Craniocerebral Trauma

(Traumatic Brain Injuury--TBI)

Neurosurgery Department
Hospital Affiliated to Nantong
University
CHEN JIANGUO
How about TBI
— Trauma the leading cause of death (under 45 years age)

— TBI the 2rd position in trauma (just less than the bone
fractrue)
— !!serious issue of the society and family
— TBI 2nd as the cause of death from injury in CNS ( 1st stroke)
— incidence: 132-367/100,000 population

— M:F ratio 2:1— 2.8:1

— Cause for TBI

1st motor vehicle accident 30-50%
2nd fall 15-35%
3rd assault and gunshot wound 5-20%
4th sport-related injury
Involved Field of TBI
Scalp Hematoma
Scalp injury Lacerate wound
Scalp avulsion
Calvarium fracture
Skull bone
fracture Skull base fracture

Primarily brain injury

Brain injury
Secondary brain injury
Pathogenesis
Three types according to the mechanism of injury

Type 1 Acceleration-Deceleration Injury

Type 2 Impact Injury

Type 3 Penetrating Injury

Pathogenesis
1.Acceleration-Deceleration Injury
High-speed motor vehicle injury

Mechanism:
-- different acceleration coefficient in different brain tissue

-- brain slosh -- tough tissue – unflatten skull base/falx/ bone ridge

-- cortical contusion/ bridge draining vein stretch and bleed (SDH)

-- transmission of kinetic force – shear injury to axon and neuron

(DAI) -- most severely in subcortical /mesencephslon
 Pathogenesis
2.Impact Injuries
Head assaulted by blunt objects – skull absorb much- brain concussion

-- skull fracture ( thin temporal squamosa)/ dura damaged

/MMA (middle meningeal artery) injury

-- epidural hematomas (EDH, meningeal vessel tear/ bleeding from bone

fracture or dura)

-- less severity of the acceleration-deceleration injury

-- typical picture: 1st loss of consciousness by concussion – recover with a

lucid period – 2nd decreased mentation ( epidural hematomas expanding )
Pathogenesis
3. Penetrating Injury

-- high-velocity and low-velocity (300 feet/per second)

--Low-velocity chopstick/pen/branch – thin skull base –

orbitocranial window– damage to vascular structure along the path

--High-velocity bullet – entry path -- away from tract – diffuse

injury – high mortality
Clinical Findings
Symptom and sign

common experience – different one by one – examination

change
--location/mechanism/severity of injury/ time after
injury

Demand FREQUENT and CAREFUL assessment and

investigate
Clinical Findings
Initial examination 1
1.ABC – emergency medical aid – airway/breathing/circulation

2.neurological examination – mental status/ pupil size/CN reflex/motor

function

1+2

ABC + D Disability
Clinical Findings
Initial examination 2
GCS (Glasgow Coma Scale)

Easy/best/objective measure for mental status

Scale from 3-15 composite score by three clinical parameters

( eye opening/ verbal response/ motor response)

Coma severity status– no more than 8

Moderate TBI status – score from 9-12
Mild TBI status -- score from 12-15
 Glasgow Coma Scale (GCS)
eye-opening verbal response moter response score
follow commands 6

normal speech with

normal content
localize pain 5
normal speech with
to ambient
stimulus
inappropriate withdraw from pain 4
content

to directed flexor posture

verbal
words without sentence
(decorticate posture) 3
stimulus
extensor posture
to pain sound without word (decrerbrate 2
posture)
no eye-opening absence of verbal output no response 1
Clinical Findings

cranial nerve and reflex assessment

depend on the patient’s lever of consciouness

Simply and directed cranial nerve examination --

Pupillary reflex , corneal reflex , gag reflex

Clinical Findings
pupillary reflex: light response , afferent information
CN2/ efferent information CN3 --
midbrain
corneal reflex: afferent information CN5/ efferent information

CN7 -- pons
gag reflex: afferent information CN10/ efferent information CN11
--medulla

Dilated/fixed pupil – transtentorial herniation (temporal

uncus) – supertentorial intracranial hypertension

Loss of corneal/gag reflex – severe brain stem injury

Clinical Findings
Assessment of motor function

1.Qualitative assessment of movement of extremities

2. Assessment of sensation / deep tendon reflex/ coordination

Depend on awake/cooperative patient

Clinical Findings

Monitor the vital sign--imperative:

• hypotension and tachycardia indicate hypovolemia
• low pulse indicate cervical injury/primary cardiac pathology
• hypertension bradycardia(Cushing reflex)indicate intracranial hypertention

Be Alert – ICP
increase blood pressure/downward drifts in heart rate
Clinical Findings
Imaging study
1. Computed tomography (CT) –
change blind neurosurgery to new bright period

Easy, fast, readily avilable, sensitive to intracranial pathologic process

2. Magnetic resonance imaging (MRI):

? Establish the severity of any intracranial pathologic process not

clear on CT

Shortcomings: procedure period longer/no metallic objects

 Medical Treatment

Dynamic and heterogeneous nature of TBI

impossible

No strict rule/no simply treatment way

 Medical Treatment
A: Hemodynamic Instability and Airway Management

common in all severe injury patients (1st)

How to do: 1. Rapid and aggressive volume resuscitation
--- crystalloid solution : 0.9% sodium chloride or Ringer’s solution
--- Blood cell or blood plasma (second step)
--- pressor agents: dopamine (third step, only after intravescular
volume been repleted)

2. secure airway ventilation/ oxygenation

--- endotracheal intubation/tracheotomy
--- never move the cervical spine separately to minimize the injury risk
Medical Treatment-- neurologic instability
2. Intracranial hypertention:

Normal intracranial contents: brain tissue, C.S.F.,blood

Fixed intracranial volume– ICP changed if any three components volume changed

ICP – volume curve : curvilinear relationship between volume and

pressure
ICP – volume curve
Causes of ICP
(Intracranial hypertension)

• Brain edema
• Mass
• Hyperemia
• Hydrocephalus
Factor influence ICP
 Head position
 Neck position
 CO2, O2
 Fever
 Nursing activity
 Pain, discomfort
 Agitation, movement
 Hyponatremia
Increased ICP
Medical Treatment
2. Intracranial hypertention:
Initially ICP is barely noticeable as V increase, slope is 0

as Vaccumulate(critical value), the curve become steep, eventually

approach vertical

ICP influence factors: brain tissue, CSF, blood volume, brain edema

Treatment target: lowering/decreasing the volume

Medical Treatment
2. Intracranial hypertention:

ICP monitor – the most useful instrument in TBI treatment

Two basic type: drainage or nondrainage type

Place in ventricle, Place within brain

subarachnoid, parenchyma
sudural space

! Risk: infection and hemorrhage

 Medical Treatment
2. Intracranial hypertention:

All treatment proposal for high ICP should target to the key factors

A. CSF volume: lower it by ventriculostomy, draining

constantly or draining only ICP reach a set threshold
Medical Treatment
2. Intracranial hypertention:
B. Brain volume:
1.lobectomy – buy extra space, it depends
2.medical management – more satisfying – control
edema
1. Monnitol most usual medicine – not cross BBB–

establish an osmotic gradient – drawing interstitial

water out of brain – limitation: hypotension, reduce

blood pressure
 Medical Treatment
2. Intracranial hypertention:
C. Blood volume: nonsurgical management focus on capillary
volume, venous volume, arterial volume
1.Capillary volume: difficult to manipulate to any significant degree

2.Venous volume: lower ICP by decreaseing venous volume

a.elevating the head of bed—increase pressure differential between intracranial venous
pressure and central venous pressure
b. Prevent intrathoracic pressure

3. Artery volume:cerebral autoregulatory mechanism—vasodilating

arterioles – increase blood flow—increase ICP
decrease PCO2 by mechanical hyperventilation—increase PH-- ￬ ICP/blood
SURGICAL TREATMENT

Treatment of
1.epidural hematomas,
2.subdural hematomas,
3.intraparenchymal contusion,
4.open skull fracture,
5.scalp lacerations
SURGICAL TREATMENT
epidural hematomas (EDH)
Location: underlie a skull fracture
—most common location temporal fossa– thinnest part/most likely
fracture and easily lacerate middle meningeal artery

--frontal/parietal convexity, occipital and infratentorial

compartment

--occasionally skull fracture cross venous sinus(sagittal

sinus/transverse sinus)—venous epidural hematoma
Operation procedure: incision should expose entire hematoma
bone window – single burr hole and then remove and turn
by cutter– evacuate hematoma, stop dural bleeding–
secure the dura to craniotomy edge– bone flap reattached
 SURGICAL TREATMENT
subdural hematomas (SDH)

SDH– resulting from tear of cortical draining vein (6 areas):

1.superior sagittal sinus at front pole,2. frontparietal junction,
3.occipital pole; 4.and shpenoparietal sinus at temporal lobe;
Operation procedure:
5.transverse – 1.incision
sigmoid junction usually
6. alonglager –2.skullpetrosal
the superior removed–sinus.

3.extending craniotomy down to the frontal/temporal floor–

dura opened totally and rapidlly – 4.evacuating hematomas

–

5.bone flap replaced

SURGICAL TREATMENT

Intraparenchymal contusion:
always presence of an overlying subdural hematoma and cerebral swelling

1.Approach is depended: with or without SDH and cerebral swelling

incision is large or small

2.Cortical incision – small and closest to surface of target—avoiding

eloquent areas ( vocal area/primary motor area)—hemostasis should
ensure
SURGICAL TREATMENT

Open skull fracture/scalp laceration

-- main objective : clean the area to minimize the risk of

infection/facilitate wound closed

-- attention must paid to underlying dural laceration/hematomas

-- devitalize tissue removed, clean and close the wound

 PROGNOSIS
Many outcome scales for long term asseeement:
cognitive function
physical disability/
emotional neuropsychologic/phychosocial/behavioral function

No one cover all spectrum of neurologic dysfunction

Glasgow Outcome Score—most popular TBI assessment way

Administered at 3,6,and 12 months after TBI

PROGNOSIS
Glasgow Outcome Score—reliable /easily applied/insensitive

Five
Categories:
1.Death
2.Persistent Vegetative State
3. Severe Disability(conscious but disabled)
4.Moderate Disability(disabled but independent)
5. Good Recovery
PROGNOSIS

Factors of Outcome following TBI:

-- initial severity of injury
-- patient age
-- presence of physiologic alteration causing

2nd brain injury

 PROGNOSIS
A. Outcome Following Mild TBI

Patients with GCS 13-15 recovery well in long term

*Most significant sequelae:

headache/fatigue/dizziness/tinnitus/nausea/diplopia/blurred
vision/memory difficulties/ irritability/difficulty concentration

* About 50% patients complain symptom at 6 weeks – 1 year after TBI

* Persistent symptom become less severe and frequent with time

PROGNOSIS
B. Outcome Following moderate TBI

Patient with GCS 9-12 – 60% good recovery,

-- 26% remain moderately disable
-- 7% severely disable
-- 7% either vegetative or dead

Factors influence outcome within this group

-- GCS
-- patient age
-- abnormal in CT and progressive change on CT
PROGNOSIS
C. Outcome following severe TBI– very difficult to predict

Often hemodynamically and neurologically unstable

/suffer significant 2nd injury

Many predictive factors influence outcome

GCS(particularly motor score) and age most significant factors

Pupillary response/size, midline shift, ICP

Prevent 2nd injury: low ICP/control ventilation/prevent complication

THANK YOU
D (Transcranial Doppler)

CBF monitor
Team work, Professional,
Right concepts and dedicate activity
Pathobiology
Cellular changes
Initial impact – biochemical alterations
--Unregulated release neurotransmitter – depolarization of neuron
--Gultamate – NMDA/gultamate receptor – cytotoxic cascade

cellular energy metabolism/ cerebral blood flow/

free radical production/harmful cytokine
Gross changes
-- intracranial hematomas/edema/hypocephalus/
-- intracranial hypertension

-- systemic problem:seizure/infection/hypoxia
Medical Treatment--neurologic instability
B.intracranial mass – intracranial hypertention –

neurologic instability (2nd)

1.seizure after TBI
– anticonvulsant medications– phenytoin -- status epileptic
(Danger) – benzodiazines – lorazepam,diazepam – even
general anesthesia
-- treatment duration 1. 7 days if no seizure 2. 6 months
reinstituted if seizure again after stop medicine
 Medical Treatment
2. Intracranial hypertention:

•Decrease cerebral metabolism—medication (barbiturate

and propofol)

•Metabolic rate ￬— ￬ metabolic demand – ￬ blood supp

-- ￬ ICP
eye-opening verbal response moter response score
follow commands 6

normal speech with

normal content
localize pain 5
normal speech with
to ambient
stimulus
inappropriate withdraw from pain 4
content

to directed flexor posture

verbal
words without sentence
(decorticate posture) 3
stimulus
extensor posture
to pain sound without word (decrerbrate 2
posture)
no eye-opening absence of verbal output no response 1