Surgical management of scalp arterio-venous malformation and scalp venous malformation: An experience of eleven cases

Abstract

Scalp arterio-venous malformation (AVM) and scalp venous malformation (SVM) are rare conditions that usually need surgical treatment. Here, we have reported our experience of the surgical management of such lesions with a short review of the literature.
In this prospective study, 11 patients with scalp AVM and SVM, who underwent surgical excision of lesion in our hospital from 2006 to 2012, were included. All suspected high-flow AVM were investigated with the selective internal and external carotid digital subtraction angiogram (DSA) ± computed tomography (CT) scan of brain with CT angiogram or magnetic resonance imaging (MRI) of brain with MR angiogram, and all suspected low-flow vascular malformation (VM) was investigated with MRI of brain + MR angiogram. Eight were high-flow and three were low-flow VM.
All lesions were successfully excised. Scalp cosmetic aspects were acceptable in all cases. There was no major post-operative complication or recurrence till last follow-up.
With preoperative appropriate surgical planning, scalp AVM and SVM can be excised without major complication.

Full text

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INTRODUCTION
A
n arterio‑venous malformation (AVM) is an
abnormal fistulous connection between the
feeding arteries and draining veins, without an
intervening capillary bed within the subcutaneous layer.
[1,2]
Its management is difficult because of its complex vascular
anatomy, high‑shunt flow (in high‑flow AVM), intracranial
connection (when present) and possible cosmetic
complications.
[3‑5]
They are relatively rare vascular lesions
present as an subcutaneous scalp lump or a large, pulsatile
mass with a propensity to skin erosion and massive
haemorrhage.
[6,7]
Several treatment options that have
been described to treat these lesions, including surgical
excision,
[2,6,8,9]
ligation of feeding vessels, transarterial and
transvenous embolization,
[8,10,11]
injection of sclerosant into
the nidus
[12,13]
and electro thrombosis.
[14,15]
Here, we have
described our experiences of surgical management of scalp
VM (SVM) and result along with a short literature review.
Surgical management of scalp arterio‑venous
malformation and scalp venous malformation:
An experience of eleven cases
Forhad Hossain Chowdhury, Mohammod Raziul Haque, Khandkar Ali Kawsar,
Mainul Haque Sarker, A. F. M. Momtazul Haque
Department of Neurosurgery, Dhaka Medical College Hospital, Dhaka, Bangladesh
Address for correspondence: Dr. Forhad Hossain Chowdhury, Department of Neurosurgery, Dhaka Medical College Hospital, Dhaka,
Bangladesh. E-mail: forhadchowdhury74@yahoo.com
ABSTRACT
Aims: Scalp arterio-venous malformation (AVM) and scalp venous malformation (SVM)
are rare conditions that usually need surgical treatment. Here, we have reported our
experience of the surgical management of such lesions with a short review of the literature.
Materials and Methods: In this prospective study, 11 patients with scalp AVM and SVM, who
underwent surgical excision of lesion in our hospital from 2006 to 2012, were included. All
suspected high‑ow AVM was investigated with the selective internal and external carotid
angiogram ± computed tomography (CT) scan of brain with Digital Substraction angiogram (DSSA)
or magnetic resonance imaging (MRI) of brain with MR angiogram and all suspected low‑ow
VM was investigated with brain MRI + MR angiogram. Eight were high‑ow and three were
low‑ow VM. Results: All lesions were successfully excised. Scalp cosmetic aspects were
acceptable in all cases. There was no major post-operative complication or recurrence till last
follow-up. Conclusions: With preoperative appropriate surgical planning, scalp AVM and SVM
can be excised without major complication.
KEY WORDS
Arterio-venous malformation; cavernous angioma; cirsoid aneurysm; scalp AVM; scalp venous
malformatiom; sinus pericranii
AQ1
AQ2
IJPS_33_13R5
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***
Indian Journal of Plastic Surgery January-April 2013 Vol 46 Issue 1 18

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Chowdhury, et al.: Surgical management of scalp AVM and SVM
MATERIALS AND METHODS
Eleven patients with scalp AVM and SVM who underwent
surgical excision of lesion in Dhaka Medical College
Hospital and few private hospitals in Dhaka, Bangladesh
from 2006 to 2012 were included. All clinical data,
investigations, surgical procedures and postoperative
follow‑up were recorded and studied prospectively. All
suspected high‑flow AVM were investigated with the
selective internal and external carotid digital subtraction
angiogram (DSA) ± computed tomography (CT) scan of brain
with CT angiogram or magnetic resonance imaging (MRI)
of brain with MR angiogram, and all suspected low‑flow
vascular malformation (VM) was investigated with MRI of
brain + MR angiogram. Eight were high‑flow lesions and
three were low‑flow VM. No scale or criteria was used
for the assessment of cosmetic appearance other than
patient’s own and his/her relatives’ appreciation of the final
appearance (excellent, good, acceptable or not acceptable).
Average follow‑up was 3.6 years (6 months to 6.5 years).
Surgical treatment
The patient was positioned according to the site of lesion
with the head elevated 20‑30° above the level of the
heart. The scalp flap was made according to the anatomy
of the VM, and the direction of the feeding arteries and
draining veins. In very high‑flow AVMs, proximal control
of external carotid artery was obtained prior to scalp
surgery. The feeding arteries were preserved at the base
of the scalp flap, and the flap incorporated one or more
normal non‑feeding vessels so as not to jeopardize its
vascularity. The skin incision line was infiltrated adequately
with lignocaine with adrenaline (1:100000 strength) only
in low‑flow SVM. The scalp was incised in short segments
with careful haemostasis using haemostatic forceps and
bipolar coagulation. The scalp flap was raised along
with the pericranium. The bleeding from the bone was
controlled with bone wax and monopolar diathermy. The
feeding arteries were identified along their course at the
base of the scalp flap, the pericranium and galea were
incised, the vessels were traced distally towards the nidus
of the scalp malformations, ligated, and/or coagulated
and then divided. As the feeding vessels were ligated, the
VM was devascularized. The pericranium and the galea
were circumferentially incised, and the VM was excised.
Where there was unavoidable skin loss with the excised
lesion, wound was closed multiple galeal incisions and
scalp mobilization and/or rotational flaps.
RESULTS
Among the 11 cases as seen in Table 1 [Figures 1‑11]eight
were high‑flow AVM and three were low‑flow SVM (two
cavernoma and one venous malformation‑sinus pericranii).
Age rang was 04 months to 72 years. Four were female and
seven were male. Commonly involved areas were frontal,
parietal and temporal. More than one area was involved in
four cases. Only two patients had history of trauma, and two
patients had history of prior surgery for their lesions. In five
patients, the AVM extended on the both side of midline.
Common clinical features were swelling, headache, skin
changes and recurrent bleeding. Common feeders were
superficial temporal, supraorbital and occipital artery.
There was no supply to AVM from MCA, Anterior cerebral
AQ3
Figure 2: (a and b) Pre-operative picture of lesion and patient. (c and d)
Post-operative picture patient with good cosmetic outcome
AQ6
a b
c
d
Figure 1: (a) Per-operative picture of lesion. (b) Post-operative picture of
patient
AQ6
b
a
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Chowdhury, et al.: Surgical management of scalp AVM and SVM
Table 1: Details of all cases
No Age/sex Size
cm
Site C/F Investigation Feeder Types Blood
transfusion
Surgery **Cosmetic
app
Complication
Figure 1 19 yr/M 5×10 Fr (midline) HA, Fr Swelling,
cosmetic problem
DSA, MRI and
MRA
ST, SO (bilateral) AVM 1 unit CE Excellent Nil
Figures
2 and 3
8 months/M 9×11 Fr (midline) Fr swelling,
cosmetic problem
CT and CTA Not identied,
connected with normal
SSS
LF SVM
(sinus
pericranii)
150 ml blood CE Excellent Nil
Figure 4 72 yr/M 5×6 Pa (Lt) H/o trauma,
swelling, recurrent
bleeding
DSA, CT and
CTA
STA, OA (Lt) AVM 1 unite CE, ruptured during
anaesthesia.
Excellent Nil
Figure 5 34 yr/F 3×4 cm Te (Rt) Pain, swelling MRI and MRA Not identied Cavernoma Nil CE Excellent
Figures
6-8
43 yr/M 15×19 Te+Pa (Rt) Increasing size
after operation
4 year back, HA,
Tinitus, ulceration,
recurrent bleeding
DSA, CT *ST, SO, STA, PA, OA,
MA and it’s branches
(Rt) *OA, STA, SO, ST
(Lt) *multiple intracranial
small AVM (ow related)
*Rt te and pa bony
indentation and erosion
by meningeal vessels
AVM 3 unit CE with ulcerated skin
excision, rotational
ap closure (Rt ECA
ligation at neck,
during ligation there
was rupture of ECA)
Good Minor infection
Figure 9 9 mo/F 11×13 Occ+Pa
(Rt>Lt)
Swelling, cosmetic
problem
MRI, MRA
and CT
Not identied Cavernoma 100 ml CE Excellent Nil
Figure 10 18 yr/F 7×18 Fr+pa
(midline)
Hair loss, swelling,
HA, cosmetic
DSA, MRI and
MRA
STA, SO, ST, PA
(bilaterally)
AVM 1 unit CE Good Wound infection
(secondary
Healing)
17 yr/M 6×7 Te+Pa (Lt) H/O trauma (5Yr
back, H/O operation
2 yr back, HA,
Recurrent bleeding
DSA, MRI and
MRA
STA, PA, OA (Lt) AVM Nil CE Excellent Nil
35 yr/M 10×12 Te (Rt) HA, swelling DSA, MRI STA, SO, PA (Rt) AVM 1 unit CE Excellent Nil
Figure 11 39 yr/M 10×13 Fr (Lt>Rt) HA, swelling DSA, MRI SO, ST, STA (Bilateral) AVM 1 unit CE Aceptable
by the
patient
Infection, Large
wound gap
(secondary closure
by rotational ap)
47 yr/F 7×5 Te (Rt) HA, swelling DSA STA, SO, PA AVM 1 unit CE Excellent Nil
Fig: Figure, Yr: Year, Mo: Month, M: Male, F: Female, Fr: Frontal, Pa: Pareital, Te: Temporal, Occ: Occipital, Lt: Left, Rt: Right, H/O: History of, C/F: Clinical feature, HA: Headache, MRI: Magnetic resonance imaging,
CT: Computed tomography, CTA: Computed tomography angiogram, MRA: Magnetic resonance angiogram, DSA: digital subtraction angiogram, ST: Supratrochlear artery, SO: Supraorbital artery, STA: Supercial
temporal artery, PA: Posterior auricular artery, MA: Maxillary artery, OA: Occipital artery, AVM: Arterio venous malformation, CE: complete excision, ECA: External carotid artery, **No Scale or criteria was used for the
assesment of cosmetic appearance. Only patient’s (where applicable) +/one of his/her close relative’s comment on cosmoses (Excellent, good, acceptable or not acceptable) was taken for judgment
Indian Journal of Plastic Surgery January-April 2013 Vol 46 Issue 1 20

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Chowdhury, et al.: Surgical management of scalp AVM and SVM
Figure 5: Peroperative picture of temporal cavernomaAQ5
(ACA) or vertebro‑basilar system. In one case (case 5),
there was some intracranial venous communication. In
case 2, sinus pericranii was connected with superior sagital
sinus (SSS). Per‑operative bleeding was not a problem in
ten cases where blood transfusion was one unit or less.
In case 5, three unit blood was required due to external
carotid artery (ECA) partial rupture and intracranial venous
communication. Complete excision was done satisfactorily
in all cases without any recurrence until the last follow‑up.
Minor infection occurred in one case (case 5), and wound
infection and wound dehiscence occurred in two cases. In
case 7, wound infection and dehiscence were managed
conservatively with antibiotic and regular dressing. In case
10, the dehiscence was very big, and a second operation was
needed to close it with local scalp rotational flap. Excellent
Figure 3: (a and b) CTA of head showing frontal venous malformation (sinus
pericranii) with normal intracranial venous sinuses. (c) Per-operative picture
of low‑ow lesion after exposure. (d) Per‑operative picture after complete
excision of lesion
b
a
c
d
cosmetic result was observed in nine cases. In two cases,
wound healing was acceptable with scar formation in hairy
area. We faced no brain oedema or intracranial hematoma
after operation. There were no recurrence in any case until
the last follow‑up.
Representative cases
Case 2
An 8‑month‑old male child presented with a 9 × 11 cm
swelling in mid‑frontal region extending more to the
right up to the supra‑orbital region. Swelling increased
in size during cry and prone position of the baby, and
it was compressible and non pulsatile. There was no
other prominent vessel on face and scalp. The right
orbit was a little downward and outward placed.
Right half of his face was little hypoplastic. CT scan of
brain showed extra‑calvarial soft tissue mass in frontal
region, and there was no apparent bony gap infront
of anterior fontanel. CT angiogram showed soft tissue
mass was vascular lesion connected with SSS through
emissary veins and intracranial dural sinuses including
SSS. There were no prominent veins of face or scalp
connected with vascular lesion. The lesion was excised
completely by elevation of a bi‑frontal flap through a
post‑hairline bi‑coronal incision. Connecting emissary
veins were coagulated and cut to remove the lesion.
Figure 4: (a and b) CTA of extracranial vessel showing left posterior parietal
AVM with feeder from supercial temporal and occipital artery
a
b
Figure 6: (a and b) CT scan of head showing huge diffuse extracranial soft tissue
swelling and multiple vascular marking (guttering and erosion by AVM vessels)
a
b
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Chowdhury, et al.: Surgical management of scalp AVM and SVM
The lesion was well‑defined capsulated without
septation and filled with venous blood. Histopathology
reported venous malformation‑sinus pericranii. The
patient recovered unevavtfully (Figures 2 and 3) and has
remained asymptomatic for last 5 years (until the last
follow‑up).
Case 5
A 43‑years‑old male patient presented with right‑sided
pulsatile, progressively increasing fronto ‑parieto ‑temporal
swelling measuring about 15 × 19 cm. He had headache
and tinnitus. The swelling was diffusely serpentine.
There was skin changes (ulceration and healed ulcerated
areas). He had a history of surgery 5 years back in
another institution. According to the patient, the lesion
progressively increased in size after the operation. He also
had recurrent attack of haemorrhage from the ulcerated
area But none were of serious nature to cause shock and
were controlled by pressure dressings. CT scan showed
large soft tissue swelling [Figure 6] and the bony windows
showed multiple erosions and prominent vascular
marking. Right‑sided common carotid artery and ECA
angiogram showed huge dilatation of branches (occipital
artery, posterior auricular artery, superficial temporal
artery and maxillary artery and its branches, including
meningeal and middle temporal arteries) of ECA supplying
the AVM. Left ECA angiogram showed enlargement and
tortuousity of left occipital, posterior auricular and
superficial temporal arteries supplying the AVM crossing
the midline. Both internal carotid artery (ICA) angiograms
showed prominent ophthalmic and supraorbital and
supratrochlear arteries supplying the AVM. ACA, middle
cerebral (MCA) and vertebro‑basilar arterial systems were
normal and intracranial venous drainage system seemed
to be normal [Figure 7]. Right‑sided ECA was ligated at the
beginning of operation through a neck incision (During
ligation, partial rupture of ECA occurred, which was
immediately controlled). Then, AVM was excised
completely with some part of skin (ulcerated and infected
area). At the posterior part of AVM, there was some
intracranial venous connection through bony erosion.
There was also some significant pericranial component
Figure 7: (a-i) DSA of ECA and internal carotid artery (ICA) showing bilateral feeding vessels from branches of ECA and ICA through supratrochlear and
supraorbital arteries. There was aneurysmic and ecstatic dilatation of right ECA and its branches
a b
c
d
i
h
c
g
b
f
a
e
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of AVM. Wound was closed with a transposition scalp
flap. Postoperatively, there was minor wound infection
that was controlled by regular dressing and antibiotic.
Cosmetic appearance improved after 2 months [Figure 8].
The patient has remained free of recurrence of AVM for
last 1.5 years (until the last follow‑up).
DISCUSSION
The scalp AVM is an abnormal arteriovenous communication
situated within the subcutaneous fatty layer of the scalp.
In low‑flow VM (i.e., cavernoma, cavernous hemangioma,
venous malformation and sinus pericranii), usually,
no arteriovenous shunt is present and they are seen as
well‑demarcated lesions.
[1,15,16]
The origin of AVM of
the scalp is still uncertain, but trauma is an important
factor in most of the patients,
[3,5]
though some are
congenital (spontaneous) in origin.
[6]
The post traumatic
ones generally develop in patients over 30 years of age.
Spontaneous AVM of the scalp may present at birth, but,
in most patients, it is asymptomatic until adulthood.
[3,16,17]
Low‑flow SVM are usually congenital in nature. Trauma,
pregnancy or hormonal change causes deterioration of the
symptoms. Traumatic AVM of the scalp develops months
or years after the scalp trauma. About 10‑20% of scalp
AVMs develop following penetrating or non‑penetrating
trauma to the scalp.
[15,16,18]
They are equally distributed in
the frontal, parietal and temporal areas.
[6]
Various names
being used to describe the VMs of the scalp include
aneurysm cirsoide, aneurysma serpentinum, aneurysm
racemosum, plexiform angioma, arteriovenous fistula and
AVM.
[5,19,20]
The origin of the main feeding arteries is in the
subcutaneous tissue of the scalp. The origin of these main
feeders, most frequently, arises from the external carotid,
occipital and supraorbital arteries. The STA is frequently
involved in traumatic cirsoid aneurysm.
[18,21,22]
In this series,
two patients had blunt injury to the head. However, these
patients noticed the swelling many years later. Most of the
Figure 8: (a-c) Immediate pre-operative picture of AVM. (d-f) Immediate post-operative picture of operative site. (g and h) Post-operative picture of 9
th
post-operative day. (i) Post-operative picture 4 week after operation with good cosmetic outcome
a
b c
d
g
h
i
e
f
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Chowdhury, et al.: Surgical management of scalp AVM and SVM
necrosis, ulcer and/or haemorrhage.
[3,21,22]
Patients with high
flow lesions also present with loud bruit.
[10]
Haemorrhage
is generally uncommon and may develop in the event of
large VMs. Recurrent haemorrhage, from necrotic areas
may be seen in some patients.
[1,3,16]
Three patients in this
series had recurrent haemorrhage from their lesions.
Angiography is the gold standard investigation to delineate
the lesion and to exclude an intracranial component;
[15]
it is of great importance for diagnosis and treatment
selection. It is particularly employed for the determination
of cranial feeders. Selective angiography should be carried
out for differential diagnosis of the vascular lesions, such
as aneurysms, sinus pericranii, venous malformation
and cavernous hemangioma.
[2,15,16]
Brain MRI is also of
significance for establishing the diagnosis. Scalp high‑flow
AVMs are needed to differentiate from low‑flow AVMS as
the latter are more susceptible to sclerotherapy. AVMs
show flow void signs on MRI due to the rapid flow in the
lesions.
[1,4,15,16]
Management of scalp AVM is difficult because of its high
shunt flow, intracranial communication, complex vascular
anatomy and cosmetic problems. When sinus pericranii
or venous malformation associated with intracranial
sinus occlusion or congenital absence of sinus, then
treatment become difficult. The indication of treatment
patients had a history of progressive increase in the size
of the lesion and had become symptomatic in the third
decade of life.
[2,20]
Their clinical features are associated
with the size of the AVM. The patients may present with
a pulsatile mass, headache, local pain, tinitus, numbness,
Figure 9: (a and b) Pre-operative picture of patient and lesion. (c) CT scan
of head showing extracranial lesion. (d) Per-opeartive picture after complete
removal of low‑ow vascular malformation
AQ6
a
c
d
b
Figure 10: (a) Pre-operative picture of lesion and patient. (b and c) Immediate pre-operative picture of lesion. (d) Post-operative picture of operating site with
infection. (e and f) Post-operative picture of patient with ultimate outcome of operating site 2.5 months after operation
AQ6
a
d
e f
b c
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Chowdhury, et al.: Surgical management of scalp AVM and SVM
includes cosmetic relief of the pulsatile or non‑pulsatile
mass, prevention of haemorrhage and other symptoms
such as headache and tinnitus. The treatment options
include surgical excision
[2,6‑9]
ligation of feeding vessels,
transarterial and transvenous embolization,
[3,8,10,11]
injection
of sclerosant into the nidus
[8,9]
and electro thrombosis.
[14,23]
Surgical excision is the most common and successful
method of dealing with scalp vascular lesion.
[1,3,13]
Surgical
treatment is particularly indicated in order to rule out
bleeding and for the resolution of cosmetic problems,
as well as treat the accompaning issues of tinnitus and
headache.
[5,18,21]
AVM is generally located in the periosteal
and temporal fascia or under the galea. Thus, pre‑operative
radiological evaluation should be used for the assessment
of feeding arteries, drainage vessels, numbers of fistulas,
connected vascular structures and shunt flow volume in
order to prevent any possible complications.
[3,18,23]
Various techniques have been used to control the
haemorrhage during surgery including percutaneous
sutures of the feeding vessels,
[3]
interlocking suture along
Figure 11: (a and b) Post-AVM excisional wound infection and large wound gap. (c and d) Pictures of wound 12 day after second operation (wound closure by
rotational ap of scalp). (e and f) Pictures 1 year after operation showing acceptable cosmetic outcome
a b
c
e
f
d
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Chowdhury, et al.: Surgical management of scalp AVM and SVM
the line of incision and use of tourniquet and intestinal
clamp over the base of the flap.
[22]
A step‑wise incision
with careful pressure control is a useful method to control
the scalp bleeding.
[6]
Reflection of the pericranium along
with the scalp flap prevents inadvertent rupture of the
nidus. In AVM, there may be significant pericranial
component of the malformation
[6]
as was evident in one
of our cases.
Due to the anomalous arteriovenous communication, AVM
must be completely eliminated because recurrence or
enlargement is reported after an incomplete treatment.
[9,20]
Infection, sepsis, haemorrhage and necrosis may
occur as complications.
[1,15,23]
Endovascular treatment
may be applied in order to decrease the haemorrhage
and facilitate the surgical treatment or in the direct
treatment of AVMs.
[5,18,24]
Pre operative embolization
of nidus and feeders especially prevents massive
haemorrhage. Embolization of both feeders and nidus
before surgery is safer than embolization of the feeders
alone to reduce the risk of excessive haemorrhage.
[8]
Three different approaches have been used to access the
fistula, namely femoral transarterial, femoral transvenous
and direct percutaneous catheterization of the feeding
arteries or draining veins.
[8,10,11,13,23]
Direct percutaneous
catheterization of the fistula has been used whenever
access through the artery or vein was not possible.
[10]
The percutaneous placement of thrombogenic coils is a
simple and effective method to produce thrombosis of
cirsoid aneurysm of the scalp, especially after slowing
down the blood flow through transvascular intra‑arterial
embolization.
[15]
Embolization and endovascular treatment may not
be sufficient in the treatment of large scalp AVMs.
Incomplete surgical resection is also insufficient for
the treatment. This may cause scalp haemorrhage and
necrosis, especially in elderly patients.
[15,16,18]
Due to
feeding collaterals, recurrence is possible even after
a long time. The most important step is total surgical
excision without causing scalp necrosis and excessive
blood loss. Furthermore, in this way, a better cosmetic
result may be obtained.
[1,3,15]
The low‑ and high‑flow scalp AVMs have different
management protocol. A thorough clinical evaluation for
differentiation of high‑flow malformation from low‑flow,
should be followed by either a CT angiogram or MR
angiogram and/or DSA. A high‑flow AVM with large size,
multiple feeders, skin changes, skin necrosis/ulceration
and haemorrhage are the right candidate for surgical
treatment as it gives best chances of cure with better
cosmetic result and less chance of recurrence. Feeding
arteries should be identified clinically and confirmed by
imaging. Appropriate management plan should be made on
the basis of clinical data, investigation findings, available
treatment options (surgery, embolization + surgery or
embolization alone) and surgical expertise. In scalp AVM,
usually there are multiple feeders, even with single feeder
cure without recurrence is probably rare. Moreover,
per‑operative feeder control is very easy for a skilled
surgeon even if it needs a separate incision. The scalp
flap should be planned in such a way that the feeding
arteries are preserved in the base of the scalp flap and
the flap incorporate one or more normal non‑feeding
vessels so as not to jeopardize the flap blood supply once
the feeding vessels are ligated. In case of unavoidable
skin excision with AVM, one should keep option/s for
scalp reconstruction. The scalp incision should be in
short segments with appropriate haemostasis. The flap
should be raised along with the pericranium, the feeders
should be identified, the pericranium and galea incised,
the vessels traced distally towards the nidus and ligated,
and/or coagulated and divided. The pericranium and the
galea should be circumferentially incised for excision of
AVM. Wherever needed, scalp should be reconstructed
with scalp mobilization or rotational flap.
In the management of low‑flow VM patient age, size
of lesion, presenting complains, skin thickness and
intracranial venous sinus communication with direction
of venous blood flow are important factors. In our series,
among the three low‑flow VMs, two were under 1 year of
age with a large lesion and the skin overlying the lesion
was thin. In one case, scalp lesion was connected with
superior saggital sinus. In the remaining case, patient
wanted removal of mass. Due to possible intracranial
complications, and chances of scalp necrosis, bleeding,
ulceration, and scarring scarring and other systemic
complication, we did not use interventional radiology
or sclerosants in our series but with expert interveninal
radiologists these are very valuable tools of management
of such lesions.
CONCLUSION
With pre‑operative appropriate surgical planning, scalp
AVM and SVM can be excised safely without any major
complication. Though some cases may be treated with
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Chowdhury, et al.: Surgical management of scalp AVM and SVM
percutaneus or endovascular embolization, surgery
remains the mainstay of treatment. In the event of scalp
ulceration and haemorrhage, total excision is the only
option. CT/MR angiography and/or DSA helps us to
differentiate between low flow and high flow lesions as
well as identify the feeders and the nidus.
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2. Muthukumar N, Rajagopal V, Manoharan AV, Durairaj N. Surgical
management of cirsoid aneurysms. Acta Neurochir (Wien)
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6. Domingo Z, Fisher-Jeffes ND, de Villiers JC. Surgical
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9. Shepard RH. Proceedings: Cirsoid arteriovenous malformations
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13. Hendrix LE, Meyer GA, Erickson SJ. Cirsoid aneurysm treatment
by percutaneous injection of sodium tetradecyl sulfate. Surg
Neurol 1996;46:557-60.
14. Gardner AM, Stewart IA. Treatment of arteriovenous malformation
by endarterial electrocoagulation. Br J Surg 1972;59:146-8.
15. Matsushige T, Kiya K, Satoh H, Mizoue T, Kagawa K, Araki H.
Arteriovenous malformation of the scalp: Case report and review
of the literature. Surg Neurol 2004;62:253-9.
16. Fisher-Jeffes ND, Domingo Z, Madden M, de Villiers JC.
Arteriovenous malformations of the scalp. Neurosurgery
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17. Li F, Zhu S, Liu Y, Chen Y, Chi L, Chen G, et al. Traumatic
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18. Gupta AK, Purkayastha S, Bodhey NK, Kapilamoorthy TR,
Krishnamoorthy T, Kesavadas C, et al. Endovascular treatment
of scalp cirsoid aneurysms. Neurol India 2008;56:167-72.
19. Khodadad G. Familial cirsoid aneurysm of the scalp. J Neurol
Neurosurg Psychiatry 1971;34:664-7.
20. Khodadad G. Arteriovenous malformation of the scalp. Ann Surg
1973;177:79-85.
21. Burrus TM, Miller GM, Flynn LP, Fulgham JR, Lanzino G.
NeuroImages. Symptomatic left temporal arteriovenous
traumatic stula. Neurology 2009;73:570.
22. Hochberg J, Ardenghy M, Pait TG. Scalp tourniquet. Br J Plast
Surg 1994;47:194-8.
23. Heilman CB, Kwan ES, Klucznik RP, Cohen AR. Elimination of a
cirsoid aneurysm of the scalp by direct percutaneous embolization
with thrombogenic coils. Case report. J Neurosurg 1990;73:296-300.
24. Tiwary SK, Khanna R, Khanna AK. Craniofacial cirsoid aneurysm:
2-stage treatment. J Oral Maxillofac Surg 2007;65:523-5.
Editorial Commentary
Not too long ago I had the privilege of reviewing a
book ‘The Management of Haemangiomas and Vascular
Malformations of the Head and Neck’ authored by
Prof. K.S. Goleria and I will rely solely on the contents of
this book while writing this commentary. These lesions
owe their identity to the presence of various channels, it
is the behaviour of the dominant channels that decides
the behaviour of a particular lesion, which in turn is
dependent upon their location in the vascular tree, their
size and the rate of flow through them. This in turn
decides both ‑ the investigative modalities to identify
these lesions and the therapeautic modalities they would
respond to like lasers, radio frequency (RF), embolization
and surgery.
Investigative modalities like Ultrasound, Doppler, CT, MRI,
angiography and DSA can readily differentiate the various
types of vascular malformations and haemangiomas into four
clinically identifiable management oriented groups – the
small channel high flow lesions (congenital haemangioma
of infancy or CHI), small channel low flow lesions (capillary,
lymphatic, venule combination CLVC), large channel low
flow lesions (vascular malformations – VM) and large channel
high flow lesions (arterio‑venous malformations ‑ AVMs).
How to cite this article: ???
Source of Support: Nil, Conict of Interest: None declared.
Indian Journal of Plastic Surgery January-April 2013 Vol 46 Issue 127

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In Venous Malformations‑ the large channel low flow
lesions it is of vital importance to arrive at a correct
diagnosis of the predominant component of the lesion
in order to avoid surprises like profuse bleeding per
operatively. In venous malformations the input must be
ligated before the output and the dissection should be in
a centripetal fashion. Sclerotherapy has been advocated
for small and residual lesions in this group.
The large channel high flow lesions however grow
relentlessly and treating them by blocking the main
blood vessels without treating the nidus spells doom
as it results in a severe re growth with multiple new
feeders. Ablation of the feeders along with the nidus by
embolization, surgery or a combination of both is a must
for results to be lasting and recurrence free. The nidus,
which is a fast flow system involving both arteries and
veins, a conglomeration of many A‑V fistulae is the cause
of ‘steal’, which in turn promotes the nidus. Hence, the
only way to treat AVM is to totally eliminate the nidus.
Another modality that we should not forger is the
laser. This causes photocoagulation resulting in
thrombosis of the channels and involution of the
lesions with less morbidity and minimal scarring. The
target chromophores ‑ haemoglobin, oxy‑haemoglobin,
melanin and water get hit by lasers and the heat energy
thus produced coagulates blood, chars vessel walls and
produce thrombosis best in small channel low flow
lesions.
S. Bhattacharya
Editor, Indian Journal of Plastic Surgery
E-mail: surajitbh@yahoo.co.in
AQ7
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IJPS_35_13R5
INTRODUCTION
I
schemia reperfusion (I/R) injury can be devastating
during flap reconstruction. Some described metabolic
alterations such as capillary narrowing, leukocyte
sequestration, neutrophil infiltration, dysfunction of
endothelium, end‑organ membrane dysfunction and
enzymatic defects of mediators take place in I/R injury.
[1]
Free oxygen radicals play key role in reperfused tissues,
thus causing detrimental effects
[2]
.
Tadalafil is a competitive and potent inhibitor of
cyclic guanosine monophosphate (cGMP)‑specific
phosphodiesterase type 5 (PDE‑5).
[3]
PDE‑5 specifically
inhibits nitric oxide (NO)/GMP pathway in vascular
smooth muscles inducing vasodilatation and in platelets
inhibiting aggregation.
[4]
Among PDE‑5 inhibitors like
silenafil, verdenafil, tadalafil, udenafil, avanafil, tadalafil
has longest half‑life.
There is little data existing in flap surgery field for PDE‑5
inhibitors. In this experimental study, local response to
Tadalal signicantly reduces ischemia reperfusion injury
in skin island aps
Oguz Kayiran, Suat S. Cuzdan
1
, Afsin Uysal
2
, Ugur Kocer
3
???, Izmir Ekol KBB Hospital, Plastic and Reconstructive Surgery Clinic, Izmir,
1
M.D. Sanmed Hospital, Plastic and
Reconstructive Surgery Clinic, Sanliurfa,
2
TOBB ETU Hospital,
3
Ankara Training and Research Hospital, Plastic and
Reconstructive Surgery Clinic, Ankara, Turkey
Address for correspondence: Oguz Kayiran, Mavisehir Modern 2 Sitesi, F Blok D: 4, Karsiyaka, Izmir, Turkey. E-mail: droguzk@yahoo.com
ABSTRACT
Introduction: Numerous pharmacological agents have been used to enhance the viability of
aps. Ischemia reperfusion (I/R) injury is an unwanted, sometimes devastating complication in
reconstructive microsurgery. Tadalal, a specic inhibitor of phosphodiesterase type 5 is mainly used
for erectile dysfunction, and acts on vascular smooth muscles, platelets and leukocytes. Herein,
the protective and therapeutical effect of tadalal in I/R injury in rat skin ap model is evaluated.
Materials and Methods: Sixty epigastric island aps were used to create I/R model in 60 Wistar
rats (non-ischemic group, ischemic group, medication group). Biochemical markers including total
nitrite, malondialdehyde (MDA) and myeloperoxidase (MPO) were analysed. Necrosis rates were
calculated and histopathologic evaluation was carried out. Results: MDA, MPO and total nitrite
values were found elevated in the ischemic group, however there was an evident drop in the
medication group. Histological results revealed that early inammatory ndings (oedema, neutrophil
inltration, necrosis rate) were observed lower with tadalal administration. Moreover, statistical
signicance (P < 0.05) was recorded. Conclusions: We conclude that tadalal has benecial
effects on epigastric island aps against I/R injury.
KEY WORDS
Free radicals; ischemia; island ap; reperfusion injury; tadalal
AQ5
AQ6
Original Article
Access this article online
Quick Response Code:
Website:
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DOI:
***
Indian Journal of Plastic Surgery January-April 2013 Vol 46 Issue 129