Dermatology & Vascular Surgery & Pediatrics & Family Medicine
Angioma
The term «angioma» refers to a heterogeneous group of benign tumors or malformations of the blood and lymphatic vessels. The modern classification, proposed by ISSVA (International Society for the Study of Vascular Anomalies) in 1996 and revised in 2018, basically distinguishes two main categories: vascular tumors (with active cell proliferation - infantile hemangiomas, congenital hemangiomas, tufted angiomas, hemangioendotheliomas) and vascular malformations (static structural anomalies without cell proliferation - capillary, venous, arteriovenous, lymphatic or mixed malformations). This distinction is clinically essential, as it determines prognosis and therapeutic strategy: infantile hemangiomas have an active growth phase followed by spontaneous involution, whereas vascular malformations persist and evolve with the patient. In everyday family practice, the most frequently encountered lesions are ruby angioma (senile hemangioma - a small, bright red lesion, benign and extremely common in adults over the age of 30), spider or stellate angioma (associated with cirrhosis or pregnancy), infantile hemangioma (most common vascular tumor in children - 4 to 10 % of infants) and plano angioma (capillary malformation - congenital wine stain). Treatment varies considerably according to type: from simple monitoring (asymptomatic ruby angioma), to oral propranolol (complicated infantile hemangioma), to pulsed dye laser (PDL) or Nd:YAG laser (plano angioma, symptomatic ruby angioma), to surgery or embolization for extensive or dangerous forms.
Classification, types, and pathophysiology
- Classification ISSVA 2018 and Pathophysiology of Vascular Anomalies international reference classification (ISSVA 2018 - update of Mulliken and Glowacki 1982 classification): category 1 - vascular tumors (active endothelial cell proliferation): infantile hemangioma (IH): most frequent vascular tumor of childhood + growth phase + involution phase → GLUT-1 positive (specific immunohistochemical marker - North 2000 - Microcirculation) + Rapidly Involuting Congenital Hemangioma (RICH): present at birth + involution in 12-14 months + GLUT-1 negative + Non-Involuting Congenital Hemangioma (NICH): persists throughout life + GLUT-1 negative + Partially Involuting Congenital Hemangioma (PICH) + Tufted Angioma + Kapositic Hemangioendothelioma (KHE) : rare + associated with Kasabach-Merritt phenomenon (thrombocytopenia + DIC + microangiopathic hemolytic anemia → significant mortality) → treatment with vincristine + sirolimus → category 2 - vascular malformations (structural anomalies - no active proliferation): capillary malformations (CM): plane angioma (port-wine stain - nevus flammeus) + telangiectasias + spider angioma + arteriovenous malformations (AVM): abnormal connection between arteries and veins without intermediate capillary bed → high-velocity flow → progressive → expansion under the effect of hormones + trauma + pregnancy + venous malformations (MV): slow flow → local thrombosis + pain + thrombophlebitis + lymphatic malformations (ML): former «lymphangioma» → lymphatic cyst + neonatal hygroma colli → mixed malformations (capillaro-venous + capillaro-lymphatic + etc.).); pathophysiology according to type: infantile hemangiomas: cellular origin controversial - placental hypothesis dominant : Barnés 2005 - Placenta: placental endothelial stem cells (GLUT-1+) → migration in utero → VEGF-dependent proliferation (vascular endothelial growth factor) in the first months of life → VEGF + IGF-2 + bFGF → proliferation → then apoptosis-mediated involution + increased TGF-β + reduced VEGF + HI risk factors: prematurity (75 years → genetic factors + sun exposure + immunosuppression + pregnancy + spider angioma (angiome stellaire - spider angioma - spider nevus): dilated central arteriole + radiating capillaries → reddens at central pressure + whitens → origin: hyperoestrogenism (pregnancy + estroprogestogenic contraceptives + hepatic cirrhosis) + spider angioma → clinical sign of advanced chronic liver disease + Foutch 1988 - American Journal of Gastroenterology: >5 spider angiomas → significant association with cirrhosis and portal hypertension
- Clinical Presentation of the Main Types of Angiomas: infantile hemangioma (IH) - vascular tumor of infants: epidemiology: 4-10 % of Caucasian infants + premature infants up to 30 % + F/H = 3:1 → localizations: head and neck (60 %) + trunk (25 %) + limbs (15 %) + superficial forms (formerly «strawberries»): bright red + relief + well delimited + deep forms (formerly «cavernous hemangioma»): subcutaneous bluish nodule + mixed forms → natural evolution in 3 phases: proliferation: birth to 6-9 months → rapid growth + plateau: 9-12 months → involution: 1-7 years → complete involution in 50 % of cases at 5 years + 70 % at 7 years + residual sequelae in 20-40 % of cases (fibrosis + telangiectasias + flaccid skin - especially if HI ≥2 cm) → Leaute-Labreze 2008 - NEJM : discovery of the effect of propranolol (non-selective beta-blocker) in the treatment of complicated HI → therapeutic revolution → complicated HI requiring active treatment (15-20 % of HI): periorbital location (risk of amblyopia) + nasal location (Cyrano - risk of permanent distortion) + labial location (risk of scarring + functional discomfort) + ulcerated HI (pain + superinfection) + extensive facial segmental HI (risk of PHACE syndrome : Posterior fossa anomalies + Facial hemangiomas + Arterial + Cardiovascular anomalies + Eye + Sternal/Endocrine anomalies) + Subglottic HI (stridor + respiratory distress) + Multiple hepatic HI (hypothyroidism + shunt heart failure) + HI >5 cm (risk of LUMBAR or PELVIS syndrome - spinal dysraphism + anal imperforation + genitourinary anomalies) ; angioma planus (capillary malformation - port-wine stain) : present from birth + pink to dark red macule + often unilateral + geographic contours + frequent facial localization (V1/V2 territory of trigeminal) → darkens + thickens with age + may develop nodules + complications: glaucoma (if V1 + periorbital) + Sturge-Weber syndrome (4 % of V1 facial plane angiomas) → cerebral MRI + fundus recommended if plane angioma in ophthalmic territory + Klippel-Trenaunay: lower limb plane angioma + varicose veins + limb hypertrophy → clinical diagnosis; ruby angioma (senile hemangioma / cherry angioma): bright red to purple papule or macule + 1-5 mm + smooth surface + well delimited + whitens on incomplete vitropression (vascular flow) + preferential location: trunk + arms + shoulders + increases in number with age + benign + no malignant degeneration + clinical diagnosis (dermoscopy: homogeneous red lacunae separated by whitish septa - «red globules» in dermoscopy) → treatment if cosmetic discomfort or post-traumatic bleeding; spider angioma (spider nevus): red punctiform central arteriole + 0.5-1 cm radiating capillaries + clears on central compression + localizations: face + décolleté + upper limbs + children: physiological in small numbers + adults: >5 spider angiomas → liver check-up + pregnancy: physiological (hyperoestrogenism) → post-partum regression; essential telangiectasias: permanent dilatations of small superficial vessels (capillaries + venules) + face (couperose) + legs (reticular veins + telangiectasias) + Rendu-Osler-Weber (hereditary hemorrhagic telangiectasia - HHT) : ENG (endoglin) or ACVRL1 (ALK1) mutation + autosomal dominant → mucosal + digestive telangiectasias + recurrent epistaxis + pulmonary + hepatic + cerebral AVMs → to be evoked if epistaxis + unexplained hemoptysis + iron-deficiency anemia without obvious cause → family genetic screening
Diagnosis, treatment and follow-up
| Type / intervention | Diagnostic and therapeutic modalities | Evidence and recommendations |
|---|---|---|
| Infantile hemangioma (IH) — diagnosis and treatment GLUT-1 — propranolol — timolol — corticosteroids — laser — PHACE — Ulcerated Hemangioma — pediatric follow-up |
Diagnosis of HI: clinical in the vast majority of cases + no biopsy necessary if typical presentation → ultrasound-Doppler (high flow - intra-lesional arterial flow) if doubt → MRI if deep HI + undetermined subcutaneous localization + suspicion of PHACE syndrome + extensive segmental HI → GLUT-1 immunohistochemistry if biopsy performed → GLUT-1 positive = HI (excellent sensitivity and specificity - North 2000 - Microcirculation) → to be distinguished from: congenital hemangioma (RICH/NICH - GLUT-1 negative) + venous malformation + tufted angioma + kaposiform hemangioendothelioma → systemic workup if multiple hepatic HI (>5 skin lesions → hepatic HI screening by ultrasound) → TSH dosage (hypothyroidism by overexpression of iodothyronine deiodinase type 3 by HI cells) → risk of profound hypothyroidism + neurodevelopmental delay ; oral propranolol - reference treatment for complicated ICH (since Leaute-Labreze 2008 - NEJM): mechanism: vasoconstriction + reduction in VEGF and bFGF expression + promotion of apoptosis of HI endothelial cells → Leaute-Labreze 2015 - NEJM (PRIDE trial): international multicenter RCT n=456 infants → propranolol 3 mg/kg/d × 6 months vs placebo → success at 24 weeks: 60 % vs 4 % → worldwide standard of care → initiation scheme: in hospital or specialized consultation → ECG + blood glucose before initiation + cardiac workup if pathology suspected + contraindications: PHACE with severe arterial abnormalities (risk of stroke due to vasoconstriction) + asthma + AV block + bradycardia + neonatal hypoglycemia → dose: 1 mg/kg/d × 1 week → 2 mg/kg/d × 1 week → 3 mg/kg/d (maximum dose) → monitoring: HR + BP + blood glucose when dose is increased → duration: 6 months (generally until age 12-15 months) → adverse effects: hypoglycemia (take with meals - fasting to be avoided) + bradycardia + bronchospasm + sleep disorders → recurrence on discontinuation: 10-25 % → resumption of propranolol → timolol gel 0.5 % ophthalmic topical use: alternative to oral propranolol for localized superficial IH + superficial periorbital IH → Püttgen 2016 - JAMA Dermatology: timolol gel 0.5 % × 2/d → partial to complete response in 60-70 % of superficial thin IH → low but not zero systemic absorption → systemic corticoids (prednisone 2-3 mg/kg/d): 2nd-line option if propranolol contraindicated or in combination → recognized efficacy but adverse effects (hypertension + Cushing's + growth retardation) → pulsed dye laser (PDL 585/595 nm): treatment of residual post-involution sequelae + telangiectasias + very thin superficial HI in involution phase → not very effective on thick HI in growth phase → ulcerated HI: local care (oily dressings + vaseline + oily tulle) + oral propranolol (accelerates healing of ulceration) + topical antibiotic therapy if superinfection (fusidic acid) + analgesia (paracetamol + oral sucrose in infants) + PDL laser if persistent | Key data on propranolol in IH: Leaute-Labreze 2008 - NEJM: initial case report → propranolol 2 mg/kg/d → rapid, dramatic regression of IH → chance discovery → therapeutic revolution → Leaute-Labreze 2015 - NEJM (PRIDE trial): RCT n=456 → propranolol 3 mg/kg/d × 6 months → success rate 60 % vs 4 % placebo → p<0.001 → worldwide standard of care → Drolet 2013 - Pediatrics: multicenter cohort → propranolol → response from the first weeks → plateau at 6 months + Solman 2018 - British Journal of Dermatology: meta-analysis → oral propranolol superior to topical timolol + oral corticosteroids for complicated IH → consensus indication: localized periorbital + nasal + labial + subglottic + ulcerated + PHACE IH without vascular contraindication; position of Hypertension Canada and pediatric societies: CPS (Canadian Pediatric Society) 2023: propranolol = 1st-line treatment of complicated IH → initiation by physician specialized in pediatric dermatology or pediatric surgery → close follow-up for first few weeks + Hoeger 2015 - Journal of the American Academy of Dermatology: algorithm for management of IH → indications for treatment + contraindications for propranolol + specialized referral criteria |
| Angioma plan — laser treatment and follow-up PDL — Nd:YAG — laser 532 nm — Sturge-Weber — glaucoma — results — recurrence — number of sessions |
Planar angioma treatment with vascular laser: reference laser: pulsed dye laser (PDL - Pulsed Dye Laser) 585/595 nm: principle of selective photolysis (Anderson and Parrish 1983 - Science): the laser is selectively absorbed by oxyhemoglobin (absorption peak at 577-585 nm) → coagulation of dilated vessels in the dermis → epidermal sparing → parameters: wavelength 585 or 595 nm + pulse duration 0.45-40 ms + energy density (fluence) 6-12 J/cm² + spot 5-10 mm → results: partial to complete whitening in 60-80 % of cases + Renfro 1993 - Journal of the American Academy of Dermatology: PDL → complete response 15 % + partial response (>50 % improvement) 60 % → variable results depending on location (central face best response) + thickness (thick angioma → less good response) + color (pinkish → better response than dark red or violet) + age (early treatment in infants → best results - Enjolras 1990 - Pediatrics) → number of sessions: 5-20 sessions or more depending on response → spacing: 6-8 weeks → insufficient results from PDL alone if: very thick angioma (nodules) + dark violet angioma + resistant angioma → alternatives and complements to PDL: Nd:YAG 1064 nm laser: deeper penetration → treatment of thick angiomas + resistant to PDL + PDL + Nd:YAG combination: better response for resistant angiomas + KTP (potassium-titanyl-phosphate) 532 nm laser: effective on telangiectasias and small flat angiomas + IPL (Intense Pulsed Light): intense pulsed light - less effective than PDL for flat angiomas, but useful for diffuse rosacea + Nd:YAG 1064 nm long pulse: treatment of choice for venous malformations + deep angiomas; eye protection mandatory (leaded glasses or eye cones) if periorbital treatment + local or general anesthesia in infants and children; post-laser care: ecchymoses (purpura) for 10-14 days (unavoidable with PDL - photolysis of intravascular red blood cells) + erythema + edema → local care: vaseline + avoid the sun 4-6 weeks + SPF 50+ sunscreen → post-inflammatory hyperpigmentation (dark skin - Fitzpatrick IV-VI): increased risk → test on a small area → recurrence after treatment: frequent (neoformed vessels) → maintenance sessions → long-term results: whitening maintained in 50-70 % of cases at 5 years if early and complete treatment; Sturge-Weber syndrome - multidisciplinary management: systematic screening: planar angioma in ophthalmic territory (V1) → cerebral MRI with gadolinium (leptomeningeal angioma) + fundus + intraocular pressure (glaucoma) + EEG + neuropsychological assessment → Comi 2011 - Neurology: MRI + planar angioma V1 → leptomeningeal angioma in 8-26 % of cases depending on laterality → treatment: aspirin 3-5 mg/kg/d (prophylaxis of ischemic strokes related to stasis in leptomeningeal angioma) + antiepileptics (comitiality) + glaucoma: topical beta-blockers + trabeculectomy if refractory + early PDL laser (as early as the first months) for planar angioma → better results than offline | Selective photolysis - physical foundations of laser processing : Anderson and Parrish 1983 - Science: theory of selective photolysis → wavelength selectively absorbed by chromophoric target (oxyhemoglobin) → pulse duration less than thermal relaxation time of target vessel → sparing of adjacent tissue → physical basis of all vascular lasers → Tan 1992 - Archives of Dermatology: PDL optimized for pediatric planar angiomas → best results if initiated early (before 1 year) + Renfro 1993 - JAAD: PDL results in planar angiomas → complete whitening 15 % + partial 60 % over 8-10 sessions → localization + depth-dependent efficacy + Nguyen 2012 - Lasers in Surgery and Medicine: PDL vs Nd:YAG in resistant planar angiomas → superior combination + Rohrer 2010 - Dermatologic Surgery: IPL vs PDL → superior PDL for planar angiomas; treatment of glaucoma associated with Sturge-Weber syndrome: Sujansky 1993 - American Journal of Medical Genetics: prevalence of glaucoma in SWS: 30-70 % → congenital or juvenile glaucoma + medical treatment (beta-blockers + carbonic anhydrase inhibitors) then surgical if refractory + Comi 2011 - Neurology: early MRI recommended in any child with V1 planar angioma → presence of leptomeningeal angioma → predictive factor for neurological severity + aspirin + early neurological management |
| Cherry angiomas and spider angiomas — treatment and clinical significance Laser — electrocoagulation — cryotherapy — liver function test — pregnancy — couperose — IPL |
Ruby angioma - management: therapeutic abstention justified if asymptomatic (benign lesion + no malignant potential) → indications for treatment: aesthetic discomfort + repeated bleeding (rubbing or shaving trauma) + troublesome localization (finger + face); treatment options: pulsed dye laser (PDL 595 nm): 1st intention if lesion <3 mm → one to two sessions → KTP 532 nm laser: very effective for flat + small lesions → Nd:YAG 1064 nm long pulse laser: for larger or deep ruby angiomas + electrocoagulation (monopolar electrosurgery): classic in-office treatment → fine needle + high-frequency current → coagulation of the central arteriole → high efficacy on small lesions → risk of scarring if too intense → advantage: accessible + inexpensive + without laser equipment → liquid nitrogen cryotherapy: less effective than laser or electrocoagulation for ruby angiomas → risk of hypopigmentation on dark skin → may leave a white scar → IPL (intense pulsed light): effective for diffuse multiple ruby angiomas (trunk + shoulders) → single-session surface treatment of large areas; couperose (erythematotelangiectatic rosacea) and facial telangiectasias: IPL + PDL + KTP laser → very effective for facial telangiectasias + Nd:YAG laser for reticular leg veins (1-3 mm) + foam sclerosis (polidocanol) for varicose veins and telangiectasias of the lower limbs + fine electrocoagulation on isolated nasal telangiectasias; spider angioma - clinical significance and management: in children: often physiological + in small numbers (<5) + disappears spontaneously before puberty → no systematic workup if 5 + outside pregnancy → systematic liver workup: ASAT + ALAT + GGT + PAL + bilirubin + albumin + PT + CBC (thrombocytopenia → portal hypertension) → echo-abdominal if workup abnormal → Foutch 1988 - American Journal of Gastroenterology: >5 spider angiomas → sensitivity 75 % + specificity 84 % for cirrhosis or severe liver disease → pregnancy: physiological + regression within 3 months postpartum → estroprogestative contraceptives: partial regression on discontinuation → treatment if persistent or cosmetically bothersome: PDL or KTP laser on the central arteriole → one session often sufficient + fine electrocoagulation of the central arteriole → immediate efficacy → slight scarring possible if too intense; hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber - HHT): Curaçao diagnostic criteria (Shovlin 2000 - American Journal of Medical Genetics): recurrent epistaxis + mucosal and cutaneous telangiectasias + visceral AVMs (pulmonary + hepatic + cerebral) + 1st-degree family history → HHT certain if 3 criteria + probable if 2 + improbable if 1 → screening for visceral AVMs: thoracic CT (pulmonary AVMs → risk of paradoxical stroke + cerebral abscess) + cardiac echo with contrast (right-left shunt) + cerebral MRI (cerebral AVMs) + hepatic angioscan (hepatic AVMs - high-flow heart failure) → HHT treatment: bevacizumab (anti-VEGF) → reduction of epistaxis (Dupuis-Girod 2012 - JAMA) + thalidomide → embolization of pulmonary AVMs + embolization or surgery of cerebral AVMs | Data on treatment efficacy for ruby and spider angiomas: Sommer 2002 - Dermatologic Surgery: PDL vs electrocoagulation for ruby angiomas → PDL superior in terms of aesthetic results + less scarring → electrocoagulation: comparable efficacy but slightly higher scar rate → both effective in daily practice + Hedelund 2006 - Lasers in Medical Science: KTP 532 nm laser → highly effective for ruby angiomas and facial telangiectasias → excellent results in 1-2 sessions + Goldberg 2011 - Dermatologic Surgery: IPL + multiple angiomas + rosacea → improvement in 70-80 % of cases → less precise than PDL on individual lesions but useful for extensive surfaces; HHT - therapeutic data: Dupuis-Girod 2012 - JAMA: RCT bevacizumab IV in HHT + epistaxis → significant reduction in duration and frequency of epistaxis → low NNT → bevacizumab = validated option in severe HHT + Faughnan 2011 - Annals of Internal Medicine: HHT guidelines → systematic screening for pulmonary AVMs by chest CT recommended in any HHT patient from diagnosis → embolization if AVM >3 mm → reduction in paradoxical strokes and brain abscesses by 80 % |
| Complex vascular malformations — multidisciplinary diagnosis and management MAV — venous malformation — lymphatic — KHE — Kasabach-Merritt — sirolimus — embolization — surgery |
Cutaneous and subcutaneous arteriovenous malformations (AVMs): clinical presentation: warm pulsatile mass + palpable quivering + systolic murmur on auscultation + local hyperthermia + distal ischemia if vascular steal + high-flow heart failure if voluminous → evolution: progressive (worsening under hormones + trauma + pregnancy + incomplete exeresis attempt → recruitment of new vessels) → Schobinger classification (1990 - Seminars in Vascular Surgery): stage I (quiescence): pinkish + warm + symptomless AV arteriole → stage II (expansion): pulsation + tremor + varicosities → stage III (destruction): ulceration + bleeding + pain + osteolysis if bony → stage IV (decompensation): heart failure + diagnosis: MRI with gadolinium (arterial flow-void) + angioscanner → conventional angiography: gold standard before embolization → treatment: endovascular embolization (feeder arteries) + surgical excision within 24-72h post-embolization → excision alone or embolization alone → almost certain recurrence + contraindicated injection of sclerosant alone → sirolimus (mTOR inhibitor): effective in complex AVMs + Parkes-Weber syndrome → Venot 2018 - Nature: sirolimus → lesion reduction in PIK3CA-related overgrowth spectrum (PROS) → somatic PIK3CA mutations → alpelisib treatment (PI3K inhibitor) + cerebral AVMs: see neurosurgery / interventional neuroradiology; venous malformations (VMs): presentation: bluish mass + compressible + non-pulsatile + increases in declive position + painful on pressure → phleboliths (round calcifications) = pathognomonic + localized intravascular coagulopathy (localized DIC - fibrin + elevated D-dimers) in extensive forms → risk of VTE + diagnosis: T2 MRI (hypersignal) + echo-Doppler (low flow) + treatment: percutaneous ethanol or polidocanol sclerotherapy + intravascular 1064 nm Nd:YAG laser (EVLT - endovenous laser treatment) + surgical excision if localized + sirolimus (rapamycin) in extensive or complex forms : Hammer 2018 - Pediatric Blood and Cancer: sirolimus → reduction in coagulopathy + volume + pain in complex venous malformations; lymphatic malformations (ML): presentation: macrocystic (large logettes - former «cystic lymphangioma») + microcystic (superficial vesicles) + mixed → frequent localization: neck (neonatal hygroma colli) + axilla + mediastinum + tongue + orbit → prenatal diagnosis possible (hygroma colli → T21 + Turner to be excluded) → treatment: percutaneous sclerotherapy with OK-432 (inactivated streptococcus) or doxycycline + surgical resection + sirolimus: reduction of complex MLs (Adams 2016 - Pediatrics); kaposiform hemangioendothelioma (KHE) and Kasabach-Merritt phenomenon: KHE = childhood vascular tumor + intratumoral platelet resorption → profound thrombocytopenia + DIC + microangiopathic hemolytic anemia → mortality 10-30 % without treatment → treatment: sirolimus (rapamycin) - Kai 2014 - Pediatrics: sirolimus 0.8 mg/m²/d → resolution of Kasabach-Merritt phenomenon in 80-90 % of cases → current gold standard → corticosteroids + vincristine as 2nd-line treatment if sirolimus insufficient; reference center for vascular anomalies: complex forms → refer to a specialized multidisciplinary center: CHU → team: dermatologist + vascular surgeon + interventional radiologist + hematologist + neurologist depending on involvement | Data on sirolimus in complex vascular anomalies: Venot 2018 - Nature: sirolimus + PIK3CA mutations (PROS - PIK3CA-related overgrowth spectrum) → reduction of vascular lesions + functional improvement → PIK3CA mutations found in infantile hemangiomas + planar angiomas + AVMs + CLOVES syndrome + Kai 2014 - Pediatrics: sirolimus in KHE + Kasabach-Merritt → resolution of thrombocytopenia in 80-90 % → sirolimus = standard of care in KHE → Hammer 2018 - Pediatric Blood and Cancer: sirolimus in complex venous malformations → significant reduction in coagulopathy + volume + pain → Adams 2016 - Pediatrics: sirolimus in lymphatic malformations + clinical improvement in 85 % of cases; Schobinger 1990 - Seminars in Vascular Surgery: classification of AVMs into 4 stages → guides therapeutic decisions + fundamental precautions in AVMs: never perform incomplete excision alone without prior embolization → certain aggravation + recruitment of new arterial pedicles → Rosen 2009 - Seminars in Interventional Radiology: embolization + surgery within 48h → better results than delayed surgery |
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Vascular tumor or vascular malformation: a clinically essential distinction: Infantile hemangiomas (vascular tumors) have a growth phase and then spontaneously involute—the majority do not require treatment. Vascular malformations (port-wine stains, venous malformations, AVMs) do not involute and evolve with the patient. A facial port-wine stain in the V1 territory requires screening for Sturge-Weber syndrome. More than 5 spider angiomas in a non-pregnant adult warrant hepatic evaluation. Complicated infantile hemangiomas (periorbital, nasal, ulcerated, subglottic) should be treated rapidly with oral propranolol under specialized supervision.
Situations Requiring Urgent Medical Attention or Emergency Room Visit
Infant with rapidly growing peri-orbital, nasal, or labial infantile hemangioma, or with stridor -> Functional or life risk -> Urgent consultation with pediatric dermatology or pediatric surgery -> Immediate initiation of oral propranolol -> Subglottic location: risk of airway obstruction -> Pediatric emergency if stridor + respiratory distress.
Infant or child with large hemangioma + thrombocytopenia + DIC + hemolytic anemia (pallor + jaundice + purpura) → Kasabach-Merritt phenomenon on kaposiform hemangioendothelioma → pediatric hematologic emergency → hospitalization in a specialized center → sirolimus + corticosteroids + vincristine according to protocol → mortality 10–30 % without treatment.
Infant with facial port-wine stain in the ophthalmic (V1) territory + seizures + neurological deficit or developmental delay → Sturge-Weber syndrome → pediatric neurological emergencies → MRI of the brain with gadolinium + EEG + fundus examination + intraocular pressure → multidisciplinary management (neurology + ophthalmology + dermatology).
Patient with recurrent epistaxis, mucosal telangiectasias, and a family history of pulmonary or cerebral AVMs. → suggest hereditary hemorrhagic telangiectasia (HHT) → risk of paradoxical stroke due to pulmonary arteriovenous malformation (AVM) → semi-urgent thoracic CT + brain MRI + contrast echocardiogram → if pulmonary AVM confirmed: endovascular embolization without delay.
Consult at Clinique Omicron
Clinique Omicron doctors evaluate cutaneous vascular lesions, differentiate between benign lesions (cherry angioma, physiological spider angioma) and forms requiring specialized investigation or treatment, prescribe appropriate investigations (liver function tests if multiple spider angiomas, ophthalmological and neurological assessments if V1 facial port-wine stain), and refer to competent specialists (dermatologists, pediatricians, vascular surgeons). Consultations are available at several service points in Quebec and via telemedicine. To book an appointment, visit cliniqueomicron.ca.
The content of this page is provided for informational purposes only and does not replace the advice of a doctor or specialist. Any vascular anomaly in an infant or child, or any rapidly evolving lesion or one associated with systemic symptoms, should be evaluated by a qualified healthcare professional.
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