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ARTERIOVENOUS MALFORMASI

(Tinjauan kepustakaan)
Kepanitraan Klinik Madya

Oleh :
1. Krisnasari Dwi Marlati.
2. Tommy. J. Numberi.

Pembimbing :
1. dr. I. B Indrajaya,Sp. S.
2. dr. Meike Karema, Sp.S.

BAGIAN NEUROLOGI
PROGRAM PENDIDIKAN DOKTER
UNIVERSITAS CENDERAWASIH
JAYAPURA PAPUA
2008

LEMBAR PENGESAHAN
Telah dipersentasikan dihadapan para Pembimbing Kepanitraan Klinik Madya
pada Bagian Neurologi di RSUD Jayapura.

Pada
Hari

Tanggal

Tempat

Pembimbing/ Penguji
1.

dr. I. B Indrajaya,Sp. S.
1..................................

1.

dr. Meike Karema, Sp.S.


2...................................

DAFTAR ISI
Halaman
LEMBAR JUDUL............................................................................................
LEMBAR PENGESAHAN.............................................................................
DAFTAR ISI.....................................................................................................
DAFTAR GAMBAR .......................................................................................
BAB I PENDAHULUAN .............................................................................
BAB II PEMBAHASAN ...............................................................................
II.1. DEFINISIS .....................................................................................
II.2. PATOFISIOLOGI..........................................................................
II.3. MANIFESTASI KLINIS..............................................................
II.4. DIAGNOSIS................................................................
II.5. DIAGNOSIS BANDING...................................................
II.6. KOMPLIKASI...........................................................................
II.7. PENATALAKSANAAN................................................................
II.8. PROGNOSIS..............................................................................
BAB III PENUTUP..........................................................................................
DAFTAR PUSTAKA.......................................................................................

BAB I
PENDAHULUAN

Arterio-Venous Malformation atau AVM, adalah kumpulan pembuluh darah yang


abnormal. Normalnya, darah yang berisi oksigen di pompa oleh jantung melalui
pembuluh darah arteri menuju ke otak, yang akan masuk dan menjadi cabang-cabang
kecil dari pembuluh darah yang disebut kapiler. Di bagian akhir kapiler ini darah akan
memberikan nutrisi ke jaringan. Darah yang telah mengalami deoksigenasi akan
terdorong menuju pembuluh darah vena yang sangat kecil kembali ke jantung. Arterivena Malformasi adalah area tempat pertukaran pembuluh darah kapiler yang sangat
kecil. Tempat dimana ada hubungan antara arteri dan vena ini yang disebut shunt. Area
dari jaringan disebut nidus dari AVM. AVM dapat merupakan suatu "Sirkuit Pendek"
dimana darah tidak menuju ke jaringan tetapi terpompa melalui shunt dan kembali ke
jantung, tanpa memberikan nutrisi ke jaringan.1
Struktur yang abnormal dari pembuluh darah kepala dan otak telah lama di
ketahui. William McCormick, MD, menyampaikan

empat sistim klasifikasi dalam

tulisannya di tahun 1966 yang berjudul, "The Pathology of Vascular ('Arteriovenous')


Malformations."5
Sejarah
Luschka and Virchow secara jelas menggambarkan AVM pada pertengahan abad
1800. Olivecrona melakukan pembedahan yang pertama di tahun 1932. 5. 2% dari stroke
hemoraghic di sebabkan oleh perdarahan yang diakibatkan AVM. Pemahaman yang baik
tentang diagnosa dan alogaritma terapi sangat dibutuhkan karena AVM merupakan
penyebab dari perdarahan cerebral pada usia muda.5
Harvey Cushing pada tahun 1928 menulis pengalaman mengoperasi cerebro
vasculer malformasi, ia mengatakan bahwa catatan operasi yang dilaporkan tidak hanya
menunjukkan kesia-siaan dari operasi angioma, tetapi juga resiko yang serius dari
gangguan fungsi cortical. Bila lesi ini ditemukan secara tidak sengaja sebaiknya
dibiarkan. Sejak pengalaman Harvey Cushing yang kesulitan menangani operasi cerebro
vasculer malformasi, teknik operasi cerebro vasculer berkembang sedikit demi sedikit
sehingga banyak operai yang sulit dilaporkan dapat dilakukan dengan sukses, sesuai
dengan perkembangan microsurgical teknik, neuro anestesiologi endovascular therapy
dan streotactic radio surgery, tidak kalah pentingnya adalah pengetahuan Biology dan
Pathology anatomy.6

BAB II
PEMBAHASAN
II.1. DEFINISI
Lesi dari perkembangan vascular cerebral seperti aliran darah yang langsung dari
sistim arteri menuju ke sistim vena tanpa melalui kapilari sistim. Arteriovenous (AV)
shunt yang menunjukan bentuk karakteristik yang khas.5
II.2. EPIDEMOLOGI
AVMS adalah suatu kondisi yang jarang mempengaruhi sekitar 250,000 orang di
dalam Amerika Serikat.
Pernyataan tentang insiden terjadinya AVM di masyarakat AS adalah sekitar
0.14% (140 kasus per 100,000 orang atau 1 kasus per 700 orang). Hal ini menunjukan
kira-kira satu dari 50 atau satu dari 70 orang ada yang menderita anurisma intracranial.5
Suatu arteriovenus malformasi merupakan suatu kelainan bawaan dari pada
pembuluh darah otak, khas dengan adanya hubungan arteri dan vena. Arteriovenus
malformasi dapat berada di tempat lain di tubuh manusia.2
II.3. ETIOLOGI
Kita tidak mengetahui apa yang menyebabkan AVM. AVM ada yang dibawa sejak
lahir tapi tidak diturunkan. AVM dapat berada pada laki-laki maupun perempuan ataupun
pada ras yang berbeda. Suatu penilaiaan dari 3 juta orang di Amerika Serikat lahir dengan
kelainan vasculer, 10% dari kasus adalah AVM. AVMS bisa disebabkan oleh suatu
pecahan suatu pembuluh darah selama pengembangan saat janin. Biasanya

tidak

berhubungan dengan permasalahan lain saat kelahiran1


Arteriovenous Malformasi (AVM) adalah cacat-cacat dari sistem peredaran darah
yang secara umum dipercaya untuk muncul selama pengembangan embreriologi janin
atau yang berkenaan dengan perkembangan saat janin atau segera setelah kelahiran.
Terjadi kekacauan pada peredaran darah arteri dan vena. Arteri yang membawa darah
yang kaya oksigen keluar dari jantung menuju ke sel jaringan tubuh dan vena yang
menerina darah dari jaringan dan mengantarkannya ke paru-paru dan jantung. Kehadiran
dari suatu AVM mengganggu proses penting siklis ini. Meski AVM dapat berkembang di

dalam berbagai lokasi, tetapi yang terutama di otak dan tulang belakang kedua bagian ini
merupakan bagian terpenting dari sistim saraf dan akan memberikan efek yang cukup
luas dan berarti pada tubuh.3
Embriology pembuluh darah otak

Gestational Age

Developmental Event

Week 3

Appearance of primordial endothelium-lined vascular plexi

Week 4

Internal carotid arteries begin to form

Week 5

Basilar and vertebral arteries begin to form; Primitive head veins


and dural plexus form

Week 6

Development of carotid and basilar arterial branches;Pial veins


appear

Week 7

Circle of willis complete; first indication of adult pattern dural


sinuses; capillary precursors begin to penetrate the emispheres

Week 8-12

Vein of galen appears, primitive capillaries branch, anastomose,


and then regress to complete the internal vascularization of the
brain

Adanya satu atau lebih hubungan langsung arteri atau vena sistim. AVMs
dianggap suatu lesi kogenital dengan karakteristik adanya kegagalan saat emberiologi
vaskular pada pembelahan sel pembentukan pleksus dan berkembang menjadi jaringan
kapiler yang matur pada area-area tertentu. Struktur ini munkin terbentuk dan tumbuh
pada saat postnatal yang berhubungan dengan lesi pada saat perinatal. Faktor biologi
molecular yang dianggap berpengaruh pada terjadinya AVM, melibatkan vascular
endothelial growth factor (VEGF) dan basic fibroblast growth factor (bFGF). Keadaan
jaringan yang dengan adanya AVM adanya hipoxia jaringan yang persisten, karena
malformasi yang terjadi berasal dari jaringan vaskular yang sehat, kedepannya akan
terbentuk angiogenesis.5
II.4. PATOFISIOLOGI
Kebanyakan pasien-pasien tidak mengetahui bahwa mereka mempunyai satu
AVM. Sejumlah pasien-pasien dengan AVMs mempunyai seizures atau sakit kepala yang
terus menerus. Satu AVM dapat menambah ketegangan di pembuluh darah dan

melingkupi jaringan. Untuk usia muda (di bawah usia dari dua puluh) ini bukan suatu
masalah. Aliran darah yang meningkat yang disebabkan oleh shunt memperlemah
pembuluh darah. Pembuluh darah yang lemah dapat pecah. Hal ini dikenal sebagai suatu
hemorrhage atau suatu perdarahan. Jika satu AVM berdarah, pasien mengalami sakit
kepala sangat berat. Hal ini dapat menjadi suatu stroke dan bahkan kematian. Mengenai
4% dari orang-orang dengan AVM luar cetak yang awal masing-masing tahun.
Kemungkinan munculnya perdarahan pada pendeita dengan AVM tidak diketahui. AVM
yang luas dapat menyebabkan gangguan neurologist progresif dengan adanya penekan
jaringan otak dan terjadinya perubahan aliran darah.1
Penyebab AVM sementara ini tidak diketahui pasti, Resiko terbesar adalah
perdarahan intra serebral. Resiko yang muncul sulit untuk diketahui. Kira-kira 40% dari
kasus

cerebral AVM ditemukan melalui gejala yang disebabkan perdarahan yang

mendadakpada pembuluh darah yang rapuh karena struktur yang abnormal di otak. Lagi
pula pada beberapa penderita ada yang asimtomatik atau adanya keluhan lokal tergantung
pada daerah mana yang terkena AVM. Jika terjadi ruptur atau perdarahan, maka darah
akan penetrasi masik kedalam jaringan otak (cerebral hemorrhage) atau masuk kedalam
ruang subarachnoid. Ruang ini terletak antara selaput (meninges) yang mengelilingi otak
(subarachnoid hemorrhage).2
Satu kali AVM berdarah, akan sangat mungkin terjadi perdarahan ulang.
Bagaimanapun, selama AVM tidak ruptur resiko terjadinya perdarahan relative lebih
rendah.2
AVM yang tidak berdarah dapat menyebabkan gejala seperti epileptic seizures,
nyeri kepala, atau gejala neurologic yang fluktuasi. Kebanyakan dari kasus bersifat
asimtomatik.2
Resiko perdarahan dari AVM:1
10 years ---33.5%
20 years ---55.8%
30 years ---70.6%
40 years ---80.3%
50 years ---86.8%

Tidak ada aktivitas yang dapat diketahui dapat melindungi atau menyebabkan
perdarahan.Ada beberapa hal yang harus diperhatikan dalam aspirin, aspiring-containing
compounds, or non-steroidal anti-inflammatory agents.1
AVMs memberikan gejala hanya bila terjadi kerusakan yang
mengenai otak atau medulla spinalis pada level kritikal tertentu. Ini
yang

menjadi

penyebab

mengapa

pada

beberapa

orang

yang

mempunyai relatively small fraction pasien dengan lesi ini menunjuka


masalah kesehatan yang signifikan yang tergantung dari kondisi nya.
Kerusakan AVMs pada otak dan spinal cord dapat melalui 3 mekanisme
dasar: dengan menekan peningkatan kebutuhan oksigen oleh jaringan
saraf, dengan menyebabkan perdarhan (hemorrhage) pada jaringan
sekitar,

dan dengan kompresi dan displacing bagian dari otak dan

medulla spinalis.3
Kompromi pada AVMs pengiriman oksigen ke otak atau ke
medulla spinalis melalui

pola alternative normal peredaran darah.

Arteri dan vena secara normal terhubung oleh beberapa pembuluh


darah kecil yang progressiveyang mengontrol dan memperlambat laju
aliran darah. Oksigen dikirimkan ke jaringan sekitar melalui pembuluh
darah yang halus ini, , bagaimanapun, kekurangan ini yang campur tangan jaringan
kapiler. Celah dari pembuluh darah kapiler ini saling berhubungan dengan
vascular yang dikenal dengan capillaries, dimana aliran darah disana
paling lambat. Arteri dan vena yang membentuk AVM, bagaimanapun,
tidak terlepas dari campur tangan jaringan kapiler. Yang mana, arteri
membuang darah secara langsung ke vena melalui jalan pintas yaitu
fistula. Aliran darah yanmg sangat ekstrime dan tidak terkontrol dan
sangat

cepatakan

menyebabkanterbuangnya

oksigen

kejaringan

sekitar. Saat kebutuhan oksigen sangat tinggi, sel yang menyusun


jaringan ini mulai memburuk dan kadang benar benar sekarat.3

Frekuensi aliran darah yang sangat cepat dapat meningkatkan tekanan


dalam lumen pembuluh darah

yang terletak ditengah AVMThis

abnormally rapid rate of blood flow frequently causes blood pressure


inside the vessels located in the central portion of an AVM directly
adjacent to the fistulaan area doctors refer to as the nidus, from the
Latin word for nestto rise to dangerously high levels. The arteries
feeding blood into the AVM often become swollen and distorted; the
veins that drain blood away from it often become abnormally
constricted (a condition called stenosis). Moreover, the walls of the
involved arteries and veins are often abnormally thin and weak.
Aneurysmsballoon-like

bulges

in

blood

vessel

walls

that

are

susceptible to rupturemay develop in association with approximately


half of all neurological AVMs due to this structural weakness.3
Bleeding can result from this combination of high internal pressure and
vessel wall weakness. Such hemorrhages are often microscopic in size,
causing limited damage and few significant symptoms. Even many
nonsymptomatic AVMs show evidence of past bleeding. But massive
hemorrhages can occur if the physical stresses caused by extremely
high blood pressure, rapid blood flow rates, and vessel wall weakness
are great enough. If a large enough volume of blood escapes from a
ruptured AVM into the surrounding brain, the result can be a
catastrophic stroke. AVMs account for approximately 2 percent of all
hemorrhagic strokes that occur each year. 3
Even in the absence of bleeding or significant oxygen depletion, large AVMs can damage
the brain or spinal cord simply by their presence. They can range in size from a fraction
of an inch to more than 2.5 inches in diameter, depending on the number and size of the
blood vessels making up the lesion. The larger the lesion, the greater the amount of
pressure it exerts on surrounding brain or spinal cord structures. The largest lesions may
compress several inches of the spinal cord or distort the shape of an entire hemisphere of
the brain. Such massive AVMs can constrict the flow of cerebrospinal fluida clear

liquid that normally nourishes and protects the brain and spinal cordby distorting or
closing the passageways and open chambers (ventricles) inside the brain that allow this
fluid to circulate freely. As cerebrospinal fluid accumulates, hydrocephalus results. This
fluid buildup further increases the amount of pressure on fragile neurological structures,
adding to the damage caused by the AVM itself.3
The direct connection between the arterial and venous systems supplies a low-resistance
shunt for arterial blood and exposes the venous system to abnormally high pressures. This
results in a system of enlarged feeding vessels, the tangled nidus of the AVM itself, and
enlarged draining venous structures.5
II.5. MANIFESTASI KLINIS

Hemorrhage (53% of cases)


o

Acute onset of severe headache

May be described as the worst headache of the patient's life

Depending on the location of hemorrhage, may be associated with new


fixed neurologic deficit

Seizure (46%)

Headache (34%)

Progressive neurologic deficit (21%)


o

May be caused by mass effect or ischemia resulting from local vascular


steal phenomenon

Presence and nature of deficit depend on location of lesion

Pediatric patients
o

Heart failure

Macrocephaly

Prominent scalp veins

Hemorrhage is more likely to be caused by small lesions, while seizures are more likely
to be caused by large lesions. 5
An increasing number of lesions now are found incidentally upon brain imaging. 5

The annual risk of intracranial hemorrhages associated with AVMs is 2-3%. The mortality
rate associated with the initial bleed is 10%. The mortality rate associated with the second
bleed is 13%, and the rate increases to 20% for each subsequent bleed. The incidence of
new neurologic deficit occurring with each bleed is 50%. These numbers are generalized
for all AVMs. The location and size of each patient's lesion greatly affects their risk of
morbidity and mortality. 5
Patients with an AVM have an increased risk of developing a cerebral aneurysm.
Approximately 7.6% of patients with an AVM develop an aneurysm. Alternatively, 1.1%
of patients with an aneurysm are found to have an AVM. Most commonly, aneurysms are
found on arteries feeding the AVM. 5
Rare case reports describe multiple intracranial AVMs and/or concomitant intracranial
and intraspinal AVMs, but these are too rare to be well characterized. AVMs may present
as part of a neurocutaneous syndrome, including Sturge-Weber syndrome or RenduOsler-Weber syndrome.5
II.5. DIAGNOSIS
Semua pasien yang dicurigai AVM harus dilakukan CT scan atau MRI sebagai
pemeriksaan awal. Pada CT scan akan tampak bercak-bercak kalsifikasi dikelilingi oleh
malformasi, dengan pemberian kontras, feeding arteri atau vena yang dilatasi biasanya
tampak gambaran anatomi yang detasan tampak pada MRI. Angiografi merupakan
pemeriksaan yang utama untuk diagnosa AVMS dan perencanaan operasi. Angiografi ipsi
dan kontralateral diperlukan.(iskandar Japardi)
An AVM diagnosis is established by neuroimaging studies. A computed
tomography scan of the head (head CT) is usually performed; this can reveal the site of
the bleed. More detailed pictures of the tangle of blood vessels that compose an AVM can
be obtained by using radioactive reagents injected into the blood stream, then observed
using a fluoroscope or Magnetic Resonance Imaging (MRI). A spinal tap (lumbar
puncture) can be used to examine spinal fluid for red blood cells; this condition is
indicative of leakage of blood from the bleeding vessels into the subarachnoid space. The

best images of an AVM are obtained through cerebral angiography. This procedure
involves using a catheter, threaded through an artery up to the head, to deliver a contrast
agent into the AVM. As the contrast agent flows through the AVM structure, a sequence
of X-ray images can be obtained to ascertain the size, shape and extent of that structure.2

II.6. DIAGNOSIS BANDING

II.7.KOMPLIKASI

The most dreaded complication of the AVMs' natural history is intracerebral


hemorrhage (see Prognosis). Treatment decisions are based on the natural historyrisk of first or subsequent hemorrhage versus the risk-benefit ratio of treatment.

Surgical complications
o

Surgical complications may include persistent neurological deficits


associated with hemorrhage and stroke.

Surgical outcome risk correlates with score on the Spetzler-Martin scale;


higher scores, seen with large-sized AVMs, deep venous drainage, and
location of the AVM in eloquent brain regions, increase the surgical risk.

A recent meta-analysis reports a morbidity of 8.6% and mortality of 3.3%


after mostly surgical treatment in a series of 2452 patients. The surgical
risk for morbidity and mortality for Spetzler-Martin grade of less or equal
to 3 has been reported to be 2-6.3% and 0-2%, respectively. The surgical
risk for morbidity and mortality for Spetzler-Martin grade IV and V has
been reported to be 9-39% and 0-9%, respectively.

Complications of endovascular embolization

Complications

of

endovascular

embolization

include

persistent

neurological deficits related to inadvertent embolization of arteries


supplying normal brain tissue or obliteration of the venous outflow leading
to intracerebral hemorrhages. The procedure carries an associated risk for
morbidity and mortality in the range of 9-22% and 0-9%, respectively.
o

No long-term outcome studies are yet available; however, as endovascular


techniques continue to improve, complication rates are likely to diminish.

Complications of radiosurgery
o

Complications depend on the size and location of the AVM. AVMs located
in eloquent areas and in central locations are more prone to radiationinduced complications.

White matter edema and radiation-induced necrosis may occur during the
1- to 3-year treatment period. Persistent neurological deficits after
radiation have been reported in 8% of treated patients.
Patients with hemorrhagic presentation have a higher mean annual risk for
hemorrhage until radiation-induced obliteration of the AVM is achieved
compared to patients with a nonhemorrhagic presentation (6.3% vs 3.9%).
The risk for hemorrhage seems to be lower after radiation therapy in
patients with hemorrhagic presentation compared to the period before
gamma knife radiotherapy was initiated.

Seizure frequency may increase in the first days to weeks after


radiosurgery.

The potential for late effects from radiation, such as accelerated


atherosclerosis in surrounding blood vessels, does exist.

II.8. PENATALAKSANAAN
Penatalaksanaan malformasi arteri vena adalah penatalaksanaan yang "paling lambat"
mengalami kemajuan. Saat ini, masih tidak ada bukti bukti yang valid, untuk menjawab,
penatalaksanaan apa yang paling tepat untuk kasus ini, apakah reseksi oleh bedah saraf,
radiasi stereotaktik, ataupun embolisasi. Saat ini sedang dilakukan suatu penelitian secara
komphrehensif dengan nama ARUBA (A Randomized trials of Unrupturs Brain AVM),
dimana pada saat ini rencana penelitian tersebut masih dalam pengujian teori dan
protokol.
Sementara itu, tindakan embolisasi sendiri yang saat ini menjadi pilihan utama untuk
penatalaksanaan terapi malformasi arteri vena, memiliki angka komplikasi sebesar 10%15%. Untuk saat ini injeksi yang biasa digunakan para interventionist pun masih berkisar
pada senyawa n-butyl cyanoacrylate, onyx, dan polivinil alcohol, yang disuntikan
langsung melalui mikro kateter ke pembuluh darah feeder malformasi tersebut.
Treatment planning for AVMs depends on risk of subsequent hemorrhage, which
is determined by the demographic, historical, and angiographic features of the individual
patient as discussed above. Prior hemorrhage, smaller AVM size, deep venous drainage,
and relatively high arterial feeding pressures make subsequent hemorrhage more likely.
No randomized clinical trial comparing invasive treatment (staged embolization
followed by either neurosurgical resection or radiosurgery) versus medical management
alone of patients with a known brain AVM is available. There is little disagreement that
patients with an AVM-related hemorrhage need treatment to avoid subsequent
hemorrhages given the high recurrent hemorrhage rates. However, until recently, most
patients with a diagnosis of an unruptured brain AVM were also considered candidates for
invasive treatment to prevent a devastating hemorrhage. This concept has been
challenged because of the low annual hemorrhage rates in patients who did not present
with a brain hemorrhage.
To answer this question, the NIH-sponsored, multicenter Unruptured Brain
Arteriovenous Malformations Trial (ARUBA) is conducted in the United States, Canada,

Europe, and Australia. A total of 800 patients will be randomly assigned in 90 centers to
invasive therapy (endovascular, surgical, and/or radiation therapy) versus medical
management alone. Patients will be followed for a minimum of 5 years and a maximum
of 7.5 years (mean, 6.25 y) from randomization. Final study results will not be available
until 2012.
Until the ARUBA study results are available, treatment is recommended for the
younger patient with one or more of the high-risk features for a AVM rupture, whereas an
older individual or a patient with no high-risk features may be best treated by managing
the medical aspects of the illness alone. In such patients, anticonvulsants for seizure
control and appropriate analgesia for headaches may be the only treatment
recommendations necessary.

Anticonvulsants
o

Standard anticonvulsant therapy, pursuant to the type of seizure, is


generally sufficient to bring seizures under control.

In many patients, seizures are well controlled with phenytoin,


carbamazepine, valproic acid, or lamotrigine. Please see the article
Complex Partial Seizures.

Headache management
o

Headache of acute onset without localizing neurological signs may be the


presenting sign of a hemorrhage, either intraventricular or subarachnoidal,
and need immediate assessment by neuroimaging.

For AVM-associated headaches that are not associated with an intracranial


hemorrhage, standard analgesia for headache may be used, either
nonspecific or migraine specific. Serotonin agonists are not specifically
contraindicated, unless focal neurological symptoms appear as a part of
the migraine. Please see the article Migraine Headache. (emedicine)

Terapi Bedah
Invasive treatment of AVMs may include endovascular embolization, surgical
resection, and focal beam radiation, alone or in any combination. The surgical treatment
risk has traditionally been estimated by the Spetzler-Martin grade. This grading system
assigns 1 point to AVMs smaller than 3 cm in largest diameter, 2 points to AVMs between
3 and 6 cm in largest diameter, and 3 points for AVMs larger than 6 cm. A further point is
added if the AVM is located in functionally critical brain (eg, language, motor, sensory, or
visual cortex), and another point if the AVM has a deep venous drainage.
Selama terjadinya embolisasi pasien tetap sadar dan dibuat nyaman dengan
pertolongan tim anastesi yang memonitor dan memberikan obat melalui jalur intravena.
Setelah embolisasi pasien menginap/ dirawat di Neurological Intensive Care Unit (NICU)
dimana pasien dapat dimonitor secara ketat. Pasien biasanya rawat inap untuk satu malam
untuk setiap embolisasi dan biasanya membutuhkan 2-3 embolisasi dengan interval
selama 2-6 minggu intervals. Pasien biasanya dapat langsung segera melakukan aktivitas
setelah tindakan. Mungkin akan ada nyeri kepala sedang setelah embolisasi dihubungkan
dengan sistim cloting pembuluh darah AVM, atau adanya mual yang berhubungan dengan
obat yang diberikan. Pada pemeriksaan neurologik dilakukan sebelum atau sesudah
injeksi di lakukan. Hal ini dapat memberitahukan apakah pembuluh darah yang
mensupplai AVM juga mkendapat supplai secara normal dan sesuai dengan kebutuhan
dari otak.Setelah ini, agent permanent akan disuntikan melalui AVM dan kateter di pin
dahkan. Hal ini dilakukan berulang kali pada pembuluh darah yang menyuplai AVM.1
The current American Heart Association multidisciplinary management guidelines for
the treatment of brain AVMs recommend the following approach:
1. Surgical extirpation is strongly suggested as the primary treatment for SpetzlerMartin grade I and II if surgically accessible with low risk.

2. Radiation therapy alone is recommended for Spetzler-Martin grade I or II if the


AVM is less than 3 cm in size and surgery has an increased surgical risk based on
location and vascular anatomy.

3. Brain AVM of Spetzler-Martin grades III can often be treated by a multimodal


approach with embolization followed by surgical extirpation. If the lesion has a
high surgical risk based on location and vascular anatomy, radiation therapy may
be performed after embolization.

4. AVMs of Spetzler-Martin grade IV and V are often not amenable to surgical


treatment alone because of the high procedural risk. These AVMs can be
approached by a combined multimodal approach of a combination of
embolization, radiosurgery, and/or surgery.

5. In general, embolization should only be performed if the goal is complete AVM


eradication with other treatment modalities. The only exception is palliative
embolization in patients with an AVM of Spetzler-Martin grade IV or V with
venous outflow obstruction or true steal phenomenon in order to reduce arterial
inflow to control edema or to reduce the amount of shunt, respectively.

Surgical resection
o

Surgical resection is the mainstay of definitive treatment and is most


effective with more easily accessible lesions of smaller size.

AVMs may be approached with craniotomy over the cerebral convexity,


via the skull base, or via the ventricular system.

Arterial feeders and draining veins are isolated and ligated, then the nidus
is resected. Arterial aneurysms may be clipped surgically as well.

Postsurgical angiography is done routinely to ensure that no residual AVM


exists; however, cases of reappearance of AVMs, years after a negative
postresection angiogram, have been reported.

Endovascular embolization
o

Superselective endovascular treatment includes delivery of thrombosing


agents such as quick-acting acrylate glue (N-butyl cyanoacrylate
[NBCA]), thrombus-inducing coils, Onyx liquid embolic fluid, or small
balloons into the AVM nidus.

The goal of embolization is to block the high-velocity shunting of blood


from the high-pressure arterial system into the venous system. Serial
embolization sessions may whittle the AVM down to a fraction of its
original size; the reduced AVM size and the presence of embolic material
within the AVM make surgery and radiosurgery safer and more accurate.
Embolization may be embarked upon to produce relief of neurological
symptoms caused by a large lesion, even if the goal of treatment is not
complete obliteration. In most cases, embolization alone is not sufficient
to completely obliterate the AVM. However, isolated case series have
reported

11-40%

of AVM

obliteration

with

only

endovascular

embolization.

Radiosurgery
o

Radiosurgery is an option to treat AVMs that are approximately 3 cm in


diameter or less. Proton beam, linear accelerator, or gamma knife methods
are used to deliver a high dose of radiation to the AVM, while minimizing
the effects to surrounding brain tissue; a single dose generally is given.
Proton beam irradiation sometimes is attempted with larger lesions.

Radiotherapy is thought to work by inducing thrombosis. This approach is


appealing because of its apparent noninvasiveness.
o

MRI often shows high signal in surrounding brain white matter following
treatment; actual mass effect from edema can be seen when larger
territories are covered. Radiosurgery may take 1-3 years to achieve
thrombosis of an AVM, thus the patient remains at risk for hemorrhage
from AVM during the treatment period.

II.9. PROGNOSIS

With an overall risk of intracerebral hemorrhage of 2-4% per year, angiographic


assessment is recommended to further define prognosis for patients with AVM.

Those with superficial, moderate-sized AVMs have a good long-term prognosis


and may not have any additional benefit with interventional treatment.

Lifetime risk of hemorrhage may be substantial for young patients with AVM.

Prognosis after AVM hemorrhage is generally better than that after intracerebral
hemorrhage from other causes. Better prognosis may be due to the relatively
younger age of patients and a greater potential for reorganization of brain
function. More accurate prognosis awaits the results of currently active, longterm, population-based outcome studies.

BAB III
PENUTUP

DAFTAR PUSTAKA
1. Anonim. Arterio-Venous Malformation, http//www. AVM com.htm. Diakses
tanggal 23 Januari 2008.
2. Anonim. Cerebral arteriovenous malformation, http//www.Wikipedia, the free
encyclopedia.htm. Diakses tanggal 23 Januari 2008.

3. Arteriovenous Malformations and Other Vascular Lesions of the Central Nervous


System Fact Sheet National Institute of Neurological Disorders and Stroke
(NINDS).htm
4. Arteriovenous Malformation Information Page National Institute of Neurological
Disorders and Stroke (NINDS).htm
5. eMedicine - Intracranial Arteriovenous Malformation
Smith, MD.htm

Article by Michael L

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