CEDERA KEPALA

Iskandar Japardi
Departemen Ilmu Bedah Saraf
Fakultas Kedokteran USU / RS.H.Adam Malik
MEDAN

ANATOMI KEPALA
KULIT
TULANG TENGKORAK
DURAMATER
ARACHNOID
PIAMATER

PEMERIKSAAN CEDERA KEPALA DI UGD

PRIMARY SURVEY

Airway
Breathing
Circulation
Disability
Exposure

SECONDARY SURVEY

KEPALA DAN LEHER

THORAKS
ABDOMEN
EXTREMITAS

TERMINOLOGI YANG DAPAT DIPAKAI

UNTUK MEMBAWA PENDERITA KE RUMAH
SAKIT
Primary care: dilakukan pada tempat kejadian
Primary hospital : perawatan pertama pada

rumah sakit (rural)

Primary transport : pertama dipindahkan ke
rumah sakit terdekat
Secondary transport : dipindahkan dari primary
hospital ke secondary center untuk perawatan
definitive
Tertiary transport : antara rumah sakit besar,
penderita multiple trauma, pindah ke pusat
dialisis

MANAJEMEN AWAL CEDERA KEPALA,

HINDARI
HIPOKSIA
HIPERKARBIA
HIPOTENSI
HIPOVOLEMIA

GELISAH
HYPOXIA
RETENTION URINE
NYERI
PROSES INTRACRANIAL

Intracranial contents,
Brain (including the neurological elements
[70%] and interstitial fluid [10%] ) ;
volume 1400 ml or 80%
Blood (arterial and venous) ;
volume 150 ml or 10%
Cerebrospinal fluid (CSF) ;
volume 150 ml or 10%

PEMERIKSAAN NEUROLOGIS

TINGKAT KESADARAN
PUPIL DAN GERAKAN BOLA MATA
REAKSI TERHADAP RANGSANG DARI
LUAR
REAKSI MOTORIK
POLA PERNAFASAN
SINDROMA HERNIASI
BRAIN DEATH

 Motor
Response. (6)
GLASGOW COMA
SCALE

Eye Response. (4)

1.No eye opening
2.Eye opening to pain
3.Eye opening to verbal

command
4.Eye open spontaneously

Verbal Response. (5)

1.No verbal response
2.Incomprehensible sounds
3.Inappropriate words
4.Confused
5.Orientated

1.No motor response

2.Extension to pain
3.Flexion to pain
4.Withdrawal from pain
5.Localizing pain
6.Obey Commands
Klasifikasi
Mild
14 - 15
Moderate 9 - 13
Severe
3-8

SYMPTOMS AND
SIGNS
Headache, worse at night or recumbent

position, because of the increase in CO2

tension and increased venous pressure
Nausea and vomiting
Ataxia, papilledema, and cranial nerve
paralysis
Irregular breathing patterns
Decorticate or decerebrate
Pupillary inequality

PEMERIKSAAN RADIOLOGIS

FOTO POLOS KEPALA

FOTO CERVICAL
FOTO THORAX
FOTO LUMBAL
CT SCAN / COMPUTED TOMOGRAPHY
MRI / MAGNETIC RESONANCE IMAGING

Indikasi CT Scan

Kesadaran menurun (GCS<15).

Skull fracture.
Tanda fraktur basis kranii.
Sakit kepala menetap/ muntah.
Cedera penetrasi.
Kejang.
Neurologic defisit (lateralization).

Indikasi rawat

Kesadaran menurun
Sakit kepala (sedang sampai berat).
Riwayat kesadaran menurun > 15 minute.
Fraktur tulang tengkorak.
Rhinorea otorhea.
Cedera penetrasi.
Alkohol/drugs intoxication.
Significant multiple trauma.
Abnormal CT Scan.
Amnesia.
No family at home.

CEREBRAL BLOOD FLOW

Normal 55 to 60 ml/100 gr brain tissue/minute
In the gray matter is 75 ml/100 gr brain tissue/minute
In the white matter 45 ml/100 gr brain tissue/minute
The most significant factor that determines CBF is the

CPP which is the effective blood pressure gradient

across the brain
MAP is the diastolic pressure plus one-third of the
pulse pressure ; increased ICP is tendency for the CPP
to decrease

MACAM MACAM FRAKTUR

FRAKTUR
FRAKTUR
FRAKTUR
FRAKTUR
FRAKTUR
FRAKTUR

LINEAR
DIASTASE
COMMUNITED
DEPRESSED
KONVEKSITAS / KUBAH
BASIS CRANII

ANTERIOR - ANOSMIA, RHINORRHOE

MEDIA - OTORRHEA, HEMATYMPANI, BATTLES

SIGN
POSTERIOR - INFRA TENTORIAL

TANDA FRAKTUR BASIS KRANII

HAEMOTYMPANUM
OTORRHEA
RHINORRHEA
RACOON EYES
BATTLES SIGN

CEREBRAL EDEMA
VASOGENIC EDEMA
Increased permiability of capillaries ; the tight
junctions between the endothelial cell become
incompetent, allowing plasma filtrate to escape
into the intercellular space
Contrast enhancement because of the
breakdown of the BBB
Edema is more marked in white matter than in
gray matter
Edema is seen with trauma, tumor, and abscess

CYTOTOXIC EDEMA
Hypoxia of the neural tissue and water intoxication
Hypoxia affects the ATP-dependent sodium pump
mechanism in the cell membrane, promoting an
accumulation of intracellular sodium and subsequent
flow of water into cell to maintain osmotic
equilibrium
Edema is intracellular and affects all cells :
endothelial cells, astrocytes, and neurons (interstitial
space is narrowed)
Subtle or no changes in CT scan, indicative in early
phases of ischemic stroke

INTERSTITIAL EDEMA
Transudation of CSF in obstructive
hydrocephalus
Best observed on CT or MRI as periventricular
low density areas because of the retrograde
transependymal flow of CSF into the interstitial
space of the white matter (mostly in frontal
region) , indicates active hydrocephalus
requiring surgical therapy

TYPES OF BRAIN
HERNIATION
CINGULATE HERNIATION
Focal mass lesion in the supratentorial
compartement pressure locally on the ipsilateral
hemisphere
The mass lesion may displace the cingulate gyrus,
which is next to the free edge of the falx cerebri,
and cause it to herniate under the falx to the
opposite side
Usually displacement of the ventricular system
Arterior cerebral artery, tight, sharp edge of the falx
No clinical signs and symptoms specific

UNCAL HERNIATION
When lesions of the middle cranial fossa, such as
acute epidural hematoma, subdural hematoma,
temporal lobe contussions, or temporal lobe
neoplasms
An expansile mass of the middle fossa cause the
uncus, the inferomedial structure of the temporal
lobe, to herniate between the rostral brainstem
and tentorial edge into posterior fossa
The medial displacement of the brainstem may
cause compression of the brainstem againts the
opposite tentorial edge, producing a notch called
Kernohans notch (ipsilateral hemiplegia)

CENTRAL TRANSTENTORIAL HERNIATION

Mass lesions located to the tentorial hiatus
Bilateral mass lesions, such as bilateral subdural
hematomas, can also cause herniation
Downward displacement of the diencephalon
and midbrain centrally through the tentorial
incisura
Clinical symptom,
Bilaterally small, reactive pupils
Cheyne-Stokes respirations
Loss of vertical gaze

TONSILLAR HERNIATION
The tonsil of the cerebellum herniates through
the foramen magnum into the upper spinal
canal, compressing the medulla
Manifestations of acute medullary compression
are,
Cardiorespiratory impairment
Hypertension
High pulse pressure
Cheyne-Stokes respirations
Neurogenic hyperventilation
Impaired consciousness
Stiff neck or opisthotonic position
Decorticate or decerebrate posturing

INDIKASI OPERASI
Epidural Hematoma (EDH)

- EDH >30 ml
- EDH,Koma,GCS <9, pupil anisokor
- Bila EDH <30 ml dan ketebalan <15 mm
serta midline shift <5 mm dan GCS >8 tanpa
fokal defisit ------ tidak operasi
Akut Subdural Hematoma (SDH)

- ketebalan >10 mm atau midline shift >5 mm

pada CT Scan
- koma (GCS<9), ketebalan <10 mm dan
midline shift <5 mm,operasi bila GCS
menurun 2 atau lebih (waktu antara kejadian
dan masuk RS) atau ICP >20 mmHg
- koma (GCS<9) ----- monitoring ICP

 Traumatic parenchymal lesions

- GCS 6-8 dengan kontusi frontal atau
temporal <20 ml, midline shift >5 mm
dan kompresi sisterna pada CT Scan
- lesi >50 ml
Lesi fossa posterior
lesi dengan distorsi,dislokasi, atau obliterasi
ventrikel IV, sisterna basalis, atau obstruksi
hidrosefalus
Depressed skull fractures

luka terbuka dan lebih dari 1 tabula

TREATMENT
MANNITOL
It increases serum osmolality and to draw fluid

from the brain parenchyma into the vascular

space
The osmotic effect of mannitol is
Decrease CSF production
Increases cerebral blood flow and cerebral oxygen
consumption
Decrease blood viscosity, thereby improving
perfusion

INDIKASI EVAKUASI HEMATOMA

Tidak semua lesi intrakranial cedera kepala

berat tertutup dilakukan kraniotomi

Traumatic Coma Data Bank
37% penderita koma dilakukan operasi
intrakranial hematoma
25% keadaan klinis menurun pada penderita
dengan lesi intrakranial atau gambaran
radiologi menunjukkan bertambahnya
hematoma

Explorasi
burrhole
Tidak dilakukan bila ada fasilitas CT

Scan
Life saving : rural area, jarak transfer
ke lokasi CT Scan cukup jauh atau
tidak memungkinkan

Lokasi burrhole
frontal,parietal dan temporal
dilatasi pupil ipsilateral
hemiparesis .. kontralateral
fraktur . ipsilateral
bila tidak ada didaerah temporal,

dilakukan burrhole didaerah frontal, dan

parietal
bila ketiga tempat ini tidak ada,
dilakukan pada sisi berlawanan

LOKASI BURR
HOLE

INSIDENCE DEPRESSED FRACTURE

3% fraktur tulang tengkorak pada

cedera kepala ringan

65% fraktur tulang tengkorak pada
cedera kepala berat, dengan atau tanpa
kerusakan dura atau otak
>50% fraktur frontal dan memerlukan
perbaikan kosmetik

fraktur depressed

fracture depressed

INSIDEN EPIDURAL HEMATOMA

2%-6% dari cedera kepala, dengan atau

tanpa fraktur tulang tengkorak

30% penderita, hematoma bertambah dalam
6 jam pertama setelah cedera
10%-50% berhubungan dengan hidrosefalus
bila lokasi hematoma fossa posterior

SUBDURAL HEMATOMA
Simple atau intradural hematoma
Complicated atau mixed subdural

hematoma
Akut
Subakut
kronik

CHRONIC SUBDURAL HEMATOMA

(CSDH)
Subdural hematoma is older than 3 weeks
Result of rupture of small bridging veins
Caused by minor head trauma or fall, often not

remembered by the patient or relatives

Bilateral clots about 20% of cases
Risk factor
Old age
Alkohol abuse
seizures
CSF shunts
Anticoagulation
Patients at risk for falls

DATA KEMATIAN AKIBAT TRAUMA

(Meislin,Rogers,et.al.,1997)

Very early deaths, 35%-50% dari total ;

kerusakan CNS permanen

Early deaths (dalam 4 jam), 18%-30% dari
total; biasanya karena perdarahan atau
problem jalan nafas
Hospital deaths dalam 24 jam, 20% dari total
Hospital deaths setelah beberapa hari atau
minggu, 20% dari total; multiple system
failure dengan sepsis

KESIMPULAN
Tidak ada obat atau miracle treatment

untuk memicu penyembuhan saraf

paska trauma kepala
Penanganan konservatif dan operatif
sesuai indikasi
Pengobatan terbaik mencegah cedera
sekunder
Pengetahuan molekuler penting,
menyusun kombinasi terapi penanganan
cedera otak sekunder

TERIMA KASIH