VASCULAR SURGERY e I
Vascular anomalies
Vimal J Gokani
Branavan Sivakumar
Loshan Kangesu
Abstract
Vascular anomalies are vascular lesions that are present from child-
hood. They are classified into tumours or malformations based on clin-
ical and histological features. Benign infantile haemangiomas are the
most common vascular tumour and have a predictable self-limiting
course. Rarer vascular tumours exist, and some may cause platelet
consumption. Management is usually conservative, with active treat-
ment reserved for functional or cosmetic complications (ulceration,
or obstruction and distortion of vital structures). Oral propranolol is
useful for troublesome lesions.
Vascular malformations are structural anomalies of vascular morpho-
genesis present at birth without cellular proliferation that, in general,
grow with the patient. They are sub-classified by vessel type as ‘low
flow’ (capillary, lymphatic and venous) and ‘high flow’ (arteriovenous)
or lesions with a combination of vessel type. They become problem-
atic under certain circumstances, usually puberty and also pregnancy.
The most troublesome are extensive lesions, especially venous and
arteriovenous. Their effects may be cosmetic, those of a space-
occupying lesion, infection, bleeding, pain or coagulopathy. Venous
lesions cause consumptive coagulopathy, sometimes with life-threat-
ening risks. Treatment options include medication and symptom con-
trol with antibiotics, analgesia, control of menses, compression
garments and intervention with laser (capillary type), sclerotherapy,
embolization and/or surgical excision. Patients with complex lesions,
are best managed by a multidisciplinary team and all surgical sub-
specialties may be involved.
Keywords Arteriovenous malformations; capillary malformations;
haemangiomas; lymphatic malformations; multidisciplinary team;
vascular anomalies; vascular malformations; venous malformations
Introduction
Vascular anomalies are vascular lesions of childhood that result
from abnormal cell proliferation (tumours) or abnormal cell ar-
chitecture (malformations) of vascular endothelia. They may
affect any organ and traverse tissue planes. They were classified
Vimal J Gokani MSc(Dist) MRCS MFSTEd is a Specialist Registrar in
Plastic Surgery at Imperial Healthcare Trust, London, UK. Conflicts of
interests: none declared.
Branavan Sivakumar BSc MD(Res) FRCS(Plast) is a Consultant Plastic
Surgeon at Great Ormond Street Hospital and the Royal Free
Hospital Foundation NHS Trust, London, UK. Conflicts of interests:
none declared.
Loshan Kangesu MS FRCS(Plast) is a Consultant Plastic Surgeon at St
Andrews Centre for Plastic Surgery, Mid Essex Hospitals NHS Trust,
And Great Ormond Street Hospital, London, UK. Conflicts of
interests: None declared.
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by Mulliken and Glowacki in 1982 into infantile haemangiomas
(vascular tumours) and vascular malformations, based on clin-
ical and histological characteristics.1 The International Society
for the Study of Vascular Anomalies (ISSVA) is now a large body
of clinicians and scientists at which the latest research and
treatments are presented. ISSVA modified the terms to tumours
and malformations in 1996. This simple structure for classifica-
tion was suitable for over 90% of lesions (Figure 1). The clas-
sification is now more comprehensive, includes malignant
lesions, and assimilates knowledge about genetic defects asso-
ciated with some of these lesions (2014) (Table 1).2 It is regularly
updated online (see http://www.issva.org/).
Vascular anomaly assessment is based on clinical features and
special investigations such as duplex ultrasound (DUS),
gadolinium-enhanced magnetic resonance imaging (MRI) and
histology. Angiography is only needed during treatment (i.e.
embolization), rather than for diagnosis.
Complex lesions should be managed by a multidisciplinary
team (MDT) including surgeons (of all disciplines), interven-
tional radiologists, dermatologists, paediatricians and histopa-
thologists. Specialist nurses are invaluable in supporting parents,
and parent support groups are important. Lesions vary in size
from isolated small anomalies to complex lesions, with second-
ary effects that cause significant morbidity and even mortality.
Much of the management is supportive with the emphasis on
disease control rather than cure.
Vascular tumours
The majority of vascular tumours are benign. Malignant tu-
mours, like angiosarcoma, may occur in infants. More details
were described previously.3
Infantile haemangiomas
Ninety-five per cent of vascular tumours are infantile hae-
mangiomas. These benign, self-limiting vascular tumours have
been called ‘strawberry naevae’. They are more common in
Caucasians and are the most frequent tumours of infancy,
affecting 10% of full-term babies and have up to a 20% incidence
in prematurity.4 There is a female predominance of 2:1 but
higher rates have been reported. There is a predilection for the
Simple classification of vascular anomalies into
tumours and malformations
Vascular anomalies
Vascular tumours Vascular malformations
Infantile haemangioma (95%) Slow flow
Venous (VM)
Lymphatic (LM)
Capillary (CM)
Fast flow
Arteriovenous (AVM)
Combined
Figure 1
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 VASCULAR SURGERY e I

The 2014 ISSVA classification for vascular anomalies

Vascular tumours
Simple Combined Malformaons associated with other anomalies (<5% of cases)
Klippel-Trenaunay syndrome CM + VM +/- LM + limb overgrowth (PIK3CA)
Benign Slow Flow Combined channel Parkes Weber syndrome CM + AVF + limb overgrowth (RASA1)
Capillary (CM) Servelle-Martorell syndrome limb VM + bone undergrowth
Congenital haemangioma Venous (VM) e.g.: Sturge-Weber syndrome facial + leptomeningeal CM + eye anomalies
CVM
CLM Limb CM + congenital non-progressive limb hypertrophy
High Flow LVM Maffucci syndrome VM +/- spindle-cell hemangioma + enchondroma (IDH1/2)
Arteriovenous CAVM Macrocephaly - CM (M-CM / MCAP) (PIK3CA)
Others Others Microcephaly - CM (MICCAP) (STAMBP)
Locally aggressive or borderline (AVM) CLOVES syndrome LM + VM + CM +/- AVM + lipomatous overgrowth (PICK3CA)
Proteus syndrome
Kaposiform haemangioendothelioma Arteriovenous
(AKT1)
Kaposi sarcoma fistula Bannayan-Riley-Ruvalcaba syndrome AVM + VM +macrocephaly,
Others (AVF) lipomatous overgrowth (PTEN)
Malignant CLAPO syndrome lower lip CM, face&neck LM, limb overgrowth (PIK3CA)
Angiosarcoma
Of major named vessels
Others
Associated with other lesions Anomalies of origin [course, number, length, diameter (aplasia, hypoplasia, stenosis, ectasia /
aneurysm), valves]
PHACES syndrome*
Modified from Dasgupta& Fishman, 20142.
supraumbilical raphe

Table 1
head and neck, but this may be due to referral bias, as these are
more visible.
Haemangiomas are usually not present at birth, although a
subtle premonitory red mark (herald patch) may be present.
They are first noticed at about 2 weeks of life and undergo a
three-stage cycle of rapid proliferation, a slow phase of
involution and then leave lifelong residue of a fibrofatty
deposit and attenuated surrounding tissue in the involuted
phase (Figures 2 and 3).5
Most infantile haemangiomas are superficial and managed
conservatively in primary care. The large or dangerous ones may
be referred to dermatology, paediatrics, paediatric surgery or
plastic surgery. Treatment is again mostly expectant. In rare
circumstances, if the diagnosis is uncertain or a differential
diagnosis with malignant lesions is required, a biopsy is indi-
cated with a request for GLUT-1 immunostaining.6 For atypical
haemagiomas a full blood count is done to exclude thrombocy-
topenia (see below). MRI or ultrasound is indicated to look for
internal lesions if there are 8 or more skin lesions in order to
predict the likelihood of cardiac failure. Active intervention is
necessary in the presence of complications such as:
 large size or causing disfigurement
 multiple lesions causing high-output cardiac failure
 obstruction of vital structures
 eye, can cause amblyopia and patching may be indicated
 airway, may require urgent ENT intervention (e.g., tra-
cheostomy or excision)
 persistent ulceration.

Figure 2 Infantile haemangioma in the same child showing the different phases: (a) the early proliferating (child aged 3 months); (b) early involuting
(aged 16 months); (c) involuted phase (child aged 4½ years); and (d) following excision of excess skin (aged 12 years). Due to the use pf pro-
pranolol, such extensive proliferation is now seen less frequently.

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 VASCULAR SURGERY e I
A diagrammatic representation of growth patterns of the various types
of haemangioma
NICH
Size
RICH
1st 2nd 3rd
Trimester Birth 1 year 2 years 3 years 4 years 5 years 6 years 7 years
NICH, non-involuting congenital haemangioma;
PICH, partially involuting congenital heamangioma;
RICH, rapidly involuting congenital haemangioma
Adapted from Mulliken & Enjolras 2004
Figure 3
Propranolol (1e2 mg/kg per day in three divided doses) has
replaced prednisolone as systemic therapy to which most pa-
tients respond;7 shared care with a paediatrician is ideal
(Figure 4). Steroid injections (triamcinolone max 1 mg/kg) are
still useful for small, well-circumscribed haemangiomas, where
treatment is indicated.
Other benign vascular tumours
Kaposiform haemagioendothelioma (KHE) is an infantile tumour
that is slightly darker and firmer to touch than an infantile hae-
mangioma.8 It is associated with thrombocytopenia (the
Kasabach-Merrott phenomenon), a potentially life-threatening
complication due to serious bleeding.
Rarely, benign haemangioma may be present at birth, i.e.
‘congenital’. All of the above tumours are negative on Glut-1
staining. They are described by their clinical pattern (Figures 2
and 3), as:
 rapidly involuting congenital haemagioma (RICH)9
 non-involuting haemangioma (NICH)10
 partially involuting congenital haemangioma (PICH).11
Vascular malformations
Vascular malformations are vascular anomalies that, in contrast
to haemangiomas, are present at birth, although some present
later in life. They do not regress, and show normal endothelial
cell mitotic rate unless stimulated, but abnormal vascular
morphology.1 The different types of vascular malformation are
classified according to their flow characteristics and vessel type:
capillary, venous, lymphatic and arterial components, or a
combination of these (Table 1).
Ectatic vessels enlarge from pressure and flow changes. They
are stimulated by hormonal changes, as seen during puberty and
pregnancy. Vascular malformations may be associated with limb
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PICH
Infantile haemangioma
overgrowth, soft tissue and skeletal hypertrophy, obstruction as
space-occupying lesions, or secondary effects such as infection,
bleeding and blood dyscrasia. They present in childhood to
paediatrics, dermatology or surgery (paediatric, plastic, ortho-
paedic and vascular). Adult patients tend to be followed up in
orthopaedic, vascular surgery and plastic surgery clinics. A
multidisciplinary clinic is the ideal.
Interventional radiology (IR) is key to the management of
vascular malformations and may involve percutaneous sclero-
therapy, embolization and endovascular laser therapy. More
complex procedures involve temporary balloons and filters in the
main feeding and draining vessels. Preferred sclerosing agents
are sodium tetradecyl sulphate, bleomycin, doxycycline, ethanol,
Ethibloc (a viscous mixture of propylene glycol, corn protein and
other agents) and polydocanol microfoam. Embolic agents
include ethanol, cyanoacrylate (glue), coils, polyvinyl particles
and Onyx (a liquid ethylene vinyl alcohol copolymer). Emboli-
zation is also an adjunct to excision surgery to reduce the risk of
haemorrhage or distal embolization of thrombi.
Complications of sclerotherapy and embolization include:
 tnecrosis
 extravasation of sclerosant with damage to adjacent tissue
 systemic thrombosis or embolization
 systemic toxicity
 complications from fragmentation of devices (i.e.
catheters).
Capillary malformations
This most common type of vascular malformation is often known
as a ‘port-wine stain’ that affects the skin and occurs in 0.3% of
newborns.12 They present as a macular patch that are pink in
infants, later becoming red and eventually purple in adulthood.
Skin temperature and Doppler signal are largely normal. There is
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 VASCULAR SURGERY e I
Figure 4 A capillary malformation (‘port-wine stain’) of the right side of
the face on a 19-year-old boy. Note the skeletal and soft tissue hy-
pertrophy of the affected area. He had two operations to reduce the
lips in his early teenage years.
secondary tissue hypertrophy, skin nodules and an increased
incidence of pyogenic granuloma. On the face, the distribution
may correspond to the dermatomes of the trigeminal nerve
branches (V1, V2, V3) (Figure 4). Histologically, there are ectatic
capillaries to venule-sized dermal channels. They may be asso-
ciated with syndromes such as Klippel-Trenaunay syndrome
(KTS), Sturge-Weber and Parkes-Weber.
Management is a combination of supportive care, with
involvement of a clinical psychologist where beneficial,
Figure 5 (a & b) Extensive venous malformation extending across the chest, into the axilla, and into the intrathoracic cavity; and (c) venous
malformation of the right side of the tongue, which had been treated once with sclerotherapy.
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camouflage and use of pulse dye laser therapy. Laser therapy can
lighten the colour for a number of years. Surgery may be useful
for reducing hypertrophied areas such as on the lower lip.
Venous malformations
These low-flow lesions are blue, compressible soft tissue masses
that empty on elevation (Figure 5). They can affect most tissues.
Histologically, they are composed of abnormal venous channels
with flat endothelium and normal cellular turnover. They cause
disfigurement and an aching pain, which is thought to be due to
release of mediators from formation and dissolution of thrombus.
In larger lesions, there is a localized intravascular coagulopathy
detected by elevated D-dimer levels as well as low serum
fibrinogen (<1.5 g/L). Extensive lesions have a recognized
mortality from thromboembolism, internal bleeding and
disseminated intravascular coagulopathy (DIC) that may trigger
multi-organ failure. Such patients may paradoxically require
anticoagulation to interrupt the clotting cascade and insertion of
a filter in the inferior vena cava.
Rarely (5%), venous malformations are associated with ge-
netic abnormalities and mutations have been discovered in the
Krit-1, TIE-2 and Glomulin genes.13,14 Blue rubber bleb syndrome
is associated with a sporadic mutation in the TIE-2 gene. It is
characterized by multiple lesions over the skin and gastrointes-
tinal (GI) tract. GI tract lesions cause melaena and chronic
anaemia and are best treated surgically. Mutations in the glo-
mulin gene cause a subtype of venous malformation that is
known as glomangioma where the lesions are dark, tender,
venous nodules characterized at histology by the presence of
smooth muscle-like glomus cells.
The emphasis of management is on symptom control. It is
seldom possible to completely remove these lesions. Compres-
sion garments and non-steroidal anti-inflammatory drugs such as
ibuprofen provide good pain relief. The next line of treatment is
sclerotherapy (i.e. sodium tetradecyl sulphate) carried out under
ultrasound guidance. Repeat sclerotherapy is frequently needed
over the years.
Surgical excision, with preoperative sclerotherapy, has a
lesser role and is complicated by an increased risk of haemor-
rhage that is exacerbated by the consumptive coagulopathy and
poor wound healing. Therefore, it is reserved for a minority of
cases with ongoing functional issues despite conservative mea-
sures and/or interventional radiology treatment. In these cases,
close liaison with haematologists is important as these patients
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 VASCULAR SURGERY e I

Figure 6 Lymphatic malformations: (a) Macrocystic lymphangioma of the neck that respond well to sclerotherapy; and (b) microcystic lesions of
the lip that bled and caused infections and hence the area was excised.

can benefit from preoperative replenishment of low clotting
factors.
Lymphatic malformations
These may be microcystic (as seen in superficial lesions
described as lymphangioma circumscriptum) or macrocystic (as
in the classic neck lesions that were called cystic hygroma), but
combined types also exist (Figure 6). Microcystic lesions appear
as small raised cutaneous vesicles full of lymphatic fluid. Mac-
rocystic lesions are larger, soft subcutaneous swellings that easily
transilluminate (an easy to perform bedside test). Both may be
complicated by infection or intralesional haemorrhage. Histo-
logically, they are composed of abnormal dilated lymphatic
channels without connection to the normal lymphatic system.
The emphasis of treatment is on disease control. Long-term
relief of symptoms can be achieved, unlike in venous lesions.
Microcystic cutaneous lesions are more prone to infections, good
skin care is essential, and sometimes long-term antibiotics are
needed.
Sclerotherapy or surgery is effective for treatment of macro-
cystic lesions and the options are best discussed in a specialist
MDT. The sclerosants that are used are similar to those for
venous malformations. Many lymphatic lesions are mixed with a
fibro-fatty matrix causing a large mass and surgical excision is
the ideal treatment. The most common postoperative complica-
tions are wound seroma and secondary infection. Postoperative
pressure garments and suction drains help reduce these
problems.
Arteriovenous malformations (AVM)
These are the most aggressive vascular malformations (AVMs),
causing progressive deformity and posing a systemic risk
(Figure 7). High-flow malformations have a characteristic ‘nidus’
with multiple arterial feeders, arteriovenous fistulas and enlarged
draining veins. These malformations continue to recruit new
vessels and are seldom cured. They may be quiescent at birth,
mimicking innocent lesions such as capillary malformations or
haemangiomas of infancy, but their behaviour is usually
aggressive in later life sometimes triggered by pubertal changes,
pregnancy or trauma. They may present with throbbing pain or
ulceration with bleeding and may cause high-output cardiac
failure. The lesions are warm to touch with a loud Doppler signal
(indicating arterial flow); later stages have a pulsatile mass with
a bruit, overlying purple discolouration and engorged, tortuous
veins.
Cure is seldom achieved. The symptomatic stages may war-
rant treatment with a combination of interventional radiology,
excisional surgery and reconstruction. Some lesions can be

Figure 7 A large arterio-venous malformation of the right buttock in a

15-year-old with ulceration and causing hypotension from shunting. Figure 8 Combined vascular malformation demonstrating features of
This was surgically resected with vascular control using intravascular limb overgrowth and a mixed vessel type lesion with a significant
balloons (with thanks to Dr Alex Barnacle and Dr Derek Roebuck). lymphatic component.

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 VASCULAR SURGERY e I
controlled with repeated embolization. The nidus must be
treated.
Combined lesions
Patients also present with vascular malformations with a mixed
vessel type. These lesions occur either isolated or associated with
overgrowth disorders such as Klippel-Trenaunay syndrome
(Figure 8) and Proteus syndrome. Those affected often have
significant morbidity with heavy, painful areas especially when
involving a limb. They are also troubled by episodes of infection
and ulceration. Life-long care and support are required.
Drug therapy
In the past decade there is interest in sirolimus and other in-
hibitors of the mTOR pathway particular for those combined
lesions associated with overgrowth.15,16
Conclusion
Vascular anomalies are challenging to manage. Advances in
basic science, drug therapy and interventional radiology are
improving our understanding of these lesions and giving hope of
treatment options. Visible and extensive lesions cause consider-
able physical and emotional distress for patients and their fam-
ilies. Large venous lesions carry a significant risk of mortality. It
is important for all doctors to understand this subject and hos-
pital treatment should be planned by a specialist multidisci-
plinary team. A
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15 Al-Olabi L, Polubothu S, Dowsett K, et al. Mosaic RAS/MAPK
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Practice points
C The term vascular anomalies refers to both vascular tumours and
vascular malformations
C Benign, self-limiting, infantile haemangioma is the commonest
vascular tumour and presents soon after birth
C Oral propranolol is used to treat infantile haemangioma that are
causing problems
C Vascular malformations are classified into ‘low flow’, ‘high flow’,
or ‘combined’ types; this is important for management
C Vascular malformations are always present from birth but can
enlarge and cause symptoms especially at puberty or during
pregnancy
C Venous lesions may cause a consumptive coagulopathy by
depleting fibrinogen
C Treatment of vascular malformations is mainly conservative, with
intervention reserved for pain, loss of function, disfigurement,
pressure effects or risk of ulceration
C Sclerotherapy or embolization may be effective in managing
vascular malformations
C Complex lesions are best managed by a specialist multidisci-
plinary team
Acknowledgements
The authors are grateful to Dr Samira Syed and Dr Alex Barnacle and
Dr Derek Roebuck, Great Ormond Street Hospital (GOSH) for the
images in Figures 3 and 7, respectively and all members of the
multidisciplinary vascular anomalies’ teams past and present at both
GOSH and Broomfield Hospital; and the patients and families from
whom we continue to learn.
312 Ó 2021 Published by Elsevier Ltd.