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Identifikasi Dan Tata Laksana

Peningkatan Tekanan Intrakranial


Dengan Cairan Hiperosmolar Pada
Stroke Akut

Oleh:

dr. Pinto Desti Ramadhoni, SpS

Pendahulua
n
Ruang rigid yang terdiri dari:
Jaringan otak (80%)
CSS (10%)
Darah (10%).

Intrakranial

Hipotesis Monro Kellie

Hubungan
volume dan
TIK

Isi dari kranium


tidak dapat
dikompresi
dan peningkatan
volume
menyebabkan
peningkatan
tekanan secara
cepat.

AWAL
TIK

Kompli
en
rendah

TIK

AKHIR

Komplian Intrakranial

tor yang mempengaruhi komplien

Menin
gkat

Hipokarbia
Hiperoksia
(paO2>100%)
Hipotermia
Barbiturat

Menur
un

Hiperkarbia
Hipoksia
Hipertermia
Anestesia

Mekanism
e
kompensa
si TIK

Etiologi peningkatan TIK


Patologi Primer
SOL
(space occupying
lesion)
Akumulasi CSS
Vaskuler

Contoh Kasus
Tumor, hematoma, air, abses, benda asing

Hidrosefalus: obstruktif atau komunikans


Gangguan input (peningkatan CBF atau
CBV
yang
disebabkan
gangguan
autoregulasi,
hiperkarbia,
dll)
atau
gangguan output (kongesti vena atau
trombosis sinus)

Edema Serebral
Vasogenik

Kerusakan pembuluh darah akibat tumor,


infeksi, abses, kontusio

Sitotoksik

Kerusakan membran sel/pompa

Hidrostatik

Tekanan transmural pada hidrosefalus

Edema Serebral
Edema Vasogenik:
Peningkatan cairan
ekstrasel
Edema Sitotoksik:
Pembengkakan sel
Edema Interstitial:
Peningkatan
cairan
dan
natrium
periventrikel
(hidrosefalus
obstruktif)

Injuri intrakranial
(stroke)

Hipertensi
intrakranial akan
menyebabkan
kompresi terhadap
jaringan sekitarnya
dan batang otak

Edema otak
TIK
Kompressi p.d. otak
dan batang otak
Gangguan fungsi
otak dan batang
otak

Peningkatan TIK akan

Herniasi
Otak

eningkatan TIK akan menyebabkan iskem


TIK meningkat

CBF menurun
CPP tidak adekuat menimbulkan iskemia otak
(berakibat memburuknya outcome pada
stroke)

CBF
CPP

= CPP / CVR
= MAP ICP

STROKE menyebabkan peningkatan TIK

Perdarahan
intraserebral

Infark serebral luas

Sakit kepala
(memburuk pada pagi
hari)
Muntah proyektil
(tanpa didahului mual)
Perubahan tingkat kesadaran
(PALING SENSITIF)

Gejala Klinis

Cushings triad
(hipertensi, bradikardi, pola
nafas ireguler)

Ocular signs
(refleks pupil melambat dan anisokor akibat
penekanan N III,
diplopia, paresis N VI, edema papil)

Perubahan fungsi motorik


(hemiparesis, dekortikasi,
deserebrasi)

Gejala Klinis

Normal Papil

Edema Papil

Gejala Klimis

T
N
E
M
T
A
TRE
Terapi terbaik untuk menurunkan TIK
adalah:

Menatalaksana
PENYEBABNYA

Monitoring
Adekuat

Tinggikan posisi kepala (HOB)


30
Atasi hipokapnia
Atasi demam
Atasi kejang
Analgesik
Sedasi atas indikasi
Jaga keseimbangan cairan dan
elektrolit
Drainase LCS
Terapi hiperventilasi

Terapi cairan
hiperosmolar
Tata Laksana Konservatif & Operatif
Peningkatan TIK

Cairan
hiperosmolar

Manitol

Efek utama:
Menurunkan
TIK
Neuroprotekta
n
Prinsip kerja manitol dalam menurunkan TIK:
Membentuk gradien osmotik antara parenkim
otak dan plasma untuk menghasilkan penurunan
kadar air otak, serta meningkatkan CPP dimana
akan terjadi vasokonstriksi serebral sehingga

Pantau fungsi ginjal, osmolaritas


serum, tanda vital, dan kadar
elektrolit

Kontraindikasi:
Gangguan ginjal,
gangguan hati berat,
syok hipovolemia,
gagal jantung
kongestif.
Efek samping:
Gagal ginjal akut,
hiperosmolaritas,
hipovolemia, dan
imbalans elektrolit.

Rekomendasi dosis:
0.25 1 gr/kgBB (diulangi setiap 6 8 jam) dengan
pemberian cepat untuk meningkatkan osmolaritas serum
sebesar 300 to 310 mOsm/L.

Manitol
Most investigations found beneficial
effects of intravenous mannitol with
respect to infarct volume, edema
formation, and elevated ICP.
Single doses of 40-g mannitol in 8 patients
with hemispheric stroke and massive edema
were effective in temporarily (up to 4
hours) reducing elevated ICP in 10 of 14
episodes. Effects on long-term outcome
were not investigated.
Similarly, in another observational study with
21 patients with severe MCA infarction, mannitol
was effective in reducing ICP in most
patients. This was associated with substantial
increase in CPP and brain tissue oxygen
pressure
in both the ischemic
and the non-ischemic
From Department of Neurology, University of Erlangen, Germany.

Kontroversial Manitol
Given the lack of systematic clinical trial in
stroke patients, there is no clear
information on optimal timing, dosing,
and application schedule of mannitol. A
range between 310 and 320 mOsm/L has
been commonly recommended as target
serum osmolality.

From Department of Neurology, University of Erlangen, Germany.

Despite the facts that mannitol has been


widely used to
decrease elevated ICP, and that both
ischemic and hemorrhagic strokes are
associated with some cerebral edema, very
few randomized trials were performed to
study the effects of mannitol in acute
stroke.

Kontr
overs
ial
Manit
ol

There is currently not enough evidence


to decide whether the routine use of
mannitol in acute stroke would result in any
beneficial or harmful effect. The routine use
of mannitol in all patients with acute stroke
is not supported by any evidence from
From the Department of Neurology, University of Debrecen, Medical School,
randomized
controlled
clinical
trials.
Debrecen,
Hungary (D.B., I.F.); Department
of Neurology, First University
From the Department of Neurology,
Hospital, West China University of Medical Sciences, Chengdu, Sichuan,
University
Further trials
areand Department
needed
confirm
or of California, San Francisco, CA
China (M.L.);
of Internal to
Medicine,
Federal University of
Sao Paulo,, Sao Paulo, Brazil (G.F.P.)
refute whether
the routine use of mannitol
is beneficial in acute stroke.

Salin Hipertonik

Prinsip kerja:
Salin hipertonik

manitol

Infusion of 75 mL hypertonic (10%) saline


decreases elevated ICP and increases
cerebral perfusion pressure in stroke
patients in whom mannitol had failed.
The effect on the ICP and cerebral perfusion
pressure reaches its maximum after the end
of infusion and is seen for 4 hours. No
unexpected side effects were noted.
From the Departments of Neurology and Neurosurgery (A.A.),
University of Heidelberg, Heidelberg, Germany

Hypertonic saline is more effective than mannitol


for the treatment of elevated intracranial
pressure. Our meta-analysis is limited by the small
number and size of eligible trials, but our findings
suggest that hypertonic saline may be superior to the
current standard of care and argue for a large,
multicenter, randomized trial to definitively establish
the Department
of Neurology,
the first-line medical therapy From
for
intracranial
University of California, San Francisco, CA
hypertension.
(Crit Care Med 2011; 39:554 559)

anitol VS Salin hipertoni


From the Department of Neurology,
University of California, San Francisco, CA

KESIMPULAN
Penambahan volume patologis pada ruang
intrakranial akibat stroke akut dapat berupa
hematoma,
edema
cerebri,
dan
hidrosepalus.
Hal tersebut akan memberikan gejala
peningkatan tekanan intra kranial, dan
gejala klinis akan terjadi setelah
mekanisme kompensasi gagal.

Kesimpulan
Peningkatan tekanan intrakranial akan menyebabkan
iskemia jaringan akibat penurunan tekanan perfusi
serebral, kompresi pada jaringan di dalam
intrakranial, serta herniasi.
Gejala berupa sakit kepala, muntah proyektil,
penurunan tingkat kesadaran, gejala okuler,
Cushings triad, dan gejala motorik.

Kesimpulan
Tata laksana utama peningkatan TIK adalah mengatasi
penyebabnya.
Berbagai upaya menurunkan TIK dan meningkatkan
komplien, diantaranya: elevasi kepala 30 0, atasi nyeri,
terapi barbiturat, hiperventilasi, dll (non farmakologis),
drainase LCS, dan pemberian cairan hiperosmotik.

Kesimpulan
Manitol merupakan cairan hipertonik yang banyak
digunakan dalam upaya menurunkan tekanan intra
kranial, akan tetapi masih kontroversial.
Salin hipertonik sebagai terapi alternatif pengganti
manitol dikatakan lebih efektif dibandingkan
manitol, akan tetapi masih belum memiliki evidence
yang cukup.

THANK
YOU

or your attention...