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358
J. Valakkada et al.
a
e
Fig. 28.8 A patient with end-stage renal failure on hemodialysis
through left BCF presented with left upper limb edema. CT venogram
(not shown) showed a long segment left brachiocephalic vein occlusion
and severe stenosis at the right brachiocephalic and SVC junction.
Venogram obtained after simultaneous contrast injection through both
cephalic veins and SVC showing long segment complete occlusion of
left brachiocephalic vein (arrows in a) with failure to cross the lesion
despite multiple attempts. Balloon angioplasty of the stenotic segment
at the right brachiocephalic vein–SVC junction (arrows in b and c) was
bc d
f
g
done. Post-angioplasty check venogram showed good opening (arrow
in d) with good antegrade ow across the stenosis. Later, the left BCF
was closed and a new right RCF was created. DSA images showing
long segment occlusions in bilateral brachiocephalic veins (arrows in e
and f) with failure to cross the lesions. An axillary interloop graft (diagram in g) was planned for the patient as he had occlusions of both
femoral veins due to venous catheter placements with no alternate sites
for AV stula creation
28.6 Distal Hypoperfusion Ischemic
Syndrome (DHIS)
DHIS can occur due to true steal caused by the shunting of blood
into low-pressure outow veins causing ischemia distal to the
anastomotic site, arterial stenosis (above or below anastomotic
site), failure of vascular adaptation, or development of collaterals
in forearm preventing compensation for increased ow into stula (Fig.28.9) [33]. Angiogram can differentiate true steal syn-
drome from arterial disease. It also delineates the anatomy distal
to the stula for planning surgical correction. Arterial stenotic
lesions causing steal can be treated with balloon angioplasty.
However, surgery is indicated in true steal syndrome. The surgical procedures include banding/ligation of the outow vein, distal revascularization with interval ligation (DRIL), and revision
using distal inow (RUDI) [33]. Endovascular techniques like
partially covering an anastomotic site with a stent graft have also
been tried with a limited success [34].
28 Endovascular Interventions inHemodialysis Access Fistulas
359
a
e
Fig. 28.9 Distal hypoperfusion ischemic syndrome. A 45-year-old
patient on hemodialysis through left BCF presented with ischemic pain
and gangrene of the distal rst and second ngers. Sheath venogram
showed normal opacication of the cephalic vein (arrow in a) with nonopacication of the radial and ulnar arteries distal to the anastomotic
site. Angiogram with catheter in brachial artery proximal to the stulous anastomotic site showing shunting of blood into the venous side
(curved arrow in b) without lling of the distal radial and ulnar arteries.
Angiogram obtained after compression of the AV stula showing lling
of both radial artery and ulnar artery. No obvious stenosis was noted in
b
f
c
d
g
the proximal or distal ends of the AV stula indicating true steal syndrome. The patient was managed surgically using distal inow (RUDI)
which involves ligation of the stula (arrowhead in d) at its origin followed by reestablishment of the stula via bypass from a more distal
arterial source to the venous limb (arrow in d). Figure28.9e–f shows
distal ischemia in 56-year-old patient with diffuse steno-occlusive disease involving the ulnar artery (arrowhead in e). Balloon angioplasty of
the stenotic segment (arrowhead in f) was done with moderate increase
in distal ow (arrowhead in g)
28.7 Pseudoaneurysm
It occurs in both native and graft stulas but is most common
in graft stulas. It can occur at dialysis access puncture sites
or proximal to venous stenosis. They can be left alone if the
stula is functioning well and the patient is asymptomatic.
Surgery is the preferred treatment for pseudoaneurysms.
Stent graft has been tried in cases of recurrent thrombosis,
overlying skin compromise, and difcult puncture sites [31].
However, stent graft is less preferred due to the high chance
of infection [35].
In summary, a comprehensive understanding of the hemodynamics and structure of natural arteriovenous stulae,
along with their associated complications and interventional
radiology methods for addressing them, is vital for an interventional radiologist.
360
J. Valakkada et al.
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IR Management ofVascular
Malformations
AmitGupta, AnkurGoyal, andAbantiDas
29
Key Messages
1. Vascular malformations can be classied into low-ow
and high-ow types based on their ow characteristics
and presence of an arterial component.
2. For low-ow vascular malformations (venous and lymphatic malformations), percutaneous imaging-guided
sclerosant injection into cystic spaces is the preferred
management.
3. Detergent-based sclerosant agents are the most commonly used agents for sclerotherapy.
4. For high-ow arteriovenous malformations, endovascular
therapy including embolization for ow occlusion and
glue/ethanol injection is the preferred treatment, and the
approach is based on its architecture on angiography.
5. Fibro-adipose vascular anomaly is a recently described
distinct vascular anomaly seen in young adolescent
patients; treatment strategies include ablation for focal
lesions and surgical excision or systemic sirolimus therapy for diffuse extensive lesions.
29.1 Introduction
Vascular anomalies are a complex group of entities and are
broadly classied into (a) vascular tumours and (b) vascular
malformations based on their histopathological features and
clinical behaviour. This classication is endorsed by the
International Society of Vascular Anomalies (ISSVA), allowing a systematic approach to diagnosis as well as management of this heterogeneous group of disorders.
Vascular malformations are further classied into simple,
combined, anomalies of major named vessels and those with
A. Gupta · A. Goyal (*)
Department of Radiodiagnosis and Interventional Radiology,
All India Institute of Medical Sciences, Delhi, India
A. Das
Department of Radiodiagnosis, All India Institute of Medical
Sciences, Kalyani, West Bengal, India
syndromic associations. In addition, they can also be classied based on their ow characteristics into low-ow and
high-ow types depending on the presence or absence of an
arterial component [1]. While any part or organ of the body
can be affected, the current discussion shall be limited to the
management of peripheral vascular anomalies excluding
those involving the pulmonary, visceral and central nervous
systems.
29.2 Low-Flow Vascular Malformations
Low-ow vascular malformations include venous malformation (VM), lymphatic malformation (LM), capillary malformations (CM) and combined lesions. Other than lymphatic
malformations, these vascular anomalies do not regress with
time and tend to grow, commensurate with age. When unifocal or small in size, they may remain asymptomatic and can
be followed up. However, larger lesions or lesions with transspatial, multifocal or diffuse involvement of limb or trunk
warrant treatment. Table29.1 highlights the common indications and relative contraindications for the treatment of lowow vascular malformations [2]. There are no absolute
contraindications. It may be noted that proximity to vital
structures like nerves, airways or orbit may be considered a
contraindication to endovascular treatment if symptoms are
minor. However, if the lesion is signicantly symptomatic
due to its mass effect, it needs to be treated.
The venous malformations are composed of stagnant
blood in abnormal cystic spaces or channels, leading to
recurrent thrombosis resulting in pain and swelling. Longstanding thrombi may calcify over time to form phleboliths.
Some of the diffuse or extensive lesions may develop localized intravascular consumption coagulopathy [3]. Lymphatic
malformations usually present in the paediatric age group as
soft cystic lesions or poorly dened solid-appearing lesions
with multi-compartmental involvement. Capillary malformations are not amenable to endovascular interventions.
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2024
S. H. Chandrashekhara (ed.), Textbook of Interventional Radiology, https://doi.org/10.1007/978-981-97-9601-4_29
361
362
A. Gupta et al.
Table 29.1 Common indications and relative contraindications for
endovascular treatment of low-ow vascular malformations
Indications Relative contraindications
Recurrent pain, swelling:
Most common complaint
Physical deformity,
interference with daily
routine activity, abnormal gait
Recurrent sepsis Involvement of deep venous
Thromboembolic
complications
Mass effect on major nerves Extensive skin involvement
Mass effect on airway and
orbit
Proximity to major nerve bundle
Proximity or involvement of
airway and orbit
system of lower limb
Presence of severe consumptive
coagulopathy
Presence of right to left shunt
Chronic pulmonary
thromboembolism
Treatment strategy for low-ow vascular malformations
includes a two-pronged approach: symptomatic relief and
addressing the lesion. While both goals may be achievable in
focal and sequestered lesions, management is more challenging in diffuse or extensive lesions. In these cases, the primary
aim is to offer maximum symptomatic relief rather than
complete lesion obliteration (which may not be possible) [4].
Oral analgesics and anticoagulants can minimize pain associated with episodes of thrombosis. Local compression garments can be used to reduce limb swelling and discomfort
and should be worn in the daytime to reduce the pooling of
blood.
Treatment of the lesion includes either surgical resection
or obliteration of cystic spaces using sclerosant injection or
laser photocoagulation [4]. We shall focus the discussion on
sclerotherapy here.
29.2.1 Sclerotherapy forLow-Flow Vascular
Malformations
Sclerosant agents cause damage to the endothelium of
venous channels eventually leading to inammation and
brosis. This results in obliteration of spaces and improvement in symptoms. However, they do not alter the inherently
abnormal vascular channels and adjacent soft tissues.
29.2.1.1 Pre-procedural Requirements
1. Adequate immobilization and analgesia are warranted
during the procedure. Hence, use of sedation or general
anaesthesia is needed to alleviate patient discomfort and
pain, especially in the paediatric age group.
2. Ensuring adequate hydration of the patients in peri-
procedural period is highly desirable, especially when
large volume of sclerosant is planned to be used, to avoid
associated haemoglobinuria [5].
3. Sometimes pre-procedure corticosteroids at a dose of
0.1 mg/kg dexamethasone intravenously may be used,
especially those undergoing ethanol sclerotherapy or in
those with lesions involving or in proximity to airway to
minimize post-procedure inammation and swelling
which can potentially compromise airway [4].
4. Targeting the area of compressible anechoic cystic spaces
has the potential to yield maximum results.
29.2.1.2 Procedure
1. The ultrasound probe is properly cleaned and covered
with sterile probe cover prior to the procedure. The compressible cystic anechoic spaces or abnormal vascular
channels are selected for cannulation under ultrasound
guidance. Preferably, 21–23G needles are used to cannulate the lesion [2]. Care should be taken to ensure adequate penetration to the desired depth and proper
stabilization of the needle throughout the procedure to
prevent inadvertent dislodgement and extravasation of
sclerosant.
2. After cannulation, once blood/serous uid return is
obtained, diluted iodinated non-ionic contrast (1:1 dilution) is injected slowly under low-pulse rate uoroscopy
(typically 1–2 frames/second). This preliminary step also
referred to as phlebogram is very crucial (especially in
the rst treatment session) as it allows delineation of
lesion anatomy, morphology of interconnecting spaces
(cavitary, spongy or dysplastic veins), communication
with nearby vascular structures, if any, and the speed of
venous outow (Fig. 29.1). The total dose of contrast
needed to completely opacify the lesion and allow visualization of the draining vein (early or late) also provides an
estimate of the amount of sclerosant to be injected in the
lesion.
3. From a management point of view, morphology of the
lesion on phlebogram has a signicant implication. Focal
lesions that are either sequestered or have late draining
small venous outow usually respond well to sclerotherapy [6]. Also, patients with LMs have been shown to have
a better symptomatic response as compared to VMs
(>60% alleviation of symptoms in 87% cases of LM as
compared to 51% cases of VM) [6]. On the other hand,
diffuse lesions communicating with deep venous system
through large draining veins and showing rapid drainage
on phlebogram pose a challenge. These lesions predispose the patients to systemic side effects of sclerosant,
more often than sequestered lesions, due to rapid transit
of sclerosant into systemic circulation. Passage of sclerosant into the deep vein can result in deep vein thrombosis and pulmonary embolism. Consequently,
recanalization is also observed more often in these lesions
leading to treatment failure. Multifocal lesions are usually seen in syndromic patients [6].
29 IR Management ofVascular Malformations
363
abc
Fig. 29.1 Various morphologies of low-ow venous vascular malformations (arrows) on phlebograms. (a) Spongy intercommunicating spaces,
(b) cavitary spaces and (c) dysplastic veins
abc
*
*
*
Fig. 29.2 Ultrasound appearance during sclerotherapy of low-ow
malformation. (a) Ultrasound image shows the multi-septated appearance of the malformation with anechoic cystic spaces (asterisks). (b)
On injection of the foamed sclerosant into one of the cystic spaces, the
lesion appears hyperechoic (arrows) with dirty posterior acoustic shad-
4. After the phlebogram, the sclerosant is adequately mixed
with air (usually 1:1) into a foam and is injected slowly
under ultrasound/uoroscopic roadmap guidance until
the lesion is lled or there is visualization of draining
vein (Fig.29.2). The dose of sclerosant is usually kept as
two-thirds of the total dose of contrast injected in the
phlebogram [2]. For lesions showing early or rapid drainage into large veins, venous outow must be occluded
either manually by local compression or embolized using
endovenous coil placement or glue, before injecting sclerosant. For cutaneous lesions, sclerosant can be diluted
with normal saline. Some authors practise “double- needle
technique” wherein one needle is used to inject the sclerosant while the other allows egress of contrast, blood and
owing (dotted arrows) obscuring the posterior margin of the lesion. (c)
With time, the sclerosant (hyperechoic content) is seen to diffuse further into the inter-communicating cystic spaces (arrows) of the
malformation
excess sclerosant [2] (Fig.29.3). This may reduce the side
effects related to sclerosant extravasation.
5. Once the lesion is completely lled or there is drainage of
sclerosant into normal veins, injection is stopped. While
injecting sclerosant, overlying skin colour of the must
also be observed and injection must be stopped in case of
erythema or blanching. Care should be taken to prevent
sclerosant leakage along the needle track while removing
the needle.
6. In case of large lesions, multiple punctures may also be
done so that more parts of the lesion may be simultaneously treated (Fig.29.3).
7. The sclerotherapy procedure for LMs has some differences from that of VM.In these cases, the individual cys-
364
ab
A. Gupta et al.
c
Fig. 29.3 Sclerosant preparation and injection. (a) Tessari method for
mixing detergent sclerosant with air using two leur lock syringes
(arrows) and a three-way stopcock (rectangle). (b) Multiple needle
puncture sites (arrows) used for sclerosant injection in large lesions
with multiple internal septated compartments. (c) Double-needle technique (arrows) for sclerosant injection with one needle allowing egress
of contrast, blood and extra sclerosant
tic spaces in a macrocystic LM are cannulated separately,
starting with the largest. Before injecting the sclerosant,
uid is aspirated for better contact of the sclerosant with
patients may require prolonged intubation due to acute postprocedural swelling. Sclerotherapy is usually performed as a
series of multiple sessions at an interval of 6–8weeks [4].
the cavity lining (Fig. 29.4). For larger lesions, pigtail
catheter can be kept in situ for drainage with daily reinjections and drainage of sclerosant solution. Care
29.2.1.4 Choice ofSclerosant Agent
(Table29.2)
should be taken not to over-distend the cystic spaces
while injecting since these are sequestered lesions without any drainage. In general, macrocystic LMs respond
better to sclerotherapy than microcystic LMs [7].
Ethanol
Absolute ethanol (95–98%) is the most potent sclerosant
agent available. It causes rapid precipitation of proteins of
endothelial cells and thrombosis [7]. However, serious side
29.2.1.3 Post-procedure Care
After removal of needle or cannula, mild local compression
is given to stop bleeding and to allow adequate contact of
sclerosant and endothelium. Light compression dressing
may also be applied around the lesion. Topical antibiotic
ointment is usually not required. Local cold compression and
limb elevation are advised to reduce pain and swelling along
with oral analgesics. Vascular malformations close to airways must be observed carefully for up to 72 h as some
effects can occur in certain cases and include tissue necrosis,
nerve injury, hypoglycaemia, haemolysis, hyperthermia,
hypertension, pulmonary embolism and cardiac arrhythmias.
Pulmonary artery hypertension is a potentially fatal complication that can occur with the use of large volumes of ethanol. Hence, it should only be used by experienced trained
personnel in a hospital setting. Injection should be avoided in
lesions that are in close proximity to major nerve trunks and
in cutaneous lesions [4].
b
a
29 IR Management ofVascular Malformations
Fig. 29.4 Lymphatic
malformation. (a) Phlebogram
showing large cavitary
contrast-lled space (arrow)
in the lymphatic malformation
with no opacication of
draining veins. (b)
Ultrasound-guided aspiration
of the lymphatic uid content
using a needle (arrows). (c)
Yellowish lymphatic uid
aspirated from the cavitary
space
c
365
Table 29.2 Agents used for sclerotherapy of low-ow vascular malformations
Name Mechanism of action Dosage/technique Uses Complications
Ethanol Aggressive sclerosant
Sodium
tetradecyl
sulphate (STS)
Bleomycin DNA cleavage triggering
Doxycycline Tetracycline antibiotic Solution of 10mg/mL
OK-432
(Picibanil)
causing rapid
denaturation of
endothelial cell proteins
and thrombosis
Anionic detergent-based
sclerosant, endothelial
damage by reducing
surface tension
single- and double-strand
breaks
Lyophilized preparation
containing killed group A
streptococci in penicillin
Maximum dose 1mg/
kg or 60mL in a single
session
3% commonest
strength used, injected
as foam (STS/air
mixture)
Maximum single
session dose—0.5U/
kg, lifetime cumulative
dose <300mg
mixed with iodinated
contrast, up to a
volume of 100mL
1–2 KE (Klinische
Einheit) units every
2months
The procedure must be performed under general anaes-
thesia with continuous patient monitoring. As a general rule,
Venous malformations,
macrocystic lymphatic
malformations
Venous malformations,
macrocystic lymphatic
malformations
Microcystic lymphatic and
venous malformations
(especially in areas
sensitive to swelling)
Macrocystic lymphatic
malformations
Macrocystic lymphatic
malformations
maximum dose of 1 mg/kg or 60 mL per session should
never be exceeded [2].
Signicant local site pain and
swelling (requires general
anaesthesia), nerve damage,
pulmonary artery hypertension (with
large volumes)
Local site pain and skin staining,
haemoglobinuria (with large
volumes)
Pulmonary brosis (related to
cumulative dose)
Safe agent, may cause hypoglycaemia
in neonates
Post-injection u-like illness,
contraindicated in patients allergic to
penicillin
before injecting any sclerosant, the appropriate position of
cannula in the lesion must be conrmed with contrast injection or USG.Ethanol can be injected in undiluted form or
diluted with an oily contrast medium in 10:1 or 10:2 dilution
under digital subtraction angiography mode [8]. However, a
Detergent Sclerosant
This category includes sodium tetradecyl sulphate (STS),
polidocanol, sodium morrhuate and ethanolamine. This
group of drugs have a milder sclerosant action than ethanol.
366
ab
Fig. 29.5 Lymphatic
malformation showing good
response following
sclerotherapy with
polidocanol. (a) Coronal
T2-weighted MRI image
shows a lobulated T2
hyperintense lymphatic
malformation (arrows) in the
right supraclavicular location
with T2 shading representing
bleeding in one of the loculi.
(b) Coronal T2-weighted
fat-suppressed MRI image
shows signicant reduction in
the size of the malformation
(arrows) after three sessions
of sclerotherapy with
polidocanol
A. Gupta et al.
They too damage endothelial cells and cause thrombosis but
are slower than ethanol. Unlike ethanol, they do not have
cumulative doses over 100U are never attained. Flagellate
dermatitis is another rare side effect with multiple sessions.
neurolytic action [4]. Thus, staged treatment with detergent
sclerosants is now being used by the majority of practitioners
for low-ow vascular malformations, given their similar efcacy as ethanol and signicantly reduced systemic complications (Fig.29.5).
These sclerosants are usually administered as a form by
either mixing with air alone or with air and an oily or watersoluble contrast medium [9]. The use of foam allows better
and prolonged contact between the sclerosant agent and the
endothelial lining of the vessel wall by delaying the transit
across the lesion. The foam can be generated by mixing
detergent sclerosant and air in 1:1 proportion by the Tessari
Doxycycline
Although the exact mechanism of action of doxycycline in
vascular malformations is still unclear, it has been found to
be effective as a sclerosant in macrocystic LMs. It is especially useful since a large volume can be used for distending
cystic spaces without signicant toxicity [7]. Doxycycline
can be used as a solution of 10mg/mL mixed with iodinated
contrast, up to a volume of 100ml. It can also be used in
conjunction with other sclerosants (e.g., STS) for better efciency. Peri-procedural corticosteroids should not be used if
doxycycline is used as a sclerosant [7].
method using two leur lock syringes and a three-way stopcock [7]. Patients should be kept well-hydrated during and
after the procedure to avoid renal impairment associated
with haemoglobinuria, especially when a large volume of
detergent sclerosant is injected [5].
OK-432 (Picibanil)
OK-432 is an immune stimulant consisting of killed group A
streptococci in a suspension containing penicillin. It has
been shown to cause an inammatory reaction that causes
subsequent shrinkage of cystic spaces in macrocystic LMs.
Bleomycin
Bleomycin is effective for the treatment of microcystic LMs.
It is a cytotoxic anti-tumoural antibiotic which acts by trig-
Minimal side effects have been reported aside from post-
procedural swelling. However, its use is contra-indicated in
patients allergic to penicillin due to risk of anaphylaxis [7].
gering DNA cleavage causing single- and double-strand
breaks [10]. Bleomycin is associated with the least amount
of post-treatment swelling as compared to ethanol and foam
sclerosants as it does not cause thrombosis. Thus, it is useful
in areas which are sensitive to swelling (e.g., intramuscular,
close to nerves/orbit/airway, etc.) (Fig.29.6). However, pulmonary brosis is a major complication related directly to its
cumulative dose. Thus, the maximum single session dose of
Bleomycin should not exceed 0.5 U/kg to a maximum of
15U [2]. Also, a record of cumulative doses over multiple
sessions should be kept, and the maximum lifetime dose of
Bleomycin must not exceed 5U/kg or 300U [7]. Practically,
29.2.1.5 Complications
Skin necrosis is the most common complication occurring
secondary to sclerotherapy of VMs. Blanching or discoloura-
tion of overlying skin during sclerosant injection are indica-
tors for development of skin necrosis at a later time point.
The treated area should be kept clean with application of
antibiotic ointment. Cases with deep ulceration should be
referred to a wound care centre.
Transient numbness is common with ethanol and usually
resolves in a few weeks. In case of suspicion of compartment
syndrome, emergency surgical fasciotomy may be required.
ab
29 IR Management ofVascular Malformations
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367
Fig. 29.6 Venolymphatic low-ow vascular malformation showing
good response following sclerotherapy with polidocanol and bleomycin. (a) Axial T2-weighted fat-suppressed MRI image shows a large
lobulated multi-septated T2 hyperintense low-ow vascular malformation (arrows) in the right lower neck encasing the right neck vessels
Haemoglobinuria may occur after large-volume sclerotherapy of large VMs. To minimize renal toxicity, the patient
should be aggressively hydrated and alkalinization of urine
with IV sodium bicarbonate infusion should be done [2].
Deep venous thrombosis and pulmonary embolism are
dreaded complications of sclerotherapy of VMs with rapid
drainage into deep veins. Prophylactic low-molecular-weight
heparin therapy may be given post-procedure for a duration
of 2weeks [2].
Delayed infection is uncommon unless there is skin compromise. To minimize contractures following sclerotherapy
(asterisks). (b) Axial T2-weighted fat-suppressed MRI image shows
signicant reduction in the size of the malformation (arrows) after
sclerotherapy with polidocanol in the lateral part and bleomycin in the
medial part of the lesion
Endovascular/percutaneous interventions have become
the rst-line treatment for these high-ow lesions on account
of high rates of recurrence and the morbidity associated with
surgical resection. The goal of endovascular embolization in
AVM is to obliterate the nidus and simultaneously prevent
non-target embolization. This requires super-selective positioning of the catheter within the nidus or as close to the
nidus as possible. Flow reduction prior to injecting the
occluding agent increases the likelihood of obliterating the
nidus. Other management options include surgery, oral thalidomide and radiotherapy for osseous lesions.
of intramuscular VMs, early stretching or physiotherapy
should be started (within 2weeks after procedure) [2].
29.3.1 Endovascular Therapy forHigh-Flow
Vascular Malformations
29.3 High-Flow Vascular Malformations
29.3.1.1 Pre-procedure Evaluation
Arteriovenous malformations (AVMs) are true high-ow
vascular malformations characterized by abnormal communication between arteries and veins through an intervening
nidus without a normal capillary bed. Arteriovenous stulas,
on the other hand, represent direct communication between a
single artery and vein and usually occur secondary to trauma
or surgery.
The usual clinical presentation is with warm, erythematous pulsatile swelling with superimposed features of local
site ischaemia, bleeding and high-output cardiac failure in
large lesions. On imaging, AVMs are seen as tangle of vessels showing high-velocity, low-resistance arterial ow, supplied by one or more feeding arteries with prominent draining
veins [11].
1. Patients should be counselled regarding the prognosis
prior to the procedure planning. Outcomes of endovascular therapy are highly variable in cases of AVMs, and
large AVMs are usually not curable. However, most
patients experience bleeding control and symptomatic
improvement in pain following embolization.
2. Review of patient history, physical examination ndings
and imaging ndings (including CT/MRI angiography
images) is an essential pre-requisite before the procedure
to conrm the diagnosis, extent of the lesion, prominent
arterial feeders and draining veins.
3. The embolic agents used for AVM embolization (alcohol,
EVOH and NBCA glue) are usually painful and patients
may require general anaesthesia.