Traumatic Head Injury

Petra O.P. Wahjoepramono, Sp.B.S., B.Med.Sci.(Hons.)

Siloam Hospitals, Universitas Pelita Harapan
Introduction
• Head trauma: injury to the head,
which could cause structural or
functional damage to the brain.
• Indications:
• History of injury to the head,
lacerations, hematoma
• Visible wound on the head:,
lacerations, hematoma
• Abnormal radiological findings
• Clinical evidence of brain injury:
decrease of consciousness, amnesia,
neurological deficits, seizures
Penting kah?
Bagaimana secara global?

• Global: 69 Juta Kasus Per Annum

• Di U.K :
• Head Injury : 300.000 – 500.000
• 20%  perawatan
• 10%-nya dalam kondisi koma
• 50%-nya memiliki tekanan tinggi intrakranial
• 35% Severe HI : meninggal
• 18% Severe HI : sequelae (+)
Brain Injury is a leading cause of death
and disability worldwide.
Injuries to the brain are among the most likely
to result in death and permanent disability
Anatomy of Head Injury
Anatomy
• The head contents can be divided into the following:
1. Scalp.
2. Skull.
3. Meninges.
4. Brain.
5. Cerebrospinal fluid.
Anatomy

S : Skin (epidermis, dermis)

C : Loose connective tissue
A: Epicranial aponeurosis
(galea aponeurotica)
L: Loose areolar tissue
P: Pericranium (periosteum)

Bleeding from scalp laceration can result in major blood loss,

especially in children
 Anatomy

 Composed of:
• Cranial Vault
• Cranial Base
 The floor of the cranial cavity is
divided into 3 parts:
- Anterior fossa → frontal lobe
- Middle fossa → temporal lobe
- Posterior fossa → brain stem and
cerebellum
Anatomy

Meninges
1. Dura mater
• Subdural space is a potential space, where
hemorrhage can occur
2. Arachnoid mater
• Cerebrospinal fluid circulate between the
arachnoid and pia matter in the subarachnoid
space
3. Pia mater
• Pia mater connects directly to brain
parenchyme
Anatomy
 Pathophysiology of Head Injury
• Brain Movement During Impact
• Acceleration and Deceleration
• Coup and Countrecoup
• Rotational Injury
• Impact between brain and skull
Newton’s Law
• Inertia: Newton’s law: force = mass x acceleration
• Slow heavy object
• Hit on the head
• Light accidents
• Fast light object
• Bullets
• Fast, heavy objects: not good.
• Shear forces  Traction on neurons
• Effect on microvasculature
• Brain swelling and edema
What happens?
• Concussive force temporarily disturbs activity within brain stem
• Loss of consciousness
• Amnesia: retrograde or anterograde
• Post-Concussion syndrome
• Headache
• Memory
• Irritability
• Inability to concentrate
 You can have skull fractures
• Skull X-Ray is useful

•Linear
•Depressed
•Diastatic

•Basilar  cannot be seen

Skull Base Fractures
• Basal skull fractures usually require CT scan
with bone window
• Clinical signs of basal skull fracture
• Periorbital ecchymosis (Raccoon eye)
• Local trauma or not?
• Retroauricular ecchymosis (Battle’s sign)
• CSF leakage (rhinorrhea, otorrhea)
• Halo Sign, litmus paper, β-transferrin
• 7th nerve palsy
Brain Injury
Primary Brain Injury
• Extraaxial
• Epidural H
• Subdural H
• Subarachnoid H
• Intraaxial
• Diffuse axonal injury
• Contusion
• Intracerebral H
 Epidural Hematoma
• Collection of blood between dura mater and
calvarium
• Commonly from torn dural vessel, middle
meningeal artery, bone fracture
• Sharp margins, biconvex shape, limited by
suture lines
• “Swirl sign”  shows ongoing bleeding
Subdural Hematoma
• Collection of blood between dura and arachnoid
membrane
• Crescent-shaped mass, crossing suture lines, does not
cross the falx, does not displace dural venous sinus
• Usually countercoup injury
• Clinical signs: lateralization on opposite side of
trauma
• Occur most frequently from tearing of a bridging vein
between the cerebral cortex and a draining venous
sinus
• May also be caused by ICH, contusion. Contusion
present in 50% acute SDH cases
• May cover the entire surface of hemisphere
• Prognosis is much worse than epidural
Subarachnoid hemorrhage
• Bleeding into the subarachnoid space, usually from contusion
• Usually over convexities, followed by fissure/sulci, or basal cistern
• 2-fold increased risk of poorer outcome
 Diffuse axonal injury
• Loss of consciousness >6 hours without
intracranial mass
• Major cause of unconsciousness
and persistent vegetative state after head
trauma
• Result of traumatic shearing forces
Cerebral contusion

• Multiple small bleeds in the cerebral

parenchyme
• Usually forms high-density area < 1 cm in
diameter
• Due to direct impact with calvarium, most
common at bony protuberances (frontal
poles, frontal base, temporal poles,
temporal base)
 Intra Cerebral Hematoma
• Result from shearing or rapid
deceleration injuries
• Blood vessels burst, gathers
in parenchyme
• Traumatic ICH usually
superficial, rarely in deep
structures
• Delayed ICH: Injury to vessel
wall due to hypoxia, CO2
accumulation, acidic PH.
•a

Brain is Beautiful
Secondary Brain Injury
• Damage to the brain AFTER the trauma: because of inadequate
management.

Pathological
Edema, Infarction
Secondary and chemical
ischemia,
Brain Injury changes to the
hypoxemia Herniation
BRAIN
Brain Edema
• Causing a repeated cycle of cell death
Increased ICP ICP (mmHg) No of Patients Mortality

0-20 95 (47%) 19%

21-40 67 (33%) 28%

• Head Injury can cause change in
intracranial pressure (ICP) 41-80 39 (20%) 79%
• Ruled by Monroe-Kelly doctrine
Total 201 (100%) 34%
• Intracranial bleeding is a
complication of head injury, found in
25-45% of severe head injuries, 3-
12% of moderate head injuries, and
1 in 500 mild head injury patients.
• Cushing Triad:
• High blood pressure
• Decreased pulse rate
• Abnormal respiratory type
Monroe-Kelly Doctrine
Change of Intracranial Compartment

Compensation:
Increased ICP Reduce CSF Fail: herniation
Reduce Venous blood
Brain herniation
• Types of brain herniation:
1. Uncal herniation
2. Central herniation
3. Cingulate herniation
4. Transcalvarial herniation
5. Upward herniation
6. Tonsillar herniation
Herniation causes Neurological Signs
• Cingulate
• Frontal lobe under falx cerebri: compresses ACA
• Hypoxia, edema, infarct frontal lobe
• Uncal
• Temporal lobe presses n. III, mesencephalon
• Anisocoria  motoric paresis
• Central
• Brain into hiatus tentorium: compressing PCA
• Bad.
• Tonsillar
• Cerebellar tonsil pressed into foramen magnum, compressing medulla
• Dead.
Field Guide to Head Injury
Cedera Kepala:
Apa yang bisa anda lakukan?
• Primary survey
• Airway : Bebaskan jalan nafas
• Breathing : Pernafasan harus adekuat: perhatikan
saturasi O2
• Circulation : Pertahankan sistolik >90 mmHg
• Disability : GCS, lateralisasi
• Exposure : Adanya cidera lain: Multiple trauma!

• Secondary survey dan pemeriksaan tambahan

Communication is important
• Triage
• Know which patients to prioritize
• Clinical management
• What resources to use
• Communication
• To other care providers
• Referring the patient
• Outcome
• Know the future (probability).
How you should report:
• Identity of patient
1) Mechanism of injury
2) Classification of the injury
3) Morphology of the injury
1) Mechanism

• Blunt head injury

• High-velocity: motor vehicle
accident
• Low-velocity: falls, assault
• Penetrating head injury
• Gunshot wounds or other
penetrating wounds
 Classification of Head Injury
Type Stimulus Type of Response Points

• Classified according to Eyes Open Spontaneously 4

To verbal command 3
Glasgow Coma Scale To pain 2
into: No response 1
Best Motor To verbal command Obeys 6
1) Mild (GCS 14-15) Response To painful stimulus Localized pain 5
2) Moderate (GCS 9-13) Flexion-withdrawal 4
Flexion-abnormal 3
3) Severe (GCS 3-8) Extension 2
No response 1
Best Verbal Oriented and converses 5
Response Disoriented and converses 4
Inappropriate words 3
Incomprehensible sounds 2
No response 1
Secondary Survey
• The wounds of the patient
• Head: hematoma? Skull base fractures?
• Body: bruising on chest? Abdomen? Pelvis?
• Extremities: maybe something happened
Initial Trauma Management
• Head up 15-30 derajat.
• Airway assured : prevent hypercarbia and hypoxia.
• Assisted ventilation : mild hyperventilasi 15-30 mnt, PCO2 >30
mmHg
• Circulation: maintain CPP, MABP minimal 50 mmHg.
• Mild hypothermia
 Do you need imaging?
• Moderate/severe HI: always!
• Neurological signs
• Fracture on plain film  400x more likely for intracranial hematoma
• DO NOT let medical management delay diagnosis!

Foto polos kepala Foto servikal CT Scan

• Riwayat pingsan & amnesia
• Gejala neurologis: lateralisasi!
diplopia, vertigo, muntah
• Adanya otorea & rhinorea
• Kecurigaan luka tembus kepala
• Intoksikasi alkohol/obat
• Penderita dengan penurunan
kesadaran
• Penderita sadar dan mengeluh
adanya nyeri pada leher
• Adanya jejas diatas klavikula
• Setiap penderita dengan kecurigaan
trauma servikal
• GCS <15 / terdapat penurunan
kesadaran > 1 point selama observasi
• CKR dengan fraktur tulang tengkorak
• Ada tanda klinis fraktur basis cranii
• Disertai dengan kejang
• Gejala neurologis: lateralisasi!
diplopia, vertigo, muntah
• Kecurigaan luka tembus kepala
• Sakit kepala menetap
Perlukah dirawat?
• Cedera kepala ringan : GCS 14-15
• Penurunan kesadaran
• Gejala dan tanda defisit neurologis: sakit kepala berat, muntah, lateralisasi
• Alkohol, obat, usia tua
• Fraktur tulang tengkorak
• Tidak ada pengawas di rumah
• Jarak jauh ke RS
• Cedera kepala sedang, berat: tentu saja.
Dalam Perawatan Anda, Strategi
Apa Yang Terpenting?
Mencegah secondary brain injury!
Monitoring dan tatalaksana tekanan tinggi intrakranial (TTIK)
Monitoring Intracranial Pressure
Critical to determine action
Tanda Peningkatan TIK
• Pasien sadar:
• Gelisah, nyeri kepala, mual, muntah, pandangan kabur,
• Anak: fontanel cembung dan tegang
• Pasien tak sadar
• Dilatasi pupil unilateral, nonreaktif + hemiparesa kontralateral
(emergensi).
• Postur abnormal : deserebrasi atau dekortikasi
• Papilledema dan perdarahan retina, sering disertai paresa n.VI
• Hipertensi, bradikardi, respirasi abnormal (periodic, hiperventilasi,
irreguler)  Cushing Triad
Bagaimana menurunkan TIK?
• Posisi pasien: tirah baring, dengan elevasi kepala 30° diatas dada
• Memperbaiki venous return
• Target: normotensi (MAP: 90-100 mmHg), normovolemi (CVP: >6 cm H2O),
normotermi (T: 38° C)
Farmakologi

CPP = MAP – ICP

Hipothermia
= 100 mmHg – 15 mmHg
= 85 mmHg (Normal) Kontrol Gula Darah

Hiperventilasi
Manajemen Farmakologis
• Cairan isotonik
Manajemen Cairan

• Mannitol 20%: 0.25 - 1.5 gr/kg

Osmoterapi
• NaCl 3%

• Kurangi metabolisme otak

Agen Farmakologis
• Sedasi: propofol, pentobarbital

• Tidak efektif dalam kasus trauma

Kortikosteroid
Bagaimana jika TIK tidak
terkontrol secara konservatif?
Manajemen Operatif Bedah Saraf!

• Time Is Brain!
• Multiple trauma?
• Persiapan kelayakan operasi
• Lab: Hemoglobin, trombosit, faktor koagulasi, elektrolit
• Rontgen thorax
• Pada orang muda dengan trauma, mungkin dapat ditunda
• Craniotomy/Craniectomy
• Mengeluarkan lesi intrakranial
• Pemasangan drainase LCS
Decompressive Craniectomy
 Bila tekanan intrakranial tidak terkontrol  senjata terakhir
Contoh Kasus
Saat anda bertugas, datang pasien trauma.
• Laki-laki, 32 tahun. Penurunan kesadaran
• 2 hari yang lalu tabrakan motor, tanpa helm, sempat pingsan, sadar
lagi. Dibawa ke puskesmas. Sehari kemudian, meminta pulang.
• Pelan-pelan mengantuk, susah bangun, lalu dibawa ke RS anda.

• !!! Kemungkinan cedera kepala !!!

• Anamnesis riwayat pingsan, kemudian turun kesadaran
• Lakukan sesuai ATLS
• Primary survey, secondary survey
Pemeriksaan Fisik

• Primary:
A : Clear + C-Spine control
B : RR : 18x/mnt, gerakan dada simetris, nafas vesikuler
C : P : 68x/mnt, BP : 120/80 mmHg
D : GCS E3M5V2= 10, Pupil : isokor Ø 3 mm, RC +/+. Tanpa
paresis.
E : tidak tampak luka lain di sekujur badan

• Secondary:
Tampak hematoma di frontoparietal kanan. Ekskoriasi di wajah
kiri.
• Tekanan tinggi?
• Patologi apa yang
terlihat?
• SDH
• EDH
• ICH
• SAB
• Midline shift?
Manajemen pasien
• Cedera kepala sedang
• Jejas di kepala
• Tirah baring, elevasi kepala 30°
• Oksigen, cairan
• Monitoring ICP?
• Hyperventilasi?
• Apakah butuh pemeriksaan tambahan?
Manajemen Operatif
• Adanya lesi intrakranial
• EDH
• SDH
• ICH
• Membutuhkan pembedahan untuk menurunkan TTIK
EDH kanan
SDH Kiri
Semuanya sulit dilakukan bila sejak IGD,
penanganan tidak baik
• Apakah pasien bisa survive sampai kamar operasi?
• Bagaimana kondisi otak saat dioperasi?

• Penanganan yang baik, maka pasien dapat pulih seperti sediakala

Take home message
• Penanganan tepat & cepat  menurunkan angka morbiditas dan mortalitas
penderita!!
• Dibutuhkan pemahaman klinis dan patofisiologi TTIK, mengenali adanya kondisi
gawatdarurat di bidang bedah saraf
• Kemampuan menangani pasien trauma, untuk stabilisasi kondisi pasien
berdasarkan primary survey dan segera konsul ke dokter bedah saraf untuk
diagnosa dan penanganan definitif.
 morphology
Skull • Vault •Open / closed
Fracture •Avulsed
•Linear
•Depressed
•Diastatic

•With/without CSF leakage

• Basilar
•With/without nerve palsy
Intracranial •Diffuse •Concussion
lesions •Contusion
•Diffuse axonal injury

•Epidural Hemorrhage
•Focal •Subdural Hemorrhage
•Intracerebral Hemorrhage
•Subarachnoid Hemorrhage
management