TRAUMA KEPALA

TUJUAN

Setelah menyelesaikan bab ini peserta

diharapkan dapat menjelaskan:
1.Anatomi kepala & otak.
2.Patofisiologi cedera kepala.
3.Pemeriksaan pasien cedera kepala.
4.Penatalaksanaan pasien cedera kepala.
 PENDAHULUAN

PREVENTING
SECONDARY
BRAIN INJURY IS
THE MOST
IMPORTANT
ASPECT OF
TRAUMA TO THE
BRAIN
 EPIDEMIOLOGI

Data di Bagian Syaraf RSUPNCM tahun 2000, dari 929

penderita cedera kepala :
- CKR 570 orang
- CKS 231 dengan kematian 3 %
- CKB 128 dengan kematian 50%.
Di US 2 juta insiden kasus trauma kepala per tahun, 52 ribu
meninggal , 220 ribu MRS dan 100 ribu terdapat kecacatan
temporer/permanen (Data tahun 1993).
Sejak mulai diberlakukannya Safety On The Road terjadi
penurunan hingga 22% lebih terhadap angka kematian
trauma kepala.
34 ribu meninggal dalam perjalanan ke UGD RS (data tahun
1995)
 EPIDEMIOLOGI
Angka Survival di UGD ( US tahun 1993) adalah :
80% pada Cedera kepala ringan (GCS 13 15)
10% Cedera Kepala Sedang (GCS 9 12)
10% pada Cedera Kepala Berat (GCS 8 )
PENYEBAB
 ANATOMI

Kulit kepala. 1.Kulit Kepala (SCALP)

Tulang tengkorak. S kin atau kulit
Selaput otak/meningen, C onnective Tissue
Jaringan otak. A poneurosis
Cairan serebro spinal. L oose areolar tissue
Kompartemen vaskuler. P erikranium
 ANATOMI

Tulang Tengkorak :
1. Calvaria
2. Basis Cranium

Lapisan Meningen
1. Duramater
2. Arachnoid Mater
3. Pia mater
 MECHANISME OF BRAIN INJURY
2 Mekanisme yaitu : Cedera Primer dan
A. Direct (Langsung ) Sekunder
B. Indirect (Tidak Primer (timbul segera
Langsung)
pada
Direct --- initial saat terjadinya trauma):
impact tulang kepala 1. Lokal
dengan obyek 2. Difus
Indirect - Robekan
pembuluh darah dan
terganggunya Sekunder (Timbul dan
integritas akson, shg berkembang beberapa
terjadi subdural waktu
hematoma, diffus
axonal injury dan setelah trauma)
gegar otak. 1. Lokal
2. Difus
 DIAGRAM MOI

CEDERA OTAK

TRAUMA SKULL FRACTURE

CEDERA PRIMER CEDERA SEKUNDER

LOKAL : DIFUS : LOKAL : DIFUS :

DAI Komosio HSD subakut/kronik Iskemi, Hipoksi
Kontusio PSA Infeksi Edema,TIK naik
Laserasi, HSD akut EDH Infark Batang Otak Difus Vaskuler Injury
 COUP VS CONTRA COUP

COUP -- Direct Contra Coup -

Lacerasi SCALP Direct & Indirect
Fraktur tulang
tengkorak
Epidural Hematoma
Contusio Otak
 PENYEBAB CEDERA OTAK
SEKUNDER
ISCHEMIA
Cerebral Perfusion Pressure.
Another simple but vital principal that must be kept in mind
when dealing with intracranial pathologies.
The CPP is just as important as the intracranial pressure.
CPP 70mmHg> is generally associated with a poorer outcome
following head injury.
Hyperventilation and low C02 are no longer recommended.
Causes arterial vasoconstriction that reduces the ICP but also
the CPP.
EXCITOTOXICITY
 CEDERA OTAK SEKUNDER

Sistemik : Intracranial
Hipoxemia TIK
Anemia Edema cerebri
Hipotensi Lesi massa
Hiperthermia Kejang
Hiper/hipocapnea
Komplikasi respirasi
Elektrolyte
imbalance
KARAKTERISTIK CEDERA KEPALA
GCS
E + M + V = 3 to 15
Less than or equal to 8
at 6 hours - 50% die
Initial
"postresuscitation"
score most accurate
predictor of future
outcome.
KARAKTERISTIK CEDERA KEPALA
CONT
PENATALAKSANAAN
 CASE 1

Ditemukan seorang laki -

laki muda terbaring
dibawah tangga,
mengerang kesakitan,
lupa ingatan, tidak ada
yang mengetahui
insidennya . Korban
tampak pucat dan dingin
dengan muka penuh
darah, dan terdapat
lacerasi dan udem di
bagian kiri kepala.
 What do yo do now ?

ABCs
AIRWAY / BREATHING

Most important and the primary concern is if

the patient is able to maintain an airway.
How do you assess the airway?
Rapid assessment of the neurological state.
How do you assess the neurological state?
Korban suara hanya mengerang dan respon
menghindari rangsangan nyeri. Mata tidak
membuka

What is his GCS ?

GCS = 7
What do you need to now ?
GCS < 8 --- Intubasi pasien
 What do you want to check next ?

Breathing:
Exclude conditions that will impair breating and rapidly
correct.
look for:
exposure
inspection of chest
chest wall movement
tracheal deviation.
percussion may be helpful but
Auscultation
Conditions that have to be excluded:
tension pneumothorax
flail chest
massive haemothorax
open pneumothorax
 CIRCULATION
Now you can finally deal with the head laceration.
How do you deal with it?
In this category you also need to look for:
Blood volume and cardiac output.
Level of consciousness
Skin color
Pulse.
Bleeding: expose patient fully.
 C - SPINE
What do you do to protect the C-spine?
All patients with head trauma or maxillofacial trauma should
be presumed to have an unstable cervical spine injury until
positively excluded.
Absence of neurological deficit does not exclude cervical
spine injury.
Examination of the c-spine is impaired in a comatosed
patients.
Decubitus ulcers may develope quickly.
Waiting for several hours to exclude c-spine injury is poor
management.
leaving patient in hard color and on spinal board for
several hours is very poor management. Serious full
thickness skin ulcers will develope.
Early attention to excluding c-spine injuries is important.
What are the investigations you would do?
 FOTO CERVICAL

This injury is known

as a extension teardrop
fracture. This injury is
secondary to a
hyperextension
mechanism and
usually involves the
second cervical
vertebrae. It is seen
most often in the
elderly.
This injury is
potentially unstable.
 This is known as a
hangman's fracture and
consists of fractures
through the pedicles of C-2
(traumatic
spondylolithisis of the
axis). The injury occurs
with hyperextension and
commonly occurs following
car
accidents.
In this patient with little
dispacement, the anterior
and longitudinal ligaments
are intact and the injury is
relatively stable. With
marked anterior
displacement, the ligaments
are ruptured and the injury
is unstable
 THE PATIENT IS NOW STABLE

Good oxygen saturation,

Breathing 100% oxygen and on ventilator.
Abdomen is soft (but this may be misleading in head
trauma)
There is no x-ray finding of fracture or any clinical
signs of fracture.

What is your next step?

Reassess the GCS.
pupillary changes - (fixed, dilated) - a late finding
due to brainstem compression.
Continuous Neuro OBS is vital the detect early
changes in the patient.
 The patient is now intubated and paralysed, you did
not get a chance to do the neurological examination
prior to intubation.
Your findings at this stage:
Slightly dilated pupil on the right but reactiv.
Previously equal pupils.
GCS of 3T
More brisk reflexes on the left.
 What is the next step ?

Patient needs urgent CT scan.

Neurosurgeon needs to be contacted at
an early stage.
 TEKANAN INTRA KRANIAL

Many Intracranial pathologies

affects intracranial pressure
Normal ICP <10mmHg (136 mm water)
20 mmHg < is abnormal.
40 mmHg < severe elevation.
The higher the ICP after head injury the worst
the outcome
DOKTRIN MONROE-KELLIE
 ICP value gets elevated
at point of
decompensation.
When ICP starts going
up the patient will
rapidly decompensate
and herniation is
imminent
Every effort should
therefore be made to
keep the patient on the
flat part of the curve
 Signs of increased ICP:
Headache:
Worse on waking in the
morning,
relieved by vomiting.
(Intracranial pressure
increases during sleep,
some carbon dioxide
retention?)
Nausea and vomiting,
usually worse in the
morning.
Drowsiness. Important
clinical sign not to be
dismissed.
Papilloedema.
CONCLUSION
TREATMENT STRATEGIES
DEFINITIVE TREATMENT
CT SCAN