Manajemen Penderita

Penderita
Manajemen
Cedera Kepala
Kepala
Cedera

Endro Basuki S.
Disampaikan pada seminar clinical update FKUGM
2012

dr. ENDRO BASUKI S., Sp.BS, M.Kes

Jakarta, 8 Januari, 1953

Dokter Umum FK UGM, 1979
Spesialis Bedah Saraf FK UNPAD, 1989
Vrije Universiteit Amsterdam, 1987 1988
Magister Kesehatan FK UGM, 2000
Puskesmas Kec. Lamuru, Bone, 1979 1982
Staf SMF Bedah Saraf RS Dr Sardjito
KPS Bedah Saraf FK UGM / RSUP Dr
Sardjito
Bendahara CE&BU RS Dr Sardjito/FK
UGM
Pengurus Harian Komite Medik RS Dr
Sardjito/Ketua Sub Komite Disiplin Profesi
Presiden elect PERSPEBSI, 2009 2013
Medical Advisory Board PT. ASKES

TERJADI TIAP 15 DETIK

MATI TIAP 12 MENIT

CEDERA KEPALA

50 % KEMATIAN PADA TRAUMA

60 % KEMATIAN AKIBAT KLL

TATALAKSANA
P
R
I
M
A
R
Y
S
U
R
V
E
Y

AIRWAY & C-SPINE CONTROL

BREATHING

CIRCULATION

KONSEPNYA
RESPONSIBILITAS TERPENTING
MANAJEMEN ABC : CEGAH

HIPOVENTILASI DAN HIPOVOLEMIA

POTENSIAL TERJADINYA
SECONDARY BRAIN DAMAGE

ANATOMI FISIOLOGI
CEDERA KEPALA

SCALP
SCALP

SKIN
CONNECTIVE TISSUE
APONEUROSIS/GALEA
LOOSE AREOLAR TISSUE
PERICRANIUM

vaskularisasi sangat baik,

perdarahan hebat potensial menimbulkan syok

SCALP
SKULL
MENINGES
BRAIN
LCS
TENTORIUM
GCS
ICP

MENINGES
Tiga lapis : duramater, arachnoid, piamater
Arteri Meningea Media, potensial terlibat pada kasus EDH

CAIRAN SEREBROSPINAL
Diproduksi oleh pleksus koroideus
Rata-rata 30 ml per jam
Bersirkulasi

TENTORIUM
Membagi 2 ruangan intrakranial
Supratentorial dan Infratentorial

CEREBRAL PERFUSION PRESSURE ( CPP )

Merupakan PRIORITAS UTAMA
Rumus : CPP = Mean Arterial Pressure - ICP

CEREBRAL BLOOD FLOW ( CBF )

Normal : 50 ml/100 gram otak/ menit
Bila mencapai 5 ml/ menit :
cell death & irreversible damage

TEKANAN INTRAKRANIAL
Normal : 10 mmHg ( 136 mm air )
Makin tinggi TIK makin jelek prognosis

HUKUM MONRO-KELLIE
Prinsip : total volume intrakranial bersifat TETAP,
Oleh karena kranium merupakan NON EXPANSILE BOX

Monro Kellie
Vk = V darah + V likwor + V
parenkim
mmHg
100

Tekanan
Intrakranial

Fatal

60
50

Disfungsi
Otak
50

40
30

Obati
Volume Intrakranial

Normal

20
10
0

SECONDARY SURVEY
Whole Examination

ANAMNESIS
ANAMNESIS
PEMERIKSAAN FISIK
FISIK
PEMERIKSAAN
PENUNJANG
PENUNJANG

INFORMASI PENTING

USIA DAN MEKANISME TRAUMA

STATUS RESPIRASI & KARDIOVASKULER
KESADARAN, REAKSI PUPIL, LATERALISASI
ADANYA TRAUMA NON SEREBRAL
HASIL PEMERIKSAAN DIAGNOSTIK

TANDA TANDA PENTING

PUPIL ANISOKOR
LATERALISASI MOTORIK
LUKA TERBUKA DGN KEBOCORAN LCS
PERBURUKAN NEUROLOGIS
FRAKTUR DEPRESI TULANG TENGKORAK
SAKIT KEPALA HEBAT

KOMPONEN GLASGOW COMA SCALE

E:: BUKA
BUKA MATA:
MATA: 11 44
E

V:: SUARA
SUARA :: 11 55
V
M :: GERAKAN
GERAKAN :: 11 -- 66
M

KOMPONEN MATA

KOMPONEN MOTORIK

KOMPONEN VERBAL

KLASIFIKASI
TUMPUL

KLL

MEKANISME
MEKANISME
TAJAM
(PENETRATING)

TRAUMA TEMBAK
TRAUMA TUSUK

SEVERITY
SEVERITY

RINGAN :GCS 14 - 15
SEDANG :GCS 9 - 13
BERAT :GCS 3 - 8

FRAKTUR KRANIUM
linear
terbuka/tertutup
depresi
MORFOLOGI
MORFOLOGI
basis cranii
Berdasarkan
Patofisiologi
Berdasarkan Patofisiologi
LESI INTRAKRANIAL

LESI INTRAKRANIAL
1. Primary Brain Injury:
a. Vocal Brain Injury:
- Cerebral Contusions,
- Cerebral Laceration,
b. Diffuse Brain Damage:
- Diffuse Axonal Injury,
- Diffuse Vascular Injury.
2. Secondary Brain Injury:
a. Traumatic Intracranial Haematoma,
Extradural Haematoma,
Subdural Haematoma (Akut, Sub-akut, dan Kronik),
Subdural Hygroma,
Intracerebral Haematoma,
Intraventricular Haematoma,
Subarachnoid Haemorrhage,
b. Post Traumatic Brain Swelling,
c. Focal Brain Damage Secondary to Brain Shift and Herniations

Primary Brain Injury:

Vocal Brain Injury

Diffuse Brain Damage

Cerebral Contusions

Diffuse Axonal Injury

Cerebral Laceration

Diffuse Vascular Injury

Subdural Haematoma

Secondary Brain Injury:

Traumatic Intracranial Haematoma

Sub-akut

Akut
Extradural Haematoma
Subdural Hygroma

Kronik
Intraventricular Haematoma

Intracerebral Haematoma

Subarachnoid Haemorrhage

Focal Brain Damage

Secondary to Brain Shift
and Herniations
Post Traumatic Brain Swelling

PRINSIP
MEMELIHARA KEBUTUHAN METABOLIK OTAK
CEGAH/OBATI HIPERTENSI INTRAKRANIAL
HIPOKAPNEA
KONTROL CAIRAN
DIURETIK ( MANNITOL )

MANNITOL
The mechanism by which mannitol
provides its beneficial effects is still
controversial, but probably includes some
combination of the following:
1. Lowering ICP
2. Supports the microcirculation by
improving blood rheology
3. Possible free radical scavenging

Lowering ICP
A. Immediate plasma expansion: reduces the
hematocrit and blood viscosity (improved
rheology) which increases CBF and O2 delivery.
This reduces ICP within a few minutes , and is
most marked in patients with CPP < 70 mmHg
B. Osmotic effect: increased serum tonicity draws
edema fluid from cerebral parenchyma. Takes 1530 minutes until gradients are established. Effect
lasts 1.5-6 hrs, depending on the clinical
condition.

 bolus administration : onset of ICP

lowering effect occurs in 1-5 minutes; peaks
at 20-60 minutes.
In urgent reduction of ICP : an initial dose
of 1 gm/kg should be given over 30
minutes.
for long-term reduction of ICP : infusion
time should be lengthened to 60 minutes
and the dose reduced (e.g. 0.25-0.5 gm/kg q
6 hours.

Cautions with Mannitol

1. mannitol opens the BBB , and mannitol
that has crossed the BBB may draw fluid
into CNS (this may be minimized by
repeated bolus administration vs. continous
infusion) which can aggravate vasogenic
cerebral edema. Thus, when it is time to
D/C mannitol, it should be tapered to
prevent ICP rebound

 2. caution: corticosteroids + phenytoin +

manitol may cause hyperosmolar
nonketotic state with high mortality
3. overenthusiastic bolus administration
may HTN and if autoregulation is
defective increased CBF which may
promote herniation rather than prevent it

 4. high doses of mannitol carries the risk of

accute renal failure (acute tubular necrosis),
especially in the following: serum
osmolarity > 320 mOsm/L, use of other
potentially nephrotoxic drugs, sepsis, preexisting renal disease

 5. large doses prevents diagnosing DI by

use of urinary osmols or SG
6. because it may further increase CBF, the
use of mannitol may be deleterious when
IC-HTN is due to hyperemia

RINGKASAN
JAGA PATENSI JALAN NAFAS
JAGA VENTILASI
ATASI SYOK
PERIKSA NEUROLOGIS
CEGAH CEDERA OTAK SEKUNDER
CARI CEDERA YANG TERKAIT
BILA STABIL, PERIKSA PENUNJANG
BILA PERLU KONSUL BEDAH SARAF
TERUSKAN ASESMENT

ILUSTRASI KASUS
ILUSTRASI
CEDERA KEPALA
KEPALA
CEDERA

Fraktur Impresi

CT scan
Impresi Fraktur

TINDAKAN OPERATIF FRAKTUR DEPPRESI

BASILAR SKULL
FRACTURES

EPIDURAL
HEMATOM
Epidural

PERJALANAN KLINIK EDH

ACUTE
EPIDURAL
HEMATOMA

Subdural hematom

Pre operasi

Pasca Operasi

Intraserebral
hematom

Korpus
Alienum

FUNGSI OTAK
Sisi dominan untuk yang tidak kidal adl
yg
sebelah kiri
Orang kidal, 75 % sisi dominan adalah
kiri
Fungsi sisi dominan adalah untuk bahasa
dan memori yang berdasarkan bahasa
Sisi kanan untuk memori visual

LOBUS FRONTALIS
1. PRE-SENTRAL GIRUS
Pusat motorik untuk muka, tangan,
kaki, badan, dsb.
2. AREA BROCA
Pada sisi dominan adalah pusat
bicara ekspresif motorik
3. AREA MOTOR TAMBAHAN
Untuk gerakan mata dan kepala sisi
yang berlawanan
4. AREA PRE-FRONTAL
Untuk inisiatif dan personalitas
5. PARASENTRAL LOBUS
Pusat penahan BAK dan BAB

Pustaka Baru :
Selladurai, Ben dan Reilly, Peter, Initial Management of Head Injury a Comprehensive Guide,
McGraw-Hill Australia, 2007.