di/biphosphonates, disodium etidronate, surgery (12-18
mo)
Hydrocephalus NPH or hydrocephalus ex vacuo
Post traumatic epilepsy MC type: complex partial
seizure
Late, early, immediate (> 7 days, 1-6, within 24 hrs)
Med: anticonvulsants (prophylaxis for 7 days for
penetrating injuries & GCS < 12)
DVT
Pulmonary embolism, post-phlebitic syndrome
(chronic DVT)
Doppler US, Venography (gold standard)
Prophylaxis: mobility, graded compression stockings,
anticoagulants (heparin & warfarin, safe period 24-72
hrs post TBI, w/o prior surgery or active bleeding)
Spasticity
Eliminating irritants, ROM & positioning

Modalities, splinting & casting

Systemic medications (dantrolene sodium, baclofen),
neurolytics (Botox, phenol)
Intrathecal baclofen pumps
Surgery
GIT Complications dysphagia, gastroparesis (meds:
erythromycin), gastric ulcers
Increased metabolism & catabolism post TBI
Aspiration risks npo thin liquids use of NGT
(indicated only for <3 weeks) gastrotomy,
jejunostomy
Respiratory complications pneumonia respiratory
failure
Bowel & Bladder incontinence, dyssynergia, retention
Meds (anticholinergics)
Endocrine
SIADH volume-expanded
DI
Cerebral salt-wasting syndrome volume contracted
Anterior pituitary ACTH (Addison like),
hypothyroidism (cold intolerance), gonadotropin
(impotence, amenorrhea), GH
Cognitive
Arousal
tonic fluctuations in relation to diurnal rhythm, food
intake, and activity level
phasic modulated over brief intervals by demands
in the environment
Selection focused attention
Strategic control modulation of attention
Processing speed
Behavioral
Agitation Craig bed, meds: antipsychotics
diazepam (Valium)
Hypoarousal
Depression - Psychological: depression, substance
abuse, PTSD, OCD, panic
Dermatologic ulcers
Fracture femur (supracondylar)
GCS

Scores of 8 or less are classified as severe

scores between 9 and 12 are defined as
moderate
scores of 13 to 15 are classified as mild brain
injury
postconcussional syndrome
have persistent symptoms
require outpatient follow-up evaluation
objective evidence:cognitive deficits,
three or more subjective symptoms
for at least 3 months
Symptoms: 3-12 mos.
athletes should be free of symptoms before
returning to competition
labyrinthine concussion
o sudden onset of hearing loss and
vertigo after TBI in the absence of
temporal bone fracture
Child Athletes: MC in Mild TBI

Shaken baby syndrome/inflicted childhood

neurotrauma:
risk factors:
maternal factors such as
o mothers less than 19 years old
o education less than 12 years
o single marital status
o African American or Native American
o limited prenatal care
o newborns less than 28 weeks old.
Military TBI/military blast injuries
M>F (80%)
leading causes of military TBIs include:
o blast injury (72%)
o falls (11%)
o vehicular incidents (6%)
o injuries caused by fragments (5%)
o other injuries (6%)

high-order explosives (HE)

produces a supersonic
overpressurization shock wave that is
associated with primary injury.
low-order explosives (LE)

angular acceleration result in

diffuse axonal injury (DAI)
Traumatic subarachnoid hemorrhage (SAH)
Bridging veins are susceptible to shear and
rupture
Translational acceleration result in
Cortical contusions
Epidural hematomas (EDHs)
result from local injury of underlying dural veins
and arteries. The meningeal artery is commonly
the source
damage to dural sinuses can also cause EDH
EDH develops from a disrupted artery
a neurologic emergency occurs because the
EDH quickly expands-rapidly causing neurologic
deterioration.
Subdural hematomas (SDHs)
result from:
o inertial forces
o tearing of bridging veins
Bridging veins: susceptible to shear/rupture
from angular accelerations assoc c falls

Traumatic subarachnoid hemorrhage (SAH)

occurs when angular acceleration shears vessels
located in the subarachnoidspace.
Return to Play Guidelines in athletes sustaining
Concussion

CONCUSSION