Vascular Lesions: Hemangiomas, Angiokeratoma, Pyogenic Granuloma, Glomus Tumor
Red, blue, and purple lacunae, white septae, ulceration with collarette, and characteristic vascular morphologies define a broad spectrum of benign vascular lesions and the dermoscopic differential against amelanotic melanoma and Kaposi sarcoma.
In brief
Vascular lesions form a heterogeneous group sharing one dermoscopic motif: structureless red, blue, or purple zones organized as discrete lacunae, lakes, or diffuse homogeneous color. The diagnostic challenge is to map the dermoscopic morphology to the histopathologic compartment (capillary, venular, lymphatic, glomus, or reactive proliferation) and to recognize the dangerous mimics (amelanotic melanoma, Kaposi sarcoma, angiosarcoma) that hide within the vascular vocabulary. The most useful clinical-dermoscopic anchors are the depth and color of the vascular spaces, the presence or absence of a whitish veil over the surface, the presence of a peripheral collarette, and the rapidity of growth.
Must-remember points
Clinical content
01Cherry (senile) angioma is the prototypical adult vascular lesion. Multiple bright-red papules develop on the trunk and extremities from the third decade onward, increasing with age. Dermoscopy shows red or red-blue lacunae arranged across a sharply demarcated lesion, often with white septae separating the lacunae. Larger or older cherry angiomas may thrombose and appear blue-purple to black. The differential against angiokeratoma centers on the absence of a whitish veil and the absence of corkscrew vessels in cherry angioma.
02Angiokeratoma encompasses solitary and multiple variants. Solitary angiokeratoma typically arises on the lower extremity as a dark blue-purple to black papule with hyperkeratotic surface. Dermoscopically, blue-purple lacunae predominate, often partially obscured by an overlying whitish veil corresponding to compact orthokeratotic stratum corneum. Corkscrew vessels (looped, twisted vessels visible at the lesion margin or within thinner regions) are characteristic. Black homogeneous areas correspond to thrombosed vessels. The differential against melanoma is real and important: a thrombosed angiokeratoma may show black homogeneous areas, blue color, and irregular borders, all of which can mimic nodular melanoma. The whitish veil, the corkscrew vessels, and the peripheral lacunae favor angiokeratoma.
03Pyogenic granuloma (lobular capillary hemangioma) presents most often on the face, hands, and oral mucosa as a rapidly growing red papule, often ulcerated, sometimes pedunculated, with a peripheral collarette of scale (the white-yellow rim where the surrounding epidermis grows up around the lesion base). Dermoscopy typically shows a homogeneous red structureless area with peripheral white collarette, sometimes with white intersecting lines (white rail lines) corresponding to collagen strands separating tumor lobules, and frequent ulceration. The history of rapid growth (days to weeks) and frequent bleeding with minor trauma raises the diagnosis. The major differential is amelanotic melanoma, which can also present as a rapidly growing pink-red papule with ulceration; the absence of any pigment criterion in pyogenic granuloma and the youth of typical patients lean toward the benign diagnosis, but in adults excision and histology are routine because the cost of misdiagnosis is high.
04Glomus tumor is a rare benign neoplasm of glomus body (specialized arteriovenous shunt) cells, most often subungual, presenting with the classical triad of severe paroxysmal pain, exquisite cold sensitivity, and pinpoint tenderness on the Love test. Dermoscopically, a subungual blue-purple to red discoloration is visible through the nail plate; longitudinal erythronychia (a single red longitudinal nail band) is a recognized clue. Imaging (ultrasound or MRI) confirms the deep vascular tumor before surgery. Multiple glomus tumors (glomangiomas) occur familially, sometimes associated with the GLMN gene. Outside the nail unit, glomus tumors arise on the digits, palms, soles, and rarely deep soft tissue.
05Spider angioma (nevus araneus) presents as a central pulsating arteriole with radiating telangiectatic legs, classically on the face, neck, and upper trunk. Dermoscopy shows the central red dot with branching small vessels. Multiple lesions in adults raise the differential of liver disease, pregnancy, estrogen therapy, or hyperthyroidism. In children, multiple spider angiomas can be physiologic. The differential is rarely difficult: the central pulsating arteriole and radiating pattern are highly characteristic.
06Infantile hemangioma is the most common vascular tumor of infancy, with a phase of rapid postnatal proliferation followed by spontaneous involution. The spectrum includes superficial (strawberry, bright red), deep (blue, soft, compressible), and mixed lesions. Dermoscopy of superficial lesions shows red and red-blue lacunae arranged in lobules with intervening pale septae (lobular pattern). Involuting lesions develop white scar-like areas, fibrofatty residual changes, and persistent telangiectasia. PHACES syndrome (large facial hemangioma plus posterior fossa malformations, hemangioma, arterial anomalies, cardiac defects, eye abnormalities, and sternal cleft) is the most important syndrome to consider when a large segmental hemangioma is present.
07Lobular capillary hemangioma is the histopathologic name for pyogenic granuloma. The term is preferred in pathology because the lesion is neither pyogenic (not infectious) nor a true granuloma. Histopathology shows lobules of capillaries with intervening fibromyxoid stroma, often with surface ulceration and collarette. Recent literature describes intravascular pyogenic granuloma and disseminated pyogenic granuloma as rare variants.
08Vascular malformations differ from hemangiomas biologically. They are present at birth, grow proportionally with the patient, and never involute spontaneously. Capillary malformations (port-wine stain) appear as flat red-purple patches following dermatomal or unilateral patterns; the GNAQ R183Q mutation drives most cases and the recognition has clinical implications (Sturge-Weber syndrome screening with brain MRI in V1 distribution port-wine stains). Venous malformations appear as soft compressible blue lesions; lymphatic malformations show clear or hemorrhagic vesicles (lymphangioma circumscriptum) with characteristic frog-spawn appearance. Arteriovenous malformations are pulsatile, warm, and have a rapid filling pattern. Dermoscopy of capillary malformations shows uniform red coloration with a pebble-like or globular pattern.
09Glomeruloid hemangioma is a rare hemangioma morphologically distinct because of intravascular capillary tufts resembling glomeruli; it is characteristically associated with POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, skin changes). Recognition of multiple glomeruloid hemangiomas should prompt POEMS screening with serum protein electrophoresis and skeletal survey for sclerotic bone lesions.
10The dermoscopic differential against amelanotic melanoma is the most clinically important. Milky-red areas, polymorphic vessels (multiple morphologies in one lesion), and white shiny structures are the melanoma cues that should not appear in benign vascular lesions. Pyogenic granuloma is the single most common amelanotic melanoma mimic in routine practice, and adult-onset rapidly growing red papules should be excised, not monitored, even when pyogenic granuloma is the leading diagnosis. Kaposi sarcoma presents as red-purple to brown macules, plaques, or nodules, often on the lower extremities or in HIV-positive patients on the face; dermoscopy shows the rainbow pattern (multiple colors radiating across the lesion under polarized light) plus polymorphic vascular structures. Angiosarcoma in elderly patients on the scalp and face shows ill-defined erythematous to bruise-like patches that progress to nodules and ulceration; dermoscopy is often non-specific (red-purple structureless areas, white shiny streaks, polymorphic vessels), and any ill-defined bruise on the scalp of an elderly patient deserves biopsy.
Key dermoscopic features
High yield clinical points15 pearls in 4 groups
Recognition & pattern analysis
7 pointsManagement & treatment
2 pointsPitfalls & mimics
3 pointsWhen to biopsy
3 pointsLectures covering this topic7 lectures
Notable updates & conceptual milestones5 updates
Propranolol for infantile hemangioma
2008The serendipitous discovery that systemic propranolol arrests proliferation and accelerates involution of infantile hemangiomas transformed treatment, replacing systemic corticosteroids and surgery as first-line management for problematic lesions.
GNAQ mutations in capillary malformations and Sturge-Weber
2013The 2013 identification of recurrent GNAQ R183Q mutations in port-wine stains and Sturge-Weber syndrome confirmed a unifying somatic mosaic mechanism and opened molecular avenues for targeted therapy.
Rainbow pattern as Kaposi sarcoma marker
2009Cheng's 2009 description of the rainbow pattern under polarized dermoscopy provided a high-specificity dermoscopic marker for Kaposi sarcoma that has since been incorporated into routine vascular-lesion analysis.
GLMN germline mutations in familial glomangiomas
2002Loss-of-function mutations in GLMN underlie autosomal dominant familial glomuvenous malformations (glomangiomas), allowing genetic counseling and screening of affected families.
Polymorphic vessels and milky-red areas as amelanotic melanoma cues
2008Menzies and colleagues defined the dermoscopic vocabulary of amelanotic and hypomelanotic melanoma, establishing polymorphic vessels and milky-red areas as the high-yield melanoma cues that must be excluded in any pink lesion.
Bottom line
Most benign vascular lesions are recognized confidently by lacunae of characteristic color, whitish veil or collarette features, and clinical course (acute growth in pyogenic granuloma, slow accumulation in cherry angioma, congenital persistence in vascular malformation). The clinical anchor is to exclude amelanotic melanoma in any rapidly growing pink-red papule, Kaposi sarcoma in lower-extremity violaceous lesions or HIV-positive patients, and angiosarcoma in elderly patients with progressive scalp or face bruise-like patches.
Molecular characterization of vascular anomalies (GNAQ in capillary malformations, TIE2 in venous malformations, PIK3CA in lymphatic malformations) is enabling precision targeted therapy with mTOR inhibitors and PI3K inhibitors. Beta-blockers for infantile hemangioma will remain standard, but molecular agents will increasingly address malformations that previously required only surgical or laser management.
References
Sources cited in the lecture content or that underpin the clinical points above. Verify with primary sources before practice changes.
- [1]Zaballos P, Daufi C, Puig S, et al. Dermoscopy of solitary angiokeratomas: a morphological study. Arch Dermatol 2007;143:318-325.PubMed: 17372096DOI: 10.1001/archderm.143.3.318· Foundational morphologic study defining the dermoscopic vocabulary of angiokeratoma.
- [2]Zaballos P, Carulla M, Ozdemir F, et al. Dermoscopy of pyogenic granuloma: a morphological study. Br J Dermatol 2010;163:1229-1237.PubMed: 20846306DOI: 10.1111/j.1365-2133.2010.10040.x· Defining series on the collarette, white intersecting lines, and ulceration features of pyogenic granuloma.
- [3]Cheng ST, Ke CL, Lee CH, Wu CS, Chen GS, Hu SC. Rainbow pattern in Kaposi's sarcoma under polarized dermoscopy: a dermoscopic pathological study. Br J Dermatol 2009;160:801-809.PubMed: 19067686DOI: 10.1111/j.1365-2133.2008.08940.x· Original description of the rainbow pattern in Kaposi sarcoma, now incorporated into vascular-lesion analysis.
- [4]Leaute-Labreze C, Hoeger P, Mazereeuw-Hautier J, et al. A randomized, controlled trial of oral propranolol in infantile hemangioma. N Engl J Med 2015;372:735-746.PubMed: 25693013DOI: 10.1056/NEJMoa1404710· Pivotal trial establishing oral propranolol as standard therapy for problematic infantile hemangiomas.
- [5]Shirley MD, Tang H, Gallione CJ, et al. Sturge-Weber syndrome and port-wine stains caused by somatic mutation in GNAQ. N Engl J Med 2013;368:1971-1979.PubMed: 23656586DOI: 10.1056/NEJMoa1213507· Identification of GNAQ R183Q as causal mutation in port-wine stains and Sturge-Weber syndrome.
- [6]Brouillard P, Boon LM, Mulliken JB, et al. Mutations in a novel factor, glomulin, are responsible for glomuvenous malformations ("glomangiomas"). Am J Hum Genet 2002;70:866-874.PubMed: 11845407DOI: 10.1086/339492· Identification of GLMN germline mutations underlying familial glomuvenous malformations.
- [7]Menzies SW, Kreusch J, Byth K, et al. Dermoscopic evaluation of amelanotic and hypomelanotic melanoma. Arch Dermatol 2008;144:1120-1127.PubMed: 18794455DOI: 10.1001/archderm.144.9.1120· Defining study of dermoscopic features of amelanotic and hypomelanotic melanoma; vascular-lesion mimickers excluded by polymorphic vessels and milky-red areas.
- [8]Piccolo V, Russo T, Moscarella E, Brancaccio G, Alfano R, Argenziano G. Dermatoscopy of vascular lesions. Dermatol Clin 2018;36:389-395.PubMed: 30201148DOI: 10.1016/j.det.2018.05.006· Comprehensive review of dermoscopic features of vascular lesions and their differential against amelanotic melanoma.