EDUCATION EXHIBIT
1519
Soft-Tissue Venous
Malformations in Adult
Patients: Imaging and
Therapeutic Issues1
ONLINE-ONLY
CME
See www.rsna
.org/education
/rg_cme.html.
LEARNING
OBJECTIVES
After reading this
article and taking
the test, the reader
will be able to:
䡲 Discuss the current roles of US, CT,
MR imaging, and
direct phlebography
in the evaluation of
soft-tissue venous
malformations.
䡲 Recognize the imaging features of softtissue venous malformations.
䡲 Discuss the various therapeutic options for soft-tissue
venous malformations.
Josée Dubois, MD ● Gilles Soulez, MD ● Vincent L. Oliva, MD ● MarieJosée Berthiaume, MD ● Chantale Lapierre, MD ● Eric Therasse, MD
Venous malformations are the most common vascular malformations.
However, confusion with respect to terminology and imaging guidelines continues to result in improper diagnosis and treatment. An appropriate classification scheme for vascular anomalies is important to
avoid the use of false generic terms. Adequate imaging in association
with clinical findings is crucial to establishing the correct diagnosis.
Doppler ultrasonography should be the initial imaging modality and
demonstrates absence of flow or low-velocity venous flow. Computed
tomography and magnetic resonance (MR) imaging are used primarily
for pretreatment evaluation of lesion extension. These lesions are usually hypointense on T1-weighted MR images and markedly hyperintense on T2-weighted images with variable gadolinium enhancement.
Direct phlebography helps confirm the diagnosis and exclude other
soft-tissue tumors. Three distinct phlebographic patterns (cavitary,
spongy, dysmorphic) have been identified. In most cases, conservative
treatment is recommended. Sclerotherapy with or without surgery is
useful in cases of functional impairment or significant aesthetic prejudice, even if recurrences are frequent. Direct phlebography is performed when a more detailed assessment of the vascular pattern is
needed or as part of sclerotherapy. Use of the appropriate imaging
technique is critical in establishing the diagnosis, evaluating extension,
and planning appropriate treatment.
Abbreviation: FISP ⫽ fast imaging with steady-state precession
Index terms: Arteriovenous malformations, 9*.1422 ● Arteriovenous malformations, therapeutic radiology, 9*.124, 9*.1291, 9*.12941, 9*.12984
Veins, abnormalities, 9*.142
RadioGraphics 2001; 21:1519 –1531
1From the Department of Radiology, Ste-Justine Hospital, 3175 Côte Ste-Catherine, Montréal, Québec, Canada H3T 1C5 (J.D., C.L.); and the Department of Radiology, Centre Hospitalier de l’Université de Montréal, Québec, Canada (G.S., V.L.O., M.J.B., E.T.). Recipient of a Magna Cum
Laude award for an education exhibit at the 2000 RSNA scientific assembly. Received February 27, 2001; revision requested May 2 and received June
28; accepted July 2. Address correspondence to J.D. (e-mail: joseedubois@compuserve.com).
29*
©
indicates vascular system, location unspecified.
RSNA, 2001
1520
RG f Volume 21
November-December 2001
●
Number 6
ISSVA Classification of Vascular Anomalies
Vascular Malformations
Vascular Tumor
Simple
Hemangioma
Proliferative phase
Involutive phase
Other tumors
Capillary malformation
Lymphatic malformation
(macrocystic, microcystic, mixed)
Venous malformation
Combined
Arteriovenous fistula, arteriovenous malformation,
capillary-venous malformation, capillarylymphatic-venous malformation (KlippelTrenaunay syndrome)
Lymphatic-venous malformation, capillaryarteriovenous malformation (Parkes-Weber
syndrome), capillary-lymphatic-arteriovenous
malformation
...
Note.—ISSVA ⫽ International Society for the Study of Vascular Anomalies.
Source.—Reference 2.
Introduction
Venous malformations are part of a spectrum of
vascular malformations commonly found in
adults. A venous malformation is defined as a
simple malformation with slow flow and an abnormal venous network. However, confusion in
terminology, with misnomers such as hemangioma, cavernous hemangioma, phlebangioma, and
phlebangiomatosis, continues to be responsible for
improper diagnosis and illogical treatment.
Venous malformations can be distinguished by
their characteristic imaging findings at Doppler
ultrasound (US), computed tomography (CT),
magnetic resonance (MR) imaging, and direct
phlebography. Interventional radiologic techniques play an important role in the management
of venous malformations.
In this article, we describe the imaging features
of venous malformations that permit accurate
classification and review the therapeutic options
currently available for these lesions.
Classification
of Vascular Anomalies
The most helpful classification scheme for vascular anomalies was described by Mulliken and
Glowacki in 1982 (1). They have classified vascu-
lar anomalies as either vascular tumors with endothelial hyperplasia or vascular malformations secondary to an error of embryonic development
with normal endothelial turnover. This classification scheme is supported by clinical, histologic,
histochemical, and biochemical differences as
well as imaging features.
A classification scheme for vascular anomalies
based on cellular features, flow characteristics,
and clinical behavior was updated during the
1992 meeting of the International Society for the
Study of Vascular Anomalies (ISSVA) (Table)
(2).
Vascular malformations are also classified as
slow-flow malformations (capillary, venous, lymphatic, capillary-venous, and capillary-lymphaticvenous malformations) and high-flow malformations (arteriovenous fistulas, arteriovenous malformations).
Clinical Characteristics
Venous malformations are characterized by a soft,
compressible, nonpulsatile tissue mass. The overlying skin usually has a bluish tint, but occasionally it may appear normal. The main locations are
the head and neck (40% of cases), extremities
(40%), and trunk (20%). Venous malformations
typically expand after the Valsalva maneuver and
may be flattened with applied pressure. They tend
to grow over time in proportion to the growth of
the patient. They often enlarge during puberty
RG f Volume 21
●
Number 6
Dubois et al
1521
Pathologic Features
Histopathologic examination of venous malformations reveals thin-walled, dilated spongelike
channels varying in size from capillary to cavernous dimensions, with sparse smooth muscle cells,
adventitial fibrosis, thrombosis, and phleboliths
(3). Smooth-muscle actin staining reveals muscle
in clumps instead of the normal smooth-muscle
architecture. The mural muscular anomaly is
probably responsible for the gradual expansion
(3).
Genetic Features
Figure 1. Venous malformation of the right parotid
gland. Conventional radiograph demonstrates phleboliths (arrows).
and pregnancy (due to hormonal influence) and
do not regress. Symptoms are related to size and
location. Although most venous malformations
are in the skin and subcutaneous tissues, they also
frequently involve underlying muscle, bone, and
abdominal viscera. Most venous malformations
are solitary, but multiple cutaneous or visceral
lesions can occur.
Deep cutaneous or intramuscular lesions usually cause discomfort, often in the early morning
on awakening or with exertion. Intraoral venous
malformations can bleed, distort dentition, cause
speech problems, and obstruct the upper airway
and pharynx. Thrombosis, swelling, and pain are
common in venous malformations. Only symptomatic malformations or lesions causing important aesthetic prejudice require treatment.
Coagulopathic Features
A coagulation profile should be performed for any
patient with an extensive venous malformation,
especially if there is a history of easy bruising or
bleeding. Stagnation within a venous malformation can cause localized intravascular coagulopathy (3).
Venous anomalies usually occur sporadically, but
families with dominant inheritance have been
identified. In these families, a linkage to chromosome 9p21 has been established (4). This mutation causes ligand-independent activation of an
endothelial cell–specific receptor tyrosine kinase,
TIE-2. Familial forms of venous malformations
with glomus cells (glomangioma) have also been
linked to chromosome 1p21-p22 (5). Consequently, venous anomalies could be caused by
gene mutations that regulate angiogenesis.
Imaging Features
Conventional Radiography
Conventional radiography usually demonstrates a
soft-tissue mass with occasional phleboliths and,
occasionally, adjacent skeletal anomalies (Fig 1).
Doppler US
Doppler US is essential in differentiating venous
malformations from other vascular anomalies. US
should be performed with a high-frequency lineararray transducer (5–10 MHz). Exploration begins
with a gray-scale examination to delineate the
margins of the malformation. Venous malformations appear as hypoechoic or heterogeneous lesions in 80% of cases (6,7). Anechoic channels
can be visualized in less than 50% of cases (Fig
2a). Sometimes, isoechoic thickening of the subcutaneous tissues without a solid mass or discernible channels is the only feature. Hyperechoic foci
1522
November-December 2001
RG f Volume 21
●
Number 6
Figure 2. Venous malformation of the cheek. (a) Gray-scale US image shows hypoechoic structures (arrows).
(b) Doppler US image helps confirm the presence of low venous flow within the malformation.
with posterior acoustic shadowing are seen in less
than 20% of cases (6).
In most cases, Doppler US demonstrates
monophasic, low-velocity flow (Fig 2b). In 20%
of lesions, no flow is demonstrated. This absence
of flow may reflect thrombosis or be caused by
equipment limitations (6).
Computed Tomography
At CT, venous malformations are hypoattenuating or heterogeneous lesions that enhance slowly
and peripherally after bolus injection of contrast
material (Fig 3a). CT usually demonstrates lesion
extension, but MR imaging is more accurate in
assessing the extension of venous malformations
owing to its superior contrast resolution (Fig 3b,
3c). Phleboliths are more clearly depicted and
fatty components are sometimes demonstrated at
CT (Fig 4).
Figure 4. Venous malformation of the left
thigh. CT scan demonstrates a heterogeneous
lesion in the vastus lateralis muscle. The hypoattenuating peripheral portion of the lesion (arrows) suggests the presence of fat.
RG f Volume 21
●
Number 6
Dubois et al
1523
Figure 3. Venous malformation of the right masseter
muscle. (a) Contrast material– enhanced CT scan
shows a heterogeneous mass of the right masseter
muscle with faint peripheral enhancement surrounding
hypoattenuating areas. The presence of a phlebolith
(arrow) confirms the diagnosis of venous malformation. (b) Fast spin-echo T2-weighted MR image depicts a cavitary lesion with septation. The lesion is
clearly hyperintense. (c) Gadolinium-enhanced T1weighted MR image shows the lesion with partial heterogeneous enhancement, a finding that suggests partial
thrombosis of the venous malformation.
MR Imaging
MR imaging is excellent for defining the extension of venous malformations and their relationship to adjacent structures. Examination protocol
should begin with spin-echo or fast spin-echo T1weighted imaging for basic anatomic evaluation
(Fig 5a). The extension of the malformation
should be assessed with short-inversion-time in-
version recovery (STIR) T2-weighted imaging
with a 512 matrix (Fig 5b).
Fat-suppressed fast spin-echo T1-weighted
imaging should be performed after contrast material injection to evaluate perfusion of the malformation (Fig 5c, 5d). Gradient-echo T2*-
1524
November-December 2001
RG f Volume 21
●
Number 6
Figure 5. Venous malformation of
the right plantar region. (a) Spinecho T1-weighted MR image shows
diffuse enlargement of the medial
plantar muscles. The lesion is hypointense and is difficult to differentiate from the normal muscular
structures. (b) STIR T2-weighted
image (512 matrix) clearly demonstrates the malformation within the
plantar muscles. (c, d) Unenhanced
(c) and contrast-enhanced (d) coronal T1-weighted images show perfusion of the malformation, which involves the first three layers of the
plantar muscles.
weighted imaging can also be used to demonstrate calcification or hemosiderin (Fig 6). The
examination can be completed with three-dimensional fast imaging with steady-state precession
(FISP) phlebography to appreciate the drainage
of the malformation (Fig 7) (8).
Venous malformations are usually hypo- or
isointense at T1-weighted MR imaging. In cases
of hemorrhage or thrombosis, heterogeneous signal intensity can be observed on T1-weighted
images. Abnormal veins can be observed in the
area of the malformation (Fig 8). At T2-weighted
MR imaging, venous malformations display
bright signal intensity. Areas of hypointensity related to thrombosis, septation inside the malformation, or phleboliths can also be observed (Fig
9). On T2-weighted MR images, the extension
of the malformation into adjacent structures is
Figure 6. Venous malformation of the right parotid
gland. Gradient-echo T2*-weighted MR image clearly
demonstrates a malformation within the right parotid
gland with extension into the right parapharyngeal
space. Phleboliths are well visualized as areas of hypointensity (arrows).
RG f Volume 21
●
Number 6
Dubois et al
1525
Figure 7. Venous malformation of the right thigh. (a) Coronal STIR MR image demonstrates dysmorphic veins (arrows). (b, c) Gadolinium-enhanced MR phlebograms obtained with three-dimensional
FISP show dysmorphic veins in the territory of the deep femoral vein (arrows).
Figures 8, 9. (8) Venous malformation of the left arm. (a) Clinical photograph of the left arm demonstrates a softtissue lump. The bluish discoloration of the overlying skin suggests a venous malformation. (b) Sagittal spin-echo
T1-weighted MR image reveals infiltration of the subcutaneous fat by a low-signal-intensity mass. Dysmorphic veins
are present in the vicinity of the mass (arrow). (9) Venous malformation of the hand. T2-weighted MR image shows
dysmorphic veins (arrows).
1526
November-December 2001
RG f Volume 21
●
Number 6
Figure 10. Venous malformation with extension. (a) Axial T1-weighted MR image shows a venous malformation
infiltrating the fat surrounding the femoral vessel in the right inguinal region (arrows). (b) On a STIR T2-weighted
MR image, the malformation is clearly demonstrated in the inguinal region (arrow). Involvement of the parametrium
is also noted.
Figure 11. Venous malformation of the elbow.
(a) Spin-echo T1-weighted MR image shows an isointense mass (arrowheads) infiltrating the periarticular fat
and the triceps muscle. Subtle infiltration of the subcortical bone medulla is also seen (arrow). (b) Axial
T2-weighted MR image clearly demonstrates the malformation with involvement of the distal humeral bone
and infiltration of the olecranon fossa and the distal
portion of the triceps muscle. (c) Gadolinium-enhanced T1-weighted MR image demonstrates perfusion of the entire malformation.
RG f Volume 21
●
Number 6
Dubois et al
1527
Figure 12. Venous malformation in a middle-aged woman with dysphagia and dysphonia. (a) Sagittal T2weighted MR image shows a large venous malformation of the cervical prevertebral region inducing compression of
the pharynx. (b) T1-weighted MR image obtained after three sessions of sclerotherapy with alcoholic solution of zein
and alcohol reveals significant shrinkage of the malformation, which now demonstrates heterogeneous signal intensity
with small hyperintense areas. This finding may be related to recent thrombosis. (c) Gadolinium-enhanced MR image shows the malformation with heterogeneous enhancement (arrows). This finding may be related to a posttherapeutic inflammatory reaction and to residual perfusion of the malformation.
usually clearly delineated (Fig 10). Gadoliniumenhanced T1-weighted imaging is useful in evaluating the circulatory portion of the malformation
(Fig 11).
After sclerotherapy, venous malformations
demonstrate heterogeneous signal intensity on
both T1- and T2-weighted images. A delay of up
to several months is necessary to evaluate the
therapeutic response after sclerotherapy, allowing
time for the transient inflammatory reaction to
resolve. In most cases, progressive shrinkage of
the malformation is observed (Fig 12a, 12b).
Gadolinium-enhanced imaging is useful in demonstrating residual perfusion of the malformation
and directing additional treatment (Fig 12c).
Although MR imaging is very sensitive for
identifying and assessing the extension of venous
malformations, it is not very specific. Findings
must be correlated with clinical findings and
Doppler US findings to make the diagnosis. In
cases of atypical clinical or imaging findings, percutaneous phlebography must be performed to
confirm the diagnosis. If phlebographic findings
are inconclusive, percutaneous or surgical biopsy
must be performed to rule out malignant disease.
In summary, a standard MR imaging examination should include fast spin-echo T1-weighted
imaging with and without fat saturation. STIR is
the preferred T2-weighted sequence, and gradient-echo T2*-weighted imaging is useful in evaluating bleeding or thrombosis or demonstrating
calcification. Gadolinium-enhanced fat-suppressed fast spin-echo T1-weighted MR imaging
is mandatory. Phlebography is optional and can
be used if dysplastic veins are suspected. During
posttreatment follow-up, MR imaging should be
performed with the same specifications as those
used for the baseline examination.
Direct Percutaneous Phlebography
Direct percutaneous phlebography can be performed as a diagnostic procedure in cases of
atypical venous malformation. Opacification of
abnormal venous cavities allows confirmation of
the diagnosis of venous malformation and exclusion of other diagnoses such as benign or malignant soft-tissue tumors. Direct percutaneous
phlebography is also frequently performed as the
initial step during sclerotherapy. Direct needle
puncture of the malformation is performed with a
20- or 21-gauge needle. US or CT can be useful
1528
November-December 2001
RG f Volume 21
●
Number 6
Figure 14. Direct phlebography and sclerotherapy of a venous malformation of the foot. (a) Clinical photograph
shows a sclerotherapeutic procedure. Because the lesion was superficial, we used a 21-gauge butterfly needle. Venous
return was observed, confirming the proper positioning of the needle. (b) Direct phlebogram demonstrates a venous
malformation with a cavitary portion (straight arrow) and drainage into dysmorphic veins (curved arrow).
Figure 13. CT scan demonstrates direct needle
puncture of the venous malformation in the same patient as in Figure 12.
in guiding the needle, especially if the malformation is located deep in the soft tissues (Fig 13).
The needle is connected to a syringe through a
length of extension tubing and is progressively
withdrawn while applying slight suction (Fig
14a). Once blood return is observed, a small
Figure 15. Venous malformation of the elbow. Direct phlebogram demonstrates a venous malformation
with a cavitary pattern.
amount of low-osmolarity iodinated contrast material is injected to obtain a phlebogram (Fig
14b).
Three different phlebographic patterns can be
observed with venous malformation opacification.
The most common of these is a cavitary pattern
with late venous drainage without evidence of
abnormal veins (Fig 15), the second is a spongy
RG f Volume 21
●
Number 6
Dubois et al
1529
Figure 16. Venous malformation of the right thigh.
Direct phlebogram demonstrates a venous malformation with a spongy pattern.
Figure 18. Venous malformation of the anterior
portion of the elbow. Peripheral phlebogram demonstrates a malformation and its venous drainage.
pattern with small “honeycomb” cavities and late
venous drainage (Fig 16), and the third is rapid
opacification of dysmorphic veins (Fig 17).
Peripheral Phlebography
In most cases, peripheral limb phlebography is
not helpful in the diagnosis of venous malformations of the upper or lower limbs because most of
these malformations will not demonstrate opacification. In cases of venous malformations composed of dysmorphic veins, peripheral phlebography is helpful in demonstrating the venous drainage of the malformation (Fig 18).
Arteriography
Arteriography is usually not required for the diagnosis of venous malformations. Findings can be
normal or demonstrate dysmorphic veins in the
late venous opacification phase. Arteriography
may be useful in cases of complex malformations
such as capillary-venous malformations or in
Figure 17. Venous malformation of the hand.
Direct phlebogram demonstrates a venous malformation with dysmorphic veins and early drainage.
1530
November-December 2001
RG f Volume 21
●
Number 6
Figure 19. Complex venous malformation of the temporal area. (a) External carotid angiogram demonstrates progressive filling of venous structures. (b) Delayed-phase angiogram shows stagnation of the
contrast material in the venous lakes. Because no washout of the dysmorphic veins was observed, the
term microfistula is probably not appropriate. This malformation demonstrated high venous flow at
Doppler US. Arterial embolization was performed to decrease the flow, followed by direct embolization
with alcohol.
demonstrating microfistulas (Fig 19). The pathophysiology and clinical significance of these microfistulas are unclear.
Treatment
Medical Treatment
Lower-extremity venous malformations should
first be treated with elastic stockings. Low doses
of aspirin seem to minimize phlebothromboses.
Preoperative control of intravascular coagulopathy with heparin should be considered before the
resection of large venous malformations (3).
Sclerotherapy
Treatment of venous malformations is indicated
when they cause aesthetic problems, pain, or
functional problems. Absolute ethanol is the most
commonly used agent (9). Alcoholic solution of
zein (Ethibloc; Ethicon, Norderstedt, Germany),
a mixture of zein (a corn protein), alcohol, and
contrast medium, is commonly used in Europe
(10). The main drawback of this agent is its propensity to induce cutaneous fistulization with extrusion of the agent. In cases involving very superficial cutaneous or oromucosal lesions, sodium
tetradecyl sulfate is preferred to minimize the risk
of superficial necrosis.
Sclerotherapy should be performed under fluoroscopic control by a skilled interventional radiologist. The amount of sclerosing agent required
is evaluated with percutaneous phlebography. It is
important to avoid filling drainage veins with the
sclerosing agent. A tourniquet or manual compression is useful in minimizing passage of the
sclerosing agent into the systemic circulation.
The main complications of sclerotherapy are
cutaneous necrosis and neural toxicity, especially
with alcohol. Systemic complications are rare and
are related to the passage of alcohol into the systemic circulation. These include hemolysis with
potential renal toxicity and cardiac arrest.
Sclerotherapy induces an inflammatory reaction that will worsen the symptoms during the
week following intervention. Analgesics and antiinflammatory agents (nonsteroidal anti-inflam-
RG f Volume 21
●
Number 6
matory agents or corticoids) must be given to
minimize the symptoms. There should be a time
delay of 1–3 months between each sclerotherapy
session.
Venous anomalies have a propensity for recanalization and recurrence (11). We have observed
better results with sclerotherapy in cases involving
cavitary lesions and dysmorphic vein patterns,
although the latter are more prone to recurrence.
Spongy patterns, especially when they are intramuscular, are more difficult to treat.
Because of the significant inflammatory reaction that follows sclerotherapy, it is recommended
that a control MR imaging examination not be
performed until 6 months after the last session.
Surgical Resection
Surgery is generally contemplated after sclerotherapy when treatment is incomplete or when an
aesthetic prejudice requires correction.
Laser Therapy
Laser therapy can be useful in very superficial
forms of venous malformations and in oromucosal lesions. Photocoagulation can be performed
with argon, yellow dye, or a neodymium yttrium
aluminum garnet laser. For deeper lesions, laser
probes can be inserted subcutaneously. Satisfactory results with minimal scarring have been reported (12), but recurrences and repeated treatments are common.
Summary
Venous malformations are relatively easy to recognize. Radiologists play a key role in avoiding
inappropriate treatment of these lesions. The first
rule is to refer to a proper classification scheme
for vascular anomalies and avoid the use of false
generic terms such as hemangioma (which is not
seen in adult patients). Absence of flow or lowvelocity venous flow is observed at Doppler US.
MR imaging is very useful in assessing the extension of venous malformations. These lesions are
usually hypointense on T1-weighted images and
markedly hyperintense on T2-weighted images.
Gadolinium enhancement is present but variable.
Direct phlebography is useful in confirming the
diagnosis and excluding other soft-tissue tumors.
Dubois et al
1531
Three distinct phlebographic patterns (cavitary,
spongy, dysmorphic) have been identified. Conservative treatment is recommended in most
cases. In cases of functional impairment or significant aesthetic prejudice, sclerotherapy with or
without surgery is useful even if recurrences are
frequent.
References
1. Mulliken JB, Glowacki J. Hemangiomas and vascular malformations in infants and children: a classification based on endothelial characteristics.
Plast Reconstr Surg 1982; 69:412– 422.
2. Enjolras O. Classification and management of the
various superficial vascular anomalies: hemangiomas and vascular malformations. J Dermatol
1997; 24:701–710.
3. Mulliken JB, Fishman SJ, Burrows PE. Vascular
anomalies. Curr Probl Surg 2000; 37: 517–584.
4. Boon LM, Mulliken JB, Vikkula M, et al. Assignment of a locus for dominantly inherited venous
malformations to chromosome 9p. Hum Mol
Genet 1994; 3:1583–1587.
5. Boon LM, Brouillard P, Irrthum A, et al. A gene
for inherited cutaneous venous anomalies (“glomangiomas”) localizes to chromosome 1p21-22.
Am J Hum Genet 1999; 65:125–133.
6. Trop I, Dubois J, Guibaud L, et al. Soft-tissue venous malformations in pediatric and young adult
patients: diagnosis with Doppler US. Radiology
1999; 212:841– 845.
7. Paltiel HJ, Burrows PE, Kozakewich HP, Zurakowski D, Mulliken JB. Soft-tissue vascular
anomalies: utility of US for diagnosis. Radiology
2000; 214:747–754.
8. Li W, David V, Kaplan R, Edelman RR. Threedimensional low dose gadolinium-enhanced peripheral MR venography. J Magn Reson Imaging
1998; 8:630 – 633.
9. Dubois JM, Sebag GH, De Prost Y, Teillac D,
Chrétien B, Brunelle FO. Soft-tissue venous malformations in children: percutaneous sclerotherapy
with Ethibloc. Radiology 1991; 180:195–198.
10. Berenguer B, Burrows PE, Zurakowski D, Mulliken JB. Sclerotherapy of craniofacial venous malformations: complications and results. Plast Reconstr Surg 1999; 104:1–11.
11. De Lorimier AA. Sclerotherapy for venous malformations. J Pediatr Surg 1995; 30:188 –193.
12. Derby LD, Low DW. Laser treatment of facial
venous vascular malformations. Ann Plast Surg
1997; 38:371–378.
This article meets the criteria for 1.0 credit hour in category 1 of the AMA Physician’s Recognition Award. To obtain
credit, see www.rsna.org/education/rg_cme.html.