Trauma

kepala
(head
injury)

Trau ma
ma ra u l
kapi
tis
T
s erebra
io
kran

Ci u ma
d a
ot era Tr tak n
ak o ai
r
(b ury)
inj

Traumatic Brain Injury (TBI)

AKBAR PATUTI, MD, NEUROSURGEON
 Objectives

 Describe basic intracranial

physiology.
 Recognize the importance of
limiting secondary brain injury.
 Perform a focused neurologic
exam.
 Stabilize and arrange for
definitive care.
 Incidence

Traumatic Brain Injury, or TBI, is the leading cause of death and disability in children and adults from
ages 1-44

Most often caused by motor visual crashes, sports injuries, or simple falls on the playground, at work,
or in the home

Approximately 52,00 deaths occur from TBI annually

An estimated 1.5 million head injuries are seen yearly in Emergency Departments

An estimated 1.6 to 3.8 million sports related TBIs occur each year
 Causes

Motor vehicle accidents

Firearm-related injuries
Falls
Assaults
Sports-related injuries
Recreational accidents
 Prevention

 The best way to treat TBI is prevention

 Seat belt use
 Helmets
 Skateboarding
 Rollerblading
 Scooters
 Bicycle/Motorcycle
 At risk behaviors
 Males 2 times > injury rate than females
 Anatomy and physiology

 Rigid, nonexpansile skull filled with

brain, CSF, and blood
 CBF autoregulation
 Autoregulatory compensation
disrupted by brain injury
 Mass effect of intracranial
hemorrhage
©ACS
7
ICP : Intra Cranial Pressure

 ICP is influenced by relatively fixed volumes

 The brain 80%
 The blood 10%
 The CSF 10%

 Monroe-Kellie Hypothesis
 to maintain a normal ICP, a change in the
volume of one compartment must be offset by a
reciprocal change in the volume of another
compartment
Intracranial Pressure (ICP)

 10 mm Hg = Normal
 > 20 mm Hg = Abnormal
 > 40 mm Hg = Severe
 Many pathologic processes affect
outcome
 Sustained  ICP leads to  brain function
and outcome
 Increased ICP

 Etiology – Any condition that:

 Increases brain volume
 space occupying lesions
 SDH, masses, cerebral edema, EDH, ICB

 Increases blood volume

 Venous outflow obstruction, hyperemia (HTN), hypercapnia
 Increases CSF
 Hydrocephalus, SAH, lack of absorption of CSF
 Monro-Kellie Doctrine

Venous Art. Brain CSF

Volume Vol.

Ven. Art.
Brain Mass CSF
Vol. Vol.

75 mL Arterial 75 mL
Brain Mass CSF
Volume

©ACS
 Increased ICP

 Sign
Cefalgia • Medical History
Nausea • Neuro disease
• Trauma
Vomiting • Fainting
Seizures • Substance abuse
• Especially cocaine,
Decrease Level of Consciousness heroin
Personality Changes • Medications
Motor deficits • Allergies
Visual changes
 Patofisiologi Cedera Otak
TRAUMA KEPALA Norm
al

CEDERA OTAK
Tx
adequad
PRIMER

INTRA KRANIAL EXTRA KRANIAL

SECONDARY INSULT SECONDARY INSULT

CEDERA OTAK
SEKUNDER AIRWAY
BREATHIN
G
CIRCULATI
•  ICP, CPP ON
• ISKEMIK-
HIPOKSIK
• Kerusakan sel

• MORTALIT
AS
Management
 Early Management

 ABCDE
Airway & C-Spine control
Breathing
Circulation & Haemorhagic control
Disability: Neurologic Evaluation
Exposure/Environmental Control
 Minimize secondary brain injury
 Administer O2
 Maintain blood pressure (systolic > 90 mm Hg)
 Early Management

 Airway should be secured in pts with GCS<9, the inability to

maintain an adequate airway
 Endotracheal intubation is the most effective
 Oxygenation and Blood Pressure
 Hypoxemia (<90% O2 Sat) or hypotension (<90 mm Hg SBP)
are significant parameters -> a poor outcome
 Fluid resuscitation should be administered to avoid hypotension
and/or limit hypotension to the shortest duration possible
 IV’s with NaCl 0,9%
 Sistolik BP > 90
Neurologic Examination

 GCS Score
 Pupils
 Lateralizing signs
 Glasgow Coma Score (GCS)

 pre-hospital measurement of GCS is a significant and

reliable indicator of severity of head injury
 A GCS score of 3 to 5 has at least a 70% positive
predictive value for poor outcome
 Note that the phrase 'GCS of 11' is essentially
meaningless, and it is important to break the figure down
into its components, such as E3V3M5 = GCS 11.
Teasdale G., Jennett B., LANCET (ii) 81-83, 1974.
 GCS

Eye Response. (4)

1. No eye opening. Motor Response. (6)
2. Eye opening to pain.
3. Eye opening to verbal command. 1. No motor response.
4. Eyes open spontaneously. 2. Extension to pain.
3. Flexion to pain.
Verbal Response. (5) 4. Withdrawal from pain.
1. No verbal response 5. Localizing pain.
2. Incomprehensible sounds. 6. Obeys Commands.
3. Inappropriate words.
4. Confused
5. Orientated
 23

23
Pupillary Assessment

 Pupil examination is a standard component of the pre-hospital neuro

exam
 Pre-hospital pupil exam should consist of:
 The pupil size and light reflex
 Assess and document
 The duration of the pupillary dilation and fixation should be
assessed and documented
 Brisk reaction to light
 Sluggish reaction to light
 No reaction to light
Anisocoria
Classification of TBI

Mild TBI (GCS 13-15)

Moderate TBI (GSC 9-12)
Severe TBI (GCS 3-8)
 Mild Brain Injury

 GCS Score = 14–15  X-rays as indicated

 History  Alcohol / drug screens as
indicated
 Exclude systemic injuries
 Liberal use of head CT
 Neurologic exam

Observe or discharge based on findings

 Moderate Brain Injury

 GCS Score = 9–13  Admit and observe

 Initial evaluation same as  Frequent neurologic exams
for mild injury  Repeat CT scan

 CT scan for all

Deterioration:
 Manage as severe head
injury
 Severe Brain Injury

 GCS Score = 3–8

 Evaluate and resuscitate
 Intubate for airway protection
 Focused neurologic exam
 Frequent reevaluation
 Identify associated injuries
 Admission or Discharge?

 GCS < 15
 GCS 15, but
 Continuing amnesia
 Continuing nausea/vomiting
 Severe headache
 Any seizure
 Focal neurological signs
 Skull fracture
 Abnormal CT

 Significant medical problems

 Social problems/no supervision at home
  Patients with severe TBI and a GCS <9
 Immediate CT Scanning
 Prompt neurosurgical care
 Ability to monitor ICP and treat increased
ICP
 Abnormal CT scan

Transfer/Consul  Clinical features which warrant neurosurgical

assessment, monitoring or management:
t to  Persisting coma (GCS 8/15)

Neurosurgery 


Persisting confusion
Deteriorating GCS
 Progressive focal neurology
 Seizure without full recovery
 Depressed skull fracture
 Penetrating injury
 CSF leak/BOS fracture
Discharge from A/E

 None of the above exclusion criteria

 Patient must be given head injury advice
 Responsible adult to supervise the patient
 Easy access to a telephone
 Reasonable access to a hospital
 Easy access to transport
 Assessment
Skull x-ray indications

 CT scanning resources are unavailable

 GCS < 15 or
 GCS 15, but:
 MOI not trivial
 Losse of conciousness
 Amnesia or has vomited
 Full thickness scalp laceration/boggy haematoma
 Inadequate history
 Skull X-ray

Advantages
Quick
No need for radiologist
Low dose of radiation
(0.14mSv)
Inexpensive

Disadvantages
Increased workload
Inconclusive
 Assessment
Head CT Scan

 CT is a vital tool in the assessment of

patients with serious head injury,
 It remains the investigation of choice even
following the advent of MRI, due both to the
ease of monitoring of injured patients and
the better demonstration of fresh bleeding
and bony injury.
3
6
36
 CT Indications

 GCS less than 13 at any point since the injury

 GCS 13 or 14 at 2 hours after the injury
 Suspected open or depressed skull fracture
 Any sign of BOS fracture
 Post-traumatic seizure
 Focal neurological deficit
 >1 episode of vomiting
 Amnesia > 30 minutes before impact
In patients with some LOC or amnesia since the injury:
 Age > 65
 Coagulopathy
 Dangerous MOI
 Classification of Brain Injury

By Mechanism

 Blunt: High and low

velocity
 Penetrating: Gun
Shot Wound and
other
©ACS
 Classification of Brain Injury

By Morphology: Skull Fractures

Depressed /
Vault nondepressed
 Open / closed
 With / without CSF
Basilar leak
 With / without cranial
palsy
Classifications of Brain Injury
By Morphology: Brain

 Epidural (extradural)
Focal  Subdural
 Intracerebral

 Concussion
Diffuse
 Multiple contusions
 Hypoxic / ischemic injury
Anatomy Head and brain
Epidural Hematoma
 Epidural Hematoma (EDH)

 Collection of blood between the skull and dura

 10-20% of all patients with head injuries : EDH
 Approximately 17% of previously conscious patients who deteriorate
into coma following a trauma have EDH
 Etiology
 Usually from a laceration of the middle meningeal artery
 dural venous sinuses, superior sagittal sinus . venous lakes,
diploic veins, arachnoid granulations, and the petrosal sinuses.
 commonly associated with calvarial fractures
 The arterial bleed in under high pressure – it does not
tamponade, but rather progresses to become a space occupying
lesion causing ↑↑ ICP, brain shift and herniation
 Mortality = 50% if not treated
Epidural Hematoma (EDH)

 Assessment
 Mechanism of injury
 Previous trauma, previous head injury (most common cause)
 PATTERN of unconsciousness

 Initially unconscious, followed by a lucid period , then followed by rapid

unconsciousness
 The classic lucid interval occurs in 20-50.
 the concussive force -> head injury -> alteration of consciousness -> recovering hematoma expand -> mass
effect -> increased intracranial pressure
-> a decreased level of consciousness
-> herniation syndrome.
Epidural Hematoma (EDH)

 Physical exam
 Altered LOC, pupils with unilateral dilation, fixed and/or dilated, contralateral
paresis or paralysis which leads to posturing
 Cushing’s triad
 Abnormal respirations
 Hypertension
 Bradycardia

 Diagnostics
 Rapid CT exam at trauma center
 Epidural Hematoma (EDH)

Lesi hiperdens
bikonveks
EDH

 ABC’s

 hypertension, bradycardia,
The classic Cushing triad:

and respiratory depression

 Frequent neuro checks
 Prepare for emergency surgery
 Transport to a facility with neurosurgery capabilities
 TRUE Neurosurgical emergency!
 Perdarahan epidural
Surgery

 Indikasi radiologi
 Volume lebih 30 cc, berapapun nilai GCS
 Tebal lebih 2 cm
 Midline shift > 0,5 cm
Timing

as soon as
Any patient with acute EDH/GCS <9 / anisocoria should undergo operation “

possible”
Prognosis baik
Non Operative Operative
Subdural Hematoma
 Subdural Hematoma (SDH)

 SDH is a collection of blood between the dura matter and the

subarachnoid layer of the meninges
 most common type of traumatic intracranial mass lesion.
 Acute SDH is the most common type of traumatic intracranial
hematoma -> 24% of patients comatose
 overall mortality rates around 60%.
 Usually caused by trauma or as the extension of an intracerebral
hematoma into the subdural space
Subdural Hematoma (SDH)

 Mechanism :
 a high-speed impact to the skull.
 accelerate or decelerate-> tearing blood vessels, bridging veins,
cortical vessel
 Three classifications
 Acute - onset within 48 hours of presentation
 Sub-acute – onset 2-14 days
 Chronic – more than 14 days
 Subdural Hematoma (SDH)

 Assessment
 Mechanism of injury, time interval, trends in neuro status
 Chronic SDH common : less severe head injuries, elderly,
secondary to multiple falls and abnormal bleeding tendencies
secondary to impaired liver function
 Use of blood thinners or anti-platelet agents
 have minor trauma or low mechanism
 Subdural Hematoma (SDH)

 Physical Exam
 Acute
 Headache, drowsiness, confusion
 Steady decline in LOC
 lucid intervals: up to 38% of cases
 Ipsilateral , unilateral pupil dilation with lack of response to light –
LATE finding
 Contra lateral hemiparesis
 Chronic and sub acute
 Gradual and non-specific changes
 Altered mentation
 Altered motor status
 Ipsilateral pupil dilation and sluggish to light
Subdural Hematoma (SDH)

Acute:
hyperdens
crescent
shape

Acute SDH with left to right shift

 Subdural Hematoma (SDH) chronic

Subacute: hyperdens-
Subacute: hypodens hypodens crescent
crescent shape shape
Subdural Hematoma (SDH)

 Morbidity / mortality due to underlying

brain injury
 Rapid surgical evacuation recommended,
especially if > 5 mm shift of midline
 Acute Subdural Hematomas
Surgery

 Indikasi radiologis
 Tebal > 10mm/midline shift > 5mm -> evacuated regardless of GCS
 Patients with acute SDH and GCS < 9 -> ICP monitoring

Timing “As soon as possible”

 “Four hour rule” operated < 4 h -> mortality 30%, if delay > 4 hour ->
mortality 90%
 Methods
 Craniotomy decompresi
Non operative Operative
 Large frontal
Cerebral Contusion contusion with shift
Subarachnoid haemorrhagic
 Laserasi SCALP

 Perdarahan masif
 Syok
hipovolemik
 Bebat tekan
 Jahit luka
 Resiko infeksi
 Debridement
 Fraktur kalvaria

 Tipe
 Linear
 Paling sering, sekitar 70%
 Tidak menimbulkan gejala, kecuali jika garis fraktur melewati struktur vena
 Depressed
 Menekan jaringan otak
 Kejang/epilepsi pasca trauma

 Merusak struktur otak/pembuluh darah

 Laserasi korteks, perdarahan intrakranial
 Menyebabkan robekan duramater
 Kebocoran cairan LCS

 Infeksi
 Fraktur Kalvaria

 Pemeriksaan fisis
 Jejas/luka eksoriasi, lacerasi,
hematoma
 Hematom > 5 cm -> resiko fraktur
 Deformitas tulang
 Defisit fokal
 Perikranium intak/robek->
terbuka/tertutup
 Pemeriksaan penunjang

Foto X-Ray :
Skull AP/Lat
Garis fraktur
Double kontour
CT Scan
Penatalaksanaan

 Debridement
 Kontrol perdarahan: Bebat tekan/jahit luka
 Antibiotik
 Toxoid tetanus
 Fraktur depres terbuka : rujuk < 24 jam
Basis Cranii
 Fraktur Basis Cranii

 Periorbital
bruising/raccoon Eyes
 Subconjunctival
haemorrhage
 CSF rhino/otorrhoea
 Epistaxis
 Haemotympanum
 Battle’s sign
 Komplikasi
 Infeksi
 Hematoma
 Kebocoran liquor
 Gangguan penciuman
 Gangguan pendengaran
 Pneumocephalus
 Gangguan gerakan bola mata
 Kejang
 Fraktur Basis Cranii

 Diagnostics
 Halo Test (ottorrhea or
rhinorrhea)
 Using a 4X4 collect fluid leak
from nose or ear
 Set on the bedside table for a
few minutes
 Positive when there is a
circular separation of blood
and clear fluid or a “halo”
 Indicative of a CSF leak
 Penatalaksanaan

 Mengurangi kebocoran likuor

 Bed flat
 Never suction orally;
 Hindari pemasangan NGT;
 caution patient not to blow nose
 Pasang sterile gauze/cotton ball
 Monitor pernafasan. Obstruksi jalan nafas
 Antibiotik
 Rujuk
Traumatic Intracerebral
haematoma
 Perdarahan intracerebral

 Terjadi kerusakan vaskular pembuluh darah otak

 Mekanisme cidera : Coup / contracoup
 Menyebabkan edema dan iskemik fokal yang berpotensi
menyebabkan infark/nekrosis jaringan otak
 Perdarahan, dan edema meningkatkan tekanan intrakranial
 Etiologi
 Trauma, acceleration/deceleration, benturan kecepatan tinggi,
rotasi kepala
Perdarahan intracerebral

Diagnosis
 Anamnesis
 Mekanisme cidera
 gejala peningkatan tekanan intrakranial
 Penurunan kesadaran
 Gejala fokal tergantung lokasi perdarahan
 Pemeriksaan fisik
 Penurunan GCS
 Jejas cidera pada kepala
 Pemeriksaan neurologis
 Pemeriksaan Penunjang

 CT Scan kepala :
Golden standar
 Lesi hiperdens
 Perifokal edema
 Efek massa: penekanan
pada struktur eloquen
 Lokasi tersering:
 Frontal / temporal
lobes
Perdarahan intracerebral

Large frontal
contusion with
shift
Difise Axional injury
Traumatic Subarachnoid
Hematoma
 Perdarahan Subarachnoid

Penyebab :
- cidera kepala
- Arteri Vena Malformation (AVM)
- aneurisma pecah
- gangguan fungsi hemostasis
- unknown
Perdarahan Subarachnoid

 Insiden berkisar 26% - 53% pada pasien cidera kepala

 Mekanisme :
(1) accelerasi rotational kepala menyebabkan gerakan osilasi singkat otak
rotational;
(2) regangan arteri vertebrobasilar akibat hiperekstensi;
(3) peningkatan tiba-tiba tekanan intrakranial dari aliran arteri cervical carotid
(4) robekan bridging veins atau pial vessels; dan
(5) diffusi darah kontusio ke ruang subarachnoid.
Gejala klinis

 "worst headache ever”

 Penurunan kesadaran
 Photophobia, gangguan visus
 confusion and irritability, gangguan mood
 Nyeri leher dan bahu
 Mual, muntah
 Hipostesi
 Seizure
Pemeriksaan Penunjang
CT Scan/CT Angiografi
Komplikasi

 Vasospasm
 Hydrocefalus
 Ischemia
 Pulmonary embolism
 Hyponatremia
 Seizures
 Cardiac problem
Penatalaksanaan