Version May 2024
INTRODUCTION — Capillary malformations (also called port wine birthmarks or nevus flammeus, MIM #163000) are congenital low-flow vascular malformations of dermal capillaries and postcapillary venules. They are most often isolated skin anomalies but may rarely occur as part of complex malformation syndromes. (See 'Associated syndromes' below.)
Capillary malformations are present at birth as blanchable, pink to red patches and may be located anywhere on the body, typically with a unilateral or segmental distribution that respects the midline. They should not be confused with infantile hemangiomas, common vascular tumors of infancy that only in a minority of cases are present at birth. In contrast with infantile hemangiomas, capillary malformations do not regress with time but grow in proportion to the child's growth and become thicker and darker in color during adulthood. (See "Infantile hemangiomas: Epidemiology, pathogenesis, clinical features, and complications".)
The pathogenesis, clinical presentation, and associated syndromes of capillary malformations will be discussed here. Laser treatment of capillary malformations is discussed separately. An overview of vascular lesions in newborns and venous malformations are also discussed separately.
●(See "Vascular lesions in the newborn".)
●(See "Venous malformations".)
EPIDEMIOLOGY — In a prospective study and literature review, capillary malformations occurred in 0.1 to 2 percent of newborns without sex predilection [1]. They are generally sporadic, but familial cases have been reported [2-4].
PATHOGENESIS — The etiology and pathogenesis of capillary malformations are unknown. Several mechanisms may be involved in their development, including vascular ectasia, lack of neuronal control of blood flow, overexpression of vascular endothelial growth factor (VEGF) and VEGF receptor, and development of compensatory, collateral passageways for venous drainage [5-7].
In a genome-wide study, a specific somatic mosaic activating mutation in the GNAQ gene on chromosome 9q21,2, encoding the guanine nucleotide binding protein G-alpha-q, was found in skin samples of 12 of 13 participants with nonsyndromic port wine birthmarks and in skin or brain samples of 23 of 26 participants with Sturge-Weber syndrome (a rare congenital disorder characterized by facial capillary malformation and capillary-venous malformations affecting the brain and eye) but in none of six control subjects [8]. This mutation (c.548G→A, resulting in the p.Arg183Gln amino acid substitution) may be involved in abnormal cell proliferation through the activation of the extracellular signal-regulated kinase (ERK) pathway. (See "Sturge-Weber syndrome".)
Nonsyndromic port wine birthmarks may represent a late origin of the somatic GNAQ mutation in vascular endothelial cells, whereas in Sturge-Weber syndrome mutation may occur earlier during embryogenesis in progenitor cells that are precursors to a larger variety of cell types and tissues, leading to the syndromic phenotype.
Inactivating mutations in the RASA1 gene, which cause the autosomal dominant capillary malformation-arteriovenous malformation syndrome, may be involved in hereditary cases of capillary malformations without arteriovenous malformations [2,9]. The RAS gene family encodes membrane-associated proteins that are involved in the control of cell proliferation and differentiation and organization of endothelial cells into highly organized networks [10].
PATHOLOGY — Histologic examination of port wine birthmarks reveals ectatic capillaries and postcapillary venules in the papillary and reticular dermis. The number of vessels is not increased and there is no endothelial proliferation. Later-stage lesions develop progressive fibrosis around the vessels and dilatation of the channels. Decreased nerve density has been demonstrated within affected areas [5,11].
CLINICAL FEATURES
Clinical presentation — Capillary malformations are present at birth as partially or completely blanchable, pink to red or reddish-brown patches, with unilateral or segmental distribution that respects the midline (picture 5B). Lesions are flat, painless, and the same temperature as surrounding skin.
The face is a common location, but capillary malformations can occur anywhere on the body (picture 1). On the face, they tend to follow the distribution of the trigeminal nerve branches (segments V1 [ophthalmic], V2 [maxillary], and V3 [mandibular]) (picture 5C and figure 1). It has also been suggested that the pattern of capillary malformations may correspond to areas of somatic mosaicism or follow the embryonic vasculature [12,13]. Facial lesions may extend into the mucosal surfaces of the lips and gingivae.
In most cases, capillary malformations are isolated cutaneous anomalies. However, they may be associated with other abnormalities (eg, glaucoma and occult spinal dysraphism) or be a component of complex malformation syndromes (eg, Sturge-Weber or Klippel Trenaunay syndrome). (See 'Associated abnormalities/complications' below and 'Associated syndromes' below.)
Clinical course — Capillary malformations do not regress over time but grow proportionally with the child's growth. Untreated lesions may become thicker, darker in color (port wine), and nodular in adulthood (picture 2).
Associated abnormalities/complications
Glaucoma — In a retrospective study of 216 children with periocular capillary malformations, 18 percent had glaucoma at presentation or developed glaucoma during a median follow-up of three years [14]. Glaucoma was more common in patients with bilateral port wine birthmarks or involvement of the upper and lower eyelids (distribution areas of V1 and V2 trigeminal branches). A higher prevalence of glaucoma of 40 to 60 percent has been reported in case series of patients with facial capillary malformations associated with Sturge-Weber syndrome [15,16]. Early-onset glaucoma occurs before age four and causes eye enlargement (buphthalmos), whereas late-onset glaucoma may be delayed until adolescence and is not associated with buphthalmos [17]. (See "Overview of glaucoma in infants and children", section on 'Secondary glaucoma'.)
In patients with facial capillary malformation and glaucoma, brain imaging studies are recommended to exclude leptomeningeal involvement and Sturge-Weber syndrome. (See "Sturge-Weber syndrome", section on 'Diagnosis'.)
Occult spinal dysraphism — The association between isolated capillary malformations located over the lumbar spine and spinal dysraphism is controversial [18-21]. However, imaging studies to rule out occult spinal dysraphism are recommended when capillary malformations occur in conjunction with other cutaneous abnormalities (eg, hypertrichosis, dermal sinus or pit, lipomas, or deviated gluteal cleft) in the midline lumbosacral area. (See "Closed spinal dysraphism: Pathogenesis and types".)
Soft tissue and bone overgrowth — Soft tissue and/or bone overgrowth are complications of capillary malformations. Maxillary bone and gingival hyperplasia, lip enlargement, and abnormal bite may occur with facial capillary malformations in the V2 distribution [22]. Overgrowth of digits or limbs also may occur with reticulated or extensive lesions localized to the limbs. [23]
Thickening and nodularity — In large case series, skin thickening or "cobblestoning" with nodular growths within the capillary malformation occurs in up to 65 percent of lesions, especially within those located on the face (picture 3) [24-26]. On histologic examination, most nodules are pyogenic granulomas (picture 4), arteriovenous malformations, or vascular ectasias [27-31]. Easy bleeding within these lesions is common.
Early treatment may prevent thickening and development of nodularity. (See "Laser and light therapy for cutaneous vascular lesions", section on 'Capillary malformations (port wine birthmarks)'.)
DIAGNOSIS
Clinical — The diagnosis of capillary malformations is in most cases clinical and based upon the appearance, time of onset, and temporal evolution of the skin lesion:
●In newborns and children, blanchable, pink to reddish patches, often with unilateral distribution and midline demarcation (picture 5A-C); in adults, red to purple plaques with "cobblestoning" and nodular growths (picture 3). Soft-tissue and bone overgrowth may be noted in children and adults. (See 'Clinical features' above.)
●Presence at birth without regression over time.
●Growth in proportion to body growth; hyperplastic changes of the skin and underlying tissues over time in untreated lesions. (See 'Clinical course' above.)
Imaging studies — Imaging studies (ultrasonography or magnetic resonance) are not routinely performed in children with capillary malformations. However, imaging studies may be necessary in the evaluation of associated syndromes including:
●In children with facial capillary malformation involving more than one trigeminal segment (figure 1) or with neurologic symptoms and in those with facial capillary malformation and glaucoma, magnetic resonance imaging (MRI) of the brain is indicated to exclude Sturge-Weber [17,32,33]. (See "Sturge-Weber syndrome", section on 'Diagnosis'.)
●In children with symptomatic capillary malformations (warm to the touch or painful), ultrasonography can identify venous varicosities associated with Klippel-Trenaunay syndrome (KTS) or exclude an associated fast-flow arteriovenous malformation. (See 'Klippel-Trenaunay syndrome' below and "Klippel-Trenaunay syndrome: Clinical manifestations, diagnosis, and management" and 'Capillary malformation-arteriovenous malformation syndrome' below.)
●MRI or computed tomography to exclude occult spinal dysraphism in children with midline lumbosacral capillary malformations associated with other cutaneous abnormalities (eg, hypertrichosis, dermal sinus or pit, lipomas, or deviated gluteal cleft). (See 'Occult spinal dysraphism' above.)
DIFFERENTIAL DIAGNOSIS — The differential diagnosis of capillary malformations includes:
●Nevus simplex – Nevus simplex, also called salmon patch or stork bite, is a common birthmark occurring in up to 80 percent of newborns [1]. It is similar in appearance to capillary malformations but has more indistinct borders and is usually located in the midline. The most common locations are the glabella, upper eyelids, and nape of the neck (picture 6), but they can also be present in other locations including the forehead (picture 7), nose, upper and lower cutaneous lip, philtrum, scalp, and the upper, mid, and lower back [34]. Unlike capillary malformations, these lesions (with the exception of those located on the nape of the neck) fade spontaneously over time. (See "Vascular lesions in the newborn", section on 'Nevus simplex (macular stain)'.)
●Infantile hemangioma – In approximately one-third of cases, infantile hemangioma is present at birth as a macular telangiectatic patch similar in appearance to a capillary malformation (picture 8). Hemangiomas with this presentation often have surrounding pallor representing vasoconstriction, which can help to differentiate them from capillary malformations early on. However, in contrast with capillary malformations, hemangiomas quickly begin to develop small vascular blebs and become raised (picture 9). (See "Infantile hemangiomas: Epidemiology, pathogenesis, clinical features, and complications".)
●Arteriovenous malformation – Arteriovenous malformations may present as macular vascular birthmarks (picture 10C). However, they are often warm to the touch, and a thrill may be felt on palpation. A distinguishing feature on dermoscopy may be reticular pigmentation with reticular vessels seen in arteriovenous malformations but not in capillary malformations [35]. Over time, arteriovenous malformations become progressively raised and develop a deep component (picture 10A-B). (See "Arteriovenous malformations of the extremities".)
●Linear scleroderma – Linear scleroderma (morphea) of the face, particularly the "en coup de sabre" form, may rarely present at birth as an erythematous patch and mimic a capillary malformation (picture 11A) [36,37]. Over time, these lesions develop induration and atrophy typical of scleroderma (picture 11B). (See "Juvenile localized scleroderma".)
INDICATIONS FOR REFERRAL — Neonates presenting with a capillary malformation involving the upper and lower eyelids and the frontotemporal region (V1 and V2 segments) should be referred for ophthalmologic examination to rule out glaucoma. (See 'Glaucoma' above.)
Children with a facial capillary malformation and neurologic symptoms, particularly seizures, should be referred for neurologic examination and neuroimaging studies to exclude Sturge-Weber syndrome. (See "Sturge-Weber syndrome", section on 'Diagnosis'.)
TREATMENT — Capillary malformations may be disfiguring and a source of significant psychologic stress for patients [38]. The goals of treatment are cosmetic improvement (reduction of skin redness) and prevention of complications (eg, thickening, nodularity, or bleeding) [39-42].
Pulsed dye laser (PDL) therapy is considered the standard of care for the treatment of capillary malformations [43]. It is based on the concept of selective photothermolysis with oxyhemoglobin as the target [44]. PDL treatment irreversibly damages the capillary vessel wall with minimal damage to the overlying epidermis, which leads to lightening of the port wine birthmark without scarring [45]. (See "Laser and light therapy for cutaneous vascular lesions", section on 'Capillary malformations (port wine birthmarks)'.)
Lesions may recur after treatment. In a 10-year follow-up study of 51 patients treated with PDL for port wine birthmarks, lesions were significantly darker at follow-up than at the time of the last treatment [46]. However, treated lesions remained significantly lighter than they were prior to the start of treatment, supporting the existence of long-lasting, beneficial effects of treatment.
The efficacy of PDL is supported by several uncontrolled studies:
●In a retrospective study of 197 patients, the mean age at time of first treatment was 3.4 months [47]. After an average of 9.8 treatments, 26 percent achieved 100 percent clearance, and an additional 41 percent achieved 76 to 99 percent clearance. None of the patients experienced permanent pigment change or scarring. Of note, all patients were treated without topical or general anesthesia.
●In a retrospective study of 49 infants ≤6 months of age, treatment with a 595 nm PDL with dynamic cooling led to an average percentage of lesion clearance of 89 percent. No patients developed atrophy or scarring [48].
●In a prospective study of 12 children ages 6 to 30 weeks treated with PDL, 10 had greater than 50 percent lightening of port wine birthmarks after 2.9±1.4 treatments [49]. No patients experienced scarring, atrophy, or dyspigmentation.
PDL therapy for capillary malformations is reviewed in detail separately. (See "Laser and light therapy for cutaneous vascular lesions", section on 'Capillary malformations (port wine birthmarks)'.)
ASSOCIATED SYNDROMES
Sturge-Weber syndrome — Sturge-Weber syndrome (SWS) is a rare congenital disorder characterized by the classic triad of facial port wine birthmark, leptomeningeal angiomatosis, and ocular involvement. The capillary malformation associated with SWS usually occurs in the distribution area of the ophthalmic and/or maxillary branch (segments V1/V2) of the trigeminal nerve (figure 1), involves both the upper and lower eyelids, and is often bilateral [50]. The discovery of the somatic mutation in GNAQ associated with SWS has raised the hypothesis of somatic mosaicism in SWS [8]. In a multicenter prospective study of 66 infants with upper facial port wine birthmarks larger than 1 cm2 located in the ophthalmic division (figure 1) of trigeminal nerve distribution, 11 (17 percent) were diagnosed with SWS [12]. Hemifacial and median (including median linear) distribution pattern were associated with a high risk of SWS.
Mutations in GNA11 have also been reported in several cases of SWS with distinct characteristics [51,52]. These patients have the typical, large, facial capillary malformation and glaucoma but have less severe neurologic symptoms. A distinguishing feature in this phenotype is diffuse, reticulated capillary malformations of the trunk and limbs with associated hyper- or hypotrophy.
The clinical features, diagnosis, and treatment of SWS are discussed in detail separately. (See "Sturge-Weber syndrome".)
Klippel-Trenaunay syndrome — Klippel-Trenaunay syndrome (KTS) is characterized by capillary malformations, venous and lymphatic malformations, and soft tissue and bone hypertrophy involving a limb [53,54]. The lower limbs, sometimes with extension to the trunk, are more frequently involved than the upper limbs.
The capillary malformations are present at birth as extensive, geographic patches located on the trunk or extremity (picture 12). Limb hypertrophy, resulting from soft tissue and bone overgrowth and underlying lymphatic abnormalities, may be apparent at birth or may develop later and progress until the end of puberty (picture 13). KTS is caused by somatic mutations in the PIK3CA gene [55].
The pathogenesis, diagnosis, and management of KTS are discussed in detail separately. (See "Klippel-Trenaunay syndrome: Clinical manifestations, diagnosis, and management".)
Parkes Weber syndrome — Parkes Weber syndrome is characterized by a large capillary malformation on an extremity; soft tissue and bone hypertrophy of the affected limb; and multiple microscopic, fast-flow arteriovenous shunts. The capillary malformation of Parkes Weber syndrome is indistinguishable from the port wine birthmark seen in KTS. Ultrasonography, MRI, and magnetic resonance arteriography are helpful in differentiating Parkes Weber syndrome from KTS. Parkes Weber syndrome has been associated with germline and somatic variants in RASA1 [56,57] and, in a minority of cases, with germline variants in EPHB4 [58].
Patients with Parkes Weber syndrome have progressive overgrowth of the affected limb and complications related to the arteriovenous shunts, including ulcerations and high-output cardiac failure, especially in the neonatal period. (See "Klippel-Trenaunay syndrome: Clinical manifestations, diagnosis, and management", section on 'Parkes Weber syndrome'.)
Servelle-Martorell syndrome — Servelle-Martorell syndrome is a rare congenital angiodysplastic disease [59]. It manifests with capillary malformations and varicosities similar to KTS but is associated with progressive limb hypotrophy rather than overgrowth.
Proteus syndrome — Proteus syndrome is an extremely rare disorder characterized by asymmetric and disproportionate overgrowth of body parts (picture 14) [60]. Mosaicism for a somatic activating mutation in the AKT1 oncogene is thought to be the cause of Proteus syndrome.
Cutaneous findings are present in approximately 40 percent of neonates and include capillary, lymphatic, or venous malformations; linear and nonlinear epidermal nevi; cerebriform connective tissue nevi; lipomatous tissue overgrowth or lipoatrophy; café-au-lait macules; and nail abnormalities [61]. The vascular malformations are usually extensive, covering a large portion of the body, and may be associated with visceral vascular malformations. Cerebriform epidermal nevi occur predominantly on soles and palms (picture 15). Overgrowth is evident at birth in approximately 20 percent of cases and is asymmetric, disproportionate, and progressive. It may involve many tissues including bone, cartilage, muscle, and connective tissue.
CLOVES syndrome — CLOVES (congenital lipomatous overgrowth, vascular malformations, epidermal nevi, spinal/skeletal anomalies/scoliosis) syndrome is a very rare congenital disorder caused by somatic mosaic activating mutations in the PIK3CA gene [62-64]. (See "Klippel-Trenaunay syndrome: Clinical manifestations, diagnosis, and management", section on 'CLOVES syndrome'.)
Bannayan-Riley-Ruvalcaba syndrome — Bannayan-Riley-Ruvalcaba syndrome, which is incorporated into Cowden syndrome-1 (MIM #158350), is an autosomal dominant disorder caused by mutations in the tumor suppressor gene PTEN [65]. Cutaneous features include capillary, venous, and lymphatic malformations as well as lipomas and pigmented macules on the genitalia. Associated findings include macrocephaly, pseudopapilledema, intellectual disability, and juvenile intestinal polyposis.
Cowden syndrome-1 is discussed separately. (See "PTEN hamartoma tumor syndromes, including Cowden syndrome", section on 'Bannayan-Riley-Ruvalcaba syndrome'.)
Capillary malformation-arteriovenous malformation syndrome — Capillary malformation-arteriovenous malformation (CM-AVM) syndrome is an autosomal dominant disorder characterized by atypical, cutaneous capillary malformations in conjunction with an arteriovenous malformation. It is caused by pathogenic variants in the RASA1 gene (CM-AVM1; MIM #608354) or in the EPHB4 gene (CM-AVM2; MIM #618196) [9,58]. RASA1 encodes a guanine nucleotide-binding protein (p21) involved in the control of cell proliferation and differentiation and organization of endothelial cells into highly organized networks [10]. EPHB4 encodes the ephrin receptor EphB4, a transmembrane tyrosine kinase.
Capillary malformations occur in nearly 100 percent of patients with either CM-AVM1 or CM-AVM2. They are usually multiple round to oval, pink-red or tan patches of 1 to 2 cm in size, sometimes with a pale halo, scattered randomly on the body (predominantly on the face and limbs). New lesions may continue to appear throughout childhood.
Fast-flow arteriovenous malformations have been reported in approximately 30 and 20 percent of patients with CM-AVM1 and CM-AVM2, respectively [58,66]. They can be located in the soft tissues, muscles, bones, brain, or spine [67,68]. Arteriovenous malformations in the central nervous system are more common in CM-AVM1 than in CM-AVM2 (10 versus 3 percent, respectively). Of note, vein of Galen aneurysmal malformations have been reported in CM-AVM2 [58].
Approximately 8 percent of patients have a Parkes Weber syndrome phenotype (see 'Parkes Weber syndrome' above). Other clinical findings include telangiectasias, lymphatic malformations, and cardiac failure due to volume overload [66].
In patients with clinical findings that suggest CM-AVM syndrome, genetic testing for a heterozygous pathogenic variant in RASA1 or EPHB4 is necessary to confirm the diagnosis.
Macrocephaly-capillary malformation syndrome — Macrocephaly-capillary malformation (M-CM) syndrome (previously named macrocephaly-cutis marmorata telangiectatica congenita) is a genetic syndrome characterized by an enlarged head circumference and patchy, reticular capillary malformations [69-71]. It is caused by mutations in the PIK3CA gene, leading to gain of function and activation of the PI3K-AKT pathway, which is involved in cell growth, proliferation, survival, and apoptosis [72,73].
The diagnosis is based upon the presence of two major clinical criteria and at least two minor criteria.
Major criteria are:
●Macrocephaly
●Capillary malformation
Minor criteria are:
●Asymmetry or overgrowth
●Developmental delay
●Hypotonia
●Syndactyly or polydactyly
●Frontal bossing
●Hydrocephalus
●Connective tissue abnormalities such as joint hypermobility or hyperelastic skin
●Midline facial nevus simplex
The capillary malformations are usually reticulated and widespread on the trunk and extremities. Cardiac abnormalities including aortic coarctation have also been described [74,75]. Neuroimaging findings include white matter abnormalities, ventriculomegaly, cerebral asymmetry, cortical dysplasia, polymicrogyria-like changes, and cerebellar tonsil herniation [76].
Microcephaly-capillary malformation syndrome — Microcephaly-capillary malformation (MIM #614261) is an autosomal recessive syndrome due to mutations in the STAMBP gene on chromosome 2p13.1, encoding a deubiquitinating enzyme [77-80]. It presents with:
●Severe progressive microcephaly
●Diffuse small capillary malformations of the skin
●Profound global developmental delay
●Severe spastic quadriparesis
●Neonatal-onset intractable epilepsy
●Hypoplastic distal phalanges
●Poor growth
The capillary malformations range in size from 2 to 15 mm and are scattered on the trunk, extremities, and head. Minor heart malformations, including small atrial and ventricular septal defects, have also been reported [78]. Neuroimaging findings include diffusely reduced number of gyri with shallow sulci consistent with a severe simplified gyral pattern, and moderately enlarged extra-axial space [78].
Beckwith-Wiedemann syndrome — Beckwith-Wiedemann syndrome is a congenital overgrowth syndrome with major features including anterior abdominal wall defects, macroglossia, gigantism, and a propensity to develop specific tumors (hepatoblastoma, Wilms tumour, neuroblastoma, and rhabdomyosarcoma) [81,82]. Infants have centrofacial capillary malformations similar to nevus simplex in the majority of cases. Vascular lesions may extend to the upper eyelids, upper lip, and nose. Characteristic-associated findings are an anterior ear lobe crease and posterior helical ear pits.
Beckwith-Wiedemann syndrome is discussed separately. (See "Beckwith-Wiedemann syndrome".)
Phakomatosis pigmentovascularis — Phakomatosis pigmentovascularis is a syndrome associated with mosaic activating variants of the GNA11 and GNAQ genes and is characterized by the association of a widespread capillary malformation with pigmented lesions including dermal melanocytosis, nevus spilus, mosaic hyperpigmentation, and epidermal nevus [83]. Nevus anemicus and café-au-lait spots can be associated findings. Extracutaneous findings include visceral, muscular, neurologic, or ocular abnormalities.
Five types of phakomatosis pigmentovascularis have been identified based upon the type of pigmented lesion associated with the capillary malformation; for each type, subtype "a" denotes absence and subtype "b" presence of extracutaneous findings (table 1) [84-86]. (See "Vascular lesions in the newborn", section on 'Phakomatosis pigmentovascularis'.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Vascular anomalies".)
SUMMARY AND RECOMMENDATIONS
●Clinical presentation – Capillary malformations (port wine birthmarks or nevus flammeus) are low-flow vascular malformations of dermal capillaries and postcapillary venules that are present at birth. Characteristic clinical features include blanchable, pink to red patches located anywhere on the body (picture 1), typically with a unilateral or segmental distribution that respects the midline (picture 5A-C). On the face, capillary malformations tend to follow the distribution of the trigeminal nerve branches (picture 5C and figure 1). (See 'Clinical presentation' above.)
●Clinical course – Lesions do not regress spontaneously and, if left untreated, may become thicker, darker in color (port wine), and nodular in adulthood (picture 3). (See 'Clinical course' above.)
●Diagnosis – The diagnosis of capillary malformations can be made with a history and examination in patients with characteristic clinical features (picture 5A-C). Imaging studies (ultrasonography or magnetic resonance) may be necessary in the evaluation of associated syndromes or abnormalities. (See 'Diagnosis' above.)
●Differential diagnosis – The differential diagnosis of capillary malformations includes nevus simplex (salmon patch or stork bite) (picture 7), infantile hemangioma (picture 9), arteriovenous malformation (picture 10A-C), and linear scleroderma (picture 11A-B).
●Treatment – For children and young patients with capillary malformations who desire treatment, we suggest treatment with pulsed dye laser (PDL) over other lasers as first-line treatment (Grade 2C). PDL therapy for capillary malformations is discussed in detail separately. (See "Laser and light therapy for cutaneous vascular lesions", section on 'Capillary malformations (port wine birthmarks)'.)
●Associated syndromes – In most cases, capillary malformations are isolated cutaneous anomalies. However, they may be associated with other abnormalities (eg, glaucoma and occult spinal dysraphism) or be a component of complex malformation syndromes (eg, Sturge-Weber or Klippel Trenaunay syndrome). (See 'Associated abnormalities/complications' above and 'Associated syndromes' above.)
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